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MIIM20002 - Microbes, Infections, Responses > Lectures 7, 8 & 9 - Gastroenteritis > Flashcards

Lectures 7, 8 & 9 - Gastroenteritis Flashcards

0
Q

What are the types of bacteria that make pre-formed toxin, bringing about intoxication?

A

Bacillus cereus

Staphylococcus aureus

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1
Q

What are the broad categories of how bacteria can cause gastroenteritis?

A

Intoxication (pre-formed toxin)

Toxin production

Invasive pathogens

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2
Q

What are the two different types of B. cereus?

How do the symptoms vary?

A

Emetic type: vomiting and cramps in every case, sometimes diarrhoea

Diarrhoeal type: diarrhoea seen in most cases

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3
Q

What is the source of b. cereus toxin?

A

Vegetables, soups, dairy

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4
Q

What is the source of Staphylococcus aureus?

A

Skin (it is part of the natural flora)

Food high in sugar and salt (ham…)

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5
Q

What are the general sequelae of intoxication?

A

Mild, self-limiting

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6
Q

Describe the Pathogenesis of S. aureus intoxication

A
  1. Toxin produced in the food
  2. When the food is eaten, the toxin binds to receptors in the upper GIT.
  3. Vomiting region of the brain is affected
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7
Q

Describe the Pathogenesis of emetic B. cereus intoxication

A
  1. Spores in food
  2. Spores survive cooking and germinate as food is cooled slowly at room temperature
  3. Spores produce cereulide peptide
  4. Peptide survives flash frying
  5. The toxin induces the symptoms once consumed
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8
Q

Describe the Pathogenesis of diarrhoeal B. cereus intoxication

A
  1. Spores in food
  2. Post cooking, the spores germinate and the numbers of bacteria rise
  3. Once in the body, a heat labile toxin
  4. Toxin activates Adenylate cyclase
  5. Fluid secretion into the intestine
  6. Diarrhoea
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9
Q

Compare the incubation period of the different bacteria that cause intoxication

A

B. cereus emetic - 1-5 hours
B. cereus diarrhoeal - 6-15 hours

S. aureus - 2-6 hours

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10
Q

What is the Pathogenesis of Clostridium perfringens?

A
  1. Spores in food survive cooking
  2. Germination
  3. Heat labile Toxin produced
  4. Glucose transport inhibited, epithelium damaged
  5. Watery diarrhoea
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11
Q

What is a common source of C. Perfringens intoxication?

A

Meat

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12
Q

What are the common sources of bacterial intoxication?

A

Meat: clostridium perfringens

Rice / cereals: B. cereus emetic

Soup, vegetables, dairy: B. cereus diarrhoeal

Sugary, salty, processed food: S. aureus

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13
Q

Which organisms cause attaching and effacing lesion, but do not invade?

A 
Vibrio cholerae
Vibrio parahaemolyticus
E. coli:
- ETEC
- EHEC
- EPEC
- EAggEC
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14
Q

Which bacterium is often found in marine water, and thus shellfish?

A

Vibrio parahaemolyticus

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15
Q

What is the source of the E. coli and V. Cholerae bacteria?

A

Faecally contaminated food or water

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16
Q

What is the Pathogenesis of V. Cholerae?

A
  1. Consumption of faecally contaminated food / drink
  2. Gets through mucus with flagella and mucinase
  3. Attaches with Tcp
  4. Cholera toxin: B5 binds, A enters the cell
  5. A turns on GTPase
  6. GTPase upregulates Adenylate cyclase
  7. Icreased cAMP in cell
  8. Na+, Cl- and H2O loss from cells
  9. Rice water stools
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17
Q

What are the virulence determinants of V. Cholerae?

A

Tcp (toxin co-regulated pilus)

Ctx (cholera toxin)

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18
Q

What is the structure of cholera toxin?

A

AB5

A: active, turns on GTPase

B5: binds to GM1 gangliosides

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19
Q

What is the pathogenesis of V. parahaemolyticus?

A

Not well understood

Invades intestinal cells, but does not produce a toxin

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20
Q

How can V. cholerae and V. parahaemolyticus be differentiated on a TCBS medium?

