EQUINE DISEASES

This page is meant to give you information about the most common diseases we vaccinate against. It is by no means meant to be a complete list of diseases. it just gives you the basics about diseases we vaccinate against. I have included Equine Infectious anemia in this list because it can be controlled and prevented through constant testing. Click the link to read about each disease. Click your "Back" button to return to this menu.

Transmission: Mosquito-borne disease. The cycle starts with infected birds, which can travel long distances in a short amount of time. When a mosquito bites a bird carrying the West Nile virus, it too becomes infected. The mosquito then feeds on another bird, a horse, human or other mammal. Once a horse has been bitten, it may take only 5 to 15 days for signs of West Nile virus to appear.

Clinical Signs: Muscle weakness or twitching, partial paralysis, stumbling or tripping, loss of appetite, depression or lethargy, head pressing or tilt, impaired vision, wandering or circling, inability to swallow, inability to stand up, fever, convulsions, coma and death. These symptoms can be confused with rabies, EPM ("Possum Disease), equine encephalitis, and other serious neurological diseases. Not all animals contracting the disease will show signs. Of those animals showing signs about 1/3 will die if untreated.

Diagnosis: A serum sample is submitted to confirm West Nile. Sometimes, if the sample is tested early in the disease, a negative result may be seen. Retesting in a few days to weeks will reveal a positive sample.

Treatment: Treatment is aimed at controlling inflammation in the nervous system. We use steroids early, nonsteroidal anti-inflammatory drugs, DMSO, and interferon. A serum is also available that contains antibodies to the disease.

Prevention and Control: There is are several vaccines available for West Nile. There are many rumors out there about abortions when it is used in pregnant mares. I have never had a problem. ANY potential stress can lead to abortion.

Transmission: Equine influenza is spread via aerosolized respiratory secretions and contaminated objects and people moving between infected and uninfected horses. The most common source of infection and outbreak is the introduction of a new animal into the herd. The incubation period is usually one to three days (but up to 7 days). Infected horses shed virus in their respiratory secretions during the incubation period, and continue to excrete the virus for four to five days after clinical signs are observed. It is also possible for an infected animal to shed the virus for 7-10 days after the animal has appeared to recover. Viral shedding is thought to reach its peak during the first 24 to 48 hours the animal has a fever. Infected droplets may be able to spread as far as 50 yards. Virtually 100% of horses that are exposed become infected. Nearly 20% of infected horses do not exhibit clinical signs of disease, but still shed virus and can spread the infection. Up to 60 - 90% of a herd may show signs if a diseased animal is introduced into your herd. .

Clinical Signs: Equine influenza virus causes clinical disease of the upper respiratory tract. The virus spreads rapidly. Clinical signs include fever, coughing, nasal discharge, depression, muscle soreness, lack of appetite, and enlarged regional lymph nodes. Colic (abdominal pain) and swelling of the legs and scrotum have also been observed with influenza infection. If there are no secondary complications, healthy, adult horses usually recover from influenza within one to two weeks; however, coughing may persist for a longer period. Young foals lacking adequate maternal antibodies are at risk of developing a rapidly fatal viral pneumonia. Secondary bacterial infections can greatly prolong recovery or lead to death. The mortality rate is from 1 -20% depending on secondary infections. Higher death rates are seen in foals, horses with depressed immune systems and donkeys

Diagnosis: A tentative diagnosis of influenza is often made based on clinical signs. Diagnosis can be confirmed by detection of the virus in samples from nasal swabs or tissue samples.

Treatment: As for all viral disease, treatment is largely supportive. Good husbandry and nutrition may assist horses in mounting an effective immune response. Rest reduces viral shedding. Rest is recommended for several weeks following infection. Medications are used to control fever, fight secondary infections and to boost the immune system. Secondary infection is a real problem. In a recent outbreak of influenza locally, lung culture from an animal that died revealed Strep equi pneumonia. (See Strangles).

