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Intestinal tuberculosis and schistosomiasis presenting like Crohn's disease

A diagnosis of Crohn’s disease (CD) in a migrant from a tuberculosis endemic region is often difficult to make. This is further complicated by a resurgence of tuberculosis (TB) worldwide. The epidemiology of CD is also changing, with increasing incidences in the Asian Pacific region, India, Eastern Europe and South Africa. A migrant from the Asian Pacific region is also at risk of contracting schistosomiasis – caused by parasitic blood flukes known as schistosomes. Crohn’s disease, intestinal TB (iTB) and chronic schistosomiasis are all chronic granulomatous conditions. Therefore, diagnosis in a migrant from an endemic region requires careful interpretation of clinical history and signs as well as histopathological assessment. In this report, we describe a case with delayed diagnosis of intestinal TB with chronic schistosomiasis, and an initial presentation and histology similar to that of CD. A 52-year-old Laotian woman immigrated to Australia in 1980. Since living in Australia, the patient still had regular travel to south-east Asia and China. She initially presented to a gastroenterologist in March 2004 with 1-week history of fresh per-rectal bleeding and right flank pain. She did not display any of the typical constitutional symptoms of TB. She denied any respiratory symptoms. Her weight was stable and her appetite was normal. There was no nausea or vomiting observed. The only significant medical history was of hypertension controlled with antihypertensives. She did not have any known TB contacts or any previous Bacillus CalmetteGuérin vaccination. Chest X-ray was normal. Colonoscopic biopsy demonstrated colonic mucosal ulceration in her caecum and ascending colon (Fig. 1, left). Acid Fast Bacilli was not seen on the Ziehl-Neelsen stain. Given the clinical and histopathological findings, a diagnosis of CD was made and salazopyrin was commenced. Three monthly progress colonoscopies were performed till June 2005. These showed gradual resolution of the mucosal ulcerations. Colonic biopsies showed occasional cryptitis and remaining epithelioid granulomas. In June 2007, the patient returned for repeat colonoscopy. She was asymptomatic with no per rectal bleeding, weight loss, fever or night sweats. Her vital signs were normal. On colonoscopy, polypoid lesions and ulcers were seen in the caecum, ascending and transverse colon. Histopathology reported presence of multiple schistosome ova. Focally suppurative granulomatous inflammation was also seen (Figs 2 and 1, right). The schistosome ova were non-viable and calcified suggesting an old infection, and the granulomatous inflammation was not centred on the schistosome ova. One course of praziquantel was given for schistosomiasis. Retrospective review of histopathology for 2004 revealed presence of calcified schistosome ova. TB culture and polymerase chain reaction (PCR) eventually returned positive for Mycobacterium tuberculosis. Anti-Tb treatment consisting of isoniazid, rifampicin, pyrazinamide and ethambutol was commenced. After 6 months of therapy, ethambutol and pyrazinamide were ceased and isoniazid and rifampicin were continued. After 9 months of treatment, colonoscopy was performed and a small rectal polyp was noted. No mucosal ulceration or colonic polyps was seen. Histopathology and TB culture of caecal biopsies returned negative TB growth and negative PCR. At the time of publication, she remains well and due to complete a full 12 months of anti-TB treatment.