Disease - utcom2014

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					      Disease               Caused by                       Pathophysiology

                                                 transmitted through the bite of a rabid
                                               animal or inhalation of aerosolized virus,
      Rabies               Rabies virus       virus replicates locally then travels through
                                              the axon (the longer the axon, the greater
                                                          the time to disease)

                                                entry through the stratum corneum (dry,
                                              tough, low pH, has bacteriostatic lipids on
                                             it), infection of the dermis or subcutaneous
                                               tissues, potentiated by poor lymphatic or
                                               venous drainage/poor arterial or capillary
                       staph aureus or staph
      Cellulitis                                        blood supply/neutropenia/
                                             hypogammaglobulinemia, staph has alpha
                                              toxin (dermonecrotic hemolytic toxin) and
                                               leukocidins (kill neutrophils), strep has M
                                                   proteins (escape phagocytosis) and
                                                          hyaluronidase (spread)

    Paronychia          bacteria or fungus         mild skin infection around the nail

                                                 fungal nail infection, usually affecting
  Onychomycosis               fungus
                                               trapping of fibrin outside of vasculature
                                              due to increased leaks (fibrin cuffs), blood
                                               pools due to poorly functioning valves in
Lipodermatosclerosis      chronic venous       veins and causes chronic inflammation,
 (Stasis Dermatitis)       insufficiency       get tissue hypoxia, venous hypertension
                                                 due to decreased lymphatic flow and
                                                    fragmentation of the cutaneous
     Impetigo              group A strep           infection of superficial skin layers
                                               acute infection of the dermis resulting in
     Erysipelas            group A strep
                                                furuncle is a skin infection involving an
                                               entire hair follicle and nearby skin tissue,
Furuncle/Carbuncle            bacteria
                                                carbuncle is a skin infection involving a
                                                          group of hair follicles
                                                 for pre-septal an infection from outside
                          staph and group A
                                                    enters deeper tissue but doesn't go
                          strep for preseptal,
 Preseptal/Periorbital                         beyond the septum eye isn't affected, just
and Postseptal/Orbital                            swollen eyelid), for orbital an infection
                          mixed aerobic and
      Cellulitis                                   from the sinus progresses to deeper
                         anaerobic/fungus for
                                               tissues and can cause a cavernous sinus
                                                           thrombosis (serious!)
                                                      can be secondary to sinusitis/tooth
  Septic Cavernous       Orbital Cellulitis (see   infection/facial furuncles, abscess forms
  Sinus Thrombosis              above)                 and affects the bone forming the
                               mixed flora
                         (anaerobes and non
                          group A strep and               may be secondary to minor
 Necrotizing Fasciitis
                         enterobacteriaceae)               trauma/surgery/furuncle
                          for type 1, group A
                            strep for type 2

                            reactivation of
                         varicella zoster virus

                          staph aureus,
                       Eikenella corrodens
                      (humans), anaerobes
Bite Wound Infections   porphyromonas),
                      pasteurella multocida
                           (dogs, cats),
                       canimorsus (dogs),
                        staph intermedius

                                                   superantigen toxic shock syndrome toxin
                                                   or enterotoxins produced by strep activate
                                                       many clones of T cells due to direct
                                                   bidning to the invariant region of the class
                                                     II MHC molecule --> huge amounts of
Toxic Shock Syndrome        staph or strep
                                                    cytokines released into the bloodstream,
                                                    agr gene regulates toxin production and
                                                     requires elevated protein level/ neutral
                                                         pH/elevated partial pressure of
                                                      CO2/elevated partial pressure of O2

                             streptococcal          streptococcal erythrogenic (pyrogenic)
    Scarlet Fever
                              pharyngitis                           toxins
    Scalded Skin                                   caused by exfoliative toxins A (ETA) or B
     Syndrome                                                       (ETB)
                         mostly bacterial,
                       rarely fungal, staph
                      aureus causes more
                                              bacteria from a distant site goes through
                         than 50% of all
                                                the blood to the bone, infection is soft
                         cases, group B
                                             tissue goes to infection in bone AND bone
  Osteomyelitis         strep/E. coli/other
                                                   marrow, infection leads to bone
                      enterics in neonates,
                                              destruction and new bone formation, can
                      group A strep in kids,
                                                 lead to bone necrosis (sequestrum)
                      pseudomonas in drug
                       users, salmonella in
                            sickle cell

                                              infection of the fallopian tubes produces
Pelvic Inflammatory         chlamydia
                                               severe salpingitis, adhesions, scarring,
      Disease              trachomatis
                                                         and tubal occlusions
                                               transient autoimmune disease causing
Reiter's Syndrome                             peripheral reactive arthritis lasting longer
                                                            than 1 month

                                               enters through skin breaks or crosses
                                                     epithelial cells of MUCOUS
                                                  MEMBRANES, causes painless
Lymphogranuloma                                  herpetiform ulceration at the site of
                      trachomatis serovars
   Venereum                                   inoculation, travesl via the lymphatics to
                          L1, L2, and L3
                                              multiply within mononuclear phagocytes
                                                (macrophages and dendritic cells) in
                                                        regional lymph nodes

                                              bacterial eye infection, highly infectious
                                                 through personal contact (hands or
                            chlamydia        clothing), can be carried by flies that have
                           trachomatis       contacted the discharge from an infected
                                              eye/nose, transmission through vaginal

                          natural toxic
                        compound from         inhibits protein synthesis (phytotoxin is a
                       seeds of the rosary          ribosome inactivating protein)
                         (jequinty) pea
                              toxic compound in
                               castor beans, 5%
                              ricin content bean
                              mash is produced              inhibits protein synthesis (holotoxin is a
                                during castor oil                ribosome inactivating protein)
                                production, can
                             extract ricin from the

                                                           endocardial surface is disrupted (from turbulent
                                                            blood flow or direct injury) causing collagen to
                                    infection of the        come into direct contact with the blood stream,
                               endocardial surface of     platelets and fibrin are deposited on the collagen
                             the heart or heart valves,           forming a sterile thrombus (marantic
                              NVE is most commonly           endocarditis), transient bacteremia can then
                              caused by viridans strep       cause infection of the sterile thrombus (some
                              and staph aureus (staph     bacteria are intrinsically stickier to the thrombus),
                                aureus causes most             bacteria can come from direct inoculation
Infective Endocarditis (IE):
                                    cases of acute              (brushing teeth, catheter) or invasion of
can be native valve (NVE)
                              endocarditis), early PVE         anatomical barriers, bacteria resistant to
 or prosthetic valve (PVE)
                                  is most commonly               complement killing are likely to cause
                             caused by coag negative       endocarditis, staph aureus can directly injure the
                              staph, late PVE is most         endocardium and adhere to the underlying
                                commonly caused by        collagen, the thrombus grows due to the bacteria-
                             viridans streph and staph    platelet-fibrin interaction, bacteria stick to the low
                               aureus (like NVE) but          pressure side of the valve (mitral or aortic),
                             also coag negative staph      antibodies are produces against the antigen and
                                                              form immune complexes but are unable to
                                                                          eradicate the disease

                                            preformed antibodies against blood group
                                                  or HLA antigens occurs within
                      pre-formed antibodies     minutes/hours of transplantation,
Hyperacute Transplant
                         and complement       comparable to type III hypersensitivity
                             fixation         (immune complex deposition causes
                                            complement activation within blood vessel
                                                   T-cells attack the graft and destroy it,
                                                occurs within 5-7 days of transplant (must
                                                    have time for activation and clonal
                                                   selection to occur), memory cells are
                                                      formed, comparable to type IV
                                                     hypersensitivity reactions (T-cell
  Acute Transplant        alloreactive T-cell
                                                mediated), CD4 T helper cells (specifically
     Rejection                 activation
                                                 TH1 cells) are directed against the graft
                                                   MHC-II molecules, TH1 release IFN-
                                                 gamma/IL-2/TNF-beta which activated a
                                                 cellular T-cell mediated response, CD8
                                                cytotoxic T-cells are directed against MHC-
                                                                1 molecules

                           reactions in the
                         vasculature of the
                          graft that causes
                         thickening onf the
 Chronic Transplant                              narrow lumina result in ischema, loss of
                          vessel walls and
     Rejection                                       function, and death of the graft
                          narrowing of the
                           lumina (indirect
                              pathway of
                                                occurs when a bone marrow transplant
                         donor T cells attack
                                               replaces the host immune system, if not
Graft vs. Host Disease   the transplantation
                                              all allograft T cells in the graft are depleted
                                                         they can attack the host
                            cancer of the        involves primarily cells of B cell origin in
                            lymphocytes         the lymph nodes (usually isolated without
 Hodgkins lymphoma         beginning in the        metastisis) and lymphatics, no single
                         lymph nodes (B+T          known cause, moves systematically
                                cells)                  through the lymph nodes
                            cancer of the
                            lymphocytes            T or B cells isolated, can be found in
                           beginning in the      lymph nodes but is more systemic than
                         lymph nodes (B+T                  Hodgkins lymphoma

    acute/chronic      cancer of the WBC in overproduction of immature lymphocytes
lymphoblastic leukemia        blood                     (lymphoblasts)

acute/chronic myeloid cancer of the WBC in
                                                      overproduction of myeloblasts
      leukemia               blood
                                                 produce copious amounts of non-
                        cancer of plasma (B)
      myeloma                                functional antibodies (M protein), occurs in
                                                          the bone marrow

                                                  amantin toxin (amatoxins) is rapidly
cyclopeptide mycetism      amatoxins or        absorbed by the GI tract and inhibits RNA
(mushroom poisoning)       phallotoxins             pol II, it undergoes enterohepatic
                                                recirculation and is excreted in the ruine

                                               tetrahydroxylated di-N oxidized bipyridin
                                                  causes formation of radical oxygen
mycetism (mushroom      corinariaceas family
                                               species (peroxide and superoxide ions)
                                                     that are harmful to the cells

                                                 consumption of flase morel containing
                                                  gyromatirin (MMH is hydrolyzed from
                                               gyromitrin during cooking), poisoning can
monomethylhydrazine                             occur from inhaling fumes from cooking
  (MMH) mycetism                               mushrooms (it's an irritant), MMH inhibits
(mushroom poisoning)                            enzymes having a pyridoxal phosphate
                                                  cofactor which is important in GABA
                                                    synthesis, hydrazines inhibit the
                                                     metabolism of folic acid to THF

                         clitocybe dealbata
                                                activates acetylcholine receptors on the
 muscarine mycetism         and inocybes
                                               heart/apocrine glands/smooth muscle and
(mushroom poisoning)    patouillardii found in
                                                      causes cholinergic poisoning
                         lawns/public parks

                        psilocybe mexicana
 psilocybin mycetism
                          and conocibes                psychoactive mushrooms
(mushroom poisoning)
                                                  resembles glutamic acid and acts on
                                                    glutaminergic recptors to produce
ibotenic acid mycetism   amanita muscaria A         excitatory effects (anticholinergic
(mushroom poisoning)        pantherine           symptoms), if converted to muscimol it
                                                competes with GABA receptors (sedative

                         Claviceps purpurea       synthesizes lots of biologically active
   ergot mycetism
                           (a grain fungus      agents (acetylcholine, histamine, tyramine
(mushroom poisoning)
                          especially in rye)                       acid)

systemic inflammatory systemic response to
                                                   generalized inflammatory reaction in
 response syndrome       a wide range of
                                                   organs remote from the initial insult
       (SIRS)               stressors

                                                    infection most commonly starts as a
                                                   respiratory infection, blood infection is
                                                      second most common, bacterium
                                                 breaches an epithelial barrier and enters
                                                   underlying tissue where it encounters
                                                  macrophages/mast cells/dendritic cells,
                                                these cells recognize the bacteria through
                                                TLRs (TLR4 for G- and TLR2 for G+) and
                                                 secrete mediators that activate the local
                                                       inflammatory response AND the
                             staph aureus       coagulation cascade, TLR activates NFkB
                          (MRSA), candida,            which produces pro-inflammatory
       sepsis              resistant hospital      cytokines TNF-alpha and IL1 causing
                            acquired gram         coagulation, NO is involved and causes
                               negatives         dilation, IL-10 is anti-inflammatory and is
                                                also secreted, prostaglandins cause fever
                                                 (COX2/3 produce PGE2 which shifts the
                                                 body temperature set point, also causes
                                                    myalgia and arthralgia), coagulation
                                                activated by tissue factor and happens all
                                                   over if there's not enough protein C to
                                                counteract, DIC results when coagulation
                                                 factors are depleted leading to bleeding,
                                                    peripheral vasoconstriction and body
                                                         thermogenesis causes fever

                                                 sepsis + organ dysfunction distant from
    severe sepsis
                                                           the site of infection
                                                severe sepsis + hypotension unresponsive
    septic shock
                                                   to fluids and requiring vasopressors
                                                  acute development of severe hypoxemia
                          oxygen not getting to
                                                   and diffuse pulmonary infiltrates in the
   acute respiratory       circulation, can be
                                                absence of over heart failure, exudatio nof
  distress syndrome           secondary to
                                                 fluid rich in large molecular weight protein
        (ARDS)              trauma/surgery/
                                                in the alveolar space (hyaline membranes)
                            distant infection
                                                         causes surfactant impairment
                                                      enhanced cytokine expression and
                                                   release (TNF, IL-1, IL-6, IL-8) promote
    disseminated                                     tissue factor exposure, this leads to
                          coagulation followed
    intravascular                                 thrombin generation and suppression of
                              by bleeding
  coagulation (DIC)                                   fibrinolysis and procoagulant state,
                                                  consumption of platelets and coagulation
                                                            factors causes bleeding
                          C1 inhibitor deficiency kallikrein/bradykinin/C2 may be involved,
Hereditary angioedema          (overactive         attacks triggered by minor trauma/cold/
                              complement)                            stress

                            defect in bacterial
   C5-9 deficiency
                        mutation in PIGA
                     gene causes deficit in
                       regulating surface   complement-induced hemolytic anemia
                     proteins (DAF decay- due to cell membrane defect, red cells are
paroxysmal nocturnal
                      accelerating factor     destroyed, increased intravascular
                     and CD59), this gene hemolysis at night, thrombosis due to lack
                         encodes for an               of CD59 on platelets
                     anchor that attaches
                         proteins to the
 C3 (major opsonin)
 C1/C4/C2 defects

                              IgA deficiency

transient hypogamma-
globulinemia of infancy
   common variable

                                                    multiple myeloma, chronic lymphocytic
secondary hypogamma-                              leukemia, or loss of lobulins through skin
    globulinemias                                  (burns)/kidney (nephrotic sydnrome)/gut
                                                          (protein-losing enteropathy)
                                                acquired (drugs, autoimmune, cancer) or
                        defects in neutrophil
                                                   hereditary (familial, cyclic, infantile
                          function, can be
                                                 agranulocytosis), or qualitative defects
     neutropenia           acquired after
                                                (adhesion defects, chemotactic defects,
                         infections or from
                                                 opsonin defects, defects in intracellular

   hereditary cyclic      ELA2 (neutrophil
     neutropenia         elastase) mutation

                          bacteremia with
                                                    inflammation/ulceration of mucous
      mucositis           streptococci and
                                                       membranes lining the GI tract
                             enteric flora

                                                 invasion of vessels and tissue infarction
                                                (necrotisin vasculitis), may be associated
ecthyma gangrenosum        pseudomonas
                                                 with extensive infarction in other organs
                               fever and
                         inflammation of the
       typhlitis                                           thickened cecum wall
                              cecum in a
                         neutropenic patient

                                                affects lungs/kidneys/liver/spleen/skin/ eye

                           fungus found in           usually pulmonary, may involve
                               nature                       brain/skin/kidneys

                                                giant and dysmorphic lysosomes, affects
                           mutation in LYST
  Chediak-Higashi                               melanocytes/Schwann cells/renal tubular
                        (lysosomal trafficking
    syndrome                                   cells/throid cells/all leukocytes, ineffective
                            regulator) gene
                                                   granulopoiesis leads to neutropenia

Job's syndrome (hyper
                         mutation in STAT3          defect in chemotactic response of
  IgE with impaired
                                gene                            neutrophils
                                                 MPO normally catalyzses conversion of
                                                   H2O2 (peroxide) to HOCl (bleach) in
                                                   neutrophils, if there's a deficiency in
                                                   neutrophil granules and macrophage
  (MPO) deficiency
                                                lysosomes there's impaired production of
                                                    HOCl, only significant if there's an
                                                            additional disease
                      heterogenous group
                      of molecular defects,       defective NADPH oxidase causes failure
chronic granulomatous inherited autosomal             of phagocytic cells to generate a
      syndrome         or X-linked causes          respiratory burst, defect in intracellular
                        defective NADPH                             killing

                                                         indications: trauma, idiopathic
                                                  thrombocytopenic purpura, spherocytosis,
                                                    thalassemia major, hairy cell leukemia,
                                                             malignancies, abscess

                           inherited T cell
DiGeorge's syndrome                                 defective development of pharyngeal
                         defiiency caused by
  (velocardiofacial                               pouches, causes agenesis of thymus and
                              deletion on
     syndrome)                                                  parathyroids
                          chromosome 22
                        multiple gene defects:
                          cytokine receptor
                        genes (Il-2RG, Jak3,       combined B and T cell deficiency, ADA
   severe combined
                          IL-7Ra), antigen            and PNP are involved in purine
                           receptor genes            degradation, the accumulation of
                         (RAG1/2, artemis,           metabolites is toxic to lymphocytes
                         CD3-delta, CD3e),
                          ADA/PNP, CD45
   Wiscott-Aldrich                                 cytoskeletal reorganization needed for
                        WASP protein defect
     syndrome                                          cytokine production is impaired
CD4 T-cell deficiency     HIV or idiopathic
   T-cell defieincy
                                                   transmitted by aerosols or hand-to-nose
                                                  contact, self-limited viral infection causing
rhinitis: common cold    parainfluenza, RSV,
                                                  rhinorrhea, ciliated cells infected but have
                                                                  little damage
                         viral (rhono, adeno,
                             corona, HIV),
                                                  strep that produces pyrogenic toxin may
     pharyngitis            bacterial (beta-
                                                    give scarlet fever rash/desquamation
                            hemolytic strep
                              can be viral
                        (rhinovirus, influenza,
      laryngitis             coronavirus),                   involves vocal cords
                           chlamydia, beta-
                            hemolytic strep
                       usually viral etiology
                            (flu, adeno,
  acute bronchitis
                        chlamydia) unless
                         there's underlying
                       illness (COPD, CF)

                                                enters through the nose and settles in the
                                                  lungs and trachea, damages ciliated
     influenza                                     mucosa, paralyzes defense against
                                                bacteria, normal flora can cause disease,
                                                         get secondary infections

                       community-acquired        nasopharynx can be colonized with S.
                        pneumonia, can be        pneumo, lots of serotypes that vary in
                       caused by aspiration           virulence and prevalence

klebsiella pneumonia

                                                 often occurs after influenza, in IV drug
S. aureus pneumonia
                                                      users, and hospital-acquired

  atypical/walking                                intracellular pathogen, incubation is 3
    pneumonia                                                      weeks

aspiration pneumonia         oral flora         common in alcoholics, anesthesia, stroke
                         cholera toxin formed     cholera toxin (on an encoded phage)
                          in vivo (in patient's    binds to cells and acts as an ADP-
                          body), consumption ribosylating enzyme locking the cyclase on
                            of contaminated      and increasing cAMP, increased cAMP
    vibrio cholera
                         water/food (person-to- turns off Na absorption and increases Cl
                           person spread is     secretions resulting in a net loss of water,
                         unlikely), needs high cholera is able to adhere to prevent being
                            infectious dose                    washed out

                            consumption of
vibrio parahemolyticus    improperly cooked           toxin and/or tissue invasion
                           seafood (oysters)

                            consumption of          protein capsule protects against
   vibrio vulnificus      improperly cooked      phagocytosis and complement-mediated
                           seafood (oysters)                     killing
                                                  toxins formed in vivo (in the patient),
                                                labile toxin results in permanent activation
                                                   of adenylate cyclase and increase in
ETEC (enterotoxigenic        contaminated
                                                  cAMP causing osmotic diarrhea, stabile
      E. coli)                food/water
                                                   toxin increases cGMP stimulating Cl
                                                 secretion and inhibiting NaCl absorption,

       EPEC                                       effacing of microvilli and attaching cell
(enteropathogenic E.                              membrane leads to activation of signal
        coli)                                               tranduction, motile

                         shiga-like or vero-
                       toxin cytotoxin (Stx),
                                                 adhesing and effacing causes diarrhea,
                        contaminated meat
        EHEC                                       Stx is necessary for bloody diarrhea,
                      (burgers, apple juice,
(enterohemorrhagic E.                                hemolytic uremic syndrome from
                      salami, mayonnaise,
         coli)                                    intravascular dissemination of Stx and
                          radish sprouts),
                                                        damage to glomeruli, motile
                                                      dysenteriae has Shiga toxin (hihgly
                                                  specific enzyme that reversible inactivates
                                                      mammalian 60S ribosomal subunit
                                                  resulting in cessation of protein synthesis,
                                                     organisms invade (tissue invasion)
                                                    intestinal epithelium (colonic mucosa),
                          direct contact, sex,
                                                  multiply intracellularly and spreads cell-to-
       shigella            food (egg salad,
                                                    cell, structural damage to the intestine,
                             lettuce), water
                                                    inflammatory leukocyte reaction in the
                                                   lamina propria, inflammatory mediators
                                                     are released, vascular abnormalities
                                                     results in bloody stool, leads to focal
                                                    mucosal ulcers and inflammation, non-

                                                      dysenteriae has Shiga toxin (hihgly
                                                  specific enzyme that reversible inactivates
                                                      mammalian 60S ribosomal subunit
                                                  resulting in cessation of protein synthesis,
                                                     organisms invade (tissue invasion)
                                                    intestinal epithelium (colonic mucosa),
                          from humans, food,
                                                  multiply intracellularly and spreads cell-to-
   salmonella typhi         water, zoonosis
                                                    cell, structural damage to the intestine,
                           (turtles, chickens)
                                                    inflammatory leukocyte reaction in the
                                                   lamina propria, inflammatory mediators
                                                     are released, vascular abnormalities
                                                     results in bloody stool, leads to focal
                                                    mucosal ulcers and inflammation, non-
                                                    damage to vascular endothelium (can
     salmonella                                       adhere to endothelium) can cause
    choleraesuis                                  endocarditis and intravascular infections,
                                                            (tissue invasion), motile
                                                  multiply in the lamina propria, induce fluid
                                                    secretion by increasing cAMP and the
                                                    release of prostaglandings, enters the
   diarrhea causing                                bloodstream where it is normally rapidly
                          poultry, eggs, dairy,
salmonella (salmonella                               killed by phagocytes, conditions that
      enteritidis)                                   impair the function of the phagocytic
                                                  system (HbSS, AIDS, leukemia) enhance
                                                         the susceptibility to salmonella
                                                                bacteremia, motile
                          contaminated food
yersinia (enterocolitica (milk, meat, water,        plasmids with virulence genes, resist
          and            belgian chocolates),      phagocytosis, non-motile, toxin and/or
 pseudotuberculosis) blood transfusions                      tissue invasion
                           (can grow at 4C)

yersinia enterocolitica   tofu, milk, raw pork
                                                     blocks acid secretion (bacterial acid-
                                fecal-oral        inhibitory proteins) and prudces urease to
                             transmission,         neutralize acid, motile bacteria can then
  heliobacter pylori
                            humans are the          pass through the gastric mucosa and
                            primary source         cause epithelial cell damage, stimulates
                                                          and inflammatory response

                            ham, poultry, egg      preformed toxin (ST toxins) affects the
    staph aureus
                             salad, pastries            sympathetic nervous system

                          fried rice kept warm,
                           meats, vegetables,
   b. cereus (short)                                 preformed toxin (heat stable toxin)
                           dried foods, cereal,

                                                  preformed toxin, botulinum toxin inhibits
clostridium botulinum
                                                              ACh release

                          recent campylobacter
    Guillan Barre           infection (within 3

                          beef, poultry, gravy, toxin formed in vivo (in patient's body),
clostridium perfringens
                           Mexican food, raw      heat labile enterotoxin damages brush
  (only type A strains)
                                 meat             borders, net secretion of Na and fluids

                                                  toxin formed in vivo (in patient's body-
                              fried rice and
   b. cereus (long)                                   intestine), heat labile enterotoxin
                                                         activates adenylate cyclase

                                                  toxin formed in vivo (in patient's body),
clostridium botulinum
                                                   spores and subsequent toxin production,
                                                     botulinum toxin inhibits ACh release

 verotoxigenic E. coli                            toxin formed in vivo (in patient's body)

                             most common
                           pathogen found in
       c. jejuni                                              tissue invasion
                          poultry (chicken) and
                                 raw milk
                             beef, raw milk,
        EIEC                                                  tissue invasion
                             salads, cheese

listeria monocytogenes                                        tissue invasion
                           heavy metals
                         (copper, zinc, tin,
                        cadmium), chinese
                       restaurant syndrome
 nonbacterial toxins                                       gastric irritations
                           (MSG), niacin
                       poisoning, histamine
                       fish poisoning (tuna,
                            mahi mahi)

   ciguatera fish

 paralytic shellfish
                        improperly cooked
     norovirus                                            preformed toxins
   calicaeviridae       improperly cooked
    (sapovirus)               food
      Giardia                                   lines microvili and prevents absorption

mushroom poisoning

                                                transmitted by aerosol (risk of acquiring
     congenital                                  from other kids), worse if mom is non-
  cytomegalovirus                                   immune (primary infection): 40%
                        (intrapartum), post
                                                      transplacental transmission
                        natal transmission

                       perinatal transmission
 congenital herpes
                         (maybe post-natal

congenital parvo B19   prenatal transmission

 congenital rubella    prenatal transmission
                           transmission, cats
                                                      humans can get infected from
                             are reservoir in
                                                intermediate hosts (farm animals take up
                            nature and shed
                                               the fecal cysts and transmit tissue cysts to
     congenital              protozoa in their
                                                    humans)/blood products/directly by
   toxoplasmosis         feces, rats/birds are
                                               ingesting fecal cysts (in contaminated food
                           intermediate hosts
                                                  or changing cat litter), tissue cysts are
                          infected with tissue
                                                 transmitted transplacentally to the fetus
                          cysts via fecal-oral

  congenital syphilis
                      prenatal transmission
(treponema pallidum)

                             perinatal and
congenital group B

                          prenatal, perinatal,
   congenital HIV              post natal

                                                    health-care associated strains are more
                                                   difficult to treat (beta-lactam resistance),
staph aureus/MRSA         nasal colonization
                                                      exotoxins such as Panton Valentine
                                                  leukocidin (PVL) is a good virulence factor

                         GI tract colonization,    urinary catheter colonization is common
vancomycin-resistant          survives on              and difficult to eradicate but only
    enterococci            enevironmental            occasionally progresses to invasive
                               surfaces                              disease

 clostridium difficile
                                                         not all strains are pathogenic

                          E. coli, klebsiella,
                                                   enterococci and candida often colonize
         UTI                pseudomonas,
                         enterococci, candida
                        usually gram positive    having a central venous catheter is a
                         cocci, can also be     major risk, other risks include prolonged
                        gram negative bacilli    hospitalization/colonization at catheter
nosocomial infections
                         (pseudomonas) or          site/femoral catheter/mechanical
                                fungi                        ventilation/TPN

health care associated
 pneumonia (HCAP)
                       klebsiella, multi-drug
                       resistant organsism,

