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Medical Microbiology > Gastrointestinal Infections > Flashcards

Gastrointestinal Infections Flashcards

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1
Q

What percentage of the population is affected by GI infections per year?

A

20%

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2
Q

Where does the GIT span?

A

From mouth to anus

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3
Q

What are the host defence mechanisms?

A 
Stomach pH <4
Innate immunity
Digestive enzymes
Peristalsis
Tight junctions between epithelial cells
Commensal microbiota
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4
Q

What environment is the GIT?

A

Anaerobic - strictly anaerobic bacteria outnumbers anaerobes

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5
Q

What are the normal inhabitants of the stomach?

A

Lactic acid bacilli (small number)

Helicobacter pylori

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6
Q

What are the normal inhabitants of the small intestine?

A

Mainly Gram-positive

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7
Q

What are the normal inhabitants of the large intestine?

A

E. coli

Gram-positives (Bacteroides, Clostridium

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8
Q

What are the symptoms of GIT infections?

A 
Diarrhoea
Vomiting
Abdominal pain
Nausea
Fever
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9
Q

What abilities does a GI pathogen need?

A 
Survive the gastric acid
Attach to epithelium
Get food
Survive in environment
Invade
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10
Q

Which Gram-negative bacteria infect the GIT?

A 
Campylobacter jejuni
Salmonella enterica
Helicobacter pylori
Vibrio cholera
Escherichia coli
Shigella spp (sonnei)
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11
Q

How is Helicobacter pylori transmitted?

A

Person-to-person

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12
Q

How does Helicobacter pylori survive in the stimach?

A

Motility- flagella allows it to swim through gastric mucus

Urease - catalyses hydrolysis of urea yielding CO2 and NH3 to raise local pH

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13
Q

What can Helicobacter pylori cause?

A

Gastritis
Gastric ulcer
Gastric cancer

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14
Q

What are the pathogenicity factors of Helicobacter pylori?

A 
Urease
Flagella
VacA (pore forming)
Blood group antigen-binding adhesin (BabA)
Type IV secretion system (on cag)
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15
Q

What is T4SS?

A

Transports DNA or protein in Either a 1-step or 2-step mechanism

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16
Q

What do cag strains cause?

A

Stringer inflammatory response in stomach and greater risk of developing peptic ulcers and cancer

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17
Q

What is the most common E. coli strain?

A

K12

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18
Q

What is the infective dose of Enterohaemolytic E. coli?

A

Approximately 10 cells

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19
Q

How does Enterohaemolytic E. coli affect the body?

A

Bloody diarrhoea

Shiga toxin -> haemolytic uraemic syndrome (HUS) -> acute kidney failure

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20
Q

What is shiga toxin?

A

Protein complex encoded by stxAB genes located in prophage
Toxin released from bacterial cell by lysis
Formed from A and B subunits in AB5 complex

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21
Q

What does the A subunit of shiga toxin do?

A

Inhibits protein synthesis after release in host cytosol by removing adenine from 28S RNA of 60S ribosomal subunit

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22
Q

What does the B subunit of shiga toxin do?

A

Cell surface binding to host with Gb3 receptor found mainly on kidney cells

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23
Q

Which toxins have AB family?

A

Shiga

Cholera

24
Q

What are features of Clostridium difficile?

A

Toxin producer
Resistant spores (alcohol hand gel)
Disturbs normal bowel flora
Diarrhoea

25
Q

What are the major toxins of Clostridium difficile?

A

TcdA and TcdB

26
Q

What do the major toxins in Clostridium difficile cause?

A

Diarrhoea
Inflammation
Damage of colonic mucosa

27
Q

How are the toxins of Clostridium difficile internalised to host cell?

A

Endocytosis

28
Q

How do Tcd toxins work?

A

Toxin binds to unknown receptor
Internalised
Enzymic domain proteolytically cleaved from binding domain
Endosomes acidified
Enzymic component transported to cytoplasm
Glucosylates Rho proteins

29
Q

Why is acid resistance an important pathogenicity mechanism?

A

Survival

30
Q

How does toxin production affect host cells?

A

Can disable via pore formation in cytoplasmic membrane
Disrupt actin cytoskeleton
Increase intracellular levels of cyclic AMP
Inactivation of signalling pathways (GTPases)

31
Q

What are three types of toxin groups in GI disease?

A

Neurotoxins
Enterotoxins
Cytotoxins

32
Q

What are some examples of neurotoxins?

A 
Staphylococcus aureus (toxin B)
B. cereus (emetic toxin)
33
Q

How does a neurotoxin enter the body?

A

Consumed (intoxication)

34
Q

What is an example of a enterotoxin?

A

V. cholerae

35
Q

How does V. cholera affect the body?

A

Direct effect on gut epithelium
Water transferred from blood to gut
Catastrophic fluid loss

36
Q

What are some examples of cytotoxins?

A 
Shiga toxin (Shigella, EHEC)
Helicobacter pylori VacA toxin
37
Q

What do cytotoxins do?

A

Destroy intestinal cells

May cause inflammatory diarrhoea

38
Q

What are effector proteins?

A

Typically enzyme that disrupts host cell signalling pathways for pathogen’s benefit

39
Q

How do effector proteins work?

A

Either by mimicking host endogenous cellular proteins or covalently modifying host cell proteins

40
Q

What are some examples of effector proteins?

A

E. coli Map

Helicobacter pylori CagA

41
Q

What are the features of a chromosomal genome?

A

Pathogenicity islands (present in pathogen absent in commensal)

42
Q

What are the features of a mobile genome (mobilome)?

A

Transmissible (conjugative) plasmids

Phage

43
Q

What are the features of viral GI pathogens?

A 
Usually mild gastroenteritis
Self limiting 
Short lived (1-2 days)
Person to person transmission/aerosols from vomiting
Food bourne outbreaks
44
Q

What are the features of noroviru?

A 
Winter vomiting disease
Affects all ages
Low infective dose
Aerosol spread
Good survival in environment
45
Q

Who does rotavirus affect?

A

Young children <2

46
Q

How can norovirus and rotavirus be detected?

A

Electron microscopy

PCR

47
Q

What are some examples of protozoan GI pathogens?

A

Cryptosporidium parvum
Giardia lamblia
Entamoeba histolytica

48
Q

What is a common feature of Cryptosporidium parvum, Giardia lamblia and Entamoeba histolytica?

A

Cysts

Often contaminate water surfaces

49
Q

What pathogens would xylose lysine desoxycholate agar be used for?

A

Salmonella and Shigella spp

50
Q

What is the morphology of Salmonella and Shigella on xylose lysine desoxycholate agar?

A

Red colonies

Salmonella spp also have black centre

51
Q

How is Salmonella and Shigella differentiated from non-pathogenic bacteria of the same apperance?

A

Urease test - they are both negative

52
Q

What pathogen is Sorbitol MacConkey agar used for?

A

E. coli O157 (EHEC)

53
Q

How is E. coli differentiated?

A

O157 does not ferment sorbitol therefore has pale colonies

Other E.coli ferment sorbitol and therefore have red colonies

54
Q

What is the treatment for most GI pathogens?

A

Rehydration/electrolyte balance
Pain relief (cramps)
Antipyretics (fever)

55
Q

What is the therapy for peptic ulcer from Helicobacter pylori?

A

Calrithromycin or metronidazole

Resistance is common

56
Q

What is the therapy for C. difficile?

A

Metronidazole

for other diarrhoeal pathogens antibiotic treatment should be avoided - can make worse

Medical Microbiology (7 decks)

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