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Gluck Center > Equine Disease Quarterly > January 2006


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Influenza is in the news with predictions of a global catastrophe from Avian Influenza (Bird Flu) in Southeast Asia. Meanwhile, canine flu has caught the attention of American dog owners.  What is going on?

Influenza is a viral disease of many species, primarily waterfowl and poultry, but also humans, horses, and pigs. With the exception of pigs, these different species ordinarily have their own flu viruses—human flu does not spread to horses. But on rare, unpredictable occasions, a flu virus of one host species crosses into a different host, causing alarm bells to ring.

The last emerging equine flu virus was a bird flu that broke out in 1989 in horses in China; it was gone by 1991. No case of the subtype equine-1 (H7N7) influenza has been confirmed since 1980. Recommendations on equine flu vaccines are made by an international surveillance panel consisting of experts from OIE (World Organisation for Animal Health) laboratories in Newmarket, England, and Lexington, Kentucky, plus others from the World Health Organization. The panel has recommended the equine-1 subtype be removed from equine vaccines. There remain the twin families, or lineages, of subtype equine-2 (H3N8) influenza. The “Eurasian” lineage circulates but lately has not caused major outbreaks. The “American” lineage is predominant in both the Western Hemisphere and Europe and was responsible for large outbreaks during 2003 in Newmarket and South Africa. Some affected horses in Newmarket were vaccinated, a sign that vaccines needed updating to catch up with mutations in the American lineage virus. Accordingly, the panel recommends the American lineage constituent of equine flu vaccines should be similar to the South Africa/2003 strain. Viruses meeting this criterion have been supplied to manufacturers. A need remains for continued and improved surveillance for equine flu to assess ongoing vaccine effectiveness and also to spot any emergence of brand new flu viruses in horses (or re-emergence of old ones like equine-1). International air transport makes spread of flu remarkably easy, but the success of Australia and New Zealand in keeping flu out of their horse populations demonstrates the effectiveness of strict quarantine regulations.

Canine flu started around 2000 as a typical equine flu virus that dogs probably acquired by consumption of raw horse viscera. A separate outbreak occurred in England, probably with the same cause. In the United States, the equine virus adapted to dogs. Canine flu virus has several characteristic mutations absent in equine flu and now appears to be highly contagious for dogs. Canine flu vaccines will be forthcoming.

Bird Flu has not yet taken the critical step of developing high contagiousness for humans. Thanks to 40 years of research on the causes of flu pandemics (worldwide epidemics) a potential pandemic was spotted in advance. This gives an opportunity to nip the pandemic in the bud, if resources including vaccines, antiviral drugs, and effective quarantine can be brought into play early enough. There are other possibilities: Bird Flu might be unable to take the critical step to become highly contagious and fizzle out, or it might combine genetically with the usual human flu virus and become a human contagion. Betting on what the flu will do next is a risky business.

Dr. Tom Chambers, (859) 257-4757,
Maxwell H. Gluck Equine Research Center, University of Kentucky, Lexington, Kentucky.

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Third Quarter 2005

The International Collating Centre, Newmarket, England, and other sources reported the following disease outbreaks:

Anaplasma phagocytophilia (formerly Ehrlichiosis) was diagnosed among non-Thoroughbred horses on three premises in Switzerland. Respiratory disease attributable to equine herpes virus (EHV) was reported on multiple premises among several breeds of horses in France and several premises in the United Kingdom.

The paralytic form of EHV-1, involving two fatalities, was confirmed on a combined thoroughbred stud farm and racing stable in Ireland. South Africa reported two outbreaks in KwaZulu-Natal Province among performance horses, and in Switzerland, two fatal cases were recorded among Warmblood riding horses. Two limited outbreaks of Coital Exanthema (EHV-3) were reported among mares and stallions in the United Kingdom.

A case of Equine Infectious Anemia (EIA) was reported in Southwest Queensland, Australia, and four cases were reported at an equestrian center in France among various breeds. Two fatal cases of Grass Sickness were diagnosed among draught horses in Switzerland in a region that had experienced previous cases. Equine influenza was confirmed on several premises in France and one premise in the United Kingdom.

Outbreaks of Piroplasmosis affecting Thoroughbred performance horses were diagnosed on two premises in Eastern Cape Province, South Africa, and among non-Thoroughbred horses on six premises in Switzerland. Turkey reported a single case of equine rabies. Strangles cases were confirmed on premises in Ireland, South Africa, Sweden, and Switzerland.

