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I am a scientific bricklayer helping to build, through new information that my colleagues and I discover, a sound foundation of knowledge about heaves (formerly called Chronic Obstructive Pulmonary Disease, or COPD) in horses. I rely on colleagues at my own and other universities to provide the skills I lack. My labor is like that of masons building ancient cathedrals, who knew that they might not see the edifice completed in their lifetime but that one day it would be complete, with a spire. My “spire” is a heaves susceptibility marker (HSM). With HSM, foals could be managed to prevent heaves, an informed decision could be made about purchasing a horse, or selective breeding might eliminate the disease.
We have used many approaches to gain clues about HSM, which I suspect is a result of a gene mutation. Primarily, we have used a scientific process known as hypothesis testing to investigate the etiology, or cause of, heaves. Many of these hypotheses were based on published research undertaken by other laboratories that we trust had undertaken careful and skilled studies. We investigated the effect of heaves on lung function, determined the time course of inflammation, and asked why muscle spasms occur around air passages and why excess mucus accumulates. Once it became clear inflammation is the basis of the lung dysfunction in heaves, we needed to find the signaling molecules involved, which required an understanding of the immune response. After 20-plus years, we can say with confidence that exposure of susceptible horses to high particulate loads from hay and other sources activates signaling molecules in lung cells. This response initiates neutrophilic inflammation, which is associated with increased activity of nerves and causes the muscle around airways to contract. Simultaneously, mucus accumulates as a consequence of increased activity of mucin genes and stiffening of the mucus. As long as inflammation persists, mucus persists, and structural changes in the airway muscle and surrounding fibrous tissue develop. Because excessive inflammation is at the core of the problem, HSM will most likely be a regulator of inflammation.
Our group has been able to generate this knowledge because of consistent funding (around $300,000 annually) for many years. A critical mass of faculty, graduate students, and technicians maintains the level of intellectual activity and technical expertise. We have developed skill in studying heaves. If our funding had been intermittent, we would lack experienced personnel as we diverted our research away from the horse to other endeavors.
As a horse person, you might say “Heaves is no threat to our industry, so do we really need HSM?” That is a valid criticism, but instead of heaves, think about the emergence of a “new” infectious disease or a syndrome such as Mare Reproductive Loss Syndrome (MRLS). When a new problem occurs for which a foundation of knowledge must be built, you need skilled “masons” in that field, with all their tools. These problems cannot be solved with a short-term financial fix utilizing individuals with little experience or knowledge in the relevant disciplines.
Dr. N. Edward Robinson, (517) 353-5978, firstname.lastname@example.org
College of Veterinary Medicine, Michigan State University, East Lansing, Michigan.
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Second Quarter 2005
THE INTERNATIONAL COLLATING CENTRE, Newmarket, and other sources reported the following disease outbreaks:
Cases of African Horse Sickness caused by serotypes 1, 2, 5, 6, and 7 affecting different breeds and types of horses were reported from seven provinces in South Africa. The first cases were reported in January, with most occurring during March and April. The highest mortality was recorded in KwaZulu-Natal Province, attributable primarily to serotypes 5 and 7.
Atypical Myoglobinuria was reported in France during April at eight premises, with nine deaths among 15 cases. A single case of Contagious Equine Metritis (CEM) was reported from Japan in a Thoroughbred animal. Eastern Equine Encephalitis (EEE) was prevalent in the United States in Florida.
The various clinical manifestations of Equine Herpes Virus (EHV) infection were extensively reported during this period. Thirty-two cases of EHV-1 abortion and early foal death were reported from Ireland, primarily among unvaccinated mares. On nine premises there was more than one case. A limited number of abortion cases were reported from Argentina, Japan, and the United Kingdom. The paralytic form of EHV-1 occurred on two premises in Switzerland and one in the United Kingdom. In the USA, EHV-1 paralysis was diagnosed at a boarding facility in Maryland and among Thoroughbred racehorses in three barns at Churchill Downs’ racetrack in Louisville, Kentucky, resulting in three animals being euthanized. The respiratory form of EHV was widely reported in France. Cases of coital exanthema attributable to EHV-3 were diagnosed on four premises in the United Kingdom, involving mares and stallions of a variety of breeds.
Influenza was reported from France and Sweden, and clinical cases of Equine Piroplasmosis were reported from South Africa, Switzerland, the United Arab Emirates, and Turkey. Strangles was reported on 20 premises in Ireland and 12 premises in Sweden. Vesicular Stomatitis attributable to the New Jersey strain of virus was confirmed in the United States in Arizona, Colorado, New Mexico, Texas, and Utah in April and most recently in Montana and Wyoming during August.
