Skin bone and joing infections gangrene

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					Infectious Disease Emergencies

      Charles S. Bryan, M.D.
        December 3, 2007
            William Osler, 1897

 “Humanity has but three
  great enemies: fever,
  famine, and war; of these
  by far the greatest, by far
  the most terrible, is
  fever.”
                  Review
 Most common cause of meningitis, all ages
  considered: Streptococcus pneumoniae
 Right-sided staphylococcal endocarditis:
  injecting drug use, positive blood cultures,
  bilateral pulmonary infiltrates
 Left-sided staphylococcal endocarditis:
  underlying valvular disease (variable),
  positive blood cultures, systemic emboli
  often with skin lesions
              West Nile virus
 Meningitis or encephalitis in about one in every
  150 patients
 Most common in late summer or early fall—
  associated with mosquitoes and corvids
 Muscle weakness is often severe
 Flaccid paralysis suggesting Guillain-Barre
  syndrome sometimes occurs
 Unlike HSV, does NOT favor the temporal lobe
            22 year old WM
   10 days PTA: injured right chest wall in
    fight
   3 days PTA: presents with severe pain.
    Physical examination essentially benign.
    Spiral CT scan of chest negative for
    pulmonary embolism. Rx: NSAIDs
   On admission: Hypotensive, severe pain in
    right pectoral area
        Necrotizing fasciitis

