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Gastrointestinal infections Flashcards

1
Q

What are different classes of peritonitis?

A

Primary - also known as SBP. Usually arises from translocation of bacteria from gut

Secondary - e.g due to surgery, malignancy or peritoneal dialysis

Treat for 5-7 days usually. But may change depending on patient condition, or organism isolated.

Requires surgical review, as may need surgery/ drainage for source control

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2
Q

Patient with peritonitis.

How important is empiric cover against enterococci?

A

Most common causes are gram neg bacilli, so enterococci less likely cause

amox/ met/ gent will cover the most common causes, including enterococci (although not optimal)

if culture results show enterococci, then add cover

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3
Q

Patient with peritonitis.

Blood cultures show ESBL.

Patient on co-amoxiclav/ gent/ metro

Should antibiotics be changed?

A

Not necessarily

Co-amoxiclav has clavulanic acid, so can resist ESBL in principle. Better to check MIC to see if is resistant or not.

If so, may need to use meropenem

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4
Q

Options for peritonitis -

amox/met/ gent
taz/ gent
vanc/ gent
cephalosporin/ metro

What are limitations of using cephalosporin in this case?

A

Does not cover pseudomonas
Does not cover enterococci

Taz does have pseudomonal/ enterococci cover

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5
Q

What bacteria can be implicated in bacterial hepatic abscess?

What is duration of therapy?

A

Klebsiella pneumoniae

Abscess requires drainage.
Approx 4-6 weeks of antibiotics, usually continued for few weeks after radiological resolution

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6
Q

When is C. Difficile infection classified as

Healthcare associated

Community associated

A

Healthcare associated -

  • symptoms appear on day 3 or later in hospital admission
  • symptoms within 4 weeks of discharge

Community associated
- symptoms without being in healthcare facility in past 12 weeks

Unknown association
- symptoms occurring 4-12 weeks after being in healthcare facility

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7
Q

After how long since C. Difficile infection, is it re-occurrence?

A

if returns within 8 weeks of first episode

occurs in 20% patients

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8
Q

What are treatment options for first recurrence of C. difficile?

A

If had metronidazole, then give first course of vancomycin

If had vancomycin, then give 14 days, with reducing course

Also consider fidaxomicin, rifaximin, nitazoxinide

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9
Q

Which microbes are associated with travellers diarrhoea?

A

E. Coli - ETEC. EAEC
Campylobacter
Salmonella - non-typhi
Shigella

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10
Q

Travellers can take antibiotics if at high risk of developing travellers diarrhoea, or would be high risk if developed diarrhoea

What are options?

A

Azithromycin 500mg OD 3 days - most universally used choice

Ciprofloxacin - 500mg BD 3 days - resistance in SEA

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11
Q

What are most common causes of viral gastroenteritis?

A

Caliciviruses - norovirus, sapovirus
rotavirus
astrovirus
adenovirus - serotypes 40/41

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12
Q

Describe structure of norovirus

Which genotype causes most infections

A

+ssRNA

7 genogroups based on VP1 - major capsid protein

within genogroups, there are genotypes

genogroup 2 genotype 4 is most common cause worldwide

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13
Q

Patient with norovirus.

36 hours later, patient in bay has diarrhoea/ vomiting.

12 hours later, further 4 cases are reported within the ward.

What are criteria for identifying outbreak of viral gastroenteritis?

A

Kaplan criteria can be used to determine probability that cause is viral gastroenteritis

sensitivity 70%
specificity 99%

  • vomiting >50%
  • mean incubation period 24-48 hours
  • mean duration illness 12-60 hours
  • no bacterial cause identified
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14
Q

What are the Kaplan criteria, used to identify an outbreak of viral gastroenteritis?

A
  • mean illness duration 12-60 hours
  • mean incubation 24-48 hours
  • > 50% people with vomiting
  • no bacterial agent found

usually triggered if two patients develop diarrhoea and vomiting

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15
Q

Viral gastroenteritis outbreak.

What are some infection control measures

A

Handwashing - superior than alcohol

Isolate patients

Close bays

Enteric precautions

Do not move suspect patients until 48 hours symptom free

Staff not to return until 48 hours symptom free

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16
Q

HEV infection in immunocompromised can become chronic.

What are treatment options for chronic HEV infection?

A

Reduce immunosuppression

ribavirin

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17
Q

Which HEV genotypes infect in resource rich, and resource poor countries?

A

Resource poor -
genotype 1/2 - contaminated water

Resource rich -
genotype 3/4 - zoonosis pigs

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18
Q

What are complications of HEV infection?

A

Chronic infection - immunocompromised

Fulminant hepatitis - particularly pregnant women infected with genotype 1/2

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19
Q

HCV

What are general drug targets for treating virus?

A

NS3/4A protease inhibitor - suffix -previr

NS5A inhibitor - suffix - asvir

NS5B inhibitor - suffix - buvir

NS - non-structural

20
Q

HCV DAA

What are examples of NS3/4A inhibitors?

A

Simeprevir

Grazoprevir

21
Q

HCV DAA

What are examples of NS5A inhibitors?

A

Elbasavir

Ledipasavir

Velpatasvir

22
Q

HCV DAA

What are examples of NS5B inhibitors?

A

Sofosbuvir - nucleoside analogue

Dasabuvir - non-nucleoside analgoue

23
Q

What are functions of these proteins?

NS3A/4A

NS5A

NS5B

A

NS3A/4A - NS3 is protease and helicase. NS4A is a co-factor

NS5A - key role in viral replication, including release of new virions

NS5B - RNA dependent RNA polymerase

24
Q

How are HCV genotypes defined?

A

If they have >30% difference in nucleotide sequence across whole genome

25
Q

Patient with abdominal pain, cramping, non-bloody diarrhoea. Stool samples shows some white cells.

