1538 I 49 N. Service Road · Sunset, LA · (337) 662-5930
HomeAboutServicesFacilityStaffNewsroomAsk the VeterinarianFAQContact
Latest News:
Disaster Preparedness.
Order Maximum Performance Products Online
Emergency Preparedness.
Immunization Program.
West Nile Virus/Eastern Equine Encephalitis: The Importance of Vaccination . Read More...
Health & Maintenance|Diseases & Conditions|Breeding & Reproduction|Prepurchase
Equine Diseases & Conditions

What is Pigeon Fever?

Though Pigeon Fever is not commonly seen in Louisiana, several area horses have been diagnosed with this disease in the past few months. In the face of this apparent outbreak, we hope the following information will help answer some general questions.

Pigeon Fever results following infection with a bacteria (Corynebacterium pseudotuburculosis) in horses. In more than 90% of affected horses, infection causes external abscesses (pus-filled pockets) involving the skin and underlying tissues. The underside and front of the chest are the most common places for these variably sized abscesses to develop, resembling the chest of a pigeon, hence the lay term “Pigeon Fever.” Signs of systemic illness (fever, loss of appetite, decreased energy level) are not common with external abscesses. However, C. pseudotuburculosis may uncommonly cause internal abscess or infection of the lymphatic vessels; horses with these types of infection will show generalized clinical signs. It is important to note that these are 3 different and unrelated manifestations of the same disease – horses with external abscesses will not likely develop internal abscesses, and vice versa.

Any horse with a newly developed bump anywhere on the body should be evaluated by a veterinarian, as there are many other causes of external lesions, all of which should be addressed appropriately. The only way to definitively prove that an abscess is caused by C. pseudotuburculosis is to culture the lesion – collect tissue or fluid and try to grow bacteria from it in a laboratory setting. It is more difficult to get a culture result if a horse has been treated with antibiotics, so it is important to have an affected horse seen by a veterinarian before any medications are given. Blood tests may also be performed, but only evaluate the horse’s exposure to the bacteria, not infection with it.

The most important aspect of treating Pigeon Fever is opening the abscesses once they mature (meaning they have formed one or two big pockets of pus within the capsule, instead of several small ones, resembling a honeycomb) and allowing them to drain. Treatment beyond this varies depending on a veterinarian’s preferences, and may include daily flushing with fluid, infusion of antibiotics into the wound, or oral antibiotics. Horses rarely need to be hospitalized.

The pus that is drained from abscesses contains large quantities of bacteria, and is therefore very contagious. These bacteria can survive very well in the environment, and can easily be passed to other horses, entering the body through open wounds. Flies, bedding, ointments, clippers, buckets, blankets, or brushes may all transfer bacteria if it comes in contact with infected pus. Though no specific cleaning agent has been proven to kill this bacteria, practicing good hygiene and isolation procedures should be sufficient to minimize infection on a farm. Horses with draining lesions should be kept separate from healthy horses, and should be treated in an area that is not used by other horses. Equipment used should be cleaned with soap and water or a dilute bleach solution and allowed to dry in the sun. Hands, clothing and boots should be clean before handling any healthy horses. This bacteria is not transmissible to humans, though other farm animals may also develop abscesses (especially sheep).

Pigeon Fever is a contagious bacterial disease amongst horses, most commonly causing external abscesses of the chest. All horses with external lesions should be evaluated by a veterinarian. Good hygiene and isolation practices are paramount to prevention of infection in healthy horses.

What are gastric ulcers?

Ulcers of the stomach and or intestine can occur in adult horses as they do in people. Two of the more common causes are stress and the use of nosteriodal anti-inflammatory drugs (NSAIDs) such as phenylbutazone or banamine.

The horse's stomach continually secretes acid. When the horse is denied access to food for intermittent periods, large ulcers may develop within 48 hours. Horses turned out to graze usually do not develop gastric ulcers. The following situations warrant careful observation for the development of gastrointestinal ulcers:

* Weight loss
* Poor performance
* Recurrent back pain
* Loss of condition
* Shipping the horse while it is receiving NSAIDs
* Chronic problems requiring long term NSAIDs
* Laminitis
* Chronic colic
* Dehydration
* Behavioral abnormalities

Signs of gastrointestinal ulcers in adult horse include low-grade intermittent colicky behavior, unthriftiness, decreased performance, and possibly some diarrhea. Gastric ulcers can be confirmed by video endoscopy of the stomach. This procedure requires the horse be fasted for 12 hours and held without water for 2 to 4 hours prior to the endoscopic examination. At Baronne Veterinary Clinic all horses are sedated and examinations are performed utilizing video endoscope. Gastric lesions are recorded onto a CD for documentation and future comparison.

