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Where can I get more information about the West Nile Virus?

The USDA APHIS web site has a page with all sorts of links. Check out http://www.aphis.usda.gov/oa/wnv/index.html.

Fact Sheet on Strangles

Cause: The bacterial organism Streptococcus equi.

Transmission: Transmission may be direct from one horse to another through nasal discharge or by drainage from either active or recovering cases. Transmission may also be indirect via contaminated housing, water sources, and feeders or from handler’s clothing and equipment.

It is increasingly recognized that transmission may originate from outwardly healthy animals. These may be animals that are incubating the disease and who later develop symptoms or from recovering animals that appear to be fully recovered but may still be shedding the organism. A recovered horse may be a potential source of infection for at least 6 weeks after clinical signs have resolved.

A chronic carrier state may develop in up to 10% of horses affected. These horses appear normal clinically but harbor the organism primarily in the guttural pouches. The guttural pouches are large air-filled cavities on either side of the horse’s pharynx. Roughly 50% of the horses with these low-grade guttural pouch infections will have an occasional cough and intermittent unilateral nasal discharge.

No good studies have been conducted to determine the length of time the organism can persist in the environment. The organism is unlikely to persist more than 4 weeks on pasture. Feeding, watering utensils and horse trailers should be thoroughly cleaned and disinfected.

Symptoms: Some horses may show no outward signs of the disease or develop only a single abscess with no other symptoms of illness. A typical case will develop firm, painful swelling of the intermandibular lymph nodes which eventually burst and drain white pus. Lymph nodes also break into the guttural pouches and throat which then drain out the nose. Bastard strangles is the term used to refer to cases where lymph nodes in the chest or abdominal cavity may develop abscesses. These animals have rather vague symptoms of illness that when remain undetected until they culminate in colic, peritonitis or sudden death when an abscess ruptures inside a body cavity.

Some horse immune response to Strep infections is exaggerated resulting in an inflammation of the blood vessels know as vasculitis. This condition, also knows as purpura hemorrhagica, is manifested by swelling of the extremities and occasionally rupture of small blood vessels on the mucous membranes.

Diagnosis: The classical form of Strangles can be diagnoses based on symptoms alone. Veterinarians do face a diagnostic challenge when presented with an otherwise healthy horse with a single abscess in the throat or between the jaws. In these cases the veterinarian will most likely refrain from a diagnosis but assume it I until a culture of the organism can be obtained. Cultures of nasal swabs, nasal washes, or aspirated pus from abscesses remain the gold standard for detection of S. equi. The organism is normally not present on the mucous membranes until 24-48 hours after the onset of fever. Twice daily monitoring rectal temperatures may be used to detect and isolate new cases early in an outbreak.

Nasal or guttural pouch washes are used to:

  1. detect asymptomatic carriers
  2. establish S. equi status before transport or reintroduction with susceptible horses either on the premise or the general public
  3. establish the S. equi status of horses after transport and before commingling
  4. determine the success of eliminating S. equi from the guttural pouch of chronic carriers

A blood test that detects a specific antibody for S. equi in the horse is used to:

  1. detect recent infection
  2. determine need for vaccination
  3. ID animals with existing high levels of the antibody that may predispose them to purpura
  4. support a diagnosis of purpura associated with S. equi infection; and
  5. support diagnosis of bastard strangles

Vaccination: Over 75% of horses that recover from strangles develop a solid immunity for 5 years or more. However, attempts to stimulate solid immunity through vaccination have been disappointing.

Earlier intramuscular vaccines had a high rate of soreness and occasional abscess formation at the injection site. These same vaccines were only protective in 50% of horses challenged a few weeks after vaccination.

A new intranasal vaccine contains a live, attenuated, and non-encapsulated strain of Strep equi. This vaccine has provided a high level of resistance against experimental challenge. Safety issues include residual virulence with formation of slowly developing abscesses in a small percentage of vaccinates nasal discharge, and occasional cases of purpura. Since this is a live vaccine contamination of remote injection sites will result in abscess formation at these locations.