Prevention: Vaccination is by intranasal or intramuscular injection. We recommend vaccination AT LEAST every 6 months (2-3 months in very high risk animals). Vaccine may not completely protect an animal but will decrease the severity of infection. The virus is easily killed by 10% bleach solutions. The most common source of infection is the introduction of a new animal into the herd; therefore, isolation of newly acquired animals is recommended. Animals should be isolated for 21 days after the last horse has appeared to recover from the infection. Clothing, equipment, surfaces, and hands should be cleaned and disinfected after exposure to horses known or suspected to be infected.

Cause: Strangles is caused by a highly contagious bacteria -- Streptococcus equi.

Transmission: Strangles is very contagious, especially with foals, spreading easily from horse to horse and often leading to large outbreaks with many horses affected. It is spread in the discharges (pus) from the nose and burst abscesses. Objects such as water troughs, feed buckets, brushes, reins and other equipment, if contaminated with infected pus, can also spread the disease. Recovered horses can spread the disease for up to eight months, even though they can appear clinically healthy and normal.

Clinical Signs: Typically, horses suffering from strangles have pus discharging from the nostrils and swellings (abscesses) forming in the lymph glands under the jaw. These abscesses often burst and exude a thick yellow pus. Affected horses can have fever, cough, be depressed and may stop eating. Some horses will just have a fever and nasal discharge. While not considered strangles, Strep equi is also commonly a bacteria that invade as a secondary infection following any disease that lowers the bodies resistance including influenza, rhinopneumonitis and viral arteritis. It may be also seen in infections of the skin, uterus and pneumonia. Most animals recover, but horses that contract even a mild case of strangles must be isolated and removed from training or heavy work for up to 3 months. In some cases the infection can cause chronic illness or even death.

Diagnosis: Clinical signs are usually enough for diagnosis. Bacterial cultures of pus or nasal discharges will grow Strep equi .

Treatment: This is a subject of debate. Current recommendation is if the horse is still eating, keep them off antibiotics. Antibiotics can actually make the disease worse in some cases. We use anti inflammatory drugs, immune stimulants and sometimes hot packs to bring abscesses to the surface. Most abscesses are allowed to break without lancing. Extreme depression, high fever, and not eating usually prompt me to start them on antibiotics.

Prevention: In common with other respiratory diseases, such as canine cough and feline respiratory disease, immunity is short lived and incomplete. In fact 25% of horses infected with strangles do not appear to develop immunity. We have found the best vaccine is an intranasal product. This product is given every year to maintain immunity. The disease is highly infectious. Clean everything thoroughly. Infected animals should be isolated

Cause: Tetanus is caused by a bacteria, Clostridium tetani. The toxins produced by the bacteria cause the clinical signs.

Transmission: Tetanus occurs when a wound becomes infected with bacterial spores of Clostridium tetani.. These spores germinate, multiply and produce a very powerful poison which affects the muscles. Some cases of tetanus occur from wounds that are so small they are not noticed. These spores can be found in the soil (it is more prevalent in cultivated than uncultivated soils) and organisms are routinely isolated from the feces of many domestic animals, including the dog and cat, and also from humans. Clostridial infections are anaerobic infections, meaning they grow where there is no oxygen. Puncture wounds are ideal for this. I have also seen it in mares with an unaborted dead fetus.

Clinical Signs: An affected horse moves with a stiff-legged gait, often with the tail held out stiffly and the ears pricked. The 3rd eyelid moves across the eye from the inside corner. Loud noises will make the animal spasm or convulse. As the disease progresses the muscles become so rigid and stiff that the horse may fall and not be able to get up again. Convulsions may occur and death is caused by paralysis of the breathing muscles. Most cases will show clinical signs weeks or longer after the initial infection.

Treatment: Treatment includes opening the infected area if possible, very high doses of tetanus antitoxin, muscle relaxants, sedatives, penicillin and other supportive measures. While we have saved animals with tetanus, far more have died.

