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Medical Microbiology and Virology > 23 Gastrointestinal tract infections > Flashcards

23 Gastrointestinal tract infections Flashcards

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1
Q

What is meaning of these terms -

Gastroenteritis

Dysentery

Enterocolitis

A

Gastroenteritis - nasuea/ vomiting/ diarrhoea usually due to enterotoxin in small bowel. Causes increased fluid/ electrolyte loss

Dysentery - inflammation of GI tract causing blood in stool - indicating invasive infection causing mucosal destruction. Causes pain, fever, abdominal pain

Enterocolitis - inflammation of both small and large intestine

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2
Q

Why is food poisoning a bad term?

A

Food poisioning correct if describing disease due to heavy metal, or toxin e.g botulism

Food-associated infection is better as organisms may be transported in via food (campylobacter), or can provide vessel to multiply within (salmonella)

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3
Q

What are host defenses against GI pathogens?

A

Saliva - lysosyme
Normal bacterial flora

Stomach acid
bile
Shedding epithelium

secretory IgA
Lymphoid tissue - Peyer’s patches

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4
Q

What are physiological outcomes from initial GI infection?

A

Local disease - e.g shigella/ amoebiasis causing diarrhoea

Systemic disease e.g fever, myalgia, jaundice

  • spread - hepatitis A/ enteric fever
  • toxin - cholera/ staph
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5
Q

E. Coli species can be grouped into six pathogtypes, based on mechanisms of pathogenicity.

What are their names?

Most E. coli species are part of normal GI flora

A

EPEC

ETEC

VTEC - sometimes termed STEC/ EHEC

EIEC

EAEC

DAEC

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6
Q

How does EPEC E. Coli cause disease?

A

Does not produce toxin

Has pili to bind to epithelial cells, leading to disruption of microvillus

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7
Q

How does ETEC E. coli cause disease?

A

Common cause Traveller’s diarrhoea

Bind to villi of small intestine - disrupting barrier

Produce enterotoxin - either heat labile HT or heat stabile ST

Heat-labile enterotoxin LT1 is similar to cholera toxin

Heat-stabile entertoxin activate guanylate cyclase activity causing increase cyclic guanosine monophosphate which results in increased fluid secretion

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8
Q

How does VTEC E. coli cause disease?

Notifiable disease

A

Binds to villi of small intestine - disrupting barrier

Produce a verotoxin which is similar to shiga-toxin, and causes direct damage to intestinal epithelium.

Also damages renal epithelium, as veroreceptors seen there

Toxin causes destruction of mucosa and haemorrhagic colitis. Can lead to haemolytic-uraemic syndrome

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9
Q

What is most common VTEC E.coli species?

A

O157:H7

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10
Q

How to identify case of HUS?

A

Usually children aged 0-5

Fever/ abdo pain/ vomiting diarrhoea which becomes bloody

Contact with farm animals

Microangiopathic haemolytic anaemia (Coombs’ test negative).

Thrombocytopenia.

Acute kidney injury - most common cause of childhood renal failure

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11
Q

How does VTEC toxin cause HUS?

A

Verotoxin 1 + 2

circulating toxin which binds to endothelial receptors, particularly in the renal, gastrointestinal and central nervous systems.

Thrombin and fibrin are deposited in the microvasculature. This occurs early in the disease, prior even to the development of HUS and may be why antibiotics confer no benefit.

Erythrocytes are damaged as they pass through partially occluded small vessels and subsequent haemolysis occurs.

Platelets are sequestered but without the cascade of clotting factors as in disseminated intravascular coagulation

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12
Q

What are investigations for HUS?

A

FBC and film: evidence of haemolysis, anaemia and thrombocytopenia. Raised white cell count and low platelet count are early indicators of development of HUS.

LDH raised

CRP raised

Clotting screen (reduced values may be seen during active HUS).

Stool culture: stool sample should be sent for culture and phage typing of the E. coli. Genes for virulence factors may be confirmed by polymerase chain reaction (PCR).

Urinalysis - haematuria

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13
Q

How to manage HUS?

A

Report to public health

Supportive management - may include dialysis

No evidence of antibitotics/ FFP helping

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14
Q

How does EIEC cause disease?