   T-cell mediated
  immune defense
  NK cell mediated
  immune defense
 phagocyte mediated
  immune defense
complement mediated
  immune defense

                            mutation in the
                         common gammag-
                                                those IL receptors are needed for T-cell
                         chain gene (part of
                                                survival, so gamma-chain gene mutation
   X-linked severe        the IL-2 and other
                                               results in complete depletion of T-cells, T-
      combined          receptor complexes),
                                                 cells are needed to activate B-cells so
  immunodeficiency      same abnormalities in
                                                    there's also no antibody-mediated
        (SCID)           protein kinase Jak3
                                                  response, B-cells are present but not
                         mutation (involved in
                                                      functional, NK cells are absent
                                                      ADA and PNP catalyze purine
                         mutation in ADA or           degradation, mutation leads to
    ADA and PNP
                         PNP gene results in    accumulation of nucleotide metabolites in
                           no T or B cells       all cells, these metabolites are toxic to
                                                        rapidly proliferating T cells
                           RAG enzymes are
                             responsible for        mutation in RAG results in no
                         recombination of the recombination, missense mutations result
 RAG gene mutation
                           Ig gene and T-cell in partial impairment of enzymatic activity
                          receptor gene (VDJ            called Omenn syndrome

                           mutation in DNA      mutation in DNA helicase gene results in
  Bloom's syndrome
                            helicase gene               defects with DNA repair

                                                ATM protein is a signaling molecule in
Ataxia Telangiectasia      mutaiton in ATM
                                                  cellular responses to DNA damage,
        (AT)                    gene
                                               mutation results in defects with DNA repair

                                                   WASP (protein) is involved in the
                                                reorganization of the actin cytoskeleton
                                                  and is expressed in leukocytes and
  Wiskott-Aldrich         mutaiton in WASP
                                               megakaryocytes, WASP plays a role in T-
Syndrome (X-Linked)             gene
                                                cell receptor-dependent activation of T
                                                 cells, mutation results in cytoskeletal
                                                     defects and thrombocytopenia
                       (hemizygous) deletion
                             of a piece of
                                              deletion of this gene results in incomplete
DiGeorge's Syndrome        chromosome 22
                                                   development of thymic epithelia
                        containing the TBX1
                         transcription factor
                           mutation in TAP
                           associated with
                                                 mutation results in no MHC class I
                        antigen processing)
                                               expression, MHC class I expression is
MHC Class I deficiency      genes which is
                                                  required for positive selection and
                           required for the
                                                       activation of CD8 T-cells
                       surface expression of
                             MHC class I
                                                 MHC class II transactivator (CIITA) is a
                                               transcription factor binding to the promoter
                            MHC class II
    MHC Class II                                    region of the MHC class II genes,
                         transactivator gene
     deficiency                                    mutation results in no MHC class II
                                                 expression, MHC class II is required for
                                                     positive selection of CD4 T-cells

                      Bruton's tyrosine
                                             Btk plays a role in the intracellular
                   kinase (Btk) mutation
                                          signaling from the B-cell receptor and is
    X-linked            results in the
                                          required for the differentiation of pre-B-
Agammaglobulinemia   blockade of B cell
                                         cells to B-cells, mutation results in lots of
                    development at the
                                         pre-B-cells and no B-cells, lack antibodies
                     pre-B-cell stage
                                                 IgM is much less efficient than IgG in
                                               neutralization and opsonization, antibody
                         mutation in CD40L     isotype switching requires help from CD4
 X-linked hyper IgM          gene on X           T-cells which is provided by molecular
      syndrome            chromosome or        interaction between CD40 on B-cells and
                          chromosome 20         CD40 ligand on T-cells, mutaiton of the
                                               CD40L gene results in a defect in isotype

                                               antigen-activated B-cells diversify via
 Activation-induced                          somatic hypermutation (leading to affinity
 cytidien deaminase     mutation in AID gene maturation) and isotype switching, AID is
   (AID) deficiency                          required for both somatic hypermutation
                                                       and isotype switching

                                                 NFkB essential modulator (NEMO, aka
                                              IkB kinase IKK-gamma) plays a role in the
                                              NFkB activation pathway, ligation of CD40
X-linked hypohydrotic                          on B-cells with CD40L on T-cells triggers
                         mutation in NEMO
ectodermal dysplasia                              NFkB activation in B-cells leading to
       with ID                                  isotype switching, NFkB cascade is also
                                               involved in TLR signaling and ectodermal
                                              development, mutaiton of NEMO results in
                                                      a defect in isotype switching

                                              SH2-domain containing gene 1A encodes
                                              a protein called SLAM-associated protein
                                             (SAP), SAP interacts with cytoplasmic tails
                                              of SLAM on T-cells and NK cells leading
                                                 to the recruitment of Fyn/activation of
                                              killing machinery/inhibition of IFN-gamma
 lymphoproliferative    mutation in SAP gene
                                                production, mutation in SH2S1A gene
   syndrome (XLP)
                                                results in defective killing by T and NK
                                               cells/dysregulated cytokine production/
                                              uncontrolled lymphocyte proliferation, get
                                                an increase in IFN-gamma and a Th1-
                                                           skewed response

                                              NK cells kill virally-infected host cells by
                                             recognizing downregulated expression of
   NK cell defect        defective NK cells
                                              MHC class I (such as in herpes simplex
                                               CD18 integrin binds to 3 different CD
                                                molecules that function as adhesion
                                              molecules mediating leukocyte adhesion
 leukocyte adhesion     mutation in the CD18   to counter-receptors (ICAMs) and as
     deficiency                 gene         complement receptors, mutation results in
                                                 defective leukocyte migration and
                                             imparied uptake of opsonized bacteria by
                                               mutation results in impaired killing of
                                           ingested bacteria because this complex is
                      mutation of the gene
                                           responsible for oxidative burst (production
chronic granulomatous encoding one subunit
                                             of reactive oxygen species), granuloma
       disease           of the NADPH
                                             formation occurs when microorganisms
                        oxidase complex
                                               are ingested by phagocytes but the
                                                     infection can't be cleared
                                infection of brain
                             parenchyma, almost
                               always viral origin
                             (togavirus, flavivirus,
                                                          pathogen enters brain parenchyma
                                                           hematogenously (viral infections,
                                                           rickettsia, bacteria, fungi, TB), by
      encephalitis               retrovirus/HIV,
                                                        retrograde peripheral transport (rabies,
                                                       varicella), or by exposed olfactory nerves
                                                         (viral), often enters through the nose
                                  can have non-
                                infectious cause
                               (drug reactions or

                                                               presentation within 24-48 hours,
                                                         nasopharyngeal colonization leads to local
                                    infection of         invasion then bacteremia (listeria starts as
                              letpomeninges due to      bacteremia), bacteremia leads to meningeal
                                    bacteria (S.          invasion and bacterial replication causing
acute bacterial meningitis       pneumoniae, N.        subarachnoid space inflammation, this causes
                                  meningitidis, H.       increased BBB permeability and increased
                                   influenza, L.       CSF outflow resistance which leads to edema
                                 monocytogenes)              and increased intracranial pressure,
                                                       subarachnoid space inflammation also causes
                                                                cerebral vasculitis or infarction

                                                        mucosal colonization leads to viremia, the
                                   infection of
                                                           virus crosses the BBB and enters the
                              leptomeninges due to
                                                       subarachnoid spaces where it can spread in
  acute viral meningitis          viral infection
                                                        the CSF, an inflammatory response (less
   (aseptic meningitis)      (enteroviruses are most
                                                      intense than response to bacteria) is specific
                              common, can also be
                                                     for the virus and consists of lympocytes (T-cell
                             arbovirus, herpes, HIV)
                                                            response needed to clear the CSF)
                            infections (TB,
                            nocardia, CMV,
 chronic meningitis
                       toxoplasmosis, syphilis,
                           Lyme), Behcet's,
                         carcinoma, vasculitis

                         infection of spinal
                             cord tissue
                       infection of peripheral

                                                from contiguous foci/hematogenous
                                             dissemination/direct inoculation/primary
                         abscess in brain
                                                 abscess, frontal lobe abscess from
intracranial abscess                         teeth/sinuses/direct, temoral from otitis/
                       depends on source of
                                            mastoiditis/sphenoid sinusitis, cerebellum
                                              from otitis/mastoiditis, MCA circulation
                                                    from hematogenous source

                           pyogenic (pus)
                       infection of the space     the subdural space is crossed by
                       between the dura and numeous small veins (emissary vessels)
                          arachnoid, often    and divided into anatomic compartments
                         caused by aerobic    by falx cerebri/tentorium cerebelli/base of
subdural empyema
                           strep/staph/ S.      brain, organisms reach the subdural
                           pneumo/H. flu/      space through the emissary vessels or
                          anaerobes/other      direct extension of osteomyelitis of the
                           gram negative             skull (from epidural abscess)

                                               in the spinal canal the dura mater is not
                                                adherent to the vertebra so there's an
                         abscess between
                                              epidural space (fat-filled anatomic space)
                        bone and dura mater
                                                without emissary vessels, bacteria can
 epidural abscess      (usually staph aureus,
                                               enter the epidural spinal space by direct
  (usually spinal)       followed by strep,
                                              extension from vertebral osteomyelitis or
                       anaerobes, and gram
                                                  hematogenous dissemination, easy
                           negative rods)
                                                longitudinal sperad (not easy subdural
                                                   perinatal transmission and sexual
                                              intercourse, infects primarily columnar or
                                                  cuboidal epithelium, attachment to
                                                epithelium (may have pili that increase
                           neisseria          virulence by better attachment to mucosal
                          gonorrhoaea              surfaces), penetrates through and
                                                  between epithelial cells, neutrophil
                                                response results in purulent discharge,
                                                 primary infection in women occurs in

                                                attaches to epithelial cells and enter the
                           chlamydia          cell by pinocytosis or endocytosis, resides
                          trachomatis             in the intracellular membrane-bound
                                               inclusions, growth and replication begins

  trichomoniasis      trichomonas vaginalis

                      gardnerella vaginalis
bacterial vaginosis      or mobiluncus

     herpes               HSV I/HSV II
                                                spirochetes penetrate skin or mucous
      syphilis          treponema pallidum      membranes then enter lymphatics and
                                                    hematogenously disseminate

  congenital syphilis
                        treponema pallidum
(treponema pallidum)
                        infection with G- rod
                             H. ducreyi
                                              transmission depends on amount of infectious
                                                  virus and exposure time as well as host
                                                 suceptibility, most transmission is through
                                                 genital fluids/ blood/breast milk, persistent
                                                  viremia and decreasing immune system
        AIDS                    HIV            function, able to mutate rapidly, death of CD4
                                              T-cells, infects CD4 T cells and macrophages,
                                              viral entry requires a B-chemokine co-receptor
                                                 (CCR5 or CXCR4), can have lytic or latent
                                              infection, loss of T-cell part of immune system
                                                      results in clinical manifestations

                                                      bacteria enter urinary tract by
                                                bacterial virulence/host defenses/host-
                                              organism interactions determine whether
                                E. coli           infection develops, urethra becomes
                          (uropathogenic),   colonized prior to UTI, bacteria ascend the
                             usually not     urethra to the bladder where they multiply
                            polymicrobic          and start an inflammatory response,
lower UTI (lower pole
                         (polymicrobic with   UPEC carries multi-gene DNA segments
                              structural         that allow them to grow in urine (allow
                          abnormalities or    synthesis of certain AA) and carry genes
                        catheters), other G-   to synthesize adhesins, adhesins make
                           rods (proteus)     filamentous surface organelles (fimbriae)
                                                 or pili to better adhere to uroepithelial
                                               cells, P fimbriae (P pili) allow enhanced
                                               colonization and binding to uroepithelial
                                              cell by binding to blood group P antigens

  cystitis (bladder


      urethritis        often due to an STD
                         bacteria, usually G-
   acute bacterial
                         rods (especially E.           inflammation of the prostate
  chronic bacterial
                                                  bacteria can continue to ascend to the
                                                     ureters and kidneys, certain pili (P
upper UTI (upper pole
                                E. coli            fimbriae) adhere and ascend better,
                                                  uretovesicular reflux can contribute to
                                                             ascent of bacteria

                        usually E. coli, can be

                         rare complication of
   renal abscess          UTI, usually staph

                           E. coli, proteus,
                                                  bacteria enter bladder from inside the
catheter-related UTI       pseudomonas,
                                                       lumen or outside the lumen

  UTI in pregnancy
                                transmission from infected aerosolized droplets
                                    small enough to get directly inhaled into the
                                   alveoli, replicates in the alveolar space in the
                                 middle/lower lobes, spreads to the hilar lymph
                                nodes through resident macrophages within 2-3
                               weeks, can then disseminate to the bloodstream,
                                 PPD skin test will turn positive 3-9 weeks after
                                 exposure, infection normally controlled by cell-
               mycobacterium           mediated immunity (T-cell) within the
                tuberculosis     traceobronical nodes, lymph or hematogenous
                                dissemination leads to disease (can be through
                               reactivation), once infected risk of progressing to
                               active disease within the first year is 3-4% and 5-
                                  15% over a lifetime, if infected with HIV these
                                  rates are higher (40% within the first year and
                               10% every year following), progression depends
                               on the TB strain/inoculant dose/immune status of
                                                      the patient
                         Symptoms                                         Lab Findings

incubation period is 10-60 days, local irritation and swelling
    shortly after the bite, prodromal signs (fever, nausea,
                                                                   milk peripheral leukocytosis,
vomiting, headache, malaise, anxiety, pain or paresthesias
                                                                      CSF shows protein and
  at the bite site) within 2-7 days, acute neurological phase
                                                                   leukocytosis, elevated CPK,
     for 2-7 days (anxiety, agitation, confused, delerium,
                                                                 arrhythmias and ST changes on
      hallucinations, aphasia, incoordination, dysphagia,
                                                                     ECG, brain shows diffuse
  pharyngeal spasms, hydrophobia, marked hyperactivity,
                                                                 involvement with an increase in
      hyperventilation, fatigue, areflexia develops), coma
                                                                 inflammatory cells, perivascular
 (pituitary dysfunction, hypoventilation, apnea, arrhythmia,
                                                                 mononuclear cell accumulation,
 cardiac arrest), death follows due to CNS failure of control
                                                                  collections of virus in neuronal
        functions or secondary complications (ARDS,
                                                                     cells called Negri Bodies
  pneumothroax, superinfection, DIC), animals show hind-
                          limb weaknses

 mild redness, severe pain, swelling, skin break and fluid
     leak with loss of tissue, skin is warm to the touch

          painful red swollen area around the nail

nail may appear brittle and change shapes/color, nail may
                    become thickened

 decreased sensation, red/yellow skin changes, areas of
  chronic inflammation and fibrosis, loss of hair, cool to
           touch (cellulitis is warm), not painful

honey colored crusts, localized and more superficial than
             cellulitis (upper layers of skin)
upper dermis and superficial lymphatics are affected, may
         involve ears, borders are well defined

in a carbuncle the infected material forms a mass deep in
                                                                           can culture
   the skin, forms a small pocket of pus or an abscess
 in preseptal vision and ocular movements are intact but
  the eyelid is swollen, in orbital eye function may not be
                 intact and 10% lose vision

  abrupt onset with diplopia/photophobia/orbital edema/
               progressive exophthalmos

involves superficial fascia, crepitus (gas in tissue produced
  by bacteria), can spread quickly and cause bacteremia
                      and lead to sepsis

 lesions don't cross midline and usually stay in a single
dermatome, lesions stay on skin surface (no induration of
                                                                 virus can be recovered from
  underlying tissue), lesions are painful and may leave
      scars, can get postherpatic neuralgia or staph

pasteurella multocida shows rapid swelling at the bite site,      gram stain and culture for
  it can cause arthritis/septicemia/endocarditis, only see            aerobes/anaerobes,
       signs of infection 8 hours after bite, see fever/           radiographs to assess for
            cellulitis/purulent drainage/abscess                  osteomyelitis if bite is older

     sepsis, liver damage, heart failure, renal failure,        can detect toxin production and
                    desquamating rash                                     antibodies

 Pastia lines (red skin folds), diffuse erythema, small red
  papules spreading centrifugally from the chest to the
                extremities, sandpaper skin
                                                                  skin lesions do not contain
                                                           use MRI to rule it out, WBC and
                                                               platelets may be normal,
                                                            nuclear medicine studies may
                                                             be helpful, culture from deep
                                                           bone to find cause, bone biopsy
may start from a penetrating wound, suggestive if ulcer is
                                                               necessary, staph aureus
   larger than 2cm/if probe touches bone/high ESR/
                                                               growing in the sinus tract
   abnormal radiograph, may see Charcot foot, see
                                                            correlates well to staph aureus
               inflammation in periosteum
                                                            growing in the bone, use ESR
                                                           and C reactive protein (CRP) to
                                                             monitor progression, imaging
                                                              will retain changes beyone
                                                           clinical and microbiological cure

        infertility, ectopic pregnancies, pelvic pain

arthritis triggered following enteric or urogenital infections,
                 urethritis, cervicitis, diarrhea

painless ulcers, inguinal syndrome in men (painful inguinal

chronic conjunvtiviits that can lead to blindness, entropion
(distortion of eyelids), trichiasis (in-turning of eye lashes),
  repeated infections lead to scarring as the eyelashes
                     scratch the cornea

  ingestion (symptoms from 6 hours to 1-3 days, nausea,
diarrhea, dehydration, hallucinations, seizures, organ shut-
  down), inhalation (symptoms within 8 hours, respiratory
   distress, fever, nausea, cough, tight chest, pulmonary
 edema, cyanosis, low blood pressure, respiratory failure),
  skin exposure (redness, pain), large amounts are lethal
       ingestion (nausea, vomiting, diarrhea, gastric
   hemorrhaging, shock, hallucinations, death), injection
    (severe internal necrosis and hemorrhage leading to
   systemic collapse), inhalation (irritation of airways and
           lungs, pulmonary edema, pneumonia)

                                                                           culture negative endocarditis is often
                                                                                caused by HACEK organisms
                                                                                (haemophilus, actinobacillus,
          clinical presentation occurs slowly and is due to the host
                                                                            cardiobacterium, eikenella, kingella)
  inflammatory response (immune complexes)/cardiac abnormalities
                                                                           or intracellular pathogens/fungi, more
        due to dysfunctional valve/emboli/consistent and persistent
                                                                               often find G+ bacteria (because
 bacteremia, FEVER AND MURMUR (mitral or aortic regurg), classic
                                                                              they're more likely to stick to the
 manifestations (fever, fatigue, myalgia, arthralgia, weight loss, night
                                                                             heart valves), diagnosis based on
    sweats, strokes, splenomegaly, petechia, clubbing of digits, olser
  (painful) or janeway (not painful) nodes/lesion on palms/soles, roth
                                                                            BACTERMIA, majority of 3-6 blood
   spots (retinal hemorrhage with central pallor) cancause blindness,
                                                                                cultures are positive, may see
    retinal/conjunctival/subungal splinter hemorrhages, with insidious
   onset) aren't often seen today because we catch IE much sooner,
     renal involvement (diffuse glomerulonephritis with uremia, renal
       infarction with hematuria) is common, neurologic involvement
                                                                                  echocarediography shows
   (strokes), cardiac involvement (CHF, arrthymia, pericarditis) often
                                                                           vegetations, need 2 major, 1 major +
   leads to death, underlying heart disease or recent procedures are
                                                                           3 minor, or 5 minor criteria, major are
      risk factors, cytokine release (host response) causes systemic
                                                                           positive blood culture and evidence of
       symptoms (fever, arthralgia, myalgia), in prosthetic valves the
                                                                             endocardial involvement on echo,
   infection at the site of surgical attachment (annulus) can lead to a
                                                                                      minor include fever/
 ring abscess, the valve is unable to close well due to the thrombus,
this causes regurtitation which can then cause heart failure or emboli
                                                                                    evidence/echo findings
GVHD primarily affects the skin/liver/intestines

                                                   Reed-Sternberg (giant cells with
                                                    2 nuclei) cells in lymph node
                                                     biopsy, presence of EBV or
                                                        measles is common

                                                     NO Reed-Sternberg cells in

                                                   lack of other blood cells due to
                                                   overproduction of cancer cells
                                                    (low platelets and hematocrit)
                                                               can affect bone density and
                                                               cause bone weakening, see
                                                              reduced number of RBCs and
                                                              other WBCs due to excessive
                                                                production of plasma cells

    long incubation period, hepatotoxic, nephrotoxic,
erythomelagic (blood problems), hepatic and renal failure,
may develop chronic hepatitis, stage 1 (latent, 0-24 hours)
                                                            may be detected in vomitus and
  is asymptomatic, stage 2 (gastroenteritis, 6-24 hours)
                                                                  feces, increased
shows n/v/d/hematuria, stage 3 (apparent convalescence,
                                                            AST/ALT/bilirubin in advanced
      24-72 hours) is asymptomatic but shows rising
   AST/ALT/bilirubin, stage 4 (hepatic, 4-9 days) shows
               heaptic failure/renal failure/
cardiomyopathy/encephalopathy/convusions/coma/ death

long incubation period (6 horus to 3-14 days, depends on
number ingested), nephrotoxic (unexplained acute renal
   failure, non-golmerular renal injury), n/v/d, anorexia,
abdominal cramps, thirst, decreased urine output, chronic
                    renal insufficiency

       long incubation period (6-24 hours), affects the
 liver/kidney/CNS, can see convulsions, n/v/d, abdominal
              cramps, delirium, seizures, coma

 short incubation period (1 hour) and last for 4-24 hours,
   PSL (perspiration, salivation, lacrimation), SLUDGE
       (salivation, lacrimation, urination, defecation,
 gastrointestinal distress, emesis), bradycardia, miosis,

short incubation period (2 hours), hallucination, euphoria,
  flushing, hypertension, rapid heart rate, arrhythmia,
          seizure, CNS symptoms, hyperpyrexia
short incubation period, anticholinergic symptoms (mimics
atropine), midriasis (pupil dilation), muscular spasms, CNS
    stimulant, neurotoxic, if converted to muscimol see
                 prolonged coma-like sleep

  short incubation period, dementia, florid hallucinations
(being pinched/bitten), burning sensation, vasospasm,
 uterine muscle stimulation, early stage shows abnormal
 sensation in limbs (ants crawling over legs), then local
    pain develops in the limbs, late manifestations are
   separated into gangrenous and convulsive patterns

   two or more: temperature >38 or <36, heart rate >90,
respiratory rate >20, PaCO2 <32, WBC >12,000 or <4000,
                       >10% bands

    fever (>100.4 oral or 101 rectal), clotting and bleeding
(DIC), if you have sepsis you must have SIRS, bacteremia
     is not required for sepsis to develop, cardiovascular
      dysfunction (sinus tachycardia, hypotension due to          nonspecific markers of
        vasodilation, abnormal distribution of blood flow,      inflammation (acute phase
       decreased in ventricular preload, fluid losses from    reactants: platelets, fibrinogen,
 diarrhea/vomiting/fever, capillary leak and third spacing,      C-reactive protein, ESR),
venodilation from NO, increased pulse pressure/bounding          procalcitonin is a specific
 pulses, decreased contractility due to cytokines and NO, marker (precursor of calcitonin
  coronary ischemia due to microvascular obstruction by        and is selectively induced by
   leukocytes), acute respiratory distress syndrome, DIC,       severe bacterial infection),
        renal involvement (azotemia and olyguria due to        procalcitonin increases within
hypovolemia, vasoconstriction, and toxins) GI involvement the first 24 hours, TNF-alpha
 (increased permeability, bleeding due to erosions, ileus),    and IL-6 are dropping by this
      liver dysfucntion (cholestatic jaundice, failure), skin               point
involvement (cellulitis, thrombophlebitis, palpable purpura,
gangrene, erythroderma), adrenal insufficiency (ischemic),
                      neuropathy, myopathy
  severe inflammation, impaired air exchange, righ-left
  shunting (blood leaves lungs without enough oxygen),
                      rapid scarring

                                                                  fibrin degradation products like


    Neisseria bacteremia infections (more likely to get
             infections but less likely to die)

      hematuria, renal failure, NO depletion due to
 oversaturation of haptoglobin (pulmonary hypertension),             flow cytometry, Ham test
     bone marrow failure, hemolytic anemia, clots

 severe recurrent pyogenic infections with encapsulated
        associated with immune disorders (SLE)

  common variable immunodeficiency, rarely upper/lower
respiratory tract infections and atopy (dietary allergies), not
    severe because there's compensation by other Igs

   small for gestational age, recurrent upper respiratory
  infections/otitis media/bronchitis/meningitis, some are                     low IgG
  onset age 15-25, prone to malabsorption/autoimmune              low Igs (most importantly IgG),
        disorders/large joint arthritis/gastrointestinal                normal number of B
    malignancies/lymphoma, recurrent sino-pulmonary                lymphocytes but low levels of
       bacterial infections, chronic enteric infections                  soluble antibodies
  infections are common (usually G- bacteremia), high
      mortality, most frequent in patients undergoing             severe <500 PMNs

                                                             normal granulocyte precursors,
episodes of 5-8 days of neutropenia followed by 2-5 weeks      aphtous stomatitis (mouth
      of low-normal ANC (absolute neutrophil count)           ulcers), fever, malaise, skin
                                                               ulcers on fingers/perineum

                     no pus formed

     high mortality due to bowel perforation, can get
              bacteremia, can see ulcers

  small round nodules in liver/spleen, nodules can grow
 when neutropenia is corrected because of inflammation

                                                             diagnosed by galactomannan
        NOT FOUND IN BLOOD, grows in tissue
                                                             antigen/halo sign/tissue biopsy

  many die in childhood from infection, oculocutaneous
                                                                     huge granules
              albinism, low IQ, neuropathy

       staph skin abscesses, sinusitis, otitis media,
pneumatoceles, eczema, typical facies, scoliosis, retained
                                                             elevated IgE and eosinophilia
  decidual teeth (2 layers of teeth), x-ray shows blebs in
              lungs from repeated infections

                   candida infections                             affects neutrophils
 infections with catalase positive organisms (S. aureus,
                                                               NBT (nitroblue tetrazolium) test
   serratia, burkholderia, nocardia, aspergillus), strep
                                                                or dihydrorhodamine (DHR)
           produce peroxide and lack catalase

                                                                  howell-jolly bodies (nuclear
                                                                remnants of erythrocytes seen
increased risk of infection, risk of sepsis (most infections
                                                               in periphery- clusters of DNA in
   occur within the first year), commonly caused by S.
                                                                 cicurlating RBC), number of
 pneumoniae and haemophilus, encapsulated bacteria
                                                                  circulating activated B cells
  cardiac abnormalities, abnormal facies, cleft palate,
   hypocalcemia, mental retardation, schizophrenia,                       no T cells
            susceptible to lots of infections

 first presents with persistent diarrhea/pneumonia/otitis
    media/sepsis/cutaneous infections, lymphopenia,