As of the end of November, the USDA reported that the only premises confirmed with Vesicular Stomatitis that remained under quarantine were in the states of Colorado, Idaho, and Wyoming. Recent cases were confirmed in early November on two premises in Colorado and one premise in Wyoming.

The USDA reported in mid-November a total of 1,061 clinical equine cases of West Nile Virus infection throughout the United States for 2005. States reporting the highest number of cases were California (454), Idaho (114), Utah (68), Nevada (47), Oregon (46), Arizona (37), and Oklahoma (32), with many states on the eastern seaboard reporting no cases.  

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New Insights into Equine Herpesvirus-1 (EHV-1) Neurological Disease

Outbreaks of neurological disease caused by hypervirulent strains of EHV-1 have been reported with increasing and near-alarming frequency during the past several years (see July 2003 issue of the Equine Disease Quarterly). This disease is characterized by high morbidity and case fatality rates, resistance to prevention by vaccination, and the ability to affect horses of all breeds, ages, and vaccination status. EHV-1 neurological disease has the potential for causing catastrophic losses to both the welfare of horses and the economy of equine-based businesses.

Figure 1A major milestone in our understanding of the neurological form of EHV-1 infection recently has been achieved following a five-year, internationally collaborative research effort by scientists at the Maxwell H. Gluck Equine Research Center in the United States and the Animal Health Trust in the United Kingdom. With an eye toward identifying a genetic basis for the neuropathogenic phenotype of EHV-1, the DNA sequence of several key genes of the herpesvirus was determined for virus isolates collected from 48 outbreaks of EHV-1 neurological disease and 82 outbreaks of EHV-1 abortion without accompanying neurological involvement. The disease outbreaks occurred over a 35-year time span in eight different countries. An unanticipated outcome of the comparative genomics study was the finding of a single point mutation uniquely present in EHV-1 isolates from 83% of the neurological disease outbreaks and uniquely absent from 95% of EHV-1 abortion outbreaks. Importantly, the identified mutation that is highly associated (p<0.0001) with the capacity of an EHV-1 strain for causing neurologic signs in the horse is located in the catalytic subunit of the gene encoding the viral DNA polymerase. This discovery of a mutation-associated, monogenic determinant of EHV-1 neuropathogenicity has given rise to the hypothesis that underlying the pathogenetic basis of a neurologic EHV-1 strain is the acquired viral attribute of enhanced replicative aggressiveness made possible by a single, mutation-induced alteration of the enzymatic properties of its replicative polymerase. Recent empirical support of the hypothesis was provided by studies, supported by the Grayson-Jockey Club Research Foundation, Inc., demonstrating a fivefold greater level of virus delivered by viremic leukocytes to the blood vascular endothelium of the central nervous system of horses infected by paralytic strains of EHV-1 (Figure 1).

Two practical benefits have resulted from this first genetic characterization of neuropathogenic strains of EHV-1 and the ensuing discovery of a disease-conferring mutation that can be used as a genetic marker for identifying and tracking such mutant strains of the virus. First, the Maxwell H. Gluck Equine Research Center at the University of Kentucky, in partnership with the University's Livestock Disease Diagnostic Center (LDDC), is providing real-time surveillance of the prevalence and distribution of neuropathotype strains of EHV-1 as latent viral DNA in Kentucky's large Thoroughbred population. Submandibular lymph nodes collected from horses submitted to the LDDC for postmortem examination are being tested for the presence of latent neuropathotype strains of EHV-1 by polymerase chain reaction and subsequent DNA sequencing of the amplified polymorphic region of the latent EHV-1 DNA. The collaborative effort is part of the LDDC’s new epidemiology initiative designed to monitor disease trends and to identify and track emerging infectious disease threats to Kentucky’s livestock-based economy (see October 2005 issue of the Equine Disease Quarterly). Second, a molecular diagnostic technique has been developed for antemortem detection of mutant EHV-1 DNA present in tissue biopsies from the submandibular lymph nodes of latently infected carrier horses. These lymph nodes may act as reservoirs for the potential spread of neuropathotype strains of EHV-1. The neuropathotype carrier-identification procedure provides the option of an additional, test-and-segregate approach for minimizing the risk of outbreaks of EHV-1 neurological disease resulting from latent virus reactivation in carrier horses.