A

Attach to mucosa of large intestine

Invade cells by endocytosis

Lyse endocytic vacuole, multiply, spread to adjacent cells causing destruction.

Results in blood and mucus in stools

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15
Q

How does EAEC cause disease?

A

Attach to small intestine mucosa

Produces heat labile toxins

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16
Q

Which species of E.coli are more common in resource rich/ poor countries?

A

Poor/ traveller diarrhoea - EPEC/ ETEC

Rich - EHEC

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17
Q

What is treatment of E.coli diarrhoea? excluding HUS

A

Supportive

No role for antibiotics - antibiotics actually increase risk of HUS

E. coli bacteraemia will require treatment

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18
Q

Acute onset diarrhoeal illness within 1 day.

What are possible pathogens?

A

Bacillus cereus

Clostridium perfringens

S aureus enterotoxin - 30mins - 8hours

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19
Q

What are causes of bloody diarrhoea?

A

Amoebiasis

Campylobacter

Shigella

Yersinia entercolitica

EHEC/ EIEC

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20
Q

Which species of salmonella cause enteric fever?

After infection, people can carry typhoid providing ongoing source of infection e.g Typhoid Mary

A

Typhoidal Salmonella -

  • Typhi
  • Paratyphi A/B/C

Rest of species are known as non-typhoidal salmonella

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21
Q

How are salmonella species differentiated?

A

O antigen - cell wall

H antigen - flagella

Over 2000 serotypes classified as typhoidal/ non-typhoidal

O/H antigens also used to classify E. coli

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22
Q

What are sources of salmonella/ how is it spread?

A

Large animal reservoir in poultry/ dairy/ reptiles

Initial infection usually via contaminated food - faecal-oral spread

Then human-human spread occurs

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23
Q

What is path of salmonella through the body?

A

Ingestion

Absorbed by epithelial cells small itnestine

Penetrate to lamina propria in ileocaecal region

Macrophages confine infection to GI tract

Inflammatory response causes release of prostaglandins, which stimulate cAMP

This stimulates fluid secretion and diarrhoea

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24
Q

Salmonella usually causes mild self-limiting diarrhoea

Salmonella can become invasive and spread beyond small intestine

Who is at risk?

A

Immunocompromised

Elderly

Children

Sickle cell

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25
Q

What conditions are caused by invasive salmonella?

Fever is sign of systemic illness, and may require admission

A

Bowel perforation

Osteomyelitis

Pneumonia

Meningitis

Endocarditis

Cholecystitis - can form reservoir here

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26
Q

How to test for invasive salmonella?

A

Blood culture

Widal test - agglutination assay detecting antibodies ahainst O/ H antigens

Stool culture to confirm that salmonella has caused enteric infection

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27
Q

What is treatment for salmonella?

A

Usually self-limiting

Fluid replacement

No antibiotics, unless signs of invasion.
Azithromycin + ceftriaxone
Ciprofloxacin - resistance emerging
Ceftriaxone

Surgical intervention may be required if complications occur

If food handler, cannot work until three specimens of faeces have failed to grow salmonella

Vaccination live attenuated available for travellers - up to 80% protection

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28
Q

What is source/ transmission of campylobacter?

A

Large animal reservoir

Consumption of contaminated food - faecal-oral

Person-person spread is less common

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29
Q

Campylobacter has similar life cycle to salmonella.

Except it can cause bleeding of mucosal surface, and production of cytotoxins by C. jejuni

What clinical manifestations can occur?

A

Meningitis

Guillain-Barre

Endocarditis

IBD/ IBS?

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30
Q

What is treatment of campylobacter infection?

A

Usually self-limiting

If unwell/ fever -
Azithromycin
Ciprofloxacin - resistance emerging

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31
Q

V cholerae can live in free water. It has flagella so is motile

Common cause of infection in Asia/ Africa/ SA

How is it spread/source?

A

Contaminated water

Contaminated food

Shellfish grown in polluted estuaries

Person-person transmission rare

Natural disasters such as floods/ earthquakes can disrupt public health facilities and cause outbreaks

32
Q

How are cholera species classifed?

