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MICR2209 > 15 - Food & Water borne bacterial diseases > Flashcards

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
Q

Clinical symptoms of Botulism

A
  • 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
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26
Q

Epidemiology of Botulism

A
  • 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
Q

Main virulence factor of botulism

A
  • Botulinum toxin
  • neurotoxin binds to motor neurons, prevents release of
    neurotransmitter acetylcholine, muscles unable to contract, hence paralysis
28
Q

Diseases that arise through adherence and secretion of toxins

A
  • Cholera (Vibrio cholerae)
  • Enterotoxigenic Escherichia coli
  • Clostridium perfringens
29
Q

Clinical symptoms of Cholera

A
  • 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
Q

Treatment of Cholera

A

Rehydration (fluids and electrolytes), antibiotics

31
Q

Virulence factors of Cholera

A
  • Tcp pilus adhesins allow colonisation of intestinal
    epithelium
  • Cholera toxin (Ctx)
32
Q

What encodes for Tcp pilus adhesions

A

Mobile DNA element Vibrio Pathogenicity Island (VPI) in chromosome

33
Q

What encodes for Cholera toxin (Ctx)

A

Encoded by bacteriophage (Ctx phage) which infects the
V. cholerae cells

34
Q

Epidemiology of Cholera

A
  • 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
Q

Clinical symptoms of Enterotoxigenic Escherichia coli (ETEC)

A
  • watery diarrhoea, traveler’s diarrhoea
  • Serious in infants, traveler’s diarrhoea self-limited 1-3 days
36
Q

Virulence factors of ETEC

A
  • Heat labile LT and heat stable ST enterotoxins
  • LT is highly similar to cholera toxin (but infection much less serious than cholera)
37
Q

Clostridium perfringens

A

Gram positive endospore-forming anaerobic bacillus

38
Q

Clinical symptoms of Clostridium perfringens

A
  • Diarrhoea and abdominal cramps
  • Usually no fever or vomiting
39
Q

Epidemiology of Clostridium perfringens

A
  • 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
Q

Main virulence factor of Clostridium perfringens

A
  • Enterotoxin CPE
  • forms pores in mammalian cell membranes
41
Q

Different types of protein secretion systems

A
  • Type 2 secretion (T2SS)
  • Type 3 and 4 secretion (T3SS and T4SS)
42
Q

Type II secretion T2SS

A

exports proteins into medium (e.g. Cholera toxin)

43
Q

Type 3 and 4 secretion (T3SS, T4SS)

A

Export proteins (effectors) into host cell

44
Q

Effect of T3SS and T4SS proteins on host cell

A
  • 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
Q

Diseases that arise through injection of effectors

A

Escherichia coli (EPEC and EHEC pathways)

46
Q

Enteropathogenic E. coli (EPEC)

A
  • Watery diarrhoea following vomiting
  • Problem in infants of developing countries
47
Q

Enterohaemorrhagic E. coli (EHEC)

A
  • Haemorrhagic colitis (bloody mucoid diarrhoea)
  • Haemolytic uremic syndrome (HUS)
48
Q

Haemolytic uremic syndrome

A

Shiga toxin diffuses into blood stream and damages kidney function: stops protein synthesis in kidney cells: may be fatal

49
Q

Common reservoir of EPEC and EHEC

A
  • cattle/cattle products (meat, salami)
  • Raw alfalfa sprouts and tomatoes also source of infections
50
Q

Treatment of EPEC and EHEC

A

antibiotics, but increasing multi-drug resistance

51
Q

Diseases arising from invasion

A
  • Salmonellosis
  • Typhoid
  • Shigellosis (bacterial dysentery)
  • Campylobacter jejuni
52
Q

Clinical symptoms of Salmonellosis

A

gastroenteritis, nausea, diarrhoea, low grade fever

53
Q

Epidemiology of Salmonellosis

A
  • Salmonella enterica (gram negative rod)
  • Intestinal tracts of birds and animals, water and food become contaminated e.g. eggs, chicken
54
Q

Typhoid clinical symptoms

A

diarrhoea, high fever 40ºC, severe cases are fatal

55
Q

Virulence of Salmonellosis

A
  • Salmonellae infect cells of the small intestine using a
    T3SS
  • Cross the epithelial cell membrane and enter the
    bloodstream and lymphatic system
56
Q

Epidemiology of Thypoid

A
  • 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
Q

Shigellosis epidemiology

A
  • S. dysenteriae, Gram negative rod
  • Transmitted by faecal-oral route
  • Infectious dose only 10-100 cells
58
Q

Virulence of Typhoid

A
  • 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
Q

Shigellosis clinical symptoms

A

bloody diarrhoea, cramps

60
Q

Shigellosis virulence

A
  • 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
Q

Campylobacter jejuni clinical symptoms

A

Fever, diarrhoea, blood in stool. Usually self-limiting

62
Q

Epidemiology Campylobacter jejuni

A
  • 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
Q

Virulence Campylobacter jejuni

A
  • Invade cells of the lower intestinal tract/colon
  • Cytolethal distending toxin is produced

MICR2209 (26 decks)

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