Hosam Mohamed-
broad spectrum; cephalosporins, clindamycin, fluroquinolones, extended-coverage penicillins
What kind of Antibiotics are usually the cause of AAD?
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suppressed anaerobic flora interferes with carbohydrate & bile acid metabolism; a short chain acid is secreted; induced osmotic/secretory diarrhea
Explain the pathogenesis of AAD.
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anaerobic Gm+ rod
What kind of bacterium is Clostridium difficile?
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pseudomembraneous enterocolitis
-C.diff that produces toxins
-
transfer of spores via caregiver-patient or patient-patient
How is Pseudomembraneous Enterocolitis spread?
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enterotoxic; cytotoxic
C.difficile toxins A & B are potent _____& _______.
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attract neutrophils & monocytes to the area; increasing capillary permeability, tissue necrosis, hemorrhage, and edema
What do Toxins A & B cause the immune system to do?
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IgG & IgA
Which C.diff antibodies were found in asymptomatic & mild infected patients?
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b
Which stage of C.diff involves focal epithelial necrosis that has fibrin-rich exudates?
a) Third
b) Initial
c) Second
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c
Which stage of C.diff is characterized by a mucosal ulceration that looks like a volcano lesion with exudate protruding out?
a) Third
b) Initial
c) Second
-
a
Which stage of C.diff has more severe mucosal ulceration, necrosis, and a pseudomembrane composed of fibrin & cellular debris?
a) Third
b) Initial
c) Second
-
b
Neutrophils are present in which stage of C.diff?
a) Third
b) Initial
c) Second
-
a
Leukocytes are present in which stage of C.diff?
a) Third
b) Initial
c) Second
-
yellow coalescent plaques in the colon
What are typical findings for pseudomembraneous enterocolitis?
-
flat raised lesions
What are hyperemic findings for pseudomembraneous enterocolitis?
-
NAP-1
-this strain of C.diff produces more toxin A & B and is AB resistant.
-
10%
What is the infection rate 2 weeks after hopsitalization?
-
50%
What is the infection rate 4 weeks after hopsitalization?
