Anaerobic Infections Flashcards

1
Q

Skin Infections

A

Result from 3 mechanisms:

  • Primary infection of healthy tissue
  • Primary infection of devitalized, traumatized tissue (wound infections)
  • Infection secondary to systemic disease
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2
Q

Soft Tissue Infections

A
  • Non-necrotizing infections of fascia and muscle
  • Can involve subcutaneous CT, fascia and/or muscles
  • Fasciitis ⇒ most cases are caused by β-hemolytic Strep
  • Pyomyositis ⇒ usu. caused by S. aureus, occasionally Group A Strep
  • Tissue necrosis is a prominent feature of progressive soft tissue infections
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3
Q

Intra-Abdominal Infections

A

Abscesses and Peritonitis

  • Primary peritonitis rarely involves anaerobes
  • Secondary peritonitis and intra-abdominal abscess ⇒ involve bacteria found in the GI tract
  • Infections are usu. mixed ⇒ contains both non-anaerobes and anaerobes
    • ~ 90% of infections involve anaerobes
    • ~ 10-35% show anaerobes only
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4
Q

Intra-Abdominal Infections

Pathogens

A
  • Non-Anaerobes
    • E. coli (dominant)
    • Other Enterobacteriaceae, Strep, Enterococci, S. aureus and Pseudomonas
  • Anaerobes
    • Bacteroides fragilis group (dominant)
    • Bacteroides, Fusobacterium, Clostridium, Peptostreptococci
    • Gram-⊕ non-spore forming rods
    • Eubacterium, Lactobacillus, Bifidobacterium, Actinomyces
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5
Q

Infections of Bone

A

Osteomyelitis

  • Most commonly affect long bones and vertebrae
  • Result from hematogenous or contiguous spread
  • Staph causes 50-60% of osteomyelitis
    • Majority (90%) occurring in children
  • Neonates (1 month)
    • Staph. aureus, group b Strep (S. epidermidis)
    • E. Coli, Klebsiella, Proteus, Pseudomonas
  • Older infants, children, adults
    • Staph. aureus
    • Pseudomonas aeruginosa
  • Sickle cell pts ⇒ often due to Strep. pneumoniae and non-typhoidal salmonella
  • Other special settings favorable for osteomyelitis are cat or dog bites (pasteurella multocida), human bites, periodontal infections and cutaneous ulcers
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6
Q

Anaerobic Infections

A
  • Predominant bacteria primarily responsible for the clinical symptoms are anaerobic
    • Are often mixed
    • May contain a variety of aerobic types
  • Excellent example of opportunism
    • Compromising factors strongly favor the establishment of anaerobic infection
      • Trauma, surgery, immunosuppressive drugs, vascular insufficiency and diabetes
    • Tissue hypoxia due to lack of blood supply and/or presence of contaminating aerobes (utilize O2)
      • Aids in creating conditions
      • Contributes to the rapid development of anaerobic infections
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7
Q

Spore-Forming Anaerobes

A
  • Organisms of medical importance all belong to the genus clostridium
    • Clostridium tetani
    • Clostridium botulinum
    • Clostridium perfringens
    • Clostridium difficile
  • All are obligate anaerobic, large gram-⊕ rods, saprophytic
  • Usu. found in soil or air and intestinal tract of various animals
  • Source of clostridium involved in anaerobic infections is usu. exogenous
    • Can be endogenous
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8
Q

Clostridium perfringens

Skin and Soft Tissue Infections

A
  • Infection - mixed infections common
  • Exogenous - infections of wound from soil, water, sewage etc.
  • Endogenous - C. perfringens may be normal flora of GI tract and female genital tract
  • Infections secondary to abdominal surgery or trauma
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9
Q

Clostridium perfringens

Disease

A
  • Organisms grow in traumatized tissue, especially muscle
    • Occurs in contaminated deep wounds / membranes
  • Produce a variety of exotoxins
  • Pain, edema and cellulitis occur in the wound area
  • Crepitation due to gas in tissue
  • Manifestation include:
    • Localized cellulitis ⇒ amputations
    • Suppurative infections and abscesses ⇒ abdomen, gall bladder, uterus, fallopian tubes
    • Severe necrotizing disease of the intestines
    • Gas gangrene/myonecrosis
      • Most serious
      • Characterized by rapidly progressive, extensive necrosis, gas, foul smell
      • Fever, hemolysis, toxemia, jaundice
      • Can lead to shock and death
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10
Q