Ulcers of the stomach and or intestine can occur in foals as they do in people. Neonatal and suckling foals are more likely to develop an ulcer if subject to such risk factors as:

* Complications at delivery
* Minor or major illness
* Unusual environmental factors (adverse weather during foaling; foaling in an undesirable location)
* Chronic problems associated with casting or splinting procedures, pneumonia, gastrointestinal problems, etc…
* An unusual response to the use of NSAID's for the relief of inflammation
* Transport

Signs of gastrointestinal ulcers in foals are depression, grinding of the teeth, salivation, rolling and colic. For most foals diarrhea, poor growth, rough haircoat and a pot bellied appearance may be typical signs of intestinal ulcers. Affected foals sometimes find comfort by rolling onto their back and propping themselves against the stall wall. Diagnosis is aided by observing these signs and can be confirmed by gastroendoscopy. This procedure requires sedation and an examination using a video endoscope.

What is EPM?

Equine protozoal myeloencephalitis (EPM) is an infection of the brain and spinal cord of horses by single-celled parasites known as protozoa. EPM, which is the most commonly diagnosed neurological disorder in horses, can be a permanently debilitating or fatal disease.

The disease is most commonly (probably > 95% of cases) caused by the protozoa Sarcocystis neurona; occasionally, another protozoa known as Neospora hughesi also can cause EPM. EPM is a disease of North, Central and South America, and is only observed in horses outside this region among horses that have been exported from the Americas. This infection is acquired by ingestion of the intermediate stages of the S. neurona parasite, which are passed in the feces of opossums and which contaminate feed and forage consumed by the horse. After the parasite is ingested, it is eliminated by the immune response in most cases.

In a small minority of cases (probably less than two percent), the organism invades the spinal cord or brain of the horse and grows, resulting in the clinical signs recognized as EPM. The organism is carried to the nervous system either directly by the blood stream, or within white blood cells that have engulfed the organism. Horses do not appear to be able to transmit the infection directly to other horses.

The clinical signs of EPM in the horse are quite variable and depend upon the anatomic location in the nervous system in which it resides. Chance seems to favor the spinal cord, and the most common clinical signs expressed are stumbling, a weak, weaving gait, and atrophy of muscles. If the brain is affected, which is far less common, the clinical signs may include blindness, inability to chew or swallow, atrophy of muscles of the head (such as the masseter in the cheek that closes the jaw during chewing), head tilt or seizures.

Diagnosis of EPM is challenging because of the variability of the clinical signs. Veterinarians depend upon three criteria for diagnosis; 1) the presence of clinical signs which are consistent with EPM; 2) ruling out other diseases of the nervous system which can look similar; and 3) laboratory tests to demonstrate that the horse has mounted an immune response to the organism. These tests, including the Western blot (WB), immunofluorescent antibody test (IFAT), and enzyme-linked immunosorbent assay (ELISA) tests, are offered commercially by various laboratories. Positive tests indicate exposure to the organism, but when the reactions are strong, and in the presence of clinical signs, these tests are considered supportive of clinical disease. Of the commercially available tests, there is no clearly superior choice. Because of the limitations of EPM diagnostic testing, other diagnostic testing (such as radiography of the neck, if deemed appropriate) should be performed to help exclude other diseases that result in similar clinical signs from consideration.

Treatment of EPM can be achieved using a variety of pharmaceuticals. Ponazuril, marketed as Marquis®, was the first licensed drug for the treatment of EPM. Diclazuril, a very similar compound to ponazuril, has received FDA approval, but has not been released by the company as of this writing. Nitazoxanide, marketed as Navigator®, and a trimethoprim-sulfadiazine combination product, Re-Balance®, have also been approved for the treatment of EPM. In similarly constructed studies, all of these compounds have demonstrated a very similar effectiveness (about 60 to 65 percent success) in treating EPM. It is often necessary to treat for EPM beyond the recommended period on the product label of FDA-approved products. Other treatments including acupuncture or chiropractic manipulations, various herbal remedies, immune modulators or hormonal drugs have no scientific support at this time.