Prevention: Vaccination is the only way to provide safe, effective long-term protection against tetanus. Vaccinate mares with tetanus toxoid within 30-60 days before foaling to give immunity to the foal. Unvaccinated horses that become injured need a dose of tetanus toxoid AND a dose of tetanus antitoxin. Vaccinated horses need a booster of tetanus toxoid.

Transmission: The Eastern and Western encephalomyelitis viruses are transmitted mainly by mosquitoes. Normally, these two viruses cycle between birds and mosquitoes. Humans and horses are incidental, dead end hosts. The Venezuelan equine encephalomyelitis viruses are also spread mainly by mosquitoes. The enzootic subtypes of VEE cycle between rodents and mosquitoes. Birds may also be involved in some cycles. Humans and horses are incidental hosts. The Western, Eastern and Venezuelan encephalomyelitis viruses are found in North, Central and South America. The WEE viruses occur in western Canada, Mexico, parts of South America, and west of the Mississippi in the United States. The EEE virus is found in eastern Canada, all states east of the Mississippi, Arkansas, Minnesota, South Dakota and Texas. It also occurs in the Caribbean and regions of Central and South America, particularly along the Gulf coast. VEE viruses are endemic in South and Central America and Trinidad. Enzootic subtypes of VEE are also found in Florida, the Rocky Mountains and northern plains of the United States. Most epidemics of VEE occur in northern and western South America, but some may spread into adjacent countries, including the United States.

Clinical Signs: Eastern and Western equine encephalomyelitis are very similar in horses. The initial clinical signs are usually fever, anorexia and depression. In severe cases, this prodromal stage is followed by neurologic signs; the symptoms may include involuntary muscle movements, impaired vision, aimless wandering, head pressing, circling, an inability to swallow, incoordination, paresis, paralysis and convulsions. Periods of excitement or intense itching can also be seen. Down animals may develop a characteristic 􀂳paddling􀂴 motion. Both EEE and WEE can also cause asymptomatic infections or mild disease without neurologic signs. The enzootic subtypes usually infect horses subclinically. The epizootic subtypes can cause asymptomatic infections or two clinical syndromes. The clinical signs of all these can be confused with those of other diseases that affect the central nervous system. These include West Nile equine encephalitis, EPM, African horse sickness, rabies, tetanus, and bacterial meningitis. They may be mistaken for toxic poisoning. EEE is often fatal in horses; the mortality rate is 50 to 90%. WEE is more likely to be asymptomatic or mild, with mortality rates of approximately 20 to 30%.

Treatment: Treatment is directed at supportive therapy. Anti-inflammatory, fluids, etc. are used to support the animal to allow its own immune system to try to overthrow the infection.

Cause: Potomac horse fever is caused by a type of tiny bacteria, Neorickettsia risticii.

Transmission: The PHF organism is harbored inside flukes that parasitize water snails. When the water becomes warm, the flukes hatch immature forms, called cercaria, which carry the PHF organism, and pass out of the snail into the water. Experimentally, this water can infect horses. Currently, the most important transmission route is believed to be these immature flukes which are ingested by a variety of aquatic insects. The larval stages of the insects then molt into flying insects, carrying the immature fluke and PHF organisms into the horse’s environment. The horse then becomes infected when it eats or drinks anything contaminated with these insects. Most of the research has focused on 2 types of insects: caddis flies and mayflies, which carry the organism. Direct transmission of the disease from one horse to another is remotely possible, but requires consumption of a very large amount of manure from a sick horse. As diarrhea can be caused by a number of other organisms as well, such as Salmonella, and Clostridia, you should isolate any horse with diarrhea to minimize transmission of possible contagious microbes to other horses, animals or humans.

Clinical Signs: After the organism is ingested, it multiplies in the intestinal tract, where it can cause marked inflammation (colitis). This leads to the clinical signs of fever, depression, poor appetite, and in most cases, diarrhea. Colic may be seen. Some horses will founder and pregnant mares can abort. Some will also develop swelling of their lower limbs or body wall.

