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MD3002 > Bacterial and Viral Infections of the Gastrointestinal Tract > Flashcards

Bacterial and Viral Infections of the Gastrointestinal Tract Flashcards

1
Q

Identify the main ways in which GI pathogens can damage the GI.

A
  • Local inflammation
  • Ulceration / perforation of mucosal epithelium
  • Disruption of normal microbiota
  • Pharmacological action of bacterial toxins
  • Invasion to blood or lymphatics
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2
Q

Identify different ways in which pathogens can cause local inflammation.

A

1) Bacillus bacillus interferes with the tight
junctions through E cadherin cleavage (so bugs can get through).

2) E coli damages top of epithelium by causing attaching and effacing lesion.
3) Salmonella invade M (microfold) cells, specific to gut. M cells grab salmonella and drives it through into body tissues, so it can recruit other immune cells (e.g. secretory IgA) so it can get rid of salmonella.

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3
Q

What diagnostic test would be necessary to detect ulceration ?

A

Endoscopy

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4
Q

Describe how epithelial perforation occurs. How is this treated ?

A
  • Lining of the mucosa wall is perforated due to untreated ulcers (ruptured ulcer)
  • May result in leaking of food and gastric juices (and potentially bacteria) to the peritoneal or abdominal cavities.

Treatment requires surgery

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5
Q

What is a potential consequence of bacterial growth ?

A

Villous atrophy

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6
Q

Identify the main bacterial diarrhoeal pathogens.

A 
Gram negative: 
• Vibrio cholerae
• Escherichia coli
• Campylobacter jejuni 
• Salmonella spp.
• Shigella spp.

Gram positive:
• Listeria monocytogenes

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7
Q

Are all diarrheas infectious ?

A

No, e.g. due to IBD

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8
Q

Distinguish between the incubation period, duration, and symptoms of diarrhea caused by campylobacter, and shigella respectively. Also identify the symptoms of E. Coli and Cholera diarrhea.

A

1) Campylobacter
Longer incubation period (up to 11 days), longer duration (up to three weeks), bloody stools

2) Shigella
Shorter incubation (up to 4 days), shorter duration (2-3 days), bloody stools

3) E. Coli and diarrhea
Watery stools

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9
Q

V. CHOLERAE

  • Classification of bacteria, including shape and other structural specificities
  • Animal-only ? Human-only ? etc.
  • Vaccines
  • Serotypes
  • Epidemiology
  • Other
A

V. CHOLERAE

  • Gram negative, comma shaped rod, flagellated.
  • Human-only pathogen
  • Vaccines: parenteral vaccine (low protective efficiency) and oral vaccine (effective and suitable for travellers)
  • Serotypes: Based on O antigens (O1 associated with early pandemics, non-O1 e.g. O139 associated with recent outbreaks)
  • Epidemiology: Flourishes in communities with no clean drinking water/sewage disposal (associated with poor hygiene)
  • Other: characterised by epidemics and pandemics.
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10
Q

Describe the pathogenesis of V. cholerae.

A
  • Only infective in large doses
  • Many organisms kille in stomach
  • Colonisation of small intestine, involving flagellar motion, mucinase (breaks down mucus, to help weaken immune system, but doesn’t damage the cell, so it has somehwere to live), attachment to specific receptors
  • Production of multicomponent toxin
  • Loss of fluid and electrolytes without damage to enterocytes
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11
Q

Describe the structure of the Cholera Toxin and actions. Which symptom is this toxin responsible for ?

A

Cholera Toxin (CTx)

Oligomeric complex of six protein subunits:

  • 1 copy of A subunit (enzymatic)
  • 5 copies of B subunit (responsible for receptor binding)

GM1 receptor, which sits on cell surface, internalises toxin through retrograde endocytosis, leading to increase in cAMP, so CFTR (Cystic fibrosis transmembrane receptor, chloride channel) stimulates Cl leaving body so water and electrolytes come out of body, hence diarrhea

Responsible for the characteristic, watery cholera diarrhea.

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12
Q

Identify the main consequences of Cholera infection.

A
  • Fluid loss of up to one liter per hour (white, rice water stool)
  • Electrolyte imbalance leading to dehydration, metabolic acidosis, and hypokalemia
  • HypoV shock
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13
Q

What is the mortality rate of Cholera infection ?