The ideal prevention would be an effective vaccine against S. neurona. Though substantial research has been directed at this, no effective vaccine has been developed. Evidence from clinical trials also is lacking for other recommended preventive strategies. Based on observational studies, it is proposed that methods including preventing exposure to S. neurona through keeping feed in a sealed bin, cleaning up spilled grain so that opossums are not attracted to the feed area, and feeding horses off the ground may help prevent EPM.

Application of products directly to feed to kill the S. neurona organism have no basis for effectiveness, and are not advised. Pretreatment of horses with ponazuril has been shown to decrease the risk of infection with S. neurona, and may in some circumstances be beneficial. For example, shipping stress is a known risk factor for development of EPM, and pretreatment with ponazuril prior to and during periods of similar stress may decrease the risk of disease.

The EPM story is truly a success story for modern veterinary research. Twenty-five years ago, we became aware of an enigmatic parasitic infection of the nervous system of the horse. Since then, veterinary and affiliated scientists have determined the cause of the illness, worked out a complicated life cycle, described the epidemiology of the disease, developed specific tests to diagnose infection and developed pharmaceutical agents to treat the infection. This highlights the importance of research in all aspects of an illness, and its contribution toward the final goal of effective means of prevention or treatment in individual animals.

By Martin Furr, DVM, PhD, Dipl ACVIM

What is colic?

"Colic" isn't a specific illness. It's abdominal pain. Intestinal problems are the most common cause, but it could also be related to urinary tract, reproductive tract or liver disease, as well as tumors or abscesses.

Having a colic "plan" will help get you efficiently through the scary period between noticing your horse has colic and when the vet gets there. Successful treatment directly depends on the amount of time that elapses between the appearance of symptoms and the beginning of treatment.

Owners notice the horses are not eating. They seem sluggish and preoccupied or irritable. Note for your vet any recent changes in hay/feed or recent access to pasture (new green grass or round bales put out suddenly); changes in drinking, urinating, or manure; stage in the estrus cycle if the horse is a mare; recent breeding; recent de-worming, medicines, or vaccinations; access to natural water sources such as ponds.

The next warning signal usually observed indicates the horse's pain level. Some colicky horses will start pawing; standing stretched out as if trying to urinate; glancing or biting at flanks; or wanting to lie down and get up frequently. As severity increases, sweating may appear and the horse may begin to lie down, then roll.

Vital signs can indicate pain associated with colic. The heart rate will increase (normal is 28-44 bpm), and respiratory rate will become rapid with flared nostrils (normal is 8-20 breaths per minute). The color of the horse's gums will change from their usual light pink color to white, red or purplish/bluish.

The more complete picture of your horse's health you can provide, the better the chances for correct treatment.

After assessing the horse, your vet will probably prescribe an anti-inflammatory drug. This drug can provide comfort in as little as 15-30 minutes. He will use a stethoscope to listen for gut sounds as an indication of intestinal motility. The next option is for the vet to pass a naso-gastric tube to see if fluid is backing up from the small intestine into the stomach. Drainage of this gastric reflux can ease intestinal pressure. Another diagnostic test is a rectal exam. This allows the vet to palpate abdominal structures to see if they are displaced or distended and further help in the diagnosis. Several laboratory tests can be of immediate benefit to assess hydration and vascular integrity. Your vet may recommend an additional lab test to evaluate abdominal fluid, which can be helpful in diagnosis.

Mineral oil is traditionally used as a lubricant to help relieve impaction and it appears to soften feces. When other vital signs appear stable this treatment along with intravenous (IV) fluids hydrates the impaction to assist the evacuation of the impaction.

Rapid diagnostics are vital to treating a colicking horse properly and quickly for a better prognosis. The decision as to whether a patient is a surgical candidate or not isn't always easy to make. Factored into the decision is the history of the case, examination of the patient, and consideration of the patient as a surgical risk.
We are equipped to perform colic surgery 24-hours a day, 365 days a year. Our surgical team effort consists of experienced surgeons, assistants, anesthetists, and technicians. Every surgical patient receives intensive monitoring from the pre-op to the recovery period. Our intensive care units accommodate IV therapy, and 24-hour patient monitoring.
Successful colic treatment depends on early recognition and rapid action. Studies show as little as a 2 hour time delay between the appearance of colic symptoms and the beginning of vet treatment can mean the difference between horses that survive and those that don't.

