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Intro to STDs Ali

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Intro to STDs Ali Powered By Docstoc
					10-Intro to STDs-Ali
11-Syphillis-David
12-Gonococcus and Chlamydia-Nichole
13-Herpes-Amanda
14-HPV-John
15-HIV/AIDS-Ali
16-UTI's-David
17-Skin Infections-Nichole
18-Chicken Pox, Shingles-Amanda
19-Wounds, Staph-John
20-Fungal Infections, Antifungals-Ali

QUESTIONS: Introduction to Sexually Transmitted Infections

1. What three factors influence the rate of transmission of an STD?

2. What populations are disproportionately affected by STDs? Why?

3. What common features are shared by most STD agents?

4. What is pelvic inflammatory disease?

5. What role do condoms play in STDs?

6. What synergy is seen between bacterial STDs and HIV?
ANSWERS: STD’s
1. What three factors influence the rate of transmission of an STD?

   R0 = b  D  C

   R0 = rate of transmission
   b = transmissibility
   D = duration of infectiousness
   C = rate of new partner acquisition
        STDs sustained by small # of individuals who have a large # of partners

2. What populations are disproportionately affected by STDs? Why?

      Women
       o ignorance or misinformation about STDs
       o physiologically more susceptible to infection

      Minorities: African Americans > Hispanics > Whites
       o poverty
       o access to quality health care
       o health care seeking behavior
       o illicit drug use
       o living in communities with high prevalence of STDs

      Adolescents
       o ignorance or misinformation about STDs
       o physiologically more susceptible to infection

3. What common features are shared by most STD agents?

          Sensitive to physical and chemical factors so never found free in environment
          Obligate human pathogens with no human reservoir
          Asymptomatic disease common
          No effective vaccines (exceptions: HBV and HPV)
              o Organisms highly adapted to human host
              o Inability to culture bacteria in vitro
              o Lack of knowledge about how to stimulate mucosal responses
              o Lack of immunity after natural infection

4. What is pelvic inflammatory disease?

          Symptoms (only 1/3 of the time): lower abdominal pain, fever, unusual
           vaginal, discharge with foul odor, painful intercourse, painful urination,
           irregular menstrual, bleeding
          Risk factors: < 25 years age, # of sex partners; douching, IUD
          Largest complication: ectopic pregnancy
5. What role do condoms play in STDs?

      o reduce transmission risk of HIV, gonorrhea, chlamydia, trichomoniasis,
        genital herpes, syphilis, and chancroid
      o promote the regression of HPV lesions
      o reduce risk of cervical cancer and PID

6. What synergy is seen between bacterial STDs and HIV?

      o Bacterial STD  inflammation  activates chemokines  attracts HIV-
         infected cells  increases transmission of HIV
      o Ulcerative STDs (syphilis and chancroid)  break mucosa  facilitate entry
         of HIV
      o Non-ulcerative STDs (gonorrhea and chlamydia)  higher concentration of
         CCR5 co-receptors  increases infectability
      Back to Table of Contents
QUESTIONS: Syphilis Treponema pallidium
1. Describe the etiology of syphilis including site of invasion, motility mechanism,
   destructive product and dissemination method.


2. Describe Primary Syphilis in terms of its duration, characteristic lesion, clinical sign
   visible upon inspection, resolution.


3. What are the clinical symptoms of secondary syphilis? How long after the
   disappearance of primary chancre do these appear?


4. What are the differences between early and late latent syphilis (including relapse,
   infectious potential, and treatment duration)?


5. What are the three complications associated with tertiary syphilis? On what time scale
   do these symptoms present?


6. Describe the logic of syphilis testing using words like treponema, non-treponema, the
   chronology of the tests, what are RPR/TRUST and TP-PA and FTA.


