An 11-year-old male castrated 5.7-kg domestic shorthair cat presented to the internal medicine service after experiencing two seizures (believed to be tonic-clonic). The medical record information prior to this presentation is limited. The patient was feline immunodeficiency virus (FIV) positive and had been seen at the referring veterinarian 3 months prior with a presenting complaint of fever and ataxia. Pulmonary nodules were identified on thoracic radiographs at that time. A diagnosis of systemic blastomycosis was made based on fine-needle aspiration (FNA) of an enlarged popliteal lymph node. A Blastomyces urine antigen enzyme immunoassay (Blastomyces quantitative antigen EIA; MiraVista Diagnostics; range of quantification 0.2-14.7 ng/ml) was performed and was highly positive (above the limit of quantification). The clinical signs and lung nodules had improved with treatment (itraconazole and amphotericin B; dose regimen unknown). The reported tonic-clonic seizures occurred after the most recent antifungal treatment had been administered. At presentation, no abnormalities were noted on physical and neurologic examination.
On MRI of the brain, three separate intra-axial lesions were identified (Figure 1). A round  0.8-cm diameter nodule was associated with the ventral aspect of the left temporal lobe. This lesion was iso-to-slightly hypointense to gray matter, with a hyperintense rim on T2-weighted and T2-FLAIR images, was slightly hypointense on T1-weighted images, did not show evidence of susceptibility artifact on T2*-weighted images, and was strongly homogeneously contrast enhancing. There was moderate indistinct perilesional T2 hyperintensity, consistent with perilesional edema. A second well-circumscribed  0.4-cm diameter T2 hypointense and T1 isointense lesion was associated with the right cerebellar hemisphere and exhibited moderate ring enhancement following contrast medium administration. A third  0.2-cm diameter ring-enhancing lesion was noted in the cerebellar vermis, not seen on precontrast images. There was no evidence of perilesional edema associated with the cerebellar lesions. There was no evidence of meningeal enhancement or any abnormalities of the ventricular system, skull, nasal cavity, paranasal sinuses, tympanic bullae, orbits, ocular structures, and soft tissues of the head and cranial neck including regional lymph nodes.
A cisternal cerebrospinal fluid (CSF) tap was obtained and yielded a diagnosis of probably iatrogenic hemorrhage without other cytologic abnormalities. A Blastomyces urine antigen EIA was moderately positive (3.04 ng/ml).
Corticosteroid treatment was initiated (prednisolone 5-mg/head PO q 24 h x 3 days, 2.5-mg/head PO q 24 h x 3 days, and 1.25-mg/head PO q 24 h x 3 days) for treatment of perilesional edema and to help manage the inflammatory effects caused by fungal die-off. The patient was also started on phenobarbital (2.5-mg/kg PO BID of 20-mg/ml suspension), levetiracetam (20-mg/kg PO of 100-mg/ml suspension q 8 h), and fluconazole (50-mg/head PO q 12 h). Amphotericin B was discontinued. Phenobarbital was discontinued the following day due to the patient being very lethargic.
The cat showed improvement over the next months and was considered clinically normal aside from an occasional cough and unrelated chronic gingivitis 2 months after the MRI examination (5 months after initial diagnosis). The previously seen pulmonary abnormalities had resolved. There was no recurrence of seizures, and no other neurologic abnormalities were reported. A Blastomyces urine antigen EIA was greatly improved but still mildly positive (0.73 ng/ml).
The patient remained neurologically normal. Levetiracetam was gradually tapered from 5 to 8 months after the initial diagnosis without recurrence of seizure activity. A Blastomyces urine antigen EIA was still mildly positive after 7 and 9 months. Fluconazole was discontinued 15 months after the initial diagnosis (12 months after the first MRI examination) based on 2 consecutive negative Blastomyces urine antigen EIA tests.
The cat represented 3 years later (4 years and 7 months after initial diagnosis) to the emergency service for a 24-h history of circling to the right and behavior changes. On neurologic examination, the patient was circling to the right and had a bilaterally absent menace response. Possible hyperesthesia of the head was also noted. Neurolocalization was to the right forebrain. Thoracic radiographs did not reveal any significant abnormalities.
Magnetic resonance imaging was repeated. There was a new finding of an  1.2 x 1.4 cm ovoid mass in the right temporal lobe (Figure 2) which was predominantly T2 and T1 isointense to gray matter with a small centrally located T2 hyperintense and T1 hypointense focus which did not suppress on T2-FLAIR. The lesion was hypointense on both DWI and ADC maps. There was marked perilesional T2 and FLAIR hyperintensity following the white matter tracts of the right cerebral hemisphere with a moderate to marked mass effect characterized by compression of the right lateral ventricle, leftward midline shift, and caudal transtentorial and foramen magnum herniations. Following contrast medium administration, the mass displayed marked heterogeneous contrast enhancement. Mild focal pachymeningeal contrast enhancement was identified adjacent to the lesion. An  0.2-cm diameter well-defined T1, T2, and T2-FLAIR hypointense ovoid nodule was observed in the region of the previously seen cerebellar hemispheric lesion and was decreased in size. This lesion was associated with a susceptibility artifact on T2*-weighted images and had mild rim contrast enhancement. The lesion within the cerebellar vermis was no longer visible. An incidental small amount of fluid was noted within the bilateral tympanic bulla. The remaining structures of the head and cranial neck remained normal.
The patient received a tapering dosing regimen of prednisolone (5-mg/head PO q 24 h x 3 days, 2.5-mg/head PO q 24 h x 3 days, and 1.25-mg/head PO q 24 h x 3 days). Fluconazole treatment was resumed empirically (50-mg/head PO q 12 h) while awaiting urine antigen testing results. A repeat Blastomyces urine EIA test was positive (4.24 ng/ml), and fluconazole treatment was continued. The patient improved, and the client reported the cat as being back to normal 5 weeks after the second MRI examination. On neurologic examination at that time, menace response was noted in both eyes. The pupillary light responses were decreased. Additional findings during this visit included weight loss, hypoalbuminemia, anemia, a soft heart murmur, and an irregular heartbeat. The patient represented for a work-up of these new problems to the internal medicine service 2 weeks later and at that point was diagnosed with large cell gastrointestinal (GI) lymphoma. Chemotherapy was started and initially well-tolerated. The owners did not report a recurrence of neurologic abnormalities, and the physical examinations performed by the oncology service over the next weeks did not reveal any obvious neurologic abnormalities. A full neurologic exam was not performed. Urine blastomycosis antigen tests were also not repeated during that time due to the inability to acquire sufficient urine samples. The patient started declining  2 months after the diagnosis of GI lymphoma and was euthanized 3 months later. An autopsy was not performed. The overall survival time after the initial diagnosis of systemic blastomycosis was  5 years.