Teaching Case

An immunocompetent 40-year-old man presented with high grade fever and passage of dark-coloured urine. Laboratory markers revealed elevated total leukocyte count, elevated s. bilirubin (2mg/dl) and mildly elevated liver enzymes. Blood culture for bacterial growth was negative. Clinical examination revealed tender hepatomegaly.

Contrast enhanced CT of abdomen revealed an enlarged liver with multiple peripherally enhancing fluid-attenuation cystic lesions with associated perilesional oedema. Note was also made of a short segment of circumferential mural thickening involving the ascending colon with loco-regional mesocolic lymphadenopathy. Remaining colon was unremarkable. No free fluid was seen in the abdomen.

Concomitant involvement of the colon in a patient with liver abscesses suggested the possibility of invasive amoebiasis. The patient, on carefully eliciting the clinical history, reported on-and-off diarrhoea for the past month. Serological assay for amoebiasis was ordered, which was reactive (positive). A diagnostic US-guided fluid tap revealed characteristic anchovy-sauce pus.

Amoebiasis is the infection of the human gastrointestinal tract caused by a protozoan parasite Entamoeba histolytica which is transmitted by fecal-oral route. It is the second leading cause of death from parasitic disease worldwide. Approximately 50 million cases of invasive amoebiasis occur each year, with as many as 100,000 deaths. Amoebiasis is rampant in the developing world with a rising incidence in the developed nations due to increased travel to endemic regions and increased prevalence of HIV-AIDS patients.

At CT, amoebic colitis typically involves the right colon i.e. the caecum and/or ascending colon [3-5]. Terminal ileum is characteristically spared. Skip-lesions and pancolitis have been reported. As in any other infective colitis the involved segment shows wall thickening with or without pericolonic fat stranding, local lymphadenopathy, and ascites. Rarely, excessive proliferation of granulation tissue can present as an ameboma which is an uncommon pseudo-tumoural lesion presenting as a fungating or necrotic colonic mass [4, 5]. Since the imaging findings are non-specific, laboratory studies are necessary for definitive diagnosis which include microscopic identification of E. histolytica trophozoites in stools or in samples collected during rectosigmoidoscopy. Serological testing for antiamoebic antibodies is highly sensitive and is positive in approximately 75% of patients with invasive colonic amoebiasis. Invasive amoebiasis constitutes almost 10% cases of amoebiasis wherein the amoebae enter the bloodstream and travels to other body organs. Liver is the most frequent extra-intestinal site of infection [1, 2]. Amoebic liver abscess is characteristically solitary subacapsular lesion located in the right postero-superior segment displaying low-level internal echoes and lacking significant wall-echoes at ultrasonography. At contrast-enhanced CT, it appears as a rounded, well-marginated lesion with thick enhancing walls (average wall thickness 3–15 mm) and variable amount of perilesional oedema) [1, 2]. Intralesional multiple septae or debris levels and, rarely, air bubbles or haemorrhage can be seen. Lesions can be multiple especially in immunocompromised patients. The subacaspular location of the abscess predisposes them to rupture and extension into the peritoneal cavity, chest wall, pleural cavity, pericardium, or adjacent viscera. Amoebic serology has been reported to be positive in over 90% of patients with amoebic liver abscesses. Differentiation of amoebic and pyogenic abscess can be confounding based on imaging findings alone. Hence, epidemiologic information, clinical details, stool tests and positive amoebic titers, are of utmost importance for arriving at an appropriate diagnosis. It is important to remember that liver abscesses can occur even without previous development of amoebic dysentery.