* large, GPR spore forming * ubiquitous (soil) * aerotolerant: histolyticum, tertium, carnis * fluoro: c. diff, innocuum = chartreuse; ramosum = red * exogenous infections: wounds, organism, toxin ingestion (except c.diff) * antibiotics can prevent growth on artificial media
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fluorescence
* wood’s lamp * may need longer incubation or exposure to O2 * a. odontolyticus red * veillonella brick red
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c. perfringens diseases
* food poisoning * gas gangrene (clos myonecrosis)
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food poisoning - c. perfringens
* ingestion of spores from contam food = enterotoxin made in GI * beef, poultry, gravies, dried/precooked foods * large amts of food made (hospitals, cafeterias, events) * watery diarrhea, adb cramps, 8-12 hrs, self resolving
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clostridial myonecrosis - c. perfringens
* traumatic injury, entry of vegetative bacteria/spores in wound * vascular damage = improper perfusion = lack of O2 = anaerobic * sudden pain, skin pale = bronze = purple red * bullae develop (black bubbles) * tachy, fever, shock, organ failure, IV hemolysis, jaundice, renal failure, hypotension, liver necrosis
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c. perfringens toxins
* alpha toxin: phospholipase C and sphingomyelinase * theta (perfringolysin O): pore forming
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morphology of c. perfringens
* boxcar GPR with rare subterminal spores * double zone hemolysis (inner = theta) (outer = alpha)
* determine metabolic activity of microbes in milk (esp for clos) * skim milk substrate, azolitmin pH (pink acid; blue alk) * no change: no carb ferm * alk: proteolysis of lactalbumin (pos) * acid: ferm of lactose and/or dextrose (stormy - gas) * clot formation: coag of casein * clot dissolution: peptonization of milk protein
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spore induction - heat method
* inoculate 2 tubes of starch broth and heat 1 for 10 min at 70C * incubate both 37C anaerobic * if growth in both = spores induced
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spore induction - ethanol test
* mix week old TG broth with 95% EtOH * sit at RT 30 min and sub to anaBAP (incubate anaerobically 48 hrs) * growth = spores produced
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tetanus - c. tetani
* spores enter tissue and vegetate, producing tetanospasmin * four types: generalized, local, cephalic, neonatal
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tetanospasmin
* 2nd most toxic sub * carried thru to nerves, spinal cord, brain stem * binds to neuronal receptors irreversibly, blocks signals to inhibit motor responses (GABA) = spastic paralysis
* botulism: spores enter body thru wounds, ingestion, inhalation which vegetate in tissue and make exotoxin * five types: infant, foodborne, wound, adult infectious, bioterrorism assoc
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botulism toxin
* most potent toxin to man * carried to nerves, spinal cord, brain stem * moves across presynaptic nerve terminal membrane * breaks down neuronal SNARE proteins that are supposed to release Ach to stimulate motor responses = flaccid paralysis
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infant botulism - floppy baby syndrome
* ingestion of clostridial spores move to GI tract and germinate and produce toxin * common form in US * constipation, weakness, feeding difficulties, hypotonia, drooling, anorexia, irritability, weak cry, dyspnea
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foodborne botulism
* ingestion of preformed toxin in contam food (canned goods) * 2nd most common in US * nausea, vomiting, adb pain, diarrhea, dry mouth, sore throat * blurred vision, diplopia, nystagmus, dysphagia, muscle weakness, dyspnea
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wound botulism
* bacteria/spores enter thru skin and tissue trauma * same symptoms as foodborne w/o prodromal
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adult infectious botulism
* arises from enteric colonization by the bacteria * symptoms like infant form * botex used for cosmetics and migraines
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bioterrorism assoc botulism
* theoretical delivery of botulinum toxin via aerosol or food * similar symptoms to generalized
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morphology of c. botulinum
* GPR w subterminal or eccentric spores * large, rough appearing on anaBAP
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c. botulism lab dx
* based on symptomology (cx done by ref lab) * sero or molecular methods * phenotypically similar to c. sporogenes, but makes a neurotoxin * ELISA, PCR, PGFE, GLS * lipase pos (so is c. noyvi) * dx from stool (organism or toxin)
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c. diff
* no O&P after 3 days in hospital (CAP requirement) * after taking antimicrobials (clindamycin, fluoroquinolones) * advanced age and proton pump inhibitors also inc risk
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c. diff toxins
* toxin A enterotoxin: causes inflammation leading to fluid secretion, mucosal injury * toxin B cytotoxin: induces cellular apoptosis, necrosis
* normal flora in oral cavity and GI tract; bacteria enter thru trauma sites * form a mass in affected area, usually in mandible (misDx as cellulitis) * bluish/red swelling progressing to abscess, fistulae, draining sinus tracts * sulfur granules in yellow exudate
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a. israelii
most common isolate, slow grower, molar teeth
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a. odontolyticus
red pigment enhanced with air exposure
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a. naeslundii
colonies produce tan pigment with prolonged incubation
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a. visocosus
pos catalase
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a. meyeri
small GPR, strict anaerobic (QA organism)
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actinomyces ID
* branching GPR, stain from exudate, sulfur granules * differentiation not done
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bifidobacterium
* normal GI, vaginal, oral flora * rare resp, UTIs, dental caries * assoc w probiotics * bifurcated ends, Y shaped GPR
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eubacterium
rare infections (oral flora) teeth, human bite, polymicrobic vaginal infections
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lactobacillus
* bacteremia, endocarditis, dental caries in IC * normal vaginal flora * some aerotolerant * long thin GPR in chains * cat neg * vanc R