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Year 3 Infections > 1. Infectious Diarrhoea > Flashcards

1. Infectious Diarrhoea Flashcards

1
Q

Define Diarrhoea.

A

Fluidity and frequency of stools.

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2
Q

Define gastro-enteritis.

A
  • Three or more loose stools/day

- Accompanying features (fever, abdominal pain, vomiting, blood/mucus in stools).

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3
Q

Define dysentery.

A

Large bowel inflammation, bloody stools.

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4
Q

What chart is used to classify faeces into groups?

A

Bristol stool chart. Classifies faeces into 7 groups. Group 1-2 = constipation.
Group 3-4 = ideal stools as easier to pass.
Group 5-7 = may indicate diarrhoea and urgency.

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5
Q

Outline epidemiology of gastro-enteritis.

A

Contamination of foodstuffs: Intensively farmed chicken (commonly contaminated by campylobacter)

Poor storage of produce: Bacterial proliferation at room temperature

Travel-related infections e.g. Salmonella

Person-to-person spread: norovirus

Viruses are commonest cause with campylobacter being the commonest bacterial pathogen.

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6
Q

Trends in food poisoning:

  1. T/F: Campylobacter is the most common foodborne pathogen.
  2. Which pathogen causes the most hospital admissions?
  3. What kind of food is linked to the most cases of food poisoning?
A
  1. True
  2. Salmonella
  3. Poultry meat
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7
Q

What defences do we have against enteric infections?

A
  1. Hygiene: washing very important for viral gastroenteritis. Adequate cooking important for bacterial enteritis.
  2. Stomach acidity: patients on antacids have higher risk of developing gastroenteritis as they don’t have protection from the stomach acid.
  3. Normal gut flora: Cl. Difficile diarrhoea seen in patients prescribed antibiotics that disrupt normal gut flora.
  4. Immunity: salmonella gastroenteritis seen in HIV (immuno-compromised) patients.
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8
Q

What are the 3 broad clinical features of diarrhoeal illness?

A
  1. Non-inflammatory/secretory: e.g. cholera
  2. Inflammatory (inflammatory toxin damage and mucosal destruction): e.g. bacterial infection/ shigella dysentery / amoebic dysentery
  3. Mixed picture: e.g. C. difficile (produce toxins that can lead to increased secretions (secretory toxins) and toxins that can lead to inflammation).
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9
Q

Non-inflammatory diarrhoeal illness:

  1. Which organisms is the common cause of this?
  2. What are the clinical features of it?
  3. How is it treated?
A
  1. Secretory toxins released by:
    - Cholera (Increased cAMP results in loss of Cl from cells along with Na and K. Osmotic effect leads to massive loss of water from the gut).
  • Enterotoxigenic E. coli (travellers’ diarrhoea) - not routinely tested in the lab.
    2. frequent watery stools with little abdominal pain.
    3. Rehydration mainstay of therapy.
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10
Q

Inflammatory diarrhoeal illness:

  1. What are the clinical features of it?
  2. How is it treated?
A
  1. Pain and fever

2. Antimicrobials may be appropriate but rehydration alone is often sufficient.

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11
Q

How would you assess a patient presenting with possible GI infection?

A

History:

  • Symptoms and their duration : >2/52 unlikely to be infective gastro-enteritis
  • Risk of food poisoning: Dietary, contact, travel history

Examination:

  • Assess hydration: postural BP (patient my collapse etc.), skin turgor, pulse
  • features of inflammation (SIRS): fever, raised WCC

Children: sunken eyes and cheeks, sunken frontanelle, sunken abdomen few or no tears, dry mouth or tongue, decreased skin turgor.

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12
Q

What kind of investigations would you do for a patient suspected of GI infection?

A
  1. Stool culture +/- molecular (e.g. detecting toxins from c. diff) or antigen testing (e.g. Ab against antigen produced by some parasites).
  2. blood culture
  3. renal function (requirement for fluid replacement etc.)
  4. Blood count - neutrophilia, haemolysis (E. coli O157)
  5. abdominal X-ray/CT if abdomen distended, tender
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13
Q

List some differential diagnosis in a patient presenting with diarrhoea suspected to have gastroenteritis?

