Clostidium Flashcards
2 ways a bacteria causes disease
toxins or invasions
two ways to establish infection via ingesting toxin
toxins preformed in food (c. botulism, S aureus)
ingestion and toxin formed in gut (infant botulism, v. cholerae)
general properties of clostriudium
gram positive rods
spore forming- spore location is diagnostic
obligate anerobes
catalse negative
oxidase negative
clostridium tetani epi
soil, puncture wounds
very rare in US. immigrants and developing countries
clostridium tetani pathogenesis
toxin mediated- tetanus toxin = neurotoxin. toxin has 2 subunits. one subunit binds neurogangliosides, the other has toxin activity
toxin inhibits release of NTs glycine and GABA, resulting in spastic paralysis
“convulsive contractions”
only 1 serotype
clostridium tetani syndromes
violant muscle spasms, clenched teeth, neck and back
no fever or sensory deficits
complications w/ pulmonary infection, aspiration, or respiratory failure
clostridium tetani diagnosis
clinical
culture positive in only 40%
clostridium tetani incubation period
4 days - weeks. vague
clostridium tetani treatment
immunization w/ human tetanus IgG.
penicillin plus wound debridement
resipratory support
clostridium tetani mortality rate
60%
clostridium tetani vaccine
3 doses in first 6 months of life w/ toxoid in part of DPT
booster every 10 years
clostridium botulism epi
very low incidence
soil organism. spores very resistant to chemical/physical agents
found in canned food, wounds. or infant botulsim (honey)
clostridium botulism pathogenesis
extremely potent but heat labile
acid resistance
7 types of toxin, A, B, E most common
toxin has A and B subunits. carried to nerves via blood and acts as neurotoxin. enters synapse and blocks release of ACh
clostridium botulism syndrome
no fever
normal mental status
no sensory deficits
symmetrical weakness or flaccid paralysis- can affect cranial nerves and respiratory muscles
clostridium botulism incubation period
18-36 hr
clostridium botulism diagnosis
detect toxin in food or serum/vomit/feces
clostridium botulism differential
myasthenia gravis or guillan barre syndrome
clostridium botulism therapy
removal of toxin, antitoxin from horse serum
12% mortality
clostridium botulism prevention
canned food cooked for 10 min at 100 C
infant botulism
1-8 months
eat honey- no immune in gut
symptoms- constipation, weak head control, cranial nerve deficits
diagnosis- find toxin
treatment- antitoxin Abs for types A and B, supportive
wound-associated botulism
spores from soil contaiminate
diagnose via wound culture or toxin in serum
clostridium difficile epi
Ab associated diarrhea
found in GI tract, espcially in hospital
virulent strain 027 recently emerged
clostridium difficile pathogenesis
Ab induced suppression of normal flora allows clostridium difficile to proliferate and make 2 toxins
exotoxin A- enterotoxin binding to gut receptors
exotoxin B- cytotoxin, damaging colonic mucosa via ADP ribosulating Rho, a GTP binding protein
damage via exotoxin B leads to pseudomembrane formation
clostridium difficile syndromes
diarrhea w/ pseudomembranes (plaques on colonoscopy)
