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55 terms

oral/gut anaerobes

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obligate anaerobes
require reduced oxygen tension for growth (<10%). do not durvive in ambient air.
extremely oxygen sensitive species
like some clostridia, cannot survive even 0.5% oxygen.
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.
dental plaque
microbial biofilm of complex composition. more than 700 species that can colonize.
oral colonization timing
neonates oral cavity is sterile, but is colonized soon after birth. microbiota stable in composition.
biofilm development
pellicle forms from saliva proteins. serves as scaffold for biofilm. Then comes primary, secondary, and tertiary colonizers.
primary colonizers
Strep and actinomyces. Have adhesins that directly atach to salivary proteins.
secondary colonizers
allow coadhesion and coaggregation between bacterial species. "bridge" species, usually fusobacterium.
tertiary colonizers.
G-, including porphyromonas. Tend to be strict anaerobes, depend on 1 and 2 colonizers to deplete oxygen. more proinflammatory.
plaque removal
removes biomass but no evidence that it changes bicrobiot over time.
gut flora
different in different parts of the gut. highest in the large intestine (500-1000 species). Dominated by bacteriodes and firmicutes.
aerobic/anaerobic synergy
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.
Bacteriodes
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.
B. fragilis
most important opportunistic Bacteriodes pathogen. 1-2% of normal flora, but 80% of anaerobic infections.
bacteriodes treatment
most produce beta-lactamases, so treat w/ beta-lactam and inhibitor (ampicillin + sublactam), or metronidazole. most are resistant to aminoglycosides.
actinomyces
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.
actinomycosis
abscess formation when oral health is compromised.
actinomyces diagnosis
may be confused w/ nocardi. differentiation important because of treatment.
actinomyces treatment
long term penicillin treatment. resistant to metronidazole.
clostridia
G+ spore forming rods. vary in O2 sensitivity. clostridial spores ubiquitous in the environment
C. perfingens/C. septicum
produce gangrene.
polysaccharide capsule
produced by B. fragilis and peptrostrep, can protect from phagocytocis, enhances abscess formation, increase liklihood of systemic infection. Important in peritoneal abcess formation.
LPS
G-, some like B. Fragilis have LPs that is less toxic and thus less immunostimulatory.
superoxide dismutase
often produced by anaerobes to protect them from reactive O2 species created by the host.
succinic acid.
fatty acid produced by B. fragilis, decreases phagocyte function and neutrophil migration. enhances not only B. fragilis but other nearby species.
lumpy jaw
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"
lumpy jaw treatment
long term treatment w/ penicillins. (4-6 weeks IV followed by oral therapy).
brain abscess
oropharynx usual source of anaerobes in brain. caused by anatomically adjacent infection, or septic emboli from the lung. prevotella, porphyromonas, peptrostrep most common.
aspiration pneumonia
follows aspiration of lung or gut contents. pneumonitis first, then abcess in 1-2 weeks if untreated.
fetid breath
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.
perotinitis
intra abdominal infection usually following trauma or necrosis w/ GI flora entering peritoneum. Most frequently B. fragilis and E. coli.
peritonitis synergy
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.
stages in development of chronic infection
contamination, colonization, local infection, infection.
contamination stage
organisms present but not replicating
colonization stage
organisms present in the wound but are not causing tissue damage.
local infection stage
transition between colonization and infection stages, infectious signs absent but wound healing is delayed
infetion
bacteria are replicating at high numbers and are causing tissue damage.
traumatic gas gangrene
C. perfingens, crush type injury reducing perfusion. Spores from enviroment germinate, producing myonectoric factors, mass myonecrosis/shock
traumatic gas gangrene treatment
debridement, wound vacuums, hyperbaric O2, antimicrobials.
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
abscess treatment
need to debride, drain pus for abx to reach site. broad spectrum abx. aminoglycosides no good because anaerobic, no proton motive force.
C. perfingens
produces lectithinase (phospholipase) and other myonectrotic factors that can degrade tissue and cause myonecrosis.
lecithinase
reffered to as alpha toxin, hemolysin on agar plates,
C. septicum
also produces lecithinase, comparatively aerotolerant to C. perfingens.
β toxin
cytotoxin produced by C. perfingens that affects endothelial cells, allows rapid destruction of host tissues.