Fulminant diffuse cerebral toxoplasmosis as the first manifestation of HIV infection

Individuals with HIV may present to the emergency department with HIV-related or HIV-unrelated conditions, toxicity associated with antiretroviral therapy or primary HIV infection (seroconversion). In individuals with HIV infection, central nervous system toxoplasmosis occurs from reactivation of disease, especially when the CD4+ count is <100 cells/μL, whereas in those taking immunosuppressive therapy, this can be either due to newly acquired or reactivated latent infection. It is a rare occurrence in immune-competent patients. Vertical transmission during pregnancy can manifest as congenital toxoplasmosis in the neonate and is often asymptomatic until the second or third decade of life when ocular lesions develop. Toxoplasmosis is an infection caused by the intracellular protozoan parasite Toxoplasma gondii and causes zoonotic infection. It can cause focal or disseminated brain lesions leading to neurological deficit, coma and death. Typical radiological findings are multiple ring-enhancing lesions. Histopathological examination demonstrating tachyzoites of T. gondii and the presence of nucleic material in the spinal cerebrospinal fluid (CSF) confirms the diagnosis. The authors present the case of a 52-year-old male UK resident, born in sub-Saharan Africa, with a 3-week history of visual hallucinations. He attended the emergency department on three occasions. Laboratory investigations and a CT head were unremarkable. He was referred to psychological medicine for further evaluation. On his third presentation, 2 months later, a CT head showed widespread lesions suggestive of cerebral metastasis. Dexamethasone was initiated and he developed rigours. An MRI head showed multiple ring-enhancing lesions disseminated throughout his brain parenchyma. CSF analysis and serology confirmed the diagnosis of HIV and toxoplasmosis, respectively. His CD4 count was 10 and his viral load (VL) was 1 245 003. He was then initiated on Biktarvy 50 mg/200 mg/25 mg, one tablet daily, which contains 50 mg of bictegravir, 200 mg of emtricitabine and tenofovir alafenamide fumarate equivalent to 25 mg of tenofovir alafenamide. After 3 months of antiretroviral therapy, his HIV VL reduced to 42. However, his abbreviated mental test remained at 2/10. Despite presenting with neurocognitive impairment and being born in a HIV prevalent region, an HIV test was not offered. This case highlights missed opportunities to request HIV serology and raises awareness that cerebral toxoplasmosis can occur as the first manifestation of HIV. Prompt diagnosis and early initiation of antiretroviral therapy reduces morbidity and mortality in this patient cohort.