Fatal Granulomatous Amoebic Encephalitis Caused by Acanthamoeba in a Patient With Kidney Transplant: A Case Report Downloaded from

Abstract

Granulomatous amoebic encephalitis (GAE) due to Acanthamoeba is almost a uniformly fatal infection in immunecompromised hosts despite multidrug combination therapy. We report a case of GAE in a female who received a deceased donor kidney graft. She was treated with a combination of miltefosine, pentamidine, sulfadiazine, fluconazole, flucytosine, and azithromycin. Keywords. Acanthamoeba; encephalitis; granulomatous amoebic; immunosuppression; transplantation. CASE REPORT A 64-year-old woman underwent deceased donor kidney transplantation due to diabetic nephropathy with uneventful recovery postoperatively and who had no known episodes of rejection. Seven months after transplantation, she presented with an episode of confusion that was attributed to a recurrent urinary tract infection and after treatment she was discharged home. A noncontrast computed tomography (CT) head scan and magnetic resonance imaging (MRI) of the brain at this time were normal. She returned 10 days later with intermittent confusion and word-finding difficulty. A physical examination was notable for a nontoxic-appearing woman with stable vital signs. She was awake and alert but oriented to person only. Speech was intact: language evaluation revealed expressive aphasia with impaired naming, intact repetition, and ability to follow simple commands. Cranial nerves and motor function were intact: deep tendon reflexes were 2+ and symmetric. She had downgoing toes bilaterally. Sensory function was intact except for decreased vibration bilaterally in the distal lower extremities. Cerebellar function was intact and gait was normal. Home transplant-related medications included tacrolimus, mycophenolate mofetil, prednisone, and valganciclovir for cytomegalovirus prophylaxis. Noncontrast CT head scan revealed hypodensity with mild mass effect in the left temporal lobe and insular cortex with the radiological differential diagnosis including encephalitis and acute stroke. An MRI of the brain with contrast showed diffuse, T2 hyperintense lesion of the left temporal lobe, and insular cortex. This was associated with patchy cytotoxic edema and focal, subtle enhancement with a tiny single focus of necrosis. There were multiple microhemorrhages within and remote from this region. Appearances were of atypical infectious encephalitis with microhemorrhages secondary to either a necrotizing vasculitis or arising from a central embolic source