                                                               high IgA, hihg-normal IgE, low
pyogenic infections, thrombocytopenic purpura, eczema
   opportunistic infections (pneumocystis pneumonia,
     mycobacterium avium complex, cryptococcus)
     viral, fungal, and some bacterial infections
 symptoms peak at day 3-4 and persist for 1-2 weeks,
cough is one of several symptoms but isn't predominant,
             cough subsides after a week

sore throat, fever, headahce, chills, white exudate (pus),     rapid strep test and culture or
                     lymphadenopathy                                    identify cause

  respiratory tract infection with hoarseness, dry cough
  persistant cough with colored sputum, flu-like illness,
severe cough becomes the predominant compaint, cough
   persists for a month, may progress into adult-onset

   rhinorrhea, fever, cough, malaise, cough become
predominant, respiratory distress, symptoms peak around
 day 3 when the virus peaks, can cause viral pneumonia
       (fine interstitial infiltrate at the base of lung)

                                                                  lancet-shaped diplococci, G+,
acute onset of rigors/chills/chest pain, initially just cough,
                                                                 dense infiltrate in lungs, usually
                but then get rusty sputum
                                                                      only one lobe involved

                                                                 usually in upper lobe, lots of pus
  "currang jelly" sputum, cough up necrotic lung tissue            plus necrosis (bulging fission
                                                                          hainging down)
                                                                    bigger than strep pneumo,
                                                                     grape clusters, can cause
                                                                     pneumatocele (cyst) that
       right-sided endocarditis --> embolize lungs
                                                                  destroys lung tissue and bone,
                                                                   secretes enzymes that digest
                                                                    cold agglutination, huge
                                                                     infiltrate on chest x-ray,
bronchitis, headache, dry cough, sore throat, may cause
                                                                    diagnosed by ELISA and
           hemolysis because low hemoglobin
                                                                 complement fixation or serology
                                                                             and culture
mental status change and/or decreased cough, aspirated            G+ and G=, different shapes
            anaerobes can cause abscesses                                 and forms
  dehydration, severe secretory rice water diarrhea, no
 fever, no invasion, no damaged cells, no inflammation,
 enterotoxigenic shows abdominal cramps and diarrhea
  within 16-72 hours (profuse diarrhea, some vomiting,
             cramps, resolves within 5 days)

    gastroenteritis year round, septicemia and wound
       infections in warm months, fever/abdominal
     cramps/diarrhea within 16-48 hours of ingestion
                  (incubation is 1-7 days)

           severe wound infections and sepsis

 incubation is 14-50 hours, weanling diarrhea, traveler's
   diarrhea, secretory diarrhea, enterotoxigenic shows
   abdominal cramps and diarrhea within 16-72 hours                lactose fermenter
 (profuse diarrhea, some vomiting, some fever, cramps,
                resolves within 3-4 days)

                                                             diagnose by culture on HeLa
 infant diarrhea, vomiting, no WBC present in stool (not
                                                              cells or genotype by PCR,
                                                                   lactose fermenter

first see diarrhea/fever/cramps, then bloody diarrhea lasts lactose fermenter, stool culture
 for 4-10 days, hemorrhage and edema in the transverse on sorbitol MacConkey within 2
      and ascending colon, HUS consists of hemolytic         days of diarrhea to diagnose,
           anemia/oliguric renal failure (little urine       non-O157:H7 strains detected
                 output)/thrombocytopenia                     by Stx (PCR or DNA probes)
mild watery diarrhea to dysentery (frequent small volume        does not ferment lactose,
       stools with gross pus, with or without blood,           bacillus, leukocytes in stool
 fever/abdominal cramps/diarrhea within 16-48 hours of        (invasive), diagnose via DNA
            ingestion (incubation is 1-7 days)                          probe/PCR

typhoid fever, daily high fevers for 4-8 weeks, invasion of     does not ferment lactose,
   gallbladder leads to carrier state, can invade kidney,     diagnosed based on isolated
  reinvasion of gut mucosa results in inflammation and         organism from stool/blood/
                      causes diarrhea                                     urine

       causes osteomyelitis in sickle cell patients             does not ferment lactose

 fever/abdominal cramps/diarrhea within 16-48 hours of
                                                                does not ferment lactose
           ingestion (incubation is 1-7 days)

incubation is 1-10 days, diarrhea/fever/abdominal pain for
  2 weeks, chronic disease can develop (terminal ileum),
invasion of the gut mucosa results in bloody diarrhea, can      does not ferment lactose
    mimic appendicitis if mesenteric lymph nodes are
 dysentery (fever and abdominal cramps within 16-48
hours), fever and mesenteric adenitis, lasts 24 hours-14       mimics acute appendicitis
                                                              spiral gram negative rod with
                                                             corkscrew motility and urease
                                                                production, IgM/IgG/IgA
   gastritis, peptic ulcers, gastric carcinoma, mucosa-     antibody with elisa, titers do not
    associated lymphoid tissue associated lymphoma            correlate with severity, silver
                                                             stain can be used to visualize,
                                                            biopsy specimens show urease
                                                               activity, urease breath test

symptoms begin within 6 hours of ingestion, vomiting and
 diarrhea, rarely fever, symptoms resolve over 12 hours

symptoms begin within 6 hours of ingestion, vomiting and
      cramps, symptoms resolve over 12 hours

 descending paralysis, acute GI symptoms (diarrhea then
   constipation), double/blurred vision, slurred speech,
 weakness, symmetrical (nausea, vomiting, diarrhea, and
               paralysis within 18-36 hours)

  ascending paralysis, sensory findings, abnormal nerve

symptoms begin within 8-16 hours of ingestion and resolve
within 24 hours, abdominal cramps and diarrhea, no fever

symptoms begin within 8-16 hours of ingestion and resolve
within 24 hours, abdominal cramps and diarrhea, no fever

 descending paralysis, acute GI symptoms (diarrhea then
   constipation), double/blurred vision, slurred speech,
 weakness, symmetrical (nausea, vomiting, diarrhea, and
               paralysis within 18-36 hours)

 fever/abdominal cramps/diarrhea within 16-48 hours of
                                                                 fecal WBC and colitis
           ingestion (incubation is 1-7 days)

 fever/abdominal cramps/diarrhea within 16-48 hours of
                                                                 fecal WBC and colitis
           ingestion (incubation is 1-7 days)

 fever/abdominal cramps/diarrhea within 16-48 hours of
    ingestion (incubation is 1-7 days), watery diarrhea
nausea/vomiting/abdominal cramps within an hour, short
  incubation (5-15 minutes), histamine fish poisoning
   (scombroid, big fish) shows burning in mouth and

paesthesias within 1-6 horus, abdominal cramps, nausea,
       vomiting, diarrhea preceded or followed by
tongue/lips/throat numbness, sharp shooting leg pains,
                sensations of loose teeth
                     transient paralysis

            vomiting/diarrhea, sometimes fever

    vomiting/diarrhea, sometimes fever, 24-48 hours
chronic diarrhea, bloated, stool floats (fatty stool), no fever
                       (no invasion)
  botenic acid/muscimol (mimics acute EtOH poisoning,
   confusion, restlessness, visual disturbances, mild),
   muscarine (parasympathetic hyperactivity, salivation,
      diaphoresis, blurred vision, diarrhea, cramps),
   psilocybin/psilocin (acute psychosis, hallucinations),
   amatoxins (liver/kidney failure, gastroenteritis, bad)

     small birth size, hepatosplenomegaly, jaundice,
   thrombocytopenia, purpura, CNS defects, hearing
      defects, mental retardation, microcephaly,
              periventricular calcifications

     small birth size, hepatosplenomegaly, jaundice,
thrombocytopenia, purpura, CNS defects, hearing defects

     small birth size, hepatosplenomegaly, jaundice,
thrombocytopenia, purpura, CNS defects, hearing defects,
      causes spontaneous abortion in 2nd trimester

      small birth size, hepatosplenomegaly, jaundice,
thrombocytopenia, purpura, CNS defects, hearing defects,
 cardiac anomalies (patent ductus arteriosus, mental
     retardation), cataracts, blueberry muffin rash
    half of infections are asymptomatic in the mother,
  symptomatic infections in the baby show neurological
       defects with diffuse cerebral intracranial
     calcifications, chorioretinitis, small birth size,
    hepatosplenomegaly, jaundice, thrombocytopenia,
  purpura, CNS defects, hearing defects, microcephaly

    hepatosplenomegaly, jaundice, thrombocytopenia,
                                                        CSF should be screened to rule
                                                         out neurosuphilis in any baby
   extensive skin lesions, interstitial keratitis, bone
                                                         born of a seropositive mother
 lesions, can initially be asymptomatic but manifest
          with neurological sumptoms later

     small birth size, hepatosplenomegaly, jaundice,
thrombocytopenia, purpura, CNS defects, hearing defects,
   worry about sepsis and meningitis in the newborn

     small birth size, hepatosplenomegaly, jaundice,
thrombocytopenia, purpura, CNS defects, hearing defects

  skin infections, can get rapidly lethal pneumonias after
                 respiratory viral infections

                                                              diagnosed by toxin assays (both
  watery diarrhea with pungent smell, large volume stools,       A and B toxins) or nucleic
leukocytosis (high WBC- invasive), fever, prior exposure to      amplification, culture is not
                  antibiotics, megacolon                          useful, don't normally do
                                                            >102 cfu from the catheter
                                                           means it's colonized, positive
                                                             peripheral blood cultures
                                                            indicate infection, culture
                                                           exudate around catheter tip

            extracellular pathogen infections
 clear intracellular pathogens and help B cells produce
 antibodies, so intracellular and extracellular pathogen
    viral infections (intracellular pathogen infections)

            extracellular pathogen infections

            extracellular pathogen infections

     no T cells, reduced NK and B cells, combined
    immunodeficiency, infections by intracellular and
                 extracellular pathogens

SCID-like phenotype, underdeveloped thymus on chest x-
    SCID-like phenotype, susceptibility to oppotunistic
     infections, rash, diarrhea, lymph node swelling,
              eosinophilia with elevated IgE

 SCID phenotype, premature aging (rapidly dividing cells
 including T and B lymphocytes), photosensitivity, cancer
       mild SCID phenotype, premature aging, cancer
     development, neurodegeneration (causing ataxia),
    telangiectasia (small dialated blood vessels near the
   surface of the skin and mucous membranes, seen on
                face), reduced T-cell number

mild SCID phenotype, thrombocytopenia, abnormally small
platelets, cytoskletal defects, recurrent bacterial infections

mild SCID phenotype, incomplete development of thymus
                  and parathyroids

 no CD8 T cells, sustained respiratory infections, chronic
  respiratory inflammation, strong antibody response to
   other viruses and bacteria via overlap (not too sick)

 no CD4 T-cells, no B cells (because CD4 is required for
activation of naïve B-cells), impaired antibody responses,
      repated pyogenic and opportunistic infections

increased susceptibility to extracellular bacterial pathogens
     (haemophilus influenza, strep pneumoniae, strep
  pyogenes, staph aureus) and pyogenic infections, upper
                                                                 no CD19, low levesl of all Ig
     and lower respiratory infections (pneumonia), skin
   abscesses (H. influenza, S. pneumo, S. pyogenes, S.
      aureus) leads to permanent tissue damage and
            bronchiectasis, recurrent diarrhea
                                                              normal levles of circulating B
  only produce IgM, recurrent infections with pyogenic         cells, defect in T cells (lack
    bacteria, opportunistic infections (pneumocystis,        CD40 ligand so they can't bind
    cryptosporidium, cryptococcus, candidda, CMV)             to B cells and induce isotype

produce only IgM (with low affinity), recurrent infections
                with pyogenic bacteria

  recurrent infections, abnormal development of sweat

develop B cell lymphomas because B-cell transformation
         is usually prevented by NK and T cells

        increased susceptibility to HSV infection

       recurrent infections with pyogenic bacteria
 granuloma formation, persistent infections with bacteria
           and fungi, granulomatous lesions

                                                            EEG, MRI shows temporal lobe
     alterations in consciousness and mental status,           involvement with HSV or
personality changes, focal neurological findings, seizures, general inflammation/edema,
                   fever is less common                     LP has mild pleocytosis, PCR is

                                                                   CSF examination (can't be done if
                                                                       increased ICP, low platelets,
   CSF leukocytosis, fever, neurologic symptoms, cerebral
                                                                     severe scoliosis, infection over
 dysfunction, headahce, lethary, confusion, vomiting, stiff neck,
                                                                      lumbar spine) with WBC and
 acute mental status change, increased respiratory rate is first
                                                                  diff/glucose/ protein/gram stain and
sign of sepsis, nuchal rigidity/Kernig's sign (bend knee, leg is
                                                                    culture, WBC >1000 and >60%
        passively extended, this is resisted in meningeal
                                                                     PMNs, glucose <45 or <2/3 of
   inflammation)/Brudzinski's sign (passive flexion of neck
                                                                        serum glucose, protein >80
       causes passive flexion of hips/pelvis), papilledema
                                                                   (elevated), gram stain and culture
                                                                               are positive

                                                                     LP shows <1000 cells that are
entervirus meningitis in kids >2 weeks old (acute fever, frontal
                                                                     usually lymphs/mildly elevated
   headache, photophobia, nucal rigidity, myalgia, comiting,
                                                                     protein/normal glucose, WBC
diarrhea, anorexia, cough, sore throat), initial episode of HSV2
                                                                    <1000 and usually PMN, PCR of
associated with asepctic meningitis and genital tract infection,
                                                                   HSV from CSF, difficult to culture
  initial episode of HIV assocated with aseptic meningitis but
                                                                   (gram stain and culture negative),
                     antibodies are negative
                                                                           mononuclear cells
                                                               diagnosed via thorough history and
                                                                 physical plus LP, fungal causes
 neurologic abnormalities or CSF abnormalities for >4 weeks,      (WBC <500, glucose normal,
insidious onset, symptoms wax and wane, gradual neurologic       prtoein >60, special smears and
       decline, increased lethargy, decreased cognition        culture), TB (WBC <1000, glucose
                                                                       <45, protein >>100),
                                                                        mononuclear cells

  space occupying lesions cause headache/nausea/
                                                                 diagnosis by MRI or CT with
vomiting/mental status change/focal neurological deficit/
                                                                   contrast, NO LP (causes
   fever, 4 stages: early cerebritis from 1-3 days, late
                                                               herniation), culture the abscess,
cerebritis from 4-9 days, early capsule from 10-13 days,
                                                               gram/AFB stain, fungal smears
                late capsule after 14 days

 acts like a rapidly expanding mass lesion, fever, focal
  headache that generalizes, vomiting, altered mental
 status, focal neurologic signs appear then spread and             MRI is diagnostic, no LP
 expand rapidly, hemiparesis, seizures, papilloedema,
                usually quick progression

intracranial show inflammation of face/scalp, spinal forms
    show abscess that usually cover 4-5 vertebra, focal         MRI, myelogram to see cord
   vertebral pain, radiculopathy, motor/sensory deficits,      compression, positive cultures,
     increasing paralysis, may or may not have fever,                 elevated SED
      symptoms progress more slowly, nuchal rigidity
  incubation is 4-14 days, females are often asymptomatic        non-motile, non-spore forming
  and men are symptomatic, acute urethritis in men, rectal            rod, G- intracellular
   and pharyngeal infections are often asymptomatic, men          diplococci in urine, must be
          have abrupt onset of copious discharge and                   kept moist or plated
    dysuria/anorectal infection is associated with proctitis,     immediately (Thayer-Martin),
   women are usually symptomatic but may have vaginal            diagnosed by gram stain from
       discharge/pruritis/pain, can cause PID in women           male urethral discharge, culture
    (abdominal pain, cervical tenderness, fever, scarring,         used for rectal/pharyngeal
infertility, ectopic pregnancy), Fitz-Hugh Curtis syndrome               infections, DNA
         (perihepatitis associated with PID, RUQ pain),              probles/NAAT/PCR for
       disseminated infection more common in women               urine/endocervical specimens/
    (tenosynovitis, dermatitis, polyarthraliga syndrome or       urethral swabs (better on male
                          septic arthritis)                                   urine)

    LVG has 3 stages: painless ulcer/papule on genitals
    (heals without scarring) then lymphadenopathy and
   systemic complaints (fever, headache, myalgia) then
                                                                   diagnose serovars D-K by
   ulceration of external genitalia, urogenital infections
                                                                  culutre or amplifications tests
(serovars D-K) causes urethritis after 7-14 days incubation
                                                                     on urine/vagine/urethral
       (dysuria, urethral discharge stains underwear),
               complications include proctitis/
 epididymitis/endometritis/cervicitis/salpingitis/PID/ ectopic
 pregnancy/ infertility/reactive arthritis (Reiter's syndrome)

     yellow vaginal discharge, dysuria, vulvar itching,      flagellated motile protozoan, pH
dyspareunia (pain with intercourse), lower abdominal pain,      >5, organisms seen on wet
      purulent copious frothy discharge with foul odor                    mount
 vaginal discharge, thin gray adherent, itching, with odor,
requires 3 of 4 criteria (homogenous thin adherent vaginal
 discharge with string test on culture, clue cells which are
 squamous stippled with bacteria and obscured borders,
    ph>4.5, positive wiff test with fischy smell of vaginal
                     secretions in KOH)
 most are asymptomatic with primary infection, incubation
is 2-20 days, grouped vesicular lesions form painful ulcers,
  often affects urethra (burning/tingling on penis), look like   Tzanck smear with Wright stain
water blisters, can ulcerate in immunocompromized hosts,         of scraped base of lesion shows
     primary disease (regional lymphadenopathy, fever,           multinucleated giant cells and
    malaise, anorexia, aseptic meningitis) lasts 3 weeks,        is diagnostic, viral culture media
  recurrence in 90% of patients (itching, tingling, burning,
                     vesicle appearance)
                                                             can't culture, darkfield exam not
       incubation is 3 weeks, 3 clinical stages: primary/
                                                                usually available, serology:
secondary/tertiary, latency occurs after secondary stage,
                                                                     treponemal (tests for
primary (ulcerated non-tender ulcers, chancres with hard
                                                               antibodies against T pallidum
        smooth clean base, nontender bilateral inguinal
        lymphadenopathy, serology not always positive,         antigens directly, FTA-ABS is
      generalized dissemination leads to appearance of           fluorescent Ab test used to
       chancre), secondary (3-6 weeks after chancre,          confirm a positive RPR/VDRL,
                                                               remains positive for life, more
    generalized rash including palms/soles/oral mucosa/
                                                                   useful in primary/tertiary
  genitals, minimally pruritic, sore throat, myalgia, patchy
                                                                syphilis) or non-treponemal
  alopecia, generalized lymphadenopathy, condylomata
                                                                    (measure IgM and IgG
    lata flat warts in moist areas and oral ulcers are very
                                                                antibodies formed against a
contagious), late/tertiary (meningitis, dementia, hearing
                                                             lipoidal antigen that forms when
 loss, tabes dorsalis with posterior column demyelination
                                                             the organism interacts with host
    causing pain and ataxia, aorta problems, aneurysm,
                                                                 tissues, non-specific, gives
  arthralgia), gumma (granulomatous-like lesion causing
                                                                 false-positives, negative in
   local destruction in any organ), ocular findings (Argyll
                                                                primary/ tertiary syphilis, titer
 Robertson pupil- small pupil that accomodates to near
                                                                   drops with treatment and
  vision but doesn't react to light, gun-barrel sight- optic    becomes negative, used for
nerve atrophy causing progressing concentric destruction screenign and efficacy, VDRL
                        of visual fields)
                                                                           and RPR)
affects muscle/skin/bones, saber shins (bowing of legs),
saddle nose (loss of cartilage), Hutchinson's teeth (peg
             shaped upper central incisors)
4-7 days of incubation, painful ulcer with ragged edges,
           painful inguinal lymphadenopathy
inguinal granuloma, painfless destructive ulcers without
               regional lymphadenopathy
 incubation period is around 2 weeks, primary infection leads to
                                                                              virus found in semen and
        an acute self-limited febrile illness (flu-like or mono-like
                                                                        vaginal/cervical secretions as well
    symptoms prior to seroconversion, fever, adenopathy, rash,
                                                                         as CSF (in both cellular and free
    pharyngitis, myalgia, arthralgia), CD4 count >500 is usually
                                                                        compartments), seroconversion is
                 asymptomatic, CD4 count 200-500 has
                                                                            detection of antibodies after
  thrust/shingles/pneumococcal pneumonia (gradual increase in
                                                                       infection (takes weeks), initially see
        dyspnea on exertion, dry cough, weight loss, interstitial
                                                                           lymphopenia followed by CD8
     infiltrates), CD4 count <200 shows opportunistic infections
                                                                        lymphocytosis, HIV antibody (IgG)
(PCP, candida esophagitis, toxoplasmosis), toxoplasma causes
                                                                       may be negative but p24 antigen is
    focal encephalitis/weakness/seizures/confusion/coma, CD4
                                                                           positive early, ELISA used for
   count <50 at risk for CMV (chorioretinitis, colitis, esophagitis)
                                                                           screening with confirmation by
 and MAC (mycobacterium avium complex, fever, night sweats,
                                                                       western blot (2 out of 3 bands must
 weight loss, diarrhea, diagnosed by culture), clinical findings to
                                                                       be positive: p24, gp41, gp120/160),
   suggest HIV infection include generalized lymphadenopathy/
                                                                         viral load measured by PCR and
   unexplained anemia/leukopenia/thrombocytopenia/ recurrent
                                                                          predicts outcome, PCP mimics
     pneumonias/Kaposi's sarcoma/thrush/ wasting/TB without
                                                                           walking pneumonia (interstitial
        positive PPD/other STDs/CNS neuropathy and memory
                                                                          infiltrates, on staining looks like
 loss/fever, AIDS is severe immunodepression characterized by
                                                                           deflated footballs), toxoplamsa
      one of 23 clinical illness or CD4 >200, cryptosporidia is a
                                                                         shows ring-enhancing lesions on
 parasitic cause of diarrhea in AIDS patients (n/v/d, weight loss,
                                                                                 CT with contrast, see
       RUQ pain, biliary tree involvement), candida esophagitis
                                                                           cryptosporidia by AFB stain of
(dysphagia, retrosternal pain on swallowing, treated with empiric
                                                                       stool, PML diagnosed by MRI, treat
      flucoanzole), progressive multifocal leukoencephalopathy
                                                                                  lots of stuff by fixing
   (papovavirus JC, rapid progression of focal changes causing
                 ataxia, hemiparesis, speech difficulties)

    cystitis, urethritis, prostatitis, can be confused with
     vaginitis, can result in sepsis in debilitated hosts,
  symptoms depend on age, babies and elderly display
 nonspecific syptoms, hematuria (micro or macro) in 50%

dysuria (burning or pain during/after urination), frequency
  (need to urinate more), urgency (decreased ability to
           consciously/comfortably hold urine)
   >10 luekocytes per high power field on a spun urine
      sample or urine dipstic for leukocyte esterase
>105 bacteria per milliliter for G- rods from a clean catch or
catheter specimen, urine is usually sterile but will get some
 contamination when obtaining the spcimen, presence of
 one bacteria per oil field in an unspun G- specimen, can
       be associated with acute urethral syndrome
 can be confused with vaginitis (suspect vaginitis if odor,
                  itching, discharge)
 abrupt onset of fever, chills, low back/perineal pain with
                                                                 urinalysis and culture organism

   can be asymptomatic or have back/perineal pain qith           urine reveals pyruia, bacteruria,
              dysuria/frequency/urgency                           culture identifies the organism

    pyelonephritis, renal abscess, fever, suprapubic
 tenderness, hematuria (gross or microscopic), flank

    n/v/d, elderly may look septic (fever, hypothermia,      pyuria, bacteruria, positive urine
hypotension, tachycardia, respiratory distress), "urosepsis"    culture and blood cultures

                                                                   urine cultures can be sterile,
         insidious onset of fever, chills, flank pain
                                                                  diagnose by CT or ultrasound

 bacteruria, cystitis, pyelonephritis, bacteremia, urosepsis

asymptomatic bacteremia in 5%, symptomatic UTI, acute
                                                                     screen urine throughout
 pyelonephritis, low infant birth weight, premature labor,
 in controlled infections see calcified area on chest x-ray, there are 2
      clinical forms of TB which can occur concurrently: pulmonary
      (cavitary, pneumonia, pleurisy, miliary) and extrapulmonary
    (meningitis, pericarditis, osteomyelitis, lymphadenitis, laryngitis),
  symptoms progress gradually, fever, chest pain, productivce cough
       with/without hemoptysis, arthralgia, weight loss, night sweat,       tubercle acid-fast bacillus, weakly G+
     Rasmussen's aneurysm, non-specific effusion or consolidation,          (must treat mycobacterium with heat/
   alveolar or patchy nodular pattern of infiltrates on chest x-ray, can       detergent/acid to get it to take up
  have pleural effusion, hilar adenopathy (occasional cavities), young        dyes), aerobic, non-spore forming,
      children are more likely to have hilar node involvement, large          non-motile, grows slowly, produces
     amounts of sputum with PMN and AFB, tuberculous pleurisy                 niacin and can reduce nitrates, use
  (pleural effusio due to TB, rupture of subpleural component into the      BACTEC blood cultures, PPD is often
    pleural space, usually self-limited and resolve in a few months, 5         negative in primary TB, diagnose
     year risk of reactivated TB is high, nonproductive cough, fever,                    through clinical
   pleuritic chest pain, diagnose from pleural fluid or biopsy, cultures    presentation/cultivation from tissue or
usually positive, fluid smears uusally negative, low communicability),      fluid/AFB with symptoms/smears and
pleurisy with miliary TB (can have efusion), cavitary TB can occur             cultures, have quick liquid culture
   wiht reactivation or during primary pneumonia when upper lobe is           media (7-10 days to diagnose) and
     seeded during lymphohematogeouns dissemination (productive                direct amplification tests (3 days),
  cough, hemoptysis, night sweats, fever, weight loss, fatigue, highly       PPD is diagnostic of infection but
 contagious, cavities on chest x-ray, diagnosed by 3 sputum samples         doesn't differentiate between latent
          for AFB smear/PCR/ culture), miliary TB is widespread               and active infections (positive if
    hematogenous dissemination of TB and can occur after primary                      >15mm induration)
   infection or on reactivation (acute or insidious onset, fever, weight
loss, night sweats, pulmonary complains, headache, abdominal pain,
   skin lesions, genital lesions, small nodular lesions on chest x-ray,
    pleural effusion, cavitation, infiltrate, pneumothroax, cultures and
                             smears diagnose)
   Prevention/Treatment                   Other Notes

                                    can also be transmitted by
 treatment must be started         the lick of a rabid animal on
 at the time of the bite, oral       abraded skin/allographs
rabies vaccination program                    (corneal
 for wild animals (vaccines            transplants)/mucous
  dropped in by plane), use             membranes, has 5
    vaccine for domestic            structural proteins and G-
animals, also have vaccine          protein glycosylation, most
 for people (killed vaccine),      commonly transmitted from
treatment includes cleaning         bats, carried by communal
      the wound/rabies            (group of interactign species
  immunoglobulin/vaccine               sharing a populated
                                      environment) animals

                               can start as folliculitis
                            (infection of oil gland with
                           the hair follicle), associated
                            with laceration/ puncture,
     colonization with          common in diabetic
staph/strep may predispose neuropathy, risk factors:
         to cellulitis        fissures in skin/edema
                            secondary to heart failure/
                             extremities with stripped
                                   veins for CABG

    hot compresses, no
antibiotics, debride if lots of
                                  usually contained to nailbed,
anti-fungal medication, nail
                                     but may predispose to
      may be removed