7. What are the indications for a CSF exam for suspected neurosyphils? Think in terms
   of a person with less than 1 year infection, and greater than 1 year infection. What is
   the only test approved for CSF diagnosis?
ANSWERS: Syphilis
1. Describe the etiology of syphilis including site of invasion, motility mechanism,
    destructive product and dissemination method.
Syphilis invades epithelial cells, endothelial cells, and uses its periplasmic flagella to
transverse junctions b/t endothelial cells. It induces the production of matrix
metalloproteinase-1 (MMP-1) which destroys collagen in dermal cells. The bacteria
follow lymph channels and ultimately disseminate into blood stream.
2. Describe Primary Syphilis in terms of its duration, characteristic lesion, clinical sign
    visible upon inspection, resolution.
A patient will present with a red macule/chancre 10-60 days after exposure. This is
painless and described as cardboard-like. It is barely visible, but can lead to
lymphadenopathy which looks like someone has golf balls stuck around their ASIS. This
will heal in 3-6 weeks if untreated.
3. What are the clinical symptoms of secondary syphilis? How long after the
    disappearance of primary chancre do these appear?
Secondary syphilis will present with systemic symptoms (fever, malaise, myalgia)
Strange symptoms include hepatitis, patchy hair loss, and maculopapluar rash on back
and hands. Very specific to syphilis. This will show up 3-6 weeks following clearance
of primary symptoms. Can also have ocular involvement, and glomerulonephritis leading
to nephritic syndrome. Key is disseminated infection cause over immune compensation.
4. What are the differences between early and late latent syphilis (including relapse,
    infectious potential, and treatment duration)?
Early syphilis is considered less than 1 year post infection. During this time the pt. is
contagious but asymptomatic although they can relapse into secondary symptoms again.
They require a short course of tx to resolve infection during this time.
Late stage latency is considered more than one year. The pt. is no contagious but can still
transmit the disease in the case of pregnancy. Can be diagnosed using blood test for high
titers. Must be treated with long course therapy. 1/3 of patients run the risk of entering
tertiary syphilis.
5. What are the three complications associated with tertiary syphilis? On what time scale
    do these symptoms present?
Tertiary syphilis is characterized by neurosyphils, CV involvement (proximal aortic
aneurism) and Gummatous (deep, mass lesions involving bone, skin, lungs, GI, etc)
Neurosyphilis can involve meningitis (early ~1 year), stroke, dementia, lesions, and
ganglia involvement.
These complications can occur on the order of decades. Keep in mind that this is a
lifetime risk. Don‟t forget about the Tuskegee experiments from Med/Soc.
6. Describe the logic of syphilis testing using words like treponema, non-treponema, the
    chronology of the tests, what are RPR/TRUST and TP-PA and FTA.
For suspected syphilis you would first use darkfield microscopy looking for spirochetes
that are motile. For later stages when lesion samples are no longer available you use a
non-treponemal test like RPR or TRUST first. These are highly sensitive, but not
specific to T. palladium. To confirm a positive test use a treponemal test like TP-PA or
FTA. These are not quantitative like the first, but they are specific to syphilis.
7. What are the indications for a CSF exam for suspected neurosyphils? Think in terms
   of a person with less than 1 year infection, and greater than 1 year infection. What is
   the only test approved for CSF diagnosis?
You should perform a CSF exam on early latent patients if tx fails or symptoms are
present. For later patients, you still use these guidelines but also for HIV concurrence,
other tertiary signs, possibly for all late latency patients. CSF-VDRL test is the only test
approved and the test is positive if PMN‟s are >5 and protein is >40. Symptoms are still
huge factor. Negative test does NOT override clinical symptoms.
Back to Table of Contents
QUESTIONS: Gonorrhea and Chlamydia
1. True/False? Gonorrhea lack a polysaccharide capsule.