Treatment: Fluids, antibiotics and anti-inflammatory drugs are used for treatment.

Not all horses exposed to the PHF organism become ill. This disease can kill affected horses, but most respond well to treatment.

Cause: Equine protozoal myeloencephalitis (EPM) is a progressive, degenerative neurological disease of the central nervous system caused by Sarcocystis neurona. Recent investigation implies that the syndrome, in rare cases, can be caused by Neospora caninum and/or Neospora hughesi infections.

Transmission: The definitive host of Sarcocystis neurona is the opossum. Infected opossums shed sporocysts in feces which are in turn infective to the intermediate host when ingested. Many intermediate hosts are currently recognized in the life cycle of this protozoan, and the full range of hosts has yet to be identified. Current species implicated include armadillos, skunks, and raccoons. Once the intermediate host is infected, it goes on to develop sarcocysts in its skeletal muscle. When this muscle is ingested by the opossum, the life cycle is completed. The horse is considered a dead-end host of Sarcocystis neurona. (The horse cannot spread the disease.) While the horse is presumably infected by eating sporocysts in contaminated feed and water, there are many unanswered questions concerning how this organism actually infects the horse.

Diagnosis: The best diagnosis method is through testing spinal fluid. Blood tests can show exposure but may be inconclusive. New tests are being developed.

Clinical Signs: Clinical signs can be really variable with this disease. You can see muscle atrophy, uncoordination, weakness or about any neurological sign imaginable. Until West Nile hit the midwest, EPM was probably the number one neurological disease (and it still may be).

Treatment: Treatment involves a combination of anti-inflammatory drugs, antibiotics and supportive care. Studies estimate that clinical improvement can be seen in 70% of treated horses, but fewer than 25% return to original function. Relapse of disease occurs in approximately 5-28% of horses when treatment is discontinued.

Prevention: Due to the lifestyle and eating habits of the definitive host of Sarcocystis neurona (the opossum), prevention and control of EPM are potentially problematic. Current recommendations include preventing access of opossums to hay, grain, pasture, and water sources. This may be difficult, especially if food and water are in short supply for the opossum. The most reasonable and simple precaution for horse owners to take is to deny access of stored hay and grain bins to the opossum. A killed vaccine against Sarcocystis neurona has been developed, it is currently available.

Rabies

Transmission: Bats, skunks, foxes, raccoons, and other wild animals are the reservoirs of this disease. Humans, as well as horses and other domestic animals, may become infected when exposed to fluids such as saliva from rabid animals through bites or scratches.

Clinical Signs: Horses with rabies may appear sleepy or depressed; stumble; be unable to eat, swallow or drink; make unusual vocal sounds; be aggressive; or simply seem not right. Rabies should always be considered when evaluating an ill horse (especially one with neurological signs).

Transmission: Primarily a respiratory disease. Particles from acutely infected horses' nasal discharges are inhaled, often during the movement of horses at sales, shows, and racetracks. Horses are herd animals that tend to commingle, and this close contact facilitates the spread of the virus. Unlike other respiratory diseases, EVA can also be transmitted venereally during breeding, either naturally or by artificial insemination. When a mare, gelding, or sexually immature colt contracts the disease, the animal will naturally eliminate the virus and develop a strong immunity to reinfection. On the contrary, infected stallions are very likely to become virus carriers for a long time. Once stallions are in the carrier state, they transmit the virus to mares during breeding.

Clinical Signs: Many horses infected with EVA are asymptomatic. When symptoms do occur in the acute stage of the disease, they can include any or all of the following: fever, nasal discharge, loss of appetite, respiratory distress, skin rash, muscle soreness, conjunctivitis, and depression. Other clinical signs in infected animals are swelling around the eyes and ocular discharge, swollen limbs, swollen genitals in stallions, and swollen mammary glands in mares. Abortion in pregnant mares is also a symptom of EVA. Abortion rates in EVA-infected mares can be as low as 10 percent or as high as 70 percent.

