HIV-Related Toxoplasmosis Infection: A Case of Simultaneous Cerebral and Cardiac Involvement
Introduction
Toxoplasmosis, caused by the protozoan parasite Toxoplasma gondii, is a widespread zoonotic infection affecting roughly one-third of people worldwide. Its prevalence varies by geography, socioeconomic status, and diet. A recent meta-analysis estimated global seroprevalence at about 31%, with Ghana reporting the highest rates. Earlier research in The Lancet suggested that among people living with HIV (PLHIV), the infection prevalence could reach 35.8%, with most cases occurring in sub-Saharan Africa. Cats are the primary hosts, and humans usually acquire infection opportunistically, especially when immunocompromised individuals ingest oocysts from undercooked meat of intermediate hosts. The host’s immune status largely shapes how the disease presents. In people with healthy immune systems, toxoplasmosis is often asymptomatic or manifests as mild flu-like illness. In advanced HIV/AIDS, reactivation can cause severe disease, frequently when CD4 counts fall below 100 cells/µL. The disease most commonly presents as cerebral toxoplasmosis, marked by neurological deficits, seizures, and space-occupying brain lesions. Cerebral toxoplasmosis is a leading cause of focal neurological morbidity among PLHIV, particularly in settings with limited resources, where early diagnosis and prophylaxis are challenging. Cardiac toxoplasmosis is far less common and is frequently missed or diagnosed late due to nonspecific symptoms and a lack of overt imaging signs. Cardiac involvement can take the forms of myocarditis or pericarditis and may lead to heart failure or arrhythmias, complicating the clinical picture. Simultaneous cerebral and cardiac toxoplasmosis is exceedingly rare, with only a handful of documented cases. Other complications associated with T. gondii include focal neurological deficits, ocular disease, drowsiness, coma, and, in some instances, death. This report describes a unique clinical scenario: a patient newly diagnosed with HIV, initially treated for severe malaria, who deteriorated rapidly and died. An autopsy confirmed concurrent cerebral and cardiac toxoplasmosis, underscoring diagnostic complexity, the need for heightened clinical suspicion, and the critical role of timely diagnosis and appropriate referrals to prevent fatal outcomes.
Case Report
April 30, 2025: A 50-year-old man newly diagnosed with HIV presented to a peripheral health center with severe frontal and temporal headaches and nausea of unknown duration. He was a known alcoholic and hypertensive with a history of poor adherence to antihypertensive therapy. There was no fever or neck stiffness. It was unclear when his HIV diagnosis occurred.
On examination, he looked ill but not in acute distress. He was oriented to time, place, and person, with mild pallor. Blood pressure was 145/90 mmHg. Initial management included intramuscular diclofenac 75 mg, intravenous antibiotics (X-pen) 2 million units every 6 hours, and fluid resuscitation with 500 mL normal saline followed by 500 mL of 5% dextrose. He was started on a first-line HIV regimen (tenofovir/lamivudine/dolutegravir) and received prophylaxis with cotrimoxazole 960 mg.
May 1, 2025: Laboratory results showed negative serum cryptococcal antigen (CrAg) and negative Lipoarabinomannan (LAM) tests in serum and urine. Malaria rapid diagnostic testing (MRDT) was positive, and intravenous artesunate was administered (130 mg at 0 hours and at 12 hours; the 24-hour dose was missed). Paracetamol 1 g was given every 8 hours for pain. Notably, there was no recorded fever or recorded temperature.
May 2, 2025: The patient showed marked improvement. He became afebrile, a repeat MRDT was negative, and he reported complete relief of headaches. He subsequently left the facility without the medical team’s knowledge. On the morning of May 3, his condition markedly deteriorated. He was brought back by friends in a severely emaciated state, unable to walk, and appeared intoxicated with a strong smell of alcohol. He was vomiting with tremors in the upper limbs. His pulse was 58 bpm, and random blood glucose was 8 mmol/L. He received IV metoclopramide 10 mg for vomiting.
Later that evening, around 6:40 PM, he developed several generalized tonic-clonic seizures, remained unconscious between episodes, and his Glasgow Coma Scale dropped to 8/15. Oxygen saturation on room air fell to 85%, and his pulse rose to 112 bpm. Diazepam 10 mg was given urgently, and a nasogastric tube was placed. Plans were made for urgent review by a medical officer.
Despite resuscitative efforts, the patient’s condition worsened. By 9:25 PM, he developed acute respiratory distress with severe desaturation and subsequently suffered cardiac arrest. CPR was unsuccessful, and he was pronounced dead. The body was sent for post-mortem examination at a regional hospital, where this team first engaged with a summary of the medical records.
Autopsy Findings
Gross examination revealed a severely swollen brain with flattened gyri and narrowed sulci. There were round gray-white lesions in the left temporal lobe, left thalamus, and just above the right corpus callosum at the gray–white matter junction. The largest lesion was in the left temporal region (approximately 5 cm at its widest diameter) with areas of hemorrhage and liquefactive necrosis. The heart showed multiple distinct oval infarct-like areas within the interventricular septum. No obvious lesions were seen in other organs. Tissue samples were fixed in 10% neutral buffered formalin and prepared for microscopy.
Microscopic Examination
H&E-stained brain sections showed extensive parenchymal necrosis with inflammatory infiltrates of lymphocytes and macrophages, perivascular cuffing forming microglial nodules, and meningitis with inflammatory cells in the pia mater. Bradyzoites of T. gondii were scattered at the edges of necrotic foci within gliotic tissue. Cardiac tissue showed multiple foci of myocardial necrosis with similar inflammatory infiltrates, and rare bradyzoites within myocytes.
