A 46-year-old male with a history of chronic hepatitis C and injection drug use presented to the Emergency Department of our Hospital following a generalized tonic-clonic seizure without recovery of mental status. He also had a history of heavy alcohol intake with recurrent episodes of pancreatitis and occasional epileptic fits, starting seven years prior, for which the patient did not take any medication. He was born in Portugal and had no travel exposure. One month before this presentation, the patient had an episode of acute pancreatitis and was admitted to the Surgical Department of our Hospital. At that time a type-2 diabetes mellitus was diagnosed and insulin therapy was started. During his stay in the hospital, he developed alteration in mental status with increasing agitation for which a head CT scan was performed that showed signs of left otomastoiditis, without brain lesions. A lumbar puncture was also performed with normal cerebrospinal fluid (CSF). Ear-nose-throat (ENT) specialist consultation confirmed the diagnosis of acute otitis media and left otomastoiditis, and the patient was started on therapy with ceftriaxone 2 g qd. His neurologic changes were attributed to withdrawal symptoms and he was discharged on day 20 with referral for ENT and surgical review. Following discharge, he became confused and developed ataxia and blurred vision. Two weeks later he had a new episode of generalized tonic-clonic seizure without recovery of mental status and was readmitted to our Hospital. On arrival to the emergency department, the patient was in coma, with a score of 3 (E = 1, M = 1, V = 1) on Glasgow Coma Scale (GCS). He was febrile (temperature was 38.0°C), hemodynamically stable (mean arterial pressure was 65 mmHg and heart rate was 80 beats per minute), with a normal capillary blood glucose level (110 mg/dL). The respiratory rate was 20 breaths per minute and peripheral oxygen saturation was 94%, at room air. He presented skin lesions suggestive of intravenous injections on his arms. Chest auscultation revealed rhonchi bilaterally, with no other abnormalities on physical examination. Arterial blood gas (ABG) measurement showed severe acidemia with respiratory and metabolic acidosis (pH - 7.015, PaO2 - 96.9 mmHg, PaCO2 - 64.9 mmHg HCO3− - 16.2 mmol/L) and a high lactate level of 12.07 mmol/L (normal, <1 mmol/L). Posteroanterior chest radiography was clear. The patient was intubated and invasive mechanical ventilation was started on emergency room (ER). The white blood cell (WBC) count was 15.9 × 109/L, with 58% lymphocytes. Laboratory studies showed rabdomyolisis and a creatinine of 15.1 mg/L (normal, 8.0 – 13.0 mg/L) with normal electrolytes levels. Amylase and lipase were elevated two times the upper limit of normal; liver function tests were normal, except for a slight elevation of γ-glutamyltransferase (γ-GT), and C-reactive protein (CRP) was normal. Toxicology screen was positive for opioids and benzodiazepines. Urinary antigen detection for Streptococcus pneumonia and Legionella pneumophila was negative and specimens of blood, sputum and urine were cultured. Testing for human immunodeficiency virus (HIV) was negative. Head computed tomography (CT) scan showed multiple contrast ring enhancing lesions, in left basal ganglia and right subcortical temporo-parietal region, with oedema and mass effect. A lumbar puncture was performed and analysis of the CSF showed normal levels of white-cell count, proteins and glucose (2 cels/uL, 0.10 g/L and 0.55 g/L, respectively); CSF was sent for culture, molecular tests and pathological examination. Electroencephalogram (EEG) showed non-specific encephalopathy with epileptiform activity in right frontal region. Intravenous (IV) meropenem 2 g tid was started empirically on ER for suspected bacterial cerebral abscesses, and adjunctive therapy with mannitol and dexamethasone was added. The patient was transferred to the Infectious Diseases Intensive Care Unit (ICU) with these focal brain lesions with mass effect of unknown etiology. After admission to the ICU, a transesophageal echocardiogram was performed and ruled out signs of endocarditis. Ophthalmology specialist consultation confirmed the absence of ocular involvement and chest-abdomen CT ruled out other possible foci. Brain magnetic resonance imaging (MRI) revealed multiple lesions involving basal ganglia bilaterally and subcortical right parietal white matter, with surrounding oedema, resulting in modelling of lateral ventricles, slight midline deviation and reduction of basal cisterns and sulci dimensions. These lesions were heterogeneous, some with multilayered signal differences and double-ring enhancement, and smaller ones presenting single layer ring enhancement in post gadolinium images. All lesions showed a core with restriction diffusibility to water molecules movement on diffusion weighted imaging (DWI, Figure ). No haemorrhage was seen. These imagiological findings were consistent with brain abscesses, most probably fungal or pyogenic, the latter less likely due to the double-layer pattern enhancement. On day 2, empiric anti-fungal therapy with IV fluconazole 800 mg qd was added to the therapeutic regimen. CSF studies including polymerase chain reaction (PCR) assay for toxoplasma, Epstein-Barr virus (EBV) and Mycobacterium tuberculosis were all negative, as was CSF culture. On CSF pathological examination no neoplastic cells were found. Blood, sputum and urine cultures were also negative. Neurosurgery consultation was called and a stereotactic brain biopsy was performed in order to highlight the causative pathogen. Histopathological examination of brain specimens showed a mononuclear cell infiltrate, with no evidence of tumor. Acid fast bacilli (AFB) smear of brain specimens was negative and PCR assay for Toxoplasma, Mycobacterium tuberculosis, Candida albicans and Aspergillus were also negative. Microbiologic culture of brain specimens revealed Candida albicans. Antimicrobial therapy was maintained with fluconazole and meropenem was withdrawn. The patient was extubated on day 12 and sedation was weaned off with recovery of his conscience level. Brain MRI was repeated three weeks after and showed radiological improvement with reduction of surrounding oedema but with persistent enhancing lesions. The patient recovered without neurologic disability and had a good radiological response on subsequent MRI. He was discharged home after two months of hospitalization under anti-fungal therapy consisting of oral fluconazole 400 mg bid and anticonvulsant drugs. He did well on outpatient follow-up, without new episodes of seizures and neurologic sequelae. Fluconazole therapy was maintained for 49 weeks when a complete resolution of brain abscesses was seen on follow-up brain MRI.