A

Inflammatory bowel disease (usually have diarrhoea for longer period) (also suspected if bloody diarrhoea with -ve stools?)

Spurious diarrhoea: secondary to constipation
Carcinoma (e.g. rectal)

Diarrhoea and fever can occur with sepsis outside the gut:

  • lack of abdo pain/tenderness goes against gastroenteritis
  • no blood/mucus in stools
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14
Q

How is gastroenteritis treated?

A

Rehydration - iv or oral?

  • Oral rehydration with salt/sugar solution if community setting or resource limited centre etc.
  • iv saline
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15
Q

Campylobacter gastroenteritis:

  1. Why the dietary history may be unreliable?
  2. T/F: stools negative within 6 weeks.
  3. What is the major symptom these patients present with?
  4. Is it invasive?
  5. List some complications arising after the infection?
A
  1. Long incubation period (7 days)
  2. True
  3. Abdominal pain (can be severe: confused for appendicitis sometimes)
  4. Rarely (<1%)
  5. Post-infection sequelae: Guillain-Barre syndrome, Reactive arthritis.
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16
Q

Salmonella gastroenteritis:

  1. When do the symptoms appear usually?
  2. How long does the diarrhoea last?
  3. T/F: <5% cases have +ve blood cultures weeks after the infection.
  4. T/F: 20% patients still have positive stools at 20/52.
  5. . List some complications arising after the infection?
A
  1. symptom onset usually <48 hrs after exposure
  2. diarrhoea usually lasts <10 days
  3. True.
  4. True. In some patients this is because of gallstones as stones can become chronically infected and the patients can carry on shedding salmonella for a long time (unless gallstones removed): patients may be asymptomatic but infect other people.
  5. Post-infectious irritable bowel is common.
17
Q

E. coli O157 infection:

  1. What are the sources of infection?
  2. How does it typically present?
  3. What toxin does the bacterium produce?
  4. T/F: E. coli O157 is normally present in the human gut.
  5. T/F: E. coli O157 stays in the gut but the toxin gets into the blood.
  6. What are the complications of this infection?
A
  1. Infection from e.g. contaminated meat or person-to-person spread (low inoculum so require small no. of organisms to infect another person).
  2. Frequent bloody stools, prominent abdominal pain
  3. Shiga toxin (also produced by shigella species) (aka verocyto-toxin)
  4. False. It is not usually found in the gut.
  5. True.
  6. In children <5, immunocompromised, and elderly toxin can cause haemolytic-uraemic (HUS) syndrome.
18
Q

Haemolytic-uraemic syndrome (HUS):

  1. What are the symptoms of it?
  2. What is it characterised by?
  3. How is it treated?
  4. Why are antibiotics or anti-diarrhoeal drugs not given?
A
  1. Abdominal pain, bloody diarrhoea, fever, seizures, lethargy.
  2. Characterised by renal failure, microangiopathic haemolytic anaemia (presence of schistocytes on microscopy of blood film) and thrombocytopenia (low platelet count as the toxin activates platelets leading micro-angiopathy).
  3. Treatment is supportive (e.g. dialysis), plasmapheresis/IVIG (removal, treatment, and return or exchange of blood plasma/components from and to the blood circulation).
  4. Antibiotics can destroy the bacteria therefore releasing even more toxins which can predisposes/worsens HUS.
    Anti-diarrhoea drugs e.g. loperamide (Imodium) are not recommended as they may prolong exposure to the toxin.
19
Q

When are antibiotics indicated for gastroenteritis?

A

Indicated in gastroenteritis for:

  • immunocompromised
  • severe sepsis or invasive infection
  • chronic illness e.g. malignancy

Not indicated for healthy patient with non-invasive infection.

20
Q

How long does the routine bacterial culture take and how is it done?

A

Takes 3 days to complete all tests.

