KG, a 42-year-old Indian male, presented in 1995 with abdominal pain exacerbated by eating, anorexia, and weight loss. He had travelled to India 5 years previously, and he was known to have beta thalassaemia trait. There was no history of fevers or diarrhoea. He remained afebrile during his inpatient stay. Gastroscopy, colonoscopy, small bowel meal, and barium enema were normal. Early morning urine samples, and Mantoux test, did not demonstrate evidence of tuberculosis. Furthermore, bone marrow biopsy showed leukopenia and thrombocytosis, with no organisms present on culture. His initial blood tests confirmed a thrombocytosis with a platelet count of 645 x 109/L. His haemoglobin was 12.0 g/dL, and his ESR was elevated at 64 mm/hr.
In our experience, the diagnosis of tuberculous enteritis frequently remains challenging despite the investigations described above. Several authorities recommend initiating antituberculous therapy if there is a strong clinical suspicion of tuberculosis despite nondiagnostic histological or bacteriological studies. Whilst laparoscopy and mesenteric sampling have a higher sensitivity, these patients frequently respond rapidly to medical therapy and, thus, laparoscopy is usually considered if improvement is not seen after two weeks. In this case, due to the patient's marked systemic inflammation, Indian origin, and lack of evidence for alternative diagnoses such as lymphoma or inflammatory bowel disease, he was commenced on empirical antituberculous treatment with rifampicin, isoniazid, ethambutol, and pyrazinamide. He gained weight rapidly, and his blood tests returned to normal. He received eight and a half months of treatment.
He relapsed the following year with abdominal pain, vomiting, and fever. CT of the abdomen demonstrated an abnormal terminal ileum and caecum, suggestive of tuberculosis, inflammatory bowel disease, or lymphoma. A small bowel meal confirmed an irregular thickening in the terminal ileum. However bone marrow aspirate and peripheral cultures proved unremarkable, with no evidence of mycobacteria. A diagnostic laparoscopy was recommended, but the patient declined this procedure. A further course of antituberculous therapy with the same regimen again provided a dramatic therapeutic response. He received a year of treatment. 
Five years later, a further recurrence of symptoms occurred. He was worked up in an identical fashion with colonoscopy, abdominal CT, and barium meal and follow-through. The only positive finding was on CT, which demonstrated a featureless terminal ileum, despite the wall being of normal thickness with no fat stranding. On this occasion the patient again declined diagnostic laparoscopy. Again, he responded to empirical antituberculous therapy, although a laparoscopy was not performed. A further three years later, he again presented with a recurrence of his symptoms, CT showed thickening of the terminal ileum (Figure 1), and colonoscopy demonstrated multiple erosions in the terminal ileum (Figure 2). Biopsies did not demonstrate granulomata but highlighted patchy acute and chronic inflammation with inflammatory cell infiltrate consistent with Crohn's disease. Prolonged microbiological culture of ileal specimens was also negative. On this occasion, a course of steroids for Crohn's disease was prescribed and, again, he made a dramatic recovery.