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A 26-year-old Bolivian man presented with a 3 year history of occipital headaches and bilateral papilloedema. MRI showed communicating hydrocephalus and leptomeningeal enhancement. CSF analysis revealed an opening pressure of 32cmH2O, lymphocytic pleocytosis, protein 1.9 g/dL and CSF glucose 0.4 mmol/L. CSF AFB, bacterial and fungal culture, TB-PCR, 18S rDNA PCR, serum b-d glucan, and HIV were all negative. Serum ACE was normal. Steroids and methotrexate were commenced for probable neurosarcoidosis.He had readmissions with recurrent headache, meningism, symptoms of raised intracranial pressure and development of limb spasticity and brisk reflexes. Repeat imaging demonstrated stable hydrocephalus. Despite immunosuppression and empirical TB treatment, he remained symptomatic with a persistently active CSF: maximum opening pressure 36cmH2O, protein 3.9 g/dL, WCC 205 lymphocytes and low CSF-to-serum glucose ratio on repeated therapeutic LPs.After re-evaluation and positive CSF b-d glucan, a diagnosis of Histoplasma meningitis, without systemic dissemination, was confirmed by positive serological and CSF tests: positive immunodiffusion; yeast CFT 1:16; CSF EIA antigen 0.85 ng/ml.He was treated with AmBisome, followed by oral itraconazole, with complete symptom resolution and improvement on interval imaging.We discuss challenges in reaching a diagnosis of isolated histoplasmosis, its neurological manifestations and diagnostic pathway in evaluating patients with suspected CNS fungal infection.