Discussion
Toxoplasmosis remains a major concern for immunocompromised individuals, especially those with HIV/AIDS. It usually presents as cerebral toxoplasmosis, with headaches, seizures, and altered consciousness as common features. In this patient, clinicians should have suspected T. gondii infection at the initial presentation, given the newly diagnosed HIV status and very low CD4 count. Instead, cryptococcal meningitis was suspected, and CrAg testing returned negative. Often, such patients at peripheral centers are treated for malaria, as occurred here; however, malaria diagnosis may have been a false-positive MRDT result, since a repeat test a day later was negative despite clinical improvement on antimalarial therapy.
Cardiac involvement is rare and often diagnosed post-mortem, making antemortem suspicion difficult. Myocarditis or pericarditis due to toxoplasmosis can cause severe morbidity and mortality. Histopathology identifying tachyzoites and bradyzoites remains the definitive diagnostic method. Several factors complicated management in this case: advanced disease, poor treatment adherence, and the patient’s escape from the facility to drink alcohol, which likely worsened prognosis.
What Could Have Been Done Differently?
Early referral to a higher-level facility at first presentation could have allowed diagnostic imaging (e.g., CT scans) and access to infectious disease specialists and multidisciplinary care, potentially altering the outcome. Although antiretroviral therapy (ART) and cotrimoxazole prophylaxis were started, the delay in accurate diagnosis meant limited benefit. Relying on MRDT for malaria diagnosis without confirmatory blood smear may contribute to misdiagnosis; a blood smear confirmation could reduce false positives. The patient’s later return after a binge may have been a major contributor to his rapid deterioration.
Diagnosis of T. gondii Infection
Definitive diagnosis combines clinical evaluation with laboratory tests and histopathology. Serology (ELISA for IgG and IgM; IFAT) helps distinguish acute from chronic or latent infections. Molecular methods like PCR targeting the B1 gene or the 529 bp repeat DNA fragment are particularly valuable in immunocompromised patients who may not mount reliable antibody responses. Histopathology showing bradyzoites or tachyzoites in tissue remains diagnostic. Imaging (CT, MRI, ultrasonography, and nuclear imaging) supports diagnosis but is not sufficient alone. CSF cytology from lumbar puncture or ventricular taps can also identify T. gondii.
Treatment
Cerebral and systemic toxoplasmosis are commonly treated with a combination of pyrimethamine, sulfadiazine, and leucovorin (folinic acid) to reduce pyrimethamine-induced hematologic toxicity. Therapy typically lasts 4–6 weeks or longer until clinical and radiographic improvement is observed. Alternatives, such as pyrimethamine with clindamycin or atovaquone, are used when sulfadiazine is not tolerated. In severe cerebral disease, corticosteroids may be used cautiously to manage edema, with careful monitoring due to the risk of reactivating latent infection. For HIV-positive patients, ART optimization remains essential to restore immune function. After the acute phase, secondary prophylaxis with pyrimethamine, sulfadiazine, and leucovorin is continued until sustained immune recovery (CD4 counts consistently above 200 cells/µL).
Limitations
In this setting, immunohistochemical staining for T. gondii was unavailable, though bradyzoites were clearly visible on H&E sections. Imaging and blood tests from the hospital records were not provided alongside the case report, which would have enriched the discussion.
Conclusion
This case highlights the rarity and clinical significance of concurrent cerebral and cardiac toxoplasmosis in PLHIV and underscores the value of autopsy in illuminating disease processes. Early and accurate diagnosis remains challenging yet crucial for favorable outcomes. Clinicians should maintain a high index of suspicion and pursue comprehensive diagnostic evaluations in immunocompromised patients presenting with complex syndromes. Future clinical protocols should incorporate broader differential diagnoses for acutely ill PLHIV, even in regions where certain diseases are more common.
Data Sharing
Data and materials from this case report are available from the corresponding author upon request, subject to approval by the Pathology Department and Mbarara Regional Referral Hospital.
Consent and Ethics
Written informed consent for autopsy was obtained from the next of kin. After autopsy, a provisional cause of death was provided pending histological confirmation. Two weeks after burial, the next of kin received the final cause-of-death report and a death certificate. A separate consent was obtained for use of photographic images of the body parts for academic publication. Institutional approval was not required for this case report.
Acknowledgments
Gratitude is expressed to the family for permitting the use of their relative’s specimens for educational purposes. Thanks also go to the Pathology Department of Mbarara University of Science and Technology for the opportunity to contribute to public knowledge.
Author Contributions
All authors contributed significantly to the work: conception, study design, data acquisition and analysis, drafting, revising, and final approval of the published version. They agree to be accountable for all aspects of the work.
Funding
No external funding supported this project, and it was not undertaken for profit.
Disclosure
All authors report no conflicts of interest.
References
Key sources cover toxoplasmosis epidemiology, cardiac involvement, diagnostic strategies, and treatment guidelines, including foundational reviews and case reports that emphasize the challenge of diagnosing toxoplasmosis in HIV-infected patients, particularly in resource-limited settings. These references provide context for recognizing cerebral and cardiac toxoplasmosis, the role of imaging and histology in confirmation, and best practices for treatment and prophylaxis.