2. What is the therapy for Gonorrhea?

3. Why don‟t we have a vaccine for gonorrhea?

4. What is the most common cause of preventable blindness in the world?

5. How does genital Chlamydia trachomatis present in babies?

6. What is different about the infection mechanism of C. trachomatis & C.
   Pneumoniae versus C. psittaci?

7. What is the difference between reticulate and elementary bodies?

8. How do you treat chlamydia? Explain.
ANSWERS
1. True. This means Neisseria Gonorrhea are less likely to infect the bloodstream than
Neisseria Meningitis. Also, disseminated gonococcal infection is not life-threatening,
whereas meningococcemia is often fatal.
2. ceftriaxone + Chlamydia-active antibiotic (tetracycline, ezythromycin). Often,
individuals with gonorrhea also have chlamydia.
3. Antigenic variation, poor immune responses at genital mucosa, & immunosuppressive
effects of gonococcal infection.
4. Ocular strains of Chlamydia Trachomatis, which causes trachoma. It affects the
epithelial cells, causing inflammation which interferes with tear production, and promotes
scarring. The scarred eyelid skin turns inward, eyelashes abrade the cornea (trichiasis);
cornea ulcerates and becomes susceptible to secondary bacterial infections; eventual
result is blindness. However, c.trachomatis infection can often be asymptomatic.
5. Pneumonia, conjunctivitis, failure to thrive, and/or chronic respiratory disease
syndrome.

6. In C. Pneumo and C. Trachomatis, inclusion granule with both reticulate bodies and
elementary bodies undergo REVERSE ENDOCYTOSIS, while in C. Psittaci, the
inclusion granule undergoes LYSIS of cells and the inclusions. (Slide 22 from Neisseria
Gonorrhea & Chlamydia lecture on 4/30/07).

7. Reticulate bodies are non-infectious, intracellular, grow quickly by binary fission,
divide continually until the endosome is packed with bacteria (once full, the endosome is
called an „inclusion‟). Elementary bodies are the infectious, extracellular, non-growing,
environmentally-resistant form (somewhat analagous to a spore).
8. Chlamydia are susceptible ONLY to antibiotics that can penetrate eukaryotic cells and
reach sufficient intracellular concentrations to kill the bacteria: doxycycline and
azithromycin are most commonly used.


Back to Table of Contents
QUESTIONS: Herpes Virus
1. During replication, the Herpes virus:
       a. linearizes (normally circular) and inserts into the host genome
       b. Uses host cell polymerases
       c. circularizes (normally linear), and uses its own polymerase
       d. circularizes (normally linear), and uses the host polymerase

2. Which of the following have a broad host range and are highly lytic in culture?
      a. Herpes simplex 1&2, Varicella Zoster
      b. CMV, HHV 6&7
      c. EBV and HHV8/Kaposi‟s Sarcoma – associated herpesvirus

3. Which of the following genes are expressed during both early and late times during
HSV cell infection?
      a. polymerase and thymidine kinase
      b. proteins that shut off host protein synthesis, extend life cycle of the cell, and
      modulate the immune response
      c. capsid particles
      d. viral DNA dependent DNA polymerase

4. HSV 1&2 can establish a latent or recurrent infecction in the ________ that supply the
site of the primary infection. During latency the viral genome becomes _______.

5. Why is serology not a useful diagnosis for herpes? What are other diagnostic tools?

6. Why does acyclovir not affect host cells?
ANSWERS: Herpes

1. During replication, the Herpes virus:
       a. linearizes (normally circular) and inserts into the host genome
       b. Uses host cell polymerases
       c. circularizes (normally linear), and uses its own polymerase
       d. circularizes (normally linear), and uses the host polymerase

2. Which of the following have a broad host range and are highly lytic in culture?
       a. Herpes simplex 1&2, Varicella Zoster – alpha herpes viruses
       b. CMV, HHV 6&7 (beta herpes viruses – slow growth, infected cells enlarged)
       c. EBV and HHV8/Kaposi‟s Sarcoma – associated herpesvirus (gamma
herpesviruses, these cause DNA tumors)

3. Which of the following genes are expressed during both early and late times during
HSV cell infection?
      a. polymerase and thymidine kinase (these are early genes)
      b. proteins that shut off host protein synthesis, extend life cycle of the cell, and
      modulate the immune response
      c. capsid particles (late genes)
      d. viral DNA dependent DNA polymerase (early genes)
      *There are also immediate early genes, called transactivators which intitiate txn of
      polymerase and thymidine kinase genes.

