|
|
Boden, L. A., Anderson, G. A., Charles, J. A., Morgan, K. L., Morton, J. M., Parkin, T. D. H., et al. (2006). Risk of fatality and causes of death of Thoroughbred horses associated with racing in Victoria, Australia: 1989-2004. Equine Vet J, 38(4), 312–318.
Abstract: REASONS FOR PERFORMING STUDY: Determining the risk of fatality of Thoroughbred horses while racing is essential to assess the impact of intervention measures designed to minimise such fatalities. OBJECTIVES: To measure the risk of racehorse fatality in jump and flat starts on racecourses in Victoria, Australia, over a 15 year period and to determine proportional mortality rates for specific causes of death. METHODS: All fatalities of Thoroughbred horses that occurred during or within 24 h of a race were identified from a database. The risk of a start resulting in a racehorse fatality in all races and within flat and jump races, proportional mortality rates, population attributable risk, population attributable fraction and risk ratios were calculated along with 95% confidence intervals. Poisson regression was also performed to estimate risk ratios. RESULTS: There were 514 fatalities over the 15 year period; 316 in flat races and 198 in jump races. The risk of fatality was 0.44 per 1000 flat starts and 8.3 per 1000 jump starts (18.9 x greater). The risk of fatality on city tracks was 1.1 per 1000 starts whereas on country tracks it was 0.57 per 1000 starts. Of the 316 fatalities in flat races, 73.4% were due to limb injury, 2.5% to cranial or vertebral injury and 19.0% were sudden deaths. Of the 198 fatalities in jump races, 68.7% were due to limb injury, 16.2% to cranial or vertebral injury and 3.5% were sudden deaths. The risk of fatality in flat starts increased between 1989 and 2004 but the risk in jump starts remained unchanged over the 15 year period. CONCLUSIONS: The risk of fatality in flat starts was lower in Victoria than North America and the UK but the risk in jump starts was greater. Catastrophic limb injury was the major reason for racehorse fatality in Victoria but there was a larger percentage of sudden deaths than has been reported overseas. The risk of fatality in jump starts remained constant over the study period despite jump racing reviews that recommended changes to hurdle and steeple races to improve safety. POTENTIAL RELEVANCE: This study provides important benchmarks for the racing industry to monitor racetrack fatalities and evaluate intervention strategies.
|
|
|
|
Boray, J. C. (1969). Experimental fascioliasis in Australia. Adv Parasitol, 7, 95–210.
|
|
|
|
Bourdin, P., & Laurent, A. (1974). [Ecology of African horsesickness]. Rev Elev Med Vet Pays Trop, 27(2), 163–168.
|
|
|
|
Budras, K. D., Scheibe, K., Patan, B., Streich, W. J., & Kim, K. (2001). Laminitis in Przewalski horses kept in a semireserve. J Vet Sci, 2(1), 1–7.
Abstract: Semireserves were created by the European Conservation Project for scientific research in preparation for reintroduction in the wilderness. They are defined as enclosures large enough to carry a group of Przewalski horses throughout the year without any additional feeding. The semireserve offers diverse opportunities for significant scientific research. As part of a general screening program, the hoof development in a group of Przewalski horses was investigated in the semireserve Schorfheide near Berlin. Since the foundation of this semireserve in 1992, veterinary treatment was not necessary with the exception of hoof trimming in two animals in 1993. However, major health problems were encountered in the spring of 1999, when three other mares showed signs of laminitis. The initial diagnosis by the authors and the local veterinary surgeon based on observation of behaviour, gait, stance, walk and trot of three mares whose initial weights were higher than those of the healthy mares. The initial diagnosis was confirmed by palpation and the occurrence of very deep horn rings on all hooves and a laminitic horn ring on the right front hoof of one mare. An adequate laminitic therapy was not possible under the conditions of a semireserve. The applied management aimed at two goals: 1. To reduce endotoxin production and acidosis in the horses by reducing the ingestion of carbohydrate rich food. 2. To reduce the mares level of activity and to prevent tearing of the suspensory apparatus of the coffin bone. To achieve these two goals it was decided to remove the three laminitic mares from the rich pasture in the main part of the semireserve and to confine them onto the poorer pasture of the small separately fenced area. All three affected mares had fully recovered from their laminitic condition. Prevention of grass laminitis can be achieved by the following measures: 1. Reduction in grass intake could be achieved by increasing the grazing pressure by an increase in stocking rate of the horses or mixed grazing with another species such as sheep. 2. A longer term solution to the problem may well be to sow specific varieties of grass with lower concentrations of water soluble carbohydrate.
|
|
|
|
Crans, W. J., McNelly, J., Schulze, T. L., & Main, A. (1986). Isolation of eastern equine encephalitis virus from Aedes sollicitans during an epizootic in southern New Jersey. J Am Mosq Control Assoc, 2(1), 68–72.