                                     chronic, risk factor for
                                     cellulitis (broken skin,
                                        abnormal veins)

 topical or oral antibiotics       more common in children
      and local care                      than adults
                                   beta-hemolytic streps are
                                        most common

abscess must be drained,
 antibiotics may be used
    antibiotics only for
 preseptal, orbital requires
                                 orbital is more serious than
  antibiotics and surgical
   drainage if there's an

 surgical decompression of
the source, broad spectrum
                                     rare, high mortality
      antimicrobial, no
 anticoagulation or steroids

    immediate surgical
debridement, removal of all          mortality up to 30%
dead tissue filled with toxins

zoster vaccination (10x the      immunocompromised can
dose of viral particls as the      get multiple episodes,
   varicella vaccine) for          chickenpox is itchy not
   patients over age 60                   painful

 immunize for tetanus and
                                 20% of dog bites and 50%
   rabies if bit, penicillin,
                                  of cat bites get infected
   ampicillin, sulbactam

    use antibiotic that
                                    historically related to
    decreases protein
                                  superabsorbent tampons
 production (clindamycin,
                                     made of polyester

                                    usually seen in kids,
                                   epidemics in nurseries
         risk factors:
                                   leading cause of
 procedures/injection drug
                               amputations in the US, in
  use, infections don't go
                             adults the spread is usually
  away because the bone
                              contiguous, in kids there is
doesn't have many vessels
                               hematogenous spread to
     and it's difficult for
                             long bones, TB reactivation
  antibiotics to reach the
                              can cause osteomyelitis in
  infection, no antibiotics
                                 the vertebral column
 before culture unless the
patient is septic, 6-8 weeks
        of antibiotics

                                a tertiary stage can occur
                                   years after the initial
                                infection (anogenitorectal
                                   syndrome with rectal
                               stricture or elephantiasis of
                                  the genitals, mostly in
                                 women and homosexual
                                 men), highly prevalent in
                               Africa/Asia/South America

"SAFE" strategy: surgery to
correct trichiasis, antibiotics
                                    Africa is most affected
  to treat active infection,
                                   (Ethiopia, India, Nigeria,
  face washing to reduce
                                  Sudan, Guinea), children
   disease transmission,
                                     are most susceptible
 environmental change to
                                (women are therefore more
 increase access to clean
                                likely to get it because they
    water and improved
                                        are caretakers)
   sanitation to eliminate

   no known treatment,        bioterrorism agent, stable in
supportive care, try to flush   environment as powder/
     toxin from body              mist/pellet/dissolved
                                        bioterrorism agent, stable,
  hospitalization and care,
                                        stored as either purified or
  ricin toxoid may become
                                        impure forms, used either
     available, no known
                                         as an aerosol or as food/
                                            drink contaminant

    endocarditis can't be cured
 without antibiotics, IV antibiotics
                                           average age of patient is mid-
that kill the bacteria, obtain MICs
                                           50's (associated with valvular
    and MBCs for the isolated
                                          changes such as degenerative
organism, therapy usually lasts 4
                                          lesions of atherosclerosis), low
  weeks, do NOT anticoagulate
                                       flow cardiac lesions are not a risk
  the patient, for viridans strep:
                                        factor, artificial/prosthetic valves
  penicillin + aminoglycocide for
                                       allow platelet deposition and also
   the first 2 weeks, for culture
                                        contain endocardium/underlying
   negative IE: ceftriaxone for 4
                                             collagen, PVE can be early
weeks, for MRSA/ MRSE: vanco
                                          (within 2 months of surgery) or
   + rifampin + gentamycin, for
                                         late (after 2 months of surgery),
    enterococcus: ampicillin +
                                               early PVE bacteria are
 gentamycin, for fungi: ampho B
                                          introduced during surgery, late
  + surgery, fungal endocarditis
                                          PVE bacteria are introduced in
    almost always needs valve
                                           the same mechanism as NVE
 replacement, surgery should be
                                                bacteria, polymicrobic
  considered when there's 7-10
                                         endocarditis is rare, risk factors
    days of bacteremia despite
                                        include prosthetic valves/history
       antibiotics/2+ embolic
                                          of endocardiits/non-atiral heart
   events/intractable CHF, ring
                                               and valve defects/heart
   abscesses or other signs of
                                        transplant with abnormal valves,
    extending infection require
                                           dnetal procedures can induce
  surgery, for prophylaxis: 2gm
 amoxicillin orally 1 hour prior to
     procedure (dental work)

    no known treatment,
 plasmaphoresis to remove
the plasma of the blood and
    replace it with saline
  (doesn't have antibodies)
          may work
 immunosuppressive drugs
  and anti-T-cell antibodies
   prevent T-cell activation
(donor-recipient matching is
more important in MHC-II to
   avoid T-cell activation),
corticosteroids are the drug
   of choice to treat actue
    rejection and are most
   effective if administered
    before transplantation
   because cytokine gene
  expression can be altered
 by the time of alloantigenic

                        correlated with the presence
                        of antibodies specific for the
immunosuppressive drugs HLA class I molecules of the
                          graft, suggesting a B cell

                                   this response can be
                                 beneficial when directed
                                 against leftover leukemia

                                 5 types, good survival rate

  Rituximab (anti-B cell         29 types (defined by the
  antibody), anti-idiotype      cells involved), treatment is
         therapy                        less effective

 diagnosed by blood/bone
 marrow sample, treat with
 chemotherapy and bone
    marrow transplant
  diagnosed by blood/bone
                                       often caused by
 marrow sample, treat with
                                  Philadelphia chromosome
  chemotherapy and bone
                                 (9-22 translocation forms a
marrow transplant, can also
                                fusion protein Bcr-Abl that is
use ATRA (all trans-retinoic
                                    a constitutively active
acid) which induces myeloid
   maturation (causes the
                                 kinase causing continuous
 immature cells to continue
                                         cell divisions
 chemotherapy and stem
     cell transplant

symptomatic (no lab test to
directly identify the cause),
     can pump stomach
                                  lethal, symptoms appear
   immediately following
                                    within 6-24 hours after
ingestion (too late to do it if
                                   ingestion, virotoxins are
  patient has symptoms),
                                     cyclopeptides with no
   maintain urine output,
                                toxicity, found in Europe and
   penicillin G displaces
                                    costal regions in North
   amantin from plasma
  proteins and increases
  renal excretion, silibinin
    inhibits toxin uptake

symptomatic (no lab test to
                                 lethal, symptoms appear
directly identify the cause),
                                   within 6-24 hours after
  dialysis, corticoids and
                                ingestion, found in Europe/
      antioxidants (N-
                                  Pacific Northwest in the
acetylcysterine), may need
                                    US/British Columbia
dialysis or renal transplant

symptomatic (no lab test to
directly identify the cause),
                                lethal, symptoms appear
 most recover in 2-6 days,
                                  within 6-24 hours after
  GI decontamination with
                                 ingestion, rare in North
activated charcoal in early
                                America, seen in eastern
    stages, prophylactic
 pyridoxine may prevent or
       arrest seizures

symptomatic (no lab test to
directly identify the cause),
  replace electrolytes and
                                 non-lethal, symptoms
fluids, activated charcoal if
                              generally appear within the
 the patient isn't vomiting,
                               first 6 hours of ingestion
     atropine titrated to
 pulmonary secretions and
heart rate in severe toxicity

symptomatic (no lab test to
                                   non-lethal, symptoms
directly identify the cause),
                                generally appear within the
       anxyolytic and
                                 first 6 hours of ingestion
symptomatic (no lab test to         non-lethal, symptoms
directly identify the cause),   generally appear within the
       anxiolytic and            first 6 hours of ingestion,
      anticonvulsants            found in US/Europe/Asia

                                    non-lethal, symptoms
                                generally appear within the
symptomatic (no lab test to
                                 first 6 hours of ingestion,
directly identify the cause)
                                     found in Mexico and
                                         southern US

                                SIRS is not always caused
                                       by infection

 early goal directed thearpy
    (EGDT)- place central
  venous catheter/maintain
  central venous pressure/
   mean arterial pressure/
urine output/central venous
      oxygen saturation,
 antimicrobials and control
                                 sepsis more common in
source of infection, optimize
                               men and blacks, mortality is
 tissue oxygenation, fluids,
                               20-70%, higher temperature
   vasopressors, transfuse
                                   during bacteremia is
early, nutrition, DVT/ gastric
                                  correlated with better
 ulcer prophylaxis, prevent
                               survival, worse prognosis if
     secondary infections,
       maybe low dose
                                fever/underlying disease/
                                older, positive cultures do
    recombinant activated
                                NOT correlate with worse
 protein C/glycemic control,
  activated protein C is an
anticoagulant/ antiapoptotic/
 antiinflammatory used only
    in severe sepsis, only
      patients with shock
 refractory to vasopressors
  are given low-dose long-
    course corticosteroids

                                the more organs involved,
                                 the worse the prognosis
   fresh frozen plasma

 prophylactic androgens or
C1 inhibitor concentrate, no
response to antihistamines
 vaccine with serogroups
YWCA, no vaccine against
       serogroup B

                               autosomal recessive, 65%
                                      of inherited
                                immunodeficiencies are
                                  humoral, autosomal
                                  recessive, common
                                IgG levles recover fully
                                  within months-years

treat infections, IVIG every
          4 weeks
                                 frequency of infections
                               corresponds inversely with
                                   absolute number of
 recovery depends on the
                               circulating neutrophils and
  return of normal counts
                                leukocytes, blacks have
                                normally lower neutrophil
  diagnosed by molecular
     testing (for ELA2
mutation)/periodicity/ family
                              autosomal dominant, rare
     history, treat with
 recombinant G-CSF and
prevented with keratinocyte
     growth factor and          at risk: patients going
  palifermin, treatment is    through radiation therapy/
 symptomatic with mouth stem cell transplant/ chemo

  treat with debridement

                                   chemotherapy may
                                 predispose, risk factors
    treat with antibiotics
                                include aplastic anemia/
        prophylaxis is
azoles/candins, repsonse to
                                    risk factors are
treatment is poor, mortality
    is high, resolution of
                                  spectrum antibiotics
   neutropenia improves
high mortality, combination
                                risk factors are steroids/
      of 2 antifungals:
                               collagen vascular disease/
  voriconazole/ampho B/
                              autosomal recessive, 65%
                                     of inherited
treat by stem cell transplant  immunodeficiencies are
                                 humoral, autosomal
                                 recessive, common

                               more common in females
                                     and whites

                                 many cases are silent
  prophylactic antibiotics,
  treat with bone marrow
  biopsy or gene therapy

                             functional hyposplenism
                           from autoimmune disease,
vaccination (pneumococcal,
                              neoplasia, amyloidosis,
   HiB, meningococcal)
                            alcoholism, elderly, sickle

survive only if isolated in a
pathogen-free environment
                                ADA/PNP are autosomally
   or if undergo a bone
 marrow transplant (can't
   reject foreign tissue)


                                most common from August-
                                       early spring

                                  most common in colder
treat bacterial infection with months, pharyngitis + rash =
         antibiotics           strep, group A pharyngitis is
                                        strep throat

mycoplasma or chlamydia
     are treated with                  contagious
 erythromycin or z-pack

                            leading infectious cause of
                            death in the US, influenza A
                            subtyped by neuraminidase
                             and hemagglutinin, severe
 neuraminidase inhibitors in the elderly, antigenic shift
  (zanamivir, oseltamivir)    (large changes in either
prevent infection, vaccines HA/NA) cause pandemics
     formulated yearly           because there's no
                              immunological memory,
                               antigenic drift are small
                             changes and are the basis
                                  for the flu vaccine

   pneumococal vaccine
  vaccine (conjugated for        most common bacterial
 young or polysaccharride       cause of pneumonia, can
 for older kids and adults)     get bacteremia and rapid
covers 23 serotypes based       death in splenectomized
  on prevalence in clinical      patients (can't produce
   samples, treated with             antibodies to it)

                                 often seen in alcoholics

  treated with azithromycin
                                occurs more commonly in
    (penetrates the cell) or
                                fall and winter, chlamydia
   tetracycline, makes the
                                    can cause a similar
illness disappear faster but
doesn't sterilize the sputurm
     check dentition to
                                      very common
    determine treatment
                                endemic in the Gulf of
                            America, lives in water and
 antibiotics may shorten      is halophilic (salt-loving),
duration of toxin secretion human pathogen (no animal
  and decrease spread           reservoir), pandemics
                            caused by serotypes O1 or
                                O139, bacteria levels
                             increase in warm months
                                     requires salt,
                             enterotoxigenic or cytotoxic
                               (profuse diarrhea, some
                                vomiting, some fever,
                             cramps, resolves within 3-4
                               can lead to cirrhosis and
                               renal failure especially in
                             immunocompromised hosts

 antibiotics decrease the
duration and severity of the mucosal immunity (IgA in
  diarrhea, prevention is    breastmilk), carrier states,
 bismuth subsalicylate 4x infection requires high dose
          per day

                                outbreaks in day care
                            centers and pediatric wards,
rehydration and antibiotics reservoir is asymptomatic
                             kids and adults, mortality is

                                 O157:H7 is the most
                             common strain, reservoir is
                               animals (found in meat),
                             small infectious dose, HUS
                             is more common if infected
                               with O157:H7 and have
                              bloody diarrhea and fever/
                                 very old and young/
                                  antimotility drugs/
                                  expression of Stx2
                              4 species (s. dysenteriae is
                               the most severe, s. sonnei
                               is most common in the US
                              and is mildest), infects only
                                humans, small infectious
                                 dose (resistant to acid),
  antibiotics reduce the
                               most common in kids <15,
  duratio nof illness and
                                     endemic in male
  period of infectivity but
                              homosexuals, epidemics in
  resistance is common
                                  day care centers and
                              institutions, enterotoxigenic
                                  or cytotoxic (profuse
                                diarrhea, some vomiting,
                                  some fever, cramps,
                                resolves within 3-4 days)

  ampicillin, ceftriaxone,
                                 human host, mainly in
Bactrim (carriers are given
                               patients with proton pump
ampicillin + probenecid and
   Bactrim for 6 weeks)

                                      host is pigs
 patients must be treated

                              enterotoxigenic or cytotoxic
                                (profuse diarrhea, some
    NO ANTIBIOTICS               vomiting, some fever,
                              cramps, resolves within 3-4

                              zoonotic infections, humans
   cipro, 3rd generation
                                  are incidental hosts,
cephalosporins, TMP-SMX
                                common in Scaninavia

                              common in northern Europe
                                   and Canada
                             more common in areas of
combination of proton pump
                               poor sanitiation, in US
  inhibitor + tetracycline +
                             colonization increases with
metronidazole + bismuth or
                              age, colonization protects
 amoxicillin/ clarithromycin
                             against esophageal reflux

    NO ANTIBIOTICS                mainly in summer




                             enterotoxigenic or cytotoxic
                               (profuse diarrhea, some
    antibiotics: emycin         vomiting, some fever,
                             cramps, resolves within 3-4

                             occasionally in normal host,
                              associated with pregnant
                               women and meningitis
                                  histamine fish poisoning
                                 most common in coastal
                                regions (California, Hawaii)

                                most common in Hawaii and

                                  found in the north only
                                 most common foodborne
                                pathogen, most common in
                                    late fall and winter

liver transplants in amatoxin

                                  most common congenital
  reduce transmission by         infection. Biggest cause of
 handwashing, no vaccine,       long-term morbidity in kids,
   education is important            important to reduce
  reduced transmission if
   delivered via cesarean
   section (active lesions
     present), treat with

                                 eliminated in the US, 50%
 MMR vaccine (pregnant          chance of severe disease in
 women shouldn't receive          infant in mom develops
     the vaccine)                   rubella during the first
  aggressive treatment of
    newborns for a year
                           time between infectio nand
reduces morbidity, prevent
                           safety for conception is 7-9
 transmission by avoiding
                           months, important to reduce
undercooked meat and cat
feces, wash raw fruits and
 vegetables, handwashing

  test all pregnant women,
                                   early detection and
 treat infected mother with
                                 treatment is important
penicillin during pregnancy

  prevention is maternal
screaning and treatment of         early detection and
 colonized women during          treatment is important
   reduce transmission if
 mother receives anti-HIV
therapy (zidovudine) during
  pregnancy/intrapartum,           early detection and
 newborn receives therapy        treatment is important
  for 6 weeks after birth,
  deliver by C-section, no
       breast feeding
    frequently oxacillin
    resistant, s. aureus
septicemia must be treated       nosocomial infection
     with 2 weeks of IV

                              nosocomial infection, severe
                                     infections in

resistant to quinolones and
   beta-lactams, treat by
discontinuing the causative
 antibiotics, give oral vanco nosocomial infection, severe
  with IV metronidazole or in the elderly, alcohol-based
     oral metronidazole,       solutions don't kill spores
colectomy if megacolon has
occurred, prevent spread by

treatment depends on "local
                                 nosocomial infection
 if fungal infection watch for
     fluconizale resistance         nosocomial infection,
      (candida albicans is        prevent by cleaning skin
  susceptible, C. krusei and     with chlorhexidine and not
glabrata are not), empriical     using sutures in catheter,
   treatment must cover all      use transparent dressing
 possible causes, only start      and biopatch, use teflon
treatment after cultures are     catheter, use antiseptic or
taken, narrow the spectrum         antimicrobial catheters
      once cause is found

   ventilator associated
pneumonia is prevented by nosocomial infection, more
preventing aspiration (raise common in ICU patients
head, suction, avoid gastric   especially those on
  overdistention), mouth      mechanical ventilation,
decontamination, removing leading cause of death from
   the tube as soon as        nosocomial infections
  possible, hand hygiene
   treated with gamma
      globulin (IVIG)
                              can't receive vaccines!
administration and systemic
   prone to autoimmune
    hemolytic anemia,
thrombocytopenic purpura,
 and recurrent neutropenia
  treat with acyclovir and
       supportive care

  emperic treatment based on
     age (0-4 weeks: group B
          strep/E. coli/L.                   more common in
monocytogenes, under 18: H.           underdeveloped countries,
flu/N. meningitidis/S. pneumo,     encapsulated strains (type f) of
 18-50: N. meningitidis and S.          H. flu are increasing and
       pneumo, over 50: N.            predisposing conditions are
   meningitidis/S. pneumo/ L.                    DM/CSF
monocytogenes/gram negative            leak/alcoholism/asplenia/
       rods) and underlying          hypogammaglobulinemia, N.
conditions, vaccine against N.           meningiditis serotypes
 meningiditis YWCA, vaccine             A/B/C/W135/Y, terminal
   against S. pneumo covers         complement deficiencies show
    most common serotypes,             increased attack rate but
   cephalosporins don't work           decreased fatality with N.
    against listeria (can't use       meningiditis, S. pneumo is
   vanco), ampicillin or trim-      primary cause in 18-50 yo and
                                    is associated with URI/LRTI or
    sulfa is used for listeria,
                                      endocarditis (predisposition
 begin treatment quickly, treat
                                      same as H. flu), L. mono is
  for 10-14 days with 3rd gen
                                   foodborne cause and is seen in
 cephalosporin and vanco if
     s. pneumonia resistant,
dexamethasone (steroid for

     treat enterovirus with
  gammaglobulin, emperic
                                    enterovirus meningitis more
   treatment and herpes is
                                        common in summer
acyclovir, HIV start triple drug
   treatment is not empiric,
     based on likely initial
                                  if papilledema: start treatment
    diagnosis or confirmed
                                         then get head CT
    diagnosis, always give

 for early and late cerebritis
   just treat with antibiotics,
capsules must be removed,
 treat with surgical drainage
      and management of
     increased ICP, emiric
therapy with metronidazole
 (Flagyl) + 3rd generation
 cephalosporin + nafcillin
            or vanco

  treat with neurosurgery
 (craniotomy), drain pus,
decrease ICP (may require
                            polymicrobic infections are
dexamethasone), cultures,
                            common, more common in
 debridement of sinuses/
                               males in the 2nd-3rd
  mastoid/ear, antibiotics
                                decade of life, poor
 should cover anaerobes
                              prognosis if comatose,
  gram positve and gram
                            survivors develop seizures
negatives (metronidazole
+ ceftriazone + nafcillin +

                               intracranial (not spinal)
    treat with immediate
                              forms generally spill over
      surgical drainage,
                            into the subdural space and
   antibiotics to cover S.
                           form an associated subdural
   aureus/gram negative
                                empyema, usually not
 rods/anaerobes (vanco +
                                 polymicrobial, poor
 3rd gen cephalosporin +
                               prognosis if paralysis is
     drug resistance from
   transfer of naked DNA,
  resistance to penicillins/
fluorquinolones, treat with
ceftriaxone IV or oral for
     at least a week for       can't use fluoroquinolones,
disseminated infection,         treat for chlamydia at the
 ceftriaxone IM once for        same time unless NAAT
      normal infection            tests for chlamydia are
  (including pharyngeal                   negative
        infections and
 spectinomycin IM once
    for penicillin allergy,
ceftriaxone IM followed
by amoxicillin/erythro in
      pregnant women

 treated with doxycycline
 for 21 days (erythro for
                                 venereum (LGV by L
   pregnant women), but
                              serovar, found in Africa/SE
   azithromycin once is
                              Asia/India/South America),
  preferred for everyone
                             ocular trachoma (serovars A-
       test for cure in
                               C), oculogenital disease
 pregnancy) screening in       (serovars D-K), perinatal
sexually active women and infections from any serovar,
      pregnant women,            commonly seen with
 abstinence for 1 week to              gonorrhea
  lessen risk of reinfection

 treat with metronidazole
   (even in pregnancy)

    treat with Flagyl or
clindamycin vaginally or
                               NOT AN STD, often
metronidazole/ clindamycin,
                            confused with trichomonas
 pregannt women receive

 acyclovir for 7-10 days
followed by suppressive
   therapy 5x per year
for primary/secondary/early
     latent syphilis use
benzathine penicillin G IM
   once, use in pregnant
women even if allergic, late
latent syphilis use pencillin
    G plus doxycycline,
  neurosyhpilis is IV pen G
       for 10-14 days

    azithromycin once           often associated with HIV

                                   not seen in the US
  prophylaxis for PCP if CD4
 count <200 (bactrim aka trim
 sulfa) and MAC if CD4 count
<50 (azithromycin or rifabutin,
       nuceloside reverse
transcriptase inhibitors (NRTI)
  act as nucleoside analogs,          large amounts of virus are
     non-nucleoside reverse          found in breast milk shortly
     transcriptase inhibitors       after acute infection but once
   (NNRTI) binds to RT and           the acute period is over vial
    disrupts its catalytic site,       shedding in breast milk is
       protease inhibitors           greatly decreased, low CD4
(backbone of therapy) inhibit      count and Vit A deficiency are
 HIV protease enzymes which        associated with increased viral
disrupts cleavage and packing      shedding, viral load is highest
 of the virus (use 2 NRTIs + 1        in acute infection and late
NNRTI + I protease inhibitor),     stages, 1% of peripheral blood
  treat CMV with ganciclovir/      mononuclear cells are infected,
foscarnet/cidefovir, treat MAC      amniotic fluid isn't infectious
  with azithromycin + cipro +
 ethambutal + amikacin, treat
 PCP with trim sulfa (bactrim)
and prednisone, cryptococcus
  treated with ampho + 5FC
    then lifelong fluconazole

 for uncomplicated cystitis
 treat with fluoroquinolone
    (cipro) or doxycyclin/
                               (nonpregnant, non-elderly,
ampicillin (clavulanate), for
                                healthy adult woman) vs.
  complicated cystitis get
                              complicated (all else), more
culture and treat longer (7-
                              common in males during the
   14 days) with the same
                               first 3 months of life but in
  antibiotics, UTI in males
                                females at all other ages
 needs workup to exclude
  structural abnormalities
  14 days of trim-sulfa or       avoid rectal exam because
       quinalones                 it may induce bacteremia

trim-sulf or quinolones for 6-
     12 weeks (difficult)

   14 days of antibiotics
                                 recurrence is common, if
(empirically with ampicillin +
                                  continued fever after 72
  aminoglycoside), should
                                 hours of treatment worry
  improve within 48 hours
                                  about renal abscess or
 and afebrile by day 4, urine
                                     metastatic focus
should be sterile in 2-3 days

                                    usually seen in DM/
   treatment is directed
                                   abnormal urinary tract/
 against G- rods and staph
                                  hematogenous route of
                                  infection (staph aureus)
   treat only symptomatic
    infections with broad-
     spectrum antibiotics,
                              most common nosocomial
change the catheter, use 14
                              infection, more common in
     days of antibiotics if
                                      Foley caths
toxic/bacteremia, if not use
3-5 days of antibiotics, goal
is NOT to sterilize the urine
  treat for 7-10 days with
   amoxicillin, trim-sulfa,
  cephalosporins, goal is
      should always do drug
    susceptibility testing, use
combination of drugs, treatment    surrounded by hydrocarbon
    is lengthened in HIV and    waxes like mycolic acid, isoniazid
    extrapulmonary TB, if low    has a risk of hepatitis, isoniazis
incidence of resistance can use contraindicated in previous INH
     6 months of isoniazid/           hepatotoxicity/ severe
    rifampin/pyrazidamide/             reaction/active liver
   ethambutal, or 9 months of   disease/pregnancy, precautions
       isoniazid/rifampin/      should be taken for patients over
 ethambutal, positive PPD get           age 35/alcoholics
  isoniazid prophylaxis for 9
    Bacteria              Shape Respiration   Found      Virulence factors

                                                         have genus specific
                                                      antigens and heat stable
                                                      LPS (not inflammatory),
                                                         EB is the infectious
                                                       environmentally stable
                                                      particle (lots of disulfide
    Chlamydia              diplo-
                      G-                                   links for stability),
   trachomatis             cocci
                                                       glycosaminoglycan on
                                                             the surface for
                                                       attachment, antibodies
                                                      against chlamydia have
                                                        little protective effect
                                                          against reinfection

                                                       have genus specific
                           diplo-                       antigens and heat
  pneumoniae          G-
                           cocci                         stable LPS (not

                                                       have genus specific
Chlamydia psittaci
                           diplo-                       antigens and heat
 "parrot fever" or    G-
                           cocci                         stable LPS (not
                                                                     uses outer membrane
                                                                      protein A (OmpA) to
                                                  vector is hard
                                                                    stimulate phagocytosis
                                                (wood and dog)
                                                                    or endocytosis to enter
                                                 ticks, reservoir
                              pleo-                                       the host cell,
                                     anaerobic is wild rodents,
Rickettsia Rickettsii   G-   morphic                                    phospholipase to
                                     glycolysis in North (south
                              rods                                        degrade the
                                                 US) and South
                                                                    intracellular motility via
                                                                      actin polymerization

                                                                  uses outer membrane
                                                                   protein A (OmpA) to
                                                vector is mites, stimulate phagocytosis
                                                   reservoir is  or endocytosis to enter
                              pleo-              ticks and rats,       the host cell,
  Rickettsia akari      G-   morphic            associated with      phospholipase to
                              rods                 large urban         degrade the
                                                      areas            phagosomal
                                                    worldwide           membrane,
                                                                 intracellular motility via
                                                                   actin polymerization

