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MICR > L15 food > Flashcards

L15 food Flashcards

Hard

1
Q

Gastroenteritis and diarrhoeal diseases

A
  • Leading cause of death in children
  • include bacteria, viruses and protozoa
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2
Q

gastroenteritis

A

inflammation of stomach and intestinal lining

When many bacteria that contaminate food and water cause acute

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3
Q

When food is the source of the pathogen, the condition is called

A

food poisoning

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4
Q

Some bacteria colonise the host and are non-invasive or invasive

A
  • N: bacteria remain on epithelial surface
  • I: bacteria cross the epithelium
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5
Q

Bacteria that causes food intoxication by

A
  • secreting an enterotoxin that disrupts the intestinal mucosa
  • presence of the living bacterium not required for symptoms
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6
Q

Organisation of the Gastrointestinal tract (GIT)

A
  • Stomach and small intestine: acid pH, low microbial load, few pathogens e.g.
    Helicobacter pylori
  • Large intestine: high load: 10^12 cells/gram of faeces, mainly anaerobes and facultative anaerobes, approx. 500 species isolated, but DNA (metagenomics) shows ~2000 uncultured spp.
  • essential for health and aid in digestion of food
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7
Q

Whats in the small intestine

A
  • Duodenum
  • Jejunum
  • Ileum
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8
Q

Whats in the large intestine

A

Colon

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9
Q

Defences of the GIT

A
  • Physical: tight junction btwn epithelial cells, mucins secreted from goblet cells.
  • Chemical: low pH < 3
  • Immunological: gut associated lymph tissue, paneth cells secrete antimicrobial defensin
  • Mechanical: shedding of epithelial cells and replacement enterocytes

differentiation of stem cells into enterocytes

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10
Q

How do bacterial pathogens cause disease in the GIT?

A
  1. Intoxication: preform toxin ingested (doesn’t need to live)
  2. Adherence and secretion of toxins
  3. Injection of effectors by type 3 and type 4 secretory systems
  4. Invasion and destruction of epithelia

C. botulinum, E.coli ETEC, E. coli EHEC, Listeria spp

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11
Q

GIT

Intoxication: Staphylococcal food poisoning

Symp and epidemiology

A
  • Pain, cramps diarrhoea, nausea
  • Intox period short (1-8hr) DoA < 24hr
  • [E] custards, ham, ice cream, meat
  • S. aureus may be present in nose or skin lesions (from handlers)
  • S. aureus cells are comparatively hardy

S. aureus: heat res, dry res, osmo press res

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12
Q

̶ S. aureus cells are comparatively hardy (how?)

A
  • heat resistant: survive 60oC for 30 min
  • resistant to drying: survive on skin
  • resistant to high osmotic pressure: survive in foods

Persistent

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13
Q

Intoxication: Staphylococcal food poisoning

Enterotoxins

A

– 24 different known enterotoxins -> bacteria may have one or more
– trigger the clinical symptoms
– act on gut receptors to trigger vomiting
– heat stable - survive boiling 30 min
– they are superantigens
* cause non-specific stimulation of T cells resulting in massive release of cytokines and inflammation

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14
Q

A

Intoxication: Bacillus cereus food poisoning

Symp, epid, virulence factor

A
  • Vom and diarrhoea
  • [E] Gram pos endospore forming bacillus
  • Endospore heat res so heating may not kill it
  • Found: soil and vegitation
  • spores germinate as food cools

  • emetic toxin: triggers vomiting: 2 to 5 h incubation period (an intoxication)
  • diarrhoeal toxin: diarrhoea: 8 to 16 h incubation period
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15
Q

Staphylococcal food poisoning sypm

A

– pain, cramps, diarrhoea, vomiting, nausea
– intoxication in short period (1 to 8 h); duration <24hrs

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16
Q

Bacillus cereus food poisoning
* Clinical symptoms

A
  • vomiting and diarrhoea
17
Q

A

Intoxication: Botulism- Clostridium botulinum

Symp, Epid, Virulence

A
  • Start: 12-72hrs ingestion
  • Blurred vision, difficulty swallowing, muscle weakness, flaccid paralysis
  • death if untreated
  • [E] gra pos endospore anaerobic bacillus
  • from home-canned food
  • Virulence is botulinum toxin
  • neurotoxin binds to m-neurons, prevents ACh release, muscles can’t contract, hence paralysis
18
Q

Botulism: Clostridium botulinum sypm

A
  • begin within 12-72 h of toxin ingestion
  • blurred vision, difficulty swallowing, muscle weakness, flaccid paralysis
  • death in 1/3 untreated patients from respiratory or cardiac failure
19
Q

B

Adherence and secretion of toxins
Cholera: Vibrio cholerae

Sypm, treatment, virulence

A

– acute diarrhoeal disease
– “rice water stools” contain mucous and epithelial cells
– loss of 12-20 litres fluids/day
– death due to shock, organ failure
– [T] rehydration (fluids and electrolytes), antibiotics
– [V]* Tcp pilus adhesins* allow colonisation of intestinal epithelium
* encoded by mobile DNA element Vibrio Pathogenicity Island (VPI) in chromosome
– Cholera toxin (Ctx): encoded by bacteriophage (Ctx phage) which infects V. cholerae