 Fascial necrosis with widespread
  undermining of the skin
 Typically begins with nonspecific
  symptoms such as localized pain, high fever
 Pain and toxicity often disproportionate to
  skin findings on physical examination
      Necrotizing fasciitis (2)
 Suggestive skin findings: erythema
  darkening into a reddish-purple hue;
  crepitation; local anesthesia; vesicles and
  bullae
 Other findings: toxicity, tachycardia,
  tachypnea, hypotension
      Necrotizing fasciitis (3)
 Type 1: Mixed aerobic and anaerobic
  infection (more common in patients with
  diabetes mellitus; called “Fournier’s
  gangrene” when perineum, gluteal area,
  scrotum are involved
 Type 2: Group A streptococci (S. pyogenes)
Do NSAIDs predispose to necrotizing
fasciitis while masking the evidence?
“Surgical” infections of the skin (1)
 Progressive synergistic gangrene (Meleney’s
 infection): microaerophilic streptococcus at
 periphery, S. aureus in center; a central,
 shaggy necrotic ulcer surrounded by a dusky
 margin and an erythematous periphery; often
 complicates wounds or other lesions
“Surgical” infections of the skin (3)
    Synergistic necrotizing cellulitis:
    usually in patients with diabetes
    mellitus; a painful, rapidly-
    progressing, usually-polymicrobic
    (aerobic + anaerobic) cellulitis with
    copious, foul-smelling “dishwater”
    drainage from affected areas
          Anaerobic cellulitis
 Clostridial anaerobic cellulitis: a necrotizing
  infection with impressive gas formation but
  without myositis
 Nonclostridial anaerobic cellulitis: typically due
  to a mixture of aerobic and anaerobic bacteria.
  Aerobic gram-negative rods sometimes cause
  crepitant cellulitis especially in patients with
  diabetes.
           68 year old WM
 Presents to ER with pain in right lower
  extremity (“feels heavy”) and systemic
  toxicity
 PMH: Hypertensive atherosclerotic
  cardiovascular disease
 PE: Dusky color, mild crepitance to right
  lower extremity
           Gas gangrene
 Clostridium perfringens and other species
 Spectrum of C. perfringens: wound
  contamination; crepitant cellulitis;
  anaerobic myonecrosis (true gas gangrene)
 Sudden, severe pain; gas; extreme toxicity;
  hemolytic anemia; hypotension; renal
  failure
    Infectious causes of soft tissue gas
 Clostridial myonecrosis
 Clostridial anaerobic cellulitis
 Nonclostridial anaerobic cellulitis
 Synergistic necrotizing cellulitis
 Necrotizing fasciitis
 Nonclostridial crepitant myositis
 Soft-tissue infections due to aerobic bacteria (especially in
  diabetics)
Non-infectious causes of soft-tissue gas
    Penetrating trauma
    Compressed air
    Hydrogen peroxide
    IV catheters
    Factitious
         Gas gangrene (1)
 Six species of Clostridia can cause: C.
  perfringens in about 80%
 Saprophytes widespread in soil
 May coexist with another infection
 Toxins: lecithinases that destroy cell
  membranes, alter capillary
  permeability
              Gas gangrene (2)
 Incubation period: 7 hours to 6 weeks
 Sense of increasing weight in the area progressing
  to pain and toxicity
 Gas often absent
 Can involve just about any body tissue (not just
  skin and subcutaneous tissue)
 Massive hemolysis can result from clostridial
  invasion of bloodstream
         Sphenoid sinusitis
 “The worst headache ever” (other infectious
  causes: meningitis, brain abscess, Rocky
  Mountain spotted fever, falciparum malaria)
 Complications: cavernous sinus thrombosis,
  pituitary infarction, meningitis, stroke,
  cranial nerve palsies
 Diagnosis: usually by imaging
              Pericarditis
 Complications: pericardial tamponade,
  constrictive pericarditis
 Acute pericarditis: most commonly
  “idiopathic” and presumed viral
 M. tuberculosis always an important
  consideration
Aortitis and mycotic aneurysm
 “Mycotic” aneurysm: aneurysm due to
  infection (“mycotic” suggests fungal, but
  the adjective is misleading here)
 Salmonella a common cause—affinity for
  atherosclerotic plaques
 Uniformly fatal without resection
                  Acute epiglottitis
 A life-threatening
  cellulitis of the epiglottis
  and adjacent structures
 Onset usually sudden (as
  opposed to gradual onset
  of croup); drooling,
  dysphagia, sore throat
 H. influenzae the usual
  pathogen both in
  children (the usual
  patients) and adults
               Acute epiglottitis
 In children, onset usually
  sudden with fever,
  dysphonia, difficulty
  breathing; child typically
  leans forward and drools
 Adults more likely to
  present with severe sore
  throat, odynophagia,
  sensation of airway
  obstruction
Deep fascial space infections of
      the head and neck
 Several syndromes according to anatomic
  planes
 Can complicate odontogenic or
  oropharyngeal infection
 Ludwig’s angina: bilateral involvement of
  submandibular and sublingual spaces
  (brawny cellulitis at floor of mouth)
  Deep fascial space infections of
      the head and neck (2)
 Lemierre syndrome: suppurative thrombophlebitis
  of internal jugular vein (Fusobacterium
  necrophorum)
 Retropharyngeal space infection: contiguous
  spread from lateral pharyngeal space or infected
  retropharyngeal lymph node; complications
  include rupture into airway, septic thrombosis of
  internal jugular vein
Some fascial spaces of head and neck
Retropharyngeal & prevertebral spaces
                    Tetanus
 Clostridium tetani: gram+ tennis racket
 Early symptoms may be nonspecific
 Trismus: consider other causes
 Generalized tetanus: opisthotonus, rigid abdomen, risus
  sardonicus
 Sympathetic stimulation: labile blood pressure,
  arrhythmias
 Prevention: TIG, toxoid
             Tetanus (2)
 All  of the features are due to
  tetanospasmin, an exotoxin produced
  by the vegetative form
 Spores are resistant to most agents and
  can survive in soil for years,
  converting to the vegetative form if Eh
  is low.
                  Tetanus (3)
 Tetanospasmin acts on four areas of the nervous
  system: motor end plates of skeletal muscle;
  spinal cord; brain; and sympathetic nervous
  system
 In muscle, there is inhibition of ACh release
  from nerve terminals
 In spinal cord, there is inhibition of antagonists
  (similar to strychnine)
            Tetanus (4)
        on sympathetic nervous
 Effects
 system: labile hypertension,
 tachycardia, peripheral
 vasoconstriction, cardiac arrhythmias,
 profuse sweating, hypercarbia, late-
 appearing hypotension
          Clinical forms of tetanus
 Generalized: usually from a minor wound; trismus in
  > 50%; seizures; sweating; restlessness; irritability;
  rigidity; difficulty swallowing; intense pain during
  seizures
 Localized: persistent rigidity in a group of muscles
  near the injury
 Cephalic: usually follows head trauma or otitis media;
  cranial nerves involved; poor prognosis
Potential Agents of Bioterrorism
 Category A: Organisms that are highly
  disseminated from a central source or
  transmitted from person to person, cause high
  mortality, require special action for public health
  response, and often disrupt society.
 Examples: smallpox, anthrax, plague, tularemia,
  botulism, certain viral hemorrhagic fevers (e.g.,
  Ebola, Marburg, Argentine; also, Lassa fever)
Potential Agents of Bioterrorism (2)
  Category B: Organisms that are moderately easy
   to disseminate, cause low mortality but
   considerable morbidity, and pose difficulties in
   recognition.
  Examples: Salmonellosis, shigellosis, cholera,
   cryptosporidiosis, hemorrhagic colitis (E. coli
   0157:H7), Q fever, brucellosis, glanders, viral
   encephalitis
Potential Agents of Bioterrorism (3)
  Category C: Organisms that could be
   bioengineered in the future with the potential for
   high morbidity and mortality with major public
   health impact.
  Examples: multi-drug resistant tuberculosis,
   yellow fever, hantaviruses, tickborne
   hemorrhagic-fever viruses, tickborne
   encephalitis viruses, nipah virus
  Bioterrorism, Category “A”)
 Smallpox
 Anthrax
 Plague
 Tularemia
 Botulism
 Viral hemorrhagic fevers such as Ebola,
  Marburg, and Argentine hemorrhagic fevers
  and Lassa fever
     Smallpox
 A painful pustular rash
 Individual pustules
  resemble those of
  chickenpox, but the
  pustules appear
  simultaneously and are
  concentrated most heavily
  on the face and pharynx.
                Smallpox
 Transmission does not occur until the onset
  of the rash, with the maximum being days 7
  to 10 of the rash.
 Increased infectiousness if patient is
  coughing or has a hemorrhagic form of
  smallpox.
 Vaccination does not confer lifelong
  immunity.
                      Anthrax