                                                                 uses outer membrane
                                                                  protein A (OmpA) to
                                                vector is human
                                                                 stimulate phagocytosis
                                                    body lice,
                                                                 or endocytosis to enter
                                                   reservoir is
                                                                      the host cell,
                                                                    phospholipase to
                              pleo-               squirrel/flea,
    Rickettsia                       anaerobic                        degrade the
                        G-   morphic                  found
    prowasekii                       glycolysis                       phagosomal
                              rods                  worldwide
                                                                    membrane, DOES
                                                                    NOT USE ACTIN-
                                                    regions of
                                                                   BASED MOTILITY,
                                                  Africa, Asia,
                                                                     accumulates in
                                                South America)
                                                                   cytoplasm until cell
                                                                     uses outer membrane
                                                                      protein A (OmpA) to
                                             vector is fleas
                                                                    stimulate phagocytosis
                                              and lice from
                                                                    or endocytosis to enter
                                             rats, reservoir
                          pleo-                                           the host cell,
                                 anaerobic is wild rodents,
Rickettsia typhi    G-   morphic                                        phospholipase to
                                 glycolysis seen worldwide
                          rods                                            degrade the
                                             and temperate
                                            coastal regions)
                                                                    intracellular motility via
                                                                      actin polymerization

                                                 vector is mites,
                          pleo-                    reservoir is
    Orienta                      anaerobic
                    G-   morphic                 rodents, found
tsutsugamushi                    glycolysis
                          rods                    in Asia/India/

                                                  vector is ticks,
                          pleo-                     reservoir is
                         morphic    anaerobic        mammals/       intracellular form is
Coxiella burnetii   G-
                         cocco-     glycolysis     sheep/ goats/ protected from antibodies
                         bacillus                   cattle/dogs,
                                                 found worldwide
                                                                  producing angiogenic
                                                  vector is cat      factor (vascular
                           curved               fleas, reservoir    endothelail growth
                            pleo-                  is cats (or     factor- VEGF) from
Bartonella henselae   G-   morphic    aerobic        dogs),       macrophages/PMNs
                           cocco-                 espeically in  for angiogenesis, stop
                           bacillus             warm climates       host death (inhibit
                                                 (Philippeans)      apoptosis) so the
                                                                   bacteria can survive

                                                                    producing angiogenic
                                                                       factor (vascular
                                                                      endothelail growth
                                                  vector is body     factor- VEGF) from
Bartonella quintana   G-              aerobic   lice, reservoir is macrophages/PMNs
                                                      human        for angiogenesis, stop
                                                                      host death (inhibit
                                                                      apoptosis) so the
                                                                     bacteria can survive
                                                                producing angiogenic
                                                   vector is       factor (vascular
                                                   sandfly,       endothelail growth
                                                 reservoir is    factor- VEGF) from
   Bartonella              cocco-
                      G-              aerobic      human,       macrophages/PMNs
   baciliformis            bacillus
                                                 especially in for angiogenesis, stop
                                                Peru/ Ecuador/    host death (inhibit
                                                  Columbia        apoptosis) so the
                                                                 bacteria can survive

                                                transmitted by
Anaplasmataceae       G-    cocci                ticks, globally

                                                transmitted by
                                                dog ticks/lone
                                                 star tick, wild
                                                  rodents and
                                                    deer are
     Ehrlichia                                     reservoirs,
chaffeensis (family   G-    cocci                    globally
Anaplasmataceae)                                   distributed
                                      transmitted by
                                      ticks, deer are
                       G-   cocci     major reservoir,

                                                         long and skinny, motor
                                           vector is          on each end and
                                       nymph ticks,         endoflagella wraps
                                         reservoir is     around, can travel 10-
                                         mouse/bird/          100x faster than
                                      chipmunk, deer     immune cells in tissue,
                                            are the          can penetrate any
                                        bloodmeal to      tissue, no LPS, only a
                                       keep the ticks    few lipoproteins on the
                                         alive, naïve      outside that are used
Borrelia burgdorferi   G-               ticks feed on     to sense/ adapt to the
                                       infected mice        enviornment, outer
                                           and can       membrane lipoproteins
                                           transmit       (antigenically distinct)
                                           infection         used for immune
                                       (persistance),         evasion, restrict
                                             found       access of antibodies to
                                        worldwide in        integral membrane
                                       the northern         proteins, does not
                                        hemisphere          require metabolic

                                                         long and skinny, motor
                                                              on each end and
                                                            endoflagella wraps
                                       vector is soft
                                                          around, can travel 10-
                                       ticks (sense
                             spiro                            100x faster than
                                      CO2), endemic
 Borrelia hermsii            chete                       immune cells in tissue,
                       G-             in western US
  and duttonii              (spiral                          can penetrate any
                                      and worldwide,
                            shape)                        tissue, no LPS, only a
                                      more common
                                                         few lipoproteins on the
                                      in rustic areas
                                                           outside that are used
                                                                to sense the
                                                      long and skinny, motor
                                                           on each end and
                                                         endoflagella wraps
                                      vector is human
                                                       around, can travel 10-
                                         body lice,
                             spiro                         100x faster than
                                        endemic in
                             chete                    immune cells in tissue,
Borrelia recurrentis   G-               Africa and
                            (spiral                       can penetrate any
                                      South America,
                            shape)                     tissue, no LPS, only a
                                                      few lipoproteins on the
                                                        outside that are used
                                                             to sense the

                                       reservoir is a
                                         variety of
                                      animals, most
     Leptospira              chete                         LPS-like material
                       G-                zoonotic
    interrogans             (spiral                           produced
                                      disease in the
                                         world, not
                                      common in US
                                      except Hawaii

                                                              few surface proteins,
                                                            lipoprotein anchored to
                                                            cytoplasmic memrbane
                                                                (intstead of outer
                                                             memrbane), no lipid A
                                                         (endotoxin), endoflagella (in
                                                        periplasm), coat themselves
                                       humans are the     with host proteins to evade
 Treponema pallidum    G-                only known       immune defenses, virutally
                                          reservoir        no protein exposed on the
                                                           surface, exposed proteins
                                                          (TROMPs treponemal rare
                                                           outer membrane proteins)
                                                          are rare, immunodominant
                                                           proteins are hidden in the
                                                        periplasm, have antigenically-
                                                            distinct surface proteins
                                               only in northern
                                                 vector is tick
                                                   (disease            anti-phagocytic
                                                 correlates w.    capsule, non-endotoxic
                                                  geographic         LPS (LPS tails are
                                                distribution of    tetra-acylated instead
                                               ticks), found in     of hexa-acylated and
                           pleo-   aerobic,         lots of       are longer chains than
   Francisella            morphic fastidious     animals/soil/      normal LPS) doesn't
   tularensis             cocco-    (slow         vegetation/      bind TLR-4 so there's
                           bacilli growth)     water, found in    no cytokine response),
                                                  US in every      intracellular pathogen
                                                   state but             that inhibits
                                                    Hawaii,       phagosome-lysosome
                                                  common in         fusion, escapes into
                                                   Missouri/      the cytosol to replicate

                                                                      lacks capsule and
                                                                    doesn't form spores,
                                                                      has unusal flagella
                                                                     (non-motile), LPS is
                                                                   much less stimulatory
                                                Middle East/
                                                                   than normal LPS (has
                                               Latin America/
                                                                    long acyl chains that
  Brucella ( from                                                   aren't recognized by
                           pleo-                    Africa,
most infectious to                                                       TLR-4, blocks
                          morphic aerobe,      unpasteurized
 least infectious:   G-                                           apoptosis), modified O-
                          cocco- fastidious    milk/cheese, in
melitensis, suis,                                                 antigen blocks antigen
                           bacilli              the US most
  abortus, canis)                                                         presentation,
                                                 common in
                                                                   intracellular pathogen
                                                California and
                                                                          that prevents
                                               Texas (close to
                                                                  phagolysosomal fusion
                                                                  and persists/ multiplies
                                                                       in the endosomal
                                                                  compartment, prevents
                                                                      immune detection
                                           widespread in
                                             nature and
                     coccus     aerobic,                   biofilm formation, via
                                              soil, skin,
                     (short,   fastidious                         pilus and
Acinetobacter   G+                         water, wet and
                     plump       (slow                      exopolysaccharide,
                                            dry surfaces,
                      rods)     growth)                     protective capsule
                                          normal skin and
                                           flora, Iraq and
                What it does                                 Symptoms                     Complications

   transmitted during vaginal/anal/oral sex,
  infects the single-cell columnar epithelial
 layers (endocervix or urethra), multiply and
    spread to surrounding tissues causing
                                                   may be asymptomatic, purulent
    inflammation/redness/ discharge, 2 life
                                                    discharge (green color) from
cycles: infectious and metabolic, elementary                                               can progress to
                                                       penis or cervix, pain on
     bodies (EB) are metabolically inactive                                             salpingitis and pelvic
                                                      urination, inflamed cervix
 infectious forms, reticulate bodies (RB) are                                          inflammatory disease
                                                      (mucopurulent cervicitis),
  noninfectious forms that are metabolically                                            (can cause infertility
                                                   neutrophils seen in gram stain,
       active, EB bind receptors and are                                                     and ectopic
                                                    isolation on tissue culture for
endocytosed where they reside (doesn't fuse                                            pregnancy), can pass
                                                    diagnosis, nucleic acid based
 with lysosome) in host cell surface-derived                                           to infants (infants get
                                                   tests are available but can use
 membrane vacuoles (endosomes), EB then                                                    conjunctivitis or
                                                     direct immunofluorescence
 becomes RB (initial body) which can divide                                                 pneumonia),
                                                   staining or ELISA (both test for
by binary fission, fills vacuole by EB forming                                           lymphogranuloma
                                                        antibodies), must get
an inclusion (developmental cycle takes 24-                                                   venereum
                                                   appropriate epithelial layers (it
   48 hours), intracellular parasite, kills cell
                                                          doesn't live in pus)
    when the emerge, immune response to
       dying cell causes disease, causes
      trachoma/STDs /lymphogranuloma
                venereum (LGV)

transmitted by respiratory secretions, 2
  life cycles: infectious and metabolic,    pear shaped EB with large
        elementary bodies (EB) are          periplasmic space (EBs are
 metabolically inactive infectious forms,     usually round with dense
reticulate bodies (RB) are noninfectious     internal structures), acute
    forms that are metabolically active      respiratory disease (some
intracellular parasite, kills cell when the   cases asymptomatic, or
emerge, immune response to dying cell atypical walking pneumonia),
          causes disease, causes                persistant cough and
       pneumonia/upper respiratory                     malaise,
disease/arthritis/ cardiovascular disease

   contracted by inhaling bird feces or
                                                acute infection in lower
     urine, 2 life cycles: infectious and
                                             respiratory tract (symptoms
  metabolic, elementary bodies (EB) are                                                can spread to liver
                                               for 1-2 weeks), persistent
  metabolically inactive infectious forms,                                                and spleen
                                             non-productive cough, fever,
reticulate bodies (RB) are noninfectious                                                producing focal
                                               chills, shortness of breath,
    forms that are metabolically active                                                    necrosis,
                                                     headache (CNS
 intracellular parasite, kills cell when the                                            hematogenous
                                                involvement), diarrhea,
emerge, immune response to dying cells                                                  spread to other
                                                 increasing confusion,
          causes disease, causes                                                            organs
                                              interstitial pneumonia on x-
psittacosis/abortion/arthritis/heart tissue
  damage cardiovascular disease
                                                 Rocky Mountain Spotted
     maintained in arthropod hosts by
                                                Fever, triad = fever/rash/tick
transovarian transmission, transmitted to
                                                   bite, nausea, vomiting,
 humans by tick bite (tick must attach for
                                               headache, muscle pain, loss
 24-48 hours), infects endothelial cells
                                                 of appetite, viral exanthem
  (invasive) lining the blood vessels
                                                rash appears 2-5 days after
   throughout the body, replicates in
                                               onset of fever, rash starts on
  cytoplasm or nucleus of infected host                                            skin necrosis,
                                                 extremities and is flat/pink/
cell, causes vasculitis with localization in                                         gangrene,
                                                 not itchy, abdominal pain,
        endothelial cells, the major                                               disorientation,
                                               joint pain, diarrhea, petechial
  pathophysiolgoic effect of endothelial                                         cyanotic, seizures,
                                               rash develops, rash involves
      cell injury is increased vascular                                                death
       permeability, causes edema/
                                                 thrombocytopenia, normal
                                                      WBC, petechiae,
    hypoalbuminemia, can also infect
                                                  hepatosplenomegaly, dry
      vascular smooth muscle cells,
                                                mucous membranes, pallor,
 incubation period is 5-10 days after the
                                                     elevated AST/ALT,
                    tick bite
                                                     diagnosed by PCR

    maintained in arthropod hosts by
                                              Rickettsialpox, disease is
transovarian transmission, transmitted
                                                  biphasic: red papule
    by mites, infects endothelial cells
                                            develops at site of bite after 1-
  (invasive), replicates in cytoplasm or
                                             2 weeks incubation (papule
  nucleus of infected host cell, causes
                                             develops into an eschar, get
vasculitis with localization in endothelial                                   low morbidity and
                                              fever as bacteria spreads
cells, the major pathophysiolgoic effect                                          mortality
                                              systemically) and develop
  of endothelial cell injury is increased
                                               irregular fluctuating fever
 vascular permeability, causes edema/
                                               (headache, chills, rigors,
                                             profuse sweating, myalgias,
    hypoalbuminemia, can also infect
                                                   generalized rash)
      vascular smooth muscle cells

     maintained in arthropod hosts by
                                                Epidemic typhus, 1-2 week
transovarian transmission, transmitted to
                                               incubation followed by abrupt
  humans by rubbing lice feces into bite
                                                     onset of headache/
      wounds, infects endothelial cells
                                                  chills/fever/myalgia, rash   Brill Zinsser disease-
   (invasive) and affects small venous/
                                                   develops on upper trunk     relapse of epidemic
      arterial/capillary vessels causing
                                               during day 4-7 and becomes typhus primarily seen
     multiorgan vasculitis, replicates in
                                               generalized (does not involve in immigrants from
  cytoplasm or nucleus of infected host
                                               palms/soles/face), sores that      endemic areas,
cell, the major pathophysiolgoic effect of
                                                become gangrenous (distal       usually milder and
     endothelial cell injury is increased
                                                  extremities), rotting flesh,    shorter duration
  vascular permeability, causes edema/
                                                altered mental status, stupor
                                                 to coma, hypotension and
     hypoalbuminemia, can also infect
                                                          renal failure
       vascular smooth muscle cells
    maintained in arthropod hosts by
transovarian transmission, transmitted
 by lice to humans, infects endothelial
                                             Murine endemic typhus,
cells (invasive), replicates in cytoplasm
                                            same as endemic typhus but
or nucleus of infected host cell, causes
                                            milder, incubation period is 1- can cause severe
vasculitis with localization in endothelial
                                              2 weeks, abrupt onset of      disease in elderly or
cells, the major pathophysiolgoic effect
                                                fever and chills, rash           disabled
  of endothelial cell injury is increased
                                               spreading from trunk to
 vascular permeability, causes edema/
   hypoalbuminemia, can also infect
      vascular smooth muscle cells
                                              Scrub (chigger-borne)
                                            typhus, same as endemic
                                           typhus but milder, 1-3 week
                                               incubation followed by
                                                                        older patients are
                                              abdominal pain/nausea/
transmitted to humans by larval mtie bite                               more likely to have
                                          vomiting/muscle aches, black
                                                                          serious illness
                                            eschar forms at the site of
                                             the chigger bite, regional
                                          lymphadenopathy, rash starts
                                              on trunk and spreads to

     zoonotic infection following exposure to
       livestock (aerosols are main route of
                                                                                     1-2% die, can get
      infection for humans), has a complex
                                                                                    chronic Q fever that
intracellular cycle with 2 cell forms: small-cell
                                                                                   persists for more than
    varient (metabolically inactive, resistant,      Q fever, long incubation,
                                                                                  6 months, endocarditis
      extracellular, attaches to the host cell      sudden onset of high fever/
                                                                                   of aortic heart valves
   membrane to enter phagocytic cells, after        headache/malaise/myalgia/
                                                                                  can develop in chronic
 phagolysosomal formation the pH drops and          confusion/sore throat/chills/
                                                                                   disease (most usually
    causes SCV to become active, acidity is            sweats/non-productive
                                                                                     have pre-existing
  necessary to stimulate nutrients necessary          cough/nausea/vomiting/
                                                                                  valvular heart disease
for its metbaolism, SCV divides to next form) diarrhea/abdominal pain/ chest
                                                                                     or vascular graft),
  and large-cell varient (metabollically active,    pain, fever lasts 1-2 weeks,
    intracellular, replicates until it receives a presents as atypical pneumonia,
 signal to start forming SCV again, protected            can see hepatitis
                                                                                  patients/chronic kidney
from antibodies via location), SCV enters the
                                                                                  disease are more likely
  lungs and LCV proliferates/disseminates to
                                                                                        to develop it
multiple organs, persist in macrophages and
                 disseminate more
                                                  cat scratch disease (in
                                                immunocompetent, papule
                                              develops within 1 week of cat      cat scratch disease
                                                  scratch/bite, fever, tired,          can cause
                                                  headache, no significant             Parinaud's
                                                      bactermeic phase,             oculoglandular
cat-to-cat transmiossion via flea bite (not
                                              lymphadenopathy after a few              syndrome
  ticks!), cat-to-human transmission via
                                                 weeks, self-limiting, more      (conjunctivitis, local
        direct contact/trauma, infects
                                                   common in fall/winter),        lymphadenopathy,
 erythrocytes or endothelial cells, cause
                                                  bacillary angiomatosis            granulomatous
vasoproliferative lesions (angiogenesis),
                                                           (seen in                  inflammation,
 at 5 day intervals bacteria are released
                                                   immunocompromised,            proliferation/dilation
      from the primary niche into the
                                                proliferation of small blood    of BV, coccobacilli in
  bloodstream, bloodborne bacteria can
                                                 vessels, lesions usually in      lesions, no pain or
reinfect the endothelium to start another
                                                skin but also bone/GI tract/     discharge, resolves
 infection cycle, bind to/invade/replicate
                                                  reproductive tract/lymph       in 2-4 months) and
       in erythrocytes (in intracellular
                                                node/CNS, multiple tender             encephalitis/
     membrane-bound compartment),
                                                red vascular nodules, look        myelitis/meningitis
eventually stop replicating and persist in
                                              like Kaposi's sarcoma, fever,     (children 7-12 at risk,
      erythrocytes for several weeks
                                                 chills, malaise, headache,     sudden onset, fever,
                                               anorexia, bacteremic phase          convulsion, rapid
                                               cause BA lesions to form in             recovery),
                                              several organs and mucosa),             endocarditis
                                                       peliosis (seen in

     multiplies in louse intestine and is
   transmitted to humans by lice feces
 through altered skin (not ticks!), infects
                                                                             bacteremia, can
 erythrocytes or endothelial cells, cause
                                               trench fever: recurring        cause bacillary
vasoproliferative lesions (angiogenesis),
                                              cycles of disease, sudden      angiomatosis in
 at 5 day intervals bacteria are released
                                              onset of headache/pain in          immuno-
      from the primary niche into the
                                            shins/fever, between days 3- compromised but is
  bloodstream, bloodborne bacteria can
                                            7 the fever drops, recurrence associated more with
reinfect the endothelium to start another
                                            every 5 days, often results in       bone and
 infection cycle, bind to/invade/ replicate
                                                 prolonged disability         subcutaneous
       in erythrocytes (in intracellular
                                                                             tissues than BA
     membrane-bound compartment),
                                                                           caused by henselae
eventually stop replicating and persist in
      erythrocytes for several weeks
                                              Carrion's disease: biphasic
                                              disease- Oroya fever (acute,
    transmitted by sandflies (not ticks!),      highly fatal febrile anemia,
 infects erythrocytes or endothelial cells,   massive invasion and lysis of
       cause vasoproliferative lesions          RBC via hemolysin, fever,
      (angiogenesis), at 5 day intervals           headache, shin pain,
  bacteria are released from the primary       splenomegaly) and Verruga
 niche into the bloodstream, bloodborne           peruana (chronic, from
 bacteria can reinfect the endothelium to      humoral response, bacteria
      start another infection cycle, bind          colonize the vascular
   to/invade/replicate in erythrocytes (in       endothelium and cause
        intracellular membrane-bound          vasoproliferative eruptions of
        compartment), eventually stop         the skin within 1-2 months of
replicating and persist in erythrocytes for       initial infection, persist
                 several weeks                   months-years), can also
                                               have chronic asymptomatic

  infect different leukocyte populations
   (DO NOT INFECT RBC), remain in
phagocytic vacuoles and prevent fusion
     with the lysosome, divide to form
                                               see 3-15 morulae per cell
    vacuole-bound colonies known as
  morulae, morulae will eventaully lyse
 and kill the cell, bacteria is released to
              infect more cells
                                                 Human Monocytic
   transmitted to humans by the bite of       Ehrlichiosis: symptoms
    infeted ticks that have acquired the     appear 1-21 days after tick
  infection by taking a blood meal from         bite, fever, headache,
  infected wild animals, infect primarily        pharyngitis, nausea,
monocytes (DO NOT INFECT RBC so                 vomiting, dehydration,
                                                                             human brain
   don't see rash), infected leukocytes           lymphadenopathy,
                                                                         infection is rare but
   circulate to cause systemic disease,      splenomegaly, no rash, left
                                                                           this bacteria has
    remain in phagocytic vacuoles and            shift on differential,
                                                                          been observed in
prevent fusion with the lysosome, divide          thrombocytopenia,
                                                                          CSF mononuclear
to form vacuole-bound colonies known leukopenia, anemia, elevated
as morulae, morulae will eventaully lyse      liver enzymes, see 3-15
 and kill the cell, bacteria is released to     morulae with irregular
   infect more cells, immune system is      morphology (intracytoplasmic
supressed due to infection and killing of inclusions) per cell, PCR is
                 leukocytes                  most rapid and specific for
    transmitted to humans by the bite of
                                                 Human Granulocytic
     infeted ticks that have acquired the
                                              Anaplasmosis: symptoms
   infection by taking a blood meal from
                                              appear 1-21 days after tick
   infected wild animals, infect primarily
                                             bite, fever, weakness, pain in
 granulocytes (neutrophils) (DO NOT
                                                leg muscles, dry cough,
      INFECT RBC so don't see rash),
                                               rhinorrhea, fever, intense
  infected leukocytes circulate to cause
                                                aching pain in thighs, no
 systemic disease, remain in phagocytic
                                              cutaneous rash, unsteady,
   vacuoles and prevent fusion with the
                                                 high liver enzymes, low
lysosome, divide to form vacuole-bound
colonies known as morulae, morulae will
                                                RBC/leukocyte, see 3-15
 eventaully lyse and kill the cell, bacteria
                                                morulae per cell, PCR is
is released to infect more cells, immune
                                              most rapid and specific for
system is supressed due to infection and
              killing of leukocytes

                                                                               juvenile arthritis seen
 tick must attach for 2 days to transmit
                                                   Lyme disease, early            in one larger joint
the disease, highly invasive, makes lots
                                                   symptoms (erythema              (knee or elbow)
     of different lipoprotiens which all
                                                 migrans bulls-eye rash          corresponds to re-
  possess the same lipid modification,
                                              caused by an inflammatory             emergence of
 TLR2 recognizes the lipoproteins and
                                                      response to the            spirochetes, Bell's
stimulates the immune system (causes
                                              disseminating spirochetes,             palsy (facial
  damage), diagnosed by presence of
                                               flu-like symptoms, fatigue,            paralysis),
 erythema migrans (large round lesion
                                             malaise, fever, headache, no          radiculoneuritis,
with central clearing, at least 5cm) or at
                                             respiratory complications)              sequela are
   least one subsequent manifestation
                                                 occur days-weeks after        transient, aggressive
          (nervous, cardiovascular,
                                                  infection, late disease        antibiotics treat the
    musculoskeletal) PLUS laboratory
                                             (arthritis, neurologic, cardiac           patient,
evidence of infection (isolation, antibody
                                                complications caused by             disseminated
  by ELISA or western showing 5 of 10
                                             spirochetes disseminating to        erythema migrans,
  antigens, single-tier IgG immunoblot
                                              various organs and tissues)      can get chronic lyme
 seropositivity), may get false positives
                                                occurs weeks-years after          disease (possible
due to cross-reactivity or false negatives
                                                          infection                 autoimmune-
      if antibodies haven't developed

lives in the blood, replicates in blood and
 neural tissue, get high levels of bacteria
 in blood causing a fever spike, immune                                    Jarisch-Herxheimer
   responses clear the spirochetes and      relapsing fever, reoccurring     Reaction occurs
   fever resolves, bacteria change their    fever, malaise, lower fatality when large quantities
  surface proteins (antigenicity) through    rate, increased WBC count      of endotoxins are
      genetic recombination (variable          with left shift (increased    released into the
  membrane protein, VMP), recombined          bands), can diagnose by      body as bacteria die
     bacteria replciate to high numbers              antibody titers          during antibiotic
     causing another fever spike, highly                                         treatment
    invasive, damage from the immune
lives in the blood, replicates in blood and
 neural tissue, get high levels of bacteria
 in blood causing a fever spike, immune                                     Jarisch-Herxheimer
   responses clear the spirochetes and                                        Reaction occurs
   fever resolves, bacteria change their                                    when large quantities
                                            relapsing fever, reoccurring
  surface proteins (antigenicity) through                                    of endotoxins are
                                            fever, malaise, higher fatality
      genetic recombination (variable                                         released into the
  membrane protein, VMP), recombined                                        body as bacteria die
     bacteria replciate to high numbers                                        during antibiotic
     causing another fever spike, highly                                          treatment
    invasive, damage from the immune
                                                                                           small percentage
                                                      Leptosporosis, flu-like               develop Weil's
                                                       symptoms in primary                 syndrome severe
      passed by contact with urine-
                                                      disease, diagnosed by                renal dysfunction
 contaminated water or other materials,
                                                      agglutination of patient                 caused by
spirochete gains access through the skin
                                                     serum, cultured on highly              dissemminated
     or mucous membrane, targets
                                                      enriched liquid or agar              spirochetes (high
                                                      medium (slow-growing                 mortality), can also
                                                         diffuse colonies)                  develop aseptic