4. HSV 1&2 can establish a latent or recurrent infecction in the ganglia of the nerves that
supply the site of the primary infection. During latency the viral genome becomes
chromatinized (few genes are expressed, resulting in immune evasion).


5. Why is serology not a useful diagnosis for herpes? What are other diagnosis tools?
       Because there is a high prevalence of IgG antibody in the normal population.
Only IgM can be useful in detection of primary infection.

6. Why does acyclovir not affect host cells?
        Because acyclovir is bound by the viral thymidine kinase with much more affinity
than the host thymidine kiase to become monophosphorylated. Then either the host or
the viral thymidine kinase add on 2 more phosphate groups to become a triphosphate, at
which point it mimics dGTP (however it lacks a 3‟ OH).

Back to Table of Contents
QUESTIONS: Human Papilloma Virus

1. In mid stratum spinosum, high levels of replication of HPV depend on:

a) Early promoter
b) E4
c) E1 and E2
d) E6, E7, and L1


2. What are high risk types of HPV NOT?

a) Frequent in cancer
b) Most prevalent in population regardless of disease status
c) Types 16, 18, and 45
d) Maintained as extrachomosomal DNA epitopes


3. Oncogenic HPV strains are likely to disrupt:

a) E1 ORF
b) E2 ORF
c) Rb gene
d) p53 gene


4. HPV does not cause:

a) Oral warts in some people
b) Genital warts in some people
c) Oral cancer in some people
d) Respiratory tract warts in some neonates
e) Persistent infections in most people


5. Where does HPV assemble?

a) stratum corneum
b) stratum granulosum
c) stratum spinosum
d) stratum basale
1. c
2. d
3. b
4. e
5. b

Back to Table of Contents


QUESTIONS: Human Immunodeficiency Virus: Pathogenesis and Disease

1. What is the only family of oncogenic retrovirus?

2. What diseases are associated with HTLV-1?

3. Describe the structure of the HIV virus.

4. What are M-tropic and T-tropic HIV viruses?

5. How is AIDS defined?

6. How long is the incubation period of HIV?

7. Compare the CD4+ cell counts in tissue and the CD4+ cell counts in the peripheral
   blood over the period of 20 years.

8. Describe the antiviral CTL response.

9. What is the difference between virological and clinical latency?

10. Potent inhibition of HIV viral replication can result in either a rapid or slow recovery
    of CD4+ cells. Compare these two types of CD4+ recovery processes.

11. What is the immune reconstitution syndrome? How is it treated?

12. What infections are common in AIDS patients?
ANSWERS: HIV

1. What is the only family of oncogenic retrovirus?

          human T-cell leukemia viruses (HTLV-1 and HTLV-2)

2. What diseases are associated with HTLV-1?

          adult T-cell leukemia, HTLV-1 associated myelopathy, Tropical Spastic
           Paraparesis

3. Describe the structure of the HIV virus.

   •   Envelope
          – lipid bilayer with gp41 (red) and gp120 (yellow)
   •   Capsid
          – icosahedrol Matrix (p17) and dense Capsid (p24) proteins
          – Nucleoprotein core (p6) protein
                • 2 identical ssRNA copies of genome
                • 50 copies of RT
                • A few other viral molecules: protease, integrase, Vpr, Vif, Nef, p6

4. What are M-tropic and T-tropic HIV viruses?

   •   Sequences within Env gp120 (mostly the V3 loop) determine co-receptor usage
          – CCR5 using viruses = M-tropic (R5)  causes most new inections
          – CXCR4 using viruses = T-tropic (X4)
          – R5-virus causes slower loss in CD4 T cells
          – X4-virus causes rapid loss in CD4 T cells

5. How is AIDS defined?

   •   AIDS
          – HIV-infected and CD4 count <200/µl blood
          – susceptible to opportunistic infections and cancer
               • thrush + HIV = AIDS

6. How long is the incubation period of HIV?

   •   1-4 weeks

7. Compare the CD4+ cell counts in tissue and the CD4+ cell counts in the peripheral
   blood over the period of 20 years.

   CD4 counts drop sharply in tissues with acute HIV infection and never recover. CD4
   counts in the peripheral blood drop, recover, and then drop more slowly.
8. Describe the antiviral CTL response.

