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Bacterial Infections Part II

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					       Group A Streptococcal Infections
• Also known as “flesh eaters”

• Primary pathogen is S. pyogenes
   – Can cause rapidly deteriorating
     disease and death

• Common cause of wound
  infections
   – Generally easily treated due to
     susceptibility to antimicrobials
More severe infections are called invasive
and include:

  – Pneumonia
  – Meningitis
  – Puerperal fever
  – Necrotizing fasciitis (flesh eating disease)
  – Streptococcal toxic shock
Causative Agent
  – S. pyogenes
    •   β-hemolytic, Gram-positive cocci in chains
    •   Group A Lancefield cell wall polysaccharide
    •   Some strains cause invasive infection
    •   Two extracellular products are responsible for
        virulence
         Pyrogenic exotoxin A
             Acts as a superantigen and causes streptococcal toxic
             shock
         Exotoxin B
             Destroys tissue through protein breakdown
Symptoms
 – Acute pain at the site of the wound
 – Swelling
 – Fever and confusion
 – Overlying skin tightens and becomes
   discolored
 – Shock and death
   • In the absence of treatment
Pathogenesis
  – Wound colonization enhanced through tissue binding
    proteins

  – Subcutaneous fascia is destroyed in necrotizing
    fasciitis
     • Muscle tissue is also destroyed by bacterial penetration

  – Organisms multiply and produce toxic products
     • Organisms and toxic products enter bloodstream
Epidemiology
  – “Flesh eating” infections have been described since
    the 5th century B.C.
     • 2,000 cases reported during Civil War

  – Cases generally sporadic
     • Small epidemics have occurred
     • Outbreak in San Francisco in 1996
         – Traced to use of contaminated “black tar” heroine


  – Approximately 9,000 cases of invasive S. pyogenes in
    2002
     • Resulted in 1080 deaths
     • 135 from necrotizing fasciitis
Prevention and Treatment
  – No proven prevention measures
  – Urgent surgery required due to rapidity of
    toxin spread
     • Amputation is sometimes required

  – Penicillin is still an effective treatment
     •   Must be given early
     •   Has little or no effect on bacteria in necrotic tissues
     •   No effect on toxin
     •   Surgery may still be necessary
  Pseudomonas aeruginosa Infections

P. aeruginosa is an
opportunistic pathogen


Major cause of
nosocomial infections
   Occasional cause of
   community acquired
   infections
• Community acquired infections include
  – Rash and external ear infections
       • Obtained from contaminated swimming pools and hot tubs
  –   Infection of foot bones
  –   Eye infections
  –   Heart valve infections
  –   Lung biofilms (cystic fibrosis)


• Nosocomial infections include
  – Lung infections
  – Especially burn infections
Causative Agent
  – Pseudomonas aeruginosa
    • Motile by means of single polar flagellum
    • Generally aerobic
       – Can grow anaerobically in the presence of nitrate
Symptoms
  – Change in tissue color
     • P. aeruginosa releases red, yellow and blue pigments.
     • Often, a fluorescent pigment (pyoverdin) combines with a blue
       pigment (pyocyanin) to produce the characteristic green color

  – Chills, fever, skin lesions and shock
Pathogenesis
  – Overall effect is tissue damage, prevention of healing
    and increased risk of septic shock

  – Some strains produce enzymes and toxins to
    enhance their virulence

     • Exoenzyme S (interferes with host intracellular signaling)

     • Toxin A (inhibits protein synthesis and

     • Phosphlipase C (breaks down lecithin, a component of the
                        host cell membrane)
Epidemiology
  – P. aeruginosa is widespread in nature
     • Found extensively in soil, water and on plants

  – Introduced in hospitals, on the soles of shoes, on
    ornamental plants and flowers and on produce

  – Bacteria will persist in dampness or standing water

  – Contaminates soaps, ointments, eye drops,
    swimming pools and hospital equipment
Prevention and Treatment
  – Prevention involves elimination of sources of bacteria

  – Prompt wound care

  – Removal of dead tissue from burns
     • Followed by application of antibacterial cream
         – Silver sulfadiazine

  – Established infections are extremely difficult to treat
     • P. aeruginosa is multi-drug resistant

  – Medications must be administered intravenously at
    high doses
                     Human Bites
Symptoms
  – Wound may appear insignificant

  – Eventually becomes painful and swells

  – Pus discharge
     • Pus often foul smelling

  – Most wounds are on exterior of hand
     • Swelling may involve palm
     • Movement may be hampered
Pathogenesis
  – Crushing nature of bite provides anaerobic
    conditions for infection

  – Mouth flora generally harmless
    • Produce a synergistic infection
       – Together produce numerous toxins and enzymes
       – Encapsulated flora resist phagocytosis
       – Facultative organisms reduce available oxygen allowing
         growth of anaerobic microbes
Epidemiology
  – Most serious human bite results from violent
    altercations

  – Risk of infection increases when biting
    individual has poor oral hygiene
    • Bites by small children are usually inconsequential
Prevention
  –   Avoid situations that may lead to altercation
  –   Prompt cleaning
  –   Application of antiseptic
  –   Immediate medical attention if infection becomes evident


Treatment
  – Medical treatment consists of
       •   opening wound
       •   irrigating with sterile fluid such as saline
       •   Removal of dirt and dead skin
       •   Use of antibacterial medication
             – Effective against anaerobes

				
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