Despite the success of current-generation vaccines in reducing the losses from EHV-1 abortigenic disease over the past 25 years, the mutant neuropathotype EHV-1 strains have acquired an enhanced replicative vigor that allows them to overcome the level of immune responses induced by such vaccines. Two questions remain: what selective pressures favor the emergence and continued maintenance of such virus mutants and whether a causal connection exists between vaccine refractoriness of the neuropathotype EHV-1 strains and the apparent recent upsurge in their occurrences. However, the unsettling proposition of an emerging hypervirulence of EHV-1 and its evolving toward neuropathogenicity presents a daunting challenge to both equine researchers and vaccine manufacturers: development of new-generation vaccines with an increased protective efficacy commensurate with the evolved increase in virus virulence.

Dr. George Allen, (859) 257-4757,
Maxwell H. Gluck Equine Research Center, University of Kentucky, Lexington, Kentucky.

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Equine Pregnancy Terminology

There are different terms to describe the developing foal in utero. Furthermore, certain terms are used to describe the foal when it is delivered in an abnormal condition or at the wrong time of gestation. These terms can be confusing and are often improperly applied. It is important to use the correct terms because their use allows for better communication and helps categorize the process causing the problem, allowing certain conditions to be considered as possible etiologies and others discarded.

Following fertilization of the ovum, the early developing foal is referred to as a conceptus (the tissues destined to become the embryo and placental membranes) or an embryo. The term embryo can refer to the entire conceptus, or to the portion that forms the foal. The end of the embryo stage is somewhat arbitrary. Some authors use the end of organogenesis to signal the transition from the embryo to the fetus. Others prefer to classify based on when external taxonomic features become identifiable (the single digit in horses). Even using these criteria, the time point is not clear-cut. Completion of organogenesis has been proposed to be by day 23 of gestation by some and day 30 by others. External feature development allowing classification is anywhere from day 38 to 60. In general, a conceptus prior to day 40 is referred to as an embryo, and after day 40 as a fetus. The offspring remains a fetus until delivery, becoming a foal upon birth at the end of gestation. An equine fetus near the completion of gestation is sometimes referred to as a term fetus.

Premature interruption of gestation with loss of the offspring is a relatively common occurrence. In women it is referred to as miscarriage or preterm birth, and in animals it is called abortion. Abortion in horses is subdivided by time of occurrence. At the beginning of gestation it is referred to as early embryonic loss, and during the fetal stage it is called an abortion. Most pregnancy losses in mares occur as early embryonic losses. Abortions are also called stillbirths. Technically, delivery of a dead offspring at any time of gestation is a stillbirth; however, the term is usually reserved for delivery of a non-viable offspring after the time when viability outside the reproductive tract is possible. In humans this is usually after 24 weeks of gestation (prior to 20 weeks is termed a miscarriage). Using these criteria, loss in a mare after about 310 to 320 days would be a stillbirth. Although there is obvious overlap, it is useful to think of loss of a term fetus as a stillbirth, reserving abortion for earlier losses. This allows a different set of causes to be considered in a stillbirth, many related to the delivery or birthing process. By contrast, abortions are often caused by conditions affecting the membranes, such as placentitis or torsion of the umbilical cord.

In contrast to other species, mares have a highly variable gestation length. The average length of gestation is between 320 and 370 days. Therefore, the concept of a mare being overdue when gestation goes beyond the “average” 340-day interval is erroneous. Mares have to be considered on an individual basis. A mare will typically have her own normal gestation length. Therefore, a mare that normally delivers at 360 days may have a premature foal at 335 days, while a mare that normally delivers at 330 days may have a normal-term foal at 325 days. In general, births before 320 days are considered premature, and foals rarely survive if born before 300 days.

While premature describes foals born early, there are several terms used to describe live, but abnormal, foals born beyond their expected delivery date. Some of these foals are small and appear premature. These are dysmature foals. Dysmaturity is commonly associated with placental insufficiency. Foals with extended gestation that are normal to large in skeletal size but thin are called postmature. The classical cause of postmaturity is consumption of endophyte-infected fescue grass by the mare. Each of these conditions has distinct clinical characteristics and requires special medical treatment.

Dr. Neil Williams, (859) 253-0571,
Livestock Disease Diagnostic Center, university of Kentucky, Lexington, Kentucky.

