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Gastro-intestinal system (Den 303) > Pathogens of the GI tract > Flashcards

Pathogens of the GI tract Flashcards

1
Q

The GI tract contains

A 
Ingestion
Mouth
Oesophagus
Stomach
Small intestine
Large intestine
Egestion
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2
Q

Gastroenteritis

A

Sydrome characterised by GI symptoms including

  • nausea
  • vomiting
  • diarrhoea
  • abdominal pain
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3
Q

Diarrhoea

A

Abnormal faecal discharge characterised by frequent and/ or fluid stool

  • associated with > fluid and electrolyte loss
  • often disease of small intestine
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4
Q

Dysentery

A

Abnormal inflammation of GI tract

  • often blood and pus in faeces and pain, fever and abdominal cramps
  • often disease of large intestine
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5
Q

Enterocolitis

A

Inflammation of mucosa of small and large intestine

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6
Q

Defences of mouth

A

Flow of liquids
Saliva
Lysozyme
Normal bacterial flora

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7
Q

Defences of oesophagus

A

Flow of liquids

Peristalsis

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8
Q

Defences of stomach

A

Gastric acid pH 1-2 provides effective barrier to most infections
Many bacteria transiently pass through stomach before infecting lower GI tract
-these must be able to resist the low pH during passage through OR take up residence if they can infect

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9
Q

Defences of small intestine

A 
Flow of gut contents
Peristalsis
Mucus; bile
Secretory IgA
Lymphoid tissue (Peyer's patches)
Shedding and replacement of epithelium
Normal flora
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10
Q

Defences of large intestine

A

Normal flora
Peristalsis
Shedding and replication of epithelium
Mucus

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11
Q

‘Food poisoning’

A

This strictly refers to ingestion of toxins or poisons in food
-e.g. bacterial toxins or heavy metals
Bacteria grow and multiply in food
Cooking kills bacteria but toxin still active - intoxication
Staphylococcus aureus
Botulism: Clostridium botulinum

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12
Q

Staphylococcus aureus ‘food poisoning’

A

Growth in food after human contamination
-mainly dairy products, cooked meats, pre-packed sandwiches
50% of strains produce heat-stable enterotoxins
-also resistant to stomach acid and digestive enzymes (main route of infection from food prep, naso-pharyngeal carriage)
3-6h severe vomiting - complete recovery

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13
Q

Botulism: clostridium botulinum ‘food poisoning’

A

Heat stable toxin ingested in food, leads to flaccid paralysis and death
(covered in anaerobe lecture)
Infant botulism most common

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14
Q

Bacillus cereus

A

‘Fried Rice syndrome’
Self-limiting but unpleasant
Gram +ve, spore former
Some strains are harmful to humans and cause foodborne illness, while other strains can be beneficial as probiotics for animals
-spores can survive the rice cooking process, germinate and release toxins at room temp
-re-frying rice it can remain

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15
Q

Gastric ulcers: helicobacter pylori

A

Previously thought to be solely ‘hurry, curry and worry’ but found to be bacterium 1983
Resistance to physical barriers - stomach acid
Produces urease
-protective cloud during transit to gastric mucin layer
-ammonia basis of breath test
Urea –urease–> ammonia + CO2
Confirmed link to gastric cancers cagA positive strain

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16
Q

Infective cycle of Helicobacter pylori

A

Infects lower part of the stomach (antrum)
Causes inflammation of gastric mucosa (gastritis)
-often asymptomatic
Inflammation may lead to duodenal or gastric ulcer
-severe complications include bleeding ulcer and perforated ulcer
Duodenal ulcer and gastric ulcer –> bleeding ulcer

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17
Q

Treatment for gastric ulcers

A

Now with proton-pump inhibitor PLUS metronidazole/ amoxicillin and clarithromycin

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18
Q

Food-associated infections

A

Ingestion of contaminated food that contains an infectious of bacteria (>ID50)
Faecal-oral spread - wash your hands!

19
Q

Diarrhoeal treatment

A

Fluid and electrolyte replacement is essential
Antibiotic treatment often not successful and may worsen problem
-wipes out competing organisms or stimulates toxin production (C.diff)

20
Q

Diarrhoeal disease: E.coli

A

Gram -ve motile rod
Major cause of diarrhoeal disease and gastroenteritis worldwide
Complications include hemolytic-uremic syndrome (HUS)
Many genetically distinct disease causing strains
Some strains reside in normal commensal flora
Others infect urinary tract and cause meningitis
Diarrhoea: ingested in food or via faecal-oral transmission route
Genetic diversity dependent on plasmid, lysogenic phage and transposon encoded ‘pathogenicity islands’

21
Q

Lab detection of E;coli

A

Lactose fermentation: MacConkey agar
Lactose fermented on Hektoen enteric agar
PCR/ antigen tests for stereotypes

22
Q

E.coli pathogenic strains

A 
EPEC
ETEC - toxin producing
EHEC - verotoxin producing
EIEC
EAEC
UPEC - causes of GU infections
23
Q

EPEC

A

Bundle-forming pili important in attachment
Type III secretion system injects proteins into host to manipulate cytoskeleton
-translocated intimin receptor (Tir)
-intimin mediates imtimate attachment to epithelial cells
Attaching and effacing lesion
Leads to watery diarrhoea

24
Q

ETEC

A

Attach via adhesive pili
Produce Heat Stable (ST) and Labile (LT) enterotoxins (cholera like) that cause diarrhoea
Common cause of travellers diarrhoea OR Delhi Belly
-no blood
-cholera like in some cases

25
Q

EIEC

A

Invade and destroy epithelial cells

Bloody diarrhoea

26
Q

EHEC (sometimes called STEC)

-look at diagram

A

Attachment similar to EPEC - pedestals
Produce vero-toxin (also called Shigella-like toxin) - STx
STx (verotoxin) is a potent diarrhoeal toxin (and has receptor on kidney cells) acts via damaging cells directly
EHEC infections also cause haemorrhagic colitis –> bleeding –> spread to kidneys
Can lead to HUS??

