GI Acute Non-Inflammatory Bacteria Flashcards
E. coli are (G-ve/G+ve) and facultative anaerobes
E. coli are G-ve and facultative anaerobes
E. coli are G-ve and (aerobes/facultative anaerobes)
E. coli are G-ve and facultative anaerobes
____ is the primary cause of “Traveller’s diarrhea”
Enterotoxigenic E. coli (ETEC) is the primary cause of “Traveller’s diarrhea”
Enterotoxigenic E. coli (ETEC) is transmitted via ___ and ____
ETEC is transmitted via contaminated food and water
describe the pathogenesis of Enterotoxigenic E. coli (ETEC)
ETEC reach the ___ and colonize by using ____
ETEC reach the SI and colonize by using CFA (colonization factor antigens - fimbriae)
once ETEC colonizes the SI wall, it produces ____
once ETEC colonizes the SI wall, it produces 2 plasmid-encoded enterotoxins (LT and ST)
LT activates ___
while
ST activates ____
explain how this causes diarrhea
LT (heat labile) activates adenylate cyclase
while
ST (heat stable) activates guanylate cyclase
Enteropathogenic E. coli (EPEC) can lead to ____ and is significant in ____
Enteropathogenic E. coli (EPEC) can lead to infantile diarrhea (childhood diarrhea) and is significant in developing countries
describe the steps of pathogenesis in EPEC
- ingestion of pathogen
- colonization of SI
- plasmid-borne enteric adherence factor (EAF) bundle-forming pilus (BFP)
- effacement of microvilli
- osmotic imbalance → watery diarrhea
EPEC possess ____/____ which leads to the effacement of ____
EPEC possess plasmid-borne enteric adherence factor (EAF)/bundle-forming pilus (BFP) which leads to the effacement of microvilli
the management of EPEC is with ____
the management of EPEC is with rehydration therapy
describe the family Vibrionaceae
- single curved G-ve rods
- motile (single polar flagellum)
- non-spore forming
- oxidase +ve
describe the Sketchy
Vibrio cholerae ferments ___ and ___ but not ____
is ___ sensitive
and ___tolerant
Vibrio cholerae ferments sucrose and mannose but not arabinose
is acid sensitive
and halotolerant
describe the pathogenesis of V. cholerae
- ingestion
- liquid = higher infective dose required
- solid = lower infective dose bc food helps buffer low pH of stomach (since V. cholerae is acid-sensitive)
- colonization of SI
- production of cholera toxin
- bacteriophage-encoded AB toxin
- action similar to LT toxin of ETEC
- loss of H2O, Na, K, Cl, HCO3
- profuse watery diarrhea
V. cholerae produces ___ which is ___ encoded ____
V. cholerae produces cholera toxin which is bacteriophage encoded AB toxin
the action of cholera toxin is similar to ___ of ____
the action of cholera toxin is similar to LT of ETEC
describe the pathophysiological effects of V. cholerae
- dehydration: isotonic fluid loss
- hypokalemia: K+ ion loss
- metabolic acidosis: HCO3- loss
describe the management of cholera
- management:
-
replace ionic loss
- oral and/or IV admin. of glucose
-
replace ionic loss
____ and ____ are involved in the prevention of cholera
sanitation and hygiene are involved in the prevention of cholera
describe the diagnosis and identification of cholera
describe the Sketchy
name the 2 different diseases caused by C. perfringens
- necrotic enteritis
- C. perfringens strain type C
- type A food-borne infxn (food poisoning)
- C. perfringens strain type A
describe the pathogenesis of C. perfringens
C. perfringens cytotoxic activity causes ____ in the membrane
C. perfringens cytotoxic activity causes pore formation in the membrane
describe the symptoms of C. perfringens
watery diarrhea & severe abdominal pain
NO fever, nausea, vomiting
describe Bacillus cereus
- G+ve rods
- arranged in chains
- aerobic or facultative
- spore-former
- emetic toxin & enterotoxin
compared to C. perfringens, ____ is quicker and ___ is shorter for B. cereus foodborne illness
compared to C. perfringens, onset time is quicker and duration is shorter for B. cereus foodborne illness
describe the pathogensis of B. cereus
- ingestion of pathogen
- colonization of SI and production of LT enterotoxin
- acts on adenyl acyclase-cAMP