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Reproductive Efficiency of Thoroughbred Mares in Central Kentucky

The State of Kentucky dominates the Thoroughbred breeding industry. In the 2003 foaling season, the Jockey Club reported that 26% of all registered Thoroughbred foals in the United States were from Kentucky. During the 2003 breeding season, 19,893 mares were bred to 386 stallions in Kentucky. This translates into an average book size (i.e., the average number of mares bred by a single stallion) of 51.5 mares.  The trend is toward larger book sizes. Kentucky stood 86 of the 126 stallions breeding more than 100 mares in 2005. The four stallions that bred more than 200 mares in 2005 all stand in Kentucky. Due to the large number of mares that must be bred to a single stallion during the short breeding season (February 15 to July 15), it is imperative that each mare is bred on as few reproductive cycles as possible. In addition to the necessity of getting mares in foal, it is important that these pregnant mares then carry their foals to term.

There are several methods to measure reproductive efficiency in the mare. Common measurements include live foal, pregnancy, and pregnancy loss rates. All of these measurements can be calculated per cycle or per season. Per cycle measurements look at the proportion of successful breedings over a single reproductive cycle, while per season measurements examine the proportion of successes over the entire breeding season. Per cycle measurements are better able to illustrate the influences of the stallion, veterinarian, and management on reproductive efficiency.

Several studies have examined factors that influence reproductive efficiency in the horse. These studies encompass three general categories: mare, stallion, and management factors. Many of these studies have two main limitations. First, the relationship between reproductive efficiency and each of the factors of interest are examined individually. This method of analysis does not take into account the influence of a confounder (i.e., a variable that is related to both the factor being examined and reproductive efficiency) on the results. Second, previous studies have not controlled for the correlation in pregnancy outcomes when a single mare is bred multiple times during the season.

A study to examine the influence of management and veterinary factors on reproductive efficiency is under way at the Maxwell H. Gluck Equine Research Center. Information was collected from 13 farms in Central Kentucky during the 2004 breeding season and the 2005 foaling season. A total of 1,091 mares were bred on 1,718 cycles, with 38.1% of the mares being bred more than one time during the season. Due to the sale of mares and the return of mares to their home farms, complete information on the day 15 and day 40 checks and the foaling outcome was available for 768 mares bred on 1,205 cycles.

The average pregnancy rate per cycle on day 15 and day 40 was 62.6% and 56.5%, respectively. Pregnancy loss from days 15 to 40 per cycle was 9.7%, and loss from day 40 to foaling was 9.8% (Table 1). Similar to previous studies, pregnancy rates per cycle on both days 15 and 40 decreased as mare age increased, while pregnancy loss rates increased with increasing mare age. The per cycle pregnancy rate was highest for the maiden mares and lowest for the barren mares. Pregnancy loss rate per cycle was lower for maiden mares than for barren and foaling mares (Table 2). Of the 768 mares, 79.4% produced a live foal. As in previous studies, the proportion of mares producing a live foal decreased as mare age increased.

Table 1. Influence of Mare Age on Reproductive Efficiency
  3-8 years 9-13 years 14-18 years >18 years TOTAL
No. Mares
No. Estrous Cycles
Day 15 Pregnancies/Cycle
Day 40 Pregnancies/Cycle
% Pregnancies Lost Days 15-40
% Pregnancies Lost Day 40-Foaling
% Mares Produced a Live Foal

Table 2. Influence of Mare Status on Reproductive Efficiency
  Maiden Foaling Barren
No. Mares
No. Estrous Cycles
Day 15 Pregnancies/Cycle
Day 40 Pregnancies/Cycle
% Pregnancies Lost Days 15-40
% Pregnancies Lost Day 40-Foaling
% Mares Produced a Live Foal

The influence of mare and farm level factors on pregnancy rates (days 15 and 40) and live foal rates will be examined. Statistical methods will be used to control for potential confounders and to control for the correlation among breeding outcomes from the same mare. The results will provide information regarding management and veterinary practices at the farm and mare level that significantly influence reproductive efficiency. This information will be used to examine the costs and benefits of implementing specific management and veterinary practices.

Karin Bosh, Graduate research assistant, (859) 257-4757,
Department of Veterinary Science, University of Kentucky, Lexington, Kentucky.

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Correspondence should be addressed to the editors,
Department of Veterinary Science, Gluck Equine Research Center,
University of Kentucky, Lexington, KY 40546-0099;
Phone (859) 257-4757; FAX (859) 257-8542;


Maxwell H.Gluck Equine Research Center
Department of Veterinary Science, University of Kentucky
Lexington, Kentucky 40546-0099

Main Office (859) 257-4757
Fax (859) 257-8542