A 36-year-old woman, from Los Ralos, Tucumán, northwestern province of the Argentine Republic, with a history of HIV infection 2002, with no history of indirect immunologic therapy (IFAT), hepatitis A and positive controls due to Chagas disease.
He was admitted to the Hospital de Enfermedades Infeccisos Francisco J. Muñiz de la Ciudad de Buenos Aires for an acute convulsive syndrome.
Physical examination revealed left brachio-crural and right central facial paresis, ataxia, dysmetria and nystagmus.
Laboratory tests at admission showed normal hematocrit, hemoglobin, 13.5 g/dl, leukocytes 3,200/mm3, platelets 155,000/mm, VHS 40 mm/h, GOT 187 UH.
CD4+ TL count was 79 cells/μL3 (8%).
Chest radiography, ECG and echocardiogram were normal.
Contrast-enhanced brain MRI showed an extensive area of hyperintense signal in FLAIR, T2 and diffusion with discrete mass effect and some sectors of pathological signal predominance after injecting the frontal subcortical contrast with the left side constriction mass.
Lumbar puncture was performed with opening pressure of 12 cm H2O, obtaining a cerebrospinal fluid (CSF) = 0.47 bacteria, colourless proteins, glucose 78 mg/dl, glucose 78 mg/dl, bacteriological culture and direct mycobacteria.
Molecular studies (PRC) for HSV-1 and 2, VZV, CMV, VHH-6 and EBV were negative.
A Strout micro-healing was performed on two occasions, without observation of stigmata.
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The serology for toxoplasmosis positive (Ig positive 1/64 and IgM negative by IFI), which led to the empirical initiation of a cerebral toxoplasmosis as a common mental disorder and as a common mental disorder treatment.
The patient presented clinical progression of cerebellar syndrome after two weeks of treatment, so she added benidazole 300 mg daily for assuming a probable reactivation of an infection.
A PCR for Chagas was performed in plasma and CSF, and the plasma sample was positive.
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The patient was admitted with improvement of the clinical picture and lesions observed in the images.
Contrast-enhanced brain MRI was performed 35 days after the start of antichagasic treatment, which showed a significant reduction of the lesions, with which it was decided to hospital discharge and outpatient follow-up.
After 15 days of continued treatment with benzydazol, the patient developed a platelet count increase and hepatic transaminase elevation; therefore, treatment with nifurtimox 240 mg daily was continued.
Eleven days after the last treatment, the patient developed peripheral neuropathy, so beneidazole was restarted.
The patient did not comply with the clinical controls, and one week after starting treatment with benzydazol again, she was hospitalized for fever and pancitretin.
The patient presented with multiorgan failure of septic etiology and died 24 hours after admission.