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Equine Protozoal Myeloencephalitis: Efforts to Open the Black Box
In the 35 years since Equine Protozoal Myeloencephalitis (EPM) was initially described as “segmental myelitis,” significant research advances have given us insight into this debilitating disease. An unfortunate by-product of this insight is the realization that there is still a great deal we don’t understand about EPM. It is now apparent that most cases of EPM are caused by the protozoan parasite Sarcocystis neurona, with the rare case attributed to the related parasite Neospora hughesi. Furthermore, we know that horses become infected with S. neurona by ingesting food and/or water that has been contaminated with feces from an infected opossum. That animal has picked up the parasite at its roadside smorgasbord of various small mammals (for example, raccoons and skunks).
What remains a mystery is why so many horses become infected with S. neurona—over 50% in some areas—yet patent signs of clinical disease are apparent in only a very small proportion of these infected animals. It is this central question that impedes our ability to accurately diagnose EPM and hampers efforts to rationally design new vaccines. Given its importance, the infection vs. disease dichotomy is a major focus for many investigators in the EPM research community.
The host animal and the pathogen are the yin and the yang of any infectious malady, and both facets can contribute to disease severity. For EPM, the infected horse (its genetic susceptibility, immune status, etc.) and/or the infecting S. neurona (strain virulence, inoculum size, etc.) may determine whether a simple infection will progress to acute neurologic disease. Consequently, both aspects of the EPM scenario are deserving of research attention. A number of recent and ongoing studies in horses and mice are providing a base of knowledge regarding EPM pathogenesis and the immune responses necessary to control parasite growth. By extension, these studies suggest how host immunity might become unsound, thereby leading to clinical disease. For example, the use of stress-induced immune alteration enhances the development of neurologic signs in an experimental disease model, thus supporting the hypothesis that host immunity influences the occurrence of EPM. However, the “classic” case of EPM has not been achieved in these infection studies, and attempts to further enhance the immunosuppression of experimental animals occasionally have led to puzzling results. As such, it appears that the susceptibility of the infected horse is not the sole determinant for EPM.
This evidence leads to questions about the influence on disease that might be attributed to the parasite. Studies at the gene and protein level have clearly established that molecular diversity exists between different isolates of S. neurona. Furthermore, research on the opossum has shown that this animal serves as the definitive host for a menagerie of very closely related Sarcocystis, including the prototypic S. neurona that has been recovered from EPM horses. However, it remains unclear whether these various Sarcocystis of the opossum are multiple distinct species or whether they represent strain-types of just one or a few species. Consequently, the possibility exists that not all S. neurona isolates (or S. neurona-like isolates?) are created equal, with some parasite strains having a greater capacity to cause EPM.
Ultimately, we may find that the progression to EPM is multifactorial and requires the assemblage of an unfortunate set of events. Rather than a single determinant, EPM might occur only when a susceptible horse ingests an adequate dose of a sufficiently virulent strain of S. neurona. As with any disease, continued basic research on both the host and the pathogen should eventually clarify the biological circumstances that lead to EPM. Only then will it be possible to confidently diagnose EPM and logically design new strategies for protective immunization.
Dr Daniel Howe, (859) 257-4757, email@example.com
Maxwell H. Gluck Equine Research Center, University of Kentucky, Lexington, Kentucky.
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Update on West Nile and Vesicular Stomatitis, 2005
The incidence as reported by the USDA of equine clinical cases of West Nile virus infection throughout the United States to the end of September 2005 is 805 cases. This compares with 863 cases reported for a similar period in 2004. States reporting the highest number of cases include California, Idaho, Utah and Nevada as illustrated in Figure 1 with many states on the Eastern Seaboard reporting no cases. Information on the incidence of equine cases on a state-by-state basis can be obtained from http://www.aphis.usda.gov/vs/ceah/ncahs/nsu/surveillance/wnv/wnv.htm.
A similar pattern of West Nile virus infection has emerged in the human population, with the Centers for Disease Control and Prevention reporting 2016 cases as of October 4 including 55 fatalities. The highest number of cases was reported from California 742 including 16 fatalities. This compares with 1782 human cases, including 56 fatalities throughout the United States during a similar period in 2004.
The first report of a clinical outbreak of Vesicular Stomatitis (VS) involving the New Jersey strain during 2005 occurred in Texas during April, followed by outbreaks in Arizona, Colorado, New Mexico, and Utah. During August, cases were reported in Montana and Wyoming and at the end of September among horses on a single premise in Idaho. At the beginning of October two premises in Nebraska were reported as positive with equine and bovine cases. (see Figure 2 for state by state distribution as reported by USDA). The total number of positive premises in 9 states is 389 with no new cases reported in Texas, Arizona, New Mexico and Utah. Two hundred and thirty seven premises have been released from quarantine. The ratio of equine to bovine cases is 502/140. Further information can be obtained from http://www.aphis.usda.gov/vs/ceah/ncahs/nsu/surveillance/vsv/vsv_maps.htm.