                                                                                            cardiovascular disease
                                                                                           (aortic aneurysm, aortic
                                                      low-grade fever, malaise, rash
                                                                                              valve insufficiency),
                                                      (including palms and soles),
                                                                                               neurologic disease
                                                   painless ulcers on genitalia, fever,
                                                                                          (paresis, dementia, tabes
                                                   inguinal lymphadenopathy, pustular
                                                                                                 dorsalis loss of
                                                           cutaneous lesions and
                                                                                          myelinated axons causing
                                                   condylomata lata, primary syphilis
                                                                                              wasting, pain, lack of
spread by sexual contact, very invasive (can reach     (chancres, painless ulcer with
                                                                                          coordination, disorders of
 any part of the body with blood supply), can pass    heaped edges, high number of
   across BV walls between endothelial cells like  spirochetes, neutrophils present are
                                                                                               vision), congenital
       PMNs do, lipoproteins provoke a strong       later replaced by lymphocytes and
                                                                                              syphillus caused by
  inflammatory response causing tissue damage        macrophages, disappear within a
                                                                                            transplacental infection
                                                      few weeks), secondary syphils
                                                                                          (moon's molar, bone and
                                                     (dissemination via blood, flu-like
                                                                                           tooth deformation, heart
                                                    syptoms, rash including palms and
                                                                                              and brain damage),
                                                     soles, condyolmata lata), tertiary
                                                                                            transplacental infection
                                                    syphilis (gummas, granulomatous
                                                                                           doesn't occur in the first
                                                             lesions everwhere)
                                                                                          10 weeks so there's time
                                                                                                  for treatment
                                           acute symptoms for 3-5 days
                                              (flu-like symptoms, fever,
                                              chills, malaise, headache,
  most cases are tick-mediated, rabbits          sore throat, myalgia,
      are the most likely host animals,          anorexia, prostration,
   macrophages and lymphocytes may               erythema nodosum),
 form granulomas, granulomas develop          prolonged disease day 6-
necrotic centers (sometimes caseating), death (cough, chest pain,
    infected macrophages can undergo        liver abnormalities), can get
       apoptosis or travel through the       glandular involvement with
  lymphatics to different tissues/organs,            bubo formation
 can fill the alveolar spaces of the lungs (lymphadenopathy), can get
      and cause problems with oxygen       pneumoic form (most lethal)
                 absorption                    with atypical pneumonia,
                                           pathology is mainly in lymph

                                                incubation from 6-90 days,
                                                   acute form has flu-like
                                                       symptoms (fever,
                                               malodorous sweats, malaise,
infects organs rich in erythritol (palcenta,
                                               headache, anorexia, myalgia,
    epididymis, breast, uterus), smooth
                                               back pain) and occurs within
  phenotype is more virulent and can be
                                                8 weeks from illness onset,
   diagnosed by monoclonal antibodies
                                                   undulant form (fevers,
(agglutination), replicates and perssits in
                                                      arthralgia, myalgia,
    macrophages, diagnosed by blood
                                                epididymo-orchitis in males,   sterility, abortions,
 culture (takes 2 weeks to see growth on
                                                  spontaneous abortions in        asymptomatic
enriched blood agar), colony morphology
                                                     females, neurologic        lifelong carriage,
   and agglutination test (antibodies to
                                                 symtoms) occurs within a             orchitis
     LPS) may cross react with other
                                                 year of onset, and chronic
  organisms, B. canis has rough LPS so
                                                 form (fatigue, depression,
    agglutination is not useful, can also
                                                    arthritis, endocarditis,
   diagnose by specific antibodies (IgM
  eraly or IgG late) but it also has cross-
                                                 lymphadenopathy) occurs
       reactivity, ELISA isn't specific
                                                  after a year of onset, key
                                                 symptoms are undulating
                                                fever, malodorous sweat,
LPS is potent inducer of inflammation
                                        pneumonia, burn/skin/soft
 (strong cytokine response), forms
                                          tissue wounds, UTIs,
          Other notes                  Prevention/Treatment

  rigid refractile inclusions with
      glycogen, susceptible to
                                           beta-lactam antibiotics
 sulfonamides, small, obligate
                                               (penicillins and
  intracellular parasite, human
                                       cephalosporins) don't work
          only disease, no
                                     because they're intracellular,
 peptidoglycan, disulfide linked
                                     tetracylcine for chlamydia but
 EnvB protein gives strength to
                                       also use a cephalosporin to
        the membrane, can't
                                      treat gonorrhea, risk factors:
synthesize ATP, have penicillin
    binding proteins, often see
                                     black/cervical ectopy, annual
coexisting gonorrhea, prevalent
                                          screening is indicated in
   in DC, correlates to college
                                       sexually active women with
     campuses, most females
                                        risk factors (under age 25,
  identified in non-STD clinics,
                                        inconsistent condom use,
       must differentiate from
                                      new sexual partner, multiple
  gonorrhea (gonorrhea grows
                                         partners, cervical ectopy,
 on chocolate or thayer-martin
                                      another STD). tetracycine is
     media and aren't obligate
                                        drug of choice and is only
    intracellular parasites), not
                                     effective against RB because
     seen in gram stain so use
                                       they're metabolically active
          Giemsa stain or

human only, initially isolated
  in Taiwan, small, obligate
   intracellular parasite, no
    peptidoglycan, disulfide
  linked EnvB protein gives    beta-lactam antibiotics
 strength to the membrane, don't work because they're
can't synthesize ATP, have           intracellular
 penicillin binding proteins,
  not seen in gram stain so
      use Giemsa stain or

 small, obligate intracellular
 parasite, no peptidoglycan,
disulfide linked EnvB protein
                                 beta-lactam antibiotics
     gives strength to the
                               don't work because they're
membrane, can't synthesize
                                intracellular, reservoir is
ATP, have penicillin binding
 proteins, not seen in gram
stain so use Giemsa stain or
    zoonotic vector-borne
    disease, humans are             treatment should be
    accidental hosts, stain    started early and based on
     poorly by gram stain         clinical/epidemiologic
  (minimal peptidoglycan),       presentation, Weil-Felix
 use Giemsa stain (nuclear           test detects RMSF
  stain), small, grow only in seroconversion but cross-
   cytoplasm of host cells,     reacts with Proteus, PCR
      have LPS, obligate           is quickest and most
 intracellular parasites (rely     specific, can only be
   on host for ATP), worse        cultured in host cells,
 outcomes associated with        tetracyclines are DOC
 age/men/african american/           (doxycycline), no
     alcohol abuse/G6PD              vaccine, avoid tick
deficiency, more common in                exposure

 stain poorly by gram stain
  (minimal peptidoglycan),
use Giemsa stain (nuclear
 stain), small, grow only in
                                doxycycline is DOC
   cytoplasm of host cells,
     have LPS, obligate
intracellular parasites (rely
      on host for ATP)

  occurs in cold climates,
  overcrowded unsanitary
 conditions, stain poorly by
    gram stain (minimal
peptidoglycan), use Giemsa
stain (nuclear stain), small,
 grow only in cytoplasm of
   host cells, have LPS,
    obligate intracellular
 parasites (rely on host for
  stain poorly by gram stain
   (minimal peptidoglycan),
 use Giemsa stain (nuclear
  stain), small, grow only in
    cytoplasm of host cells,
      have LPS, obligate
 intracellular parasites (rely
       on host for ATP)

                                         most patients resolve
                                        infection within several
                                      months without treatment,
                                          diagnosis based on
                                       serological test to detect
obligate intracellular pathogen,     antigens, 2 phases: phase 1
   small, gram stains poorly,          (natural form in infected
stains with Giemsa, known for          animals, corresponds to
 infecting farm animals, ticks            smooth LPS, highly
   are an important vector for      infectious) and phase 2 (less
      transmission between            infectious, corresponds to
 ANIMALS, humans acquire it         rough LPS), in acute Q fever:
  from animals who shed it in        antibody level to phase II is
feces/urine, resistant to killing    higher than phase I and can
    in nature (spore-like SCV         be detected during the 2nd
form), associated with farmers       week of illness, in chronic Q
       (lambs), animals are          fever: antibodies to phase I
 asymptomatic, bioterrorism            antigens indicate chronic
              agent!                     exposure to antigens,
                                      doxycycline is DOC, treat
                                     within first 3 days of illness,
                                      chronic requires months of
                                        treatment, vaccine not
                                           currently available
 zoonotic species, cats are
more likely to be infected in
    warm humid climates,
  poorly staining, stain with
     Warthin-Starry silver
staining (dark coccobacilli),
      fastidious (grow on
                                   cat scratch fever is
    chocolate/blood agar,
                                ususally self-limiting and
  requires hemin, takes 14
                                  antibodies produced
days to see colonies), small
                                  during infection are
 white irregular colonies on
       agar, not obligate
                              immunocompromised with
    intracellular parasites,
                                 bacillary angiomatosis
  asymptomatic in animals,
                               treated with erythromycin
 persist in host cells (often
                                     for 2-4 weeks
  WBC) and host immune
 response causes disease,
  maintained in animal and
     arthropod reservoirs,
 bacillary angiomatosis can
also be cause by bartonella

  human-specific species,
  more common in people
with poor personal hygeine,
  poorly staining, stain with
     Warthin-Starry silver
staining (dark coccobacilli),
      fastidious (grow on
    chocolate/blood agar,
  requires hemin, takes 14      erythromycin or
 days to see colonies), not doxycycline for 2-4 weeks
     obligate intracellular
 parasites asymptomatic in
animals, persist in host cells
    (often WBC) and host
 immune response causes
   disease, maintained in
    animal and arthropod
  human-specific species,
  poorly staining, stain with
     Warthin-Starry silver
staining (dark coccobacilli),
      fastidious (grow on
    chocolate/blood agar,
  requires hemin, takes 14
 days to see colonies), not chloramphenicol, penicllin,
     obligate intracellular    erythromycin, doxycycline
 parasites asymptomatic in
animals, persist in host cells
    (often WBC) and host
 immune response causes
   disease, maintained in
    animal and arthropod

 small, stain poorly, obligate
intracellular pathogens, lack
   LPS and peptidoglycan,
 pathogens of humans and

 small, stain poorly, obligate
    intracellular pathogens
(can't culture), lack LPS and
peptidoglycan (don't activate
  TLR or immune system),
 pathogens of humans and        recovery is very slow,
    animals, no transovarial tetracyclines (doxycycline),
transmission from mom tick      no vaccine, avoid tick
   to baby tick, humans are            exposure
     accidental hosts (not
 needed for life cycle), more
common in April-September
 (tick-borne), reported rates
       increase with age
  found frequently in states
     that also have a high
 incidence of Lyme disease
    Massachusettes, NY,
   Minnesota, Wisconsin),
  often see coinfection with
                                  doxycycline, recovery is
 Lyme disease, small, stain
                                  slow, no vaccine, avoid
poorly, obligate intracellular
                                       tick exposure
  pathogens (can't culture),
lack LPS and peptidoglycan
   (don't activate TLR and
      immune response),
 pathogens of humans and
  animals, more common in
spring/ summer (tick-borne)

       have inner and outer
                                 prevented by avoiding tick
membrane and thin layer of
                                 habitat/wearing protective
    peptidoglycan but don't
                                    clothing/ surveying for
gram stain, #1 vector-borne
                                   ticks on body/consuling
  illness in the US, can't be
                                       physician after tick
 passed from mom to baby
                                       bite/manage deer
       tick (no transovarial
                                 population and movement,
    transmission), deer and
                                        treated with oral
       humans aren't good
    reservoirs, Lyme cases                doxycycline/
   correlate with acorn and       amoxicillin/cefuroxime
     deer population, more        axetile for a few weeks,
     common May-August,              neurological/ cardiac
  young and old get it more           sequelae require IV
      frequently, men more           ceftriaxone/penicillin,
     common than women,            patients diagnosed late
 linear chromosome with           may require a second 4-
 21 plasmids (circular and        week course of therapy,
                                     longer courses aren't
linear) with unique genes,
                                 beneficial and may cause
   obligate parasite, treat
                                   more complications (C.
  pregnant women like all
                                        diff), no vaccine
          other patients

   have inner and outer
membrane and thin layer of
  peptidoglycan but don't
gram stain, more common
May-August, young and old
                                   penicillins for 7 days
get it more frequently, men
more common than women
   have inner and outer
membrane and thin layer of
  peptidoglycan but don't
gram stain, more common                        tetracyclines
May-August, young and old
get it more frequently, men
more common than women

  shed in urine of infected
                                         tetracyclines or beta-
host, may be asymptomatic,
associated with watersports

                                            diagnosed by rapid plasma
no known animal reservoir, can't be
                                               reagin (RPR) titer with
grown on lab media, grows in rabbit
                                        confimation by serology or PCR,
testes but no disease in rabbits, no
                                            cardiolipin found in sera of
 animal model, easily detected and
                                            infected patients but is just
    treated, most common in men
                                          caused by lysis of mammalian
ages 25-45, sexual orientation isn't
                                       cells, treponemes bind cardiolipin
  a determining factor, milder more
                                         and antibody response follows,
 chronic disease (trade-off model),
                                          use flocculation tests (purified
    origins in African skin disease
                                                cardiolipin mixed with
 called yaws (T. pallidum pertenue)
                                          dispersants, clumps appear in
  which is spread by direct skin-to-
                                         presence of cardiolipin-specific
skin contact (have cross-immunity),
                                       IgA/IgM reagin), flocculation tests
   grow slowly, can be eliminated
                                       are cardiolipin-based and include
 (humans are only host, incubation
                                          RPR/VDRL (venereal disease
      period allows prophylaxis of
                                        research labs)/TRUST (toluidine
 contacts, infectiousness only lasts
                                             red unheated serum test),
    1 year, inexpensive diagnosis,
                                           confimed by TPI (T. pallidum
      cured with a single dose of
                                        immobilization)/FTA (fluorescent
       antibiotics, no beta-lactam
                                         treponemal antibody)/TPHA (T.
  resistance), more skewed toward
                                         pallidum hemagglutination), no
   people living in poverty so less
                                            vaccine, treated with beta-
 attention from drug companies etc
                                                lactams (penicillin)
zoonotic, can be transmitted
 by arthropod vectors, non-
motile, cultures grow poorly,
    intracellular pathogens,
     diagnosed by antibody        culture of scrapings or
agglutination assays, risk of   serology used to confirm
    lab-acquired infections,      diagnosis, treated with
      bioweapon potential,            doxycycline or
        persistent in the       ciprofloxacin (levo is ok
  environment, non-spore-        too), don't use ampicillin
forming, 4 subspecies: type          (beta-lactams are
      A (most virulent, low    ineffective), live attenuated
   infectious dose, found in     vaccine is being studied
 North America) and type B          but is not available
(less virulent, found in North
  Europe/Russia/Asia, most
       cases in May-July

zoonotic, can be transmitted
 by arthropod vectors, non-
                                  treat with 2 antibiotics
motile, cultures grow poorly,
                                      (doxycycline and
   intracellular pathogens,
                                   rifampin) for 6 weeks
    diagnosed by antibody
                                 (rifampin doesn't work in
agglutination assays, risk of
                                    the dog strain used in
   lab-acquired infections,
                                vaccines, so veterinarians
bioweapon potential, causes
                                get doxy and streptomycin
     similar sypmtoms in
                                  for 3 weeks followed by
   goats/sheep/cattle, can
                                       tetracycline and
 persist in the environment,
                                streptomycin for 6 weeks),
     most common world
                                       gold standard for
   zoonosis, no person-to-
                                diagnosis is bone marrow
  person spread, extremely
infectious, more common in
        Hispanic men
   resistant to multiple
                               perform antimicrobial
antibiotics (beta-lactams,
                               susceptibility testing,
                                 sulbactam (beta-
quinolones, tetracyclines,
                             lactamase inhibitor) with
                                 ampicillin, colistin
      Drug               Class                   Mechanism                         Spectrum
                                        inhibit phospholipase A2 from
                                       releasing arachidonic acid from
                                             the membrane (blocks
                                        prostaglandin and leukotriene
                                          synthesis at this step), also
                                         block the induction of COX-2
                                           (cyclooxgenase that helps       short-term treatment of
                                           covert arachidonic acid to      inflammatory diseases
                     corticosteroids        prostaglandins --> blocks       (rheumatoid arthritis),
                                            prostaglandin synthesis),    given to transplant patients
                                        corticosteroids act by diffusing   to reduce inflammation
                                        across the plasma membrane
                                             and binding to specific
                                       receptors in the cytoplasm, the
                                         steroid receptor with steroid
                                         bound can enter the nucleus
                                          and alter gene transcription

                                                                            treatment of suspected
                                       cyclooxgenase inhibitors, blocks
                                                                            acute MI, prevention of
                                         the conversion of arachidonic
                                                                          arterial throbosis, eliminate
                                            acid to PGH2 --> blocks
                                                                           symptoms of rheumatoid
                                       prostaglandin synthesis, aspirin
                                                                           arthritis and osteoarthritis
                                        blocs COX-1 irreversibly, other
      aspirin,                                                            but don't alter the course of
                                             NSAIDs block COX-1
  indomethacin,         NSAIDs                                                  the disease, labor
                                           reversibly, prevents heart
     ibuprofin                                                             prevention (tocolysis) by
                                          attacks/strokes by inhibiting
                                                                            blocking uterine PGE2
                                            platelet aggregation (by
                                                                          syntehsis (delays the onset
                                            blocking platelet COX-1
                                                                           of labor), indomethacin is
                                            dependent thromboxane
                                                                           used to close the ductus
                                                                             arteriosis in neonates
                                                            prevention of
                       analog of a PGE1 derivative    gastirc/duodenal ulcers
                     that acts as an agonist at PGE2 in patients taking NSAIDs,
                     receptors, increases mucus and       cervical ripening,
misoprostol (PGE1)      bicarb secretion by gastric  termination of pregnancy
                     mucosa, decreases acid/pepsin     prior to the 49th day or
                       secretion by gastric parietal   pregnancy (when used
                        cells, increases blood flow      with antiprogestin

                                                         maintains blood flow
                                                          through the ductus
                                                         arteriosus (vessel that
                                                          diverts blood from the
                                                         pulmonary artery to the
                        vasodilation, relaxation of
                                                        aorta) in the last week of
                      smooth muscle of the ductus
alprostadil (PGE1)                                       pregnancy, and can be
                     arteriosis, increased blood flow
                                                       used to keep the DA open
                      to the penis treats impotence
                                                             in neonates with
                                                      pulmonary artery blocakge
                                                      so that blood can still get to
                                                      the lungs, also used for the
                                                        treatment of impotence

                                                       cervical ripening (cervix
                       effects cervix structure and
                                                         softens and becomes
                        contracts uterine smooth
                                                       distensible in preparation
                     muscle to prepare the uterus for
   dinoprostone                                         for labor), prevention of
                      labor, relaxes the cervix and
      (PGE2)                                             post-partum bleeding,
                      activates collagenase which
                                                      termination of pregnancy in
                      breaks down collagen in the
                                                            the 2nd trimester

                                                        inhibition of post-partum
                       contraction of uterine smooth
    carboprost                                           bleeding, termination of
                       muscle and vasoconstriction
(PGFalpha2 analog)                                        pregnancy in the 2nd
                      leads to decreased blood loss

                                                       used for pulmonary artery
                                                        hypertension (primary or
                        produces vasodilation and
                                                             associated with
                          inhibits clot production,
 prostacyclin/PGI2                                      scleroderma), antiplatelet
                        vasodilation of pulmonary
  (epoprostenol)                                       action used for inhibition of
                        arterial vascular beds and
                                                        blood coagulation during
                     inhibition of thrombosis in lungs
                                                        extracorporeal ciculation
                                                          (heart/lung machine)
                                               increases the drainage of
                                              aqueous humor from the eye
   latanoprost                                  via the uveoscleral route      treatment of opan angle
(PGF2alpha analog)                             through the ciliary muscle             glaucoma
                                                lowering the intra-ocular

                                                    inhibits cGMP
                                               phosphodiesterase type 5
 sildenafil (Viagra)                             (PDE5), blocking the           treatment of impotence
                                              breakdown of cGMP causes
                                               smooth muscle relaxation

                                               inhibits the function of NFkB
                                               which is a transcription factor
                                                   responsible for cellular
                                                  activation and cytokine
                                                 production in the immune
                                              response, NFkB is held in the
                                               cytoplasm in association with
                                              IkBa, upon cellular activation,
                                             IkBa becomes phosphorylated
                                              allowing NFkB to initiate gene immunosuppression, drug
      steroids                                 transcription, corticosteroids of choice for treating acute
                                                 increase IkBa production         transplant rejection
                                              preventing NFkB from gaining
                                                 access to the nucleus and
                                              preventing the upregulation of
                                                proinflammatory genes, this
                                             blocks the IL-1 signal from the
                                             APC that activates the T helper
                                             cell to secrete IL-2, suppresses
                                              the inflammatory and immune
                                               binds intracellular protein
                                           cyclophilin on T lymphocytes to
                                               form complexes that bind
                                            calcineurin (calcineurin usually
                                           activates transcription factor IL-
                                                 2), prevents calcineurin
                                            activation by Ca2+ and blocks
                                               activaiton of NFAT which
                                            normally forms a transcription
  cyclosporin A       immunosuppressant         factor that activates IL-2      immunosuppression
                                            secretion, cyclosprin prevents
                                           the dephosphorylation of NFAT
                                            by binding to cyclophilin block
                                            the IL-2 production from the T
                                           helper cell to prevent activation
                                            of cytotoxic T cells, inhibits T-
                                            cell activation by disrupting
                                             the transduction of signals
                                                      from the TCR

                                         bind intracellular protein FKBP
                                            (FK-binding proteins, aka
                                             immunophilins) to form
                                        complexes that bind calcineurin,
                                         prevents calcineurin activation
                                         by Ca2+ and blocks activaiton
tacrolimus (Prograf       macrolide     of NFAT which normally forms a
    or FK-506)        immunosuppressant      transcription factor that
                                         activates IL-2 secretion, block
                                         the IL-2 production from the T
                                         helper cell to prevent activation
                                        of cytotoxic T cells, suppresses
                                        T-cell activation by inhibiting
                                        calcineurin (and inhibits IL-2)

                                            binds FK-binding proteins like
                                             tacrolimus, but blocks T-cell
                                             activation at a later stage by
    rapamycin             macrolide         preventing signal transduction
    (sirolimus)       immunosuppressant     from the IL-2 receptor (blocks
                                           cytokine signal), block cytotoxic
                                              T-cells from proliferating in
                                                    response to IL-2
                                         prevents cell proliferation by
                                        acting as a purine antagonist,
                                         also blocks cytotoxic T-cells
                                      from proliferating in response to
mycophenolate         antimetabolite
                                        IL-2, blocks de novo purine          immunosuppression
mofetil (MMF)       immunosuppressant
                                      synthesis by inhibition of the
                                               enzyme inosine

                                                                         immunosuppression, can
                                           prevents proliferation of
                                                                        be used to treat cancers as
 cytotoxic drugs    immunosuppressant activated immune cells by killing
                                                                        well (in combo with a bone
                                        all rapidly proliferating cells
                                                                             marrow transplant)

                                      azathioprine is a pro-drug that is
                                            converted in vivo to 6-
                                       mercaptopurine and then to 6-
                                       thioinsoinic acid which inhibits
                                        the production of inosinic acid   immunosuppression in
  Azathioprine           cytoxoic
                                      (intermediate in the synthesis of solid organ transplantation
                                            adenine and guanine
                                          nucleotides), inhibits DNA
                                         replication by blocking de
                                           novo purine synthesis,
IL-2 receptor and
                    immunosuppressant     interfere with T-cell activation   immunosuppression
TCR antagonists
                                         anti-CD3 antibody that prevents
                                          TCR signaling and activates
     OKT3           immunosuppressant                                        immunosuppression
                                          complement, targets ALL T-
anti-IL2 receptor
                    immunosuppressant      only targets activated T-cells    immunosuppression

                                          block the effects of histamine
                                                                         allergy treatment, sleep-
                                         mediated by the H1 (but not H2)
diphenhydramine                                                            aids, alleviate rhinitis,
                        H1 Blocker          receptors by competitively
   (Benadryl)                                                             antinausea/antiemesis
                                         antagonizing the binding of H1
                                                                         effects (motion sickness)
                                                terfenadine undergoes
  terfenadine and                           extensive first-pass hepatic/GI
                                                                                approved for seasonal
    fexofenadine          H1 Blocker        CYP-3A4 dependent oxidation
                                                                                   allergic rhinitis
      (Allegra)                               to produce the active drug

                                                                            loratadine is only approved
  loratadine and                            loratidine undergoes extensive for seasonal allergic rhinitis
   desloratadine                             first-pass hepatic/GI CYP-3A4     while desloratadine is
                          H1 Blocker
    (Claritin and                           dependent oxidation to produce     approved for seasonal
     Clarinex)                                 the active drug desloratadin      allergic rhinitis and
                                                                              perennial allergic rhinitis

                                                                               seasonal use down to age
 cetirizine (Zyrtec)      H1 Blocker                                           2 and perinneal use down
                                                                                   to age 6 months

                         physiological       induces vasoconstriction and        used in asthma and
                          antagonist                bronchodilation                 anaphylaxis
                                            cytokines activate the immune
                                               system, for example IFN-
                                             alpha/IL-2 expand the NK cell      IFN-alpha/IL-2 used in
 cytokine therapy         anti-cancer       population and are effective on     melanoma in renal cell
                                                tumors that lower MHC                 carcinoma
                                             expression, can trigger tumor
                                                     cell apoptosis
  VEGF (vascular
                       anti-cancer, anti-
 endothelial growth                           cuts off blood flow to tumor
  factor) inhibitor
                                            recognizes proteins expressed
                                            on tumors (tumor antigens) and
                                               marks for opsonization by
monoclonal antibody                          phagocytes, can also deliver
     therapy                                 radiation or chemical therapy
                                            binding to and killing the tumor
                                            cell, or can block growth factor
                                         CD20 binds to B cells at specific
                                          developmental stages, blocks
                                         growth factor receptors inducing non-Hodgkin lymphoma,
                    anti-CD20 monoclonal    cytotoxicity or apoptosis,     can also be used in SLE/
Rituximab (Rituxan)
                           antibody       depletes all B cells (good and RA/scleroderma to get rid
                                               bad), hope that body        of autoreactive antibodies
                                             replenishes with normal

                                             inhibits cell growth, conjugate
                                                 monoclonal antibody to
                       anti-CD33 monoclonal chemical or radioisotope that is        acute myelogenous
                              antibody        site specific, radiation is only        leukemia (AML)
                                              delivered to cells expressing
  Hep B vaccine/
                                               vaccines for tumors caused by
  Gardasil (HPV           cancer vaccine
                                               enters via cytosine permease,     fungicidal, no cytosine
5-fluorocytosine (5-                          deaminated to 5-fluorouracil (5- deaminase in human cells
        FC)                                       FU), 5-FU inhibits RNA           so it targets fungi
                                              translation and DNA synthesis            specifically

                                              bind to ergosterol and form ion
                                              channels in fungal membranes,
  Amphotericin B        polyene anti-fungal    the permeability of the fungal            fungitoxic
                                                 cell wall is altered and the
                                                 intracellular contents leak

                                              bind to ergosterol and form ion
                                              channels in fungal membranes,
                                                                                 fungitoxic, mucosal or GI
     Nystatin           polyene anti-fungal    the permeability of the fungal
                                                 cell wall is altered and the
                                                 intracellular contents leak

   Miconazole,                                 inhibit lanosterol demethylase       fungistatic, candida
  Ketoconazole,               azoles              which inhibits ergosterol      species and cryptococcus
   Fluconazole                                             synthesis                   neoformans

