Bacterial infection Flashcards

1
Q

what is septic shock caused by

A

LPS on gram negative bacteria

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2
Q

what three covalently linked regions does LPS consist of

A

lipid A, core oligosaccharide, O Ag polysaccharide

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3
Q

what blocks the e. coli attachment site

A

treat cells with mannose -

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4
Q

how does Vibrio cholerae cause diarrhoel diseases

A

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…

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5
Q

what are the two main types of E.coli that cause non inflammatory diarrhoea

A

Enterotoxigenic e. coli (ETEC)

Enteropathogenic e. coli (EPEC)

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6
Q

what are the three main types of E.coli that cause inflammatory diarrhoea

A

Enteroinvasive e. coli (EIEC)
Enteroaggregative e. coli (EAggEC)
Enterohaemorrhagic e. coli (EHEC)

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7
Q

where does Ecoli 157 binds

A

large intestine in the crypts

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8
Q

what’s the hallmark of ecoli0157 infection

A

pedestal production

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9
Q

what cause production of ecoli0157 pedestals

A

actin rearrangement

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10
Q

describe the process of Gram staining

A

fixation -> add crystal violet -> add iodine (to chemically fix violet to peptidoglycan) -> decolourise (to wash unbound stain) -> add counter stain (safranin)

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11
Q

why do gram positive bacteria remain purple

A

because they have a thick peptidoglycan cell wall that is not easily penetrated by the solvent

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12
Q

what is the pathogenicity island called in EHEC

A

Locus of Enterocyte Effacement (LEE)

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13
Q

give features of EHEC Locus of enterocyte effacement

A

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

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14
Q

what is the major difference between the mechanism of non inflammatory and inflammatory diarrhoeal ecolis

A

non inflammatory ecoli attach to intestinal mucosa

inflammatory ecoli attach to colonic enterocytes

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15
Q

what characteristic structural changes do Ecoli trigger in enterocytes

A

attachment-effacement lesions (remove microvilli)

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16
Q

give examples of problems caused by enterohaemorrhagic ecoli

A

diarrhoea, haemorrhagic colitis, haemolytic uraemic syndrome, acute renal failure, hemolytic anemia, thrombocytopenia

17
Q

what is the major toxin produced by EHEC

A

shiga-like toxin (Stx1&Stx2)

18
Q

what is the structure of shiga-like toxin and what is the function of each part

A

an enzymatic Alpha subunit (depurinates adenosine in 28S rRNA) and 5 identical Beta subunits (bind to ceramide host cell receptors eg Gb3)

19
Q

where do the Stx1 and Stx2 genes come from/ what are they carried by

A

Bacteriophage lysogens in the LEE of EHEC acquired by horizontal gene transfer

20
Q

what is different about the peyers patches in the mucous membrane of the intestine

A

elongated thickened areas with surface free of projections (villi) and depressions (Lieberkuhn glands)

21
Q

what major feature of EHEC does LEE encode for

A

the ability to induce attaching and effacing lesions on the host intestinal mucosa

22
Q

where do EHECs bind and how do they form A/E lesions

A

pedestals

M cells on Peyers patches in ileum of small intestine (via long polar fimbrae adhesions