A

40-60% mortality, but <1% mortality if given fluid/electrolytes (ORT)

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14
Q

E. COLI

  • Type of bacteria, including structure
  • Other
A

E. COLI

  • Type: Gram negative bacillus, member of normal GI microbiota
  • Other: some strains possess virulence factors enabling them to cause disease (e.g. acid resistant, produces toxins, produces A and E lesions, has flagella, fimbriae, intimin which helps is attach)
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15
Q

Identify the main types of E. Coli causing GI infections, as well as the type of infection each one causes

A

EPEC (Enteropathogenic): Sporadic cases and outbreaks of infection in under 5s

ETEC (Enterotoxigenic): Travellers’ diarrhea (occurs in 20-5°% of travellers)

VTEC/STEC (Verocyototoxin-producing): Sporadic cases and outbreaks of gastroenteritis

EHEC (Enterohaemorrhagic): Sporadic cases and outbreaks of gastroenteritis

EIEC (Eneteroinvasive): food-borne infection in areas of poor hygiene (often persistent diarrhoea)

EAEC (Enteroaggregative): resource-poor countries

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16
Q

Identify some of the factors which helps E. Coli adhere.

A
  • Intimin
  • Pili/fimbriae
  • Pedestal formation (“raised actin at the site of their attachment to host cell providing an intimate host-pathogen interaction”)
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17
Q

Describe the modes of action of E. Coli enterotoxins.

A
  • LT = heat-labile toxin, increases cAMP in the enterocyte which increases secretions
  • STa = heat-stable toxin, increases cGMP in the enterocyte which increases secretions
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18
Q

C JEJUNI

  • Classification
  • Human-only ? Animal-only ?
  • Transmission
  • Mode of action
A

C JEJUNI

  • Gram negative, helical bacillus
  • Human, with large animal reservoir
  • Transmission: through consumption of raw/undercooked meat, contaminated milk (causes food associated diarrhea)
  • Mode of action: mucosal inflammation and fluid secretion
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19
Q

What pathogen is the comment cause of diarrhea in the developed world ?

A

C Jejuni

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20
Q

Describe the histological appearance of C. Jejuni infection.

A
  • Inflammation involves entire mucosa
  • Villous atrophy
  • Necrotic debris in crypts
  • Thickening of basement membrane
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21
Q

SALMONELLA SPP

  • Classification
  • Transmission
A

SALMONELLA SPP

  • Classification: Gram negative bacili
  • Transmission: Transmission through consumption of raw / undercooked meat, contaminated eggs and milk (food associated diarrhea). BUT secondary spread can be human-human
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22
Q

How many serotypes of Salmonella Spp are there ?

A

Over 2000 serotypes

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23
Q

Identify the main species of Salmonella Spp.

A

1) S. typhi
2) S. Parathypi
3) S. enteritidis

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24
Q

Describe the pathogenesis of Salmonella.

A

• Ingestion of large numbers of bacteria
• Absorption to epithelial cells in terminal section of small intestine
• Penetration of cells and migration to lamina propria
• Multiplication in lymphoid follicles
• Inflammatory response mediates release of
prostaglandins
• Stimulation of cyclic AMP
• Release of fluid and electrolytes causing diarrhoea

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25
Q

S. TYPHI and S. PARATYPHI

  • Symptoms caused
  • Human only ? Animal reservoir ?
A

S. TYPHI and S. PARATYPHI

  • Cause enteric fevers (typhoid and paratyphoid). Systemic infections are initiated in GI tract.
  • Species restricted to humans. They multiply within, and are transported around body in macrophages.
26
Q

What proportion of patients affected with typhoid fever become chronic carriers ? Where is this carried ? Are any populations especially affected ?

A

1-3% (usually carried in gall bladder)

Most common in women and the elderly

27
Q

What remnant of the disease can be seen in patients following their recovery from Typhoid fever ?

A

Patients can excrete S. typhi in faeces for several weeks after recovery

28
Q

Explain what is meant when we say that typhoid fever is a notifiable disease.

A

We must notify public health about it.

29
Q

Identify a characteristic sign of typhoid fever.

