Cerebral toxoplasmosis is a potentially fatal infectious disease of the central nervous system induced by reactivation of Toxoplasma gondii. It affects immunocompromised individuals, specifically those with severe Human Immunodeficiency Virus/Acquired Immunodeficiency Syndrome (HIV/AIDS) and CD4 T-lymphocyte counts < 100 cells/µL. Neuroimaging often reveals several ring-enhancing brain lesions, and the diagnosis is confirmed by serological tests and responsiveness to empiric treatment. Cerebral toxoplasmosis has a significant morbidity and mortality rate.
In this case study, a patient with HIV who had CD4 < 100 cells/µL experienced fever, seizures, confusion, and focal neurological deficits. Cerebral toxoplasmosis was strongly suspected based on a magnetic resonance imaging (MRI) of the brain that showed multiple ring-enhancing lesions. Pyrimethamine, sulfadiazine, and folinic acid were used in the early stages of empirical therapy, in addition to corticosteroids to lessen cerebral edema and anticonvulsants to manage seizures. After acute therapy, trimethoprim-sulfamethoxazole was prescribed for secondary prevention, and antiretroviral therapy (ART) was initiated to restore immune function.
This case emphasizes how important it is to identify and treat cerebral toxoplasmosis in immunocompromised patients as soon as possible, especially if they have an untreated HIV infection. It emphasizes the need for anti-toxoplasma therapy, ART, and secondary prophylaxis for improved survival, and high suspicion for T. gondii reactivation.

Cerebral toxoplasmosis, Toxoplasma gondii, Human immunodeficiency virus/acquired immunodeficiency syndrome, Central nervous system, Antiretroviral therapy.

Toxoplasma gondii, a protozoan parasite, causes cerebral toxoplasmosis, a severe and opportunistic infection of the central nervous system (CNS). Immunocompromised individuals are usually affected, especially those with advanced HIV/AIDS, cancer, or immunosuppressive medications. Localized brain lesions that result in a range of neurological symptoms are the condition’s defining feature. Cerebral toxoplasmosis has a high rate of morbidity and death if it is not detected and treated promptly.[1] Cerebral toxoplasmosis is the reactivation of a latent T. gondii infection in the CNS, culminating in localized necrotizing encephalitis. It appears to be as many brain lesions as possible and is the most prevalent cause of space-occupying lesions in people with AIDS.[2]

Toxoplasmosis is one of the most common zoonotic diseases with an estimated global seroprevalence of 25 to 30%, while regional rates vary greatly. Climate, food patterns, and animal exposure all contribute to the higher frequency observed in Africa, South America, and portions of Europe. In the United States, around 11% of people test seropositive, with greater prevalence among men, older adults, and those from lower socioeconomic categories.[3] While most immunocompetent people are asymptomatic, immunocompromised individuals like those with HIV/AIDS, organ transplant recipients, and cancer patients undergoing chemotherapy are especially vulnerable. Cerebral toxoplasmosis is the most common opportunistic infection in advanced HIV, especially when CD4+ numbers are below 100 cells/µL.[4]

The parasite is transmitted by the intake of contaminated food or water carrying oocysts, the eating of undercooked meat with tissue cysts, vertical transmission from mother to fetus, or, in rare cases, blood transfusion and organ donation. Untreated HIV infection, cancer treatment, prolonged steroid usage, and seropositive persons who do not get preventive prophylaxis are all major risk factors for brain involvement. When cerebral toxoplasmosis is diagnosed, neurological symptoms usually appear subacutely. Along with altered mental status and neuropsychiatric changes, patients frequently experience headache, fever, seizures, and focal neurological deficits such as hemiparesis, cranial nerve palsies, or speech problems. In severe cases, elevated intracranial pressure may also be accompanied by papilledema, nausea, and vomiting.[5]

Clinical characteristics, imaging, and laboratory tests all contribute to the diagnosis. MRI is the recommended imaging modality, which often reveals numerous ring-enhancing lesions in the basal ganglia or corticomedullary junction. Computed tomography (CT) can detect hypodense contrast-enhancing lesions. Serological testing for T. gondii IgG can establish past exposure, and cerebrospinal fluid (CSF) polymerase chain reaction (PCR) can confirm ongoing infection, but sensitivity varies. Invasive brain biopsy remains the gold standard, although it is usually reserved for instances where the diagnosis is unclear or empiric treatment fails. A significant diagnostic signal is clinical and radiological improvement in one to two weeks of starting anti-toxoplasma medication.