A

V. cholerae: yellow colonies

V. parahaemolyticus: green colonies

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21
Q

What is the Pathogenesis of ETEC?

A
  1. Faecally contaminated food / drink
  2. CFA attaches it to cells in the gut
  3. LT and ST produced
    4a. LT (identical to Ctx) disrupts osmotic balance through cAMP
    4b. ST increases cGMP –> cytotonic
  4. Watery diarrhoea
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22
Q

What are the virulence determinants of ETEC?

A

CFA (colonisation factor antigen)
ST (heat stable toxin)
LT (heat labile toxin)

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23
Q

One of the ETEC toxins is identical to another?

Which is it?

A

LT is identical to Ctx

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24
Q

How can we detect ETEC in the lab?

A

PCR for ST and LT

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25
Q

Describe the pathogenesis of EPEC

A
  1. Faecally contaminated food / drink
  2. Bfp attaches bacteria to enterocyte
  3. TIII SS injects Tir into the cell
  4. Bacteria attaches to Tir with Intimin
  5. Polymerisation of F actin
  6. Pedestal forms
  7. Attaching and effacing lesion, watery diarrhoea
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26
Q

What are the virulence determinants of EPEC?

A

Bfp (bundle forming pilus)
Tir
Intimin
TIII SS

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27
Q

How may EPEC be diagnosed in a lab?

A

PCR for eae gene
PCR for Bfp gene
Fluorescent actin staining

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28
Q

Which bacteria can be transmitted at petting zoos?

A

EHEC

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29
Q

Describe the pathogenesis of EHEC

A
  1. Faecally contaminated food / drink
  2. Unknown fimbriae attachment
  3. TIII SS injects Tir and Esp –> binds to intimin
  4. Actin rearrangement, pedestal
  5. Attaching and effacing lesion
  6. Shiga toxin passes through enterocyte to endothelium
  7. Protein synthesis stops
  8. Bloody diarrhoea
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30
Q

Describe how Shiga toxin works

A
  1. Gets into cells by binding to Gb3 receptor
  2. Removes a nucleic acid from the ribosome
  3. Protein synthesis stops
  4. Vasculature of intestine damaged
  5. Blood diarrhoea
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31
Q

What are the virulence determinants of EHEC?

A 
TIII SS
Tir
Intimin
Esp
Shiga toxin
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32
Q

How can EHEC be diagnosed in a lab?

A

PCR of eae gene (intimin)

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33
Q

Consumption of contaminated sprouts was linked to which bacterium?

A

EAggEC

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34
Q

Which bacteria are invading pathogens?

A

Salmonella
Shigella
Yersinia enterolytica
Campylobacter

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35
Q

Which viruses give rise to gastroenteritis?

Which one, that was talked about, doesn’t?

A

Norovirus
Rotavirus
Adenoviruses

Hep A doesn’t give rise to gastro

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36
Q

What is the Pathogenesis of Hep A?

A
  1. Faecally contaminated food / drink
  2. Invades blood stream via Peyer’s patches
  3. Circulates to liver
  4. Shedding in bile and faeces
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37
Q

Which groups is susceptible to rotavirus?

A

6 months - 2 years of age

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38
Q

What is the structure of rotavirus?

A
  • Icosahedral
  • Spokes
  • Double shelled capsid.

This confers acid stability and a very low infective dose

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39
Q

What is the general incubation period for viruses causing Gastroenteritis?

A

2 days

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40
Q

Describe the Replication of rotavirus

A
  1. Intestinal trypsin causes proteolysis of spokes
    - -> enhanced penetration
  2. Uncoating
  3. Produces RNA-dep RNApol (not available in host cell)
  4. Copies genome
  5. Self-assembles
  6. Lyses out of cell
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41
Q

Which cells are susceptible in rotavirus infection?

A

The mature cells of the intestine

Crypt cells are not infected

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42
Q

Why does rotavirus bring about diarrhoea?

A

The villi become blunted as the virions lyse the mature cells

Immature cells have limited resorptive capacity

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43
Q

How can rotavirus be detected in the lab?

A

Electron microscopy

Antigen detection assays

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44
Q

What preventative methods are in place to protect babies from Rotavirus?