Clostridium perfringens

Virulence

A
  • Alpha toxin
    • Lecithinase is the primary exotoxin
      • Hydrolyzes lecithin and sphingomyelin
      • Disrupts cell and mitochondrial
  • Tissue degrading enzymes
    • Collagenase
    • Hyaluronidase
    • DNase
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11
Q

Clostridium perfringens

Diagnosis and Treatment

A
  • Culture, isolation, identification by biochemical tests
  • Tissue debridement, PCN, hyperbaric oxygen
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12
Q

Clostridium tetani

Morphology and General Characteristics

A
  • Slim, gram-⊕ rod, motile
  • Forms round terminal spores (drumstick shape)
    • Spores remain viable in soil for many years
    • Prevalent in manure treated soil
  • Organism sometimes found in lower intestinal tract of man and animals
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13
Q

Clostridium tetani

Virulence

A
  • Tetanospasmin neurotoxic exotoxin
    • Causes spastic paralysis
    • Encoded by plasmid
  • Zinc-endopeptidase specific for synaptobrevins of the neuro-exocytosis machinery
    • Inhibits release of inhibitory neurotransmitters
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14
Q

Clostridium tetani

Pathogenesis and Clinical Considerations

A
  • Spores introduced into wounds contaminated by soil or foreign bodies
  • Incubation is 4 days to several weeks
  • Area of low O2 tension allows spores to germinate
  • Bacilli multiply locally
  • Tetanospasmin is produced
    • Reaches CNS by retrograde axonal transport or via the bloodstream
    • Blocks postsynaptic inhibition of spinal motor reflexes ⇒ spasmodic contractions, hyperreflexia and seizures
    • Masseter muscles usu. first affected trismus (lockjaw)
    • Untreated spasms can become generalized and extremely painful
  • Death results from respiratory failure when muscles affected
    • Untreated, mortality ranges from 15-60%
    • Highest seen in the elderly and infants
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15
Q

Neonatal Tetanus

A
  • Results from contamination of umbilicus by unclean severing implement or bandages
  • More common in developing countries
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16
Q

Clostridium tetani

Laboratory Diagnosis

A
  • Dx by clinical presentation and history of injury
    • Rabies and strychnine poisoning are differential diagnoses
  • Anaerobic culture on blood agar w/ material isolated from contaminated wounds may yield C. tetani
  • Infection remains localized, disease is entirely a toxemia
  • Treatment should never be withheld pending lab confirmation
17
Q

Clostridium tetani

Immunity

A
  • No immunity to natural infection w/ tetanus
  • Survivors do not demonstrate circulating antibody to the toxin
  • Lethal dose < immunogenic dose
18
Q

Clostridium tetani

Treatment

A
  • Tetanus immune globulin (TIG)
    • Pooled plasma containing tetanus anti-toxin
    • Can neutralize the toxin but only before it binds nervous tissue
  • Surgical debridement to remove necrotic tissue
    • Eliminates the environment essential for growth of the organism
  • Abx
    • Metronidazole is the current drug of choice
    • Historically penicillin was used as it does inhibit growth and production of toxin
      • Recent work suggests it may enhance the activity of the toxin
  • Supportive therapy ⇒ for pts who develop symptoms
    • Muscle relaxants
    • Sedation
    • Assisted ventilation
19
Q

Clostridium tetani

Prevention and Control

A
  • Tetanus is a preventable disease
  • Universal immunization w/ tetanus toxoid (DTap, Tdap)
    • Initial series is 3 shots given during 1st year of life
    • Booster shot before entry into school
    • Additional boosters every 10 years
  • Previously immunized w/ potentially dangerous wound w/o boost in past 10 yrs ⇒ tetanus toxoid
  • Immunized w/ heavily contaminated wounds w/o boost in past 5 yrs ⇒ tetanus toxoid
  • Unimmunized or incompletely immunized w/ serious wounds ⇒ anti-toxin (TIG) & tetanus toxoid
20
Q

Non-Spore Forming Anaerobes

Pathogens

A
  • Organisms belong to diverse variety of gram-⊖ and gram-⊕ rods and cocci
  • Normally inhabit mucous membranes and less commonly skin
  • Genera of major clinical importance are:
    • Bacteroides
    • Prevotella
    • Porphyromonas
    • Fusobacterium
    • Actinomyces
21
Q

