Dataset Information

Detection of canine distemper virus in cerebrospinal fluid, whole blood and mucosal specimens of dogs with distemper using RT-PCR and immunochromatographic assays.

ABSTRACT:

Background

Accurate diagnosis of canine distemper (CD), a highly contagious and acute viral disease, cannot be made solely based on clinical signs and haematological findings, but serological and molecular methods compatible with clinical signs are also required. The type of sample and method of tissue sampling are also very important. Sometimes in chronic cases, the canine distemper virus (CDV) may not be detected in blood and conjunctival specimens but can be detected in cerebrospinal fluid (CSF).

Objectives

The aim of this study was to evaluate and compare the suitability of CSF samples with whole blood and conjunctival samples in the detection of CDV.

Methods

The CDV was detected in CSF, whole blood and mucosal specimens in 20 dogs with obvious neurological with or without systemic signs congruous with CD by RT-PCR and rapid immunochromatographic (IC) antigen test kit assays.

Results

Rapid kit results were positive for mucosal swabs in 10 cases (50%) and for CSF in 17 cases (85%); RT-PCR results from whole blood were positive in 11 cases (55%) and from CSF in 16 cases (80%).

Conclusions

Our results revealed that dogs with neurological signs showing simultaneous or recent systemic symptoms, whole blood, CSF and mucosal swabs are suitable for the diagnosis of CDV by RT-PCR and rapid IC antigen test kits, but dogs with neurological symptoms that are systematically asymptomatic or have had systemic signs for a long time, whole blood and mucosal swabs are not good samples while CSF is a good one.

SUBMITTER: Sarchahi AA

PROVIDER: S-EPMC9297742 | biostudies-literature |

REPOSITORIES: biostudies-literature

ACCESS DATA

Similar Datasets

Project description:Prospective study.To identify proteins with differential expression in the cerebrospinal fluid (CSF) from 15 clinically normal (control) dogs and 15 dogs with cervical spondylomyelopathy (CSM).Canine CSM is a spontaneous, chronic, compressive cervical myelopathy similar to human cervical spondylotic myelopathy. There is a limited knowledge of the molecular mechanisms underlying these conditions. Differentially expressed CSF proteins may contribute with novel information about the disease pathogenesis in both dogs and humans.Protein separation was performed with 2-dimensional electrophoresis. A Student t test was used to detect significant differences between groups (P < 0.05). Three comparisons were made: (1) control versus CSM-affected dogs, (2) control versus non-corticosteroid-treated CSM-affected dogs, and (3) non-corticosteroid-treated CSM-affected versus corticosteroid-treated CSM-affected dogs. Protein spots exhibiting at least a statistically significant 1.25-fold change between groups were selected for subsequent identification with capillary-liquid chromatography tandem mass spectrometry.A total of 96 spots had a significant average change of at least 1.25-fold in 1 of the 3 comparisons. Compared with the CSF of control dogs, CSM-affected dogs demonstrated increased CSF expression of 8 proteins including vitamin D-binding protein, gelsolin, creatine kinase B-type, angiotensinogen, ?-2-HS-glycoprotein, SPARC (secreted protein, acidic, rich in cysteine), calsyntenin-1, and complement C3, and decreased expression of pigment epithelium-derived factor, prostaglandin-H2 D-isomerase, apolipoprotein E, and clusterin. In the CSF of CSM-affected dogs, corticosteroid treatment increased the expression of haptoglobin, transthyretin isoform 2, cystatin C-like, apolipoprotein E, and clusterin, and decreased the expression of angiotensinogen, ?-2-HS-glycoprotein, and gelsolin.Many of the differentially expressed proteins are associated with damaged neural tissue, bone turnover, and/or compromised blood-spinal cord barrier. The knowledge of the protein changes that occur in CSM and upon corticosteroid treatment of CSM-affected patients will aid in further understanding the pathomechanisms underlying this disease.N/A.