Clinic Congenital Neosporosis in a Calf.

Neosporosis is an infectious disease which is caused by a protozoan called Neospora caninum and characterized by endemic and epidemic abortions in adult cattle and congenital encephalomyelitis in calves. Our case was a female calf from the Holstein breed which was born in a farm with abortion and infertility problems and was unable to stand up after birth.. It was stated that it was the third pregnancy of the mother cow and that the previous pregnancy was aborted in the fifth month. In clinical examination, sucking reflex of the calf was present and there was spastic paralysis starting from pelvic muscle in rear limbs. Blood (EDTA and spare tube) sample was taken from the cow and from the calf before sucking first colostrum and cerebrospinal fluid was collected from the calf.. Based on the clinical and serological findings, a diagnosis of congenital neosporosis was made. As a result, neosporosis must be considered in the clinical diagnosis of calves with neurological symptoms during the neonatal period.

Detection of Nesopora caninum-specific DNA from cerebrospinal fluid by polymerase chain reaction in a dog with confirmed neosporosis.

A one-month male Greyhound dog presented with a swinging gait of the hindlimbs, and later developed muscular atrophy of the femoral region and hyperextension of hindlimbs. The dog had positive serum IFAT titers to Neospora caninum, but a negative titer in the cerebrospinal fluid (CSF). N. caninum-specific DNA was amplified from the CSF using a semi-nested polymerase chain reaction assay. Clusters of protozoa in biopsied muscle fibers were subsequently confirmed as N. caninum tachyzoites by immunohistochemical examination. Early recognition and treatment are necessary for effective recovery of clinical canine neosporosis, but antemortem diagnosis is difficult. We suggest that the detection of parasite deoxyribonucleic acid in the CSF is a useful antemortem diagnostic method in facilitating treatment of this disease.

Detection of Neospora caninum tachyzoites in cerebrospinal fluid of a dog following prednisone and cyclosporine therapy.

A 9-year-old female spayed Shetland Sheepdog was presented to the Kansas State University Veterinary Medical Teaching Hospital for evaluation following a 3-week history of left rear limb lameness that had progressed to generalized ataxia. Multifocal or diffuse brain lesions were suspected based on physical examination findings. Cerebrospinal fluid (CSF) contained 52 nucleated cells/µL composed of mixed inflammatory cells. Treatment with prednisone and cyclosporine was initiated based on a presumptive diagnosis of granulomatous meningoencephalitis. Thirteen days later the dog was nonambulatory and mentally obtunded. Repeat CSF analysis revealed 298 nucleated cells/µL with 61% eosinophils. Rare protozoal tachyzoites consistent with Neospora caninum, Toxoplasma gondii, or Sarcocystis spp. were found extracellularly and within macrophages and an eosinophil. Despite cessation of prednisone and cyclosporine therapy and provision of supportive care, the dog died 6 days later. Examination of brain tissue sections revealed multifocally extensive, necrotizing, histiocytic, and lymphoplasmacytic meningoencephalitis with numerous protozoal zoites and cysts. Immunohistochemical analysis of brain tissue using a monoclonal antibody specific for N. caninum confirmed the diagnosis of neosporosis. Similar but less severe lesions were noted in the spinal cord, although organisms were not found. This case emphasizes the value of repeated CSF analysis when therapy is ineffective and the importance of excluding infectious causes of meningoencephalitis before commencement of immunosuppressive therapy.

Effects of blood contamination of cerebrospinal fluid on results of indirect fluorescent antibody tests for detection of antibodies against Sarcocystis neurona and Neospora hughesi.

The purpose of this study was to determine the effect of blood contamination of cerebrospinal fluid (CSF) on the results of indirect fluorescent antibody tests (IFATs) for Sarcocystis neurona and Neospora hughesi. The in vitro study used antibody-negative CSF collected from non-neurologic horses immediately after euthanasia and blood samples from 40 healthy horses that had a range of IFAT antibody titers against S. neurona and N. hughesi. Serial dilutions of whole blood were made in seronegative CSF to generate blood-contaminated CSF with red blood cell (RBC) concentrations ranging from 10 to 100,000 RBCs/microl. The blood-contaminated CSF samples were then tested for antibodies against both pathogens using IFAT. Blood contamination of CSF had no detectable effect on IFAT results for S. neurona or N. hughesi at any serologic titer when the RBC concentration in CSF was <10,000 RBCs/microl. At concentrations of 10,000-100,000 RBCs/microl of CSF, positive CSF results (IFAT titer >or=5) for S. neurona and N. hughesi were detected only when the corresponding serum titers were >or=160 and >or=80, respectively. The IFAT performed on CSF is reliable for testing horses for equine protozoal myeloencephalitis caused by S. neurona or N. hughesi, even when blood contamination causes the RBC concentration in CSF to be up to 10,000 RBCs/microl.

Is it ever safe to stop azole therapy for Coccidioides immitis meningitis?

OBJECTIVE: To determine 1) whether patients with coccidioidal meningitis who had achieved remission with oral azole therapy were cured and 2) when oral azole therapy could be discontinued in these patients. DESIGN: Data were gathered on patients with coccidioidal meningitis who had successfully responded to azole therapy in previous clinical trials. SETTING: Referral centers, including university, county, and veterans' hospitals and clinics. PATIENTS: 18 patients in whom azole therapy for meningitis had been discontinued, usually because of a presumption of cure. MAIN OUTCOME MEASURES: Clinical and cerebrospinal fluid relapse. RESULTS: 14 of 18 patients (78% [95% CI, 52% to 94%]) had relapse with disseminated disease after discontinuation of therapy, for a total of 1 nonmeningeal and 15 meningeal relapses to date. Relapse occurred both soon and late (range, 0.5 to 30 months) after therapy was discontinued. The characteristics of patients who did not have relapse, including the particular azole used, the duration of therapy, the reason therapy was discontinued, and the cerebrospinal fluid indices before discontinuation, were similar to the characteristics of patients who had relapse. Relapse had serious consequences in some patients; 3 patients died. CONCLUSION: Our data suggest 1) that disease is only suppressed in patients with meningitis who achieve remission while receiving azole therapy and 2) that discontinuing azole therapy is unsafe. The alternative is lifelong treatment with azoles; this appears to be acceptable, because toxicity is uncommon with triazole therapy, even long-term triazole therapy.