Control of Outbreaks:

  1. All movement on and off the affected premise should be stopped
  2. Segregate clinical cases and their immediate contacts from unexposed horses
  3. Monitor rectal temperatures twice daily and promptly remove any horse from the “clean” population that spikes a fever.
  4. Maintain high hygiene standards throughout the premises. Affected horses should be handled last and all clothing worn while working with infected horses changed before contacting other horses.
  5. Screen convalescing cases after clinical recovery by nasopharyngeal swab or nasal wash to insure animals are no longer shedding the organism
  6. Treat carrier animals and retest until the organism is no longer present.

Treatment:

Appropriate treatment of horses with strangles depends on the stage and severity of the disease. Veterinary opinion on the use of antibiotics is markedly divided. In my opinion (Erfle) horses that have evidence of abscess formation should not be treated with antibiotics unless the animal is off feed, depressed and/or manifesting upper airway obstruction. When close monitoring of horses at risk detects a fever before an abscess has started treatment with antibiotics is a means of preventing localized abscesses. Beware however that animals treated in this manner may not develop an immune response and could still break with the disease if they have ongoing exposure to infected horses or environment.

Disinfection

Bacteria are killed by sunlight and drying. Phenolic disinfectants are recommended in facilities. Bleach and quaternary compounds are effective but are easily inactivated by organic matter. Regardless of the product used physically cleaning all surfaces before applying disinfectants is essential.

What is EVA?

Equine Viral Arteritis

Equine viral arteritis (EVA) is an infectious viral disease of horses that causes a variety of clinical symptoms, most significantly abortions. The disease is transmitted through both the respiratory and reproductive systems. Many horses are either asymptomatic or exhibit flu-like symptoms for a short period of time. An abortion in pregnant mares is often the first, and in some cases, the only sign of the disease. EVA has been confirmed in a variety of horse breeds, with the highest infection rate found in adult Standardbreds.

Breeders, racehorse owners, and show horse owners all have strong economic reasons to prevent and control this disease. While it does not kill mature horses, EVA can eliminate an entire breeding season by causing numerous mares to abort. In addition, U.S. horses that test positive for EVA antibodies and horse semen from EVA-infected horses can be barred from entering foreign countries. As the horse industry becomes increasingly internationalized, nearly all major horse-breeding countries are including in their import policies measures to reduce the risk of EVA. The U.S. Department of Agriculture's (USDA) Animal and Plant Health Inspection Service's (APHIS) Veterinary Services (VS) program provides the equine industry with EVA diagnostic and surveillance support.

History

More than a century ago, a disease fitting the clinical description of what we now call EVA was reported in European veterinary literature. However, the virus was not isolated from horses in this country until 1953 during an epidemic of abortions and respiratory disease.

The most recent EVA epidemic occurred in 1984 when this disease affected 41 thoroughbred breeding farms in Kentucky. This outbreak brought to light two very important findings about EVA: the efficiency with which an acutely infected stallion could venereally transmit the virus and the high carrier rate that immediately occurred in stallions following natural infection with the virus.

Transmission

EVA is 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.

However, 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.

While the mare will shed the virus easily, a pregnant mare infected with EVA may pass the virus to her unborn fetus. Depending on the stage of pregnancy, the fetus can become infected, die, and be aborted. If the infected foal is born, it will only live for a few days.

Symptoms

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

Fortunately, there is a way the industry can work to prevent and control EVA. A safe, effective, and low-cost 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. Strict hygiene and disinfection of instruments and equipment are essential to minimize spread of the virus. 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.

Carrier stallions should be bred only to EVA-positive mares or mares that are properly vaccinated. When breeding an EVA-positive or carrier stallion to an EVA-negative, vaccinated mare, isolate both horses for 24 hours after breeding to prevent mechanical spread of EVA from voided semen. If this is the first time the mare has been bred to a carrier stallion, she should be isolated from other horses for an additional 21 days due to potential virus shedding.

All vaccinated horses should receive yearly boosters to protect against infection and, for the stallions, to prevent the development of a carrier state. In a generation or two, these practices could all but eliminate the population of carrier stallions.

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