A

There is a vaccine that is rapidly reducing the number of cases

RotaTeq

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45
Q

What is an example of a Calicivirus?

A

Norovirus

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46
Q

What is the pathogenesis of norovirus?

A

Not well understood

  1. Faecally contaminated food / drink
  2. Binds to histo-blood group antigens
  3. Villus blunting
  4. Malabsorption of fat and lactose
  5. Diarrhoea
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47
Q

How may norovirus be detected in the lab?

A

Antigen detection assay
Electron microscopy
PCR for viral antigen

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48
Q

What symptoms result from adenovirus infection?

A

Watery diarrhoea
Vomiting
Cramps

49
Q

What diseases are caused by adenoviruses?

A

Conjunctivitis
Gastroenteritis
Respiratory tract infection

50
Q

Which protozoan pathogens cause gastroenteritis?

A

Giardia lamblia
Entamoeba histolytica
Cryptosporidium

51
Q

How are protozoan pathogens generally spread?

A

Faecal-oral spread

52
Q

Describe the Pathogenesis of entamoeba histolytica

A
  1. Cysts in food are consumes
  2. Excystation
  3. Trophozoite attaches to digalactose on intestinal cells
  4. Pre-forming toxin inserted into host cell
  5. Amoebae ingest host cells (including neutrophils and macrophages)
  6. Produce a protease that breaks down antibodies
53
Q

How may E. hytolytica be detected in a lab?

A

Microscopy : look for cysts
Immunoassay for antigen
Serology

54
Q

How may entamoeba histolytica be treated?

A

Metronidazole

55
Q

Which protozoan pathogens are zoonoses?

A

Giardia lamblia

Cryptosporidium

56
Q

What are the features of the Giardia trophozoite?

A

2 nuclei
Flagellum
Ventral sucking disk

57
Q

Describe the pathogenesis of Giardia lamblia

A
  1. Faecally contaminated food / drink
  2. Adheres to gut wall with ventral sucking disk
    - -> reduced absorptive capacity
  3. Blunting of micro villi
  4. Malabsorption of fat
    - -> wasting
58
Q

How may Giardia be detected in a lab?

A

Microscopy

Antigen detection assay

59
Q

How may Giardia infection be treated?

A

Metronidazole

60
Q

What is the life cycle of cryptosporidium?

A

Oocyst: dormant and infectious
- Excystation -
4 sporozoites

Asexual followed by sexual reproduction

Microgamont fertilises macrogamont to become oocyst

Oocyst excreted

61
Q

Describe the Pathogenesis of Cryptosporidium

A

No well understood

  1. Faecally contaminated food / drink –> cysts in GIT
  2. Surface glycoproteins and lectins –> adherence
  3. Toxin ? epithelial damage
  4. Diarrhoea
62
Q

How is Cryptosporidium detected in a lab?

A

Antigen detection assay

Microscopy

63
Q

How is Cryptosporidium treated?

A

Nitazoxanide

64
Q

Compare the sequelae of Cryptosporidium infection in healthy and immuno-suppressed individuals

A

Healthy: one or two life cycles

Immuno-compromised: indefinite life cycles, as the immune system can’t contain the infection

65
Q

Which extra cellular bacteria cause disease?

A

E. coli
V. Cholerae
V. parahaemolyticus

66
Q

Which invasive bacteria cause gastroenteritis?

A

Y. Enterolytica
Salmonella
Shigella
Campylobacter

67
Q

What are the two stereotypes of Cholera, and which is the most important?

A

Serotype O1: most important

Serotype non O1

68
Q

What are the reservoirs of V. cholerae?

A

Free living : ie water supply

Humans

69
Q

What are the sequelae of cholera infection?

A

Rice water stools

Dehydration and death within hours

70
Q

What is the infectious dose of cholera bacteria to cause disease?
Why?

