oral/gut anaerobes

Created by ehpratt 

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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.

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