                                                                                     fungistatic, candida
  Itraconazole,                                inhibit lanosterol demethylase       species/cryptococcus
  Voriconazole,               azoles              which inhibits ergosterol        neoformans/aspergillus/
  Posaconazole                                             synthesis                    blastomycosis/
                                                 inhibit squalene epoxidase      fungistatic/fungitoxic, good
                            allylamines            which inhibits ergosterol          for dermatophytes
(Lamisil), naftidine
                                                            synthesis               (ringworm infections)
                                                    inhibit beta(1,3) glucan
                                                                                     used for invasive
   caspofungin,                                 synthetase which inhibits the
                          echinocandins                                          aspergillosis and mucosal
    micafungin                                    formation of carbohydrate
                                                   polymers in hyphal walls
                                               interferes with microtubule and
                                                   spindle formation during       slow acting drug used for
                                                   mitosis, prevents hyphal        skin and nail infections
                                                penetration through skin/nails
 Whitfield ointment                                  acidifies the fungus
                                                 interferes with the action of
   trimethoprim-                                    bacterial dihydrofolate
                                                                                   pneumocystis jiroveci
 sulfamethoxazole                                  reductase, inhibiting the
                                                synthesis of tetrahydrofolate
AZT, 3TC, ddC, ddI,
                      nucleoside reverse     works at level of nuclear viral
  d4T, tenafovir,
                    transcriptase inhibitors       replication, act as
                            (NRTI)           nucleoside/nucleotide analogs
                                              works at enzymatic level and
    nevirapine,           non-nucleoside
                                                  binds to the reverse
    delavirdine,      reverse transcriptase
                                            transcriptase enzyme disrupting
efavirenz, etravirine   inhibitors (NNRTI)
                                                    the catalytic site

saquinavir, ritonavir,
indinavir, nelfinavir,
                                               inhibits HIV protease enzymes
                         protease inhibitors    which disrupts cleavage and
lopinavir, tipranavir,
                                                    packaging of the virus

                                               both prevent HIV entry into CD4
 fuseon, maraviroc        entry inhibitors        cells, maraviroc is a CCR5
                                                    coreceptor antagonist
                                                stops HIV from integrating into
     raltegravir         integrase inhibitor
    Administration        Clearance         Adverse effects             Contraindications

prednisone is reduced
in the liver to produce
  the active drug and
                                        can't be given long-term
can therefore only be
                                           because it is toxic
      used orally,
can be give orally/IM/

                                        GI effects especially if the
                                       patient drinks alcohol, PGE2
                                         normally protects gastric
                                        mucosa and increases GI
                                                                        aspirin shouldn't be
                                      motility, NSAIDs block PGE2
                                                                       given in patients with
                                        synthesis which increases
                                                                          active bleeding,
                                         H+/pepsin secretion and
                                                                        hemophilia or other
                                        decreases mucus/HCO3-
                                                                         blood coagulation
  for delaying labor:                   secretion, this can lead to
                                                                         disorders, hepatic
 indomethacin given                    bleeding/gastric or duodenal
                                                                       disease (liver makes
  rectally 50-100mg                          ulcers/perforation,
                                                                      clotting factors), renal
followed by 25-50mg                   dyspepsia, nausea, vomiting,
                                                                     disease, or active peptic
 orally every 6 hours                   damaged gastric mucosa,
                                                                     uclers, aspirin should be
     for 2-3 days                     can cause premature closing
                                                                        avoided in the last
                                         of the ductus arteriosis in
                                                                      weeks of pregnancy to
                                      fetuses during the last weeks
                                                                      avoid excessive post-
                                         of pregnancy, can cause
                                                                      partum blood loss and
                                           acute renal failure by
                                                                         the tocolytic effect
                                          inhibiting prostaglandin
                                        synthesis (prostaglandins
                                       normally act to preserve the
    1/4 100mg tablet
   inserted vaginally
   every 4 hours for
   cervical ripening,     stimulation of GI motility and
600mg of mifepristone           secretion cause
                                                           pregnancy (causes
administered on day 1      diarrhea/nausea/vomiting/
                                                           uterine contraction)
 and 400 micrograms        abdominal cramping, also
    of misoprostol is        cause uterin contraction
administered on day 3
  for abortion of early

   administration to      hypotension, priapism, penile
 maintain the ductus        pain, Peyronie's disease
    arteriosis, local        (stimulate fibrosis from
  administration for          injections into penis)
 treating impotence

   endocervical gel
  0.5mg via cervical
catheter and syringe,
   or a retrievable        increases GI motility which
    vaginal insert        can cause nausea/vomiting/
 containing 10mg of       diarrhea, hyperstimulation of
  PGE2 released at                 the uterus
0.3mg/hr for 12 hours
 (can be removed if
 active labor occurs)

                          GI effects, nausea, vomiting,
                                 diarrhea, fever,
  single IM dose of
                          vasoconstriction can cause
                           increased blood pressure
                            and bronchoconstriction

                           flushing, hypotension, GI
                           effects (nausea, vomiting,
continuous IV infusion
                                diarrhea), abrupt
 because of its short
                           discontinuation can cause
half life (3-6 minutes)
                               rebound pulmonary
                               increased brown
topical administration     pigmentation of the iris,
      once daily             increased growth of

                                                          drug interactions with
                                                              organic nitrates
                                                             nitroglycerine) for
                                                        treatment of angina can
                          headache, flushing, rhinitis
                                                          cause a rapid drop in
                           due to vasodilation, fall in
                                                          BP, drug interactions
                              BP, heartburn due ot
                                                          with alpha-adrenergic
                             relaxation of the lower
         oral                                            antagonists can cause
                          esophageal spincter, visual
                             distrubances (PDE6),
                                                            hypotension, drug
                         prolonged erection (4 hours),
                                                         interactions with drugs
                          priapism (6 hours), myalgia
                                                            that inhibit cyp3A4
                                                        increase the risk of side
                                                         effects by increase the
                                                         bioavailability and half-
                                                              life of the drugs

                           cause diabetes, thinning
                         skin, alopeica, hypertension,
                              avascular necrosis,
                         osteoporosis, fluid retention,
                          weight gain, losss of bone
 nephrotoxic because they
     suppress B cell and
   granulocyte activation,
hypertension, neurotoxicity,
 hyperglycemia, hirsutism,
    gingival hyperplasia,
gynecomastia (abnormally
  large mamarry glands in
 men), lowers magnesium

 nephrotoxic because they
    suppress B cell and
   granulocyte activation,
hypertension, neurotoxicity,
  hyperglycemia, does not
  cause hirsutism/gingival
      low magnesium

more toxic than cyclosporin
     A and tacrolimus,
 hypercholesterolemia, NO
                      NO NEPHROTOXICITY!!,
                      less bone marrow toxicity
                       than AZA but still some
                        digestive tract toxicity

                     anemia, leukopenia, diarrhea

                       damage to bone marrow/
                       intestinal epithelium/hair
                      follicles leading to anemia,   pregnant women (fetal
                               leukopenia,               development is
                     thrombocytopenia, diarrhea,       adversely affected)
                         and hair loss, but NO

                     sedation (can be sold as an
                       OTC sleep-aid), develop
                     tolerance but non-addictive,
                           anticholinergic and
                      antimuscarinic effects (dry
  half-life is 8.5      passage, blurry vision,
hours with effects        tachycardia, urinary
lasting 3-6 hours        retention, GI effects,
                       constipation), posioning/
                           overdose leads to
                                                                            certain antifungals
                                                                        itraconazole), antibiotics
                                            NO sedation, can get drug      clarithromycin), and
                     long half-life (12-24 interactions because it uses     grapefruit juice can
                       hours per dose)         CytP450 (can induce        inhibit the oxidation of
                                                    arrhythmias)         terfenadine allowing it's
                                                                           accumulation which
                                                                             blocks cardiac K+
                                                                          channels and induces

                                            some sedation at high
                                              doses, can get drug
                   long half-life (12-24
5-10 mg once a day                       interactions because it uses
                     hours per dose)
                                             CytP450 (can induce

 5mg once a day       half-life is 8 hours          some sedation

                                              flu-like symptoms, fatigue,
                                             takes a long time to respond

                                               kills normal cells too which
                                             leads to loss of normal tissue
                                                  and local inflammation
                                               get B cell depletion and no
                                               humoral immune response,
                                               kills all cells expressing the
                                                        CD20 antigen

                                               lots of accessory damage
                                               because surrounding cells
                                                        are killed

                                               bone marrow suppression
                                                     and alopecia

   intravenously or                               fever, chills, myalgia,
intraperitoneally (for                                nephrotoxic,
  systemic candida                             thrombophlebitis, anemia,
       infections)                              long-term administration

not absorbed so used
 topically for mucosal
   infections or used
    orally to treat GI
 infections (Candida)

 oral absorption and                              antiandrogenic effect,
solubility is optimal at                         adrenal supression and
  acidic gastric pH                                    dysfunction

                           metabolism is cyt
                    photosensitivity, mental
                   confusion, bone marrow
                   suppression, induces cyt
                  may be caustic, not possible
applied locally
                       to use systemic


                  peripheral neuropahty and
                  pancreatitis (DdI and d4T),
                  macrocytic anemia (AZT),
                   abacavir can cause fatal
                   hypersensitivity reaction

                  rash, efavirenz also causes
                      severe birth defects

                     ritonavir causes n/v/d,
                         indinavir causes
                     hyperbilirubinemia and
                    kidney stones, nelfinavir
                    causes diarrhea, all can
                      cause acute onset of
                    diabetes and significant

  prednisone is a synthetic
derivative of hydrocortisone
   or cortisol (the principle
steroid made by the adrenal
cortex), prednisone is a pro-
   drug with no biological
activity until it's converted in
     vivo to prednisolone

  selective COX-2 inhibitors
  are better for inflammation
  because COX-2 is directly
 involved in the process (but
 these inhibitors have worse
     side effects, like heart
   attacks), aspirin inhbibits
   platelet cyclooxygenase
    irreversibly even at low
 doses, NSAIDs don't cause
impotence because there are
 other mechanisms of sexual
      arousal (nitric oxide)
    longer half-life (20-40
 minutes) than epoprostenol
 (PGI2), is a prodrug that is
   activated by esterases,
 alternative to dinoprostone
 for cervical ripening but not
FDA approved (works faster,
       less expensive)

     longer half-life than
  dinoprostone, not drug of
choice to inhibit post-partum
  bleeding (only used when
oxytocin or methylergonovine

can be absorbed through the
          GI tract

   decreases synthesis of
prostaglandins, leukotrienes,
cytokines, platelety activating
      factor, neutrophil
   chemotactic factor, and
eosinophil chemotactic factor
   high cyclosporin levels
correlates with high toxicity,
   low cyclosporin levels
 correlates with transplant
 rejection (need balance!),
  used synergistically with

get synergy when combined
     with cyclosporin A
 cells must be attempting to
   replicate tehir DNA for
  azathioprine to work, only
 given after transplantation
    because the patient's
  immune system must be
stimulated by alloantigen for
       the drug to work

  older antihistamine, has a
   positive charge due to a
 weak basic group, lipophilic
with aromatic rings, can enter
 the CNS and cross the BBB
 newer antihistamine (more
selective for H1 so fewer side
 effects, fewer CNS effects
 due to lower lipid solubility,
  fewer antimuscarinic side
effects, longer half-life), more
   substituents on the weak

 newer antihistamine (more
selective for H1 so fewer side
 effects, fewer CNS effects
 due to lower lipid solubility,
  fewer antimuscarinic side
effects, longer half-life), more
   substituents on the weak

 newer antihistamine (more
selective for H1 so fewer side
 effects, fewer CNS effects
 due to lower lipid solubility,
  fewer antimuscarinic side
effects, longer half-life), more
   substituents on the weak

 different response rates for

naked monoclonal antibodies
  are good for non-immune
cancers because they kill all
 cells expressing the antigen
 resistance seen when not
  used in combination with
     other anti-fungals

resistance is uncommon but
 is associated with reduced
sterol in the cell membranes,
 can be used in combination
           with 5-FC

resistance in Canida albicans
(due to mutation in lanosterol
 demethylase or upregulation
of pumps exporting the drug)

 accumulates in the stratum
    corneum so good for
   resistance occurs when
there's mutations in the beta-
       glucan synthase
accumulates in the stratum
   corneum so good for

 used as a prophylactic in
      Fungus/Parasite                  Found                       Description             Disease Caused

                                grwos in soil, material
                            contaminated with bird/bat
                                                             dimorphic, tuberculate
                            droppings, natural reservoir
                                                            conidia, yeast are small
Histoplasmosis (Histoplasma   is soil/bat/avain, Central
                                                               and intracellular (in       Darling's disease
        capsulatum)              River Valleys (Ohio,
                                                            macrophages) and have
                             Mississippi, Kentucky) in
                                                             narrow-based budding
                              US/Asia/Europe/ Middle

                                                            larger, thick-walled yeast         African
    Histoplasma duboisii
                                                           cells in giant cell formation   Histoplasmosis

                                                            dimorphic (yeast at 37C
                              soil and decaying organic
Blastomycosis (Blastomyces                                   and hyphae/conidia at         North American
                               debris, Ohio-Mississippi
       dermatitidis)                                       25C), yeast are large and       blastomycosis
                                  River Valley, Africa

                              desert soil, southwestern
    Coccidioidomycosis       US, northern Mexico, parts                                    California valley
   (Coccidiodes immitis)        of Central and South                                             fever
                               America (dry climates)
                                                               dimorphic, conidia have
                                                                 septate hyphae and
                                                                                           South American
 Paracoccidioidomycosis                                       terminal chlamydospores,
                                                                                          blastomycosis and
    (Paracoccidioides         Central and South America          yeast are multipolar
       brasiliensis)                                            (multiple small buding
                                                               yeast around a big one)
                                                              and look like a pilot wheel

                                                           dimorphic, intracellular,
                                southeast Asia, imported
                                                          mold have conidia and red
   Penicillium Marneffei      cases in the US and Europe,
                                                            pigments, yeast have
                                      found in soil
                                                              transverse septa

                                                                  dimorphic, swollen
                                                                 conidiophores, tear-
Sporothrichosis (Sporothrix    Peru, tropical places in the     shaped/round conidia,  Rose-thorn or rose-
         schenkii)                         US                   sleeve shapes, rosette    gardeners
                                                              form, round/cigar-shaped

                              rare in US, found in tropical
                               regions (Americas, South         dimorphic, pigmented
 (fonsecaea, phialophora,
                               Africa, Australia), found in     (dematiaceous) fungi
                                 woody plants and soil

                               rare in US, found in soil of
  Eumycotic Mycetoma
                                 tropical regions with low     actinomyces has yellow
  (saprophytic fungi like
                                rainfall (Americas, South             granules
eumycetoma, actinomyces)
                                     Africa, Australia)
Subcutaneous Zygomycosis
(basidiobolus, conidiobolus,       leaf and plant debris

                                      soil, vegetation               black mold

                                                              acute angle branching of

                                                                  yeast are usually
                                nromal flora in tropical and unicellular, can be pseudo-
     Malassezia furfur                                                                     Tinea Versicolor
                                   subtropical regions           hyphae, looks like
                                                              spaghetti and meatballs

                               horses, dogs, rodents, cows,                                  ringworm,
     Epidermophyton                                          macroconidia in clusters of
                               monkey, birds, pigs, soil and                             Athlete's foot, jock
     Dermatophytosis                                            2-3, no microconidia,
                                      water, fomites                                             itch
                                                             green-brown to khaki color

                               horses, dogs, rodents, cows,                                ringworm,
      Microsporum                                              both microconidia and
                               monkey, birds, pigs, soil and                           Athlete's foot, jock
     Dermatophytosis                                         rough-walled macroconidia
                                      water, fomites                                           itch
                            horses, dogs, rodents, cows, usually just microconidia, if ringworm,
                            monkey, birds, pigs, soil and macroconidia are present Athlete's foot, jock
                                   water, fomites          they're smooth-walled           itch

                                                          skin and mucosal infection
                                                             with local invasion of  may see angular
                                                           mucosa, both yeasts and         chelitis
   superficial/mucosal        seen in diabetes, T-cell
                                                              filaments in infected  (inflammation at
      candidiasis                defieincies (HIV)
                                                           tissue, candida albicans corner of mouth),
                                                             has pseudohyphae in     can get vaginitis

                                                               anamorphs have
                                                                sporangia and
                                                           sporangiospores, spores
                                                          germinate to form hyphae
  invasive zygomycosis          ubiquitous in nature      and mycelium, hyphae are
                                                            wide irregular and lack
                                                          regular septa, hyphae are
                                                           angiotropic (grow in and
                                                                  invade BV)

                             ubiquitous in nature, only
rhinocerebral zygomycosis       found in uncontrolled
                             diabetes with ketoacidosis
                                                           both yeasts and filaments
                                                          in infected tissues, candida
   invasive candidiasis                                                                  (candida on dry
                                                                  albicans has
                                                                                          skin and nails,
                                                            pseudohyphae in tissue
                                                                                            masses of
                                                              very tiny "spores"
                         related to fungi, ubiquitous in
  microsporidiosis                                          detectable within cells,
                                                           spore walls contain chitin

                                                            acute branching septate
                                                            hyphae, produce conidial
                                                           heads when exposed to air
                           worldwide, ubiquitous in
invasive aspergillosis                                       (rarely seen in tissue),
                           air/soil/decaying matter
                                                            hypahe are uniform width
                                                             with regular septations,
                                                               tree-like branching

                         worldwide, pigeon droppings         encapsulated budding
                          (guano), eucalyptus trees                 yeast
                               worldwide, seen in patients
                               with AIDS and CD4 <200/       have free trophic forms,    pneumocystis
pneumocystis carinii/jirovecii
                                  transplant/immuno-           sporocyst, and cyst        pneumonia

                             Africa/Southeast Asia/ South
        plasmodium                                                                          malaria
                             America/Caribbean, vector is
                             female anopheles mosquito

                                                                 single ring forms,
                                                              Schuffner dots visible
                                                                with Giemsa stain,
     plasmodium vivax                                                                   malaria morbidity
                                                             enlarged RBC with up to
                                                               24 merozoites, larger

     plasmodium ovale
                                                          multiple rings, banana-
                             tropical and sub-tropical
plasmodium falciparum                                       shaped (crescent)

                                                             don't see large RBC
 palasmodium malariae                                     because mature RBC have
                                                              rigid membranes

                                                             dimorphic: adult is the
                                                           flagellated infective form
                                                              (free promastigote in      leishmaniasis
                                                               vector) and obligate         (visceral,
 Leishmania donovani         America/South America,
                                                          intracellular amastigote is      cutaneous,
                                  vector is sandfly
                                                                non-flagellated (in     mucocutaneous)
                                                             mammalian definitive

visceral leishmaniasis (L.   Brazil, Bangladesh, India,
                                                            multi-organ infection          kala-azar
  donovani, L. infantum)            Nepal, Sudan
                           Afghanistan, Brazil, Iran,
                                                      ulcerative skin disfiguring
cutaneous leismaniasis     Peru, Saudi Arabia, Syria,
                         focal areas in South America

    mucocutaneous                                        destruction of mucous
                         Boliva, Brazil, Peru, Central
   leishmaniasis (L.                                     membranes and related
      braziliensis)                                        tissue structures

                                                          flagellated (flagella runs
                         vector is tsetse fly, found in                               trypanosomiasis
                                                        along length) extracellular
 Trypanosoma brucei       tropical west and central                                  (nagana disease,
                                                         protozoa (no intracellular
     gambiense              Africa, reservoir is wild                                  Gambien/West
                                                         stage), much larger than
                                    animals                                           African sleeping
                                                                 the red cell

                                                           flagellated (flagella runs       African
                          vector is tsetse fly, found in
                                                         along length) extracellular trypanosomiasis
 Trypanosoma brucei      east Africa (especially cattle-
                                                          protozoa (no intracellular (nagana disease,
     rhodesiense          raising countries), reservoir
                                                          stage), much larger than       East African
                                 is wild animals
                                                                  the red cell        sleeping sickness)
                                 vector is reduviids ("kissing
                                                                   flagellated (flagella runs      American
                                 bug"), North/ Central/South
    Trypanosoma cruzi                                             along it's length), obligate trypanosomiasis
                                  America, reservoir is wild
                                                                    intracellular protozoa (Chagas' disease)

                                     worldiwde, infects cats/
                                 birds/sheep/pigs, reservoir is
                                                                       intracellular, ring
     toxoplasma gonii            house cat (domestic animals                                       toxoplasmosis
                                                                      enhancing lesions
                                   ingest infective oocysts in

                                                                  flagellated trophozoite (has
                                      worldwide, sylvatic
                                                                  an adhesive disk, 2 nuclei,
                                   (wilderness) distribution,
giardia intestinalis (lamblia)                                    four pairs of flagella, cross-     giardiasis
                                  common in urban centers,
                                                                     eyed appearance), has
                                     reservoir is beavers
                                                                            cyst form
                        worldwide, reservoir is wild     oocysts are acid-fast
  cryptosporidium                                                                    cryptosporidosis
                                 animals                       positive

                                                   have motile feeding stage
                        worldwide, more common in
                                                       (trophozoite, non-
                         underdeveloped countries,
                                                   infectious, can't survive in
entamoeba histolytica     more common in urban                                  amoebic dysentery
                                                    environment or stomach
                        centers (crowded daycares,
                                                    acid) and infective stage
                              poor sanitation)

                          worldwide, reservoir is      flagellated, extracellular,
trichomonas vaginalis                                                                trichomoniasis
                           asymptomatic men                 no cyst stage

                                                         have musculature and
 Parasitic Helminths                                   nervous system, visible by
                                                          parasitic, have tegument
                                                          that absorbs nutrients fro
                                                          mthe host, long ribbon-like
                                                             bodies, segmented,
                             adults are found in the
                                                          hermaphrodites, no body
                          intestine (no clinical effect),
  Cestoda/Tapeworms                                        cavity or digestive tract,
                              eggs are eaten by an
                                                           scolex head region has
                               intermediate host
                                                           proglottids neck region,
                                                             strobila is a string of

                                 snail is obligatgory
                          intermediate host, snail host
                           determines the geographic
                                distribution, second
                              intermediate host is the         egg morphology
     Schistosomes                                                                       Schistosomiasis
                               shellfish, contact with    differentiates the species
                           shallow freshwater leads to
                          infection through the skin by
                             infective cercaria, found
                              everywhere but the US

Schistosoma haematobium
                         ducks harbor schistosomes
                           that don't use humans as
                              hosts, molluscs are
  cercarial dermatitis                                  swimmer's itch
                         intermediate hosts, cercaria
                           penetrate through human
                                  skin then die

                            reservoir is cats/dogs,
                          prevalent in Korea/Japan/
paragonimus westermani
                            Taiwan/central China/

                          pig feces (fertilizer), raw
       fasciola           veggies like watercrest,
                            infects sheep/cattle
 Tissue Affected               Pathogenesis                          Symptoms           Diagnosis/Treatment
                                                             pulmonary are usually
                     inhale conidia (spores) or primary     asymptomatic, can see
                       cutaneous incoluation, takes 2       mild/moderate/severe/
                     weeks to grow, turns into budding           chronic/cavitary,      best diagnostic tool is
    lungs,            yeast in tissue, phagocytosis by      disseminated see RES/       direct examination of
mucocutaneous,       alveolar macrophages, restriction         liver/spleen/lymph            narrow-based
  pericarditis          of growth or dissemination to         nodes/bone marrow/         intracellular budding
                      RES (reticuloenothelial system)     mucocutaneous infections,               yeast
                      by bloodstream, suppression of       discoloration of skin, oral
                           cell-mediated immunity                lesions following
                                                                                        no treatment required
                                                                                           for asymptomatic
                                                                                          cases, itraconazole
                                                                                             used for mild
                                                                                         symptoms, ampho B
  skin and bone                                              skin and bone lesions
                                                                                        used in disseminated
                                                                                       disease, fluconazole for
                                                                                        CNS disease, surgical
                                                                                       resection of pulmonary
                           inhale conidia or primary
                                                          50% are asymptomatic,         (sputum/tissue
                     cutaneous inoculation, infiltration
                                                          acute or chronic onset,  samples, serology to
                     of macrophages and neutrophils,
                                                         see pulmonary disease or detect antibodies, urine
                      granuloma formation, oxidative
  lung and skin                                            extrapulmonary (skin,      or serum antigen
                     killing mechanisms of neutrophils
                                                           bone, prostate, liver,     testing, skin test),
                            and fungicidal acitivty of
                                                           spleen, kidney, CNS)   treated with ampho B/
                     macrophages, convert to budding
                                                                  disease                itraconazole/
                                 yeast in tissue

                                                        primary infection is usually
                                                          asymptomatic but may
                                                            include fever/chest           diagnosis by direct
                                                            pain/cough/ weight         examination (spherule),
                                                        loss/nodular lesions in the     disseminated disease
                                                             lungs, secondary             has poor prognosis,
lung, CNS, bones,                                        disseminated infection is     symptomatic treatment
                      inhale arthroconidia, converts to
 joints, cutaneous                                       chronic/ fulminant shows        for primary infection,
                     spherules containing endospores
      infection                                                  infection of          ampho B/ itraconazole/
                                                              lungs/meninges/               fluconazole for
                                                          bone/skin, can lead to         secondary infection,
                                                            chronic pulmonary          fluconazole particularly
                                                        condition, 25% of patients           for meningitis
                                                        with disseminated disease
                                                               have meningitis
                                                                                   best diagnosed by
                                                               can have           direct microscopy of
                                                         asymptomatic/latent/   budding yeast attached
  chronic single or
                                                        symptomatic infection,  to the parent cell with a
   multple organ
                    inhale conidia, convert to budding  symptomatic infection   narrow base (like histo-
involvement: lungs,
                              yeast in tissue          shows nodular lesions in      differentiate by
mouth, nose, lymph
                                                         the lungs and rarely   geography), treated with
                                                        dissemination to other    itraconazole/ampho
                                                                organs                B/fluconazole/

                                                                                       can be recovered from
       lung,                                                                               bronchial alveolar
 lymphadenopathy,      inhale conidia, convert to yeast         pulmonary or           lavage or blood/tissue
   hematogenous                      form                   disseminated infection        biopsy speciments,
   dissemination                                                                        treated with ampho B
                                                                                           and intraconazole

                                                                                        treat based on clinical
                                                                                         symptoms, diagnosis
                                                                                      based on tissue biopsy,
                                                                                        yeast are rarely seen,
                                                         insidious onset, chronic
                                                                                       can confirm by mold to
                                                         duration, nodules/ ulcers
                                                                                        yeast conversion, can
                                                        along lymphatics at site of
                                                                                       also do exoantigen test
lungs, joints, bones, infection ususally starts with      inoculation, necrosis of
                                                                                           or intradermal test
   brain, usually     trauma inoculation from soil/    skin/ subcutaneous tissue,
 confined to dermis/  plants or can inhale conidia,    follows lymphatic channels
                                                                                       spontaneous healing is
subcutaneous tissue convert to budding yeast in tissue to the lymph nodes, rarely
                                                           goes extracutaneous
                                                                                      itraconazole/ potassium
                                                        (bones, joints, meninges,
                                                                                      iodide for subcutaneous
                                                                                         infection, use ampho
                                                                                           B/itraconazole for

                                                            insidious onset, chronic
                                                               duration, verrucoid       diagnosed based on
                                                             ulcerated and crusted        sclerotic bodies in
 confined to dermis                                          lesions, flat or raised,  direct KOH microscopy,
                         infection starts with trauma
 and subcutaneous                                           satellite lesions by auto- treated with surgery and
                         inoculation from soil/plants
       tissue                                              inoculation or lymphatics,     anti-fungal therapy
                                                          extensive keloid formation,        (itraconazole,
                                                               chronic lesions are             terbinafine)

