Mobile phones (MP) and other electronic and communication devices that are used daily expose users to electromagnetic fields (EMF) and contribute to an increasing incidence of neurological disorders. Brain tissue is the closest organ to the MP as it operates, thus the influence of MP radiation on brain tissue is of particular concern, although research is still inconclusive. The present study investigated the possible effect of an EMF (1,350–1,375 megahertz (MHz)) from an MP on morphological and histopathological profiles in the mouse brain. Healthy BALB/c mice were assigned to three equal groups (a control and two experimental groups, n = 10 each). Experimental mice were exposed to EMFs continuously for 72 h, those of experimental group I to a 1,350 MHz field at a specific absorption rate (SAR) of 4.0 W/kg, and group II to a 1,375 MHz field EMF at an SAR of 4.0 W/kg. Brain segmentation and histopathological analysis were applied to detect changes in the morphometric parameters of the brain lobes and identify pathological lesions, respectively. Histopathology results revealed shrinkage of pyramidal neurons, presence of mild perivascular and perineural oedema, and some vacuolation of neurons and glial cells derived from mouse great hemispheres. The lesions also included reduction of Purkinje cells, vacuolisation of neurons and glial cells, and interstitial oedema in the cerebellum. MP distance of 3 cm from the cage may induce appreciable morphological changes in mouse brain structures; therefore, more comprehensive research is essential for assessment of safe distance. These pronounced effects may interfere with the results of laboratory tests on murine experimental models in veterinary or biomedical research.

There are numerous biomarkers of central and peripheral nervous system damage described in human and veterinary medicine. Many of these are already used as tools in the diagnosis of human neurological disorders, and many are investigated in regard to their use in small and large animal veterinary medicine. The following review presents the current knowledge about the application of cell-type (glial fibrillary acidic protein, neurofilament subunit NF-H, myelin basic protein) and central nervous system specific proteins (S100B, neuron specific enolase, tau protein, alpha II spectrin, ubiquitin carboxy-terminal hydrolase L1, creatine kinase BB) present in the cerebrospinal fluid and/or serum of animals in the diagnosis of central or peripheral nervous system damage in veterinary medicine.

Four viruses showing cytopathic effects in MDBK cells were isolated from brains of cattle showing downer cattle syndrome in 2012. The isolates were confirmed to belong to the genus Rubulavirus of the subfamily Paramyxovirinae. Isolate QIA-B1201 had the ability to hemagglutinate red blood cells from several species of animals and was capable of adsorbing guinea pig erythrocytes on the surface of infected Vero cells. Nucleotide sequence analysis showed that two isolates (QIA-B1201 and QIA-B1204) had high similarity with other human and animal PIV5 isolates ranging from 98.1 to 99.8%. The highest sequence similarity of the two isolates corresponded to strain KNU-11 (99.8% at the nucleotide and amino acid level) isolated from suckling piglets in Korea in 2012. To evaluate the virulence of strain QIA-B1201, we inoculated bPIV5 into 5 week-old mice via both the intraperitoneal and intracranial route. Body weight was not significantly altered in mice inoculated with QIA-B1201. In this study, we isolated and characterized novel bPIV5s from brain samples showing downer cattle syndrome, but were not able to elucidate the pathogenicity of the bPIV5s in mice.

An 8-month-old 3.15 kg female Cocker-spaniel with history of ataxia referred to the Veterianary Medical Teaching Hospital, Chungnam National University. There were no abnormalities in CBC and serum chemical analysis. Agenesis of dens was found on dorsoventral view in cervical radiography. Compressed cervical spinal cord and enlarged cerebral ventricle were observed in magnetic resonance imaging. It was diagnosed as atlantoaxial instability with hydrocephalus.

Four different experimental models for Streptococcus suis-induced disease were compared to find a model that closely mimics naturally occurring disease in conventional pigs. Fourteen, 2-week old pigs free of S. suis type 2 were used in 2 experiments. In experiment 1, 3 pigs were inoculated intravenously (IV) and 3 pigs intranasally (IN) with S. suis. Two out of 3 of the IV-inoculated pigs exhibited signs of severe central nervous system disease (CNS) and were euthanized. Streptococcus suis type 2 was isolated from whole blood, joints, and serosal surfaces of both pigs. No clinical signs and no growth of S. suis were detected in the IN-inoculated pigs. In experiment 2, 4 pigs were inoculated IV and another 4 were inoculated IN with the same isolate as in experiment 1. One hour before inoculation the IN-inoculated pigs were given 5 mL of 1% acetic acid intranasally (IN-AA). All the IV-inoculated pigs showed CNS disease and lameness, and 2 of the pigs became severely affected and were euthanized. All the IN-AA inoculated pigs exhibited roughened hair coats and 2 pigs developed severe CNS disease and were euthanized. Streptococcus suis was isolated from the joints and blood of 3 pigs in the IV-inoculated group. Streptococcus suis was isolated from blood of 2 pigs, meninges of 3 pigs, and joints of 1 pig in the IN-AA inoculated group. Natural exposure to S. suis most likely occurs by the intranasal route. The IN-AA model should serve as a good model for S. suis-induced disease, because the natural route of exposure is intranasal and the IN-AA model was effective in inducing disease that mimics what is observed in the field.