Selective and enrichment methods of culture necessary - variety of media (broth, agar plates) and incubation conditions.

21
Q

Campylobacter:

  1. What are two main species causing infections?
  2. What is the source of the infection?
  3. T/F: causes isolated causes rather than outbreaks.
  4. How is it grown in the lab?
A
  1. C. jejuni (90%)/ C. coli (9%)
  2. Chickens, contaminated milk, puppies
  3. True
  4. Specialised culture conditions (temp >37, grows at low O2 levels (5%).
22
Q

What is the commonest cause of bacterial food poisoning in UK?

A

Campylobacter

23
Q

Salmonella:

  1. Name 2 species of salmonella.
  2. How is it isolated in the lab?
  3. Which isolates cause commonest salmonella infections in the UK?
  4. T/F: S. typhi and S. paratyphi cause gastro-enteritis.
A
  1. Salmonella enterica, Salmonella bongori (both contain thousands of serotypes).
  2. Screened by growing it on agar with lactose - it doesn’t ferment it so agar stays beige colour. And then serotyping antigen and biochemical tests are performed.
  3. Salmonella enteritidis and Salmonella typhimurium (both subspecies of S. enterica). >50% of these imported from abroad.
  4. False. S. typhi and S. paratyphi cause enteric fever (typhoid and paratyphoid) and not gastro-enteritis.
24
Q
  1. Out of the 4 species of Shigella, which causes outbreaks in nurseries?
  2. Which other bacteria is closely genetically related to?
A
  1. Shigella sonnei

2. E. coli

25
Q

E. coli:

  1. Which one’s cause diarrhoea?
  2. How is it tested in the lab?
A
  1. Enterohaemorrhagic E. coli (E. coli O157), enterotoxigenic E. coli (traveller’s diarrhoea), enteroinvasive E. coli (doesn’t use toxins but destroys intestinal wall through adhesions etc.,
    enteropathogenic E. coli
  2. Routine diagnosis of these E. coli strains not possible – only O157 is easily distinguished from “ordinary” E. coli. Unlike other E. coli species only O157 slowly or not at all ferments D-sorbitol. So use MacConkey agar with 1% sorbitol (Sorbitol-negative colonies will appear colourless - biochemical tests are performed on these)
26
Q

Name some bacteria that occasionally causes food poisoning outbreaks.

A
  • Staph aureus (toxin)
  • Bacillus cereus (re-fried rice)
  • Clostridium perfringens (toxin) (undercooked meat/cooked food left out - toxin accumulates in spore formation)
27
Q

Clostridioides difficile diarrhoea:

  1. Patient usually gives history of which previous antibiotic treatment?
  2. How severe is it?
  3. Which toxins does it produce?
  4. How is it prevented?
A
  1. 4C’s (cephalosporins, co-amoxiclav, clindamycin, ciprofloxacin).
  2. Severity ranges from mild diarrhoea to severe colitis
  3. Produces enterotoxin (A) and cytotoxin (B) (inflammatory)
  4. Reduction in broad spectrum antibiotic prescribing (avoid 4C’s).
    - Antimicrobial Management Team (AMT) (consisting of consultants, nurses etc.) and local antibiotic policy – trying to reduce prescription of broad spec antibiotics.
    - Isolate symptomatic patients
    - Wash hands between patients (as alcohol gel doesn’t prevent c. diff transmission)
28
Q

How is C. diff infection managed?

A
  • Stop precipitating antibiotic (if possible)
  • Follow published treatment algorithm – oral metronidazole if no severity markers e.g. raised temp > 38.5, WCC >15, acute rising creatinine, suspicion of colitis/ileus/ toxic megacolon
  • Oral vancomycin if 2 or more severity markers
  • Fidaxomicin (if recurring infections with C. diff)
  • Stool transplants
  • Surgery may be required if severe
    NB: Vancomycin is normally not given orally as <10% absorbed systemically however, in this situation we need vancomycin to stay in the gut so it can treat c. diff infection.
29
Q 
Parasitology: 
If parasites (protozoa and helminths (worms)) are thought to cause the gastroenteritis or diarrhoea, how would you diagnose it?
A

Diagnosis generally by microscopy

Send stool with request “parasites, cysts and ova please” or P, C and O

30
Q

Name main UK and imported parasites causing infections.

