Table of Contents  
EPM: Equine Protozoal Myeloencephalitis   Equine Colic: Improving surgery odds   EVA: Equine Viral Arteritis
Cryptosporidium Parvum in horses    EIA: focus on genes    Fescue and poisonous plants
Grazing Yellow Star Thistle   Potomac Horse fever study results   Navicular
Melatonin and Mares: Time in a bottle    Lyme Disease   Moon Blindness
Micro Chip Identification services   Equine Cushing's Disease   DSLD


Cushing's disease in the horse is caused by hyperactivity of the pituitary gland. Researchers at the University of California at Davis Equine Research Laboratory (ERL) are studying pituitary function in horses. The pituitary gIand is responsible for the production and secretion of multiple hormones. The loss of normal pituitary gland control leads to the excessive secretion of adrenocorticotropin (ACTH) and endorphins. The excessive secretion of these hormones leads to the clinical manifestations of the disease. Because this syndrome resembles human Cushing's disease, for lack of a better term it has been called equine Cushing's disease, although the two disorders are not identical. Recent research at the University of California Davis has revealed that the abnormal hormone regulation more closely resembles Parkinson's disease.

The average age of Cushing's horses is 19 years. Mares, geldings and stallions of all breeds appear to be equally afflicted. Ponies appear to develop the disease more often than do horses.

Many horses with the disease exhibit the classic thick, long, curly coat that may not shed. Less striking coat changes are also seen, including a slightly heavier than usual winter hair coat. shedding later in the spring, patchy slow shedding and regrowing winter coats earlier in the fall than other animals housed under similar conditions. Obvious abnormalities may not be apparent early in the course of the disease, however, change in shedding behavior and/or the appearance of "guard hairs' along the chin or neck in the summer may be an early indication of equine cushing's disease.

Other clinical signs of Cushing's disease include an increased tendency to founder, excessive water drinking and urinating, excessive sweating, muscle wasting poor wound healing and elevated respiratory rates. Mares may also fail to cycle nominally or fail to conceive when bred.

The ACTH hormone controls the production and secretion of cortisol, a steroid hormone secreted from the adrenal gland. Cortisol causes a number of physiological responses including the reduction of inflammatory substances and an increased blood Sugar levels. A cyclical change in cortisol Ievels occurs throughout the day in nominal, unstressed horses. Very- low Ievels of ACTII and cortisol are present in the late afternoon and evening, but in the early morning hours ACTlI and cortisol levels start to increase in anticipation of the coming stress of the day. Horses with Cushing's disease exhibit no variation in the production of ACTH and cortisol because the abnormal pituitary control leads to continuous production of these substances. The adrenal glands of Cushing's horses are often three to four times larger than normal, indicative of increased stimulation of the adrenal glands by hormones being released from the abnormal pituitary gland.

Dexamathasone and prednisolone are synthetic copies of steroid hormones frequently used to treat a variety of musculoskeletal. respiratory and allergic problems in the horse. Prolonged use of these drugs causes undesirable side effects which match the problems seen in Cushing's horses.Excessive secretion of cortisol causes several problems. These include 1) immune deficiency, recognized as increased susceptibility to infections including pneumonia; 2) interference with normal protein metabolism, recognized as muscle wasting and pendulous abdomen (due to thinning of the skin and weakening of the abdominal musculature): and 3) resistance to insulin, responsible in part for the excessive water drinking; and urination seen in these horses. As a result of the insulin resistant effects of cortisol, horses with Cushing's disease often exhibit clinical signs of diabetes, but the high blood sugar levels cannot be corrected by treatment with insulin.

The other hormones, endorphins, produced in excess by the abnormal pituitary gland, are of importance because of their pain relieving properties. Endorphins are the body's natural opiates and are known to relieve pain by the same mechanism as morphine.They are responsible for the condition known as runner's high. Very little research on the effects of endorphins in horses has been done, but Cushing's horses make an excellent spontaneously occurring model for studying these effects.

The ERL research involves a 3 phase objective: 1) to characterize the clinical and pathological features associated with abnormal pituitary glands: 2) to investigate the potential treatment of horses with Cushings disease: and 3) to investigate the potential use of horses with Cushings disease as a spontaneous model for the study `of steroid hormones and endorphins and as a spontaneous model of human Cushing's disease.

They have tested different types of treatment with mixed results. One study was conducted on the use of cyproheptidine, an antiserotonin drug. Serotonin is one of two neurotransmitters released by neurons from the brain in the portion of the normal pituitary gland where the abnormal function occurs in diseased horses. These neurotransmitters are thought to control secretion of hormones from the abnormal part of the gland (this has proven to be true in rats). Serotonin stimulates hormone secretion, whereas the other neurotransmitter, dopamine, blocks secretion.

The mechanism by which hormone regulation is lost is similar to the mechanism in Parkinson's disease, in which dopamine containing neurons are lost from the brain. It is this loss of dopamine in Cushing's horses that leads to the similarity in Parkinson's disease. In this study, the researchers chose to block serotonin secretion rather than to increase dopamine Ievels, because of the wide safety margin associated with antiserotonin drugs. Dopamine type drugs affect the circulatory system which would increase the risk of founder.

This treatment yielded mixed results, with about 35% the horses responding with complete or partial remission of the disease. Remission was judged subjectively by an improved hair coat, weight gain and a brighter attitude. Remission was also judged objectively by the return of normal blood sugar levels and cortisol production.

Other treatments which have been attempted with unsuccessful results include: I ) the use of the drug dysodren which is used in dogs with Cushing's disease to kill the cells of the adrenal glands which produce cortisol, and 2) irradiation, both external beam and local implants. Surgical removal of the abnormal section of the pituitary gland is impractical because of the anatomy of the horse's head and the large size of the abnormal pituitary gland.

Researchers are now conducting studies to determine how the pituitary gland functions normally and what goes wrong in the brain to cause the loss of normal pituitary control. Newer methods of molecular biology are being used to accurately assess the exact sites in the brain that allows loss of secretory control. Through a better understanding of the hormone production and secretion from the pituitary gland, they hope to further understand stress adaptation in the horse and how to treat and control diseases associated with stress maladaptation. Because horses with Cushing's disease have a higher incidence of bone fractures, researchers are also looking for a possible cause of this problem.

The long term outbreak for untreated Cushing's horses is not always poor, as long as a high level of athletic or reproductive performance is not expected of them. The most important aspects of keeping these horses healthy from day to day involves basic husbandry, while keeping in mind the possible disease complications. It is critical to keep these horses, and any other horses they are exposed to, on a regular deworming program (preferably every 8 weeks but no less than every 12 weeks)

Cushing's horses are especially prone to Strongyle infestation. Teeth should be checked and floated as needed, twice per year. If weight loss is a problem the horse should be started on corn oil (up to a cup per day in the feed). Affected horses frequently do better if at least a portion of their diet is supplied as alfalfa pellets or alfalfa molasses meal.

Many horses with Cushing's disease founder easily, so care must be exercised in feeding grain supplements or leaving the horse on green pasture I f the horse has already foundered, corrective shoeing should be done to relieve pressure on the coffin bone.

Cushing's horses, particularly ones which have foundered are at higher risk than normal horses for developing sole abscesses. Care should be taken to try to prevent abscesses by keeping the feet clean, as dry as possible and well trimmed. If abscesses do occur they should be treated quickly and aggressively, as they respond poorly to treatment once the abscesses have progressed deep into the structures of the foot.

If the horse has an excessive hair coat, it should be body clipped during the hot weather to make it more comfortable. In areas with hot days and cold nights, the horse should be body clipped and then blanketed or stabled at night.

Many horses with Cushing's disease will exhibit an increased respiratory rate, which is not related to any disease process in the respiratory system. However, if an increase in respiratory rate occurs suddenly and is associated with fever, cough, opaque nasal discharge and/or loss of appetite the horse should be checked for pneumonia. Early and aggressive treatment is necessary, and even then the prognosis for recovery may be poor. The survival time of horses with Cushing's disease is greatly affected by many factors which can be controlled effectively with careful husbandry.

Recent conversation about a Peruvian Paso Horse who was diagnosed with this disease resulted in this article's submission by Peruvian Paso Owner and Veterinarian, Dr. Alice Wolf, for our educational benefit.

Update on Equine Protozoal Myeloencephalitis
Joseph J. Bertone, D.V.M., MS, Diplomate ACVIM

This article summarizes conclusions drawn from a recent symposium concerning Equine Protozoal Myeloencephalitis sponsored by the Grayson-Jockey Club Research Foundation, held March 5 through 8, 1996, in Lexington, Kentucky. Attendees were invited as experts in this or related areas. The Grayson-Jockey Club Foundation and the American Association of Equine Practitioners invited Dr. Joseph Bertone to attend this symposium as a regulatory representative, taking into account his clinical expertise.