   –   lysis of virus-infected cell before mature virions are released
   –   inhibition of viral replication (interferon-g)
   –   inhibition of viral entry into surrounding cells

9. What is the difference between virological and clinical latency?

      clinical latency: the period of time between infection with HIV and the
       development of HIV-related clinical problems (AIDS)
      virological latency: the rare state of virus in which proviral DNA is integrated into
       the host chromatin, but virus is not expressed; occurs in resting memory CD4+
       cells

10. Potent inhibition of HIV viral replication can result in either a rapid or slow recovery
    of CD4+ cells. Compare these two types of CD4+ recovery processes.

   –   Rapid but incomplete increase in CD4+ T cells
          – mostly memory CD4+ T cells
          – skewed T cell receptor repertoire (“forgotten pathogens”)
          – redistribution vs proliferation of memory CD4+ cells
          – cannot replace lost T cell specificities
   –   Slow steady rise in CD4+ T cells
          – mostly naïve CD4+ T cells
          – derived from the thymus
          – can replace lost T cell receptor specificities

11. What is the immune reconstitution syndrome? How is it treated?

   •   inflammatory systemic disease due to reawakened host response to pathogens
   •   treatment = steroids!

12. What infections are common in AIDS patients?

   –   Protozoans: Pneumocystis jiroveci pneumonia (PCP), toxoplasma gondii,
       Cryptosporidia, Strongyloides
   –   Viral infections: CMV, HSV, HHV-8, JCV
   –   Fungi: Candida, Cryptococcus, Histoplasmosis
   –   Bacteria: Mycobacterium tuberculosis, Mycobacterium avium complex,
       Treponema pallidum


Back to Table of Contents
QUESTIONS: Urinary Tract Infections
1. What are the three bacteria to be thinking about when it comes to UTI‟s? Which one
   is linked to sexual activity most directly?


2. Describe the four presentations of urinary tract infections including Cystitis,
   Pyelonephritis, Asymptomatic infections, nosocomial infections.


3. What are the pathogenic factors used by UPEC and Staph saprophyticus?


4. How do you diagnose a UTI these days? How do you treat each of the four cases?


5. What bacteria on our your differential for bacterial vaginosis? How do you diagnose?


6. What are the complications involving BV?
ANSWERS: UTI and BV
1. What are the three bacteria to be thinking about when it comes to UTI‟s? Which one
   is linked to sexual activity most directly?
UPEC, Staph saprophyticus, Enterobacteriaceae. Staph sapro is linked to sexual activity.
UPEC is believed to come from intestinal tract.
2. Describe the four presentations of urinary tract infections including Cystitis,
   Pyelonephritis, Asymptomatic infections, nosocomial infections.
Cystitis is the typical presentation of polyurea, painful unrination. The urine will include
WBCs.
Pyelonephritis-kidney infection that presents with flank pain, systemic symptoms.
Bacteremia can cause shock and death.
Many infections can be asymptomatic and be carried for years. Nosocomial infections
are VERY common for extended catheterization reaching almost 100% infection rate,
and greatly increases morbidity in elderly patients.
3. What are the pathogenic factors used by UPEC and Staph saprophyticus?
UPEC uses fimbrial adhesins to adhere to uroepithelial cells. Women who are infection
prone express more receptors that the adhesins are capable of binding too. UPEC forms a
biofilm and continually reinfects new layers as epithelium exfoliates.
Staph saprophyticus has its own attachment molecule that is not a fimbriae, but a surface
protein termed Uro-Adherence Factor A. Stap sap. has a urease that accommodates urine
environment to use urea as nitrogen source. This is associated primarily with cystitis,
debatable for pyelonephritis.
4. How do you diagnose a UTI these days? How do you treat each of the four cases?
Use urine dipstick for presence of leukocytes. Uses nitrate conversion ability of E. coli
like we talked about in case and leukocyte esterase. Cystitis receives a short course Abx
treatment. Pyelonephritis requires longer 2 week course, oral or iv. Bacteruria needs to
be treated in pregnant women. Nosocomial infections can be treated with continual
Abx‟s but you really need to get the device out.
5. What bacteria on our your differential for bacterial vaginosis? How do you diagnose?
Gardenerella vaginosis, Mycoplasma hominis, and other anaerobes. Diagnose using
culture, pH in vagina of >4.5, homogeneous discharge and a fishy odor in conjunction
with KOH test.
6. What are the complications involving BV?
Causes serious pregnancy complications, you name it. Increased risk of STD‟s and PID.

