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BMJ Case Rep. 2010; 2010: bcr1020092365.
Published online Apr 9, 2010. doi:  10.1136/bcr.10.2009.2365
PMCID: PMC3047486
Unusual presentation of more common disease/injury
Campylobacter jejuni cholecystitis: a rare but significant clinical entity
Peter G Vaughan-Shaw,1 Jonathan Richard Rees,2 Diana White,3 and Phillip Burgess4
1Salisbury District Hospital, Surgery, Odstock Road, Salisbury, Wiltshire, SP2 8BJ, UK
2Cheltenham District Hospital, Vascular Surgery, Sandford Road, Cheltenham, GL53 7AN, UK
3Great Western Road, Clinical Microbiology, Marlborough Road, Swindon, Wiltshire, SN3 6BB, UK
4Great Western Hospital, Colorectal Surgery, Marlborough Road, Swindon, Wiltshire, SN3 6BB, UK
Correspondence to Jonathan Richard Rees, j.r.e.rees/at/
Cholecystitis caused by Campylobacter is rare with only 14 cases found in the literature. This case describes a 71-year-old man who presented with right hypochondrial abdominal pain due to a gangrenous gallbladder identified at laparotomy. Culture of a bile sample identified a slow-growing gram-negative bacterium identified as Campylobacter jejuni. After a poor clinical response, this identification allowed targeted antibiotic treatment resulting in a slow but successful recovery and discharge 17 days postoperatively. This case demonstrates the importance of considering rare organisms in severe acute cholecystitis and ensuring appropriate cultures are performed, particularly in those who fail to respond to initial antimicrobial treatment.
Gallstones are one of the commonest disorders of the gastrointestinal system with nearly a quarter of women and 12% of men being noted to have gallstones in post-mortem studies.1 Altogether, 10–30% of individuals are symptomatic2 and, at the time of assessment, 12% have gallstones identified within the common bile duct or common hepatic ducts—a finding known as choledocholithiasis.3
Obstruction of the cystic duct by gallstones or biliary sludge can frequently occur and results in an acute inflammatory response. This is followed by secondary infection typically caused by Escherichia coli, Klebsiella or Streptococcus faecalis.1,4 This paper reports a case of acute cholecystitis due to Campylobacter jejuni. The Campylobacter spp. are rarely described as a cause of acute cholecystitis and more usually cause gastroenteritis and septicaemia. The literature describes just 14 cases in the last 30 years.517
A 71-year-old man presented to the emergency department at our institution with a 1 day history of epigastric and right hypochondrial abdominal pain. The pain was associated with a single episode of dark coloured vomit with one episode of black liquid stool but no rectal bleeding or haematemesis. There was no preceding change in bowel habit noted, no contact with sick people, no exposure to farm animals nor recent foreign travel. His previous medical history included hypertension, diverticular disease, ischaemic heart disease, arthritis and a laparotomy 20 years previously for peptic ulcer disease. The patient’s temperature was 37.9°C yet he was haemodynamically stable with a blood pressure of 119/53 mmHg and heart rate of 86 bpm. Cardiovascular and respiratory examinations were normal. Abdominal examination revealed severe right upper quadrant tenderness with associated percussion tenderness and guarding, abdominal distension and reduced bowel sounds.
Laboratory investigations identified a marked neutrophilia of 20.7×109/l together with a raised C-reactive protein (321 mg/l), raised urea (10.6 mmol/l) and a raised creatinine (138 μmol/l). The liver function tests were also abnormal with an aspartate transaminase of 131 U/l, a gamma glutamyl transferase of 79 U/l and a bilirubin of 35 μmol/l. Abdominal radiography showed a small number of gas-filled small bowel loops but no evidence of small bowel obstruction. In addition, no free sub-diaphragmatic gas was seen on an erect chest radiograph.
Differential diagnosis
The differential diagnosis included perforated duodenal ulcer with septic shock or severe non-responding cholecystitis +/− gallbladder perforation (without radiographic evidence of pneumo-peritoneum).
The patient was placed nil by mouth, a urinary catheter inserted and intra-venous fluids and oral and intravenous analgesia administered. However, clinical deterioration subsequently occurred, demonstrated by a reduction in blood pressure to 80/50 mmHg, an increased respiratory rate of 30 breaths a minute and a reduction in urine output to less than 5 mls/h. Given the differential diagnosis, the previous history of abdominal surgery and clinical deterioration it was decided to proceed to laparotomy. This revealed dense adhesions from the previous intra-abdominal surgery and in the right upper quadrant the gallbladder was found to be gangrenous. Adhesions were divided, a subtotal cholecystectomy was performed and the gallbladder drained using a Foley catheter as a cholecystostomy. Two Robinsons’ drains (Meddis Limited, Selby, UK) were laid and the stomach decompressed with a nasogastric tube. A sample of the bile drained during surgery was sent for culture. This was processed following UK Health Protection Agency (HPA) guidelines ( for the investigation of bile. Intravenous cefuroxime (750 mg) and metronidazole (500 mg) were administered at induction of anaesthesia and continued three times per day postoperatively as per hospital protocol for acute intra-abdominal and biliary sepsis.
Postoperatively, the gentleman was admitted to the intensive care unit (ICU). On day 3, postoperatively prolonged (72 h) microbiological culture of bile identified a slow-growing gram-negative bacterium. In view of this finding, clinical microbiological advice recommended a change to co-amoxiclav and ciprofloxacin, and a specific Campylobacter culture was set up. After 48 hours, Campylobacter growth, later identified as subtype C jejuni, was confirmed. (typed by the Campylobacter Reference Laboratory, Laboratory of Enteric Pathogens, Central Public Health Laboratory, London, UK.) The growth of Campylobacter resulted in a further change to the antibiotic treatment regime to cefotaxime (750 mg three times daily), gentamicin (5 mg/kg once daily) and metronidazole (500 mg three times daily) on microbiological advice. Blood cultures did not grow Campylobacter.
