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Anaerobes: structure
- Require less than 10% O2
- Lack catalase or superoxide dismutase
- Clostridia: spore forming, C Perfringens, C Botulinum and C Tetani, C difficile
- Propionobacteria: commensal skin flora
- Bacteriodes: Gram negative, Beta lactamase production, B Fragilis
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Anaerobes: Epidemiology
- Colozine oxygen deficient tissues
- Skin, gingival surfaces, intestinal lumen
- Usually autoinfections
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Anaerobes: pathogenesis
- Usually displaced from biological niche
- trauma, disease, aspiration
- impaired blood supply increases risk
- usually commensal adjacent to site of infection
- Some distance from site of infection and commensal site may be observed (i.e. aspiration of oral flora -> pneumonia, brain abcess)
- Additional virulence factors needed (i.e. ability to withstand O2)
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Anaerobes: manifestations
- Localized abcesses in cranium, thorax, peritoneum, live, and GU tract
- Nerve toxins as well
- Diagnosis: high quality specimen from site of infection, gram stain, isolation in anaerobic jar
- Tx: Drainage of purulent material
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C. Perfreingens
- Large gram positive rod, forms spores, produces gas in necrotic tissues, alpha toxin hydrolizes lecithin and sphingomyelin
- Epi: Gas gangrene develops in severe traumatic open lesions with muscle necrosis
- Pathogenesis: low oxidation reduction potential -> spores germinate -> alpha-toxin -> more tissue necrosis -> shock
- Food poisoning: spores survive cooking and are ingested
- Gas Gangrene: fermentation of muscle carbs -> gas (crepitation); excision of all devitalized tissue; massive doses of penicillin; surgical debridement most important
- Food poisoning: 8-24 hours -> nasua, abdominal pain, diarrhea; meat dishes
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C. Botulinum
- Environmental bacterial, gram positive rod, spore forming, toxins are heat labile and resistant to enzymes, toxins work at NM junction and black Ach release
- Epi/Patho: ingestion of home canned beans not heated sufficiently; organism multiplies in can and elaborates toxin
- Botulism: 18-96 hours; ocular, pharyngeal, laryngeal muscle paralysis which may progress to massive voluntary muscle paralysis
- infant botulism: honey; multiplesin colon; constipation, poor muscle tone, lethargy
- tx: supportive measures; horse anti-toxin
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C Tetani
- Gram positive, spore forming, environmental, toxin = tetanospasmin, heat labile, antigenic, and neutralized by intestinal proteases
- epi: introduced into wounds by contaminated soil, wounds usually small
- Patho: low redox area; germination of spores, txoin made at site of infection and reaches CNS by ascending motor nerves; acts on anterior horn cells -> unopposed neuron firing; muscle spasms
- Tetanus: 4 days -weeks; masseter muscles first affected (lockjaw), generalized convulsions
- Tx: tetanus anti-toxin
- Prevention: DPaT
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C. Diff
- Commensal organism, toxin-A=enterotoxin ->fluid secretion, hemorrhagic necrosis; toxin B=cytotoxin
- Pathogenesis: alteration of colonic flora with antibiotics; overgrowth of c. diff, psuedomembrane developes
- PMC: diarrhea (mild and watery or bloody and cramping with fever)
- Diagnosis: Toxins detected in stool
- Treatment: Vancomycin (poor adsorption)
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B. Fragilis
- Commensal intestinal flora, deep pain and tenderness below diaphragm, gram negative rod, tolerant of O2, polysaccharide capsule
- Pathogenesis: Major organism of abdominal cavity infections; capsule prevents phagocytosis, stimulates abcess formation; fever may be present
- Tx: usually resistant to beta lactams; clindamycin
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