A

Large dose required

Because it is not acid stable

71
Q

Describe the Pathogenesis of V. cholerae

A
  1. Faecally contaminated food / drink
  2. Secretes mucinase to break down mucous, flagella to tunnel though to the enterocytes
  3. Colonises the GIT with Tcp
  4. Ctx gets into cells –> cytotonic
  5. Rice water stool
72
Q

Describe the function of the cholera toxin (Ctx)

A
  1. B5 binds to GM1 gangliosides
  2. A subunit gets into the cell
  3. Binds to GTPase
  4. Turns on Adenylate cyclase
  5. Increased levels of cAMP
  6. Cl out, and Na excluded from cell, water follows
  7. Rice water stool
73
Q

Which other toxins have the same structure as cholera toxin?

A

LT of ETEC
Shiga toxin of EHEC
Shiga toxin of Shigella

74
Q

Which toxins have the same function as Ctx?

A

LT of ETEC

ST of ETEC

75
Q

Which medium is used to grow Vibrio genus?

76
Q

It Ctx cytotoxic or tonic?

77
Q

What is the Pathogenesis of V. parahaemolyticus?

A

Not well understood

It doesn’t produce a toxin like V. cholerae

78
Q

Differentiate between the groups affected by ETEC, EPEC, and EHEC

A

ETEC: worldwide (non-industrialised countries); adults, infants

EPEC: infants

EHEC: industrialised countries

79
Q

What are the different symptoms of ETEC, EPEC and EHEC?

A

ETEC and EPEC: watery diarrhoea

EHEC: dysentery, HUS

80
Q

Which bacterium causes travellers’ diarrhoea?

81
Q

Describe the pathogensis of ETEC

A
  1. Faecally contaminated food / drink
  2. CFA (fimbrial) attachment to the enterocytes in GIT
  3. LT and ST produced and enter cell
  4. Watery diarrhoea produced
82
Q

Describe the function of the toxins produced by ETEC

A

LT
1. B binds to GM1 gangliosides
2. A binds to GTPase -> AC -> cAMP -> effusion of water
PERMANENT

ST
1. Toxin enters enterocyte
2. Icreases cGMP -> effusion of water
NOT PERMANENT

83
Q

Why is the change in the cell in cholera permanent?

Hw does this differ from ETEC?

A

Once the A subunit of Ctx binds to GTPase, it is permanently on

ST from ETEC has a similar pathogenesis, but the change is not permanent

84
Q

What is the infective dose for EPEC?

A

Adults: ridiculous amount
Children: much less

85
Q

In what situation would an adult get EPEC infection?

A

If the individual were taking Antacids

86
Q

EPEC is endemic to which countries?

A

Brazil, Mexico, Sth Africa

87
Q

Describe the Pathogenesis of EPEC

A
  1. Faecally contaminated food / drink
  2. Bfp attaches the bacteria to the enterocytes
  3. T III SS injects Tir into the host cell
  4. Tir binds to Intimin of the bacterial cell
  5. Actin rearrangement
  6. Attaching and effacing lesion
  7. Blunted villi
88
Q

Which toxins do ETEC, EPEC and EHEC produce?

A

ETEC: LT, ST
EPEC: no toxin
EHEC: Shiga toxin

89
Q

Which bacterial infection is associated with undercooked meat / hamburgers?
Why?

A

EHEC

It is a zoonosis, and is found in the meat of the asymptomatic animal

If the meat is not cooked properly, the bacteria will survive the cooking process

90
Q

Which bacterium can lead to HUS?

91
Q

Describe the pathogenesis of EHEC

A
  1. Undercooked meat consumed
  2. Bacterium attaches to gut by unknown fimbrial attachment
  3. T III SS injects Tir –> intimin
  4. Attaching and effacing lesion
  5. Shiga toxin disrupts vasculature
  6. Dysentery
92
Q

Describe how the Shiga toxin functions

A
  1. Binds to Gb3 receptors on endothelial cells
  2. Gets into cells
  3. Removes a nucleic acid from the ribosome
  4. Halts protein synthesis
  5. Cells die
93
Q

Why does Shiga toxin affect the vasculature, not the epithelium?

A

Stx is thought to pass through the epithelium to the endothelium

94
Q

How is EHEC detected in the lab?

A

PCR for Intimin gene (also on EPEC, though)

Sorbitol MacConkey –> it is a sorbitol non-fermenter, so it looks different to normal E. coli

PCR for stx genes

95
Q

What is Stx?

