L15 food

Question 1

Gastroenteritis and diarrhoeal diseases

Answer 1

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

Question 2

gastroenteritis

Answer 2

inflammation of stomach and intestinal lining

When many bacteria that contaminate food and water cause acute

Question 3

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

Answer 3

food poisoning

Question 4

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

Answer 4

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

Question 5

Bacteria that causes food intoxication by

Answer 5

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

Question 6

Organisation of the Gastrointestinal tract (GIT)

Answer 6

• 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

Question 7

Whats in the small intestine

Answer 7

• Duodenum
• Jejunum
• Ileum

Question 8

Whats in the large intestine

Answer 8

Colon

Question 9

Defences of the GIT

Answer 9

• 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

Question 10

How do bacterial pathogens cause disease in the GIT?

Answer 10

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

Question 11

GIT

Intoxication: Staphylococcal food poisoning

Symp and epidemiology

Answer 11

• 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

Question 12

̶ S. aureus cells are comparatively hardy (how?)

Answer 12

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

Persistent

Question 13

Intoxication: Staphylococcal food poisoning

Enterotoxins

Answer 13

– 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

Question 14

A

Intoxication: Bacillus cereus food poisoning

Symp, epid, virulence factor

Answer 14

• 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

Question 15

Staphylococcal food poisoning sypm

Answer 15

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

Question 16

Bacillus cereus food poisoning
* Clinical symptoms

Answer 16

• vomiting and diarrhoea

Question 17

A

Intoxication: Botulism- Clostridium botulinum

Symp, Epid, Virulence

Answer 17

• 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

Question 18

Botulism: Clostridium botulinum sypm

Answer 18

• 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

Question 19

B

Adherence and secretion of toxins
Cholera: Vibrio cholerae

Sypm, treatment, virulence

Answer 19

– 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

Question 20

Cholera: Vibrio cholerae
* Clinical symptoms

Answer 20

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

Question 21

B

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

Epid, pandemics

Answer 21

• 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

Question 22

Pathogenic Vibrio O1 :

Gastrointestinal Tract

Answer 22

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

Question 23

B

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

Sypm, viru

Answer 23

• 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

Question 24

The vast majority of ____ strains are nonpathogenic

Answer 24

E. coli

Question 25

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

Answer 25

colonise

Question 26

Adherence and secretion of toxins: Clostridium perfringens | Sypm, epid, viru

Answer 26

* 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

Question 27

# C Injection of effectors by Type III and Type IV secretory systems | (T3SS) (T4SS) secretion

Answer 27

* 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)

Question 28

* Type II secretion (T2SS)

Answer 28

* exports proteins into medium * e.g. cholera toxin

Question 29

# C Injection of effectors -Escherichia coli: EPEC | Sypm, reservoir and treatment

Answer 29

* 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

Question 30

# C Injection of effectors Escherichia coli: EHEC pathotypes

Answer 30

* 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

Question 31

# D Invasion- Salmonellosis: Salmonella enterica | Sypm, epid, viru

Answer 31

* 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

Question 32

Invasion: Typhoid: Salmonella enterica serovar Typhi | Sypm, epid, viru

Answer 32

* 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)

Question 33

# D Invasion- Shigellosis or bacterial dysentery: Shigella | Sypm, epid, viru

Answer 33

* 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)

Question 34

Invasion: Campylobacter jejuni | Sypm, epide, viru

Answer 34

* 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