Campylobacter causes acute gastrointestinal illness (AGI) in millions of people internationally every year. In Ireland, 2,230 cases of Campylobacter infection were reported in 2013 with an annual incidence rate of 52 cases per 100,000 of the population.^1,2 The actual or real incidence is likely to be much higher because many cases go unreported. Most cases of infection are thought to result from handling raw poultry or eating undercooked poultry meat.

Campylobacteriosis is an infectious disease caused by Campylobacter spp. and those who become infected get diarrhoea, abdominal pain and fever within two to five days after exposure to the bacteria. It usually lasts about seven days. Most of the patients recover completely in a few days but some can develop long-term consequences such as Guillain-Barré syndrome (GBS) in one in 1,000 cases, reactive arthritis (ReA) or Reiter’s syndrome (RS), post-infectious irritable bowel syndrome (IBS), inflammatory bowel disease (IBD) and haemolytic uraemic syndrome.³

Haemolytic uraemic syndrome (HUS) is characterised by a triad of acute renal failure, microangiopathic haemolytic anaemia, and thrombocytopaenia. It was first described in 1955,⁴ and found to be secondary to Escherichia coli infection in 1982.⁵ HUS is the most common cause of renal failure in infants and young children.

HUS had been divided into diarrhoea-positive and diarrhoea-negative HUS. The former, also referred to as typical HUS⁶, primarily resulted from Shiga toxin-producing E. coli infections (Stx HUS), and it accounts for about 90% of the cases. It is more common in children who are younger than five years. All other causes of HUS or non-Stx HUS are referred to as atypical HUS or assigned to the diarrhoea-negative HUS, even though some patients with non-Stx HUS also presented with diarrhoea.⁷

Case report

A 22-year-old male was admitted with a five-day history of diarrhoea. The diarrhoea was watery, but he had one episode of bloody diarrhoea. He was going to the bathroom at least five times a day. He started to develop fever and twitching of his calf muscles and feeling weak over the next few days. He denied recent travel and the remainder of his history was unremarkable, (apart from smoking 20 cigarettes and drinking about 70 units of alcohol a week.)

On admission the patient was afebrile, BP was 90/40mmHg, PR 101/min and he was jaundiced and no evidence of purpura. His abdomen was soft and no evidence of splenomegaly elicited on examination. Cardiovascular, respiratory and CNS exams were all normal. His urine was positive for blood.

The haemoglobin was 9.1g/dl and dropped to 7.9g/dl next day, MCV 84fl, haematocrit 0.25l/l, platelet count was 31 *10^9/l, WCC count was 9.4 *10^9/l (neutrophils 7.86, lymphocytes 0.66). His urea was 33mmol/l, creatinine 497umol/l, sodium 131mmol/l, potassium 3.2mmol/l. Prothrombin time was 17.4 seconds with INR of 1.7. Lactate dehydrogenase was 305U/l (the normal range is 10-250U/l). Blood film showed schistocytes. Stool sample obtained on the second day of admission was positive for Campylobacter jejuni and negative for vero-toxigenic E. coli. He developed fever on the second day of admission and blood culture taken was negative for bacteria.

His ALT was 57U/l (5-41), total bilirubin is 54.1umol/l (2-21), hepatitis screen was negative, autoantibody screen was all negative apart from weakly positive anti nuclear AB. He had an abdominal ultrasound and it didn’t show any liver abnormality to explain his deranged liver function test.

The patient was treated with IV fluids, and started on the third day of admission on meropenem 1g tid iv after discussing the case with the microbiology consultant. He began to improve on the fourth day of admission and the diarrhoea stopped and he was discharged home six days after admission with normal renal function, platelets and haemoglobin.

Discussion

Haemolytic uraemic syndrome is a rare condition but has a significant morbidity and mortality. For Stx-HUS, about 70-85% will have a complete recovery of renal function. Patients with non-Stx-HUS have a poor prognosis, with up to 50% progressing to end-stage renal disease (ESRD) or irreversible brain damage, with 25% of patients dying during the acute phase.

Campylobacter-associated haemolytic uraemic syndrome is very rare with just a few cases reported since the first reported case in 1982. This case could be the first to be reported in Ireland. Our patient had D+HUS because his condition started with diarrhoea and then developed acute renal failure, haemolytic anaemia confirmed by low haemoglobin and schistocytes in his blood film and thrombocytopaenia with platelets 31 *10^9/l. Campylobacter jejuni was isolated from his stool and no other causative agent was detected and the stool culture was negative for STEC.

In the medical literature Campylobacter spp. can cause haemolytic uraemic syndrome but very few cases have been reported in the past 30 years. The prognosis of HUS after campylobacter infection is unknown. It is important to give more attention to the association between HUS and campylobacter infection as it may lead to serious complications.

References

1. HSE. Statutory Notifications of Infectious Diseases reported in Ireland via the Computerised Infectious Disease Reporting (CIDR) system. Ireland: HSE; 2014
2. Food Safety Authority of Ireland. Campylobacter. http://www.fsai.ie (Accessed 17/12/2014)
3. Buzby J, Roberts T, Jordan Lin T, MacDonald J. Bacterial Foodborne Disease: Medical Costs and Productivity Losses. US: USDA Economic Research Service; 1996 August. p93 report no: (AER-741)
4. Gasser C, Gautier E, Steck A, Oechslin R. Hemolytic-uremic syndrome: bilateral necrosis of the renal cortex in acute acquired hemolytic anemia. Schweiz Med Wochenschr 1955, September 20; 85(38-39):905-909
5. Chamovitz BN, Hartstein AI, Alexander SR, Terry AB, Short P and Katon R. Campylobacter jejuni Hemoltic-uremic syndrome 1983; 71(2): 253
6. Taylor C, Machin S, Wigmore S, Goodship T. Clinical Practice Guidelines for the management of Atypical Haemolytic Uraemic Syndrome in the United Kingdom. United Kingdom: Renal Association, the British Committee for Standards in Haematology and the British Transplantation Society; 2009
7. Kaplan BS, Meyers KE, Schulman SL. The pathogenesis and treatment of hemolytic uremic syndrome. J Am Soc Nephrol 1998; 9(6):1126