Abstract: Eastern equine encephalitis virus (EEE) was isolated from the salt marsh mosquito, Aedes sollicitans, collected from coastal areas of New Jersey on 3 occasions during the late summer and fall of 1982. The isolations were made at a time when local Culiseta melanura were either undergoing a population increase or exhibiting high levels of EEE virus. Although no human cases were reported during the epizootic period, the data lend support to the hypothesis that Ae. sollicitans is capable of functioning as an epidemic vector in the coastal areas of New Jersey where human cases of EEE have been most common.
|
|
|
|
Dauphin, G., Zientara, S., Zeller, H., & Murgue, B. (2004). West Nile: worldwide current situation in animals and humans. Comp Immunol Microbiol Infect Dis, 27(5), 343–355.
Abstract: West Nile (WN) virus is a mosquito-borne flavivirus that is native to Africa, Europe, and Western Asia. It mainly circulates among birds, but can infect many species of mammals, as well as amphibians and reptiles. Epidemics can occur in rural as well as urban areas. Transmission of WN virus, sometimes involving significant mortality in humans and horses, has been documented at erratic intervals in many countries, but never in the New World until it appeared in New York City in 1999. During the next four summers it spread with incredible speed to large portions of 46 US states, and to Canada, Mexico, Central America and the Caribbean. In many respects, WN virus is an outstanding example of a zoonotic pathogen that has leaped geographical barriers and can cause severe disease in human and equine. In Europe, in the past two decades there have been a number of significant outbreaks in several countries. However, very little is known of the ecology and natural history of WN virus transmission in Europe and most WN outbreaks in humans and animals remain unpredictable and difficult to control.
|
|
|
|
Dowdle, W. R., & Schild, G. C. (1976). Influenza: its antigenic variation and ecology. Bull Pan Am Health Organ, 10(3), 193–195.
Abstract: Influenza viruses have two surface antigens, the glycoprotein structures hemagglutinin (HA) and neuraminidase (NA). Antibodies to each of these are associated with immunity, but the structures themselves are antigenically variable. When an antigenic change is gradual over time it is referred to as a drift, while a sudden complete or major change in either or both antigens is termed a shift. The mechanism of antigenic drift is usually attributed to selection of preexisting mutants by pressure from increasing immunity in the human population. The mechanism of antigenic shift is less clear, but one tentative hypothesis is that shifts arise from mammalian or avian reservoirs, or through genetic recombination of human and animal influenza strains.
|
|
|
|
Endy, T. P., & Nisalak, A. (2002). Japanese encephalitis virus: ecology and epidemiology. Curr Top Microbiol Immunol, 267, 11–48.
|
|
|
|
Fulhorst, C. F., Hardy, J. L., Eldridge, B. F., Chiles, R. E., & Reeves, W. C. (1996). Ecology of Jamestown Canyon virus (Bunyaviridae: California serogroup) in coastal California. Am J Trop Med Hyg, 55(2), 185–189.
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.
|
|
|
|
Gasser, R. B., Hung, G. - C., Chilton, N. B., & Beveridge, I. (2004). Advances in developing molecular-diagnostic tools for strongyloid nematodes of equids: fundamental and applied implications. Mol Cell Probes, 18(1), 3–16.
Abstract: Infections of equids with parasitic nematodes of the order Strongylida (subfamilies Strongylinae and Cyathostominae) are of major veterinary importance. In last decades, the widespread use of drugs against these parasites has led to problems of resistance within the Cyathostominae, and to an increase in their prevalence and intensity of infection. Novel control strategies, based on improved knowledge of parasite biology and epidemiology, have thus become important. However, there are substantial limitations in the understanding of fundamental biological and systematic aspects of these parasites, which have been due largely to limitations in their specific identification and diagnosis using traditional, morphological approaches. Recently, there has been progress in the development of DNA-based approaches for the specific identification of strongyloids of equids for systematic studies and disease diagnosis. The present article briefly reviews information on the classification, biology, pathogenesis, epidemiology of equine strongyloids and the diagnosis of infections, highlights knowledge gaps in these areas, describes recent advances in the use of molecular techniques for the genetic characterisation, specific identification and differentiation of strongyloids of equids as a basis for fundamental investigations of the systematics, population biology and ecology.
|
|