A

Blanching rash (disappears when you press it)

30
Q

Describe any vaccines for the typhoid fever. Who should take this vaccine ? How effective is it ?

A

Typhoid fever:

1) Oral (live attenuated)
- booster

2) Parenteral (capsular polysaccharide)
- booster

Recommended for travellers to endemic areaas

50-80% effective

31
Q

SHIGELLA SPP

  • Classification
  • Disease caused
  • Animal reservoir ? Human-only ?
A

SHIGELLA SPP

  • Bacillus
  • Causes shigellosis (bacillary dysentry)
  • Human-only pathogen
32
Q

Identify the main types of shigella spp, classifying them by seriousness of infection caused.

A

– S. dysenteriae: most serious
– S. flexneri: severe disease
– S. boydii: severe disease
– S. sonnei: mild infections

33
Q

Describe the pathogenesis of Shigella Infection.

A
  • Attaches to mucosal epithelium of distal ileum and colon
  • Causes inflammation and ulceration
  • Rarely invasive
  • Produces Shiga toxin (STx)
  • Diarrhoea watery initially, later can contain blood and mucus
  • Disease usually self-limiting
34
Q

L. MONOCYTOGENES

  • Classification
  • Disease caused
  • Transmission
  • Populations at risk
  • Presentation
A

L. MONOCYTOGENES

  • Coccobaccillus
  • Disease caused: Listeriosis
  • Transmission: food-borne pathogen associated with paté, soft cheese, unpasteurised milk
  • Populations at risk: pregnant women (with possibility of infection of the baby in utero or at birth), immunosuppressed individuals (e.g. AIDS or immunosuppressive drugs), the elderly
  • Presentation: presents as meningitis
35
Q

What bacterial load is necessary for L. Monocytogenes to cause disease ?

A

<1000 organisms may cause disease

36
Q

Identify the main viral diarrheal pathogens.

A
  • Rotavirus
  • Norovirus
  • Enteric Adenovirus

Also:
• Calicivirus
• Coronavirus
• Astrovirus

37
Q

ROTAVIRUS

  • Structure
  • Epidemiology
  • Bacterial load
  • Transmission
  • Human only ? Animal reservoir ?
A

ROTAVIRUS

  • Genome consists of 11 separate segments of double-stranded RNA
  • Infection most common in children under 2
  • As few as 10 ingested particles can cause disease
  • Transmission: faeco-oral, but may also be faeco-respiratory. Transmission has seasonal occurrence (commoner in cooler months)
  • Infects many animals
38
Q

Describe the pathogenesis of Rotavirus Infection.

A
  • Incubation period of 1-2 days
  • Replication of virus in small intestinal epithelial cells at tips of villi
  • Results in villous atrophy
  • Damage caused to infected cells leaving immature cells with reduced absorptive capacity for sugar, water and electrolytes
  • Onset of vomiting, diarrhoea lasting 4 –7 days
  • Up to 10^10 – 10^11 virus particles/gram faeces released (very good at replicating)
39
Q

Describe any vaccines available for Rotavirus. How effective is it ?

A

• RotaRix; RotaTeq

  • Oral administration (2-3 doses)
  • First dose at 6-10 weeks of age
  • Live, attenuated virus

Very effective (large decrease in hospital admissions in US since introduction)

40
Q

NOROVIRUS

  • Human only ? Animal reservoir ?
  • Transmission
  • Bacterial load
A

NOROVIRUS
• Human only pathogen
• Transmission is faeco-oral, contaminated water / shellfish, fomites. Transmission has seasonal occurrence (commoner in cooler months)
• <100 virions can establish infection

41
Q

What virus account for the most non-bacterial outbreaks in the world ?

A

Norovirus

42
Q

What is another name for Norovirus ?

A

Winter vomiting disease

43
Q

Norovirus has a past infection of what proportion of adults ?

A

Past infection in 60% of adults

44
Q

Describe any vaccines available for Norovirus. What measure can be taken instead to reduce incidence of Norovirus infections ?

A

No vaccine for Norovirus yet (still approximately 4-5 years away).

Handwashing

45
Q

What proportion of all community acquired diarrheas in young children does enteric adenovirus account for ?