Diagnosis: Horse owners should suspect EVA when respiratory symptoms accompany an abortion in a mare. Since the clinical signs of EVA are similar to those of other respiratory disease, and no characteristic lesions are in EVA-aborted fetuses, only diagnostic tests can confirm the disease. Virus isolation can be attempted from swabs of the nose, throat, or eyes; semen, placentas, or fetal tissue; and blood samples. However, the most common method of diagnosis is testing blood for the virus' neutralizing antibodies that cause EVA. While the presence of these antibodies alone does not indicate active infection, it does indicate EVA exposure has occurred. Very high levels of antibodies on a single sample or a rising antibody titer from paired blood samples collected 14 to 28 days apart indicate active infection.

Treatment: While there is no specific treatment for EVA, treatment should include rest and in selected cases, antibiotics, which may decrease the risk of secondary bacterial infection. Adult horses recover completely from the clinical disease. However, the virus commonly persists in the accessory glands of recovered stallions, so these carrier stallions continue to shed the virus for years and remain a significant source of infection.

Prevention and Control: There is a way to prevent and control EVA. A safe and effective avirulent live virus is now available. Combining this vaccine with isolation of the vaccinated animal from noninfected horses can prevent the spread of EVA. Since properly vaccinated EVA-negative stallions do not become carriers, all EVA-negative colts less than 270 days old should be vaccinated. The vaccine is not approved for use in pregnant mares. Blood samples for EVA testing should be collected from all horses before breeding, and virus isolation should be performed on imported semen before use. EVA-negative mares should be bred only to EVA-negative, noncarrier stallions. If blood test results are positive in a stallion, but there is no official documentation of negative EVA status prior to vaccination, the stallion must be tested for the presence of a carrier state. Virus isolation can be attempted on the semen from two separate ejaculations, or by mating two EVA-negative mares with the stallion. Twenty-eight days after breeding, mares' blood should be tested for the development of the neutralizing antibodies to the EVA virus.

Cause: Equine infectious anemia (EIA)is caused by a virus that attacks red blood cells.

Transmission: Only equine species are affected. Introducing certain body fluids, usually blood, from an infected horse to a healthy horse transmits this disease. This can be accomplished by an insect (most likely horse flies) or by a variety of mechanical means (such as the repeated use of a single needle on a number of horses, one of which is infected). Once infected, horses harbor the virus for life.

Clinical Signs: The initial signs of EIA pass quickly into one of four patterns: acute, subacute, chronic, or carrier. Acute cases are more the exception than the rule. These horses rarely survive and can die within three to ten days after the virus enters their bloodstream. Subacute cases can also be very sick and then the symptoms become chronic. These horses may have no sign of disease for a long time then progress to a state of continuing weight loss, rough hair coat, and anemia. Relapses of increasing severity are also common. Chronic cases may have occasional attacks and usually have a poor haircoat, unhealthy appearance, edema, and anemia. Carrier animals appear healthy but harbor the virus. A horse may be a carrier for its entire life and never show signs of disease but can potentially transmit the disease to a healthy horse.

Diagnosis: EIA tests detect the presence of antibodies to the EIA virus in the blood of the horse. Antibodies are proteins manufactured by the horse in an attempt to fight the virus. A horse that tests positive on one occasion will do so for the rest of its life (except for young foals that absorbed antibodies from their positive dam’ colostrums but are not actually infected with the virus). The Coggins test, the original test for EIA, takes several days to run and is considered the standard test by which other more recently developed tests are evaluated. These tests, called ELISA tests, require only a few hours to complete. Positive ELISA tests are confirmed by running the Coggins test.

Treatment: There currently is no effective treatment or vaccination program available for this disease.