Vital Signs: Temperature, Pulse or Heart rate, Respirations, Gum color
· Symptoms/Behavior: What is the horse doing? sweating, pawing, rolling, agitated. Try to keep him as calm as possible. Walking him slowly may stimulate gut function. If your horse lies down, let him rest, but not roll.
· Food/Water: List any changes in grain, pasture, hay, or water intake. Remove any food and water from stall until told otherwise by vet.
· Urine/Manure: Leave passed feces in the stall for the vet to examine. Note any loose or dry stools, frequency and an approximate amount.

· Keep your horse's water clean, fresh, warm in winter, cool in summer, and available at all times.

Use quality feed. Don't feed on the ground in sandy areas. Change your horse's diet or exercise level slowly.
· Have the vet check your horse's teeth at least once a year.
· Follow the de-worming program prescribed by your vet.
· Avoid using excess drugs which can alter the intestinal function, such as Bute paste, which can result in gastric ulcers.
· Be aware that inherent physical defects can trap or strangle portions of the intestinal tract, or become strangulated by various tumors which all lead to colic.

What is strangles?

Strangles (Streptococcus equi)

Streptococcus equisubspecies equi (S. equi var. equi) is the bacterium which causes the highly contagious disease strangles (also known as “distemper”).  Strangles commonly affects young horses (weanlings and yearlings), but horses of any age can be infected. Vaccination against S. equi is recommended on premises  where strangles is a persistent endemic problem or for horses that are expected to be at high risk of exposure. Following natural infection, a carrier state of variable duration may develop and intermittent shedding may occur. The influence of vaccination on intermittent shedding of S. equi has not been adequately studied.

The organism is transmitted by direct contact with infected horses or sub-clinical shedders, or indirectly by contact with: water troughs, hoses, feed bunks, pastures, stalls, trailers, tack, grooming equipment, nose wipe cloths or sponges, attendants’ hands and clothing, or insects contaminated with nasal discharge or pus draining from lymph nodes of infected horses. Streptococcus equi has demonstrated environmental survivability particularly in water sources and when protected from exposure to direct sunlight and disinfectants, and can be a source of infection for new additions to the herd. 

Infection by S. equi induces a profound inflammatory response. Clinical signs may include fever (102-106o F); dysphagia or anorexia; stridor; lymphadenopathy (+/- abscessation); and copious mucopurulent nasal discharge.

S. equi and S. zooepidemicus are antigenically similar organisms. However, exposure to, or vaccination against, one does not confer reliable immunity to the other.
Following natural or vaccinal exposure to streptococcal antigens, certain individuals may unpredictably develop purpura hemorrhagica, an acute, non-contagious syndrome caused by immune-mediated, generalized vasculitis. Clinical signs develop within 2 to 4 weeks following natural or vaccinal exposure to streptococcal antigens. Clinical signs may include urticaria with pitting edema of the limbs, ventral abdomen and head; subcutaneous and petechial hemorrhage; and sloughing of involved tissues. Severe edema of the head may compromise breathing. Immediate medical attention should be sought for individual horses suspected of having purpura hemorrhagica. 

Vaccination in the face of an outbreak should be carefully considered, as there is significantly increased risk of adverse reactions in exposed horses.  Purpura hemmorrhagica can be associated with vaccine administration. In a recent retrospective study of 53 horses with purpura hemorrhagica, 5 cases were vaccinated with a S. equi M protein vaccine. Outbreak mitigation and the prevention of spread of S. equi infection are centered on management of horses, personnel, and facilities.

Killed vaccines
Killed vaccines are an adjunct to the prevention of strangles. Vaccination with these products should not be expected to prevent disease. However, appropriate pre-exposure vaccination with these products appears to attenuate the severity of clinical signs in affected horses, should disease occur, and has been shown to reduce the incidence of disease by as much as 50% during outbreaks.
All injectable, inactivated S. equi. vaccines, particularly the whole-cell bacterin, are associated with an increased rate of injection site reactions as compared to other equine vaccines. Due to the limited variability between commercially available vaccinal bacteria and field isolates, autogenous bacterins are not advocated.
Modified live vaccine
An intranasal product has been shown to stimulate a high level of immunity against experimental challenge. The inductive sites are the pharyngeal and lingual tonsils. Vaccinal organisms must reach these sites in sufficient numbers to trigger protective responses; therefore, accurate vaccine delivery is critical to vaccine efficacy. In a small percentage of cases, residual vaccinal organism virulence may result in formation of slowly developing mandibular or retropharyngeal abscesses.