A

10%

46
Q

ENTERIC ADENOVIRUS

  • Clinical features
  • Transmission
A

ENTERIC ADENOVIRUS

  • Asymptomatic infections common. Mild, but prolonged diarrhea also possible.
  • Transmission: no seasonal incidence
47
Q

Describe the pathogenesis of antibiotic-associated diarrhea. Give specific examples of antibiotics and the pathogens they allow the multiplication of.

A
  • Does NOT involve ingestion of pathogen or toxin
  • Can arise from disruption of gut microbiota following antibiotic therapy

EXAMPLES:
• Tetracycline- allows colonisation by Staphylococcus aureus and Candida sp.
• Clindamycin suppresses gut microbiota and allows Clostridium difficile to multiply (infection by latter now associated with resistance to vancomycin)

48
Q

Identify the main features of C. difficile infection.

A
  • Produces spores for survival
  • Produces an enterotoxin (toxin A) and cytotoxin (toxin B). More severe disease associated strain 027 produces more enterotoxin (toxin A) than cytotoxin (toxin B).
  • Causes gas gangrene
  • Clinical symptoms include diarrhea
49
Q

Are all instances of C. difficile diarrhea associated with antibiotic use ?

A

No, C. difficile diarrhea not only associated with antibiotic use.

50
Q

What is the main cause of the increase of cases of C. difficile diarrhea ?

A

Nosocomial infections largely responsible for increase in cases

51
Q

Identify pathogens associated with diarrhea resulting from overgrowth of bacterial microbiota.

A

Staph aureus and Candida sp (due to tetracycline)

C. difficile (due to clindamycin)

52
Q

Identify pathogens associated with diarrhea resulting from bacterial GI ulcers.

A

H pylori

53
Q

H Pylori

-Classification

A

H Pylori
-Gram negative, spiral, microareophillic (requires environments containing lower levels of oxygen than are present in the atmosphere) flagellated bacteria

54
Q

What is the percentage of patients with H. pylori infections who are asymptomatic ?

A

> 80% infected individuals are asymptomatic

55
Q

Identify diseases associated with H. pylori.

A
  • Duodenal ulcers
  • Gastric ulcers
  • Gastro-oesophageal reflux disease
  • Non-ulcer dyspepsia
56
Q

Identify the main virulence factors of H Pylori.

A

• Acid-inhibiting protein – survival in
stomach
• Urease – neutralisation of acid pH
• Adhesins – binding to gastric epithelium
• Cytotoxin – damage to gastric epithelium
• Flagellum – movement through gastric mucus layer

57
Q

Identify pathogens associated with diarrhea resulting from food poisoning.

A
  • Bacillus cereus (emetic toxins)
  • Staph aureus (enterotoxin)
  • Clostridium botulinum (neurotoxin)
  • Clostridium perfringens
58
Q

Define food poisoning.

A

Diseases caused by toxins elaborated by contaminating bacteria in food before it is consumed

59
Q

CLOSTRIDIUM PERFRINGENS

  • Transmission
  • Mechanism of action
  • Symptoms
  • Virulence factors
A

CLOSTRIDIUM PERFRINGENS

  • Transmission: Usually caused by type A strains from animal guts and soil. Contamination of raw meat products
  • Mechanism of action: Spores survives cooking and germination takes
    place. Multiplication in large intestine, production of spores and enterotoxin. Damage to intestinal epithelium
  • Symptoms: Diarrhea
  • Virulence factors: spores (make it very resistant)
60
Q

What is the main treatment for diarrhea ?

A

Oral Rehydration Therapy/Solutions (ORT/ORS)

  • Involves the replacement of fluids and electrolytes lost during diarrheal illness
  • ORS increases the resorption of fluids and salts into the intestinal wall
61
Q

What proportion of acute, watery diarrhea can be successfully treated with ORS ?

A

90-95% of cases of acute, watery diarrhoea can be successfully treated with an oral rehydration solution (ORS)

62
Q

Describe the composition of ORS.

A
  • Glucose (anhydrous): 13.6 g/L
  • Sodium chloride: 2.6 g/L
  • Potassium chloride: 1.5 g/L
  • Trisodium citrate dihydrate: 2.9 g/L

• In addition, fruit juices, coconut water, and other indigenous solutions can adequately approximate ORS

MD3002 (95 decks)

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