A good clinical response was achieved and the patient was discharged from the ICU on the fifth postoperative day. Inflammatory makers normalised and a cholangiogram performed on the the 15th post-operative day showed prompt passage of contrast through the cystic duct, common bile duct and into the duodenum without filling defects. The patient was discharged 17 days after surgery and remained well 4 weeks later on review in the outpatient department.
Campylobacter 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.22 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 infections;22 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
C jejuni is rarely implicated in cholecystitis with only 14 worldwide cases described in the literature517 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 cholecystitis.
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.
Learning points
  • 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.
Thanks to Denise Wright, Biomedical Scientist, Great Western Hospital, Swindon, UK; for the initial identification of the organism in this case.
Competing interests: None.
Patient consent: Patient/guardian consent was obtained for publication.
1. Godrey PJ, Bates T, Harrison M, et al. Gall stones and mortality: a study of all gall stone related deaths in a single health district. Gut 1984; 25: 1029–33. [PMC free article] [PubMed]
2. McSherry CK, Ferstenberg H, Calhoun WF, et al. The natural history of diagnosed gallstone disease in symptomatic and asymptomatic patients. Ann Surg 1985; 202: 59–63. [PubMed]
3. Motson R. Operative cholangiography. In: Motson RW, editor. , ed. Retained common duct stones Prevention and treatment. London: Grune and Stratton, 1985: 8–9.
4. Indar AA, Beckingham IJ. Acute cholecystitis. BMJ 2002. September 21; 325: 639–43. [PMC free article] [PubMed]
5. Dakdouki GK, Araj GF, Hussein M. Campylobacter jejuni: unusual cause of cholecystitis with lithiasis. Case report and literature review. Clin Microbiol Infect 2003; 9: 970–2. [PubMed]
6. Mertens A, De Smet M. Campylobacter cholecystitis. Lancet 1979. May 19; 1: 1092–3. [PubMed]
7. Darling WM, Peel RN, Skirrow MB, et al. Campylobacter cholecystitis. Lancet 1979; 1: 1302. [PubMed]
8. Pereira Mde S, Lipton SD, Kim JK. Acute cholecystitis and campylobacter fetus. Ann Intern Med 1981; 94: 821. [PubMed]
9. Costel EE, Wheeler AP, Gregg CR. Campylobacter fetus ssp fetus cholecystitis and relapsing bacteremia in a patient with acquired immunodeficiency syndrome. South Med J 1984; 77: 927–8. [PubMed]
10. Wheeler AP, Gregg CR. Campylobacter bacteremia, cholecystitis, and the acquired immunodeficiency syndrome. Ann Intern Med 1986; 105: 804. [PubMed]
11. Verbruggen P, Creve U, Hubens A, et al. Campylobacter fetus as a cause of acute cholecystitis. Br J Surg 1986; 73: 46. [PubMed]
12. Gerritsen van der Hoop A, Veringa EM. Cholecystitis caused by Campylobacter jejuni. Clin Infect Dis 1993; 17: 133. [PubMed]
13. Taziaux P, Wahlen C, Drion S. [An unusual cause of non-lithiasic acute cholecystitis: campylobacter jejuni]. J Chir (Paris) 1991; 128: 554–5. [PubMed]
14. Drion S, Wahlen C, Taziaux P. Isolation of Campylobacter jejuni from the bile of a cholecystic patient. J Clin Microbiol 1988; 26: 2193–4. [PMC free article] [PubMed]
15. Lepe JA, Guadalajara J. [Acute cholecystitis caused by Campylobacter jejuni]. Enferm Infecc Microbiol Clin 1994; 12: 364–5. [PubMed]
16. Landau Z, Agmon NL, Argas D, et al. Acute cholecystitis caused by Campylobacter jejuni. Isr J Med Sci 1995; 31: 696–7. [PubMed]
17. Takatsu M, Ichiyama S, Nada T, et al. Campylobacter fetus subsp. fetus cholecystitis in a patient with advanced hepatocellular carcinoma. Scand J Infect Dis 1997; 29: 197–8. [PubMed]
18. Smibert R. Genuc campylobacter. : Krieg NR HH, editor. , ed. Baltimore: The Williams & Wilkins Co., 1984.
19. Tauxe R. Epidemiology of campylobacter jejuni infection in the United States. : Nachamkin IB, MJ, Tompkins L, editors. , eds. Washington DC: American Society of Microbiology, 1992.
20. Atabay HI, Corry JE. The prevalence of campylobacters and arcobacters in broiler chickens. J Appl Microbiol 1997; 83: 619–26. [PubMed]
21. Blaser MJ, Taylor DN, Feldman RA. Epidemiology of Campylobacter jejuni infections. Epidemiol Rev 1983; 5: 157–76. [PubMed]
22. Wang WL, Blaser MJ. Detection of pathogenic Campylobacter species in blood culture systems. J Clin Microbiol 1986; 23: 709–14. [PMC free article] [PubMed]
23. Blaser MJ, Hardesty HL, Powers B, et al. Survival of Campylobacter fetus subsp. jejuni in biological milieus. J Clin Microbiol 1980; 11: 309–13. [PMC free article] [PubMed]
24. King O. The laboratory recognition of Vibrio fetus and closely related Vibrio species isolated from cases of human vibriosis. Annals of the New York Academy of Science 1962; 98: 700–11.
25. Blaser MJ. Campylobacter jejuni and related species. Mandell GL, Bennett JE, FDolin R, editors. , eds. Philadelphia, PA: Churchill Livingstone, 2004.
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