The goal of cerebral toxoplasmosis treatment is to keep the parasite under control and prevent recurrence. Trimethoprim-sulfamethoxazole (TMP-SMX) is the recommended prophylactic for immunosuppressed patients particularly those with HIV/AIDS (CD4 <100). Seropositive transplant patients benefit the most from focused chemoprophylaxis, whereas PCR screening may guide early medication in those who cannot tolerate prophylaxis. Empirical treatment with pyrimethamine, sulfadiazine, and folinic acid is started right away for active illness and continued for six weeks before switching to maintenance medication. TMP-SMX is a good choice. Ocular involvement or cerebral edema may be treated with corticosteroids. Early beginning and concomitant ART in HIV patients enhances survival rates.[6]

The aim of this case is to highlight the clinical presentation, diagnostic challenges, and management of cerebral toxoplasmosis in an immunocompromised patient. It emphasizes the importance of considering Toxoplasma gondii reactivation in HIV-positive individuals with CD4 counts below 100/mm³ presenting with neurological symptoms and radiological evidence of brain lesions.

A male patient, age 23, arrived with focal neurological deficits, fever, headache, and confusion. He was diagnosed with HIV two years ago and is currently receiving antiretroviral therapy. He has a history of not taking his medications as directed. The blood pressure is 112/72 mm Hg, the temperature is 38.2 °C, and the pulse rate is 103/minute. Multiple ring-enhancing lesions were found on a brain MRI, which strongly suggested cerebral toxoplasmosis. The patient was at high risk of latent T. gondii infection reactivation due to their history of HIV infection and CD4 count of less than 100/mm³. It is well known that immunocompromised people can develop opportunistic infections from toxoplasmosis, an intracellular protozoan infection spread by cat feces or undercooked meat that contains cysts. Together with the imaging findings, the patient’s constellation of neurological and systemic symptoms was consistent with toxoplasmosis.

This patient’s care was guided by clinical suspicion and imaging results consistent with cerebral toxoplasmosis. Empirical treatment was immediately commenced because postponing therapy while awaiting confirmation testing might result in rapid clinical worsening. The conventional regimen of pyrimethamine (200 mg loading dose followed by weight-based daily maintenance) with sulfadiazine and folinic acid (leucovorin) was recommended. Leucovorin was critical for reducing the danger of bone marrow suppression caused by pyrimethamine.

Because the patient showed indicators of increased intracranial pressure, corticosteroids were evaluated as an additional treatment to minimize cerebral edema and mass. Anticonvulsants were used to treat seizures, but not for prevention. Given the patient’s underlying HIV infection, ART was beginning to restore immunological function, which is crucial for avoiding recurrence. Prophylaxis with TMP-SMX was intended for long-term secondary prevention once the acute infection had been treated.

Close monitoring was conducted to measure clinical and radiological response, since any improvement within one to two weeks would corroborate the presumptive diagnosis. In the event of a poor response, other diagnoses such as primary CNS lymphoma would be considered, perhaps necessitating a brain biopsy. This management strategy emphasizes a combination of empiric medicine, supportive care, and preventative initiatives.

This case emphasizes how critical it is to identify and treat cerebral toxoplasmosis in immunocompromised patients as soon as possible, especially if they have advanced HIV infection. Although multiple ring-enhancing lesions on MRI and the clinical presentation of seizures, confusion, and focal neurological deficits are highly suggestive of toxoplasmosis, they can also coexist with other conditions like primary CNS lymphoma or tuberculoma. Because delays in starting treatment may cause rapid neurological deterioration and increased mortality, empirical therapy based on strong clinical suspicion is still lifesaving in these situations.

