Core Equine Vaccinations RecommendedEastern and Western Equine Encephalitis ”Sleeping Sickness” (EEE and WEE)
Transmission of EEE and WEE is by mosquitoes, and infrequently by other bloodsucking insects, to horses from wild birds or rodents, which serve as natural reservoirs for these viruses. Human beings are also susceptible to these diseases when the virus is transmitted to them by infected mosquitoes; however, horse-to-horse or horse-to-human transmission by mosquitoes is highly unlikely, because the amount of virus in the blood of horses affected by EEE or WEE is small. Of these 2 encephalidites, WEE has the lowest mortality (approx. 50%). Eastern equine encephalomyelitis is the most virulent for horses, with mortality approaching 90%. Epidemiological evidence indicates that young horses are particularly susceptible to disease caused by EEE.
Symptoms in horses occur one to three weeks after infection, and begins with a fever that may reach as high as 106 °F (41 °C). The fever usually lasts for 24–48 hours. Nervous signs appear during the fever that include sensitivity to sound, periods of excitement, and restlessness. Brain lesions appear, causing drowsiness, drooping ears, circling, aimless wandering, head pressing, inability to swallow, and abnormal gait. Paralysis follows, causing the horse to have difficulty raising its head.
West Nile Virus
West Nile virus (WNV) is the leading cause of arbovirus encephalitis in horses and humans in the United States. Since 1999, over 25,000 cases of WNV encephalitis have been reported in U.S. horses. Horses represent 96.9% of all reported non-human mammalian cases of WNV disease.
The virus is transmitted from avian reservoir hosts by mosquitoes (and infrequently by other bloodsucking insects) to horses, humans and a number of other mammals. West Nile virus is transmitted by many different mosquito species and this varies geographically. The virus is not directly contagious from horse to horse or horse to human. Indirect transmission via mosquitoes from infected horses is highly unlikely as these horses do not circulate a significant amount of virus in their blood.
The case fatality rate for horses exhibiting clinical signs of WNV infection is approximately 33%. Data have supported that 40% of horses that survive the acute illness caused by WNV still exhibit residual effects, such as gait and behavioral abnormalities, 6-months post-diagnosis. Thus vaccination for West Nile virus is recommended as a core vaccine and is an essential standard of care for all horses in North America.
Clinical signs of encephalitis in horses may include a general loss of appetite and depression, in addition to any combination of the following signs: fever, weakness of hind limbs, paralysis of hind limbs, impaired vision, ataxia (weakness), head pressing, aimless wandering, convulsions (seizures), inability to swallow, walking in circles, hyperexcitability and coma.
All horses are at risk of development of tetanus, an often fatal disease caused by a potent neurotoxin elaborated by the anaerobic, spore-forming bacterium, Clostridium tetani. Tetanus toxoid is a core equine vaccine and is indicated in the immunization program for all horses.
Clostridium tetani organisms are present in the intestinal tract and feces of horses, other animals and humans, and are abundant as well as ubiquitous in soil. Spores of Cl. tetani survive in the environment for many years, resulting in an ever-present risk of exposure of horses and people on equine facilities. Tetanus is not a contagious disease but is the result of Cl. tetani infection of puncture wounds (particularly those involving the foot or muscle), open lacerations, surgical incisions, exposed tissues such as the umbilicus of foals and reproductive tract of the postpartum mare (especially in the event of trauma or retained placenta ).
The earliest symptom of tetanus is extreme sensitivity. Within 10 to 14 days following injury, horses become increasingly nervous. They jump violently on being touched. Some seem unwilling to be handled and may respond with aggression. Protrusion of the third eyelid, and stiff gait are the most common clinical signs. Spasms of the masseter muscles--muscles that bring the upper jaw and lower jaw together--occur early in the disease which results in "lockjaw". Loud noises, colic, and sweating usually appear at a later stage of the disease
Rabies is an infrequently encountered neurologic disease of equines. While the incidence of rabies in horses is low, the disease is invariably fatal and has considerable public health significance. It is recommended that rabies vaccine be a core vaccine for all equines.
