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Lynch, J. J., Fregin, G. F., Mackie, J. B., & Monroe, R. R. J. (1974). Heart rate changes in the horse to human contact. Psychophysiology, 11(4), 472–478.
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Thrower, W. R. (1970). Aggression in horses. Proc R Soc Med, 63(2), 163–167.
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Friedberger, J. C. (1970). Modern horse training methods--what is justifiable? Vet. Rec., 87(8), 229–231.
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Judge, N. G. (1969). Transport of horses. Aust Vet J, 45(10), 465–469.
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Sinclair, M., Buhrmann, G., & Gummow, B. (2006). An epidemiological investigation of the African horsesickness outbreak in the Western Cape Province of South Africa in 2004 and its relevance to the current equine export protocol. J S Afr Vet Assoc, 77(4), 191–196.
Abstract: African Horsesickness (AHS) is a controlled disease in South Africa. The country is divided into an infected area and a control area. An outbreak of AHS in the control area can result in a ban of exports for at least 2 years. A retrospective epidemiological study was carried out on data collected during the 2004 AHS outbreak in the surveillance zone of the AHS control area in the Western Cape Province. The objective of this study was to describe the 2004 outbreak and compare it with the 1999 AHS outbreak in the same area. As part of the investigation, a questionnaire survey was conducted in the 30 km radius surrounding the index case. Spatial, temporal and population patterns for the outbreak are described. The investigation found that the outbreak occurred before any significant rainfall and that the main AHS vector (Culicoides imicola) was present in abundance during the outbreak. Furthermore, 63% of cases occurred at temperatures < or = 15 degrees C, the Eerste River Valley was a high risk area, only 17% of owners used vector protection as a control measure and 70% of horses in the outbreak area were protected by means of vaccination at the start of the outbreak. The study revealed that the current AHS control measures do not function optimally because of the high percentage of vaccinated horses in the surveillance zone, which results in insufficient sentinel animals and the consequent failure of the early warning system. Alternative options for control that allow continued export are discussed in the paper.
Keywords: African Horse Sickness/diagnosis/*epidemiology; African horse sickness virus/*isolation & purification; Animals; Ceratopogonidae/virology; Diagnosis, Differential; Disease Outbreaks/*veterinary; Female; Horses; Insect Vectors/virology; Male; Prevalence; Retrospective Studies; Sentinel Surveillance; South Africa/epidemiology; Viral Vaccines/administration & dosage
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Venter, G. J., Koekemoer, J. J. O., & Paweska, J. T. (2006). Investigations on outbreaks of African horse sickness in the surveillance zone in South Africa. Rev Sci Tech, 25(3), 1097–1109.
Abstract: Confirmed outbreaks of African horse sickness (AHS) occurred in the surveillance zone of the Western Cape in 1999 and 2004, both of which led to a two-year suspension on the export of horses. Light trap surveys in the outbreak areas showed that known vector competent Culicoides species, notably C. imicola, were abundant and present in numbers equal to those in the traditional AHS endemic areas. Isolations of AHS virus serotypes 1 and 7, equine encephalosis virus, and bluetongue virus from field-collected C. imicola in the surveillance zone demonstrated that this species was highly competent and could transmit viruses belonging to different serogroups of the Orbivirus genus. Molecular identification of recovered virus isolates indicated that at least two incursions of AHS into the surveillance zone had taken place in 2004. The designation of an AHS-free zone in the Western Cape remains controversial since it can be easily compromised, as evidenced by the two recent outbreaks. In light of the results reported in the present study, the policy of maintaining a large population of unvaccinated horses in the surveillance zone should be reconsidered, as it leaves them vulnerable to infection with AHS virus, which is the most pathogenic of all equine viruses.
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Sanchez-Vizcaino, J. M. (2004). Control and eradication of African horse sickness with vaccine. Dev Biol (Basel), 119, 255–258.
Abstract: African horse sickness (AHS) is an infectious but no-contagious viral disease of equidae with high mortality in horses. The disease is caused by an arthropod-borne double-stranded RNA virus within the genus Orbivirus of the family Reoviridae transmitted by at least two species of Culicoides. Nine different serotypes have been described. The nine serotypes of AHS have been described in eastern and southern Africa. Only AHS serotypes 9 and 4 have been found in West Africa from where they occasionally spread into countries surrounding the Mediterranean. Examples of outbreaks that have occurred outside Africa are: in the Middle East (1959-1963), in Spain (serotype 9, 1966, serotype 4, 1987-1990), and in Portugal (serotype 4, 1989) and Morocco (serotype 4, 1989-1991). Laboratory diagnosis of AHS is essential. Although the clinical signs and lesions are characteristic, they can be confused with those of other diseases. Several techniques have been adapted for the detection of RNA segments, antibodies and antigen. Two types of vaccines have been described for AHS virus. Attenuated live vaccines (monovalent and polyvalent) for use in horses, mules and donkeys, are currently available, as well as a monovalent, serotype 4, inactivated vaccine, produced commercially but no longer available. New vaccines, including a subunit vaccine, have been evaluated experimentally. In this paper a review of the last AHS outbreaks in Spain, occurring during 1987-1990, and affecting the central and south part of the country, is presented. The role that vaccination played for the control and eradication of the disease, as well as other aspects such as climatological conditions, number of vectors and horse management, are also presented and evaluated.
