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

Lectures 7, 8 & 9 - Gastroenteritis Flashcards

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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
How can we detect ETEC in the lab?
PCR for ST and LT
25
Describe the pathogenesis of EPEC
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
26
What are the virulence determinants of EPEC?
Bfp (bundle forming pilus) Tir Intimin TIII SS
27
How may EPEC be diagnosed in a lab?
PCR for eae gene PCR for Bfp gene Fluorescent actin staining
28
Which bacteria can be transmitted at petting zoos?
EHEC
29
Describe the pathogenesis of EHEC
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
30
Describe how Shiga toxin works
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
31
What are the virulence determinants of EHEC?
``` TIII SS Tir Intimin Esp Shiga toxin ```
32
How can EHEC be diagnosed in a lab?
PCR of eae gene (intimin)
33
Consumption of contaminated sprouts was linked to which bacterium?
EAggEC
34
Which bacteria are invading pathogens?
Salmonella Shigella Yersinia enterolytica Campylobacter
35
Which viruses give rise to gastroenteritis? | Which one, that was talked about, doesn't?
Norovirus Rotavirus Adenoviruses Hep A doesn't give rise to gastro
36
What is the Pathogenesis of Hep A?
1. Faecally contaminated food / drink 2. Invades blood stream via Peyer's patches 3. Circulates to liver 4. Shedding in bile and faeces
37
Which groups is susceptible to rotavirus?
6 months - 2 years of age
38
What is the structure of rotavirus?
- Icosahedral - Spokes - Double shelled capsid. This confers acid stability and a very low infective dose
39
What is the general incubation period for viruses causing Gastroenteritis?
2 days
40
Describe the Replication of rotavirus
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
41
Which cells are susceptible in rotavirus infection?
The mature cells of the intestine Crypt cells are not infected
42
Why does rotavirus bring about diarrhoea?
The villi become blunted as the virions lyse the mature cells Immature cells have limited resorptive capacity
43
How can rotavirus be detected in the lab?
Electron microscopy | Antigen detection assays
44
What preventative methods are in place to protect babies from Rotavirus?
There is a vaccine that is rapidly reducing the number of cases RotaTeq
45
What is an example of a Calicivirus?
Norovirus
46
What is the pathogenesis of norovirus?
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
47
How may norovirus be detected in the lab?
Antigen detection assay Electron microscopy PCR for viral antigen
48
What symptoms result from adenovirus infection?
Watery diarrhoea Vomiting Cramps
49
What diseases are caused by adenoviruses?
Conjunctivitis Gastroenteritis Respiratory tract infection
50
Which protozoan pathogens cause gastroenteritis?
Giardia lamblia Entamoeba histolytica Cryptosporidium
51
How are protozoan pathogens generally spread?
Faecal-oral spread
52
Describe the Pathogenesis of entamoeba histolytica
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
How may E. hytolytica be detected in a lab?
Microscopy : look for cysts Immunoassay for antigen Serology
54
How may entamoeba histolytica be treated?
Metronidazole
55
Which protozoan pathogens are zoonoses?
Giardia lamblia | Cryptosporidium
56
What are the features of the Giardia trophozoite?
2 nuclei Flagellum Ventral sucking disk
57
Describe the pathogenesis of Giardia lamblia
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
How may Giardia be detected in a lab?
Microscopy | Antigen detection assay
59
How may Giardia infection be treated?
Metronidazole
60
What is the life cycle of cryptosporidium?
Oocyst: dormant and infectious - Excystation - 4 sporozoites Asexual followed by sexual reproduction Microgamont fertilises macrogamont to become oocyst Oocyst excreted
61
Describe the Pathogenesis of Cryptosporidium
No well understood 1. Faecally contaminated food / drink --> cysts in GIT 2. Surface glycoproteins and lectins --> adherence 3. Toxin ? epithelial damage 4. Diarrhoea
62
How is Cryptosporidium detected in a lab?
Antigen detection assay | Microscopy
63
How is Cryptosporidium treated?
Nitazoxanide
64
Compare the sequelae of Cryptosporidium infection in healthy and immuno-suppressed individuals
Healthy: one or two life cycles | Immuno-compromised: indefinite life cycles, as the immune system can't contain the infection
65
Which extra cellular bacteria cause disease?
E. coli V. Cholerae V. parahaemolyticus
66
Which invasive bacteria cause gastroenteritis?
Y. Enterolytica Salmonella Shigella Campylobacter
67
What are the two stereotypes of Cholera, and which is the most important?
Serotype O1: most important Serotype non O1
68
What are the reservoirs of V. cholerae?
