Bacterial gastroenteritis Flashcards
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
Enteropathogenic
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.