Non-Spore Forming Anaerobes

Infections

A
  • Source of non-spore forming anaerobes involved in anaerobic infections is endogenous
    • Little evidence of person to person spread or exogenous infection
  • Majority of infections of oral cavity and maxiofacial regions are basically anaerobic
    • Actinomycosis
    • Acute necrotizing ulcerative stomatitis
    • Root canal infections
    • Periodontal diseases
    • Severe dental caries
22
Q

Bacteroides

Overview

A
  • Anaerobic, non-spore forming gram-⊖ rods
  • Most common cause of serious anaerobic infections
    • Sepsis, peritonitis, and abscesses
  • B. fragilis is the most frequent pathogenic species
    • Also predominant in the normal colonic and vaginal flora
23
Q

Bacteroides

Disease

A
  • Infections are endogenous and include intra-abdominal infections
    • Peritonitis or local abscesses
  • Metastatic abscesses may arise due to hematogenous spread to distant organs
  • Lung abscesses due to aspiration of organisms
  • Predisposing factors: surgery, trauma, chronic disease
  • Contributes to infection: local tissue necrosis, impaired blood supply, growth of facultative anaerobes (E. coli) at the site
24
Q

Bacteroides

Virulence Factors

A
  • Polysaccharide capsule ⇒ antiphagocytic, abscess promoting
  • Endotoxin ⇒ less biologically active compared to classic endotoxin due to lack of lipid A
25
Q

Actinomyces

Overview

A
  • Opportunists that produce indolent, slowly progressive diseases
  • Heterogenous group of filamentous bacteria
    • Superficially resemble fungi
    • Grow as branching organisms
    • Tend to fragment into bacteria-like pieces
  • Most are free living, particularly in soil
  • Many are part of the normal flora of the mouth or GI tract
  • Several pathogenic species
  • Actinomyces israelii most important medically
26
Q

Actinomyces

Morphology and General Characteristics

A
  • Irregular staining gram ⊕, non-spore forming rods
  • Grow in a branching filamentous pattern
  • Facultative intracellular pathogens
  • Facultative or obligate anaerobes
27
Q

Actinomycosis

Overview

A

Chronic suppurative, destructive disease of connective tissues

  • Formation of granulomas, pyogenic lesions, or abscess
  • Infections are opportunistic
    • Actinomyces found as nl flora of mouth and GI tract
  • Gain access to CT usu. following trauma of mucosal or epithelial surfaces
  • Spread via formation of interconnecting sinuses, granulomatous and pyogenic lesions
28
Q

Actinomycosis

Clinical Subtypes

A

4 clinical forms of the diseases are recognized:

  • Cervicofacial actinomycosis ⇒ 30-60% of cases
    • Usu. follows dental surgery or dental disease (poor oral hygiene)
    • ± Bone involvement
  • Abdominal actinomycosis ⇒ 20-30% of cases
    • Usu. follows rupture of appendix or cecum
    • ± Involvement of various abdominal organs
  • Thoracic actinomycosis ⇒ 20-30% of cases
    • May develop by extension from cervicofacial disease or by aspiration of sputum causing lung infection
  • Pelvic actinomycosis ⇒ associated w/ intrauterine devices
29
Q

Actinomyces

Diagnosis

A
  • In vitro: branching filaments, fragment in 24 hrs into bacillary, short chains and coccobacillary forms, stain gram ⊕
  • In vivo: microcolonies formed in infections called sulfur granules
    • When crushed, organisms appear as gram ⊕, bacillary and diphtheroid forms
    • Presence of sulfur granules in sputum, pus from draining sinuses, or exudates is diagnostic
    • Yellow color of granules d/t presence of large numbers of
  • Actinomycotic infections are almost always mixed infections
  • Material from sulfur granules
    • Inoculated into thioglycollate broth or brain heart infusion blood agar
    • Incubated anaerobically
    • Growth is slow, may take up to 2 weeks
30
Q

Actinomyces

Treatment

A
  • Prolonged tx w/ PCN (or erythromycin as an alternative)
  • Surgical excision and drainage often necessary
  • Most species are resistant to metronidazole
  • Tetracyclines have variable activity