Prevention: Prevention is accomplished through continuous testing for the disease. ALL horses should be tested that will be around other horses. Never purchase a horse or board a horse without a negative test.

Cause: Equine rhinopneumonitis is caused by the equine herpes virus. There are several types but only 2 cause clinical disease: Type 1 (EHV-1) and Type 4 (EHV-4).

Transmission: Rhinopneumonitis occurs in horses of all ages but is more common in horses less than three years old. Outbreaks come from inhalation of the virus articles. These particles are transmitted from horses spreading the infections. The virus penetrates the lining of upper and lower respiratory tracts within hours of infection, replicates, then infects the local blood vessels and respiratory lymphoid tissues within 24 hours. The immune system is suppressed, which may predispose animal to secondary lower airway bacterial disease. (See Strangles.) The incubation period is from 2 - 10 days. This means after infection it takes that long for clinical signs to appear.

Clinical Signs: EHV-4 primarily causes primarily respiratory disease in young horses. The disease is more severe in young foals. EHV-1 may present in one or a combination of the following:

Respiratory Disease This is the presentation most people are familiar with seeing. Most horses will run a low grade fever but some can run high fevers, have a runny nose and may cough. Sometimes this can cause pneumonia. Most horses continue to eat when the disease is confined to the upper airways. Secondary infections are common (see Strangles). Respiratory problems are more severe in foals, with infections near birth producing weak foals that die within 24 hours.

Reproductive Disease: This is the form most breeding farms worry about. Following a respiratory infection, the virus can cause abortions. Death of the fetus occurs two weeks to four months after exposure to the virus, or during the last three months of pregnancy. Abortion storms have a sudden onset with no additional clinical signs. The foal dies from asphyxiation by the premature separation of the placenta.

Neurological Disease: This is the part everyone is now worried about. Outbreaks have shut down barns in Florida and the Northeast US. As of 1/25/07, a barn in California is under quarantine and the University of Connecticut had their own herd under quarantine with 21 horses sick (5 with neuro disease). These animals present with a combination of neurological signs including being weak or down. Many will have bladder paralysis or urinary incontinence.

Diagnosis: Nasal swabs can diagnose the disease through the PCR test. Aborted tissues can be examined. Blood tests can show exposure but most horses are exposed.

Treatment: Supportive therapy -- anti-inflammatory drugs, immune system stimulators and teat any secondary infections. Interferon may help. In uncomplicated cases, complete recovery occurs in several weeks. However, remember that herpes infection is for life, and reactivation of the virus can cause recurrent disease or continuous shedding! REST THE HORSE AND GRADUALLY RETURN IT TO WORK. Isolate animals exhibiting signs, disinfect stable equipment, bedding (remove and burn it). Booster vaccinations during outbreak may help. Quarantine stable until 30 days after last new case is identified. Most horses recover from the respiratory infection and most mares breed back after aborting. The neurological disease has much higher death rate.

Prevention: Vaccination is the key to prevention of the respiratory and reproductive disease. The vaccines effectiveness is VERY short lived. Immunity only lasts 2 -3 months depending on the vaccine used. Vaccination does not appear to be effective in stopping the neurological form. Some evidence exists that keeping the herd vaccinated may decrease the severity of the disease. The key is once a horse is infected, it is infected for life. Stress causes it to shed the virus. These horses still shed the virus even if they have been vaccinated. A paper presented at the AAEP 2006 Convention said that 6% of the horses tested at two major horse shows were found to be shedding herpes virus. I would speculate these numbers would be considerably higher for smaller shows/events due to stress levels involved.

There are other diseases we could have included -- Rotavirus, rhodococcus, adenovirus, etc. These may be added at a later date. The above diseases can be controlled through testing and/or vaccination-management.

Copyright © 2003 Rolling Meadows Animal Hospital Last modified: November 02, 2008

Copyright © 2003 Rolling Meadows Animal Hospital
Last modified: November 02, 2008