Bacterial infection Flashcards
what is septic shock caused by
LPS on gram negative bacteria
what three covalently linked regions does LPS consist of
lipid A, core oligosaccharide, O Ag polysaccharide
what blocks the e. coli attachment site
treat cells with mannose -
how does Vibrio cholerae cause diarrhoel diseases
cholera toxin binds to GM1 receptor and is trafficked in where the A1 subunit is released
cytosolic A1 diffuses towards adenyl cyclase…. producing cAMP that opens channels…
what are the two main types of E.coli that cause non inflammatory diarrhoea
Enterotoxigenic e. coli (ETEC)
Enteropathogenic e. coli (EPEC)
what are the three main types of E.coli that cause inflammatory diarrhoea
Enteroinvasive e. coli (EIEC)
Enteroaggregative e. coli (EAggEC)
Enterohaemorrhagic e. coli (EHEC)
where does Ecoli 157 binds
large intestine in the crypts
what’s the hallmark of ecoli0157 infection
pedestal production
what cause production of ecoli0157 pedestals
actin rearrangement
describe the process of Gram staining
fixation -> add crystal violet -> add iodine (to chemically fix violet to peptidoglycan) -> decolourise (to wash unbound stain) -> add counter stain (safranin)
why do gram positive bacteria remain purple
because they have a thick peptidoglycan cell wall that is not easily penetrated by the solvent
what is the pathogenicity island called in EHEC
Locus of Enterocyte Effacement (LEE)
give features of EHEC Locus of enterocyte effacement
required for attaching and effacing lesions - ability to code the enterocyte efficient
acquired by horizontal gene transfer
lower GC content than the host cell/rest of dna
what is the major difference between the mechanism of non inflammatory and inflammatory diarrhoeal ecolis
non inflammatory ecoli attach to intestinal mucosa
inflammatory ecoli attach to colonic enterocytes
what characteristic structural changes do Ecoli trigger in enterocytes
attachment-effacement lesions (remove microvilli)
give examples of problems caused by enterohaemorrhagic ecoli
diarrhoea, haemorrhagic colitis, haemolytic uraemic syndrome, acute renal failure, hemolytic anemia, thrombocytopenia
what is the major toxin produced by EHEC
shiga-like toxin (Stx1&Stx2)
what is the structure of shiga-like toxin and what is the function of each part
an enzymatic Alpha subunit (depurinates adenosine in 28S rRNA) and 5 identical Beta subunits (bind to ceramide host cell receptors eg Gb3)
where do the Stx1 and Stx2 genes come from/ what are they carried by
Bacteriophage lysogens in the LEE of EHEC acquired by horizontal gene transfer
what is different about the peyers patches in the mucous membrane of the intestine
elongated thickened areas with surface free of projections (villi) and depressions (Lieberkuhn glands)
what major feature of EHEC does LEE encode for
the ability to induce attaching and effacing lesions on the host intestinal mucosa
where do EHECs bind and how do they form A/E lesions
pedestals
M cells on Peyers patches in ileum of small intestine (via long polar fimbrae adhesions