27
Q

HUS

A

This may lead to kidney failure (15% cases)

O157:H7 strain most well known

28
Q

Shigella (should really be classified as an E.coli)

A

Shiga toxin producing (similar to EHEC)
Shigella dysenteriae
-bacillary dysentry, bloody stools
Shigella sonnei and flexneri
-milder forms
-low infectious dose 10-100 cells - sometimes ID50
Non-lactose fermenters (Maconkey agar, Hektoen enteric - green no H2S)
Common in poorer countries
Spread faecal-orally, often via water contamination

29
Q

Salmonella

A

Historically most common food-associated pathogen in UK
Spread from food - mainly chicken and dairy products, but also person to person
Invade M-cells then spread to surrounding epithelium
Usually a severe but self-limiting diarrhoea and enterocolitis

30
Q

Salmonella enterica subspecies cause uncomplicated diarrhoea

A

typhimurium

enteritidis

31
Q

Lab detection of salmonella

A

MacConkey agar
-non-lactose fermenter (yellow)
H2S deposits on Hektoen enteric agar

32
Q

S. typhi

A

Cause of typhoid fever
Infection initiates in the intestine
Spreads systemically- transported in macrophages around body
Seed many organs before further spread
Causes increasing fever over 14 days&raquo_space; GI symptoms
Pre-antibiotics 12-16% died
Complications:
GI lesions and haemorrhage
Toxaemia- endocarditis
Meningitis
Vi antigen vaccine recommended for travel
1 – 3 % become carriers &raquo_space; gall-bladder

33
Q

Number one cause of food poisoning in UK

A

Campylobacter spp.

34
Q

Campylobacter spp.

A

Gram-negative micro-aerophiles
Campylobacter jejuni most common
Acquired by ingestion of contaminated food
Major reservoir in Chickens> 75% of all we buy have colonisation
Symptoms like Shigellosis and Salmonellosis:
-ulceration (jejunum), diarrhoea
-up to 10 movements per day…
- longer lasting illness- up to 3 weeks!
-complications: Guillame Barre and reactive arthiritis

35
Q

Cholera (biggest historical GI bug)

A

Caused by motile gram -ve comma-shaped bacterium
Cause of 8 recorded worldwide pandemics since 1817
O1 serotype most important historically: classical and El Tor (modern)
~1.3-4 million cholera cases and 21000–140,000 deaths due to cholera every year- mainly developing countries

36
Q

Cholera mechanism of infection

A

Vibrio ingested in large numbers
-can survive in fresh and sea-water
-possible marine invertebrate reservoir
-infectious dose >10^8
Sensitive to stomach acid
-large dose needed to cause disease unless pt achlorhydric or taking antacids
-in these cases infectious dose drops >10^5
Colonization of small intestine depends on motility (polar flagella) production of mucinase attachment to specific receptors –> toxin production
Massive loss of fluid and electrolytes
-no damage to enterocytes; no blood or WBC in stool

37
Q

Normal water flow in gut vs cholera toxin

A

Normal: net-flow of water is from lumen into tissue
+ cholera toxin
-ADP-ribosylation of G-protein signalling pathways causes increased secretion of Chloride ions
-this prevents influx of Sodium ions into cells
-results in rapid loss of water from tissue- massive diarrhoea

This rapid fluid loss results in loss of 1-2 litres of fluid per hour in full-blown cases
Rapid fluid and electolyte replacement required or dehydration and death result
Characteristic rice-water stool
No tissue damage, all symptoms due to
massive fluid loss

38
Q

Symptoms of cholera: no dehydration

A 
Well, alert
Normal eyes
Tears present
Moist mouth and tongue
Drinks normally, not thirsty
Skin pinch goes back quickly
39
Q

Symptoms of cholera: severe dehydration

A 
Lethargic or unconscious; floppy
Very sunken and dry eyes
Absent tears
Very dry mouth and tongue
Drinks poorly or not able to drink
Skin pinch goes back very slowly
40
Q

Prevention of cholera

A

Vaccines have been unsuccessful but several available with only temporary immunity gained
-WHO trialling 2 vaccines currently with protection 6m-2y
Best prevention method is improvement of water system and sanitation
-hard to get aid for that, especially in war-torn/ lawless regions

41
Q

Viral causes of GI infections

A

Of the 3 million infants that die from gastroenteritis 20% are viral sources
Major problem in developing countries
Children may have 60 days of diarrhoea per year – major effect on growth and nutrition
Mainly oral-fecal
Very hard to identify non-bacterial cases
Not until 1972 were viruses isolated from faeces

42
Q

Rotaviruses

A 
Wheel-like viral particle
Diarrhoea caused by tissue damage in small intestine
Dehydration main risk
Very low-infectious dose
Very contagious
V resistant to celaining products
43
Q

Winter vomiting virus

A

Norovirus (Norwalk viruses) - not cultivated
Chills, headache, fever, nausea, vomiting, v-low infectious doses (10)
Recovery in 24 – 48 hours
Common in hospital settings, Hard to clean away

Gastro-intestinal system (Den 303) (3 decks)

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