A

Over 200 serogroups

Only these serogroups cause epidemic cholera -

O1 Classical
O1 El Tor - milder disease, but longer carriage

O139

33
Q

What causes cholera symptoms?

Diarrhoea can be up to 1l/ hour

A

Enterotoxin

A subunit
B subunit

A subunit activates adenylate cyclase causing intracellular cAMP to rise, cause secretory diarrhoea - rice water

B subunit binds to eukaryotic cells

34
Q

What is treatment of cholera?

A

Fluid/ electrolyte replacement

Acidosis - loss bicarbonate
Hypokalaemia - loss potassium
Hypovolaemic shock

All contribute to high mortality without treatment

Antibiotics for severe disease -
azithromycin
ciprofloxacin

Antibiotics also reduce carriage rate

35
Q

Shigella can range from mild self limiting illness, or severe disease depending on species infecting.

Produces shiga toxin, which is similar to toxin produced by EHEC, damages intestinal epithelium.

What are names of species?

A

S sonnei - mild

S boydii - moderate
S flexneri - moderate

S dysenteriae - severe

Has no animal reservoir, so should be erradicated with good hygiene/ sanitation

36
Q

What are symptoms of shigella?

A

Starts as water diarrhoea, and changes to bloody diarrhoea with mucus

Fever

Abdominal pain

Children more commonly affected

37
Q

What is treatment of shigella?

A

Mostly self-limiting

Antibiotics for severe cases -
azithromycin
ciprofloxacin

38
Q

Yersinia entercolitica is uncommon cause of diarrhoea.

What is major reservoir?

A

Contaminated/ undercooked pork

39
Q

Yersinia entercolitica causes watery or bloody diarrhoea. Not routinely checked for on stool culture

What is incubation period?

What is duration of symptoms?

A

4-7 days - slightly longer than other pathogens

1-2 weeks

40
Q

What are causes of travellers diarrhoea?

A

Most commonly enterotoxigenic E. coli (ETEC), enteroaggregative E. coli (EAEC)

Campylobacter

Salmonella

41
Q

Which bacteria produce toxins, which cause disease when ingested?

A

B cereus

C perfringens

C botulinum

S aureus enterotoxin

42
Q

Up to 50% of S. Aureus strains produce enterotoxin to cause symptoms.

Enterotoxin A is most common

TSST-1 toxic shock syndrome toxin is not food associated

How do they cause disease?

A

Bind to MHC class II molecules resulting in T-cell stimulation, leading to production of proinflammatory mediators

Causes symptoms within 3-6 hours

Causes vomiting, but not diarrhoea.

Recover in 24h

Enterotoxins possibly implicated in pathophysiology of IBD

43
Q

C boutlinum produces exotoxin which is neurotoxic

Seven major toxins named A-G

How is infection transmitted/ reservoir?

A

Found in soil

Toxins ingested in canned/ reheated food

44
Q

What are symptoms of botulism?

A

Toxins ingested, then absorbed by gut into bloodstream.

Reach peripheral nerve synapses which it blocks

Symmetrical descending flaccid muscle paralysis, beginning with cranial nerves causing blurred vision, swallowing difficulty, slurred speech.

This then leads to paralysis of respiratory and cardiac muscles

45
Q

Three forms of botulism -

  • food-borne
  • infant
  • wound

How are they different?

A
  • food-borne - ingest toxin
  • infant - ingest bacteria, which multiply in gut and produce toxin. Does not happen as get older, as host defences mature to destroy ingested pathogen
  • wound - grow in wound

Clinical symptoms are all the same

46
Q

What is treatment of botulism?

A

Mainly supportive - airway support. Time to recovery can be from 30-100 days

Anti-toxin - stops further toxin binding, but does not remove already bound toxin

47
Q

Differential diagnosis for botulism?

blurry vision
dysphagia
slurred speech

A

Botulism

Descending form of acute inflammatory polyneuropathy.

Guillain-Barré syndrome.

Poisoning.

Myasthenia gravis.

48
Q

How to diagnose botulism?

A

Toxin detection - PCR

Bioassay - take patient serum and inject into mice which are either protected with antitoxin/ not protected

49
Q

Not practical to prevent food from being contaminated with botulism, aim to prevent spore formation.