                                                            insidious onset, chronic  diagnosed based on
                                                              duration, looks like a    tissue biopsy and
 confined to dermis    post-traumatic chronic infection   tumor, abscess formation,     demonstration of
 and subcutaneous      (from inoculation) at feet/lower         draining sinuses     granules, treated with
       tissue                 extremities/hands            containing granules, can surgery and anti-fungal
                                                          involve muscle and bones     therapy (ampho B,
                                                                     locally         azoles like fluconazole)
                                                            insidious onset and
confined to dermis                                                                    biopsy for diagnosis,
                                                         chronic duration, causes
and subcutaneous          implanted through skin                                     treat with itraconazole
                                                        large painlss masses that
      tissue                                                                                   or KI
                                                              look like tumors
                                                                                      diagnosis based on
confined to dermis                                        insidious onset and
                                                                                      biopsy and culture,
and subcutaneous                                         chronic duration, slow
                                                                                      treated by surgical
      tissue                                             growing painless cysts

                                                                                        culture must be
                                                                                    supplemented with oil
                                                                                         (oil is used for
                                                                                     metabolism), culture
                                                                                     shows white/yellow
                                                              hypo or hyper          growth, treated with
                                                        pigmentation (depends on      OTC clotrimazole/
                                                         ethnicity and skin color)  miconazole/ selenium
                                                                                       sulfide shampoo/
                                                                                   ketoconazole shampoo,
                                                                                   prescriptions in chronic
                                                                                   cases (strong selenium
                                                                                   sulfide or ketoconazole)

                      communicable from person-to-       small raised worm-like
                                                                                       scrape skin from
                     person/animal-to-person/fomites-         marks, ring of
                                                                                       margin/pluck hair/
                        to person, invades stratum      inflammation, alopecia,
                                                                                       scrape nails from
                      corneum (skin, hair, nail beds), pustules/vesicles/ papules,
                     binds keratin and breaks it down     kerion (large pustule)

                                                                                        scrape skin from
                                                                                       margin/pluck hair/
                                                                                       scrape nails from
                                                                                    nailbeds, M. audouinii
                                                                                     grows poorly on rice
                                                                                    grains and produces a
                                                                                       dark discoloration
                      communicable from person-to-       small raised worm-like      differentiating it from
                     person/animal-to-person/fomites-         marks, ring of        atypical M. canis, rice
                        to person, invades stratum      inflammation, alopecia,          grains can also
                      corneum (skin, hair, nail beds), pustules/vesicles/ papules, enhance the production
                     binds keratin and breaks it down     kerion (large pustule)        of macroconidia,
                                                                                      treatment is topical
                                                                                     (azoles, terbinafine,
                                                                                   haloprogin, benzoic and
                                                                                     salicylic acid) or oral
                                                                                        scrape skin from
                                                                                       margin/pluck hair/
                                                                                       scrape nails from
                                                                                     nailbeds, T. rubrum
                                                                                        (can use casein)
                                                                                    causes a blue/purple
                                                                                     basic end product in
                                                                                             BCP, T.
                      communicable from person-to-       small raised worm-like     mentagrophytes (can't
                     person/animal-to-person/fomites-         marks, ring of        use casein) causes a
                        to person, invades stratum      inflammation, alopecia,      colorless basic end
                      corneum (skin, hair, nail beds), pustules/vesicles/ papules, product in BCP, acidic
                     binds keratin and breaks it down     kerion (large pustule)    end product in BCP is
                                                                                      treatment is topical
                                                                                     (azoles, terbinafine,
                                                                                   haloprogin, benzoic and
                                                                                     salicylic acid) or oral
                                                         often temporary, can be
                                                               white spots or
                      predominantly T-cell response,
                                                        erythroderma that is scaly,
                       release of cytokines from Th1
   skin, mucosa                                            lesions in mouth are        see satellite lesions
                     cells stimulates epidermal growth,
                                                            usually flat, cottage
                       overgrowth of normal candida
                                                         cheese-like discharge in

                         neutropenia is predisposing
                        factor, infection via lung with                                 diagnose via fungal
                     dissemination, invasion can enter "black mold" skin lesions,          smears (from
lungs, blood vessels
                     through other routes including gut   exudate, hihg fatality       bronchoscope), treat
                       or contaminated skin wounds,                                        with ampho B
                       hyphae grow in and invade BV

                     infection via nasal turbinates and   orbital cellulitis, damage
                            sinuses into the CNS                 around orbit

                     neutrophils are essential defense,
                       neutropenia is a predisposing     maculopapular lesions,     treat albicans with
                     factor, can enter blood via normal dissemination can include    fluconazole, non-
                      GI flora penetrating through wall   eye and vitreous fluid,     albicans is often
                        (translocation) or indwelling          endocarditis       resistant to fluconazole
associated with AIDS                                                                    seen with special stains
    cholangiopathy                                                                         (calcocluor white,
                           fecal-oral transmissionobligate     severe GI disease, cause
  (infection of biliary                                                                 modified acid fast), treat
                                  intracellular fungi               lots of diarrhea
 tract causing biliary                                                                   by improving immune
      obstruction)                                                                              system

                                                                                              culture (on PAS or GMS
                                                                   allergic reactions           silver) shows hyaline
                                                               (bronchopulmonary form           molds (black, brown,
                                                              with eosinophilia or allergic      green, yellow), treat
                                                                sinusitis), colonization        allergic reactions (but
                                                                 (sinuses, obstructive            not the organism),
                                                                bronchial aspergillosis,       diagnose with isolation
                                  inhaled or transdermal          fungal ball), locally        from a normally sterile
                          transmission, inhaled conidia bind invasive aspergillosis                  stie, with tissue
                               fibrinogen/laminin alveolus,            (necrotizing           invasion, immunoassay
                           conidia germinate, macrophages        pseudomembranous                        showing
                             ingest/kill conidia, neutrophils    broncial aspergillosis,           galactomannan
                              adhere to/kill hyphae, hyphal        chronic necrotizing        antigen in serum, don't
                              forms secrete proteases and      pulmonary aspergillosis,             treat obstructive
                            invade the epithelium, vascular       locally destructive),         broncial aspergillosis,
                              invasion leads to thrombosis    invasive aspergillosis (in        treat fungal balls with
                                                                immunocompromized,                 surgery if there is
                                                                  invasive pulmonary              hemorrhage, treat
                                                                      aspergillosis,                 locally invasive
                                                                     hematogenous                  aspergillosis with
                                                                   dissemination with             surgery, treat with
                                                                     angioinvasion)                    ampho B or

                                                                                              stains with mucin stain
                                                      cerebromeningeal disease                 (mayer mucicarmine),
                                                       (fever, headaches, visual                yeast in blood, blood/
                          inhale the yeast, alveolar    disturbances, abnormal                    CSF cultures, gram
                        macrophages/inflammatory       mental status, seizures),                   stain or india ink,
                        phagocytic cells/B and T cell      menintis, increased                antigen assay serum/
                       response act in host defense,      intracranial pressure,                        CSF for
                        inhaled yeast is ingested by         fever, pulmonary                      polysaccharide
invades and lives in
                      macrophages, capsule inhibits involvement (pneumonia),                  capsule, no neutrophils
neural tissue, lungs
                     phagocytosis and suppresses the        CNS parenchyma                     (typical meningitis has
                         cellular/humoral response,            involvement                       lots of neutrophils in
                          hematogenous/lymphatic      (cryptococcoma, gattii in               CSF), treat with ampho
                      dissemination to the CNS from     competent hosts, mass                  B + fluctyosine for 2
                                    lungs                lesions), dissemination               weeks followed by 8
                                                           causes skin lesions/               weeks of fluconazole,
                                                      chorioretinitis/bone lesions                 therapeutic LP to
                                                                                                     decrease ICP
                                                                                         diagnose by cyst (4-8
                                                                                           intracystic bodies),
                                                                                         microscopic exam of
                                                                                        alveolar lavage/biopsy,
lungs, lymph nodes,   respiratory tract is main portal of  shortness of breath on           stain with Giemsa
    spleen, bone         entry, primary infection and     exertion, fever, dry cough, (trophic forms)/GMS
  marrow, liver, GI    reactivation can cause disease, diffuse interstitial infiltrates         (cyst wall)/
   tract, GU tract            slowly progressive                  in all lobes           immunofluorescence
                                                                                           (both), prophylaxis/
                                                                                          treatment with TMP-
                                                                                            SMX (bactrim), IV
                                                                                         pentamidine for sulfa

                                                             symptoms start as non-
                                                             specific flu-like symtpms
                       transmitted by blood transfusion/
                                                                due to the release of
                           needle sharing/congenital,
                                                                 massive numbers of
                         mosquito feeds and inoculates
                                                            merozoites into circulation, control programs and
                      from salivary glands, goes to liver
                                                                     each cycle of         insecticides have
                          where schizonts rupture liver
                                                              infection/replication/cell    eliminated some
    liver, RBC           cells, it can then invade RBC
                                                                lysis induces another     malaria, treatment
                       where the trophozoite (ring form)
                                                                 round of symptoms,      depends on infecting
                       matures forming schizonts, RBC
                                                              splenomegaly, anemia, species and geography
                         rupture or make gametocytes
                        which can be taken back up by
                                                            hypoglycemia, pulmonary
                                                                 or renal dysfunction,
                                                                 neurologic damage

                       invades only young immature
                        RBC containing Duffy blood
                                                                                         untreated patients can
                         group antigen, uses Duffy (a
                                                            incubation of 10-17 days,    survive, diagnosed by
                        chemokine receptor) antigen to
                                                                 flu-like symptoms,        thin blood smears,
                      invade RBC, does not cause red
    liver, RBC                                              sequelae (splenomegaly,            treated with
                      cell adherence to capillaries, can
                                                            liver and kidney damage)    chloroquine followed
                          remain dormant in the liver
                                                               results from relapses       by primaquine to
                       (hypnozoites) and relapse even
                                                                                        eliminate hypnozoites
                      after the blood has been cleared
                                of merozoites
                      like vivax, invades only immature
                          RBC but doesn't use Duffy
          infects more than 5% of RBC,
                                               shortest incubation period
         does not form hypnozoites (so no
                                               (7-10 days), most likely to
            recurrence after 6 months),
                                              result in fulminating deadly
              infects RBC of any age,
                                               disease if untreated, daily
              generates and inserts an
                                                  chills, fever, nausea,
         adhesive protein into the infected
                                                    vomiting, diarrhea,
          RBC membrane (PfEMP1) that                                             diagnosis by thin
                                                     abdominal pain,
            causes the RBC to become                                            smears, treat with
                                                dehydration, anemia due
           sticky, can bind to many host                                           chloroquine
                                               to increased inflammation
            receptors, sequestration for
                                               and rupture of RBC (toxic
         evading spleen-dependent killing,
                                                  cellular debris), renal
            antigenic variation to evade
                                                failure due to hemolysis,
             antibody-dependent killing,
                                                 hematuria, hepatic and
         obstructs capillaries, sequesters
                                                      lung pathology
                in brain and placenta

          only infects mature RBC with
                                              longest incubation period untreated infections can
         more rigid cell membranes, no
                                                    (18-40 days)               last years
           hypnozoites (no relapses)

           transmission to humans by the
               sandfly is usually zoonotic                                       diagnose based on
             (animal reservoir) but can be                                    intracellular amastigote
            from another infected human,                                     (non-flagellated form) in
         promastigotes (extracellular form-                                       macrophages by
           have flagella) are phagocytized                                     microscopy, molecular
          by macrophages, divides within                                         detection methods
            macrophages, promastigotes                                             (PCR) are most
         transform into amastigotes inside                                       accurate, treat with
         macrophages (intracellular stage-                                     antimonial compounds
         no flagella), amastigotes multiple                                  (toxic and non-effective)
          in cells including macrophages,                                            and antibiotic
            sandfly takes blood meal and                                            paramomycin
              continues cycle and spread

                                                  affects all organs,
                                                                          amastigotes in biopsy
                                              fulminating/chronic and
                                                                             samples (splenic
         grows in macrophages, invasion debilitating/ asymptomatic
                                                                          puncture, lymph node
         of the reticulo-endothelial system and self-limiting, enlarged
                                                                          aspirate, liver biopsy,
organs     causes symptoms, persistent      lymph nodes/spleen/liver,
                                                                           sternal aspirate, iliac
         inflammation and hypersplenism fatigue and weakness due
                                                                         crest bone marrow, buff
                    cause anemia               to anemia, intermittent
                                                                           coat preparations of
                                               fever/ rigor/chills, dark
                                                                              venous blood)
                                            pigmentation of skin areas
                                                       chronic sore, first as red
                                                       papule at fly's bite site (2 amastigotes in stained
                                                        weeks-2 months post-              smears fro
                                                      exposure), irritated lesion, mskin/mucous touch
      skin                                            pruritic, begins to enlarge preps or ulcer biopsies,
                                                       and ulcerate, secondary          promastigotes
                                                         infection becomes a        (flagellated) in culture
                                                       problem, skin-disfiguring,        (ulcer tissue)
                                                      slow-healing, leaves scars
                                                         progressive infection,
                                                       intially cutaneous, does
                                                                                   amastigotes in stained
                                                          not heal, secondary
                                                                                          smears fro
                                                          bacterial infections
                                                                                     mskin/mucous touch
                                                           common, severe
mucous membranes                                                                   preps or ulcer biopsies,
                                                       mutiliation, may involve
                                                        oral and nasal mucosa
                                                                                    (flagellated) in culture
                                                        causing destruction of
                                                                                         (ulcer tissue)
                                                         underlying structures
                                                       (palate, nasal cartilage)
                                                      incubation period is a few
                                                       days to weeks, starts as
                                                      inflamed red lesion at bite
                                                        site that spreads to he    diagnosed by thin and
                                                              lymph nodes         thick blood films/lymph
                                                         (winterbottom sign-       node aspirates/spinal
                         have variable surface                   cervical          fluid/serology, treated
                             glycoprotein             lymphadenopathy), fever,          with suramin/
                                                       myalgia, arthralgia, then        pentamidine/
                                                          spreads to the CNS            eflornithine/
                                                         (tremors, hemiplegia,    melasoprol, no vaccine
                                                          incontinence, coma,
                                                        death), febrile episodes
                                                            can last for years

                                                        shorter incubation period,
                                                          acute disease (fever,
                                                          rigors, myalgia) that    diagnosed by thin and
                     develops in greater numbers in      occurs more rapidly, no thick blood films/lymph
                         the blood, progresses to         lymphadenopathy, 3       node aspirates/spinal
                   fulminating/fatal illness with death     stages: chancre,       fluid/serology, treated
                      within 12 months if untreated,     hemolymphatic stage            with suramin/
                    CNS invasion occurs early, have (fever, lymphadenopathy,            pentamidine/
                      variable surface glycoprotein              pruritis),             eflornithine/
                                                         meningoencephalitic melasoprol, no vaccine
                                                            (invasion of CNS,
                                                        headaches, somnolence)
                                                                 c, early signs are
                                                            erythematous indurated
                                                            area (chagoma/bite site)
                                                               with rash and edema
                                                           aroudn the eyes and face       diagnosed by thick/thin
                                                            (Romana's sign), acute        blood films in the acute
                                                             symptoms (common in            stage, in the chronic
                                                           kids <5) usually has CNS        stage biopsy of lymph
                         passed in feces, bite ithces and
                                                           involvement, fever, chills,    nodes/liver/spleen/bone
  predilection for        feces enters, crosses mucous
                                                           malaise, myalgia, fatigue           marrow to find
  striated muscle           membrane, gets into blood
                                                          (flu-like), death after a few   amastigote, treated with
including the heart       stream and lymphatics, tissue
                                                             weeks from congestive             nifurtimox or
                                  gets infected
                                                               heart failure), chronic     benznidazol in acute
                                                            mega-syndrome after 10            phase (toxic), no
                                                          years (myocarditis, dilated      treatment for chronic
                                                          cardiomyopathy, enlarged                 disease
                                                          esophagus and colon due
                                                              to destruction of nerve
                                                             cells, granulomas, cyst
                                                             formation, autoimmune

                         usually transmitted by cat feces
                          or undercooked meat infected
                          with tissue cysts), fecal oocyst     usually asymptomatic,
                                                                                          cooking at 160F kills
                        must mature in soil for 3 days (old lymphadenitis or mono-like
                                                                                        tissue cysts, diagnosed
                           cat litter), ingested parasites      illness, progressive,
                                                                                        based on serology (IgG
                         penetrate the intestinal wall and        common cause of
                                                                                           in absence of IgM
                         enter macrophages, they spread         encephalitis in AIDS,
                                                                                          suggests immunity),
                        throughout the body via the blood congenital infection can
                                                                                               treatment is
                            and damage distant tissues        cause chorioretinitis and
                            (mono-like symptoms), get             mental retardation
                          dormant cysts, controlled by T-
                           cell mediated immunity (Th1)

                                                                                        spontaneous recovery
                                                               incubation is 10 days,
                                                                                        is possible, diagnosed
                                                                  asymptomatic, GI
                           transmitted by ingesting cysts                              by examination of stool
                                                            infection, sudden onset of
                            (water, food, hands, fomites                                      for cysts and
                                                            foul-smelling steatorrhea,
                           contaminated with cysts from                                trophozoites fro 3 days,
                                                                 abdominal cramps,
GI (spread beyond       feces) or fecal-oral transmission,                               fluorescent stain with
                                                              flatulence, non-bloody
the GI tract is rare)      ingested cyst differentiates to                              antibody-linked stains,
                                                             diarrhea, can get chronic
                         trophozoite in the small intestine                                    treatment is
                                                             malabsorption syndrome
                          and attaches to the upper small                                   metronidazole,
                                                                 (upper small bowel
                        bowel via a ventral sucking disk                                 prevention: cysts are
                                                             inflammation and villous
                                                                                       resistant to chlorination
                                                                                            (must boil to kill)
                                                           common cuase of watery
                                                                                           diagnosed by antibody-
                                                              diarrhea but usually
                                                                                           linked stains of stool or
                        transmitted by ingesting oocysts, spontaneous remission,
                         fecal-oral transmission, oocysts    asymptomatic or mild
GI (spread beyond        release sporozoites in the small    diarrhea in previously
                                                                                           treatment is supportive
the GI tract is rare)   intestine where they differentiate healthy, mild self-limiting
                                                                                               (antibiotics arent'
                          into trophozoites and attach to     enterocolitis (watery
                                                                                           effective), prevention by
                                 intestinal microvilli     diarrhea without blood), in
                                                                                            boiling (cysts killed by
                                                            AIDS get chronic lethal

                                                                     intestinal and
                                                              extraintestinal infection,
                                                                                            diagnosed by cysts in
                        transmission is fecal-oral (cysts in colitis is most common
                                                                                           stools/mucosal biopsies
                         feces), usually human-to-human,       (flask-shaped ulcers in
                                                                                           (trophozoites will ingest
                             main source is water/food      colon mucosa), numerous
                                                                                           RBC)/ serology, CT will
                              contamination from an               bloody stools daily,
                                                                                             show extra-intestinal
                              asymptomatic carrier,              abdominal pain and
                                                                                             amebiasis, treat with
                            trophozoites can invade                 cramping, liver
                            human tissues, adhere to          abscesses if it invades
                                                                                                 followed by
                            human cells, and secrete         the portal venous system,
                                                                                               paromomycin to
                          toxins and enzymes causing elevated diaphragm, RUQ
                                                                                            eliminate cysts, cysts
                                tissue destruction            pain, systemic infection
                                                                                              are killed by boiling
                                                                 (fever, leukocytosis,

                                                           asymptomatic in men (or
                                                             urethritis, prostatitis),
                                                                 women can be
                                                                                          diagnosed by wet
                        transmitted by sexual intercourse   asymptomatic or have
                                                                                          mount secretions
                        (occasional fomites), trophozoite      vaginal discharge
urogenital infection                                                                      (motile flagellated
                           resides in vagina or urethral  (profuse, foul odor, foamy
                                                                                       organism), treated with
                                       orifice            appearance) and vaginitis
                                                           (itching, burning, painful
                                                             urination), strawberry
                           CD4 T-cells (control parasitic
                        infection) preferentially produce Il-
                            4/5/12 (Th2 response), IgE
                        secretion (type I hypersensitivity),
tissue invasion by        IgE binds to the target parasite
                                                                increase eosinophils in
  larval migratory      antigen, Fc receptor binds FcE on
       stages              IgE, eosinophils degranulate
                             toward the parasite, toxic
                         produces in eosinophil granules
                           damage/ destroy/dislodge the
                          eggs hatch into larvae which
                         penetrate through the intestinal
                           wall into tissues and cause
                                damaging disease

                                                                    most infections are
                           infection by water-born cercaria
                                                                    subclinical with mild
                            penetrates the human directly,                                    diagnosis based on
                                                                anemia, abdominal pain,
                               transition from cercaria to
                                                                  diarrhea, eosinophilia,         microscopic
                            schistosomulum (lasts 2 days,
                              hyaluronidase helps in skin        continuing infection can  identification of species-
                            penetration, cercaria loses tail,   cause fibrosis (espeically specific eggs in stool or
                                 tegument takes up host              in the liver, called        ruine, ELISA,
                             components), schistosomule          Symmer's clay pipestem     prevention by avoiding
                     penetrates the epidermis and breaks                fibrosis) and         contaminated fresh
                      through it's basement membrane to         granulomatous reactions,      water, treated with
blood flukes (adults migrate through the dermis, adults           colonic polyposis with     praziquantel (single
                         live 20-30 years in the host, eggs
 in portal drainage,                                              bloody diarrhea, portal          oral dose),
                             released and migrate into the
    schistosoma)         intestinal lumen or bladder, eggs      hypertension, esophageal      oxamniquine and
                     produce proteases allowing for tissue                 varices,          metrifonate outside
                         migration, 50% of eggs die within        hepatosplenomegaly,                the US,
                         host tissue, pathology caused by           ascites, cystitis with    corticosteroids if
                     inflammatory responses to eggs that         hematuria, renal failure,        there's CNS
                          die in the tissues, schistosomule           carcinoma, CNS        involvement, vaccine
                      searches for blood vessel and coats       involvement, "swimmer's targets schistosomulum
                        itself with host factors, migrates to   itch", symptoms may not and enzymes involved
                       liver for protection from drugs, also
                                                                appear for years because      in skin penetration
                        releases stuff to make the vessels
                        dilate and decrease phagocytosis
                                                                  it depends on the egg
                                                                  buildup, eosinophilia

                                                                                             eggs in feces or urine,
                                                                                               look for location of
                                                                 hematuria in early disase,            spine,
                                                                eventual fibrosis of bladder immunodiagnosis by
                            proportional to number of
                                                                 and obstructive uropathy,    ELISA/IFAT/RIA/IHA
   bladder fluke          schistosomes and duration of
                                                                      renal failure and              (indirect
                                                                  hydronephrosis, bladder   hemagglutination), treat
                                                                         carcinoma           with praziquantel and
                                                                                            resistance is increasing
                      infection of skin by cercariae that
                          are not adapted to humans,
                                                                                             treat with topical
                       cercariae penetrate the skin (pin
                                                                                           steroids, prevent by
                        prick) but fail to form functional
                                                                                         limiting waterfowl and
                         schistosomulum and die, this
                                                                                         treat with molluscides
                           produces an inflammatory
                               reaction in th eskin

                      transmission by consumption of
                          raw/undercooked seafood,           acute symptoms related to
                       infective metacercariae (in 2nd         invasion and migration
                       intermediate host) are released       (diarrhea, abdominal pain,
                                                                                         eggs in stool/sputum
                         from the snail and penetrate             fever, pulmonary
                                                                                         (not present until 2-3
                         shellfish, they migrate to the         abnormalities, cough,
                                                                                        months after infection),
                            tissues, humans eat the            eosinophilia), chronic
lung flukes (adult in                                                                    immunodiagnosis to
                        metacercariae (lobsters, crab,       pulmonary manifestations
lung, paragominus)                                                                            differentiate
                       shrimp), they invade tissue and           (cough, discolored
                                                                                         paragonimiasis from
                      migrate to the lung cavities where        sputum, radiographic
                                                                                          TB, treatment with
                        adults mature, eggs in sputum        abnormalities) can persist
                        may be swallowed, pathology                   for years,
                         associated with inflammatory        pseudotubercules in lungs
                           response and number of                   can mimic TB
                       parasites they are infected with

                           metacercaria formed on        acute (diarrhea, abdominal
                       vegetation instead of a 2nd host,    pain, fever, vomiting,
                                                                                         diagnosed by eggs in
liver flukes (adult in  metacercaria are ingested by      heptaomegaly), chronic
                                                                                           stool, treated with
  liver of bile duct)   humans from consumption of        (intermittent blockage of
                        raw/ undercooked vegetables              bile duct and
                        (contaminated with pig feces)           inflammation)
     Other Notes

  systemic mycoses,
    fatality is more
      common in
  immunocomp, kids
(<2 years), and elderly

  systemic mycoses

  systemic mycoses

 systemic mycoses,
  seen frequently in
 systemic mycoses

 systemic mycoses,
 prominent mycotic
pathogen among HIV
     patients and

 mycoses, zoonotic,
seen in rose gardners




 superficial mycoses,
 lipophilic yeast, most
    common in young
   communicable, not
 zoonotic, some meds
(like Lipitor) that lower
     cholesterol can
interact with the drugs
      used to treat it

superficial mycoses,
communicable, can
    be zoonotic

superficial mycoses,
communicable, can
    be zoonotic
 superficial mycoses,
 most common of the
 communicable, can
be zoonotic, T. rubrub
doesn't perforate hair
     (exothrix), T.
   (endothrix) does
     perforate hair

opportunistic infection
   seen in T-cell
mediated deficiencies

opportunistic infection
     seen in PMN-
mediated deficiencies
    seeing more in
patients who received
   prophylaxis (for
aspergillosis) in bone
  marrow recipients

opportunistic infection
   seen in PMN-
mediated deficiencies
   highly flexible
 morphology due to
  genetic instability
unusual opportunist,
   found in AIDS

opportunistic infection
     seen in PMN-
mediated deficiencies
outcome depends on
      host factors,
 neutropenic patients
   (steroid use) are

opportunistic infection
      seen in T-cell
mediated deficiencies
  (CNS disease), can
grow at 37C, melanin
 cell wall responsible
    for neurotropism
 (ability to invade and
 live in neural tissue)
opportunistic infection
   seen in T-cell
mediated deficiencies

   correlates with

 benign tertian, null
Duffy antigen protects
      from vivax

    benign tertian
  malignant tertian,
causes most malaria
 deaths, people with
sickle trait have RBC
that are more readily
  eliminated by the
spleen so don't have
   severe disease

opportunistic in AIDS,
    most serious
 seen in US military

   least prevalent,
  untreated primary
cutaneous lesions can
     develop into

 more virulent than
West African sleeping
zoonotic, can also be
transmitted by blood

zoonotic, problem in
 compromized, can
also have congenital
tranmission (primary
    infection during
     pregnancy) or
  transmission from

zoonotic, can shed
cysts for years, IgA
deficient individuals
  are susceptible
 zoonotic, outbreaks
 from contaminated
   water treatment
 plants, incidence of
 diarrhea increases
 during the summer,
more common in kids

      can also be
transmitted by flies or
  sewage containing
     cysts, direct
tranmission in sexual
    encounters can
  produce cutaneous

  very common in
developed countries,
   can get passed
  through infected
 mom's birth canal,
 20% relapse rate
  (always treat the
public health concern

treatments are toxic
and can't be used as
"schistosome in
  wrong host"


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