A 45-year-old male patient was admitted for 3 weeks of behavioral and gait disturbance, headache, urinary incontinence, oral candidiasis and weight loss.
She presented corneal sepsis, impaired language and neurological focalization with decreased reflex to the right and right phciobrachio-crural paresis, without meningeal signs.
On physical examination, anemia (hemoglobin 10 g/dL), lymphoptypnea ìL), hypoalbuminemia (3.4 g/dL), and hyponatremia (126 mEq/l) stood out.
Magnetic resonance imaging (MRI) revealed hyperintense lesions in the basal ganglia with reinforcement.
A positive HIV test, a CD4 count of 25/μL and a viral load (CV) of 747,311 copies/mL were documented.
C. neoformans infection was confirmed by a Chinese ink test and positive culture in cerebrospinal fluid (CSF), which did not show increased proteins mg/mL) or pleocytosis (0 cells/mL).
The patient had daily contact with dermatomes.
The CSF study showed no bacteria with negative PCR for T. gondii.
Serology for Trypanosoma cruzi, syphilis and T. gondii (IgG) were negative.
He was treated with amphotericin B deoxylate (anfoBdeox) but presented toxicity with fever, tremors and chills that did not undergo slow infusion, saline preload and hydrocolloid premedication.
Alternatively, he received voriconazole ev with loading dose, weight-adjusted daily dose and oral change at 8 days (200 mg every 12 h).
The dose had to be increased to 200 mg every 8 h by insufficient trough plasma levels (0.7 μg/mL; desirable 1-5 μg/mL).
This adjustment allowed adequate trough plasma levels (4.5 μg/mL).
After five weeks of treatment antiretroviral therapy (HAV) was started with abacavir/metformin (HLA B5701 negative) and raltegravir.
Complete neurological and general status improvement was observed, which allowed her discharge after 39 days with ARVT, chemoprophylaxis with ARVT and strong cotrimoxazole.
Treatment with voriconazole was switched to fluconazole therapy 300 mg/day orally after eight weeks.
MRI revealed partial regression of the lesions.
The control at 11 weeks of HAART showed a decrease in viral load to 61,683 copies/mL and an increase in CD4 count to 110/μL.
Three months later, the patient was readmitted for seizure syndrome without signs of meningeal irritation, fever or neurological focalization.
Brain MRI showed new bilateral hyperintense subcortical nodules and CSF study showed a 240 mg/dL proteinorrhachia with normal cellularity (3/mL).
CSF culture ruled out new infectious agents and confirmed the eradication of C. neoformans.
CPR for tuberculosis was negative, as was the study of T. gondii, herpes virus family and JC virus.
The seizure was interpreted as SIRI by C. neoformans and treated with dexamethasone for four days (10 mg every 6 h ev), in addition to anticonvulsant therapy with levetiracetam to avoid drug interactions.
Follow-up MRI at two weeks showed almost total regression of the lesions.
The patient was discharged with HAART, fluconazole and prophylaxis with cotrimoxazole and without corticosteroids.