How is this dose?

A

Maintain food at acid pH

Store food <4degC

Cook food thoroughly

50
Q

Clostridium perfringens produces exotoxin which causes diarrhoea.

What happens if food inadequately cooked?

What other diseases does C perfringens cause?

A

Bacteria killed, but spores germinate releasing enterotoxin

Skin and soft tissue infection - gas gangrene

51
Q

Bacillus cereus is widespread in soil, and contaminates many foods

What clinical syndromes can it cause?

A

Vomiting - due to ingestion of enterotoxin (heat-stable)

Diarrhoea - due to ingestion of bacteria, and production of enterotoxin (heat-labile) in gut

52
Q

Clostridium difficile is most common cause of healthcare associated infection.

Antibiotics kill gut flora, which can then be re-colonised by other bacteria

C. difficile forms spore in environment

What exotoxins are produced?

A

Toxin A - increases intestinal permeability

Toxin B - cytotoxin causes inflammation, resulting in diarrhoea

53
Q

How to diagnose C. difficile?

Symptoms normally occur 5-10 days after starting antibiotic therapy

A

Stool culture - check if bacteria present
GDH antigen test - check if bacteria present

PCR to check for toxin A/B presence

54
Q

What are risk factors for C. difficile?

A

Prolonged/ multiple courses of antibiotics

Increasing age

Inpatient residence on ITU

Increasing duration of hospital stay; patients in long-term care facilities.

Immunocompromised patients.

PPI

55
Q

Patient with suspected C. difficile

Apart from stool tests, how should you investigate patient?

A

WCC

Creatinine

Albumin - protein loss

AXR

Sigmoidoscopy

Surgical review

Stool chart

Fluid balance chart

56
Q

What parameters make up C. diff severity score?

A

Score over 3 indicates severe CDI - increased mortality

WCC >15
Temp >38.5
5x stool motions per day
Hypotensive
Creatinine >50% above baseline
Abdominal signs indicating colitis
Radiological evidence of colonic dilation
57
Q

What is management of C. diff first episode or first recurrence?

A

Isolate patient - until 48 hours after formed stool

Medication review - Abx/ PPI

Fluids

Metronidazole

  • mild 400mg PO TDS 10-14 days
  • severe 500mg IV TDS 10-14 days

Vancomycin oral/PR - increasing risk of vancomycin resistant enterococci

  • mild - 125mg QDS 10-14 days
  • severe - 500mg QDS 10-14 days

Colectomy if severe colitis

58
Q

recurrence is termed as presenting within 8 weeks of first C. diff positive test

After first recurrence - same treatment

After second recurrence what is treatment?

A 
Vancomycin
125 QDS 14 days
125 BD 7 days
125 OD 7 days
125 alternate days for 7 days

Or

Fidaxomicin 200mg BD for 10 days

59
Q

What are options for third recurrence of C. difficile?

A

Vancomycin taper followed by rifaximin 400mg BD 14 days

IV immunoglobulin

Faecal transplant

60
Q

Viral gastroenteritis clinically looks similar to bacterial/ parasitic causes

Norovirus is most common cause of diarrhoeal illness worldwide. Previously known as Norwalk-like virus, or winter vomiting diseases. Often associated with outbreaks e.g contaminated food, or sewage contaminated shellfish

What is genetic structure?

How many genotypes?

A

uneveloped
+ssRNA

6 genotypes
GI/ GII/ GIV cause infection in human

61
Q

How to diagnose norovirus?

Why does infection not provide immunity?

A

PCR of stool

Noroviruses show high level of variability between strains, so infection does not provide cross-protection. Difficult to develop vaccine

62
Q

Rotaviruses infect many mammals. Damage gut epithelium, resulting in fluid loss into lumen, and flattening of villi

What is nuclear material?

Who is usually affected?

How to diagnose?

A

dsRNA

Children under 2.
IgA in colostrom protects until 6 months old
Vaccine given at 8 weeks old

Ag detection via PCR or ELISA in children with diarrhoea <5

63
Q

What other viruses can cause diarrhoea?