Equine protozoal myeloencephalitis (EPM) is a progressive debilitating neurologic disease of horses associated with migration of Sarcocystis falcatula (neurona). It can affect any portion of the central nervous system. Clinical signs are related to focal (single site) or multifocal (many sites) neuropathology. Varied clinical signs may be present depending on the neural anatomic location of parasite migration and the ensuing inflammatory process. Click here for 4 more articles dating back to 1994 on this subject.

EPM occurs in much of the Western Hemisphere. Over 3000 horses have been diagnosed with the condition, by immunologic analysis of cerebral spinal fluid samples, since 1992. The number of affected horses is most likely greater. Surveys in Kentucky, Pennsylvania, Ohio, and Oregon identified that 50 to 60 percent of horses are seropositive for this organism (identifies exposure). The incidence of clinical disease involving the spinal cord is far lower. Climatic factors may affect exposure rates. The frequency of seropositive horses appears to be less in areas with greater numbers of freezing days, or with hot, dry climates. EPM is often sporadic (individual cases), but herd outbreaks have been reported in Kentucky, Ohio, Indiana, Michigan, Florida, and Maryland.


Life Cycle
The clinical disease and associated pathology have been recognized for over 20 years. However, the organism was not successfully cultured until recently (J.P. Dubey, et al. 1991). Once cultured, the organism was titled Sarcocystis neurona. Strong evidence suggests that the organism is Sarcocystis falcatula. The definitive host of this organism is the opossum, and various birds (brown headed cowbird, boat tailed grackle, and probably others) act as intermediate hosts. The horse is a dead-end, aberrant host. Infectious forms of the parasite are not passed from horse to horse, or from horse to the definitive or true intermediate hosts. Recent investigation indicates that opossum feces is the major source of infection. Opossums acquire the infection by eating infected birds. Birds and insects may contribute to feed contamination, but the importance of this to equine infection is unclear. Aberrant migration of Sarcocystis falcatula has been described in free-range chickens.


Signalment and Clinical Signs
EPM often progresses to loss of neural and musculoskeletal function and may lead to death. In many cases, the abnormal neurologic deficit is so subtle that abnormal function is attributed to other causes. EPM can affect any breed or sex. To date, the youngest horse identified was 2 months of age, and the oldest was over 30 years old. Clinical signs may be triggered or worsened by physiologic stress (e.g., shipping), or the administration of corticosteroids.

Currently, treatment of EPM includes a combination of antimicrobials that inhibit folic acid metabolism. Antimicrobial treatment simply clears the organisms and their associated inflammation. It does not guarantee return to function (see prognosis). Pyrimethamine, administered orally at 1 mg/kg, once per day, acts by inhibiting dihydrofolate reductase. The most common form of this drug used for EPM is a tablet approved for use in people. However, pharmacokinetic data, which is the basis for the dose, was collected by evaluating oral administration of bulk chemical and relating that information to the effects of this drug on other similar pathogens (C.R. Clark, et al. 1992). This drug is combined with sulfamethoxazole (oral, 12.5 to 25 mg/kg, once or twice per day) or sulfadiazine (oral, 20 mg/kg, once per day). The doses of these drugs are based on pharmacokinetic analysis as well. The only veterinary formulations of the two sulfonamides are in combination with trimethoprim. Trimethoprim is not useful for treatment of this condition and may contribute to increased risk of adverse drug reactions. Folic acid metabolism inhibitors should be administered 1 hour prior to feeding hay.

The average duration of treatment is 90 to 120 days, and may exceed 6 months in some instances. The appropriate length of treatment and the methods to determine adequate treatment duration are unknown. Negative western-blot analysis, or PCR on CSF may be useful to determine the time to withdraw treatment. Premature withdrawal of treatment often leads to relapse, which is often associated with a poorer prognosis for improvement or recovery. Sub-optimal dosing or intermittent therapy (for treatment or prophylaxis) has no proven efficacy and may lead to increased resistance of the organisms within the treated individual. If resistant organisms develop, they will most likely reside in that affected horse, since they cannot multiply in aberrant hosts.

Adverse side effects of drug therapy may include anemia, abortion, diarrhea, and leukopenia (low white blood cell counts). In some cases, the initiation of therapy may be associated with worsened signs. This response is believed to be associated inflammation, secondary to death of organisms within the spinal tract. Administration of a nonsteroidal anti-inflammatory drug in the initial stage of treatment has been recommended to alleviate this situation. Folic acid supplementation, administered at 40 mg orally, once a day, may help prevent adverse side effects associated with bone marrow suppression and may also reduce the risk of abortion. This quantity of folic acid supplementation will not inhibit the effect of the absorbed drug. Supra-pharmacologic concentrations of folic acid are required to overcome the effects of drug-inhibited folic acid metabolism. Folic acid should not be administered at the same time as the antimicrobial drugs as it may inhibit antimicrobial drug absorption.

In cases with severe neurologic signs, nonsteroidal anti-inflammatory medications (labeled doses), dimethylsufoxide (intravenous, diluted 5 to 1 in saline solution), and supportive care are often added to the treatment regimen.

Antimicrobial treatment simply clears the organism and its associated inflammation and does not guarantee return to function. The specific site and extent of the lesion, the horse's use, duration of disease, and physical therapeutics are the most important contributors to prognosis once the organism has been cleared. Early detection and treatment increases the chance of success. Response to treatment is highly variable. Many treated horses return to their original level of function; however, many respond incompletely. It is estimated that approximately 10 percent of cases relapse after treatment is discontinued.

Comment from Paso Owner and Veterinarian:
Surveys checking on blood test findings in normal horses have a high rate of "positive" results from some parts of the country. Blood testing detects antibody in the circulation in response to infection by the organism. HOWEVER... as the article reports, positive blood test results indicate only EXPOSURE to the organism but not DISEASE caused by the organism. Many horses are probably infected but their immune system handles the parasite and eliminates it before it causes any problem. Very likely, they are then immune from further infection. The central nervous system (CNS = brain and spinal cord) are a very protected area of the body. The cerebrospinal fluid (CSF = the fluid that bathes the brain and spinal cord) will only have high levels of antibody against the parasite if it has been infected. Therefore, strong positive CSF antibody level (in an animal with appropriate signs of disease) is good evidence that the signs are caused by the EPM parasite. A diagnosis should not be made on the basis of peripheral blood test results alone. CSF antibody levels (along with proper examination of the protein and cells in the fluid) are required for definitive diagnosis of EPM.....Alice


Testimony of Peruvian Paso Owner:
Two horses at the barn I board at were diagnosed with EPM via CSF testing last spring/summer. One was a 13 yr old TB/QH cross and the other a 3yr old pure QH. The 3 yr old was actually more symptomatic than the 13 yr old.
As barn boarders, our first reaction was one of panic, but as we did more research and were reassured by our vets that the condition was NOT transmitable to our horses, we calmed down. The have been no recurent incidences of the disease. Both horses were relative newcomers to the barn so we like to think they were infected on arrival. However, the barn management is very careful to keep stored hay and grain covered and away from bird droppings.
Both horses underwent the 6 months + of treatment. The 13 yr old progressed rather rapidly to a point and has remained there. He is lightly usable, but that's all his owner wants. Maybe he could do more, but it isn't asked of him.
The 3 yr old was a different story. His disease would seem to go into remission, then exacerbate. This happened several times, but each time he would improve more and more. Finally after about 6 months, he began to steadily improve, until several months ago he got a clean bill of health from his vet. His owner currently has him in training as a western pleasure horse. She would like to show him in this class and he has improved his gait enough to be competitive. Her vet told her as long as the horse was not unduly stressed, he should be able to perform. ........Euel

This article was published on the "FDA Veterinarian" and it is free of copyright so may be reproduced without permission.

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If Wishes Were Horses............

More often than not, the ability to begin a research project is based on finding not on talent. We were recently asked to identify research projects that we would like to do if finds were available. The two following research projects are based on critical needs for the horse industry. Each would complement on going research and provide training opportunities for young scientists.

MELATONIN AND MARES: Time in a bottle
Equine Research & Service Report, University of Kentucky College of Agriculture
Edited from Volume X,No.2, Fall 1996 issue · 805 South Limestone · Lexington, KY 40536-0339

While the jury is still out on the use of the popular hormone melatonin in people, there is growing evidence that the hormone has the potential to revolutionize the brood mare industry.

Melatonin is a hormone which is produced in the brain and is secreted into the bloodstream during the night. This provides the individual with a chemical signal by which it can distinguish night and day. It is this signal which tells a mare when seasons are changing and when it is the optimum time to breed.

Currently, breeders who wish to get their mares bred early in the season must rely on producing an artificial photo period through expensive lighting set-ups. However, research being proposed by Dr. Barry Fitzgerald, a reproductive physiologist at the University of Kentucky Gluck Equine Research Center, may make those setups a thing of the past.

"Melatonin has often been considered to be time in a bottle," said Fitzgerald. "You can give melatonin to an animal and change its response to photo period."

