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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
What conditions are caused by invasive salmonella? Fever is sign of systemic illness, and may require admission
Bowel perforation Osteomyelitis Pneumonia Meningitis Endocarditis Cholecystitis - can form reservoir here
26
How to test for invasive salmonella?
Blood culture Widal test - agglutination assay detecting antibodies ahainst O/ H antigens Stool culture to confirm that salmonella has caused enteric infection
27
What is treatment for salmonella?
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
28
What is source/ transmission of campylobacter?
Large animal reservoir Consumption of contaminated food - faecal-oral Person-person spread is less common
29
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?
Meningitis Guillain-Barre Endocarditis IBD/ IBS?
30
What is treatment of campylobacter infection?
Usually self-limiting If unwell/ fever - Azithromycin Ciprofloxacin - resistance emerging
31
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?
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
How are cholera species classifed?
Over 200 serogroups Only these serogroups cause epidemic cholera - O1 Classical O1 El Tor - milder disease, but longer carriage O139
33
What causes cholera symptoms? Diarrhoea can be up to 1l/ hour
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
What is treatment of cholera?
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
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?
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
What are symptoms of shigella?
Starts as water diarrhoea, and changes to bloody diarrhoea with mucus Fever Abdominal pain Children more commonly affected
37
What is treatment of shigella?
Mostly self-limiting Antibiotics for severe cases - azithromycin ciprofloxacin
38
Yersinia entercolitica is uncommon cause of diarrhoea. What is major reservoir?
Contaminated/ undercooked pork
39
Yersinia entercolitica causes watery or bloody diarrhoea. Not routinely checked for on stool culture What is incubation period? What is duration of symptoms?
4-7 days - slightly longer than other pathogens 1-2 weeks
40
What are causes of travellers diarrhoea?
Most commonly enterotoxigenic E. coli (ETEC), enteroaggregative E. coli (EAEC) Campylobacter Salmonella
41
Which bacteria produce toxins, which cause disease when ingested?
B cereus C perfringens C botulinum S aureus enterotoxin
42
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?
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
C boutlinum produces exotoxin which is neurotoxic Seven major toxins named A-G How is infection transmitted/ reservoir?
Found in soil Toxins ingested in canned/ reheated food
44
What are symptoms of botulism?
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
Three forms of botulism - - food-borne - infant - wound How are they different?
- 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
What is treatment of botulism?
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
Differential diagnosis for botulism? blurry vision dysphagia slurred speech
Botulism Descending form of acute inflammatory polyneuropathy. Guillain-Barré syndrome. Poisoning. Myasthenia gravis.
48
How to diagnose botulism?
Toxin detection - PCR Bioassay - take patient serum and inject into mice which are either protected with antitoxin/ not protected
49
Not practical to prevent food from being contaminated with botulism, aim to prevent spore formation. How is this dose?
Maintain food at acid pH Store food <4degC Cook food thoroughly
50
Clostridium perfringens produces exotoxin which causes diarrhoea. What happens if food inadequately cooked? What other diseases does C perfringens cause?
Bacteria killed, but spores germinate releasing enterotoxin Skin and soft tissue infection - gas gangrene
51
Bacillus cereus is widespread in soil, and contaminates many foods What clinical syndromes can it cause?
Vomiting - due to ingestion of enterotoxin (heat-stable) Diarrhoea - due to ingestion of bacteria, and production of enterotoxin (heat-labile) in gut
52
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?
Toxin A - increases intestinal permeability Toxin B - cytotoxin causes inflammation, resulting in diarrhoea
53
How to diagnose C. difficile? Symptoms normally occur 5-10 days after starting antibiotic therapy
Stool culture - check if bacteria present GDH antigen test - check if bacteria present PCR to check for toxin A/B presence
54
What are risk factors for C. difficile?
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
Patient with suspected C. difficile Apart from stool tests, how should you investigate patient?
WCC Creatinine Albumin - protein loss AXR Sigmoidoscopy Surgical review Stool chart Fluid balance chart
56
What parameters make up C. diff severity score?
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
What is management of C. diff first episode or first recurrence?
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
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?
``` 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
What are options for third recurrence of C. difficile?
Vancomycin taper followed by rifaximin 400mg BD 14 days IV immunoglobulin Faecal transplant
60
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?
uneveloped +ssRNA 6 genotypes GI/ GII/ GIV cause infection in human
61
How to diagnose norovirus? Why does infection not provide immunity?
PCR of stool Noroviruses show high level of variability between strains, so infection does not provide cross-protection. Difficult to develop vaccine
62
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?
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
What other viruses can cause diarrhoea?
Sapovirus Astrovirus Adenovirus type 40/41 Coronavirus Some viruses may be detected in stool e.g enterovirus, but do not cause diarrhoeal disease
64
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?
Urea breath test Faecal antigen test Serology Endoscopy/ biopsy - PCR
65
What is treatment of H. pylori?
7 day course, all meds BD - PPI 40mg - first line amoxicillin 1g and clarithromycin 500mg penicillin allergy - clarithromycin 500 mg and metronidazole 400mg
66
What is pathophysiology whereby salmonella causes enteric fever?
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
What are signs of enteric fever?
Can present with constipation. Can present with rose spots on upper abdomen - maculopapular rash Faget's sign - high fever with bradycardia
68
What is differential diagnosis for Faget's sign?
``` 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
What is Lemierre's syndrome? Which organisms cause it?
Peritonsillar infection with involvement of jugular vein Fusobacterium necrophorum most common. Also oral anerobes/ strep pyogenes/ eikenella can cause
70
What is treatment of Lemierre's syndrome
Co-amoxiclav plus metronidazole Add vancomycin if associated with device e.g central line
71
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?
Gram neg - E. coli Klebsiella Gram pos- Enterococci Streptococci Staphylococci
72
What are investigations for SBP?
Ascitic tap - WCC >250 cells/mm, culture Blood cultures
73
What is treatment of SBP?
Tazocin or ceftriaxone (usually 5-7 days) albumin on day 1 and 3 Ciprofloxacin prophylaxis after first episode of SBP
74
Peritoneal dialysis Which organisms cause peritonitis in these patients?
Gram neg - E. coli Klebsiella Pseudomonas Gram pos- Enterococci Streptococci Staphylococci Staphylococci/ pseudomonas most common cause exit site infection
75
How to diagnose peritonitis in PD patients?
WCC >100/ml (0.1 x10 9/ litre) in PD fluid Repeat on day 3 of treatment if not improving
76
Treatment of PD peritonitis?
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
PD dialysis What is treatment of exit line infection?
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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