Free living : ie water supply Humans
69
What are the sequelae of cholera infection?
Rice water stools Dehydration and death within hours
70
What is the infectious dose of cholera bacteria to cause disease? Why?
Large dose required Because it is not acid stable
71
Describe the Pathogenesis of V. cholerae
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
Describe the function of the cholera toxin (Ctx)
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
Which other toxins have the same structure as cholera toxin?
LT of ETEC Shiga toxin of EHEC Shiga toxin of Shigella
74
Which toxins have the same function as Ctx?
LT of ETEC | ST of ETEC
75
Which medium is used to grow Vibrio genus?
TCBS
76
It Ctx cytotoxic or tonic?
Cytotonic
77
What is the Pathogenesis of V. parahaemolyticus?
Not well understood It doesn't produce a toxin like V. cholerae
78
Differentiate between the groups affected by ETEC, EPEC, and EHEC
ETEC: worldwide (non-industrialised countries); adults, infants EPEC: infants EHEC: industrialised countries
79
What are the different symptoms of ETEC, EPEC and EHEC?
ETEC and EPEC: watery diarrhoea EHEC: dysentery, HUS
80
Which bacterium causes travellers' diarrhoea?
ETEC
81
Describe the pathogensis of ETEC
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
Describe the function of the toxins produced by ETEC
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
Why is the change in the cell in cholera permanent? | Hw does this differ from ETEC?
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
What is the infective dose for EPEC?
Adults: ridiculous amount Children: much less
85
In what situation would an adult get EPEC infection?
If the individual were taking Antacids
86
EPEC is endemic to which countries?
Brazil, Mexico, Sth Africa
87
Describe the Pathogenesis of EPEC
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
Which toxins do ETEC, EPEC and EHEC produce?
ETEC: LT, ST EPEC: no toxin EHEC: Shiga toxin
89
Which bacterial infection is associated with undercooked meat / hamburgers? Why?
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
Which bacterium can lead to HUS?
EHEC
91
Describe the pathogenesis of EHEC
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
Describe how the Shiga toxin functions
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
Why does Shiga toxin affect the vasculature, not the epithelium?
Stx is thought to pass through the epithelium to the endothelium
94
How is EHEC detected in the lab?
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
What is Stx? | Which bacteria have it?
Shiga toxin EHEC Shigella
96
How is ETEC detected in the lab?
PCR for LT & ST
97
How is EPEC detected in the lab?
PCR for Bfp PCR for eae (intimin)
98
Shigella and EHEC both produce Stx. What distinguishes their Pathogenesis?
Shigella: invasive EHEC: extracellular
99
How many species of Shigella are there? | How are they differentiated?
The are four They are serotyped based on their cell wall (O antigen)
100
What is the infective dose of shigella? | Why?
Very low Because it is acid stable
101
What is the reservoir of shigella?
Human only oathogen
102
How is shigella spread?
Since it is human only, human - human spread is the most common - Nursing homes - Childcare - Refugee camps
103
Describe the Pathogenesis of Shigella
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
Compare the function of Ipa and IcsA. | In which bacteria are they found?
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
How does Shigella cause inflammation?
Shigella are engulfed at the Laminar propria by macrophages Macrophages release cytokines, recruiting neutrophils
106
How may Shigella be detected in a lab?
Lactose non-fermenter --> differentiated from E. coli
107
Which bacterium has a reservoir in pets?
Salmonella
108
Describe the Pathogenesis of Salmonella
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
Compare the cells that salmonella and shigella infect
Salmonella: M cells and enterocytes Shigella: M cells only
110
How is salmonella detected in a lab?
Serotyping
111
What does Y. enterocolytica typically infect? What is it sometimes mistaken for?
Mesenteric lymph nodes Appendicitis
112
Which bacterium survives at lower temperatures?
Y. enterocolytica
113
Describe the pathogenesis of Y. enterocolytica
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
How does the Yop toxin function?
- Inhibits TNF production - Inhibits phagocytosis of bacteria by the phagocytes - disrupts Monocyte signalling pathways
115
How can Y. enterocolytica be detected in the lab?
Bulls eye colonies on CIN agar
116
What is the reservoir for Campylobacter?
Meat, poultry
117
What is the infective dose of campylobacter?
Quite high, since the bacterium is not acid stable
118
Describe he Pathogenesis of campylobacter
Not well understood 1. Infected meat not properly cooked 2. Endotoxin which is cyto lytic ?
119
What are the symptoms of campylobacter infection
Bloody diarrhoea
120
He may Campylobacter be detected in a lab?
Microaerophilic conditions

MIIM20002 - Microbes, Infections, Responses (32 decks)

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