While Fitzgerald has done ground breaking work in this important field of research in the past, lack of funding may delay or prevent further proposed research. "We would like to continue to work on this line of research," he said, "because of the significant economic impact it could have for the horse industry."

Melatonin has been widely used, particularly in Europe, to manipulate the reproductive activity of sheep. Preliminary research on the effects of melatonin on the breeding cycle of mares has been carried out in France. In light of the fact that melatonin is secreted during the night, and that during the longer periods of darkness in winter months the animal is exposed to more melatonin, it would seem that the hormone would have the opposite to the desired effect in the brood mare.

"Research conducted in France has shown that when you administer melatonin for a long period of time, the animal does in fact switch off," said Fitzgerald. "But then spontaneously, it will show reproductive activity. What this tells us is that after a certain period of time, such a mare will spontaneously break away from that inhibitory signal. This is called photo refractoriness."

Fitzgerald envisions a time when breeders would have the option of inserting a small implant of melatonin every 28 days. This would relieve breeders of the need to keep their mares indoors under lights, and would enable them to maintain their mares under the same management practice year-round.

Another potential use for melatonin which may become a reality someday relates to the ability of the hormone to influence the timing of the birth of foals.

"We know that mares usually foal at night," said Fitzgerald. "Problems that arise at time of foaling necessitate calling the veterinarian in the middle of the night."

Melatonin treatment could be used to induce a sense of nighttime in the animal, thereby switching the time when it would give birth in the normal course of events.

This would be very helpful from a management standpoint as you would have foals being born during the day when people are around and help is readily available, if required," Fitzgerald noted.

Disturbances of melatonin rhythm are also of interest to Fitzgerald. The hormone is currently being investigated as a means of treating jet-lag in humans. With the racing industry becoming more globally-oriented, scientists now consider the idea that horses may also suffer from jet-lag.

"If horses travel a very long distance through a number of time zones, then they, like humans, will experience changes in their melatonin rhythms," said Fitzgerald. "We would like to know whether the change in melatonin rhythm can interfere with their potential performance capability."

Fitzgerald has a great deal of experience in studying the effect of photo period on brood mares, and was awarded a grant from the Grayson Jockey Club Foundation which has now been completed. If you would like to learn how you can help further this vital research, please contact the UK Equine Research Foundation at (606) 257-1308.

"We would like to continue to, work on this line of research," he said, "because of the significant economic impact it could have for the horse industry."

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EIA: Focus on Genes
Equine Research & Service Report, University of Kentucky College of Agriculture
Edited from Volume X,No.2, Fall 1996 issue · 805 South Limestone · Lexington, KY 40536-0339

 Dr. Charles J. Issel has battled equine infectious anemia (EIA) since 1974. Along this long road, he has worked toward developing better testing methods, developing a vaccine, and controlling the spread of this sometimes deadly virus.

But in recent years Issel, the UK Gluck Equine Research Center's Wright-Markey Professor of Equine Infectious diseases, and his team began taking a different approach in their fight against EIA, an approach at the ultra structural level with very significant potential.

"Our work has shifted in emphasis in that we are now focusing on gaining a better understanding of the genetic factors of the virus that control its multiplication and the ability of the virus to cause disease," said Issel.

"This research is really a continuum of our previous work," he continued. "We were awarded a grant from the National Institute of Health (NIH) beginning in November. These funds will support only a portion of the proposed work, which will be carried out in collaboration with the University of Pittsburgh."

The EIA virus can give rise to chronic infection and recurrent fever, and sometimes to the ultimate demise of the horse. Additionally, while it is not considered directly contagious, it is easily spread through the use of contaminated needles and, most commonly in the United States, through the transfer of infected blood by blood-feeding in sects.

The EIA research team at the Gluck Center is studying the basic components of the virus to determine how specific genes control replication. A great deal of work has already been completed by the scientists on cloning the virus so that the intrinsic properties of different genes can be established.

"We have made some progress in terms of looking at viral sequences that helped control viral replication," said Dr. Frank Cook, a molecular virologist at the Gluck Center. "These sequences, called Long Terminal Repeats (LTRs), are located at the ends of the viral genome, and essentially serve to hijack specific proteins that are important to the growth of the host cell."

"Lentiviruses, like HIV and EIAV, mutate at very high rates," explained Issel. "So we think of these as being like a cloud that is always adapting to its environment. Winds blow it, it bumps into mountains, it changes its shapes and that is what the virus does. Every time it gets into a given environment, it adapts to that environment by constant selection of more fit populations which can multiply there."

Not all strains of EIA are virulent, or in other words, have the ability to cause disease. One which is virulent is known as the Wyoming strain. This strain contains a triplet of control sequences known as ETS motifs. When scientists adapted the Wyoming strain to grow in cell culture in the laboratory rather than in the horse, they found it had lost its virulence. Gluck Center scientists have found that loss of virulence and ability to grow in cell culture appear to be Correlated with deletion of one of the ETS motifs.

While at Louisiana State University, before he came to the Gluck Center in 1990, Issel took the avirulent virus and put it back into a horse, then passed it through two more horses. He found that this virus which was grown in cell cultures can mutate and regain virulence. In the process, it gained something very similar to an ETS sequence found in the Wyoming strain.

According to Cook, graduate student John Langemeier has done a great deal of sequencing of these control elements, the results of which will soon be published.

"We think we've discovered one region of the viral genome that controls virulence," said Cook, "but it's not the only area."

To that end, the team has recently developed techniques which simplify the process of producing the virulent clones of EIA. They took one of their prototype avirulent clones grown in cell culture and substituted 40 percent of the genome from a virulent strain.

While the genetically engineered strain does not cause disease as quickly as the Wyoming strain the first time it is inoculated in a horse, the disease develops much more quickly when it is inoculated into a second horse, implying that additional mutations have taken place. With the study the team is currently proposing, this technique should allow them to better understand the inner workings of EIA virus.

As EIA virus is a lentivirus, it is comparable in many respects to the Human Immunodeficiency Virus (HIV) which causes AIDS. Understanding the way the more primitive EIA virus works could pave the way to gaining a greater understanding of the complexities of the AIDS virus.

"There are a lot of basic questions we're trying to address," said Issel. "We are trying to understand how the virus changes in its passage through cell cultures and back into animals, because it is only through a greater knowledge of what sequence changes occur that we can better understand how the virus proteins change. And in this way we can develop more effective immunization programs by tailoring our vaccines to meet the demands that the virus presents as it adapts to its environment in the horse."

To be a part of this ground breaking research at the Gluck Center, please call the UK Equine Research Foundation at (606) 257-1308.

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Cryptosporidium Parvum in horses
Morris Animal Foundation Animal News
Edited from the Volume III 1996 issue · 45 Iverness Drive East · Englewood, CO 80112-5480 · 303-790-2345 · 800-243-2345

Cryptosporidium parvum (C. parvum) is a parasite that can cause diarrhea in both horses and humans. Diarrhea is a serious health problem in young horses, affecting up to 80 percent of foals less than six months of age. Diarrhea in foals can be fatal.


Noah Cohen, VMD. PhD, MPH, and his co-investigators Dana Cole, DVM. and Karen Snowden, DVM, PhD, of Texas A&M University, are investigating three diagnostic tests to determine the presence of C.parvum in feces in a Morris Animal Foundation-sponsored study. According to Dr. Cohen, little is known about the source of this parasite or how to diagnose its presence. It is possible that the oocyte (egg-like) stage of this organism is passed in the feces of affected animals and may be passed into water supplies affecting people and other animals.

The investigators have three objectives for the study: 1) to evaluate three diagnostic tests for detecting C. parvum oocysts in feces; 2) to determine the prevalence of cryptospondial infection in three equine populations; and 3) to identify risk factors associated with fecal shedding of C parvum oocysts.

Dr. Cohen explains, "It is not yet possible to define methods of prevention or to control diarrhea in foals with C. parvum infections. Certain states in the United States are already considering legislation to restrict the activities of horses near water to prevent contamination of human water sources."

The investigators plan to compare three testing methods: a staining technique that can be performed at any veterinary clinic or laboratory with a microscope; two immunological tests that are available at many commercial diagnostic laboratories: and a newer method known as flow cytometry that is not widely available. The relative accuracy of these tests for equine samples has not been determined. The purpose of these comparisons is to determine what test works best for horses so that equine veterinarians will know the relative accuracy of these tests.

Three equine groups have been selected for this study to evaluate variations of prevalence of the disease by signalment,environment, and health status. Fecal samples will be collected, preserved, and evaluated for the presence of C. Parvum using each of the diagnostic tests. The prevalence of C. parvum shedding will be determined in each population and the results compared. The horse populations represent most areas and regions in the state of Texas, thus certain geographical factors may also be obtained in the results.

The investigators have several objectives. They want to determine how frequently infection occurs in horses, and to determine if the frequency of infection varies by age, activity, water source or other factors. The factors that are more frequently identified in infected horses may provide clues to how infection is acquired and how infection might be prevented. They also hope to determine if any association exists between infection with C. parvum and clinical signs of disease. The investigative team hopes to determine the relative accuracy of different testing methods so that equine veterinarians will be able to make informed decisions about testing methods.