20
Q

Cholera: Vibrio cholerae
* Clinical symptoms

A

– acute diarrhoeal disease
– “rice water stools” contain mucous and epithelial cells
– loss of 12-20 litres fluids/day
– death due to shock, organ failure

21
Q

B

Adherence and secretion of toxins
(1) Cholera: Vibrio cholerae

Epid, pandemics

A
  • Found: fresh/salty water
  • Form biofilms on crustaceans, algae, aquatic plants
  • Transmitted by food/water contaminated with infected faeces
  • [P] 7 recorded
  • two toxigenic serogroups but 1 cause pandemics
22
Q

Pathogenic Vibrio O1 :

Gastrointestinal Tract

A

colonizes GIT, produces Ctx, bacteria shed in diarrhoea, with poor hygiene no. of pathogens in contaminated water grows, cases increase, epidemics etc.

23
Q

B

Adherence and secretion of toxins: Enterotoxigenic Escherichia coli (ETEC)

Sypm, viru

A
  • Watery diarrhoea (infant serious)
  • self-limited 1-3 days
  • [V] heat labile (LT) and stable (ST) enterotoxin
  • LT similar to cholera toxin but infection less serious
24
Q

The vast majority of ____ strains are nonpathogenic

A

E. coli

25
Q

Environmental Vibrio cholerae are mainly non-pathogenic. They ____ aquatic plants and shellfish (bacteria form biofilms)

Aquatic

A

colonise

26
Q

Adherence and secretion of toxins: Clostridium perfringens

Sypm, epid, viru

A
  • Diarrhoea and abdominal cramps
  • No fever of nausea
  • [E] gram pos endospore forming anaerobic bacillus
  • Found: soil and GI Tract of vertebrates
  • Infection from germinating spores in cooked and cooled meat and gravy
  • [V] enterotoxin CPE: form pores in mammalian cell membranes
27
Q

C

Injection of effectors by Type III and Type IV secretory systems

(T3SS) (T4SS) secretion

A
  • export proteins called effectors
  • effectors injected into host cell
  • effectors 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 = INVASION (see D slide 17)
  • or may result in loss of absorptive capacity of host cell leading to diarrhoea: bacteria remain outside host cell (see C)
28
Q
  • Type II secretion (T2SS)
A
  • exports proteins into medium
  • e.g. cholera toxin
29
Q

C

Injection of effectors -Escherichia coli: EPEC

Sypm, reservoir and treatment

A
  • vomiting followed by watery diarrhoea
  • problem in infants of developing countries
  • [R] meat - burger/salami
  • Raw alfalfa sprouts and tomatoes
  • [T] antibiotics but there is drug res
30
Q

C

Injection of effectors
Escherichia coli: EHEC pathotypes

A
  • E. coli O157:H7 is a major EHEC
  • haemorrhagic colitis
    – bloody mucoid diarrhoea
  • haemolytic uremic syndrome (HUS)
    – Shiga toxin diffuses into blood stream and damages kidney function: stops protein synthesis in kidney cells: may be fatal

Res and treat same as EPEC

31
Q

D

Invasion- Salmonellosis: Salmonella enterica

Sypm, epid, viru

A
  • gastroenteritis, nausea, diarrhoea, low grade fever
  • [E] S. enterica, Gram negative rod
  • commensal of intestinal tracts of birds and animals: water and food become contaminated - eggs, chicken
  • [V] Salmonellae infect cells of small intestine using a T3SS
  • they cross epithelial cell membrane and enter bloodstream and lymphatic system
32
Q

Invasion: Typhoid: Salmonella enterica serovar Typhi

Sypm, epid, viru

A
  • diarrhoea, high fever 40oC, severe cases are fatal
  • [E] spread by oral-faecal root ingested comtam food water by faeces
  • [V] bacteria invade as for S. enterica
  • 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 (e.g. Typhoid Mary)
33
Q

D

Invasion- Shigellosis or bacterial dysentery:
Shigella

Sypm, epid, viru

A
  • bloody diarrhoea, cramps
  • [E] S. dysenteriae, Gram negative rod
  • transmitted by faecal-oral route
  • infectious dose only 10-100 cells
  • [V] 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)
34
Q

Invasion: Campylobacter jejuni

Sypm, epide, viru

A
  • Fever, diarrhoea, blood in stool. Usually self-limiting.
  • [E] Common gastro
  • commensal in intestinal tracts of most animals;
  • disease from ingesting undercooked meats, seafood, eggs, raw milk
  • [V] Campylobacter invade cells of the lower intestinal tract/colon
    – mechanism not well-understood
    – Cytolethal distending toxin is produced, but role unclear

MICR (18 decks)

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