spp. are motile non-spore forming gram-negative rods.18 C. jejuni
is the species most commonly associated with enteric infection. In England, Campylobacter
infections now outnumber both Shigella and Salmonella infections combined.19
Meat from infected animals is the commonest source for most human infections as Campylobacter
spp. are common in the gastrointestinal tract of cattle, sheep, swine and fowl. Furthermore, poor slaughter house procedures can amplify contamination.20,21
Consumption of unpasteurised milk, contact with infected household pets or farm animals, and human faecal oral contact may also result in transmission of C jejuni
Once ingested, C jejuni
is susceptible to hydrochloric acid;23
however, larger volumes of milk, fatty foods or water may protect the organism from gastric acid allowing it to reach the bile rich upper small intestine. Here, C jejuni
can multiply rapidly, locally colonise and cause an enteritis manifested by pyrexia, cramping abdominal pain and severe diarrhoea, sometimes blood stained.24
Diagnosis of C jejuni
is typically established by culture on a selective nutrient plate at 42°C in microaerophilic conditions. C jejuni
bacteraemia occurs in less than 1% of C jejuni
therefore, blood cultures often produce no growth. Fluid and electrolyte replacement are essential and antibiotic treatment with ciprofloxacin or erythromycin may be of value in patients with continuing pyrexia, bloody diarrhoea or stool frequency of greater than eight times per day. Most patients recover fully; however, rare complications can include Reiter’s syndrome and Guillain-Barre Syndrome and deaths do occur in the elderly or immunocompromised.25
is rarely implicated in cholecystitis with only 14 worldwide cases described in the literature5–17
and this, unsurprisingly, was the first case in our institution. Our current antibiotic protocol has recently changed in response to national advice to reduce the risk of Clostridium difficile
infection. Local guidelines now recommend that treatment for cholecystitis should include co-amoxiclav with the addition of gentamicin in a severe infection or non-responding infection. Given that Campylobacter
resistance to either of these antibiotics is extremely rare, this new protocol gives good cover against possible Campylobacter
The infrequency of identifying Campylobacter
as a cause for cholecystitis may be due to its rarity as suggested by Darling et al
who searched for Campylobacter
in the bile of 280 patients with cholecystitis and grew Campylobacter species in
none of the samples studied.7
However, because standard HPA advice for the culture of bile does not recommend selective nutrient plate culture at 42°C in microaerophilic conditions, and positive blood cultures are rare, there may be cases occurring when Campylobacter
cholecystitis is missed or under treated.
Given that C jejuni is a possible cause of cholecystitis and C jejuni bacteraemia is rare, we recommend microbiological culture of bile in all patients. Where recovery is slow or risk factors for Campylobacter infection exist, culture conditions should include those selective to this organism.
- Severe cholecystitis can cause gall bladder perforation and may need urgent surgery.
- Campylobacter rarely causes bacteraemia; therefore, microbiological culture of bile is recommended
- Poor response to treatment should precipitate extended culture of bile and extension of the spectrum of antibiotic treatment.