 20,000 to 100,000
  cases worldwide
  annually.
 In U.S., less than 1
  case per year for past
  20 years
 Gram-positive bacillus
                Bacillus anthracis
 Virulence factors
  encoded by 2 plasmids
 Polyglutamyl capsule
  inhibits phagocytosis of
  vegetative forms
 Exotoxins: “edema
  toxin” and “lethal toxin”
  (causes release of TNF-
  alpha and IL-1-beta)
                 Anthrax
 Cutaneous form: “malignant pustule”
  (papule evolves into pustule, then black
  eschar)
 Abdominal form: rare
 Inhalational form: flu-like illness followed
  in 3 to 5 days by rapid deterioration with
  hemorrhagic mediastinitis (mediastinal
  widening on chest x-ray)
Cutaneous anthrax
             Inhalational anthrax
 Biphasic illness: First
  phase looks like non-
  differentiated viral
  illness
 Second phase:
  hemorrhagic
  mediastinitis, shock,
  meningitis
Inhalational anthrax: implications
  Anthrax does not cause “cold syndrome”
   with rhinitis (runny nose) and sore throat
  However, it does look like influenza
   (malaise, myalgias, nonproductive cough,
   chest discomfort)
  Therefore, recommend liberal use of flu
   vaccine
         Plague (Yersinia pestis)

 Two principal forms:
  bubonic plague,
  pneumonic plague
 “Bubo”: enlarged,
  suppurating lymph
  node
         Plague (Yersinia pestis)
 Endemic in American Southwest (e.g., Four
  Corners Area) in ground squirrels, rock
  squirrels, prairie dogs. Has also been traced to
  domestic cats.
 Bubonic plague: fever, chills, headache,
  lymphadenopathy, progressing to sepsis
 Pneumonic plague: usually from hematogenous
  seeding from a bubo but can occur as a result of
  inhalation
                   Tularemia

 Franciscella tularensis
 Three principal forms:
  oculoglandular,
  ulceroglandular,
  typhoidal
Plague and tularemia as causes
    of bilateral pneumonia
                    Botulism

A   paralytic disease that begins with cranial
  nerve involvement and progresses caudally
  to involve the extremities caused by
  neurotoxins elaborated by C. botulinum
 C. botulinum: types A through G based on
  antigenic specificities of toxins; all but one
  of the toxins are neurotoxins
            Botulinum neurotoxin
 Is transported to peripheral cholinergic nerve terminals;
  CNS is not involved
 Steps: (1) binds to presynaptic nerve cells; (2)
  internalizes inside the nerve cells in vesicles; (3)
  translocates into the cytosol; (4) destroys by proteolysis
  components of the neuroexocytosis apparatus that
  curtails release of acetylcholine (cure follows sprouting
  of new nerve terminals)
            Types of botulism
 Food-borne   (preformed toxin)
 Wound botulism (contamination of wounds)
 Infant botulism (ingestion of spores and
  production of toxin in the intestines)
 Undetermined (some cases in older children
  and adults in which mechanism is probably
  that of infant botulism)
        Hantavirus pulmonary
             syndrome
 First described in Four Corners Area; occurs
  mainly from inhaling aerosolized rodent excreta
 Fever, malaise, and myalgia followed about 3 to 6
  days later by rapid onset of hypotension with
  pulmonary edema
 Diagnosis: high index of suspicion based on
  hypotension and pulmonary edema in a patient
  with out-of-doors exposure
“Sufficient unto the day are the
         evils thereof.”

				
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posted:1/26/2011
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