Which bacteria have it?

A

Shiga toxin

EHEC
Shigella

96
Q

How is ETEC detected in the lab?

A

PCR for LT & ST

97
Q

How is EPEC detected in the lab?

A

PCR for Bfp

PCR for eae (intimin)

98
Q

Shigella and EHEC both produce Stx. What distinguishes their Pathogenesis?

A

Shigella: invasive
EHEC: extracellular

99
Q

How many species of Shigella are there?

How are they differentiated?

A

The are four

They are serotyped based on their cell wall (O antigen)

100
Q

What is the infective dose of shigella?

Why?

A

Very low

Because it is acid stable

101
Q

What is the reservoir of shigella?

A

Human only oathogen

102
Q

How is shigella spread?

A

Since it is human only, human - human spread is the most common

  • Nursing homes
  • Childcare
  • Refugee camps
103
Q

Describe the Pathogenesis of Shigella

A
  1. Faecally contaminated food / drink
  2. Adhesion
  3. T III SS injects Ipa –> membrane ruffling –> uptake into the M cells
  4. Escape vesicle
  5. Produce IcsA
  6. Actin recruited –> burst into neighbouring enterocytes
  7. Infected cells die
  8. Stx damages vasculature
  9. Dysentry
104
Q

Compare the function of Ipa and IcsA.

In which bacteria are they found?

A

These are found in Shigella

Ipa: invasion plasmid antigens
- Induce membrane ruffling and invasion of the bacterium into M cells

IcsA: intracellular spread antigens
- Recruit the actin and burst the bacteria into neighbouring enterocytes

105
Q

How does Shigella cause inflammation?

A

Shigella are engulfed at the Laminar propria by macrophages

Macrophages release cytokines, recruiting neutrophils

106
Q

How may Shigella be detected in a lab?

A

Lactose non-fermenter –> differentiated from E. coli

107
Q

Which bacterium has a reservoir in pets?

A

Salmonella

108
Q

Describe the Pathogenesis of Salmonella

A
  1. Faecally contaminated food / drink
  2. SPI1 produces Sip –> membrane ruffling, invasion of M cells and enterocytes
  3. SPI2 produces Ssa –> survival within the vacuole
  4. Inflammatory exudate and electrolyte retention in the lumen (due to mediators of uptake)
  5. Inflammatory response: salmonella taken up by macrophages at Laminar propria and taken to mesenteric lymph nodes
109
Q

Compare the cells that salmonella and shigella infect

A

Salmonella: M cells and enterocytes

Shigella: M cells only

110
Q

How is salmonella detected in a lab?

A

Serotyping

111
Q

What does Y. enterocolytica typically infect?

What is it sometimes mistaken for?

A

Mesenteric lymph nodes

Appendicitis

112
Q

Which bacterium survives at lower temperatures?

A

Y. enterocolytica

113
Q

Describe the pathogenesis of Y. enterocolytica

A
  1. Faecally contaminated food / drink
  2. Adheres to gut
  3. T II SS injects Yop proteins into the M cell and invades
  4. Yop prevents phagocytosis of the bacterium by the macrophage
  5. Yop are cytotoxic to the host cell
  6. Spread to enterocytes via the basal layer
114
Q

How does the Yop toxin function?

A
  • Inhibits TNF production
  • Inhibits phagocytosis of bacteria by the phagocytes
  • disrupts Monocyte signalling pathways
115
Q

How can Y. enterocolytica be detected in the lab?

A

Bulls eye colonies on CIN agar

116
Q

What is the reservoir for Campylobacter?

A

Meat, poultry

117
Q

What is the infective dose of campylobacter?

A

Quite high, since the bacterium is not acid stable

118
Q

Describe he Pathogenesis of campylobacter

A

Not well understood

  1. Infected meat not properly cooked
  2. Endotoxin which is cyto lytic ?
119
Q

What are the symptoms of campylobacter infection

A

Bloody diarrhoea

120
Q

He may Campylobacter be detected in a lab?

A

Microaerophilic conditions

MIIM20002 - Microbes, Infections, Responses (32 decks)

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