A key diagnostic hallmark is improvement within one to two weeks of therapy, which serves to distinguish toxoplasmosis from other CNS pathologies. Long-term prophylaxis until immune recovery with ART is essential to prevent relapse. Importantly, initiation of ART alongside anti-toxoplasma therapy enhances immune restoration and long-term survival. Fever, neck pain, and progressive confusion were the symptoms of a hypertensive 41-year-old African American woman from Liberia. A hyperdense lesion in the left basal ganglia with edema and midline shift was seen on the initial CT scan. Multiple ring-enhancing masses that were suggestive of CNS lymphoma rather than toxoplasmosis were discovered by MRI. The workup revealed a high viral load, elevated Toxoplasma IgG, and an HIV CD4 count of 50. She was treated with TMP-SMX and supportive measures, and later started on ART, with marked neurological improvement and lesion regression on follow-up MRI.[7]

A 52-year-old man with a 3-week history of visual hallucinations was later found to have HIV infection with a CD4 count of 10 and cerebral toxoplasmosis, confirmed by MRI and serology. Initially misdiagnosed, he was started on dexamethasone and later commenced on antiretroviral therapy with Biktarvy. His viral load decreased significantly after 3 months of treatment, though severe neurocognitive impairment persisted. This case emphasizes the importance of early HIV testing and timely initiation of therapy to reduce morbidity and mortality.[8] A 30-year-old woman with no prior history presented with seizures and aggressive behaviour and was diagnosed with HIV infection (CDC stage C3) and cerebral toxoplasmosis. She was started on sulfadiazine and pyrimethamine, but within a week developed acute kidney injury due to sulfonamide crystalluria. Urinary sediment revealed crystals resembling “shocks of wheat,” confirmed by infrared spectroscopy. Sulfadiazine was switched to clindamycin, and with aggressive alkaline hydration, her renal function improved significantly.[9]

This case illustrates the complexity of managing cerebral toxoplasmosis in advanced HIV with severe immunosuppression due to therapy discontinuation. Despite initial neurological improvement with pyrimethamine, sulfadiazine, and folinic acid, the patient’s course was complicated by progressive immunodeficiency, opportunistic infections including multidrug-resistant bacterial pneumonia and cytomegalovirus (CMV) viremia, ultimately leading to respiratory failure and death. It underscores the importance of continuous ART adherence, early diagnosis, and aggressive management of opportunistic infections to improve outcomes.[10]

Cerebral toxoplasmosis remains a leading cause of focal brain lesions in patients with advanced HIV infection and other immunocompromised states. This case illustrates the critical importance of early recognition, timely initiation of empiric therapy, and integration of antiretroviral treatment to optimize outcomes. Empiric management based on clinical and radiologic findings is often lifesaving, as delays in treatment can rapidly lead to deterioration. Long-term prophylaxis and close follow-up are essential to prevent relapse and to differentiate toxoplasmosis from other CNS pathologies such as primary lymphoma. For efficient treatment and increased survival for afflicted patients, a multidisciplinary strategy integrating knowledge of infectious diseases, neurology, and radiology is essential.

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Corresponding Author:
Patel Nirali Kirankumar
Independent Researcher, Department of Content
Medtigo India Pvt Ltd, Pune, India
Email: niralipatel94291@gmail.com

Co-Authors:
Rupashi Mukhia
Department of Outcomes Research
Anesthesiology Institute, Cleveland Clinic, USA

Samatha Ampeti, Raziya Begum Sheikh, Mansi Srivastava, Shubham Ravindra Sali
Independent Researcher, Department of Content
medtigo India Pvt Ltd, Pune, India

All patient-related data were collected by Rupashi Mukhia. Patel Nirali Kirankumar contributed to the writing of the manuscript, including the original draft preparation and subsequent review and editing to refine the final version. All authors approved the final manuscript and agreed to be accountable for all aspects of the work.

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This case report is based on a clinical case published in the “Cases” section of medtigo.com. The authors declare no conflicts of interest related to this publication.

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https://doi.org/10.63096/medtigo3084237

Patel NK, Rupashi M, Samatha A, Raziya BS, Mansi S, Shubham RS. Cerebral Toxoplasmosis in an HIV-Positive 32-Year-Old Male with Poor Antiretroviral Therapy Compliance. medtigo J Neurol Psychiatr. 2025;2(3):e3084237. doi:10.63096/medtigo3084237 Crossref