Cheryl L. Chrisman

Cerebrospinal fluid analysis.

Accurate interpretation of cerebrospinal fluid (CSF) changes can only be made in the context of the differential diagnosis for each case. The routine analysis of CSF cell number and type as well as CSF total protein can provide information that suggests a specific mechanism or disease, but is often inconclusive. Further information obtained from CSF protein electrophoresis and immunoglobulin determination and calculation of an albumin quota and IgG index can lend additional support for the suspected mechanism of disease. Paired serum and CSF antibody titers for specific organisms can be useful to confirm the presence of a systemic or nervous system infection. Current research on detecting antibodies against nervous tissue components in CSF should result in better diagnostic capabilities and understanding of the pathophysiology of certain disorders in the future.

Cerebral phaeohyphomycosis caused by Cladosporium spp. in two domestic shorthair cats.

Two domestic shorthair cats presented for clinical signs related to multifocal central nervous system dysfunction. Both cats had signs of vestibular system involvement and anisocoria, and one had generalized seizure activity. Cerebrospinal fluid analysis revealed a neutrophilic pleocytosis with protein elevation in one cat and pyogranulomatous inflammation in the second. Electroencephalography and brain-stem auditory-evoked potentials in the first cat confirmed cerebral cortical and brain-stem involvement. Euthanasia was performed in both cats, and postmortem diagnoses of phaeohyphomycosis secondary to Cladosporium spp. were made based on histopathology and fungal culture in both cats.

Secondary hypoadrenocorticism associated with craniocerebral trauma in a dog

An 11-month-old, neutered female miniature schnauzer presented with a severe head injury. The dog was treated for the acute effects of craniocerebral trauma and was hospitalized for just over a week. Several weeks later, she became weak and lethargic. A diagnosis of hypoadrenocorticism was confirmed with an adrenocorticotropin hormone (ACTH) stimulation test. An endogenous ACTH assay confirmed secondary hypoadrenocorticism. The dog was tested for hypopituitarism with canine thyroid-stimulating hormone and thyroxine serum assays and an insulin-like growth factor assay. These tests could not confirm panhypopituitarism in this dog. The hypoadrenocorticism was treated with prednisone, and the dog remains controlled adequately three years later.

Acute, flaccid quadriplegia in three cats with suspected coral snake envenomation

Three cats were evaluated for acute, ascending, flaccid quadriplegia; depression; and reduced nociception. Complete or partial neuromuscular junction blockade was found on nerve stimulation studies during electromyographic examinations. Two of the cases had wounds on the chin or paw compatible with coral snake bites. Although a coral snake was found in only one case, coral snake envenomation was suspected because potential for exposure, clinical signs, and electrodiagnostic findings were similar to dogs reported with this condition and to cats with tiger snake envenomation. Only one case received coral snake antivenin. All cases recovered within seven-to-10 days.

Possible therapeutic vaccines for canine myasthenia gravis : Implications for the human disease and associated fatigue

Myasthenia gravis (MG) is caused by T cell-dependent antibodies reactive with acetylcholine receptors. These autoreactive antibodies cause muscle weakness by interfering with neuromuscular transmission via removal of acetylcholine receptors from the neuromuscular junction as well as changing the architecture of the junction itself. Consequently, muscle fatigue is a debilitating aspect of MG often leading to more general feelings of tiredness not directly due to muscle weakness. We have previously described two peptides that are mimetics of antigen receptors on certain autoreactive T and B cells that are involved in MG. When used as vaccines in the rat model of MG, these peptides prevented and ameliorated disease and muscle fatigue by blunting acetylcholine receptor antibody responses. Such disease protection resulted from vaccine-induced anergizing antibodies against acetylcholine receptor-specific T and B cell antigen receptors. The present study prospectively evaluated the efficacy of these two vaccines in spontaneous acquired MG in pet dogs. When compared to historical controls that were prospectively studied, the vaccines increased the proportion of remitted dogs from 17 to 75%. In comparison to retrospectively studied historical controls that spontaneously remitted from MG, the vaccines accelerated the rate of decline in acetylcholine receptor antibody titers which resulted in a 3-fold decrease in the mean time to remission. These results are suggestive of a new type of targeted therapy that can drive autoimmune responses into long-term remission and possibly afford a means of determining whether correction of a physical cause of muscle weakness also corrects the perception of chronic, generalized fatigue.

Clinical Evaluation of Rabies Virus Meningoencephalomyelitis in a Dog

A 6-month-old, female, mixed-breed dog presented for acute, progressive, flaccid paraplegia and bilateral pelvic-limb hyperesthesia. A lymphocytic pleocytosis with 366 mg/dL protein was found on cerebral spinal fluid (CSF) evaluation. Electromyography (EMG) demonstrated positive sharp waves and fibrillations in the left pelvic limb; the M wave of the left sciatic nerve was not obtainable by nerve stimulation. Seizures and dementia began during recovery from anesthesia. Six days after onset of paralysis, the dog was euthanized. Direct fluorescent antibody testing of the brain was positive for raccoon rabies virus. This case demonstrates clinical evaluation, CSF analysis, and EMG in an animal with rabies meningoencephalomyelitis.