Culture shows gram neg rods, slightly curved

What is most likely infectious cause?

A

Campylobacter

Differential -

Vibrio - rice water stool. No white cells as non-inflammatory

Campylobacter and vibrio are both curved rods

26
Q

What is natural host of campylobacter?

When do peak infections occur?

A

Chickens

Sometimes growth media are kept at 42degC, which is natural body temp of chickens

Usually late Spring - Summer. Possibly related to barbecues

27
Q

What is treatment of Campylobacter infection?

A

Supportive care

Macrolides/ ciprofloxacin if severe disease, or immunocompromised

Some resistance to ciprofloxacin via single mutation in DNA gyrase.
Macrolides require multiple mutations

28
Q

What is an important post-infectious cause of campylobacter infection?

A

GBS - flaccid paralysis
Requires intubation in 25% of cases

Usually occurs 3-6 weeks after illness

Molecular mimicry - antibodies targeted against lipooligosaccharide of C. jejuni cross-react with peripheral nerve ganglions, resulting in acute inflammatory polyneuropathy

Other post-infectious syndromes -

  • reactive arthritis (Reiter syndrome)
  • IBS
29
Q

What are treatment strategies for GBS following campylobacter infection?

A

Plasma exchange - remove antibodies and complement which mediate the inflammatory neuropathy

Immunoglobulin - binds to auto-antibodies inhibiting their function

30
Q

What stain is used to identify giardia parasite?

A

Lugol’s iodine useful for showing cyst

31
Q

In patients with giardia infection, why is there watery diarrhoea after meals?

A

Trophozoites adheres to intestinal mucosa, damaging the brush border.

This results in malabsorptive diarrhoea. So patient has frothy, foul-smelling stools 1-2 hours after a meal

32
Q

What are risk factors for cryptosporidium infection?

A

Poor sanitary conditions
Contact farm animals
Swimming in fresh water/ swimming pools
Contact with infected individuals

33
Q

What is treatment of cryptosporidium infection?

A

Usually self-limiting

Nitazoxanide can be used in refractory disease e.g HIV

34
Q

Child with nausea, abdominal pain, and blood in stool. Bowels moving 10x a day

What is this clinical syndrome?

A

Bacterial dysentry - if infective cause

i.e symptoms <14 days makes infection more likely

35
Q

What are major causes of bacterial dysentry?

A

Campylobacter

Shigella

Salmonella

E. coli - Shiga toxin producing STEC

Yersinia entercolitica

Non-bacterial -
Entamoeba histolytica

36
Q

Stool sample in patient with bloody diarrhoea.

Non-motile
Non-lactose fermenting
H2S negative
Grows on MacConkey agar

What is likely cause?

Campylobacter
Shigella
Salmonella
E. coli - Shiga toxin producing STEC

A

Shigella

Campylobacter will not grow on MacConkey

Salmonella is motile, and produces H2S

E. coli STEC is usually motile, and is a lactose fermenter

37
Q

What is the clinical rationale behind use/ non-use of antibiotics in dysentry?

A

Antibiotics shorten duration of symptoms, and period of infectiousness.

But in theory can upset gut mirobiota

Absolutely contra-indicated in E.coli STEC - as antibiotics are predisposing factor for HUS

38
Q

What is significance of faecal leucocyte testing?

A

If leucocytes present, suggests bacterial dysentery - invasive diarrhoea

39
Q

1 year old with rotavirus diarrhoea. What is different about the clinical course of disease compared to other ifnections?

A

Symptoms last for 1 week.

Whereas other infections symptoms last for 24-48 hours

40
Q

How does rotavirus cause diarrhoea?

A

Viral destruction of enterocytes, where virus replicates

Disruption of tight junctions - increased permeability

Enterotoxin-like molecule NSP4 stimulates enteric nervous system, which increases concentration of calcium, and results in secretion of fluid and electrolytes into lumen

These mechanisms all contribute to watery diarrhoea

41
Q

What is an adverse event associated with rota virus vaccination?

A

Intussusception - newer vaccines introduced in 2006 have even lower rate of intussusception

42
Q

Norovirus causes vomiting and diarrhoea, with rapid onset. Also called winter vomiting disease

What is the most common genogroup/ genotype which infects humans?

A

6 genogroups of norovirus - I, II, IV infected humans

genogroup II, genotype 4 is primary strain which causes outbreaks

Normally cause acute diarrhoea.
However, if immunocompromised, can have chronic diarrhoea with significant weight loss, dehydration, malnutrtion

43
Q

What toxins dose Clostridium difficile produce, and how do they work?

Called “difficile” because it is difficult to culture

A

Toxin A and Toxin B

toxins produced at epithelial surface, and taken in be cells. These toxins activates GTPases which result in damage to cells

Proinflammatory cytokines cause increased vascular permeability, contributing to diarrhoea

Pseudomembranous colitis occurs when areas of dead cells, fibrin, bacteria cause a greenish plaque to overly the colon wall

44
Q

What are usual steps in diagnosing C. difficile infection?

A

NAAT - for Toxin A/B genes. Can detect both live and dead organisms. So should only be used for initial diagnosis, not test for cure. 10-15% of true infections, will be negative, which can make diagnosis difficult as assay is insensitive

Cell wall antigen detection using antibodies - GDH. GDH is cell wall antigen. Must test for toxin in addition. As some other Clostridium difficile species can be commensals, but non-toxin producing. 10% of people are colonised

45
Q

Which HCV genotypes are most common in UK?

Which HCV genotype has higher risk of rapid progression to liver failure?

A

Genotype 1 + 3

Genotype 1b - more rapid progression

Question Bank (33 decks)

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