Ecoli Flashcards
EPEC
—>diarrhoea in infants/nurseries
mechanism
-attachment
-effacement
adhere to mucosal cells of SI
2 important facors
1) pilus encoded by EAF
2) chromosomal locus of enterocyte effacement pathogenicity island —promote tight adherance of EPEC
after attachment loss of microvilli(effacement) and formation of pedestals(cup like structures)=severe watery diarrhoea,vomitting,fever
ETEC
—> traveller diarrhoea/infants
mechanism
CFA promote the adherance of ETEC to SI
2toxins
LT-heat labile exotoxin–under plasmid control
-2 subunits
subunitB–binding to GM1 ganglioside on enterocyte facilitates entry of subunit A into the cell–activate adenylase cyclase–cAMP increased—hypersecretion of water and electrocytes & inhibition of reabsorption of sodium
antigenic and crossreact with enterotoxin of vibrio
ST of ETEC
heat stable enterotoxin
under plasmid control
activate guanylase cyclase–cGMP increased–stimulates fluid secretion
EIEC
children/travellers
similar to shigellosis
NLF/LLF
mechanism
-by invading intestinal mucosal epithelial cells
penetrate mucous layer by glycosidase produced by normal flora then attach to cell suface and induce endocytic processes–multiply ic and inhibit protein synthesis
bacillary dysentery due to tissue destruction and inflammation
resists gastric acid bile salt and pancreatic enzymes
EAEC
HIV/traveller
-adherance to human cells
exact pathogenic mechanism not known
mucosal damage, large amount of mucus, secretory diarrhoea
acute and chronic diarrhoea >14 days
Esch.coli
normal intestinal flora
not pathogenic in their normal habitat
pathogenic in UT,BT and other sites of bdominal cavity,others
enterobacteriaecae
gram(-)balli , peritrichous flagella
LF
Ag- O H K
clinical conditions caused by Esh.coli
GE
haemorrhagic colitis
HUS
UTI
appendicitis and appendicular abscess
SBE
bacteremia septicemia
pneumoniameningitis
meningitis brain abscess
wounds burns and carbuncles