Back to Table of Contents
QUESTIONS: Skin Infections: (Rubenstein lecture, no syllabus, 5-3-07…only
material on the test:)
      1. What is the most common bacterial infection of the skin? What type of patient
          does NOT get this infection?
      2. What is an example of a Type 1 Immediate Hypersensitivity Response (a.k.a
          hives)?
      3. Lichen Planus is an example of a __________ immune response to the skin.


ANSWERS:
  1. Staph Aureus. Patients with Psoriasis do not get Staph infections.
  2. Urticaria. It‟s very common, and has many causes.
  3. Cell-mediated. (it is not considered an autoimmune response despite its similarity
     to lupus in that lymphocytes attack keratinocytes).

Back to Table of Contents
QUESTIONS: Varicella Zoster Virus

1. What is the sequence of skin lesions in chicken pox infections?
      a. papules  macules  vesicles  pustules  scabs
      b. macules  papules  pustules  vesicles  scabs
      c. vesicles  pustules  macules  papules  scabs
      d. macules  papules  vesicles  pustules  scabs

2. Which of the following is FALSE about shingles (zoster) and chicken pox (varicella)?
      a. While shingles is localized to the dermatome, chicken pox is a disseminated
      disease
      b. Varicella is a reactivation of latent zoster.
      c. Initial infection of chickenpox is via respiratory aerosols
      d. Symptoms of varicella include headache, fever, malaise all within 1-2 days
      before onset of exanthem.
      e. Shingles may be extremely painful preceding and following the vesicular
      phase.

3. What are characteristics of virally infected skin/mucosal cells? Leukocytes? Neurons?

4. Which of the following is FALSE concerning VZV?
      a. Epidemics of chicken pox occur in late winter – early spring.
      b. The course of the infection and its resolution is primarily mediated by humoral
      immunity
      c. It is rare for a person to undergo more than one episode of shingles
      d. Devlopment of shingles usually results from waning of specific humoral
      immunity for VZV.
      e. Primary disease gives life long immunity to chicken pox.

5. What is the basis of the Tzank Smear? Is it a definitive identification for VZV?

6. What is a “breakthrough infection”? Is it more or less severe than normal infections?
Is it still contagious?
ANSWERS Varicella Zoster Virus

1. What is the sequence of skin lesions in chicken pox infections?
      a. papules  macules  vesicles  pustules  scabs
      b. macules  papules  pustules  vesicles  scabs
      c. vesicles  pustules  macules  papules  scabs
      d. macules  papules  vesicles  pustules  scabs

2. Which of the following is FALSE about shingles (zoster) and chicken pox (varicella)?
      a. While shingles is localized to the dermatome, chicken pox is a disseminated
      disease
      b. Varicella is a reactivation of latent zoster. (zoster is a reactivation of latent
      varicella).
      c. Initial infection of chickenpox is via respiratory aerosols
      d. Symptoms of varicella include headache, fever, malaise all within 1-2 days
      before onset of exanthem.
      e. Shingles may be extremely painful preceding and following the vesicular
      phase.

3. What are characteristics of virally infected skin/mucosal cells? Leukocytes? Neurons?
        Infected cells undergo degenerative cytopathic changes, including proming
nuclear inclusion bodies and formation of multinucleated giant cells.
        Leukocytes are infected at the lymph node and then disseminate. These virus-
infected leukocytes result in viremia.
        Neurons in the dorsal root (sensory) are infected with viruses and which then
establish a latent infection. This is a form of hiding since neurons don‟t display MHC I.

