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anaerobes as part of normal flora
obligate anaerobes outnumber facultative anaerobes in the gut, and are the prdeominant type of bacteria in the oral cavity, GI tract and genital tract.
02 solubilty and and anaerobes
02 solubility in H2O is low, and poorly diffusable, so anaerobes can live mm below the surface.
oral colonization timing
neonates oral cavity is sterile, but is colonized soon after birth. microbiota stable in composition.
pellicle forms from saliva proteins. serves as scaffold for biofilm. Then comes primary, secondary, and tertiary colonizers.
allow coadhesion and coaggregation between bacterial species. "bridge" species, usually fusobacterium.
G-, including porphyromonas. Tend to be strict anaerobes, depend on 1 and 2 colonizers to deplete oxygen. more proinflammatory.
different in different parts of the gut. highest in the large intestine (500-1000 species). Dominated by bacteriodes and firmicutes.
2/3 anaerobic infections are mixed. Abscess formation almost always mixed (E. coli and Bacteriodes).
obligate anaerobe benefits from synergy
lower redox pot of environment, necessary growth factors, impairment of local host defenses
facultative bacteria benefits from anaerobes
enhanced growth, protection from phagocytoccis as bystanders, protection from antibiotics.
G- rods, sim. to E. coli. Microflora in mouth and GI tract. Predominant genus in the GI tract.
Bacteriodes under normal conditions
involved in metabolic activities (ferment CH20, N acquisition, recycle bile), compete w/ pathogens (attachment sites, nutrients, produce volatile FA lowering pH, release free bile acids)
bacteriodes and disease
most common genus isolated from anaerobic infections, including bacteremia. Not invasive, but events compromising intestinal barrier provide access. Rely on synergism w/ aerobic for disease.
most important opportunistic Bacteriodes pathogen. 1-2% of normal flora, but 80% of anaerobic infections.
most produce beta-lactamases, so treat w/ beta-lactam and inhibitor (ampicillin + sublactam), or metronidazole. most are resistant to aminoglycosides.
G+ rods, hyphae like filaments. "ray fungus." non-motile, non-spore forming. commonly found in mouth, part of oral flora. opportunistic, esp. after dental procedure. causes periodental disease and caries. relies on synergy.
G+ spore forming rods. vary in O2 sensitivity. clostridial spores ubiquitous in the environment
produced by B. fragilis and peptrostrep, can protect from phagocytocis, enhances abscess formation, increase liklihood of systemic infection. Important in peritoneal abcess formation.
often produced by anaerobes to protect them from reactive O2 species created by the host.
fatty acid produced by B. fragilis, decreases phagocyte function and neutrophil migration. enhances not only B. fragilis but other nearby species.
actinomycosis caused by A. israelii (usually). Swelling of tissues, abcess, or mass lesion. Abcess may break through skin in chronic infections.
lumpy jaw diagnosis
inspection of abscess fluid shows yellowish granules of clumped organisms. called "sulfur granules"
oropharynx usual source of anaerobes in brain. caused by anatomically adjacent infection, or septic emboli from the lung. prevotella, porphyromonas, peptrostrep most common.
follows aspiration of lung or gut contents. pneumonitis first, then abcess in 1-2 weeks if untreated.
in many patients with lung abscess there are expectorations with horrible odor, giving patient fetid breath.
aspiration pneumo organisms
prevotella, porphyromonas, fusobacterium, peptostrep. mixed w/ strep viridians and other anaerobes.
intra abdominal infection usually following trauma or necrosis w/ GI flora entering peritoneum. Most frequently B. fragilis and E. coli.
facultative anaerobe (E. coli, enterobacter) typically responsible for early infection, and anaerobe (b. fragilis) infection leads to abcess formation.
chronic wounds in poor wound healing
individuals w/vascular disease (diabetes), typically mixed infection, w/ S. aureus, pseudomonas, peptostrep, and GBS. grow in mixed biofilms.
local infection stage
transition between colonization and infection stages, infectious signs absent but wound healing is delayed
traumatic gas gangrene
C. perfingens, crush type injury reducing perfusion. Spores from enviroment germinate, producing myonectoric factors, mass myonecrosis/shock
spontaneous gas gangrene
C. septicum enters via break in GI mucosa. Survives in blood because aerotolerant. Invades muscle tissue at multiple sites, resulting in myonecrosis. high mortality because multifocal.
diagnosis of anaerobic infections
aspirate specimens best, swabs ok, NOTHING that passed through mucous membrane. rapidly transport to avoid O2 exposure. Often just gram stain because of mixed nature of infection.
C. perfingens gram stains
spores visible, no white blood cells (cytolitic), pus does not accumulate in wounds
need to debride, drain pus for abx to reach site. broad spectrum abx. aminoglycosides no good because anaerobic, no proton motive force.
produces lectithinase (phospholipase) and other myonectrotic factors that can degrade tissue and cause myonecrosis.
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