PARACOCCIDIOIDOMYCOSIS WITH CENTRAL NERVOUS SYSTEM AND SYSTEMIC INVOLVEMENT IN AN IMMUNOCOMPETENT PATIENT

Paracoccidioidomycosis (PCM) is a systemic mycosis endemic to Latin America, especially Brazil, caused by dimorphic fungi of the genus Paracoccidioides, such as P. brasiliensis, transmitted by inhalation of spores present in soil. It predominantly affects male rural workers aged 30–60 years and often presents with pulmonary, mucosal, or reticuloendothelial involvement. Central nervous system involvement is rare and is almost universally reported in endemic areas. Hematogenous dissemination to the CNS causes neuroparacoccidioidomycosis (NPCM), which commonly presents with motor deficits, ataxia, headache, seizures, disorientation, and bradypsychia. E.S.V., a 45-year-old man from the countryside of Espírito Santo, attended an outpatient infectious disease consultation after recurrent seizure episodes accompanied by a skin lesion on the left arm. He was diagnosed with PCM after cutaneous manifestations, confirmed by histopathology of a granulomatous and abscedative lesion on the nasal bridge. He brought a head CT previously ordered due to seizures at an urgent care unit. CT showed a brain mass in the occipital lobe, initially raising suspicion of neoplasia and prompting a recommendation for confirmatory biopsy, which the patient refused. He had been treated for non-severe PCM with itraconazole for about two months without apparent clinical improvement. PCM was considered after analysis of abdominal CT and liver biopsy showing Paracoccidioides involvement, and a concordant skin biopsy, indicating significant systemic spread. Head CT revealed a granulomatous lesion with ring enhancement and perilesional edema typical of PCM with CNS involvement. He tested negative for HIV, hepatitis B and C, and other immunosuppressive diseases. Treatment was transitioned from itraconazole to amphotericin B; due to renal dysfunction, therapy was switched to liposomal amphotericin B, leading to prompt clinical improvement. Treatment was continued for two months, and follow-up CT imaging showed regression of all systemic and CNS lesions, indicating apparent clinical cure without further neurologic manifestations.