4. Which of the following is FALSE concerning VZV?
      a. Epidemics of chicken pox occur in late winter – early spring.
      b. The course of the infection and its resolution is primarily mediated by humoral
      immunity (primarily mediated by CMI)
      c. It is rare for a person to undergo more than one episode of shingles
      d. Devlopment of shingles usually results from waning of specific humoral
      immunity for VZV. (This answer is correct, but it is also presumably due to
      waning of specific CMI as well).
      e. Primary disease gives life long immunity to chicken pox.

5. What is the basis of the Tzanck Smear? Is it a definitive identification for VZV?
        The Tzanck Smear is when you scrape material from the base of the vesicular
lesions. Then you look for giant multinucleate cells in the sample. It can be more
diagnostic if you use specific VZV fluroescent antiviral Abs. However, the most
definitive test for the virus is via culture.

6. What is a “breakthrough infection”? Is it more or less severe than normal infections?
Is it still contagious?
       A breakthrough infection is when someone comes down with chicken pox more
than 42 days after receiving the vaccine. Breakthrough infections are usually mild with
much less extensive rash, often just macular lesions. However, these patients are
contagious!

Back to Table of Contents
QUESTIONS: Wounds and Staph Aureus


1. What pathogen most likely causes pyodermas?

a) GAS
b) GBS
c) staph aureus
d) strept pyogenes
e) a and c


2. What pathogen most likely causes cellulitis ?

a) GAS
b) GBS
c) staph aureus
d) strept pyogenes
e) a and c


3. What do you NOT worry about in bite wounds?

a) Eikenella corrodens
b) Pasteurella multocida
c) Actinomyces
d) Capnocytophaga canimorsus

4. What do you NOT worry about in chronic, slow-growing infections secondary to
trauma?

a) Nocardia
b) Staphlococcus aureus
c) Actinomyces
d) Mycobacterium marinum

5. What do you worry about in an enivormental contaminated wound?

a) GAS
b) GBS
c) Clostridium perfringens
d) Clostridium difficile
e) Clostridium tetani
6. What causes chronic infection especially of head and neck?

a) Actinomyces
b) Proponobacterium acnes
c) Bacteroides fragilis

7. What is often associated with infections of CNS shunts?

a) Actinomyces
b) Proponobacterium acnes
c) Bacteroides fragilis

8. Which is gram negative?

a) Actinomyces
b) Proponobacterium acnes
c) Bacteroides fragilis

9. Which often produces abscesses in female GU system?

a) Actinomyces
b) Proponobacterium acnes
c) Bacteroides fragilis

10. Match the virulence factors of Staph aureus with what they do:

a) peptidoglycan                                4. degradative enzymes; important of
b) teichoic acid                                spread of organisms through tissue
c) adhesins                                     5. binds to fibronectin; important in
d) slime layer                                  adherence to endothelial surfaces and
e) DNAse and hyaluronidase                      foreign objectives
f) hemolysins                                   6. plays a role in the desquamation seen
g) Panton-Walentine leukocidin                  in staphylococcal scalded skin syndrome
h) Epidermolytic toxin                          7. role in biofilm formation
i) Enterotoxin F                                8. pro-inflammatory
j) Protein A

1. acid component of cell wall; mediates
adherence
2. is biochemicallyidentical to toxic
shock syndrome toxin
3. forms lytic pores in membrane in
white cells, contributes to abscess
formation
ANSWERS: Wounds

1. e
2. e
3. c
4. b
5. c, but e is also probably true
6. a
7. b
8. c
9. c
10.
Peptidoglycan-pro-inflammatory
Teichoic acid component of cell wall; mediates adherence
Adhesins-binds to fibronectin; important in adherence to endothelial surfaces and foreign
objectives
Slime layers-role in biofilm formation
-DNAse and hyaluronidase-degradative enzymes; important of spread of organisms
through tissue
-Hemolysins-cytolysins
-Panton-Valentine leukocidin-forms lytic pores in membrane in white cells
        •Contributes to abscess formation
        •Commonly found in strains that cause superficial skin and infection and
        pneumonia
        •Associated with high mortality in patient with community acquired pneumonia
–Epidermolytic toxin-plays a role in the desquamation seen in staphylococcal scalded
skin syndrome
–Enterotoxins-A-F; F is biochemically identical to toxic shock syndrome toxin