Exposure occurs through the bite of an infected (rabid) animal, typically a wildlife source such as raccoon, fox, skunk, or bat. Bites to horses occur most often on the muzzle, face, and lower limbs. The virus migrates via nerves to the brain where it initiates rapidly progressive, invariably fatal encephalitis
Clinical signs can be very variable with symptoms being both general and similar to other diseases that affect the horse’s nervous system. This makes rabies very difficult to diagnose. Affected horses might go off feed or exhibit depression, excessive salivation, difficulty swallowing, lack of coordination, aggressive behavior, hyperexcitability, colic, convulsions or paralysis. Death usually occurs three to five days after the onset of clinical signs, but it can also occur in less than one day.
Equine Rhinopneumonitis Virus
Equine herpesvirus type 1 (EHV-1) and equine herpesvirus type 4 (EHV-4) can each infect the respiratory tract, causing disease that varies in severity from sub-clinical to severe and is characterized by fever, lethargy, anorexia, nasal discharge, and cough. Infection of the respiratory tract with EHV-1 and EHV-4 typically first occurs in foals in the first weeks or months of life, but recurrent or recrudescent clinically apparent infections are seen in weanlings, yearlings, and young horses entering training, especially when horses from different sources are commingled. Equine herpesvirus type 1 causes epidemic abortion in mares, the birth of weak nonviable foals, or a sporadic paralytic neurologic disease (equine herpesvirus myeloencephalopathy-EHM) secondary to vasculitis of the spinal cord and brain.
Streptococcus equi subspecies 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.
Equine influenza, caused by the orthomyxovirus equine influenza A type 2 (A/equine 2), is one of the most common infectious diseases of the respiratory tract of horses. It is endemic in the equine population of the United States and throughout much of the world, with the notable exceptions of New Zealand and Iceland. Equine influenza virus does not constantly circulate, even in large groups of horses, but is sporadically introduced by an infected horse. This epidemiologic finding and the rapid elimination of the virus by the equine immune response suggest that infection can be avoided by preventing entry of the virus into an equine population (i.e. by the quarantine of newly arriving horses for at least 14 days), and by appropriate vaccination before exposure. All horses should be vaccinated against equine influenza unless they live in a closed and isolated facility.
Flu symptoms in horses can include elevated temperature, loss of appetite, harsh dry cough, and nasal discharge which may be watery or thick
Other Equine Diseases To Be Aware Of
Other Equine Diseases To Be Aware Of
Botulism has been observed in horses as a result of the action of potent toxins produced by the soil-borne, spore-forming bacteria, Clostridium botulinum:
• Wound botulism results from vegetation of spores of Cl. botulinum and subsequent production of toxin in contaminated wounds.
• Shaker Foal Syndrome (toxicoinfectious) results from toxin produced by vegetation of ingested spores in the intestinal tract.
• Forage poisoning results from ingestion of preformed toxin produced by decaying plant material, including improperly preserved hay or haylage, or animal carcass remnants present in feed.
• Equine Grass Sickness (Equine Dysautonomia) is considered a form of botulism resulting from the overgrowth of Cl. botulinum type C in the intestinal tract, especially the ileum. There are reports of isolated cases of the disease occurring in the U.S.
Botulinum toxin is the most potent biological toxin known and acts by blocking transmission of impulses in nerves, resulting in weakness progressing to paralysis, inability to swallow, and frequently, death. Of the 8 distinct toxins produced by sub-types of Cl. botulinum, types B and C are associated with most outbreaks of botulism in horses.
Equine Anaplasma Phagocytophilum or Ehrliciosis
Anaplasmosis in horses is caused by bacteria called Anaplasma phagocytophila, which are spread by a tick-bite. This bacterium was formally known as Ehrlichia equi and the disease was previously called “equine ehrlichiosis” or “equine granulocytic ehrlichiosis” (EGE).
Ehrlichia equi was thought to be a separate bacterium unique to horses, but recently has been found to be genetically the same as Anaplasma phagocytophila and thus the name was changed. Anaplasma phagocytophila also causes “canine anaplasmosis” in dogs and “human granulocytic ehrlichiosis” (HGE) in people. Anaplasmosis is not considered contagious & is only transmitted via a tick bite or transfer of blood. We have seen several cases of Equine Anaplasmosis in our practice area.
