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15 - Food & Water borne bacterial diseases Flashcards

1
Q

Gastroenteritis

A

inflammation of stomach and intestinal lining. Called food poisoning when food is source of pathogen

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2
Q

Colonisation of the host

A

Infection may be non invasive (bacteria remain on epithelial surface) or invasive (bacteria cross the epithelium)

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3
Q

Food intoxication

A
  • Bacteria secrete an enterotoxin that disrupts the intestinal mucosa
  • Presence of the living bacterium not required for symptoms
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4
Q

Stomach and small intestine

A
  • Acidic pH
  • Low microbial load, few pathogens (e.g. Helicobacter pylori)
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5
Q

Large intestine

A
  • Mainly anaerobes and facultative anaerobes
  • ~2000 uncultured species essential for health and aid in digestion of food
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6
Q

Physical defences of the GIT

A
  • Tight junctions between epithelial cells
  • Mucins secreted from goblet cells
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7
Q

Chemical defences of the GIT

A

Low pH (<3) in stomach

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8
Q

Immunological defences of the GIT

A
  • GALT (gut associated lymphoid tissue)
  • Paneth cells secrete antimicrobial defensins
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9
Q

Mechanical defences of the GIT

A

Constant shedding of epithelial cells and replacement by differentiation of stem
cells into enterocytes

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10
Q

How do bacterial pathogens cause disease in the GIT?

A
  • Intoxication
  • Adherence and secretion of toxins
  • Injection of effectors by type III and type IV secretory systems
  • Invasion
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11
Q

Intoxication

A

preformed toxin ingested and presence of living microbes in food not required

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12
Q

Diseases that arise through intoxication

A
  • Staphylococcal food poisoning
  • Bacillus cereus food poisoning
  • Botulism: Clostridium botulinum
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13
Q

Staphylococcus aureus

A

Gram positive cocci in clusters

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14
Q

Clinical symptoms of Staphylococcal food poisoning

A
  • Pain, cramps, diarrhoea, vomiting, nausea
  • Intoxication in short period (1 to 8 hr, duration <24hrs)
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15
Q

Epidemiology of Staphylococcal food poisoning

A
  • Contaminates foods
    (custard, ham, ice cream, meats)
  • Bacteria present in nose, skin lesions, thus food may
    be contaminated by food handlers
    ̶- S. aureus cells are resistant to heat, drying and high osmotic pressure
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16
Q

Main virulence factors of Staphylococcal food poisoning

A
  • Numerous enterotoxins (24)
  • Heat stable (survive boiling 30mins)
  • Superantigens
  • Act on gut receptors and trigger vomiting
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17
Q

Superantigens

A

cause non-specific stimulation of T cells resulting in massive release of cytokines and inflammation

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18
Q

Bacillus cereus

A
  • Gram positive endospore-forming bacillus
  • Endospores are heat resistant (survive boiling)
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19
Q

Clinical symptoms of Bacillus cereus food poisoning

A

vomiting and diarrhoea

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20
Q

Epidemiology of Bacillus cereus food poisoning

A
  • Found in soil, vegetation
  • Heating food may not kill spores
  • Rice especially susceptible e.g. re-heated fried rice
  • Spores germinate as food cools
  • Vegetative cells release enterotoxins
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21
Q

Main virulence factors of Bacillus cereus food poisoning

A
  • 2 types of enterotoxins
  • Emetic toxin
  • Diarrhoeal toxin
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22
Q

Emetic toxin

A

Triggers vomiting. 2 to 5 hrs incubation period (an intoxication)

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23
Q

Diarrhoeal toxin

A

Diarrhoea. 8 to 16 hrs incubation period (an infection where bacteria colonise)