Maternal antibody interference with respect to the development of mucosal immunity needs to be studied further.

In order to avoid inadvertent contamination of other vaccines, syringes and needles, it is advisable and considered a good practice to administer all parenteral vaccines or other injectables before the handling and administration of the intranasal vaccine against S. equi.

Vaccination Schedules:

Adult horses previously vaccinated:  Vaccinate every 6 to 12 months based on risk assessment and manufacturers’ recommendations.
Adult horses unvaccinated or having unknown vaccinal history 
Killed vaccine:
Manufacturers' recommendations are for primary vaccination with a series of 2 or 3 doses administered at intervals of 2 to 4 weeks, depending on the product used, followed by annual revaccination. Revaccinate at 6- month intervals, regardless of the injectable product used. 

Modified live vaccine: 
Administer intranasally a 2-dose primary series with a 3-week interval between doses. Semiannual (6-month intervals) or annual revaccination is recommended.
Broodmares previously vaccinated 

Killed vaccine:
Vaccinate 4 to 6 weeks pre-partum with approved products that contain inactivated M-protein. Maternal antibody interference is not known to occur when injectable, M-protein vaccines are administered.

Broodmares previously unvaccinated or having unknown vaccinal history
Administer primary series of killed vaccine containing M-protein (see above, Adult horses unvaccinated) with final dose to be administered 4 to 6 weeks pre-partum.

Killed vaccine: 
For foals at high risk for exposure to strangles, administer a 3-dose primary series of an M-protein product beginning at 4 to 6 months of age. An interval of 4 to 6 weeks between doses is recommended.

Modified live vaccine: 
Administer intranasally at 6 to 9 months of age a 2-dose primary series with a 3-week interval between doses. This vaccine has been safely administered to foals as young as 6 weeks of age when there is a high risk of infection, such as occurs during an outbreak, but the efficacy of its use in very young foals has not been adequately studied. If administered to young foals in this manner, a third dose of the modified live vaccine should be administered 2 to 4 weeks before the foal is weaned to optimize protection during that time of high risk of infection. 

Horses having been naturally infected and recovered:  Following recovery from strangles, most horses develop a durable immunity, persisting in over 75% of animals for 5 years or longer. This indicates that stimulation of a high level of immunity is biologically feasible given appropriate presentation of protective immunogens. Currently, a diagnostic test is available and may be used to assess the level of immunity conferred by natural exposure or vaccination. Since natural exposure or vaccination can provide variable levels of immunity, use of this test may provide a guideline in determining the need for current or future vaccination.

What are club feet?

The increased angle of the pastern and foot along with contracted heels, suggest that your horse has too much tension in his DDF tendon (i.e. it is too "tight"). In the young horse( below 2 years of age), this generally occurs because of an increased growth rate. The bones are growing faster than the deep digital flexor tendon is able to accommodate. Subsequently, the tendons become too "tight" and increase the flexor force on the coffin bone.

Treating this condition starts out with trimming the feet with an emphasis on lowering the heels and decreasing the horses caloric intake. Lowering the heels increases the stress on the ligaments "lengthening" them. This needs to be done every couple of weeks to have success. For those who do not respond to trimming and calorie restrictive diets, there is a procedure called inferior check ligament desmotomy that can be performed. It is a surgical option where by a small ligament in the front legs can be cut below the knee which allows the tendons to relax and normal conformation can be expected. This procedure does not interfere with any athletic career in the future and recovery time is minimal.

Although this makes perfect sense, it is extremely difficult to achieve in older horses. We find that some horses develop contactural deformity(ies) in one or both thoracic deep flexor muscles/ tendons when they reach their mid to late teens. Although we are not sure as to the cause, it does appear to be a progressive problem.

One farrier and I have worked on another horse with a similar problem. We cut both deep and superficial flexor tendons which allowed us to drop the heel and reestablish a normal axis. However, within 18 months of surgery the same issues were remanifesting as a result of persistent excessive flexor tendon contraction.
Generally, dropping the heel and increasing the tension on the DDF tendon in older horses does not effectively stretch/ lengthen the tendon. Rather, it accentuates the problems occurring as a result of excessive DDF tension: laminitis, navicular inflammation, dorsal wall delamination, contracted heels, DDF tendinitis, etc. We would expect that lowering your horse's heels would do the same.

