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18 Cards in this Set

  • Front
  • Back
how do you distinguish between the spore formers bacillus and clostridium?
bacillus is catalase pos and clostridium is catalase neg
what is the basic biology of all bacillus?
gram positive, endospore forming rods, catalase positive, aerobic to facultative anaerobic, moist soil, some produce antibiotics
what do the two plasmids of B. anthracis encode?
one for toxins and one for the capsule
when do B anthracis form spores?
in well aerated cultures, rare in blood and organs, inhibited by high CO2
describe the capsule of B. anthracis
poly-D-glutamic acid (protein! not polysac), poorly immunogenic, anti phagocytic, Na and bicarb enhance production
what are the stains for the capsule of B. anthracis?
india ink and fluorescent antibody stain
describe the crazy anthrax toxin.
three part A-B toxin. 2 A's (lethal and edema factors) and 1 B (protective). protective by itself does nothing but prevent infection from other B. anthracis. If you add edema factor (an adenylate cyclase once activated by Ca-calmodulin) you get edema. If you add lethal factor (Zn metalloprotease that cleaves map kinases and thus a huge release of cytokines from macs) you get shock and then death.
how does the anthrax toxin get into the cell?
protective antigens oligomerize on surface, then either lethal or edema factor is added and then the whole thing goes through receptor mediated endocytosis
describe cutaneous anthrax.
bacs get into wound/insect bite, wound turns black (eschars) can go to lymph nodes and then blood and may result in bacteremia
how is anthrax contracted?
spores and spores alone which are from animals, no human to human transmission
describe inhalation anthrax AKA woolsorter's disease.
bacs in terminal alveoli, macs eat em, go to regional nodes, germination, toxin and capsule made, no pneumonia but do have extensive pulmonary involvement, necrotic hemorrhage, multiple organs involved, meningitis, death rapid and near 100% even with treatment...
describe GI anthrax.
eat contaminated meat, spores penetrate oropharynx/intestinal mucosa, in submucosal tissue multiply and make toxin, usually to the nodes and then blood --> systemic symptoms. Death in 50 to 90% despite treatment
lab diagnosis for B. anthracis?
culture from lesion or blood, inject into mouse, guinea pig, india ink or direct fluorescent antibody, lysis by gamma phage, PCR
what is the treatment for B. anthracis?
cipro (#1), doxycycline, penicillins, must be given before toxins! vaccine: Protective antigen alone for lab workers, military workers, sterne vaccine is better and it is acapsulated bacs used for livestock
how is B. cereus dif than anthracis in terms of biology?
B hemolytic (cereolysin), no capsule, not lysed by gamma phage, no anthrax toxin, motile (flag)
infections from B. cereus?
wound, occular, food poisoning (intoxications not infections), rare systemic (from IV-catheter)
describe emetic disease from B. cereus.
nausea vomiting, short lived, no antibiotics needed, caused by heat stable toxin (cerulide, small potassium ionophore of mitochondria), protease resistant, rice/shell pastas implicated
describe the diarrheal disease caused by B cereleus.
ab cramps and small volume to lotsa watery diarrhea, fever, pt recovers in 24 hrs, incubation is a bit longer than emetic, toxin is heat labile and protease sensitive and larger than emetic toxin, activates adenylate cyclase