Veterinarians of the Department of Veterinary Clinical Sciences at Tufts University surgically removed the granuloma in the right cerebral hemisphere. The patient was treated with fluconazole for 4 months, and was followed with voriconazole for 10 months. Both are medications used to treat fungal infections. Based on magnetic resonance imaging and cerebrospinal fluid (CSF) analysis 8 months after the surgery, the male Boxer’s outcome was considered excellent. Emphasis has been placed on how to manage this disease through careful management practices including: proper handling, preventing crowding situation with animals, and transportation. Both the animals and the environment should be treated thoroughly to hinder the spread and control the fungal infection. This is especially important since humans can also contract this disease. Research projects and implications
Phaeohyphomycosis is a disease caused by this fungus. If given the opportunity, this disease can spread to the brain and cause a painful death. There have been multiple reports of this host of fungi, but by the time the disease is recognized, it is usually too late for the animal to be successfully treated. Recent searches of databases show that there are no current projects studying the spread of this fungus in wild animals, though there are documented cases of its occurrence. In 2005, a five-month-old snow leopard (Uncia uncia) in Europe was diagnosed with phaeohyphomycosis due to Cladophalophora bantiana. This fungus caused spastic paralysis as well as the inability to defecate or urinate.
Spinocerebellar ataxia type 13 (SCA13) is a rare autosomal dominant disorder, which, like other types of SCA, is characterized by dysarthria, nystagmus, and ataxia of gait, stance and the limbs due to cerebellar dysfunction. Patients with SCA13 also tend to present with epilepsy, an inability to run, and increased reflexes. This cerebellar dysfunction is permanent and progressive. SCA13 is caused by mutations in KCNC3, a gene encoding a voltage-gated potassium channel KV3.3. There are two known mutations in this gene causative for SCA13. Unlike many other types of SCA, these are not polyglutamine expansions but, rather, point mutations resulting in channels with no current or altered kinetics. Signs and symptoms
SCA13 is typified by early onset, mildly progressive cerebellar ataxia with accompanying dysarthria, mental retardation, and nystagmus. Symptoms and age of onset can vary slightly according to the causative mutation. Pathophysiology
Mutations in KCNC3 are responsible for SCA13. This gene is expressed heavily in Purkinje cells, as is the case for some other SCA subtypes, where it is believed to play an important role in facilitating high-frequency action potential firing. There are two known mutations in this gene associated with SCA13. The first mutation, R420H, is located in the voltage-sensing S4 segment of the channel. As this mutation neutralizes a site important for voltage sensing, it is not surprising that it results in non-conducting channels. Neurons expressing such channels are unable to follow high-frequency input with adequate fidelity.The second SCA13 associated mutation, F448L, results in functional channels that have altered kinetics.