Equine Monocytic Ehrliciosis “Potomac Horse Fever”
Equine monocytic ehrlichiosis is caused by Neorickettsia risticii (formerly Ehrlichia risticii). Originally described in 1979 as a sporadic disease affecting horses residing in the eastern United States near the Potomac River, the disease has since been identified in various other geographic locations in the United States and Canada. The disease is seasonal, occurring between late spring and early fall in temperate areas, with most cases in July, August, and September at the onset of hot weather.
Clinical signs are variable but may include: fever, mild to severe diarrhea, laminitis, mild colic, and decreased abdominal sounds. Uncommonly, pregnant mares infected with N. risticii (usually in the middle trimester between 90 and 120 days) can abort due to fetal infection at 7 months of gestation.
If Potomac Horse Fever has been confirmed on a farm or in a particular geographic area, it is likely that additional cases will occur in future years. Foals appear to have a low risk of contracting the disease. Vaccination against this disease has been questioned because field evidence of benefit is lacking. Proposed explanations for this include lack of seroconversion and multiple field strains whereas only one strain is present in available vaccines.
Leptospirosis in horses is most commonly associated with uveitis or abortions. The disease is typically seen as a self-limiting mild fever with anorexia, although in severe forms hemolysis and vasculitis can result in petechial hemorrhages on mucosal surfaces, hemoglobinuria, anemia, icterus, conjunctival suffusion, depression, and weakness. Renal failure has been documented in foals. Recurrent uveitis (moon blindness) develops anytime from 2-8 mo following the initial infection. Leptospirosis appears to be a significant cause of recurrent uveitis in horses, accounting for up to 67% of the cases.
Equine Infectious Enemia (EIA)
Equine Infectious Anemia (EIA) is a contagious, viral disease. EIA affects all members of the Equine species, including horses, ponies, donkeys, and mules.
Once animals become infected they are life-long carriers of the virus.
What are the clinical forms of EIA?
There are three clinical forms of EIA, acute, chronic, and inapparant. The majority of the clinical signs of the disease are related to the reaction of the animal's immune system to the viral infection. Clinical signs of the acute form include high fever, depression, loss of appetite, small areas of hemorrhaging on the mucous membranes, stocking up (swelling of the legs), and edema (collection of fluid) along the ventral abdomen. Clinical signs of the acute form of the virus usually appear seven to 30 days after exposure to (or infection of) the virus.
Clinical signs of the chronic form of EIA include reoccurring intermittent fever, depression, lack or loss of appetite, weight loss, anemia, weakness, and incoordination of the hind legs. The severity and frequency of the reoccurring episodes decrease over time. Animals that are infected without showing detectable clinical signs are "inapparent carriers" of EIA. Mares that are infected with EIA typically fail to conceive or abort if they are pregnant.
How is the disease transmitted?
EIA is found in the blood of all infected animals even if they are inapparent carriers. Typically equines with the acute form of the disease are more infectious than others carrying the virus because of the high levels of virus circulating in the blood. The primary method of transmission is through blood sucking insects, including horse flies, deer flies, mosquitoes, and gnats. Less common modes of transmission are virally contaminated health in-struments such as needles, syringes, and dental and teeth floating equipment. Transmission may also occur between infected pregnant mares and unborn foals. About 10 percent of foals born to infected mares are infected with the virus. The virus may also be transmitted through natural service or breeding
The Coggins test is a blood test for this disease that is required of all horses bought and sold in Wisconsin and for almost every horse show. Almost every state requires this test for horses to come into their state. The blood test is usually done once per year to detect the disease. The blood sample must be drawn by a licensed and accredited Veterinarian and tested at a certified lab. Results are usually back within a week. This information is required on your interstate health papers to cross state lines.
It is a good idea to bring in a fecal sample to identify the parasite type and egg count in your horses. This information is beneficial when deciding what worming regime is best for your horse or herd.
If you have a large number of horses to deworm we have an economical and easy to use product to add to the feed. This fenbendazole can be fed at the rate of 1 lb feed for 1000 lbs body weight or at a more concentrated strength you could feed ¼ lb per 1000 lbs body weight.
Oral paste dewormers are also commonly used. These wormers are highly effective if rotated throughout the year.