Extensive Inactive Neurocysticercosis: A Case Report in Mbeya, Southern Highlands of Tanzania.

Neurocysticercosis (NCC) and Acquired Human Immunodeficiency Syndrome (AIDS) are both highly prevalent in Africa. Clinical presentation of NCC ranges from asymptomatic to manifestations, including epileptic seizures, severe progressive headache, and focal neurological deficits. It is influenced by the number, size, location, and stage of the cysts, as well as the parasite's potential to cause inflammation and the immunological response of the host. So far, little is known about how Human Immunodeficiency Virus (HIV) co-infection modifies clinical NCC presentation. We report the case of a person living with HIV presenting with extensive calcified NCC on neuroimaging without any associated signs/ symptoms.To contribute to the medical literature and enhance understanding of the disease's manifestation and progression by providing a thorough documentation of a specific case of extensive inactive neurocysticercosis.A 47-year-old male African patient was recruited in the CYSTINET Africa study at Chunya District Hospital, Mbeya. He was an artisan and has been living with HIV since 2012, and he has been compliant with antiretroviral treatment, hence with undetectable viral load during 2018, 2020, and 2021. Taenia solium serology was done by LDBIO Cysticercosis IgG Western Blot test, which tested positive for antibodies, but the apDia Cysticercosis Antigen (Ag) ELISA antigen test was negative. His computed tomography (CT) scan of the brain showed approximately 138 calcified neurocysticercosis typical lesions, 108 being located in the parenchyma, 15 in the extra parenchyma, and 15 in the subarachnoid space, consistent with a diagnosis of extensive calcified NCC. He reported no history of headaches or epileptic seizures. Neurological examination did not reveal any deficit.Intensively, patients with a large number of neurocysticercosis lesions may be completely asymptomatic throughout the disease. In our patient,the HIV co-infection might have contributed to the high lesion load and/or to less severe clinical signs/symptoms due to modulation of the immune system.