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Morris Animal Foundation Animal News
Edited from the Volume III 1996 issue · 45 Iverness Drive East · Englewood, CO 80112-5480 · 303-790-2345 · 800-243-2345

Equestrians know that colic attacks horses without warning and often causes death within hours. Colic is the leading cause of death in horses. Even horses that receive immediate medical attention may die after surgery. Jack Snyder, DVM. PhD and co-investigator Nicholas J. Vaffstas, BVSc, are beginning the second phase of a study addressing this surgical complication at the University of California at Davis School of Veterinary Medicine.

Colic is a condition where the intestine rapidly bloats with gas and often twists. Within hours the horse may die if not relieved of the gas and twisting intestine. Despite surgery to untwist the intestine, according to Dr. Snyder, 76 percent of these horses are eventually euthanized.

In a previous Foundation-sponsored study, Dr. Snyder found that tissue damage continues to occur when the blood flow is restored to the twisted segment of intestine, called ischemia reperfusion injury. This damage is likely caused by the formation of reactive oxygen-derived free radicals in the tissue and by a build-up of toxins in the blood of the damaged portion of intestine. These oxygen radicals then cause further tissue injury and the toxins are released into the horse's system when the intestine is repaired; this is often fatally poisonous to the horse.

Other studies have shown that nitric oxide prevents this type of tissue damage. Drs, and Valistas believe that nitric oxide might prevent the continuing damage that OCCI following colic surgery. Nitric oxide may regulate the permeability of toxins in the blood.

Armed with information about the role of nitric oxide in reducing tissue damage, these scientists anticipate developing a preventing intestinal damage that occurs with the reintroduction of blood flow after colic surgery. Dr. Snyder explains, "We are excited about our new model that the Comparative Gastroenterology Laboratory has developed with the Foundation support. This research tool will greatly facilitate our investigations of many important gastrointestinal problems which previously required live animals and were expensive and time consuming. Preliminary results are encouraging and I feel we will make a significant contribution to improve the survival of horses that undergo surgery for colic."

High Prairie Farms Equestrian Center and Helen Fusscas, Southern Pines International, and Morris Animal Foundation are co-sponsors of this colic study.

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Morris Animal Foundation Animal News
Edited from the Volume III 1996 issue · 45 Iverness Drive East · Englewood, CO 80112-5480 - 303-790-2345 · 800-243-2345 

Jonathan E, Palmer. VMD, completed a Morris Animal Foundation funded pilot study, "Detection of Ehrlichia risticii by PCR in Equine Tissues," conducted at the University of Pennsylvania College of Veterinary Medicine.

Potomac horse fever, caused by the bacteria Ehrlichia risticii, induces diarrhea, gastrointestinal upset and abortion in horses. The current diagnostic test relies on detection of antibodies and, according to Dr. Palmer, "Recently it has been shown to be inaccurate in many instances (falsely positive tests)." Dr. Palmer and his team tested the capability of a new genetic test, polymerase chain reaction (PCR), to detect Ehrlichia risticii in tissue and blood samples.

Dr. Palmer said, "We proved that this PCR diagnostic test is very accurate in detecting abortions caused by Ehrlichia risticii." It should also prove useful when trying to determine if an animal died from Potomac horse fever. Dr. Palmer explained, "This technology has already been adapted for use as a blood test for Potomac horse fever, which should replace the currently used blood tests."

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Grazing Yellow Star Thistle
University Of California Cooperative Extension ~ The North Central Region Livestock, Dairy & Pasture Report 

Craig Thomsen probably knows more about yellow starthistle and its control than just about anyone. Craig is a Staff Research Associate at U.C. Davis, and has been studying the effects of grazing on yellow starthistle for almost a decade. He has conducted experiments on several ranches grazing starthistle with cattle, sheep and goats.

Timing is everything: Craig has found that yellow starthistle infestations can be effectively managed or exacerbated with grazing. Timing is the key.

According to Craig, the most effective grazing strategy is to graze cattle, sheep or goats in infested pastures when plants are bolting but before spines have appeared (mid-May and June). After this initial grazing, two or three follow-up grazings about two weeks apart are generally needed to remove starthistle regrowth. The ideal timing of grazing depends on the weather, especially the amount and timing of rainfall, but Craig has found that this general sequence reduces starthistle density, height and seed production. During this period its protein content is about 13% and it is likely to be one of the few green pants on an otherwise dry range. Livestock actually selected yellow starthistle when it was bolting over other available forage on annual range.

It can backfire: Grazing starthistle in the rosette stage (March-April) does not suppress it and in fact tends to increase it relative to other pasture plants.

Grazing can keep yellow starthistle in check and take advantage of it as a late season protein source. But grazing alone will not eradicate yellow starthistle. Craig has recently started an experiment which combines grazing treatments with seeding adapted legumes to compete with yellow starthistle. We'll report the results of his work in a future issue.

While safe for ruminants (cattle, sheep & goats) yellow star thistle is toxic to horses. Prolonged consumption can cause "chewing disease", a fatal nervous disorder. A horse generally needs to eat over 100 pounds for the disease to appear.

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Lyme disease has become a serious public health threat in the U.S. The disease has now spread to 46 states. A few years ago, it was practically unknown outside a few locations in the Northeast. The disease has received considerable attention as a potential threat to human health. However, little notice has been taken of the disease in animals. Its prevention, detection, clinical signs and treatment in dogs, horses, cats, and farm animals are similar in many respect to those in humans. Yet there are some important differences to be aware of to keep your animals healthy.

Cause of Lyme Disease

Lyme disease is caused by the spirochete Borrelia burgdorferi transmitted to animals and humans through the bite of certain kinds of ticks, primarily the deer tick in the Northeast and the California black-legged tick in the West. Although the organism has been found in other kinds of ticks, it is not clear if they can transmit the disease.

Origin Of Lyme Disease

Lyme disease was first diagnosed in the U.S. in 1976 in Lyme, Connecticut, in people who lived in close proximity to wooded areas and populations of deer. The deer tick, Ixodes dammini, in its larval stage, generally feeds on the white-footed mouse, an animal that carries the Lyme disease organism with no ill effects. In the subsequent nymph stage, the tick will generally feed on larger warm-blooded animals. As an adult, the tick feeds and mates on a host animal and the females drop off, lay eggs and die. The ticks are capable of infecting humans and pets during ALL stages of their development. However, nearly 90% of human cases are caused by bites from infected nymph stage ticks. For some reason, the disease organism does not cause illness in some host animals, including deer and migratory birds. But with the arrival of people and their pets in the territory, the deer tick found new hosts, ones for whom infection with the Lyme disease spirochete has serious consequences.

Two-YearCycle Of TheDeer Tick Larval Stage

Larval deer ticks are tiny, six-legged creatures that are nearly invisible to the unaided eye. The feed on small mammals such as mice and moles, and generally pick up the Lyme spirochete from the white-footed mouse.

Nymph Stage

The following spring, larvae molt into slightly larger eight-legged nymphs which feed once on larger mammals such as dogs, deer and humans.

Adult Stage

Nymphs molt into adults in the fall, attach themselves to a host, commonly the white-tailed deer, where they mate. The males die shortly after mating, and the females continue to feed until the spring, then lay eggs and die.

Detecting Lyme Disease in Pets

Testing annually (between April-December) is ESSENTIAL for diagnosis of Lyme disease. The disease can become advanced in some animals before signs are evident. In addition, the signs in animals and man mimic many other conditions such as arthritis, heart disease and flu. In dogs there may be sudden acute lameness, fever, swelling of joints and loss of appetite. Horses may exhibit some of the same signs plus weight loss. Cats appear to contract Lyme less frequently than many other species. When they do, cats may sleep excessively, become feverish, appear arthritic or lame, and stop eating. The most common condition in all species - pain and swelling of joints - causes the animal to move as if it is 'walking on eggs.'

Progression of the Disease

Lyme disease progresses in three stages.

STAGE ONE may last for several weeks after the tick bite and may include a characteristic "bull's eye rash" at the site of the bite, and flu-like symptoms - headache, fatigue, fever, chills, nausea. The signs may disappear completely after a while, but the disease is NOT gone. It may reappear later with more serious consequences.
STAGE TWO may begin weeks or months after the tick bite. At that point, more serious complications occur, including lameness, swelling of joints, neurological and cardiac problems, such as heart arrythmias. The pets are feverish and appear to be in pain.
STAGE THREE is where permanent damage occurs. Arthritis and resulting erosion of cartilage and bone cause permanent joint damage. Kidney and neurological damage is also likely at this point. The spirochetes that cause this disease can cross the blood/brain barrier and result in brain damage. In humans this creates conditions that mimic dementia or Alzheimer's disease; in pets, it results in loss of coordination, seizures and unusual or aggressive behavior. Lyme disease is seldom fatal in humans or animals. However, it allowed to progress to STAGE THREE, the disease can result in severe joint crippling and neurological disorders and near total debilitation of the victim. In pets, such conditions cannot be corrected or alleviated and would be cause for euthanasia.