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24
Q

Clostridium botulinum

A

Gram positive endospore-forming anaerobic bacillus

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25
Clinical symptoms of Botulism
- Symptoms within 12-72 hrs of toxin ingestion - Blurred vision, difficulty swallowing, muscle weakness, flaccid paralysis - Death in 1/3 untreated patients from respiratory or cardiac failure
26
Epidemiology of Botulism
- Main source home-canned food that contains spores - Infant botulism is most common form of botulism but is not an intoxication; spores ingested from honey germinate in intestine, bacteria colonise immature gut
27
Main virulence factor of botulism
- Botulinum toxin - neurotoxin binds to motor neurons, prevents release of neurotransmitter acetylcholine, muscles unable to contract, hence paralysis
28
Diseases that arise through adherence and secretion of toxins
- Cholera (Vibrio cholerae) - Enterotoxigenic Escherichia coli - Clostridium perfringens
29
Clinical symptoms of Cholera
- Acute diarrhoeal disease - “rice water stools” containing mucous and epithelial cells - Loss of 12-20 litres fluids/day - Death due to shock, organ failure
30
Treatment of Cholera
Rehydration (fluids and electrolytes), antibiotics
31
Virulence factors of Cholera
- Tcp pilus adhesins allow colonisation of intestinal epithelium - Cholera toxin (Ctx)
32
What encodes for Tcp pilus adhesions
Mobile DNA element Vibrio Pathogenicity Island (VPI) in chromosome
33
What encodes for Cholera toxin (Ctx)
Encoded by bacteriophage (Ctx phage) which infects the V. cholerae cells
34
Epidemiology of Cholera
- Found in fresh and salty water - Form biofilms on crustaceans, algae, aquatic plants - Transmitted by food or water contaminated with faeces of infected people
35
Clinical symptoms of Enterotoxigenic Escherichia coli (ETEC)
- watery diarrhoea, traveler’s diarrhoea - Serious in infants, traveler’s diarrhoea self-limited 1-3 days
36
Virulence factors of ETEC
- Heat labile LT and heat stable ST enterotoxins - LT is highly similar to cholera toxin (but infection much less serious than cholera)
37
Clostridium perfringens
Gram positive endospore-forming anaerobic bacillus
38
Clinical symptoms of Clostridium perfringens
- Diarrhoea and abdominal cramps - Usually no fever or vomiting
39
Epidemiology of Clostridium perfringens
- Found in soil and GI tract of vertebrates - Infection from germinating spores in cooked meat/poultry/gravy dishes which have been slowly cooled at room temp.
40
Main virulence factor of Clostridium perfringens
- Enterotoxin CPE - forms pores in mammalian cell membranes
41
Different types of protein secretion systems
- Type 2 secretion (T2SS) - Type 3 and 4 secretion (T3SS and T4SS)
42
Type II secretion T2SS
exports proteins into medium (e.g. Cholera toxin)
43
Type 3 and 4 secretion (T3SS, T4SS)
Export proteins (effectors) into host cell
44
Effect of T3SS and T4SS proteins on host cell
- Interact with host cell proteins to change activity of eukaryotic cell - May force host cell to take up bacteria by controlling the host actin cytoskeleton - May result in loss of absorptive capacity of host cell leading to diarrhoea
45
Diseases that arise through injection of effectors
Escherichia coli (EPEC and EHEC pathways)
46
Enteropathogenic E. coli (EPEC)
- Watery diarrhoea following vomiting - Problem in infants of developing countries
47
Enterohaemorrhagic E. coli (EHEC)
- Haemorrhagic colitis (bloody mucoid diarrhoea) - Haemolytic uremic syndrome (HUS)
48
Haemolytic uremic syndrome
Shiga toxin diffuses into blood stream and damages kidney function: stops protein synthesis in kidney cells: may be fatal
49
Common reservoir of EPEC and EHEC
- cattle/cattle products (meat, salami) - Raw alfalfa sprouts and tomatoes also source of infections
50
Treatment of EPEC and EHEC
antibiotics, but increasing multi-drug resistance
51
Diseases arising from invasion
- Salmonellosis - Typhoid - Shigellosis (bacterial dysentery) - Campylobacter jejuni
52
Clinical symptoms of Salmonellosis
gastroenteritis, nausea, diarrhoea, low grade fever
53
Epidemiology of Salmonellosis
- Salmonella enterica (gram negative rod) - Intestinal tracts of birds and animals, water and food become contaminated e.g. eggs, chicken
54
Typhoid clinical symptoms
diarrhoea, high fever 40ºC, severe cases are fatal
55
Virulence of Salmonellosis
- Salmonellae infect cells of the small intestine using a T3SS - Cross the epithelial cell membrane and enter the bloodstream and lymphatic system
56
Epidemiology of Thypoid
- Caused by Salmonella enterica serovar Typhi - Spread by oral-faecal route i.e. ingestion of food or water contaminated by faeces of infected humans, or person-to person contact
57
Shigellosis epidemiology
- S. dysenteriae, Gram negative rod - Transmitted by faecal-oral route - Infectious dose only 10-100 cells
58
Virulence of Typhoid
- S. Typhi multiplies in phagocytic cells, spreads into spleen, liver, bloodstream - 1-3% recovered patients become carriers (harbour bacteria in gallbladder and shed it for months)
59
Shigellosis clinical symptoms
bloody diarrhoea, cramps
60
Shigellosis virulence
- Shigella invades cells of the large intestine using a T3SS - They spread to neighbouring epithelial cells but do not reach deeper tissue (unlike Salmonella) - Some strains produce Shiga toxin (like EHEC)
61
Campylobacter jejuni clinical symptoms
Fever, diarrhoea, blood in stool. Usually self-limiting
62
Epidemiology Campylobacter jejuni
- The most common bacterial cause of human gastroenteritis - Gram negative curved or spiral rod - Intestinal tracts of most animals; disease from undercooked chicken, meats, seafood, eggs, raw milk
63
Virulence Campylobacter jejuni
- Invade cells of the lower intestinal tract/colon - Cytolethal distending toxin is produced

MICR2209 (26 decks)

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