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QUESTIONS: Introduction to Mycology, Antifungals, and Superficial Mycoses

1. What are the differences between yeast and mold?

2. What is a dimorphic fungus?

3. How are fungi different from bacteria?

4. Match the following class of antifungal medications with their mechanism of action.

       1. polyenes                   a. inhibit protein synthesis by incorporation of
                                     alternative RNA nucleotides (e.g 5-fluorocytosine)
       2. azoles                     b. inhibit ergosterol synthesis by cytochrome P450
                                     inhibition (e.g. flucanazole, micanzole)
       3. anti-metabolites           c. inhibit glucan synthesis; used to treat Candida
                                     species or those unable to tolerate Aspergillus
                                     therapy (e.g. caspofungin)
       4. echinocandins              d. bind to ergosterol (e.g. amphotericin)

5. What infections are most commonly associated with Candida species?

6. What are three genera of organisms cause dermophyte infections? What is there
   shared mechanism of action?

7. Name the dermophytes that can cause each of the infections below:

   Tinea capitis
   Tinea corporis
   Tinea cruris
   Tinea pedis
   Tinea unguium

8. Describe the identifying characteristics of Candida albicans.

9. What are the 5 different types of hyphae?
ANSWERS: Mycology
1. What are the differences between yeast and mold?

   Yeast              Mold
   Unicellular        Multicellular
   Budding            Sporulation
   Pseudohyphae       hyphae

2. What is a dimorphic fungus?

   Room temp  mold
   Body temp  yeast

3. How are fungi different from bacteria?

   Fungi: Larger, dimorphic, eukaryotic, chitin cell well, sterols in cytoplasmic
   membrane, reproduction by budding, multiple spore types

   Bacteria: Smaller, no dimorphism, prokaryotic, no sterols in cytoplasmic membrane,
   reproduction by binary fission, endospores

4. Match the following class of antifungal medications with their mechanism of action.

       1. polyenes                    a. inhibit protein synthesis by incorporation of
                                      alternative RNA nucleotides (e.g 5-fluorocytosine)
       2. azoles                      b. inhibit ergosterol synthesis by cytochrome P450
                                      inhibition (e.g. flucanazole, micanzole)
       3. anti-metabolites            c. inhibit glucan synthesis; used to treat Candida
                                      species or those unable to tolerate Aspergillus
                                      therapy (e.g. caspofungin)
       4. echinocandins               d. bind to ergosterol (e.g. amphotericin)

       1. D   2. B    3. A    4. C

5. What infections are most commonly associated with Candida species?

   Nosocomial bloodstream infection (Candida albicans)
   Fungal endocarditis
   Spectrum of severity:
      [superficial] Diaper rash, oral thrush, candidal vaginitis, UTI, ocular infection,
   abscesses; infections primarily occur in immunocompetent patients
      [invasive] fugemia, endocarditis; infections primarily occur in
   immunocompromised patients
6. What are three genera of organisms cause dermophyte infections? What is there
   shared mechanism of action?

   Epidermophyton, Microsporum, Trichophyton
        possess keratinases that allows them to parasitize the fully keratinized tissues
   of the body

7. Name the dermophytes that can cause each of the infections below:

   Tinea capitis – Trichophyton (endothrix infection); Microsporum (ectothrix infection)
   Tinea corporis – most dermophytes capable of infecting humans
   Tinea cruris – Epidermophyton and Trichophytan
   Tinea pedis – Trichophyton and C. albicans
   Tinea unguium – Trichophyton and C. albicans

8. Describe the identifying characteristics of Candida albicans.

          Oval, 3-6 um
          Reproduce by budding
          Pseudohyphae

9. What are the 5 different types of hyphae?

          Septate
          Aseptate
          Hyaline
          Dematiaceous
          Pseudohyphae

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