Prevention Of Lyme Disease

The ticks that carry the disease are most common in wooded areas in moist climates. Therefore, animals that roam freely outdoors are the most likely victims. If you live in or near wooded areas and your pets spend any time outdoors, you should check them routinely once of twice a day and thoroughly after walks outside. You can protect yourself by wearing long-sleeved shirts with tight-fitting collar and cuffs, and also by tucking your trouser cuffs into your boots. Check yourself carefully for ticks. Brush (or use flea comb) on your pet's coat over a light colored surface so that you can see any ticks you dislodge. Ticks that carry the disease are quite small (pinhead size) and dark brown in color. Also check the skin for ticks that have attached themselves. Remove these by grasping the tick as close to its head as possible with tweezers (DO NOT use your bare hands) before pulling. Squeezing the body of a gorged tick can force blood back into the pet and increase the chance of infection.

Frequent Checks for ticks is the best preventive medicine, as evidence suggests that the Lyme organism is not introduced into the bloodstream of the host animal for some hours after the tick has attached itself. If pets are penned outdoors, the areas in which the run should be regularly treated in spring and summer with an insecticide approved for kennel use and/or outdoors. Tall grass, weeds and brush in the area should be cut. Insecticide powders and collars may help control ticks, as will some of the newer permethrin insecticide dips and sprays for dogs.

Consult Your Local Veterinarian for specifics on insecticides/repellents for your area. There is NO vaccination currently available for Lyme disease. The spirochetes that cause the disease have the frustrating ability to survive and multiply in the presence of the antibodies you pet develops in an attempt to ward them off. A spirochete has the ability to modify itself into a form that the antibodies do not affect. As a result, an animal that contracts the disease will develop no immunity to it.

Cures For Lyme Disease

Animals treated for Lyme disease in its early stages often appear to be cured, thought it is not entirely clear whether the "cured" or "arrested" is the proper term. Many animals continue to test positive for the disease after having been "cured." The most effective treatment will be recommended by your veterinarian and will depend largely on the stage of the disease, your pet's history and its response to treatment.

Can you be affected with Lyme Disease by your Pet?

This is unlikely. The most likely circumstance for exposure is walking in wooded areas, the habitat for the tick. Dress accordingly. However, you could become affected if you pick up an unattached tick from your pet and it attaches to you. As an added precaution, wear gloves when you brush your dog after the walk. Also, Lyme disease organisms are found in the urine of infected animals but there is some controversy over whether or not this could be the source of an infection. There have been no confirmed cases of transmission in this manner. (Courtesy Pitman-Moore, Inc., Mundelein, IL)


 Piroplasmosis (babesiosis, horse tick fever) is an acute infectious disease characterized by fever, anemia, jaundice, and edema of the legs, chest and abdomen. Recovered horses become asymptomatic carriers, capable of transmitting infection to other horses. Caused by 2 protozoan blood parasites, Babesia caballi and equi, piroplasmosis is most commonly spread by several species of tick vectors. Mortality from B. caballi is low while B. equi can be frequently fatal within 48 hours of initial clinical signs.


Piroplasmosis (babesiosis, horse tick fever) is a worldwide disease, with only the US, Canada and the UK currently free of infection. Almost all the horses coming to the 1996 Olympics come from endemic countries and are potential carriers. There is a complement fixation test for the disease that seems to fairly reliable. All Olympic equine participants will be required to be tested, however positive reactors will not be forbidden from entering the country. The latest information is that a waiver will be granted by Georgia Ag. Commissioner Erwin, and federal officials. Reactors will be directly shipped to the Olympic site and retained in special areas. Reactors will be prohibited from 3-day events.

There is a reason to be optimistic that these carriers may not cause a problem. The ticks associated with natural infections of Babesia are not found in Georgia. They are found in southern Florida however, and at least experimentally, our native ticks can become infected.


Definitive diagnosis requires observation of protozoans within RBC's in a blood smear. If the smear is negative, diagnosis is based on a negative Coggins' test and a positive complement fixation test, even in carriers. The indirect fluorescent antibody test and the complement fixation test have been recommended for identification of infected animals, but false positives and false negatives occur. DNA probes have been recently developed for detection of either organism in the blood.


Treatment is aimed at reducing the fever and halting the hemolysis in acute cases. New treatments can eliminate the parasite from carriers with a clearance rate of 95-97% for both species. Diminazene (Berenil: Hoechst), imidocarb (Imazol: Wellcome), acridine dyes (Gonacrine: May & Baker) and parvaquone (Clexon: Wellcome) are all used to treat piroplasmosis, but none is effective in eliminating B equi, and the dosages required usually approach toxic levels. Strategic tick control has been used to eliminate contact between the tick vector and the equine host. No vaccine is available.

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EquineViral Arteritis

Though the severity of the EVA is a matter of debate, thoroughbred industry leaders said it is best to be too cautious.
This item came from the August 14, 1993 "The Blood-Horse" article by K. S. Herbert & J. Duke
Restrictions Broadened in Response to EVA : Arlington Concerned about Million 

 Arlington International Race course had instituted a mandatory vaccination program to stem the spread of equine viral arteritis and to mitigate concerns about shipping in horses for the Aug. 29 Arlington Million. Meanwhile, other racing states had responded to the illness by banning horses from jurisdictions where EVA had been reported or imposed tight restrictions.

Arlington executives hoped the outbreak would have little impact on the Million field---although fields had been shorter for stakes races since themid-July outbreak---and had remained in contact with trainers on the West Coast and in Europe. "

You're always nervous about these things," said Arlington president Edward Duffy. "But we caught it early enough and we imposed our own restrictions."

An estimated 125 of the 2,000 horses stabled at Arlington had been diagnosed with EVA. To reassure the connections of out-of-town shippers, Arlington had an off-site quarantine facility in the form of chairman L. Duchossois' Hill N' Dale Farm. "It might not even be necessary by the time the Million comes," Duffy said.

The good news about that outbreak was that the virus seemed to be a mild Strain, according to Dr. Peter Timoney of the University of Kentucky's Gluck Equine Center, which first confirmed the outbreak. Since the outbreak was Reported, horses at Churchill Downs and AKsarben had been diagnosed with EVA. At Churchill and AKsarben, the affected horses had been in contact with horses from Arlington or had been at that track during the outbreak.

Kentucky had six confirmed cases of EVA at Churchill Downs, all in one barn. One horse in that barn had arrived from Illinois before the spread of the virus. Two other horses in that barn were ill with symptoms of EVA, but those cases had not been confirmed as of early Aug. 9th. One horse at AKsarben was confirmed as having EVA, and Kentucky had initiated a 21-day quarantine before allowing entry into the state of horses from AKsarben or Arlington.

New York Racing Association tracks had imposed a ban on horses shipping into NYRA tracks from affected areas, including NYRA-based horses which were trying to return home. Any horses from areas that had experienced outbreaks of EVA were be prohibited from entering NYRA ground for two to four weeks, based on relative risk of exposure and status of the clinical disease at the location where the horses were stabled. Also, a horse returning to an NYRA track must have two negative EVA tests at seven-day intervals. Any horseman wishing to ship horses to Belmont or Saratoga had to get permission from Dr. Theodore Hill, NYRA veterinarian, or Terry Meyocks, vice president of racing.

Ohio required horsemen from Kentucky and Nebraska to get permission from the Ohio state veterinarian's office before entering the state. Florida had restricted entry of horses from Arlington, Churchill, and AKsarben.

California had closed its border to all horses from Northern Illinois and had issued a broad statement that required a modified health certificate for horses coming from areas where EVA had been diagnosed. No word had been received from Europe on whether import/export requirements have been modified for horses coming for the Million.

Horsemen should check with their state veterinarian's office before shipping horses to another state to make sure the horse will not be turned away at the point of destination. Emergency regulations can be put in place in several states, and changes in those regulations, or new restrictions, can be made without warning to horsemen or shipping companies.

In 1984, an outbreak of EVA occurred in the stallion and mare population in Kentucky that literally shut down the state's breeding season. That outbreak was tentatively traced to a problem at a racetrack.

Some strains of EVA have the potential of causing abortion outbreaks, where a large percentage (sometimes up to 80%) of pregnant mares on a single farm will abort their fetuses. In stallions, the virus can become a long-term concern, with some stallions infected during the 1984 outbreak shedding the virus in their semen for several years.


RESTRICTIONS SET TO COMBAT EVA VIRUS - a venereal disease called equine viral arteritis

There is a greater chance of a horse infected with equine viral arteritis damaging his owner's bank account that to suffer personally. For this reason, restrictions on horses coming into Florida were absolutely essential in protecting the state's horse population, valued at more than $600 million.