Canada has suspended the importation of live VS-susceptible species from all states known to be infected.
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Equine Disease Surveillance in Kentucky
Classical epidemiology textbooks list “establish the existence of an outbreak” as the first step in an outbreak investigation. This would generally be accomplished by a field investigation to a specific farm that is reporting an animal health problem. Information technology is providing the tools necessary to improve on that paradigm by allowing for the real-time capture and mathematical analysis of data streams that can signal very early on that an outbreak is unfolding. In addition, it is possible to predict that an outbreak might occur based on the detection and analysis of certain risk factors (for example, above-average rainfall and leptospirosis). The Livestock Disease Diagnostic Center (Lexington), the Breathitt Veterinary Center (Hopkinsville), the State Veterinarian’s office, and the Maxwell H. Gluck Equine Research Center are working to build such a system to better serve the Kentucky equine industries.
One type of surveillance system that is being adopted for use in human medicine is known as syndromic surveillance. The Centers for Disease Control and Prevention (CDC) defines this system as follows:
Syndromic surveillance applies to surveillance using health-related data that precede diagnosis and signal a sufficient probability of a case or an outbreak to warrant further health response.
Syndromic surveillance systems utilize near-real-time reporting of clinical data reported from reliable sources. The New York City Department of Health has built such a system to monitor chief complaints of patients at 39 participating emergency departments throughout the city. From November 2001 to November 2002, over 2.5 million patient visits were captured by the system (roughly 6,780 patient visits per day). Syndromes collected included respiratory, diarrhea, fever, vomiting, and more. Citywide signals were generated by the system for fever and respiratory cases on Christmas Day, 2001, which was the earliest indication of influenza activity in New York that year. These signals coincided with an increased request for influenza testing reported by laboratories around the city. This information was used to alert the allied medical community, a service that would not have been possible without the surveillance system.
Systems that collect syndromic data are powerful, but any data stream that is related to equine health can reinforce such a system. Diagnostic laboratory testing activity and results will be an important component of any surveillance system. The near-real-time collection and analysis of weather, soil, toxic plant, environmental, and insect data will also be valuable. Other data that might be useful are over-the-counter sales of veterinary products, carcass volume at rendering plants, and farm-level animal health observations.
The first step in this project is to ensure that all of the critical agencies have the appropriate information technology infrastructure to efficiently and accurately collect the data streams necessary to drive a surveillance system analysis engine. A state-of-the-art, Web-based system will be implemented in the State Veterinarian’s office this fall, which will become the centerpiece for a statewide animal health information management system. The Lexington and Hopkinsville laboratories are aggressively evaluating existing laboratory information management software systems for their facilities.
Once these systems are in place, the two laboratories and the State Veterinarian will be able to seamlessly share data in near-real-time fashion with laboratory clients, the Kentucky Association of Equine Practitioners, the Kentucky Thoroughbred Association, the Kentucky Thoroughbred Farm Managers’ Club, and other equine stakeholders. This data-sharing capability will set the stage for a fully functional animal health information system for Kentucky. Some of the services to be offered are electronic accessioning of laboratory cases and ordering of tests, Web access to laboratory test results, electronic filing of the laboratory test results into the client’s patient record, animal disease/ syndrome distribution maps and summaries, immediate identification of farms at risk during an outbreak, and electronic medical alerts when significant adverse animal health events occur. The confidentiality of all medical and demographic information will be ensured through appropriate log-on security.
Whether dealing with day-to-day clinical cases, emerging diseases, a foreign animal disease, a natural disaster, or an agro-terrorist attack, it will be critical that our key animal health agencies and stakeholders have the necessary technology to conduct surveillance and make the appropriate response. Fortunately, Kentucky is definitely heading in that direction and will one day be able to provide the equine industries with these powerful services.
Dr. Craig Carter (859) 253-0571, firstname.lastname@example.org
Livestock Disease Diagnostic Center, University of Kentucky, Lexington, Kentucky.
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The Morris Library at the Maxwell H. Gluck Equine Research Center has bibliographies on the following topics available for distribution:
Bibliographies are focused on research material related to horse health and management. In addition, the Morris Library can do literature searches on other specific topics. Printed copies of workshop proceedings on both Mare Reproductive Loss Syndrome and the equine placenta also are available. The library can be reached by phone at 859-257-4757 ext. 81147 on weekdays between 8 a.m. and 5 p.m. The librarian may be contacted by e-mail at email@example.com.
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To receive a printed copy of the Equine Disease Quarterly in the mail, send us your name and postal mailing address (not e-mail address). There is no charge.
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; firstname.lastname@example.org.
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