The emergence of Cryptococcus gattii in temperate climates has challenged the assumption that this fungus is ‘tropical’. In Australia, C. gattii still largely causes infection in healthy hosts although a recent study identified 28% of patients with immuno-compromised/co-morbid conditions. In contrast, 40-76% of cases in the outbreaks in North America had predisposing conditions/ were immunosuppressed. Meningitis ± cerebral infection (≈85% cases) is common in Australia, whilst in the outbreaks lung infection predominated. Headache (59-88%) and neck stiffness (48%) are common. Abnormal neurological findings at presentation or arising during therapy occur in 31-58% of cases including seizures and cranial nerve deficits. Raised intracranial pressure affects 50-60% of patients and hydrocephalus 30%. Lumbar puncture, recording CSF pressure and cerebral imaging are mandatory in all patients as is fundoscopy to detect papilledema. Isolates are speciated routinely for genotyping and susceptibility testing. A new lateral flow assay has provided a valuable added resource for rapid diagnosis. Because CNS infection is severe with high morbidity, prolonged treatment is required. In Australia, physician practice often employs induction therapy with amphotericin B and 5-flucytosine for 6 weeks followed by eradication therapy with fluconazole for 18-24 months. Surgical intervention, e.g., resection of mass lesions or CSF shunting may be required. The emergence of Cryptococcus gattii in temperate climates has challenged the assumption that this fungus is ‘tropical’. In Australia, C. gattii still largely causes infection in healthy hosts although a recent study identified 28% of patients with immuno-compromised/co-morbid conditions. In contrast, 40-76% of cases in the outbreaks in North America had predisposing conditions/ were immunosuppressed. Meningitis ± cerebral infection (≈85% cases) is common in Australia, whilst in the outbreaks lung infection predominated. Headache (59-88%) and neck stiffness (48%) are common. Abnormal neurological findings at presentation or arising during therapy occur in 31-58% of cases including seizures and cranial nerve deficits. Raised intracranial pressure affects 50-60% of patients and hydrocephalus 30%. Lumbar puncture, recording CSF pressure and cerebral imaging are mandatory in all patients as is fundoscopy to detect papilledema. Isolates are speciated routinely for genotyping and susceptibility testing. A new lateral flow assay has provided a valuable added resource for rapid diagnosis. Because CNS infection is severe with high morbidity, prolonged treatment is required. In Australia, physician practice often employs induction therapy with amphotericin B and 5-flucytosine for 6 weeks followed by eradication therapy with fluconazole for 18-24 months. Surgical intervention, e.g., resection of mass lesions or CSF shunting may be required.