Equine viral arteritis, or EVA for short, does cause abortions in broodmares and once a stallion is infected, it may be able to spread the disease for years.

Infected mares don't always abort, though, and the severity of the disease is so variable that an outbreak doesn't mean doom.

"It is confusing" said Dr. Tom Little of the University of Kentucky.

"But it is irresponsible to say you can't have abortions, and it is irresponsible to get people too worked up about it."

The actual virus wasn't isolated until the 1950s. Horse owners weren't getting too excited about it until 1984 when the virus shut down breeding sheds in Lexington, Ky., and was suspected in causing several abortions. An outbreak occurred in mid-July at Arlington Race Track in Chicago, where there were 165 confirmed EVA cases. Horses shipped from this track before any action was taken to contain the virus were being blamed for subsequent cases at Churchill Downs in Kentucky, Ak-Sar-Ben in Nebraska and Prairie Meadows in Iowa.

Since then, 14 states had issued some kind of restrictions on horses crossing their borders. Some states refused to let in horses that were specifically at these tracks unless they are accompanied by two negative EVA test results taken seven days apart.

Florida issued an emergency order on August 6 that prohibited any horse from entering the state unless it was accompanied by a statement from a licensed veterinarian saying the horse had not been on any property where EVA was diagnosed within the past 14 days, nor had they been near other horses that may have been exposed.

The EVA virus responsible for the outbreak at Arlington was described as a "mild strain" and many veterinarians here agree with that assessment.

Still, there is the potential for severe problems since the Ocala area is one of the world's leading Thoroughbred breeding centers.

Local veterinarians are skeptical that existing restrictions are strong enough to prevent EVA exposed horses from entering Florida, but add that action was essential.

"We are putting too much reliance on honesty," said Dr. Edward Noble.

"We are dependent on someone writing a statement saying this horse has not come in contact with infected horses and there are so many ways around that."

Some states are requiring a horse to have a negative blood test, but this doesn't mean a horse is healthy. The test check for antibodies in blood, which are produced as part of the bodies immune system when the animal is exposed to a virus.

"A horse may have been challenged by the virus and successfully fought it off," said Dr. Gene Hill. "It may have an EVA positive test, but if you check the same horse in six months it will probably be negative." Hill said horses testing negative may be more of a problem.

"They could have a snotty nose and 106-degree fever and test negative, he said. "It takes weeks for antibodies to develop."

Still, any step needs to be taken to keep Florida's horse population as clean as possible or at least protect that perception by issuing restrictions.

EVA isn't necessarily bad and is actually endemic in standardbred horses.

When older standardbreds are tested, 60-70 percent will be positive for EVA, according to Little, also a doctorate student who is doing research on EVA.

"Most standardbred people will say, 'Hell, we never see this disease," he said.

It is also predicted that one in four standardbred stallions are infected with EVA. Some standardbreds will show signs of the disease like swollen legs, fever and hives, but there aren't wide spread abortions that one might expect with this degree of infection.

Little said it may be because a majority of the horses are already exposed to the disease so it never gets a chance "to heat up" in the population.

"They already have the antibodies, which is just what a vaccine would do," he said.

In Thoroughbreds, however, an estimated 2 percent of the population has been exposed to EVA.

The disease doesn't always cause abortions. Horses exposed to it may never show any symptoms, but there is the chance and this keeps horsemen on their toes.

The reason suggested for why EVA can linger silently for years, then jump up and cause major problems has been compared to an outbreak of influenza in people. Initial symptoms of the disease are mild, but as it spreads through the population it "learns how to do its job better" and increasingly more severe symptoms surface, including deaths.

Deaths from EVA are rare. Deaths to a stallion's career or the inability of an import/export business to move horses is very real.

A majority of breeders do blood and semen tests on their stallions every year and vaccinated annually. The vaccine has not been approved for pregnant mares, but horses in an area where there is an EVA outbreak should be treated, according to Little.

Arlington Park imposed a mandatory vaccination program and by Aug. 13, 1,700 horses were treated.

Vaccination is not as important in fillies as it is if a race horse has a potential future as a stallion.

"The virus becomes confined to the male reproductive tract," Little said. "It clears from mares and fillies, but it stays in the males from months to years."

Mares can be bred to infected stallions, but they must be vaccinated and in a market where the competition among stallion owners is tight, a mare owner may simply decide to go somewhere else.

"While the physical effects of the disease are controversial, the practical and financial effects of the disease are very real," said Dr. Phil Matthews of Ocala.

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Dee L. Cross, PhD, Clemson University, Veterinary Sciences Dept., South Carolina. Complete articles may be obtained from Dee L. Cross, PhD, ADVSC Dept., PO Box 340361, Clemson University, Clemson, South Carolina 29634-0361 phone 803-656-5155, FAX 803-656-3131
The drug, Domperidone is in the New Animal Drug Clearance process with the FDA , Investigational New Animal Drug (INAD)# 8453 A000, protected by U.S. Patent No. 5,372,818 and licensed for distribution with Equi-Tox, Inc., Center for Applied Technology MBX-2, 511 Westinghouse Rd., Pendleton, SC 29670 phone 803-646-6443.

D.L. Cross, PhD, from the proceedings of the 40th annual convention of the American Assoc of Equine Practitioners, Dec. 4-7, 1994, Vancouver, B.C. (very short summary)

Pregnant mares grazing endophyte infested (E+) tall fescue exhibit increased gestation lengths (longer pregnancies) (normal is 335-345 days), agalactia (no milk), foal and mare death, tough and thickened placentas, weak and immature foals.

Selenium, phenothiazines, or supplements such as corn or other high energy foods do not help if mares remain on E+ pastures.

According to this research, oral doses of Domperidone increase serum prolactin and progesterone levels and provide nearly complete recovery from E+ tall fescue toxicosis without drug side effects. Treated mares has live foals, milk and nearly normal gestation lengths.

Recommended doses are 5cc/500kg (1100 lbs) of mare body weight daily as oral dose starting 10-20 days prior to expected foaling date and up to foaling.

If mare remains on fescue, daily dosing should start approx. 20 days prior to expected foaling date.

Domperidone must be ordered from Equi-Tox by a veterinarian for a specific mare. The cost is $5.00 per dose plus $5.00 shipping. Domperidone must be refrigerated.Clinical Observation Forms must be completed for each mare dosed.

Further Info, complete transcript of the proceedings, & bibliography from the research papers can be provided by Dr. Cross.


Additional Info from the papers:

Fescue toxicosis dystocia: Foals usually have larger than normal skeletal frames due to prolonged gestation and are also often rotated 90-180 degrees from normal position increasing the difficulty of birth.

Agalactia: Mares on E+ tall fescue pasture often produce no milk due to reduced prolactin secretion. This is measured by serum prolactin levels.

In previous research studies, mares on infected pastures had foal mortality (death) rates of 66-100%. Mare mortality was 50-66%.

On mares removed from E+ pastures 30 days before foaling, recovery was rapid and foaling was similar to mares on clean pastures.

INEFFECTIVE treatments were phenothiazine, perphenazine, metoclopramide, fluphenazine, trifluophenazine, chlorpromazine, acrpromazine and other dopamine antagonists with neuroleptic activity. These can cross the blood brain barrier and have central nervous system activity with little or no effect on fescue toxicosis symptoms.

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Because treatment for plant poisoning is not usually effective, prevention is the best, if not the only way to control this problem. Although few poisonous plants taste good to horses, animals will eat them when very hungry, when the plants or seeds are mixed in with grain or hay, or when plant clippings are placed where horses normally eat. If certain plants in a pasture look at all suspicious, either dig them up, kill them with chemicals (and be careful of that stuff, too!), mow them down before they go to seed, or move the animals out of the pasture at the time when the poisonous plants are particularly toxic. Some plants with a salty taste may be palatable to a hungry or young horse that may not be particularly discriminating. Occasionally such plants as OLEANDER, which in large amounts can cause poisoning, are mixed in with hay; horse owners should therefore check new shipments of hay carefully.

Three different kinds of plants cause similar symptoms, each producing cirrhosis of the liver: Amsinckia intermedia (FIDDLENECK, TARWEED, FIREWEED, BUCKTHORN, and YELLOW BURR WEED), found in the West, where it is a common weed of wheat and other grain crops; Senecio jacobaea (RAGWORT, GROUNDSEL, and "STINKING WILLIE"), found in the West and Midwest; and CROTALARIA spectabilis and C. sagittalis (RATTLEBOX, RATTLEWEED, and WILD PEA), common in the Southeast. The Senecio species caused walking disease (also hard liver disease or Walla Walla walking disease). All of these plants affect the liver, causing a dysfunction of the central nervous system with symptoms including staggering, aimless walking, incoordination, mania, or delirium, often accompanied by sever intestinal irritation along with diarrhea and signs of colic. When the liver has been sufficiently damaged, loss of condition and death result, and there is no cure or treatment once the liver has been damaged. Since other causes for these symptoms, however, are rabies, abscesses, brain tumor, encephalitis, and meningitis, don't assume poisoning unless you are convinced the animal had access to any of these plants.

