1-year-old female intact Labrador retriever

Acute onset of blindness

Left to right, Top to bottom: T2W axial, FLAIR axial, Pre-contrast T1W, Post-contrast T1W

Post-contrast T1W axial

Slow T1C plus sag

Post-contrast T1W sagittal

Post-contrast T1W dorsal

A 1-year-old female Labrador retriever presented for acute onset of blindness. Owner reported she was bumping into things at home and unable to chase a ball. She was otherwise bright and alert with no coughing, sneezing, vomiting or diarrhea. On presentation the patient had a bilaterally absent menace response and resting mydriasis. No other cranial nerve deficits or abnormalities were observed on physical exam. Unremarkable electroretinography ruled out sudden acquired retinal degeneration syndrome as an underlying cause of acute blindness. Complete blood count and chemistry panel showed all values within normal reference ranges. Cryptococcus antigen titer by latex agglutination was negative. The patient had previously recovered from tetanus a year prior to presentation.

The brain was examined with standard MRI sequences including post contrast T1 weighted images in 3 planes. There are T2W/FLAIR hyperintense lesions along the gray-white matter junction of the temporal lobe bilaterally (left greater than right). On the left, there is moderate perilesional edema creating a mass-effect with bulging of the parenchyma along the internal capsule. These lesions are T1 iso to slightly hypointense on T1W precontrast images and are strongly contrast-enhancing. In addition to these more focal regions of contrast-enhancement, there is global meningeal enhancement with evidence of pachy- and leptomeningeal enhancement. There are additional regions of marked contrast-enhancement throughout the cerebral parenchyma though most severe adjacent to the gray-white matter junction. There is strong contrast-enhancement at the level of the optic chiasm. There is lateral ventricular asymmetry with the left larger than the right. There is no evidence of foraminal cerebellar herniation. No T2W GRE susceptibility artifacts are present. There is a caudal, predominantly left-sided, T2W/FLAIR hyper-, T1W hypo-intense and markedly contrast-enhancing intranasal mass. Although incompletely imaged, the mass extends into the ventral aspect of the left nasopharyngeal meatus, and there is leptomeningeal and olfactory bulb contrast enhancement adjacent to the cribriform plate, the caudal extent of the nasal mass.

Primary differentials for the intra- and extracranial lesions are fungal disease or neoplasia, with lymphoma or other round cell neoplasia thought most likely based on signalment. Given the patient’s age, fungal disease, particularly cryptococcous given the location of the patient, was thought more likely than neoplasia.

A rhinoscopic biopsy was procured from a vascular/friable lesion in the left nasal cavity. Histopathology showed yeast organisms with morphology that was consistent with Cryptococcus neoformans. The patient was started on voriconazole, terbinafine, and anti-inflammatory prednisone. At a two week recheck, owners reported the patient was doing well and had regained vision. Neurologic examination confirmed intact vision, normal resting pupillary diameter, and intact pupillary light reflexes. The patient will continue with antifungal therapy and be tapered off prednisone. Repeat imaging may be most ideal for future monitoring as a subsequent cryptococcus antigen titer continued to be negative, therefore, correlating peripheral blood titers with treatment success may not be possible in this case. Cryptococcosis is uncommon in dogs and typically presents as a systemic infection that can become life threatening as opposed to more localized disease in cats. Despite the potential for systemic disease, the nasal cavity is thought to be the initial site of infection for both dogs and cats, and the organism shows preference for the central nervous system and respiratory tissues. Clinical signs are based upon the body system affected, and over 80% of dogs with disseminated disease will display signs of CNS involvement. In the United States, particularly the Pacific Northwest, dogs are more commonly infected with Cryptococcus neoformans, while cats are more commonly infected with cryptococcus gattii. MRI characteristics of cryptococcosis are variable in both cats and dogs, though our patient showed signs similar to those reported in 7 dogs in California with cryptococcus 2010 study including meningeal enhancement and parenchymal lesions. In dogs, lesions are often more cellular and granulomatous on histopathology than cats which have less of an inflammatory reaction. This would explain the tendency for MRI lesions to have more contrast enhancement in dogs as compared to cats. Although serum antigen testing for cryptococcosis is reportedly highly sensitive (90-98%), this patient was serum negative. In a 2004 abstract, 2/7 dogs in a similar region of the country were serum negative for cryptoccosis with positive CSF titers. Therefore, CSF testing should be considered even in patients with negative serum antigen results. Treatment of cryptococcosis involves azole antifungals and careful use of glucocorticoids in dogs that have CNS involvement. Glucocorticoids are used to decrease the inflammatory response in the CNS related to organism die off, and results in improved survival rates when used in the initial phase of treatment. Prognosis of survival for canines with cryptococcosis is varied and dependent on severity of infection, strain, and financial ability of owners to pursue therapy. Altered mentation is a poor prognostic indicator. In one study, long term survival was correlated with treatment for ≥ 4 days in dogs.

Sykes J, Sturges B, Cannon M et al. Clinical signs, imaging features, neuropathology, and outcome in cats and dogs with central nervous system cryptococcosis from California. J Vet Intern Med. 2010;24:1427-38.

Trivedi S, Sykes J, Cannon M et al. Clinical features and epidemiology of cryptococcosis in cats and dogs in California: 93 cases (1988-2010). J Amer Vet Med Assoc.2011;239(3):357-69.

Vorathavorn V, Sykes J, Feldman D. Cryptococcosis as an emerging systemic mycosis in dogs. J Vet Emerg Crit Care. 2013;23(5):489-97. Lavely J, Lipstiz D. Fungal infections of the central nervous system in the dog and cat. Clin Tech Small Anim Pract. 2005;20:212-219. Stevenson TL, Dickinson PJ, Sturges BK, et al. Magnetic resonance imaging of intracranial Cryptococcosis in dogs and cats. Abstract only. Proceedings ACVIM 2004.