A 29-year-old Canadian male of Indian descent without a significant past medical history presented to the emergency department (ED) in Tucson, Arizona directly from a local optometry office after significant bilateral papilledema was noted on a routine exam required for an updated prescription for his corrective lenses. He denied nausea, vomiting, eye pain, and acute vision changes. However, he endorsed ongoing headaches for 6 months, initially starting in late spring following a job interview for a materials engineer position at a nearby mine and exploring other Sonoran Desert attractions in Arizona earlier in the year. He reported briefly living in India 4 years prior to presentation but was otherwise without notable travel history or high-risk social behaviors. He repeatedly presented to local EDs in Canada and underwent neuroimaging for his new-onset, severe headache postjob interview. Head computerized tomography (CT) and magnetic resonance imaging (MRI) during those visits revealed no acute abnormalities. At these ED visits, he was treated for migraines before discharging home. The patient also reported a 20-pound weight loss in the following months, but his weight stabilized and headache improved gradually after relocating to Arizona for his new job.
In our ED, a CT of the head showed ventriculomegaly with hydrocephalus (Figure 1A). Subsequently, an MRI of the brain confirmed extensive basilar meningeal enhancement with communicating hydrocephalus (Figure 1B). Neurosurgery was immediately consulted based on neuroimaging results. Following a successful lumbar puncture (LP), the patient was initially treated empirically for viral, fungal, bacterial, and mycobacterial meningitis, given his degree of hydrocephalus and hyperdense basilar meningeal enhancement on neuroimaging.
Initial cerebrospinal fluid (CSF) studies showed low glucose (19 mg/dL), elevated protein (279.8 mg/dL) with lymphocytic predominant leukocytosis (87% of 335 per microL), and an opening pressure of 33 cmH2O. Empiric coverage was narrowed to cover Mycobacterium tuberculosis and Coccidiosis spp. based on his international travel history and endemic exposure. Cerebro spinal fluid Gram stain did not visualize any organisms, spherules, molds, or yeasts. Bacterial and fungal cultures of CSF fluid did not yield any growth. Diagnosis of disseminated coccidioidomycosis meningitis was confirmed with positive Coccidioides enzyme immunoassay (EIA) IgG antibody, positive Coccidioides immunodiffusion (IMDF) IgM tube precipitin antibody, positive Coccidioides IMDF IgG complement fixation (CF) antibody, serum Coccidioides CF titer of 1:128, and CSF Coccidioides CF titer of 1:32. Computed tomography thorax imaging also identified a 3-mm left lower lobe pulmonary nodule without parenchymal consolidation, cavitary lesion, or pleural effusion (Figure 1C).
Our patient was treated with intravenous amphotericin B for 5 days with concurrent intravenous fluconazole until therapeutic azole levels reached blood-brain barrier penetrance concentrations. Consistent with Infectious Diseases Society of America (IDSA) Clinical Practice Guidelines, our patient was advised to undergo ventriculoperitoneal (VP) shunt surgery with neurosurgery for definitive management of symptomatic hydrocephalus.   However, he declined any invasive procedure due to his perception that his symptoms were not hindering his ability to perform his highly demanding occupational and daily activities. He was transitioned to oral fluconazole before discharging home with close outpatient follow-up in subspecialty clinics while waiting to establish care with a primary-care physician. Prior to discharge, he was educated on warning signs and symptoms (including but not limited to visual changes, new neurological symptoms, urinary or bowel dysfunction, worsening headaches, refractory nausea, and vomiting) and given strict ED return precautions. He was also scheduled for a repeat outpatient brain MRI 3 months postdischarge.
Since discharge, he has been closely monitored for any progression of his intermittent headaches or further clinical signs of neurologic impairment and completed repeat brain MRI imaging (Figure 2A-C). Thus far, our patient endorses a positive response to and tolerance of oral fluconazole treatment with symptomatic and radiographic improvement.