Ricinus communis (called the CASTOR BEAN, CASTOR OIL PLANT, and PALMA CHRISTI), common in the Southeast and Southwest, is the source of castor oil (which tastes bad but is good for you). Actually, the plant is beneficial, but the seeds, if ingested, are highly toxic, causing both humans and horses severe irritation in the intestinal tract. In addition to the plants' use in commercial production of castor oil, they are sometimes grown for ornamental effect around barns or corrals where horses - young, inquisitive ones for the most part, since the older ones are sensible enough to know that what tastes bad IS bad - can eat them. As few as 7 grams of the seeds may be fatal to a horse. Severe enteritis is the characteristic sign; at first the horse is rather dull, then uncoordinated, and then very sweaty. Spasms may be apparent, and watery diarrhea, plus other colicky symptoms, will appear. Eventually the horse goes into convulsions and dies.

Nerium OLEANDER is also grown as an ornament in the South and in California, where it has been known to poison people who used the sticks of the plant for food skewers. Lawn clippings or bales of hay containing oleander leaves are the usual source of the poisoning in horses, since they will rarely eat the shrub itself. It can be lethal; 40 to 50 grams of the green or dried leaves will kill a 1,000-pound horse. Profuse diarrhea, abnormal heartbeat, and chilled extremities are progressive signs of the poisoning, with the pulse eventually becoming imperceptible and death following shortly thereafter. If the dose was small and nonfatal, treatment must involve removal of the contents of the intestinal tract and maintenance of general good nursing care.

BRACKEN, or BRAKE FERN, is common in woodland areas all over the United States, and some species of the genus Pteridium can poison cattle and horses, with different reactions - the latter suffering disorders of the central nervous system. Since bracken stays green into the fall, animals may begin to eat it after pasture grass has browned, even cultivating a taste for it, and BRACKEN SOMETIMES SHOWS UP IN HAY. Animals must eat bracken over a period of time (one or two months) before showing such symptoms of toxicity as loss of weight, unsteadiness, swaying, and staggering. If the animal falls, it may not be able to get up.

"Chewing disease" is the colloquial term for YELLOW STAR THISTLE poisoning, from the plant Centaurea solstitialis, which grows throughout the West and is often found along roadsides and dumps. It is an attractive, yellow-flowered annual, a member of the sunflower family. As with bracken, this thistle must be consumed over a long period before signs of poisoning appear, but once they do, death is probable. A victim will have difficulty in swallowing, and food may be spat out or become lodged in the mouth; the horse will probably be unable to drink and may develop a wooden facial expression as muscles around the mouth and tongue become paralyzed. If not helped, it will die of starvation, but in any case functional recovery is unlikely since part of the brain is damaged even if the animal responds to treatment.

The short, sharp prickles of YELLOW BRISTLE GRASS (Steraia glauca and S. lutescens) cause ulcers in the stomach and irritation in the tongue and lips. Once the source is removed, healing is rapid. Many other plants, such as thistles, cacti, and thorny shrubs, will cause puncture wounds or cuts.

Some lupines are toxic, some not, and it is difficult to tell the two types apart. Poisoning occurs usually in the fall or winter in the form of gastric irritation and diarrhea, and acute poisoning will cause depression, weakness, and coma. LOCO-WEED disease, which is caused by some species of the genus Astragalus, causes horses to stagger, wander in circles, act depressed, and then fall into convulsions. Some species of the same genus (WOODY ASTER, PRINCE'S PLUM, and "GOLDEN WEED") will cause selenium poisoning, which affects the central nervous system; it also causes feces to become dark and fluid and an occasional fever to flare. The horse may die within a few hours or may linger for a few days. Other plants absorb selenium to a toxic level, causing chronic poisoning, sometimes called alkali disease. Losses of hair and hooves are characteristic, and victims become emaciated and lame. Oats, barley, and wheat grown in selenium-rich soil may be the villains here, but treatment involves simply removing the animal from the area or the feed from the animal.

There is no treatment or cure for NICOTINE POISONING, and eating the plants of the wild tobacco family is fatal. Normally paralysis precedes the death. LATHYRUS is another genus of poisonous plants; they are now rare, but there was an outbreak in 1969 affecting horses. Signs involve stiff hindquarters, unbalanced walking, and difficulty in rising. Removal of the plant (in the 1969 epidemic it was in baled hay) will relieve the symptoms.

AVOCADOS are a delicacy for humans, but their stalks, leaves, and bark can be just the opposite. Severe mastitis and lack of milk production in mares result.
Other plants, rarely eaten by horses but poisonous to them include : OAK, ERGOT (a fungus), DATURA, POISON HEMLOCK, perhaps water hemlock; members of the Nightshade family - GREEN PEPPER PLANTS, TOMATO PLANTS, POTATO PLANTS, EGGPLANT. CHOKE CHERRY leaves (green OR dead/brown) plus it's bark and fruit, BOXWOOD SHRUBS, YEWS.

This information was taken from THE WHOLE HORSE CATALOG, Steven D. Price, Editorial Director. Published 1993 by Fireside/Simon & Shuster. It's a large, softbound book which can be found at most book stores for about $20 and is an EXCELLENT reference book for everyone who is thinking of getting a horse or who already has a horse.

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Report on Navicular - Navicular Disease - What it is....... 

 The navicular bone is a small, flat, thumb-shaped bone that exists between the coffin bone and the pastern bone of the lower foot of a horse. This bone acts as a pulley for the deep digital flexor tendon.

There is a natural process of degeneration in the navicular bone that takes place in the area where the bone acts as a pulley for the deep flexor tendon. This process occurs in all horses. To neutralize the natural process of degeneration, there also exists a process in which minerals are produced and the bone regenerates itself as rapidly as it degenerates. When the process of regeneration becomes slower than the process of degeneration, areas are created on the navicular bone where the bone becomes rough, causing the deep flexor tendon to "catch" on these rough spots when the horse walks.

This condition is called navicular disease, and commonly causes pain and lameness to the horse.

Navicular disease is a common cause of forelimb lameness. Although it is possible for navicular disease to exist in any of the four limbs, it is most commonly found in the forelimbs. It is usually a bilateral disease, which means that if one of the forelimbs, say the left, is affected, the other (the right) will eventually show signs of the disease also. However, one of the limbs is nearly always affected more than the other.



The more pressure that is applied to the navicular bone from the deep flexor tendon, the higher the probability that the horse will suffer from navicular disease. Increased pressure is caused by overweight horses, and horses who have small feet (proportionally to the size of their bodies).

Therefore, certain breeds of horses, especially the quarter horse and the thoroughbred are susceptible to the disease.

Some experts believe that the disease is hereditary, which is possible.

A horse could possibly carry a gene that deprives them of regeneration of that particular section of the navicular bone. A more feasible possibility is that horses of the same families contract the disease because when a horse is bred, the genes of their bodily build are passed from the parent to its young. In other words, a horse who has a big body and small feet, and also have navicular disease, is very likely to have young that also have a big body and small feet, therefore becoming more susceptible to navicular disease.

Horses that have definite symptoms of navicular are usually detected between the ages of three and sixteen years. Horses have been found with navicular disease as early as one year old, but most commonly are found between the ages of ten and thirteen years. This is a very common time in the life of a horse to see the symptoms of navicular appear.


Diagnosis/Symptoms of Navicular Disease

Navicular disease isn't something that comes on to a horse all of a sudden. It is actually a very gradual process in which horses show the symptoms of navicular. It is usually well advanced by the time that an owner will notice his horse as having the disease.

Early cases of navicular disease may only show occasional intermittent lameness, which becomes noticeably better when the horse is rested. The animal may point his feet to relieve pressure from the deep flexor tendon, as most horses with pain below the fetlock joint point their feet. He will also walk toe-heel to relieve pressure. The horse will also take short, shuffly steps. A horse that walks in such a manner will have a shoe with a badly worn toe.

If both feet are affected by navicular, lameness will be less dramatic.

It is more easily detected, however, when the horse is turned in a short circle, where he may try to rotate on the foot rather than picking it up to take a step.

Another wat to test for navicular disease is with hoof testers. Hoof testers placed with one tong on the outside wall with the other on the sole or frog will cause pain to a navicular horse. The placement of both tongs across the outside of the heel will also cause discomfort.

The best test for navicular disease is performed by a veterinarian. He can do a procedure which is called a nerve block. He will use local anesthetic to "numb" different nerves until the horse is sound when trotted out. If the horse is sound after blocking the nerve that serves the area of the navicular bone, a good assumption is that the horse has navicular disesae.

Before beginning treatment for a navicular horse, veterinarians like to be sure that the horse definitely has navicular disease and not some other problem such as an abscess or a fracture. X-rays can be taken to show the amount of deterioration of the navicular bone, though it is often difficult to get good x-rays that will actually show the problem, especially in its beggining stages. Unfortunately, only 50% of all navicular cases can actually be diagnosed from the x-rays. Since x-rays are expensive, most diagnoses are made through an "elimination of other possibilities" process.



