Case Presentation: An 18 year old male in Florida with a history of asthma developed frontal headaches three months ago. He was diagnosed with sinusitis, and was prescribed oral amoxicillin/clavulanic acid. However, within two weeks his headaches worsened, fevers developed, and his family observed him walking into walls. At an outside hospital, his lumbar puncture (LP) revealed 492 white blood cells with lymphocytic predominance, low glucose and high protein. Computed tomography (CT) of his head was negative but magnetic resonance imaging (MRI) revealed multiple infarcts. On neurologic exam, he had aphasia, dysphagia, and left-sided weakness. Subsequently, a battery of tests was done to identify the etiology of his meningitis. This included CSF mycobacterial, fungal, viral and bacterial cultures, CSF cytology, and paraneoplastic panels, and they were all negative. He received an empiric meningitis treatment course, and some symptom improvement was observed.
During the next three months he had intermittent headaches, fevers, and neurologic deficits. Additional testing that was performed after his transfer to an academic medical center revealed the presence of serum coccidioidal antibodies. Subsequently, his CSF also tested positive for the presence of coccidioidal antibodies. Upon further questioning about his social history, the patient advised that although he currently resided in Florida, he had previously lived in Arizona. The patient’s final diagnosis was coccidioidal meningitis. He presented from the outside hospital on empiric liposomal amphotericin, but this was changed to high dose oral fluconazole after the identification of Coccidioides. He was discharged on oral fluconazole with plans for lifelong therapy. He made a full clinical recovery prior to discharge.
Discussion: Coccidioidomycosis is caused by Coccidioides immitis and Coccidioides posadasii, which are two endemic dimorphic fungi that lead to infection following inhalation of their spores. In the United States, most cases of coccidioidomycosis occur in southwestern states. Manifestations range from self-limited pneumonia to disseminated disease. Since coccidioidomycosis is often subclinical, less than half of infections are recognized. Community-acquired pneumonia is the most common manifestation of a primary infection due to Coccidioides spp. Dissemination of Coccidioides spp. occurs hematogenously, and is indicative of progression of the primary infection. The skin, skeleton, and meninges are common sites of dissemination. Meningitis is the most serious diagnosis associated with coccidioidal infection, and if untreated, within two years it leads to death in 95 percent of patients.
The diagnosis of coccidioidal meningitis is most reliably made by isolating Coccidioides spp from CSF. However, in adults the sensitivity for a positive CSF culture is low (approximately 25%). Therefore, in most instances a presumptive diagnosis is made by detecting coccidioidal antibodies in the CSF. In patients with newly diagnosed coccidioidal meningitis, the Infectious Diseases Society of America recommends high dose oral fluconazole (400-1200 mg daily) as initial therapy for patients with normal renal function.
Conclusions: Coccidioidal meningitis is the most serious diagnosis associated with coccidioidomycosis. Obtaining a complete social history, including prior residence and travel, is paramount in making the diagnosis of coccidioidal meningitis.