Abstract: Ivermectin and abamectin are two members of the group of parasiticides known as the avermectins; ivermectin was first registered as an injectable treatment for cattle in 1981. Since then, abamectin has been registered for cattle and ivermectin for horses. The relative popularity of the avermectins amongst farmers and veterinarians can be attributed to their spectrum of activity, convenience, wide margin of safety and the improved health and performance of stock following their use. Patterns of use in grazing animals apply equally to the avermectins as to other antiparasitics, particularly anthelmintics; these are based on a knowledge of epidemiology integrated with practical management considerations. For cattle, programs are commonly aimed at control of abomasal nematodes of the genera Ostertagia and Haemonchus. Use of avermectins is largely strategic in cattle, treatments being favored at the end of the period of transmission of these parasites; this frequently coincides with housing, entry into a feedlot or movement to another pasture. Simultaneous control of important ectoparasites at this time is an added benefit. Prophylactic use of avermectins at pasture is primarily targeted at the young first season grazing animal. In horses, a bimonthly treatment schedule during the period of risk has proved effective in helping prevent adverse effects of the main target parasites, including large and small strongyles and stomach bots. These patterns of use can be applied to the evaluation of the potential for avermectin residues in feces to have impact on pasture ecology. The evidence presented suggests that any effects are temporally and spatially limited. After more than a decade of practical use, there is no indication that avermectins have had a significant impact on pasture ecology and the environment.

Abstract: This paper reports the first isolation of Jamestown Canyon (JC) virus from coastal California and the results of tests for antibody to JC virus in mammals living in coastal California. The virus isolation was made from a pool of 50 Aedes dorsalis females collected as adults from Morro Bay, San Luis Obispo County, California. The virus isolate was identified by two-way plaque reduction-serum dilution neutralization tests done in Vero cell cultures. Sera from the mammals were tested for antibody to JC virus by a plaque-reduction serum dilution neutralization method. A high prevalence of JC virus-specific antibody was found in horses and cattle sampled from Morro Bay. This finding is additional evidence for the presence of a virus antigenically identical or closely related to JC virus in Morro Bay and indicates that the vectors of the virus in Morro Bay feed on large mammals. A high prevalence of virus-specific antibody was also found in horses sampled from Marin and San Diego counties. This finding suggests that viruses antigenically identical or closely related to JC virus are geographically widespread in coastal California.

Abstract: Peroxisome proliferator-activated receptor gamma (PPAR gamma) is a nuclear receptor that mediates the antidiabetic effects of thiazolidinediones. PPAR gamma is present in adipose tissue and becomes elevated in fatty livers, but the roles of specific tissues in thiazolidinedione actions are unclear. We studied the function of liver PPAR gamma in both lipoatrophic A-ZIP/F-1 (AZIP) and wild type mice. In AZIP mice, ablation of liver PPAR gamma reduced the hepatic steatosis but worsened the hyperlipidemia, triglyceride clearance, and muscle insulin resistance. Inactivation of AZIP liver PPAR gamma also abolished the hypoglycemic and hypolipidemic effects of rosiglitazone, demonstrating that, in the absence of adipose tissue, the liver is a primary and major site of thiazolidinedione action. In contrast, rosiglitazone remained effective in non-lipoatrophic mice lacking liver PPAR gamma, suggesting that adipose tissue is the major site of thiazolidinedione action in typical mice with adipose tissue. Interestingly, mice without liver PPAR gamma, but with adipose tissue, developed relative fat intolerance, increased adiposity, hyperlipidemia, and insulin resistance. Thus, liver PPAR gamma regulates triglyceride homeostasis, contributing to hepatic steatosis, but protecting other tissues from triglyceride accumulation and insulin resistance.

Abstract: The genus Thelazia (Spirurida, Thelaziidae) includes a cosmopolitan group of eyeworm spirurids responsible for ocular infections in domestic and wild animals and transmitted by different species of muscids. Bovine thelaziosis is caused by Thelazia rhodesi Desmarest 1828, Thelazia gulosa Railliet & Henry 1910, and Thelazia skrjabini Erschow 1928, which occur in many countries; T. gulosa and T. skrjabini have been reported mainly in the New World, while T. rhodesi is particularly common in the Old World. In Italy, T. rhodesi was reported in southern regions a long time ago and, recently, T. gulosa and T. skrjabini have been identified in autochthonous cattle first in Apulia and then in Sardinia. Thirteen species of Musca are listed as intermediate hosts of eyeworms, but only Musca autumnalis and Musca larvipara have been demonstrated to act as vectors of Thelazia in the ex-URSS, North America, ex-Czechoslovakia and more recently in Sweden. In Italy, after the reports of T. gulosa and T. skrjabini in southern regions, the intermediate hosts of bovine eyeworms were initially only suspected as the predominant secretophagous Muscidae collected from the periocular region of cattle with thelaziosis were the face flies, M. autumnalis and M. larvipara, followed by Musca osiris, Musca tempestiva and Musca domestica. The well-known constraints in the identification of immature eyeworms to species by fly dissection and also the time-consuming techniques used constitute important obstacles to epidemiological field studies (i.e. vector identification and/or role, prevalence and pattern of infection in flies, etc.). Molecular studies have recently permitted to further investigations into this area. A PCR-RFLP analysis of the ribosomal ITS-1 sequence was developed to differentiate the 3 species of Thelazia (i.e. T. gulosa, T. rhodesi and T. skrjabini) found in Italy, then a molecular epidemiological survey has recently been carried out in field conditions throughout five seasons of fly activity and has identified the role of M. autumnalis, M. larvipara, M. osiris and M. domestica as vectors of T. gulosa and of M. autumnalis and M. larvipara of T. rhodesi. Moreover, M. osiris was described, for the first time, to act as a vector of T. gulosa and M. larvipara of T. gulosa and T. rhodesi. The mean prevalence in the fly population examined was found to be 2.86%. The molecular techniques have opened new perspectives for further research on the ecology and epidemiology not only of Thelazia in cattle but also of other autochthonous species of Thelazia which have been also recorded in Italy, such as Thelazia callipaeda, which is responsible for human and canid ocular infection and Thelazia lacrymalis, the horse eyeworm whose epidemiological molecular studies are in progress.

Abstract: Red blood cell hypervolaemia has been used for diagnosis of overtraining in racehorses, and has been suggested as a mechanism of this cause of loss of racing performance. The effects of overload training (OLT) on the plasma, blood and red cell volumes were investigated in a prospective study in 12 Standardbred horses. Measurements of blood volumes were made after eight and 32 weeks of an exercise training study. Horses were randomly allocated to OLT and control groups (n=6) after 16 weeks of training. Training duration and intensity were increased more rapidly for the OLT group from week 16, until overtraining was diagnosed in week 32.There were no significant effects of OLT on plasma, blood or total red cell volumes between weeks eight and 32. These volumes significantly decreased with time. Maximal haematocrit after exercise was lower (P<0.05) in the OT group in week 32 (0.57+/-0.003% L/L) than in week eight (0.59+/-0.004 L/L). It was concluded that red cell hypervolaemia was not a mechanism for the decrease in capacity for exercise that occurs with overtraining.