How to treat a horse with navicular disease is a very controversial issue. Many horse owners think that the answer is to do nothing, to let time heal it, while others try every type of treatment available. The fact is that there is nor "right " or "wrong" way. The method that one chooses is dependent on what one expects from the horse and the severity of the case. There is no "cure" for navicular disesae, and time does not fix it, so each individual horse should be treated in a manner that best suits the needs of the owner and the horse.

Navicular disease will not directly shorten the length of the life of a horse; however, some owners will decide that the horse is no longer useful and will euthanize it. This is most often unnecessarily done because there are many ways to relieve the pain of a horse with navicular disease to be able to continue using him. However, if a person plans strenuous use of the animal, he may find that dealing with the disease is too much trouble. If a horse is sound other than the navicular, it seems relatively simple to continue using him as long as the pain can be relieved.


The most effective treatment of navicular disease to date appears to be simply good foot care. Numerous styles of shoes have been developed to help relieve pressure of the deep flexor tendon, therefore relieving pain in a horse with navicular disease. Navicular horses should be shod more frequently than other horses (every 6-8 weeks). According to Ruth B. James, DVM, "It is suggested that only three nails be used in either side of the hoof to allow the hoof to grow and expand."

One theory of shoeing for a navicular horse is to raise the horse's heel. By raising the heel, there is less pressure exerted by the deep flexor tendon when the horse lifts his foot to walk. A problem that comes from raising the heel of a shoe is that as one may be relieving the pain of navicular disease, the rest of the foot is strained as it is at a new, steeper angle. Some shoes that work to raise the heel include any type of wedge shoe and any type of wedge pad. The higher the angle of the wedge, the more extreme the raising of the heel.

Another theory for shoeing a navicular horse is to round the toe. By doing this, pressure is taken away from the deep flexor tendon as the animal attempts to walk. The shoe thus allows the animal to "roll" or "rock" up off of his heels instead of having to forcefully pick up his foot. Some shoes that provide "rocking" or "rolling" are a rolled toe shoe, or a rocker toe shoe.

Other common shoes used for treating navicular disease are the egg-bar shoe, polo plates, bar shoes, roll calks, and wedge calks. There are also numerous types of pads used such as leather pads, 2 degree wedge pads, and frog cradles.

Yet another common practice in shoeing a navicular horse is "setting the shoe under." This entails leaving hoof beyond the edge of the shoe, and then rounding it, acting in a way as a sort of rocker. "It's like a human wearing clown shoes versus wearin running shoes. The clown shoes, with the squared toe, make it hard to lift your foot. The running shoes, on the other hand, have a rounded toe, and when a person picks up their foot, it takes less effort and strain to move," explained farrier Uri Driscoll.


Many medications are given to navicular horses to help to relieve pain temporarily. Many drugs, both oral and injections, are available for temporary use with a horse. Prolonged use of most of these drugs can cause damage to the horse and any use of some of these drugs are illegal in most competitions.

These drugs include phenylbutazone (bute), the most commonly used bain reliever in horses, MSM, isoxuprine hydrochloride, warfarin sodium, sodium hyaluronate, corticosteroids, polysulfated glycosaminoglycan, Flex Free, Adequan, Legend, and yucca.


The last resort to treating navicular disease is a procedure called a neurectomy. This involves severing the nerve to the navicular pain. Although it is an option to euthanizing a horse, there are many problems associated with it.

When a nerve is severed, the horse loses all feeling to that area of his body. One of the many problems associated with this is that if a person is riding a nerved horse, the person is in great danger as the horse doesn't know where his foot is. The horse could stumble and fracture his leg, yet the person may not know that the horse has fracctured his leg because the horse has no feeling in that part of his leg, so he wouldn't feel any pain, and therefore wouldn't limp. A horse could get an abscess, and because he had a neurectom, he wouldn't feel any pain, and again the problem would go unnoticed. The infection could spread through the horse's body and the horse could die. What might have started out as a simple problem could become a severe one.

When severing the nerve, often times a horse will grow a neuroma, or a growth at the cut end of the nerve. It could wrap around blood vessels and prevent the removal of the growth due to obstruction to the blood vessels.

Many people have successfully used neurectomy and been able to enjoy many years of riding a horse that might have otherwise been euthanized. "Two of my own racing stockQuarterhorses had to have the nerve to the back part of both front feet cut, because the pain they suffered was too great. They both performed beautifully for many years after the 'nervin' surgery, jumping and competing," said veterinarian Nan Saye Martin, one of the fortunate people whose horses had successful neurectomies.

If a neurectomy is successful, the nerve may grow back, but can be cut as many times as necessary to keep the horse useable.

In conclusion, the best way to treat a horse for navicular is to prevent it, or at least to help a farrier work with it by providing good hoof walls.

Nutrition is the key to healthy feet. A good diet of rich alfalfa and a vitamin supplement such as biotin enrich the hooves. The better condition a horse's hooves, the more successful a person will be in battling navicular disease!


Adkins, Kirk. Farrier at U.C. Davis. Personal Interview. Nov. 11,1994.
Berry, C. "radiographic/morphologic investigation of a radiolucent crescent..." American Veterinary Medical Association. Sept. 1992, v. 53, p. 1604-1611. Carey, Susan. Internet Interview. Jan. 14, 1995.
Diseases of the Horse. U.S. Government Printing Office.Washington, c. 1942.
Driscoll, Uri. Farrier in Arcata, CA. Personal Interview. Dec.11,1994.
Hadley, Frederick B., D.V.M. The Horse in Health and Disease. Philadelphia: W.B. Saunders Co., 1915.
Honnas, C. "Anklyosis of the distal interphalangeal joint in a horse..." Journal of American Veterinarian Medical Association. Apr. 1, 1992.
James, Ruth B. How to be Your Own Veterinarian (sometimes). Mills, Wyoming: Alpine Press, 1990.
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McKibbin, Lloyd S., D.V.M. Horse Owner's Handbook.Philadelphia: W.B. Saunders Co., 1977.
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Pleasant, R. "Intraosseous pressure and pathologic changes in horses with navicular disease." American Journal of Veterinary Research. Jan. 1993
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Moon Blindness (Periodic Ophthalmia) 

Periodic ophthalmia is an inflammatory disease of the eye and is the most common cause of blindness in horses. It is characterized by the sudden onset in one or both eyes of acute clinical signs which gradually subside in a week or more, but recur after quiescent periods varying from a few days to several months. Each recurrent attack adds to the damage to the eye, usually ending in complete blindness in the affected eye. Periodic ophthalmia is often referred to as "moon blindness" since the periodic outbreaks were once thought to be affected by the lunar cycle. The disease is seen more frequently in mature horses, four years and older, and both eyes are eventually involved.

Acute signs of an attack appear suddenly and include severe photophobia, or dislike of light, and excessive lacrimation. Because the eye is extremely sensitive to light, the eyelid is held closed and sticky tears accumulate on the lower lid and cheek. The pupil is tightly contracted and fails to dilate in darkness. The cornea is intensely inflamed and the blood vessels in the sclera surrounding the cornea are so congested as to be clearly visible. After one or two days, the cornea is cloudy and yellowish at its margins. In two or three days, the lower half of the pupil becomes built up with a cheese-like exudate which partially blocks the passage of light into the eye. After about ten days the symptoms subside, and in another week the eye may seem nearly normal again. Following several relapses, the eyeball becomes atrophied and the sclera thickened, eventually resulting in complete blindness.

The cause of the disease is still unknown. There may be more than one cause, including riboflavin deficiency, Onchocerca cervicalis microfilariae (minute worm larvae), leptospirosis and hypersensitivity or allergic reaction. Nutrition studies indicate that there is an inverse relationship between the incidence of the disease and the level of riboflavin in the diet. Infection by Onchocerca cervicalis microfilariae (which die in the eye) produces symptoms of periodic ophthalmia. Affected horses often have a high level of antibodies to Leptospira pomona in their blood serum, but the nature of the relationship of leptospirosis to periodic ophthalmia is unclear. The ocular inflammation may also be a localized hypersensitivity or allergic reaction after a secondary infection or toxemia. The disease is neither inheritable nor congenital.

After diagnosis of the disease, treatment by your veterinarian involves reducing the inflammation by means of corticosteroids given topically or systemically and dilating the pupil by topical administration of mydriatics. The horse SHOULD be kept in a dark stall to decrease its discomfort during the period of photophobia and to help keep the pupil dilated. Letting the horse out for a few hours after the sun has gone down for some exercise would be allowed. Adding riboflavin to the diet and administering antihistamines appears to be ineffective.

The prognosis for the disease is poor, depending upon the severity of the inflammation and the presence of ocular damage from previous attacks. Long-term application of topical corticosteroids may be helpful, treatment which involves much time and effort.

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