We do recommend massage therapy of the flexor tendons in an attempt to discourage further contraction. Although we're still not certain as to it's effectiveness, it can only help.

What are windpuffs?

Windpuffs is a term that denotes synovial effusion (i.e. extra fluid) within the fetlock joint and/or digital flexor sheath. It can occur in the front legs, the back legs, or both. Extra fluid results in a soft fluctuant swelling behind and just above the fetlock (ankle) joint. It is more common in older horses, but can occur at any age.

Although the digital flexor sheath and fetlock joint are in close proximity with one another, effusion in one structure can be identified by its specific location. Swelling behind the suspensory ligament branches is consistent with digital flexor sheath effusion. Swelling in front of the suspensory branches suggests fetlock joint effusion.

In the vast majority of cases, the swelling is a result of extra fluid within the palmar (front leg) or plantar (back leg) digital sheath rather than the fetlock joint. The plantar digital sheath acts as a sleeve that houses the superficial and deep digital flexor tendons as they course around the back of the fetlock joint. Normally, a very small amount of synovial fluid is present within the sheath to provide lubrication to the tendons as they slide around the back of the joint.

Although plantar digital effusion can cause clinical lameness, this is rare except in severe cases (e.g. infection or tendon damage). Therefore, the problem is considered primarily cosmetic in nature. Consequently, most horses are left untreated.

Treatment options include injections (steroids/ hyaluronic acid) or surgical debridement. Injection usually dramatically reduces the size of the swelling, although recurrence is very common and usually expected. Surgical manipulation can result in the formation of scar tissue within the sheath, which in turn can cause adhesion formation and lameness. Therefore, this strategy is reserved for only the most severe of cases.

What is EVA?

Understanding Equine Viral Arteritis (EVA. Equine Viral Arteritis (EVA) is a contagious disease caused by equine arteritis virus (EAV). While it is rarely life threatening to otherwise healthy adult horses, EVA is of special concern to horse breeders because it can cause abortion in pregnant mares, death in young foals and render breeding stallions permanent carriers of the virus.

Although EVA outbreaks occur infrequently, EAV is present in horse populations in many countries. While the virus is known to infect many breeds of horses, the prevalence of infection is much higher in certain breeds, most notably, Standardbreds and Warmbloods. This may be due to the high frequency of the carrier state in stallions of these breeds.

Most horses exposed to the virus will develop no signs of the disease. If illness does occur, EVA can be difficult to diagnose because it is clinically similar to several other equine diseases, such as Equine Rhinopneumonitis, influenza, Equine Infectious Anemia (EIA) and Purpura Hemorrhagica. The clinical signs vary in range and severity and can last from 2 to 14 days. They include:

* Fever
* Swelling, most notably the legs, scrotum, sheath, mammary glands and above or around the eyes
* Loss of appetite (anorexia)
* Depression
* Conjunctivitis - inflammation and discharge
* Nasal discharge
* Skin rash (frequently localized on the head and neck, but can be generalized)
* Abortion in pregnant mares
* Pneumonia and death in young foals
* Possible short-term subfertility in stallions that experienced significant fever and scrotal edema

The only definite means of diagnosing EVA is by laboratory testing. The virus can be detected in various tissues and fluids such as nasal or conjunctival secretions, semen, blood, placenta, fetal fluids and tissues. More commonly, the blood is screened for the presence of antibodies to the virus.

Collection of samples for testing should be instigated as soon as possible after the horse is noticed ill to increase the likelihood of confirming a diagnosis. Screening for the carrier state in the stallion involves initial serological examination testing to determine if the stallion has antibodies to EAV or not. If seropositive, a sample of semen containing the sperm-rich fraction of the ejaculate should be tested for evidence of the virus. Your veterinarian will determine which laboratories are proficient in testing for EAV infection.

EAV infection can be transmitted among horses in four different ways:
1. Respiratory: An acutely-infected horse spreads the virus to other in contact horses via respiratory secretions (exposure commonly occurs at racetracks, shows, sales and other events).
2. Venereal: Virus shed in the semen of an infected stallion is transmitted to mares when they are bred.
3. Indirect contamination: The virus is transferred indirectly through the use of contaminated tack or equipment shared among horses or on hands or clothing of personnel handling animals.
4. In utero: Virus passes across the placenta from an infected mare to her unborn foal.

