Amebiasis cutis revisited

Amebiasis cutis (AC) is reported infrequently. This study assesses the clinicopathological spectrum, co-existent visceral involvement and impact of human immunodeficiency virus (HIV) co-infection on AC.

An 8-year prospective clinicopathological evaluation of patients with AC.

Thirty-one biopsies of ulcers, fistulae, fissures, abscesses, polypoid and warty lesions in perianal, penile, scrotal, vulval, buttock, chest and abdominal wall sites were evaluated. Of these, 11 had a 'superficial' (superficial AC) and 20 a 'deep' (deep AC), histopathological pattern. Superficial AC showed predominant epidermal spongiosis, liquefactive necrosis, ulceration and fissures with hematophagous amebic trophozoites (HATs). Deep AC had confluent deep dermal and subcutaneous liquefactive, coagulative or suppurative necrosis and HATs. Seven biopsies showed vasculitis or thrombosis with luminal HATs.

Fourteen patients died; 9 had concomitant visceral amebiasis, 5 had other co-infections. Six who died were HIV seropositive, three were seronegative; all had deep AC. Of the 17 survivors, 11 (8 HIV positive) had superficial AC that healed with metronidazole treatment; the remaining 6 (one HIV seropositive) required additional surgical intervention.

Deep AC is predictive of co-existent, contiguous visceral disease. The effective management, histopathological mimickers and diagnostic pitfalls of superficial and deep AC differ. The outcome in HIV-infected patients is dependent on co-existent systemic diseases.