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31 Cards in this Set

  • Front
  • Back
what are the general bio properties of clostridiums?
gram pos bacilli, anaerobes, spore formers, ubiqiutous (everywhere in environment like dirt and feces)
what diseases does C. dificile cause?
antibiotic induced diarrhea and pseudomembranous colitis (horrible ab symptoms, fever, white plaques of fibrin, inflammatory cells over colonic tissue)
what antibiotics are known to induce C. dificile?
CLINDIMYCIN, penicillin, cephalosporins
how is C. difficile transmitted.
exogenous or endogenous (5% ppl have em as normal flora), exogenous from fecal oral route
when does C difficile start producing toxins?
when there are enough bacs in there that it can hit its stationary stage and stop replicating
what are the toxins of C. dificile and what do they do?
Toxin A and B, both inactivate G proteins that regulate actin of cytoskeleton. A is an enterotoxin causes mucosal injury. B is a cytotoxin inducinng depol of actin, loss of actin cytoskeleton
how do you ID C. dificile?
culture it if you can, hard to do, then perform cytotoxicity (from pt) assays which will mean person has disease.
treatment for C. dificiel?
discontinue offending antibiotic, fluid/electrolyte replacement, avoid anti-peristaltic agents, if above do not work use oral metronidazole 1st then vanc if met doesnt work
T/F relapse of C. dificile is not common.
F, it is common bc spores are resistant to antibiotics
what can cause toxic megacolon in C. dificile?
anti peristaltic agents
what propertie of C. perfringens allow it to cause disease?
rapid growth and vigorous metabolism as well as many toxins
epidemiology of C. perfringens?
ubiqiutous, dirt, intestine of animals/humans. common infection in war
types of infections caused by C. perfringes?
most asymptomatic but can cause bad soft tissue infections: cellulitis, suppurative myositis, myonecrosis or "gas gangrene"
describe P. perfringens cellulitis:
black, min pain, gas under it, rare systemic toxicity, stinky
describe C. perfringens suppurative myositis.
pus in muscle, usually IV drug users, good prognosis with drainage and antibiotics
describe C. perfringens gas gangrene.
myonecrosis, severe, alpha toxin (lecithinase - necrotizers), thetatoxin (hemolysin: cytolytic), kills WBC's. sudden onset of pain, gas in soft tissues, fast dividing bacs, serosanguinous - foul smelling, sepsis, mortality in 40-100%
treatment for C. perfringens?
debridement and penicillin, sometimes surgical and hyperbaric O2 with gas gangrene.
describe food poisoning from C. perfringens.
spores survive meat cooking and germinate during slow cooling, ab cramps, watery diarrhea from eneterotoxin that is cytotoxin, treat symptoms, reheat food to kill vegetative bacs
epidemiology of C. tetani?
rare in US from immunization. lotsa cases worldwide and is a huge killer, esp of neonates
what are the severe disease symptoms of tetanus?
autonomic nervous system dysfunction, cardiac arrhythmias, fluctuations in BP, sweating, dehydration
what causes most tetanus deaths in neonates?
sepsis (unlike adults) and apnea
name and describe the properties of the tetanus toxin.
tetanospasmin: neurotoxin, binds at NMJ and is internalized, moves via retrograde axonal transport and is discharged in the synaptic space, goes to inhibitory interneurons of spinal cord, blocks release of GABA and gly by inhibitory interneurons, promotes over activity due to uncontrolled release of Ach
how do you diagnose C. tetani?
by symptoms only, culture is not relevant
how do you treat C. tetani?
open airways, antitoxin for systemic toxins, sedatives/anticonvulsants, surgical removal of infected tissue, antibiotics (metronidazole), recovery when new axon terminal is generated. PREVENT with the vaccine that is inactivated tetanospasm
what is the reservoir for botulism?
found in soil and water throughout US and is in anaerobic food mediums like home canned, preserved fish, fermented beans
describe the three botulism diseases.
foodbourne: weak and dizzy 2 days after eating, bilateral descending flaccid paralysis, death from respiratory failure unless you prevent this.
Infant: ingest spores in food (honey), GI tract colonized unlike adults, toxin made, same symptoms as food bourne.
wound: lacks GI prodrome, associated with black tar heroin
describe the botulism toxin.
one of most potent there is, pot. bioterror, AB, remains in neuromuscular junction unlike tetanus, A subunit inactivates proteins involved in Ach release thus understimulation and flacid paralysis.
how do you diagnose botulism?
symptoms, culture food, toxin assay of serum, stool, food
what is the treatment of botulism?
vent support, antitoxins, debridement if wound, antibiotics (metrodiazole or penicillin), immunity does not develop
prevention of botulism?
avoid buldging food containers, boiling will inactivate the toxin
mnemonic for the clostridium bugs?
tetanus causes tetanic paralysis, botulism is from bad bottles, perfringens perforates a gangrenous leg, and difficile causes diarrhea