A variable percentage of sexually mature colts or stallions infected with EAV may become long-term or permanent carriers of the virus. Since this is an androgen-dependent carrier state, EAV does not establish persistent infection in geldings, mares or sexually immature colts. Carrier stallions may/may not have exhibited prior clinical signs of EVA. The virus is harbored in certain of the accessory sex glands and shed into the semen whenever a carrier stallion is bred either naturally or by artificial insemination. Carrier stallions are clinically normal, serologically positive for antibodies to EAV and appear to experience no adverse effects on their fertility related to viral persistence in their reproductive tract. In the acutely infected stallion, EAV is shed in various secretions and excretions and also is present in white cells of the blood, usually for up to two to three weeks. Such animals can spread the virus by the respiratory and venereal routes. In contrast, the chronic or persistently infected stallion is only infectious in his semen and, therefore, can only transmit the infection by the venereal route. Mares bred to carrier stallions should be vaccinated unless shown to be seropositive from previous natural exposure to the virus.

Currently, there is no fully proven therapeutic means of eliminating the virus from a carrier stallion's reproductive tract. A small percentage of long-term carriers do, however, spontaneously clear the infection from their systems.

Using sound management practices can help prevent and control EVA:

* Isolate all new arrivals (and returning horses) to your farm or ranch for 3 to 4 weeks.
* If possible, segregate pregnant mares from other horses.
* Blood test all breeding stallions for EAV antibodies.
* Check semen of any unvaccinated, antibody positive stallions to identify carriers before breeding.
* Vaccinate all breeding stallions annually.
* Physically isolate any EAV carrier stallions.
* Restrict breeding EAV carrier stallions to vaccinated mares or those whose blood is positive for naturally-acquired antibodies to the virus.
* Vaccinate mares against EVA at least three weeks prior to breeding to a known carrier stallion.
* Isolate mares vaccinated for the first time against EVA for three weeks following breeding to an EAV carrier stallion (there is no need to revaccinate mares that need to be rebred).
* In breeds or areas with high rates of EAV infection, it is recommended that all intact males between 6 to 12 months of age be vaccinated as advised by your veterinarian.

In the event of an EVA outbreak, prompt action can prevent the disease from spreading and minimize its immediate and long-term economic impact. Follow these guidelines:

* Isolate affected horses as soon as possible.
* Notify your veterinarian immediately.
* In consultation with your veterinarian, have the diagnosis of EVA confirmed by a qualified laboratory.
* If a mare has aborted, place the fetus and placenta in a leak-proof bag, refrigerate it and send to the nearest appropriate laboratory for testing.
* Disinfect the stall, equipment and facilities using a phenolic disinfectant as advised by your veterinarian. After treatment with disinfectant, dispose of bedding by composting in an area away from horses.
* Wash down the mare's hindquarters and tail with an antiseptic solution as advised by your veterinarian and keep her separated from other horses for at least 3 weeks.
* Restrict the movement of all horses to and from the farm or ranch as advised by your veterinarian.
* Suspend breeding operations until the outbreak is over. Notify mare owners.
* Vaccinate all at-risk horses as advised by your veterinarian.
* Notify your state veterinarian or appropriate state regulatory agency of the outbreak.

Horses naturally infected with EAV develop a strong immunity against EVA, which can last for at least several years. Horses can also acquire immunity by being vaccinated against the disease.

Consult your veterinarian for information about an appropriate vaccination program to meet your individual needs. Vaccination should protect a horse against the disease for at least a year.

A blood test can confirm whether a horse has antibodies to the virus and the level of its immunity to this infection. This test cannot differentiate between a horse that is positive for antibodies to EAV as a result of vaccination or from natural exposure to the virus.

The EVA vaccine should be administered to stallions not less than 4 weeks prior to their use for breeding. There is no evidence that a vaccinated stallion will shed the virus in the semen or that the modified live virus vaccine against the disease can set up the carrier state.

A mare being vaccinated for the first time and bred to a carrier stallion should not be placed in contact with antibody negative horses for at least three weeks after her breeding date. While the vaccine will protect her from illness, she is almost certain to experience a limited re-infection cycle from the virus in the semen. During this time, she could serve as a source of infection for any unprotected horses through shedding virus via the respiratory route. This can have significant adverse consequences for pregnant mares and could result in an outbreak of abortion.

