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Viruses, including herpes viruses, can alter oxidative balance by either increasing the formation of free radicals or inhibiting synthesis of enzymes involved in oxidative defense within host cells. This study examined the occurrence of oxidative and antioxidative balance in cows naturally infected with bovine herpesvirus type 1 (BHV-1) under field conditions. Clinical history indicated that cows had been sick and showed mild to severe respiratory signs, characterized by dullness, coughing, and lacrimation, and a high febrile response. All samples obtained from the infected animals during clinical examination were confirmed as positive for bovine herpesvirus type 1 by PCR. Control cows showed no clinical abnormalities and PCR results were negative. Total antioxidative status, total oxidant status, oxidative stress index, and some biochemical parameters were measured. The level of total antioxidative status was significantly lower in infected animals, compared with the healthy control group (P = 0.025). However, there was no statistically significant difference between the 2 groups for total oxidant status and oxidative stress index levels. Furthermore, there was a significant decrease in the infected groups, with respect to concentrations of alkaline phosphatase, alanine transferase, γ glutamyl transferase, monocyte, and erythrocyte (P < 0.05). On the other hand, aspartate aminotransferase and creatinine kinase concentrations significantly increased in the cows infected with BHV-1. In conclusion, the data obtained hereby explained that animals with infected BHV-1 seemed to have more oxidative stress and low antioxidant defense. Moreover, future research conductance is needed on antioxidative and oxidative balance to understand pathophysiology of BHV-1 infections.

This paper describes a thrombosis in the vena cava caudalis of a 15 year-old cat with ascites. Trauma and eventually feline enteric corona virus infection in the cat were not detected. In the intrahepatic region, a blockage of vena cava caudalis was brought to light by ultrasonographic imaging. An aspirate of abdominal fluid revealed modified transudate. Liver enzyme levels were increased in the serum sample of the cat. The levels of total oxidant status (TOS) and total antioxidant status (TAS) were elevated in the peritoneal fluid. Liver protection diet with L-carnitine, diuretic therapy and antimicrobial drugs were administrated for treatment of the cat. During the continuous treatment, the amount of abdominal fluid decreased, but never completely absorbed. L-carnitine was administered to the cat during the time of treatment, and subsequently the levels of liver enzymes decreased. However, the cat died because of recurrent ascites and persistent thrombosis. In conclusion, ultrasonographic examination was very reliable, non-invasive and highly useful diagnostic method for BCS and L-carnitine has crucial effects on the quality of life, energy metabolism and liver enzyme levels. However, the blockage of the vena cava caudalis could not completely respond to medical treatment and thrombosis should be eliminated by surgical intervention.

This paper describes a thrombosis in the vena cava caudalis of a 15 year-old cat with ascites. Trauma and eventually feline enteric corona virus infection in the cat were not detected. In the intrahepatic region, a blockage of vena cava caudalis was brought to light by ultrasonographic imaging. An aspirate of abdominal fl uid revealed modified transudate. Liver enzyme levels were increased in the serum sample of the cat. The levels of total oxidant status (TOS) and total antioxidant status (TAS) were elevated in the peritoneal fluid. Liver protection diet with L-carnitine, diuretic therapy and antimicrobial drugs were administrated for treatment of the cat. During the continuous treatment, the amount of abdominal fluid decreased, but never completely absorbed. L-carnitine was administered to the cat during the time of treatment, and subsequently the levels of liver enzymes decreased. However, the cat died because of recurrent ascites and persistent thrombosis. In conclusion, ultrasonographic examination was very reliable, non-invasive and highly useful diagnostic method for BCS and L-carnitine has crucial effects on the quality of life, energy metabolism and liver enzyme levels. However, the blockage of the vena cava caudalis could not completely respond to medical treatment and thrombosis should be eliminated by surgical intervention.

Canine distemper, caused by Morbillivirus canis, is a highly morbid and lethal disease characterized by multiple systemic and neurological signs. In recent years, biomarkers, such as Galectin-3 and Cardiotrophin-1, have been investigated in inflammatory and degenerative diseases. However, the role of these biomarkers in neurological distemper has not been investigated. The aim of this study is to compare blood serum Galectin-3 and Cardiotrophin-1 concentrations between the neurological distemper and control group, and to evaluate the correlations of these biomarkers with hematobiochemical parameters in dogs with neurological distemper. Nineteen owned dogs (13 diagnosed with neurological distemper and 6 controls) were included in the study. Hematobiochemical analyses were performed in all dogs, and Galectin-3 and Cardiotrophin-1 concentrations were measured using ELISA. Serum concentrations of Galectin-3 and Cardiotrophin-1 were markedly elevated in dogs with neurological distemper compared to the control group (p < 0.05). A negative correlation between Galectin-3 and monocytes (p < 0.05) and a positive correlation between Galectin-3 and platelet and platelecrit levels (p < 0.05) were observed. There was negative correlation with Cardiotrophin-1 and lymphocyte percentage (p < 0.01) and a positive correlation with Cardiotrophin-1 and granulocyte percentage (p < 0.01). Galectin-3 and Cardiotrophin-1 may serve as biomarkers for the diagnosis and understanding of neurological distemper pathogenesis. Elevated serum concentrations of these biomarkers may indicate underlying neuroinflammation. This may contribute to the pathogenesis of neurological distemper.