L7 GIT Infections Flashcards

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1
Q

What is the normal human flora?

A

Microbiome on the human body where organisms naturally exist

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2
Q

Where is there an increased human microbiome?

A

Moist, protected areas of skin e.g. armpits, groin and between toes

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3
Q

Microbial cells: human cells

A

10:1

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4
Q

Commensal flora of gut (bacteria type)

A

More obligate anaerobic bacteria (e.g. bacteroides) than facultative anaerobic bacteria (e.g. E. coli) by 100:1

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5
Q

What are the beneficial effects of gut commensal flora?

A

Metabolism
Colonisation resistance
Antibody induction

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6
Q

Why does diet effect the composition of gut flora?

A

Bottle-fed babies develop adult microflora

Breast-fed babies develop ‘Bifidobacteria’ = probiotics that help to perform essential functions such as digestion

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7
Q

Most common gut commensal flora

A

Bacteroides

Prevotella

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8
Q

Obligate anaerobes

A

Clostrodia

Bifidobacteria

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9
Q

Facultative anaerobes

A

Enterobacteriacea

Enterococci

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10
Q

Bacterial gastroenteritis (enterotoxin production)

A
Vibrio cholerae
E. Coli
Shigella dysenteriae
C. perfingens
S. aureus
B. cereus
C. difficile
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11
Q

Bacterial gastroenteritis (adherence)

A

Shigella sonnei
E. coli
Campylobacter jejuni
Salmonella

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12
Q

Cholera cause

A

Vibrio Cholerae

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13
Q

Symptoms of cholera

A

Diarrhoea and vomiting

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14
Q

Transmission of cholera

A

Faecal-oral route (toxin mediated)

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15
Q

Management of cholera

A

Oral vaccine

Oral rehydration solution

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16
Q

What does salmonella enterica cause?

A

Food poisoning
Typhoid
Paratyphoid

17
Q

Serovars of salmonella enterica

A

2500 serovars

Salmonella Newport is most common

18
Q

Salmonella enterica cause

A

Contaminated foodstuff e.g. poultry

19
Q

Mechanism of salmonella enterica

A

Type three secretion systems

20
Q

Gastroentiritis treatment

A

Supportive management
Avoid antibiotics
May worsen E.coli HUS

21
Q

Pathotypes of E.coli

A

8 pathotypes

22
Q

E. coli O157

A

Cattle was a major source

Toxin causes premature destruction of RBC (clog kidneys) causing haemolytic-uremic syndrome (HUS)

23
Q

E.coli mechanism

A

Toxin activates G protein
Increase cAMP
Activates ion channels (increase chloride excretion)
Water follows out of cell

Different toxins have different mechanisms

24
Q

Common cause of C. difficile

A

From nosocomial infections

25
Q

Symptoms of C. difficile

A

Diarrhoea
Toxic megacolon
Pseudomembranous colitis (inflammation of large intestine)

26
Q

C. difficile mechanism

A

Toxin A: active component with toxic effects (increasing production of cAMP)
Toxin B: facilitate binding to certain receptor

Binary toxin

27
Q

C. difficile: Overview of intracellular modification by TcdA and TcdB

A

Both act intracellularly as glycosyltransferases
Each toxin modifies small GTPases
Effects of modification = actin condensation/ transcriptional activation/ apoptosis

Exposure of TcdA = neutrophil infiltration, substance P production, chemokine production, reactive oxygen intermediate production, disruption of tight junctions and apoptosis
Exposure of TcdB leads to disruption of tight junctions and apoptosis

Combination of one or more of these activities leads to fluid accumulation in the host and inflammatory responses

28
Q

Campylobacter complications

A

Reactive arthritis, Guillian-Barre syndrome, and BS

29
Q

Campylobacter causes

A

Raw or undercooked meat
Unpasteurised milk
Untreated water

30
Q

Outbreak of campylobacter

A

Clustering of cases due to common source e.g. recreational water/ food and water sources