The modified live virus vaccine is not approved for use in pregnant mares nor in foals less than six weeks of age unless faced with a high risk of natural infection with EAV and only then if recommended by your veterinarian.

With the exception of very young foals, EVA is rarely fatal. Most horses that contract the disease make full, uneventful recoveries. Treatment, if implemented, is directed at reducing the severity of clinical signs during the course of illness.

If fever or swelling is severe, your veterinarian will likely prescribe non-steroidal and anti-inflammatory drugs to make the horse more comfortable. Horses should be able to return to work within 14 to 28 days.

With the help of your veterinarian, EVA should never be a problem. It is a very manageable infection. By implementing a sound vaccination and/or health care program, the risk of EVA can be minimized. For more information regarding EVA, contact your local veterinarian.

Phone: 859-233-0147 ¦ Fax: 859-233-1968 ¦ e-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it

What is West Nile Virus?

The West Nile Virus is an arthropod-borne virus similar to the viruses that cause Western and Eastern Equine Encephalitis (EEE). Encephalitis cases are seen in the warm months of the year when the primary vector, the mosquito, is present. Birds are the usual host for West Nile, and it is spread from bird to bird by the intermediate host, the mosquito. Humans, horses, and perhaps other mammals are dead-end hosts, infected by the bite of an infected mosquito, and cannot transmit the virus to others. Not every individual who contracts the virus will become seriously ill. Most will have subclinical infections or develop mild symptoms such as fever, malaise, body aches, etc. similar to other viral infections.

Development of neurologic signs such as severe depression, circling, seizures, etc. occurs in a small percentage of cases; some of these cases will ultimately be fatal.

The West Nile Virus vaccine for horses currently is recommended by veterinarians annually where normal exposure to mosquitoes is expected. Mosquito control is the most important preventive measure for all species, however. Spraying, removing free-standing water, stall confinement during mosquito feeding times, etc. are encouraged.

What is a cryptorchid?

Literally, cryptorchidism means "hidden testicle". Abnormal location of the testicle occurs when one or both of the testicles fail to descend completely from the fetal position behind each kidney through their respective inguinal canals into the scrotum. An abdominal cryptorchid has testicle(s) within the abdominal cavity. A horse with testicle(s) in the inguinal canal is called an inguinal cryptorchid or "high flanker". Since cryptorchidism is heritable, cryptorchid horses are considered genetically unsound. For this reason, registration of cryptorchid horses is disallowed by many breed associations.

Cryptorchid castration requires general anesthesia and is therefore more involved than routine castration. The procedure, however, is relatively simple. By using the inguinal extension of the gubernaculum, the testicle can be retrieved without having to dilate the inguinal canal and increase the potential for herniation of bowel into the scrotum. Aftercare consists of one to two weeks of stall rest prior to resuming exercise. Surgery costs $500-$1000.

What is cribbing?

Cribbing is a common vice in which horses grasp a solid object with their upper incisors, contract ventral neck muscles and arch their necks, retract their larynx and pull backward. Cribbing is considered an unsoundness, causing excessive wear on the incisors and enlargement of ventral neck muscles. Horses that crib may exhibit weight loss, unthriftiness, poor performance, and poor performance.
Cribbing may be corrected in many cases through surgical intervention, especially when nonsurgical management (cribbing collars) is unsuccessful. Surgery involves partial removal of multiple muscles and resection of two nerves. Consequently, the act of cribbing, becomes increasingly difficult for the horse.

What is EHV-1

-Equine herpesvirus myeloencephalopathy (EHM) is caused by equine herpesvirus-1 (EHV-1). The virus most commonly causes respiratory infection, and not all infected horses will develop EHM;
-EHV-1 is a normally occurring virus found in the equine population; this outbreak is not being caused by a new virus or a new strain of a virus;
-Signs of EHM in horses may include nasal discharge, incoordination, weakness of the rear limbs and hind end, lethargy, urine dribbling, and decreased tail tone;
-Llamas and alpacas can also be infected with EHV-1 and may develop neurologic disease;
-Currently, there is no equine vaccine that has a label claim for protection against EHM;
-There is no specific treatment that has been proven effective for EHM;
-If your horse has potentially been exposed to an infected horse (or through contact with people or equipment that have been in contact with an infected horse), or is showing signs that could indicate EHM, quarantine your horse and other potentially exposed horses and contact your veterinarian.

Social Networking
Sign Up For ENewsletter
Privacy/UsageSite by Calzone