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Mellor, P. S., & Hamblin, C. (2004). African horse sickness. Vet Res, 35(4), 445–466.
Abstract: African horse sickness virus (AHSV) causes a non-contagious, infectious insect-borne disease of equids and is endemic in many areas of sub-Saharan Africa and possibly Yemen in the Arabian Peninsula. However, periodically the virus makes excursions beyond its endemic areas and has at times extended as far as India and Pakistan in the east and Spain and Portugal in the west. The vectors are certain species of Culicoides biting midge the most important of which is the Afro-Asiatic species C. imicola. This paper describes the effects that AHSV has on its equid hosts, aspects of its epidemiology, and present and future prospects for control. The distribution of AHSV seems to be governed by a number of factors including the efficiency of control measures, the presence or absence of a long term vertebrate reservoir and, most importantly, the prevalence and seasonal incidence of the major vector which is controlled by climate. However, with the advent of climate-change the major vector, C. imicola, has now significantly extended its range northwards to include much of Portugal, Spain, Italy and Greece and has even been recorded from southern Switzerland. Furthermore, in many of these new locations the insect is present and active throughout the entire year. With the related bluetongue virus, which utilises the same vector species of Culicoides this has, since 1998, precipitated the worst outbreaks of bluetongue disease ever recorded with the virus extending further north in Europe than ever before and apparently becoming endemic in that continent. The prospects for similar changes in the epidemiology and distribution of AHSV are discussed.
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Mellor, P. S. (1993). African horse sickness: transmission and epidemiology. Vet Res, 24(2), 199–212.
Abstract: African horse sickness (AHS) virus causes a non-contagious, infectious, arthropod-borne disease of equines and occasionally of dogs. The virus is widely distributed across sub-Saharan African where it is transmitted between susceptible vertebrate hosts by the vectors. These are usually considered to be species of Culicoides biting midges but mosquitoes and/or ticks may also be involved to a greater or lesser extent. Periodically the virus makes excursions beyond its sub-Saharan enzootic zones but until recently does not appear to have been able to maintain itself outside these areas for more than 2-3 consecutive years at most. This is probably due to a number of factors including the apparent absence of a long term vertebrate reservoir, the prevalence and seasonal incidence of the vectors and the efficiency of control measures (vaccination and vector abatement). The recent AHS epizootics in Iberia and N Africa spanning as they do, 5 or more yr, seem to have established a new pattern in AHS virus persistence. This is probably linked to the continuous presence of adult C imicola in the area. Culicoides imicola is basically an Afro-Asiatic insect and prefers warm climates. Therefore its continuous adult presence in parts of Iberia and N Africa may be due to some recent moderations of the climate in these areas.
Keywords: Africa, Northern/epidemiology; African Horse Sickness/epidemiology/*transmission; African horse sickness virus/*physiology; Animals; Arachnid Vectors/microbiology; Ceratopogonidae/*microbiology; Culicidae/microbiology; Horses; Insect Vectors/*microbiology; Portugal/epidemiology; Spain/epidemiology; Ticks/microbiology
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Milinovich, G. J., Trott, D. J., Burrell, P. C., van Eps, A. W., Thoefner, M. B., Blackall, L. L., et al. (2006). Changes in equine hindgut bacterial populations during oligofructose-induced laminitis. Environ Microbiol, 8(5), 885–898.
Abstract: In the horse, carbohydrate overload is thought to play an integral role in the onset of laminitis by drastically altering the profile of bacterial populations in the hindgut. The objectives of this study were to develop and validate microbial ecology methods to monitor changes in bacterial populations throughout the course of experimentally induced laminitis and to identify the predominant oligofructose-utilizing organisms. Laminitis was induced in five horses by administration of oligofructose. Faecal specimens were collected at 8 h intervals from 72 h before to 72 h after the administration of oligofructose. Hindgut microbiota able to utilize oligofructose were enumerated throughout the course of the experiment using habitat-simulating medium. Isolates were collected and representatives identified by 16S rRNA gene sequencing. The majority of these isolates collected belonged to the genus Streptococcus, 91% of which were identified as being most closely related to Streptococcus infantarius ssp. coli. Furthermore, S. infantarius ssp. coli was the predominant oligofructose-utilizing organism isolated before the onset of lameness. Fluorescence in situ hybridization probes developed to specifically target the isolated Streptococcus spp. demonstrated marked population increases between 8 and 16 h post oligofructose administration. This was followed by a rapid population decline which corresponded with a sharp decline in faecal pH and subsequently lameness at 24-32 h post oligofructose administration. This research suggests that streptococci within the Streptococcus bovis/equinus complex may be involved in the series of events which precede the onset of laminitis in the horse.
Keywords: Animal Feed; Animals; Bacteria/classification/*isolation & purification; DNA, Bacterial/analysis; Disease Models, Animal; Feces/microbiology; Foot Diseases/etiology/microbiology/*veterinary; Horse Diseases/*etiology/metabolism/microbiology; Horses; In Situ Hybridization, Fluorescence; Intestines/*microbiology; Oligosaccharides/*administration & dosage/*metabolism; Phylogeny; Polymerase Chain Reaction; RNA, Bacterial/analysis; RNA, Ribosomal, 16S/analysis
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