A

Sapovirus

Astrovirus

Adenovirus type 40/41

Coronavirus

Some viruses may be detected in stool e.g enterovirus, but do not cause diarrhoeal disease

64
Q

H. pylori is gram negative spiral bacterium, causes peptic/ gastric ulcers/ MALT lymphoma

Produces urease that breaks down urea to ammonia and CO2, increasing pH to prevent against acid

How to diagnose?

A

Urea breath test
Faecal antigen test
Serology
Endoscopy/ biopsy - PCR

65
Q

What is treatment of H. pylori?

A

7 day course, all meds BD

  • PPI 40mg
  • first line
    amoxicillin 1g and clarithromycin 500mg

penicillin allergy -
clarithromycin 500 mg and metronidazole 400mg

66
Q

What is pathophysiology whereby salmonella causes enteric fever?

A

Ingestion bacteria, penetrate gut mucosa via Peyer’s patches

Then reach intestinal lymph nodes, whereby they survive and multiply in macrophages. Lymph then drains into thoracic duct, then bloodstream

Salmonella then seeds to many organs causing disease. Particularly cells of reticuloendothelial cells e.g spleen, bone marrow, liver

Salmonella then enters gallbladder, where can survive long time as resistant to bile. Bacteria then re-enter intestinal system for second time, in larger numbers

This causes strong inflammatory response in Peyer’s patches leading to ulceration, and perforation

Chronic carriage defined as having salmonella in stool 1 year after infection

67
Q

What are signs of enteric fever?

A

Can present with constipation.

Can present with rose spots on upper abdomen - maculopapular rash

Faget’s sign - high fever with bradycardia

68
Q

What is differential diagnosis for Faget’s sign?

A 
Brucellosis
Chlamydia
Colorado tick fever virus
Coxiella burnetii
Dengue Fever
Drug fever
Legionella
Leptospirosis
Leishmaniasis
Mycoplasma
Psittacosis
Tularemia
Typhoid fever
Yellow Fever

Mostly intracellular organisms - physiology unclear

69
Q

What is Lemierre’s syndrome?

Which organisms cause it?

A

Peritonsillar infection with involvement of jugular vein

Fusobacterium necrophorum most common. Also oral anerobes/ strep pyogenes/ eikenella can cause

70
Q

What is treatment of Lemierre’s syndrome

A

Co-amoxiclav plus metronidazole

Add vancomycin if associated with device e.g central line

71
Q

Patients with liver cirrhosis at risk of SBP, as they are immunocompromised. May not have symptoms, or raised WCC or fever

What are causative organisms?

A

Gram neg -
E. coli
Klebsiella

Gram pos-
Enterococci

Streptococci

Staphylococci

72
Q

What are investigations for SBP?

A

Ascitic tap - WCC >250 cells/mm, culture

Blood cultures

73
Q

What is treatment of SBP?

A

Tazocin or ceftriaxone (usually 5-7 days)
albumin on day 1 and 3

Ciprofloxacin prophylaxis after first episode of SBP

74
Q

Peritoneal dialysis

Which organisms cause peritonitis in these patients?

A

Gram neg -
E. coli

Klebsiella

Pseudomonas

Gram pos-
Enterococci

Streptococci

Staphylococci

Staphylococci/ pseudomonas most common cause exit site infection

75
Q

How to diagnose peritonitis in PD patients?

A

WCC >100/ml (0.1 x10 9/ litre) in PD fluid

Repeat on day 3 of treatment if not improving

76
Q

Treatment of PD peritonitis?

A

Vancomycin 2g in 6 hour intraperitoneal (IP) dwell.
(1.5g if patient weighs <45kg).

And

Ciprofloxacin 500mg bd orally, or gentamicin

Then oral therapy once improved - ciprofloxacin/ rifampicin/ linezolid

14 days normal treatment duration, can be extended if slow to improve

May need PD tube change if treatment if unresponsive to antibiotics, or this is relapse from recently treated infection, or if fungal/ pseudomonal infection

77
Q

PD dialysis

What is treatment of exit line infection?

A

Flucloxacillin 500mg QDs for a minimum of 2 weeks (continue until resolution).

or

Rfampicin 300mg BD

or

Ciprofloxacin 500mg BD - also has pseudomonal activity

Medical Microbiology and Virology (60 decks)

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