Clostridia I & II Flashcards
Clostridia are: GM (+/-) ______
GM + rods
Clostridia are: obligate/facultative aerobes/anaerobes
Obligate Anaerobes
T/F: Clostridia form spores
True
Clostridia are: catalase (neg/pos)
Catalase Negative
Clostridia are: Oxidase (pos/neg)
Oxidase negative
Which clostridia species is highly invasive and causes gas gangrene?
Clostridium perfringens
Which clostridium species is generally non invasive and secretes a toxin that causes pseudommembranous enterocolitis?
Clostridium difficle
Which clostridium species is generally noninvasive and is the causeitive agent of tetanus?
Clostridium tetani
which clostridium is non invasive and causes botulism
C. botulinum
Which clostridia toxin causes flaccid paralysis?
botulism toxin
which clostridia toxin causes pseudomembranous colitis?
Exotoxin A & B
this clostridia species is the only one to form terminal spores - “tennis rackets”
C. Tetai
C. Tetani has ____ serological type(s)
ONE
The Tetanus toxin is a ______-toxin that is transported to ________
Neurotoxin, transported from infection site to peripheral and CNS nerves (anterior horn cells of S.C. + brain stem)
Tetanus toxin mechanism of action:
inhibits glycine and GABA neurotransmitter release => spastic paralysis + convulsive contractions - lockjaw
The tetanus toxin has A and B subunits: one binds ______ _______ and the other _________________
binds neuronal ganglioside, the other has neurotoxin activity
C. Tetanus infection clinical syndrome:
- Fever?
- Spasm?
- Sensory?
- Complications?
- NO FEVER
- VIOLENT MUSCLE SPASMS
- NO SENSORY LOSS
- Involvement of respiratory muscles -> failure -> aspiration, dysphagia, pulmonary infections.
C. Tetanus diagnosis made based on:
Clinical syndrome is the best way to diagnose.
Culture only positive in 39% cases. Organism not usually found in wound.
Patient has violent flexor muscle spasms, clenched teeth and jaw, no fever, and no sensory loss. They stepped on a soil-y nail a few days ago. The best treatment is:
- Human tetanus immunoglobulin
- Penicillin + wound debridement
- Resp. support
- Immunization!
Tetanus fatality rate: a - 40 % b - 50 % c - 60% d - 70 %
C - 60% fatality due to pulmonary complications
Tetanus immunization accomplished with ____ doses of _____ during the first _______ months/years of life. (Given with the DPT vaccine)
3 doses of toxoid (toxin inactivated by formaldehyde) within the first 6 months of life
T/F: Tetanus immunization requires a booster every 5 years
FALSE. Booster required every 10 years. Also, a booster is often given at 1 year and before entering school.
T/F: C. Botulinum spores are heat resistant
True
T/F: C. Botulinum toxin is heat resistant
False. Botulism toxin is HEAT LABILE
C. Botulinum spores are often found in:
Canned food (anaerobic conditions). Spore grow +germinate, form toxin in 2-3 days
T/F: botulism toxin is NOT destroyed by stomach acid
True, the toxin is not destroyed by stomach acid, but is heat labile, and thus destroyed by boiling for 10 min.
The botulism toxin has ___ types; which are most common??
7 types; A thru G.
type A, B, and E are most common
Which clostridia toxin is absorbed by the intestine, carried by blood to peripheral nerve synapses, binds to a receptor, and blocks the release of acetylcholine by interfering with proteolytic processing??
a - tetanus toxin
b - botulsim toxin
c - exotoxin A + B
d - Alpha toxin
This is the mechanism for Botulism toxin
T/F: Botulism toxin exposure will result in fever
False.
Botulsim toxin will NOT CAUSE FEVER.
T/F: botulism will cause an altered mental status
FALSE, botulsim toxin will not have any effect on mental status
the incubatio period for botulism toxin is ___ to ____ hours/days/weeks
18 to 36 hours
T/F: botulsim toxin will result in sesnory deficit
False. Botulsim = NO SENSORY DEFICIT
Which clostridium syndrome is characterized by flaccid paralysis of peripheral nerves symmetrically, dysphagia, dilated pupils, diplopia, and dry throat?
C. Botulinum, botulism
T/F: you can diagnose botulism by culturing the microorgannisms
FALSE. the preformed toxin is the culprit - better to detect the toxin in feces, vomit, serum, or via serology for diagnosis.
Patient has botulism!! - what do you do?
- Remove toxin from stomach w/ lavage
- Treat with Antitoxin (specific) - usually type A, B, + E
- May need respiratory support
Another clinical variant of botulism with more subtle symptoms and caused by honey as a source of contamination is:
Infant Botulism
In wound-associated botulism, the contamination comes from:
Spores in soil get into wound -> germinate -> toxin
A common cause of antibiotic-associated diarrhea is:
C. Difficile, due to toxin mediated coloninc inflammation
C. Difficle is found in ___% of general population GI tract
3%
___% of hospitalized patients are colonized vie the shitty-oral route from dirty hospital people
30%
C. Difficle pathogenesis:
- Antibiotic suppression of local flora -> C. Difficle proliferation
- Exotoxin A produced -> binds to gut receptor
- Exotoxin B produced -> cytotoxin -> damages colonic mucosa -> pseudo membrane formation + bloody diarrhea
Which clostridium toxin acts by ADP-ribosylating ‘Rho’, a GTP- binding protein?
a - Tetanus toxin b - Botulism toxin c - Exotoxin A d - Exotoxin B e - Alpha toxin
d - Exotoxin B
this causes the bloody diarrhea and pseudomembrane formation associated with C. Difficle infection.
Pateint has a hx of antibiotic use, and yellow-white plaque pseudomembrane on colonoscopy; what toxin might you detect in a stool sample to confirm your diagnosis?
exotoxin B. ELISA can also be used to detect toxins of C. Difficile.
You have diagnosed a pt with a C. Diff infection, you decide to treat by:
- Stopping any offending antibiotics
2. Treating with metroidazole, vancomycin, or fidaxomicin
C. perfringens organisms are primarily found in ______ but also in ________________________
Soil, but also in human GI tract + Vaginas
Two ‘syndromes’ of C. Perfringens are:
- Gas Gangrene - invasive and rapidly progressing necrosis
2. Food poisoning - self limiting diarrhea
The alpha toxin produced by c. perfringens is a _________, it damages host cell membranes including capillary walls and RBCs
Lecithinase.
The byproduct(s) of c. perfringens anaerobic growth:
- H2
2. CO2
The enterotoxin associated with C. Perfringens is part of the
Spore Coat. It is released into intesting after a large qty (10^8) of spores are consumed.
The clinical syndrome of superficial cellulitis, necrotizing cellulitis, necrotizing fasciitis, and myositis/myonecrosis is caused by which Clostridia species?
C. Perfringens; this is gas gangrene
C. Perfringens diarrhea lasts about _____ hours/days, and is characterize by abdominal cramps ad watery diarrhea.
8-22 hours
Treatment for gas gangrene would include:
- Surgical wound debridement
- Penicilliin
- Hyperbaric O2
to diagnose c. perfringens food poisoning you would need to:
detect enterotoxin by ELISA of stool or food
In addition to the Alpha Toxin - Lecithinase - what other enzymes are involved in the development of gas gangrene by C. Perfringens?
Collagenase, Hyaluronidase
