Entamoeba histolytica colitis is a classical inflammatory bowel disease (IBD) mimic. Although early misdiagnosis is common, diagnostic delay for a decade, including prolonged immunosuppressive therapy, is rare.[[1]] Here we report the unusual case of a young patient who was diagnosed with IBD and inadvertently treated with combination immunosuppression. We present several clinical practice points, which are particularly pertinent for those practicing IBD in the developed world, where amoebiasis is non-endemic and risk of misdiagnosis is high.

A previously healthy 32-year-old Caucasian male initially presented in 2009 with an 8-week history of bloody diarrhea and abdominal pain. Travel history was not documented but stool microscopy and culture, and HIV serology were negative. Colonoscopy showed severe ulcerative rectosigmoiditis, histologically consistent with ulcerative colitis. The disease followed an insidious, relapsing-remitting course for several years with partial benefit from topical and oral 5-aminosalicylates.

A colonoscopy triggered by symptom deterioration in 2017 showed severe, discrete, pan-colonic ulceration and reclassification to Crohn’s disease was made based on endoscopic appearances. Histologically, IBD subtype was equivocal but negative for infection. Treatment was escalated to combination azathioprine and weekly adalimumab, and while there was some symptomatic benefit, reassessment colonoscopy in 2018 showed persistent inflammation (Figure 1a) and biopsies revealed multiple amoebae. A short metronidazole course for the presumed superadded infection led to symptom resolution for 9 months before symptoms returned in 2019, with severe colonic inflammation and deep ulcers (Figure 1b). Repeat biopsies, positive for amoeba (Figure 1c), were reviewed in a multidisciplinary team meeting. Immunosuppression was discontinued, and further metronidazole and paromomycin led to complete symptom resolution, endoscopic healing, amoebic clearance, and no recurrence with a 2.5-year follow-up (Figure 1d–f). Close questioning a decade later revealed a history of extensive travel prior to 2009, including rural areas in South America and the Indian sub-continent, which are endemic for amoebiasis.

View Figure 1 and Table 1.

This case demonstrates several learning points. First, the challenge of diagnosing amoebic colitis in non-endemic regions due to low prevalence and index of suspicion, and similar clinicopathological features to IBD. It should be suspected in all patients presenting with diarrhoea and epidemiological risk factors, and it demonstrates that a travel history is critical in all patients. Second, our patient had negative stool microscopy throughout. Stool antigen/PCR and serum antibody tests are recommended for diagnosis, carrying significantly higher sensitivity and specificity than microscopy and culture.[[23]] Finally, that combining a nitroimidazole and a luminal agent, such as paromomycin or diloxanide furoate, is necessary to eliminate intestinal colonisation, to minimise risk of disease relapse.[[2,5]] Asymptomatic amoebiasis may be treated with a luminal agent alone. Failure to recognise infection and subsequent treatment with immunosuppression, particularly corticosteroids, can lead to life-threatening progression and dissemination.[[4]] Our patient’s poor response to multiple IBD treatments, and subsequent ulcer healing with antibiotics and discontinued immunosuppression, suggest amoebic colitis from the outset, rather than IBD.