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Flashcards in Bacterial gastroenteritis Deck (11):

Campylobacter jejuni

Most common cause of acute infective diarrhoea

Spiral, gram negative rods

Usually infects caecum and terminal ileum. Local lymphadenopathy is common

May mimic appendicitis as it has marked right iliac fossa pain

Reactive arthritis is seen in 1-2% of cases


Shigella spp.

Members of the enterobacteriaceae

Gram negative bacilli

Clinically causes dysentery

Shigella soneii is the commonest infective organism (mild illness)

Usually self limiting, ciprofloxacin may be required if individual is in a high risk group


Salmonella spp

Facultatively anaerobic, gram negative, enterobacteriaceae

Infective dose varies according to subtype

Salmonellosis: usually transmitted by infected meat (especially poultry) and eggs


E. coli


Enteroinvasive: dysentery, large bowel necrosis/ulcers

Enterotoxigenic: small intestine, travelers diarrhoea

Enterohaemorrhagic: 0157, cause a haemorrhagic colitis, haemolytic uraemic syndrome and thrombotic thrombocytopaenic purpura


Yersinia enterocolitica

Gram negative, coccobacilli

Typically produces a protracted terminal ileitis that may mimic
Crohns disease

Differential diagnosis acute appendicitis

May progress to septicaemia in susceptible individuals

Usually sensitive to quinolone or tetracyclines


Vibrio cholera

Short, gram negative rods

Transmitted by contaminated water, seafood

Symptoms include sudden onset of effortless vomiting and profuse watery diarrhoea

Correction of fluid and electrolyte losses are the mainstay of treatment

Most cases will resolve, antibiotics are not generally indicated


Staphylococcus aureus

Facultative anaerobe

Gram-positive coccus

Haemolysis on blood agar plates

Catalase positive
20% population are long term carriers

Exo and entero toxin may result in toxic shock syndrome and gastroenteritis respectively

Ideally treated with penicillin although many strains now resistant through beta-lactamase production.

In the UK less than 5% of isolates are sensitive to penicillin.

Resistance to methicillin (and other antibiotics) is mediated by the mec operon, essentially penicillin binding protein is altered and resistance to this class of antibiotics ensues

Common cause of cutaneous infections and abscesses


Streptococcus pyogenes

Gram-positive, forms chain like colonies, Lancefield Group A Streptococcus
Produces beta haemolysis on blood agar plates

Rarely part of normal skin microflora

Catalase negative
Releases a number of proteins/ virulence factors into host including hyaluronidase, streptokinase which allow rapid tissue destruction

Releases superantigens such as pyogenic exotoxin A which results in scarlet fever

Remains sensitive to penicillin, macrolides may be used as an alternative.


Escherichia coli

Gram-negative rod
Facultative anaerobe, non-sporing

Wide range of subtypes and some are normal gut commensals

Some subtypes such as 0157 may produce lethal toxins resulting in haemolytic-uraemic syndrome

Enterotoxigenic E-Coli produces an enterotoxin (ST enterotoxin) that results in large volume fluid secretion into the gut lumen (Via cAMP activation)

Enteropathogenic E-Coli binds to intestinal cells and cause structural damage, this coupled with a moderate (or in the case of enteroinvasive E-Coli significant) invasive component produces enteritis and large volume diarrhoea together with fever.

They are resistant to many antibiotics used to treat gram positive infections and acquire resistance rapidly and are recognised as producing beta-lactamases


Campylobacter jejuni

Curved, Gram-negative, non-sporulating bacteria

One of the commonest causes of diarrhoea worldwide

Produces enteritis which is often diffuse and blood may be passed

Remains a differential for right iliac fossa pain with diarrhoea

Self-limiting infection so antibiotics are not usually advised.

However, the quinolones are often rapidly effective.


Helicobacter pylori

Gram-negative, helix-shaped rod, microaerophilic

Produces hydrogenase that can derive energy from hydrogen released by intestinal bacteria

Flagellated and mobile
Those carrying the cag A gene may cause ulcers

It secretes urease that breaks down gastric urea> Carbon dioxide and ammonia> ammonium>bicarbonate (simplified!) The bicarbonate can neutralise the gastric acid.

Usually, colonises the gastric antrum and irritates resulting in increased gastrin release and higher levels of gastric acid. These patients will develop duodenal ulcers. In those with more diffuse H-Pylori infection, gastric acid levels are lower and ulcers develop by local tissue damage from H-Pylori- these patients get gastric ulcers.

Diagnosis may be made by serology (approx. 75% sensitive).

Biopsy urease test during endoscopy probably the most sensitive.

In patients who are colonised 10-20% risk of peptic ulcer, 1-2% risk gastric cancer, <1% risk MALT lymphoma.