L15 food Flashcards
Hard
Gastroenteritis and diarrhoeal diseases
- Leading cause of death in children
- include bacteria, viruses and protozoa
gastroenteritis
inflammation of stomach and intestinal lining
When many bacteria that contaminate food and water cause acute
When food is the source of the pathogen, the condition is called
food poisoning
Some bacteria colonise the host and are non-invasive or invasive
- N: bacteria remain on epithelial surface
- I: bacteria cross the epithelium
Bacteria that causes food intoxication by
- secreting an enterotoxin that disrupts the intestinal mucosa
- presence of the living bacterium not required for symptoms
Organisation of the Gastrointestinal tract (GIT)
- 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
Whats in the small intestine
- Duodenum
- Jejunum
- Ileum
Whats in the large intestine
Colon
Defences of the GIT
- 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
How do bacterial pathogens cause disease in the GIT?
- Intoxication: preform toxin ingested (doesn’t need to live)
- Adherence and secretion of toxins
- Injection of effectors by type 3 and type 4 secretory systems
- Invasion and destruction of epithelia
C. botulinum, E.coli ETEC, E. coli EHEC, Listeria spp
GIT
Intoxication: Staphylococcal food poisoning
Symp and epidemiology
- 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
̶ S. aureus cells are comparatively hardy (how?)
- heat resistant: survive 60oC for 30 min
- resistant to drying: survive on skin
- resistant to high osmotic pressure: survive in foods
Persistent
Intoxication: Staphylococcal food poisoning
Enterotoxins
– 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
A
Intoxication: Bacillus cereus food poisoning
Symp, epid, virulence factor
- 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
Staphylococcal food poisoning sypm
– pain, cramps, diarrhoea, vomiting, nausea
– intoxication in short period (1 to 8 h); duration <24hrs
Bacillus cereus food poisoning
* Clinical symptoms
- vomiting and diarrhoea
A
Intoxication: Botulism- Clostridium botulinum
Symp, Epid, Virulence
- 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
Botulism: Clostridium botulinum sypm
- 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
B
Adherence and secretion of toxins
Cholera: Vibrio cholerae
Sypm, treatment, virulence
– 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
Cholera: Vibrio cholerae
* Clinical symptoms
– acute diarrhoeal disease
– “rice water stools” contain mucous and epithelial cells
– loss of 12-20 litres fluids/day
– death due to shock, organ failure
B
Adherence and secretion of toxins
(1) Cholera: Vibrio cholerae
Epid, pandemics
- 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
Pathogenic Vibrio O1 :
Gastrointestinal Tract
colonizes GIT, produces Ctx, bacteria shed in diarrhoea, with poor hygiene no. of pathogens in contaminated water grows, cases increase, epidemics etc.
B
Adherence and secretion of toxins: Enterotoxigenic Escherichia coli (ETEC)
Sypm, viru
- 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
The vast majority of ____ strains are nonpathogenic
E. coli
Environmental Vibrio cholerae are mainly non-pathogenic. They ____ aquatic plants and shellfish (bacteria form biofilms)
Aquatic
colonise
Adherence and secretion of toxins: Clostridium perfringens
Sypm, epid, viru
- 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
C
Injection of effectors by Type III and Type IV secretory systems
(T3SS) (T4SS) secretion
- 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)
- Type II secretion (T2SS)
- exports proteins into medium
- e.g. cholera toxin
C
Injection of effectors -Escherichia coli: EPEC
Sypm, reservoir and treatment
- 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
C
Injection of effectors
Escherichia coli: EHEC pathotypes
- 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
D
Invasion- Salmonellosis: Salmonella enterica
Sypm, epid, viru
- 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
Invasion: Typhoid: Salmonella enterica serovar Typhi
Sypm, epid, viru
- 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)
D
Invasion- Shigellosis or bacterial dysentery:
Shigella
Sypm, epid, viru
- 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)
Invasion: Campylobacter jejuni
Sypm, epide, viru
- 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
