Gastrointestinal infections Flashcards
What are different classes of peritonitis?
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
Patient with peritonitis.
How important is empiric cover against enterococci?
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
Patient with peritonitis.
Blood cultures show ESBL.
Patient on co-amoxiclav/ gent/ metro
Should antibiotics be changed?
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
Options for peritonitis -
amox/met/ gent
taz/ gent
vanc/ gent
cephalosporin/ metro
What are limitations of using cephalosporin in this case?
Does not cover pseudomonas
Does not cover enterococci
Taz does have pseudomonal/ enterococci cover
What bacteria can be implicated in bacterial hepatic abscess?
What is duration of therapy?
Klebsiella pneumoniae
Abscess requires drainage.
Approx 4-6 weeks of antibiotics, usually continued for few weeks after radiological resolution
When is C. Difficile infection classified as
Healthcare associated
Community associated
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
After how long since C. Difficile infection, is it re-occurrence?
if returns within 8 weeks of first episode
occurs in 20% patients
What are treatment options for first recurrence of C. difficile?
If had metronidazole, then give first course of vancomycin
If had vancomycin, then give 14 days, with reducing course
Also consider fidaxomicin, rifaximin, nitazoxinide
Which microbes are associated with travellers diarrhoea?
E. Coli - ETEC. EAEC
Campylobacter
Salmonella - non-typhi
Shigella
Travellers can take antibiotics if at high risk of developing travellers diarrhoea, or would be high risk if developed diarrhoea
What are options?
Azithromycin 500mg OD 3 days - most universally used choice
Ciprofloxacin - 500mg BD 3 days - resistance in SEA
What are most common causes of viral gastroenteritis?
Caliciviruses - norovirus, sapovirus
rotavirus
astrovirus
adenovirus - serotypes 40/41
Describe structure of norovirus
Which genotype causes most infections
+ssRNA
7 genogroups based on VP1 - major capsid protein
within genogroups, there are genotypes
genogroup 2 genotype 4 is most common cause worldwide
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?
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
What are the Kaplan criteria, used to identify an outbreak of viral gastroenteritis?
- 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
Viral gastroenteritis outbreak.
What are some infection control measures
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
HEV infection in immunocompromised can become chronic.
What are treatment options for chronic HEV infection?
Reduce immunosuppression
ribavirin
Which HEV genotypes infect in resource rich, and resource poor countries?
Resource poor -
genotype 1/2 - contaminated water
Resource rich -
genotype 3/4 - zoonosis pigs
What are complications of HEV infection?
Chronic infection - immunocompromised
Fulminant hepatitis - particularly pregnant women infected with genotype 1/2
HCV
What are general drug targets for treating virus?
NS3/4A protease inhibitor - suffix -previr
NS5A inhibitor - suffix - asvir
NS5B inhibitor - suffix - buvir
NS - non-structural
HCV DAA
What are examples of NS3/4A inhibitors?
Simeprevir
Grazoprevir
HCV DAA
What are examples of NS5A inhibitors?
Elbasavir
Ledipasavir
Velpatasvir
HCV DAA
What are examples of NS5B inhibitors?
Sofosbuvir - nucleoside analogue
Dasabuvir - non-nucleoside analgoue
What are functions of these proteins?
NS3A/4A
NS5A
NS5B
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
How are HCV genotypes defined?
If they have >30% difference in nucleotide sequence across whole genome
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?
Campylobacter
Differential -
Vibrio - rice water stool. No white cells as non-inflammatory
Campylobacter and vibrio are both curved rods
What is natural host of campylobacter?
When do peak infections occur?
Chickens
Sometimes growth media are kept at 42degC, which is natural body temp of chickens
Usually late Spring - Summer. Possibly related to barbecues
What is treatment of Campylobacter infection?
Supportive care
Macrolides/ ciprofloxacin if severe disease, or immunocompromised
Some resistance to ciprofloxacin via single mutation in DNA gyrase.
Macrolides require multiple mutations
What is an important post-infectious cause of campylobacter infection?
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
What are treatment strategies for GBS following campylobacter infection?
Plasma exchange - remove antibodies and complement which mediate the inflammatory neuropathy
Immunoglobulin - binds to auto-antibodies inhibiting their function
What stain is used to identify giardia parasite?
Lugol’s iodine useful for showing cyst
In patients with giardia infection, why is there watery diarrhoea after meals?
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
What are risk factors for cryptosporidium infection?
Poor sanitary conditions
Contact farm animals
Swimming in fresh water/ swimming pools
Contact with infected individuals
What is treatment of cryptosporidium infection?
Usually self-limiting
Nitazoxanide can be used in refractory disease e.g HIV
Child with nausea, abdominal pain, and blood in stool. Bowels moving 10x a day
What is this clinical syndrome?
Bacterial dysentry - if infective cause
i.e symptoms <14 days makes infection more likely
What are major causes of bacterial dysentry?
Campylobacter
Shigella
Salmonella
E. coli - Shiga toxin producing STEC
Yersinia entercolitica
Non-bacterial -
Entamoeba histolytica
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
Shigella
Campylobacter will not grow on MacConkey
Salmonella is motile, and produces H2S
E. coli STEC is usually motile, and is a lactose fermenter
What is the clinical rationale behind use/ non-use of antibiotics in dysentry?
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
What is significance of faecal leucocyte testing?
If leucocytes present, suggests bacterial dysentery - invasive diarrhoea
1 year old with rotavirus diarrhoea. What is different about the clinical course of disease compared to other ifnections?
Symptoms last for 1 week.
Whereas other infections symptoms last for 24-48 hours
How does rotavirus cause diarrhoea?
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
What is an adverse event associated with rota virus vaccination?
Intussusception - newer vaccines introduced in 2006 have even lower rate of intussusception
Norovirus causes vomiting and diarrhoea, with rapid onset. Also called winter vomiting disease
What is the most common genogroup/ genotype which infects humans?
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
What toxins dose Clostridium difficile produce, and how do they work?
Called “difficile” because it is difficult to culture
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
What are usual steps in diagnosing C. difficile infection?
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
Which HCV genotypes are most common in UK?
Which HCV genotype has higher risk of rapid progression to liver failure?
Genotype 1 + 3
Genotype 1b - more rapid progression