A

UK parasites (protozoa): Giardia lamblia (aka G. duodenalis/intestinalis) and Cryptosporidium parvum.

Imported parasite (protozoa): Entamoeba histolytica

31
Q

Giardiasis:

  1. How does it present?
  2. What is the source of infection?
  3. What forms does it exist in?
  4. How is it diagnosed?
  5. How is it treated?
A
  1. abdominal cramps, bloating, nausea and bouts of watery diarrhoea, in kids malabsorption and failure to thrive.
  2. contaminated water
  3. Exists in cyst and trophozoite form. Cyst form = infectious, and it transforms into trophozoite form in the host. Trophozoite replicates within the gut and as they continue along the GIT, they convert back to their cyst form which are then excreted with faeces.
  4. Cysts - intermittent on stool microscopy
    - trophozoites –normally not identified in stool (as cannot survive for long outside host) unless diarrhoea specimen, duodenal biopsy or “string test” (gelatin capsule on absorbent string – swallowed and withdrawn)
  5. treat with metronidazole
32
Q

Cryptosporidium parvum:

  1. How does the infection present?
  2. What is the source of infection?
  3. What forms does it exist in?
  4. How is it diagnosed?
  5. How is it treated?
A
  1. Cryptosporidiosis – watery diarrhoea, nausea and vomiting, abdominal cramps, low grade fever.
  2. ingestion of oocysts in faecally contaminated water.
  3. Two forms: oocysts form (can survive in very tough conditions), trophozoites
  4. oocysts stool specimen seen on microscopy. faecal ELISA can detect the parasite as well.
  5. no specific treatment usually required just rehydration. Difficult to get rid of in immunocompromised, can try nitazoxanide (broad spectrum anti-parasitic and antiviral drug)
33
Q

Entamoeba histolytica:

  1. How does the infection present?
  2. What is the source of infection?
  3. What forms does it exist in?
  4. How is it diagnosed?
  5. How is it treated?
  6. What is the long-term complication of this infection?
A
  1. Asymptomatic = majority. Some get amoebic dysentery (severe diarrhoea with blood or milder chronic symptoms of: frequent loose stools, abdo pain.
  2. Through ingestion of contaminated water or food, or E. histolytica cysts (eggs) picked up from contaminated surfaces or fingers.
  3. cyst form, trophozoite form
  4. microscopic examination for trophozoites (symptomatic patient) “hot stool”; cysts (asymptomatic patient) seen in stools
  5. treat with metronidazole (trophozoites); then give diloxanide furoate to remove cysts in intestine
  6. Disseminated, extra intestinal disease: amoebic liver abscess may be long term complication (“anchovy pus”) – trophozoites multiply in liver cells.
34
Q

Name main viruses causing viral diarrhoea.

A
  1. Rotavirus (children <5): vaccine in 2013 given at 8 and 12 weeks. Common in winter.
  2. Adenovirus: certain strains (40/41).
  3. Norovirus (aka winter vomiting disease)
35
Q

How are rotavirus and adenoviruses diagnosed?

A

diagnosis of both possible by antigen detection – rapid test

36
Q

Noroviruses:

  1. What are the symptoms?
  2. T/F: common cause of outbreaks in hospital, community, cruise ships.
  3. T/F: it is very infectious.
  4. How is it diagnosed?
A
  1. Diarrhoea and vomiting
  2. True. Ward closures common – staff and patients affected. Strict infection control measures needed – alcohol gel not effective measure; isolation of patients suspected with norovirus.
  3. True. infectious dose only 18 virus particles (1g faeces may shed 5 billion infectious doses)
  4. Diagnosis by PCR

Year 3 Infections (4 decks)

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