LESSONS FROM PRACTICE LESSONS FROM PRACTICE Cyclospora infection masquerading as coeliac disease

THIS CASE OF PROTRACTED diarrhoea in an Australian traveller initially appeared consistent with coeliac disease. Further analysis revealed infection with Cyclospora cayetanensis, which was successfully treated with antibiotics. The increasing number of documented outbreaks of Cyclospora infection,1 and the need for special preparation of stool samples for their detection,2 highlight the importance of a high degree of suspicion in cases of traveller’s diarrhoea. C. cayetanensis is a protozoan which was first recognised as a human intestinal parasite in the early 1990s.3 In 1994, Butcher et al described the first case in an Australian traveller of explosive diarrhoea caused by a large acid-fast spherical organism that had only recently been classified as a member of the genus Cyclospora.4 Since then, reports of outbreaks of Cyclospora infection have increased,1 presumably due to greater awareness of this parasite. Outbreaks have been reported from many parts of the world, including North, Central and South America, Europe, South East Asia, India, South Africa, and the Caribbean Islands.5,6 The mode of transmission is thought to be faecal–oral, or via ingestion of contaminated water. The mechanism by which the protozoan causes villous atrophy is not well understood, but organisms have been found at the site of inflammatory changes. Like Cryptosporidium spp. (which are morphologically similar [Figure 2]), Cyclospora spp. cause nausea, profuse diarrhoea and weight loss, as well as profound fatigue. Abdominal pain and bloating can manifest as “indigestion” or “heartburn”. If untreated, symptoms last for 6 weeks to 3 months (longer in the immunocompromised), and can be mistaken for irritable-bowel syndrome. The treatment of choice is trimethoprim–sulfamethoxazole, with ongoing prophylaxis for patients with AIDS.7 Clinicians need to be aware that the histopathological appearance of the small intestine in C. cayetanensis infection culture and testing for enteric viruses, all of which gave negative results. Routine blood tests showed mild iron deficiency with no anaemia. Serum levels of vitamin B12 and folate were in the reference ranges. Serological testing for Toxoplasma and Cytomegalovirus showed no evidence of recent infection. An initial course of metronidazole for presumed Giardia infection was unhelpful, and she was referred for further gastroenterological evaluation.