African Horse Sickness

by Robert N. Oglesby DVM

Introduction

African Horse Sickness (AHS) is caused by a virus and transmitted by biting insects. Starting with fever, there is a rapid onset of severe respiratory and cardiac signs with high mortality.

African Horse Sickness (AHS) is a severe diseases of horses that has a long history. The first reports of AHS like disease go back to the 1300's and has been described periodically since. Livingston had problems exploring central, eastern, and south Africa because of the inability to use horses at times do to this infection. Major epizootics would occur every 20 or 30 years. The 1854-55 epizootic resulted in the death of over 70,000 horses representing 40% of the horse population in some areas.

In the early 1900's it became recognized this was not a bacterial disease and that there were different strains or serotypes some of which did not cross protect the horses. A horse could contract one strain and still be susceptible to other strains. Horses still die every year from AHS but in endemic areas epizootics have largely been curtailed through the use of polyvalent vaccines. Occasional outbreaks in non-endemic areas show this disease to be a threat to the rest of the world.

This article discusses the cause, transmission, clinical signs, diagnosis, treatment, and prevention of African Horse Sickness. Also discussed is the safe transport of horses in and out of endemic areas.

Cause

AHS is an Orbivirus that belongs to the Reoviridae family. Nine antigenically distinct serotypes have been described and all nine appear in the southern and eastern parts of Africa. Type nine serotype however is the most widespread and predominates in the northern aspects of Africa.

AHS predominately attacks the vascular system and the heart and clinical signs stem from this. In cases where the vessels of the lungs are predominately injured respiratory disease occurs. If the heart is the main focus of viral damage you get predominately signs of heart failure. Most infections are some mixture of these two injuries but usually one predominates.

Transmission

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Understanding the transmission, persistence, and geographical range of AHS starts with the information that zebras become infected but do not often become ill with the disease. Once infected the zebra becomes viremic, responds immunolgically, then clears the virus. AHS is transmitted almost solely by some species of the culicoides biting midge. So in the wild the virus persists in a cycle between the culicoides and zebra. It is possible that other biting flies transmit the virus but this has not been demonstrated that this occurs naturally.

Horses become infected when bit by an infected culicoides midge. There is a high seasonal incidence during the warm, moist months. AHS is endemic in Africa but a few outbreaks have occurred in Europe and the Middle East, the most recent being in Portugal (1989) and Spain (1987-1990).

Clinical Signs

The mortality rate in horses is 70-95%. The incubation period is usually 7-14 days but can be as short as 2 days. Fever is common and swelling can occur over the facial and thoracic area and cardiac or respiratory distress are the usual cause of death. Whether you get primarily respiratory or cardiac involvement determines which clinical signs predominate. The most common presentation however is the mixed form.

Respiratory Disease: "Dunkop" Form

Dunkop as a peracute disease and the form most often seen in animals that are fully susceptible. This will be horses that have never been exposed before including foals who's maternal immunity has waned. Incubation of this form is short, usually 2 or 3 days, and followed by a rapid, remarkable rise in body temperature to 104 -106 degrees F (40 - 41 degrees C) over 1 to 2 days. The horses respiratory rate rapidly rises to over 50 with remarkable expiratory dyspnea and heave line. To improve breathing horses tend to stand with the front legs apart, the head extended, and the nostrils dilated. Profuse sweating is common and terminally the horse has paroxyisms of coughing with a frothy fluid dripping from the nostrils. Once dyspnea appears most horses often die within 30 minutes to 2 hours. Fewer than 5% of the horses that develop the Dunkop form will recover.

For those few who recover the fever subsides gradually but the breathing remains labored for several day.

Cardiac Disease: "Dikkop" Form

The incubation for the Dikkop form is longer, usually 5 to 7 days after which a fever ranging from 102 to 106 degrees F (39-41 degrees C). The fever persists for 3 or 4 days at which time the typical symptoms of swelling around and above the eyes that spreads to the other tissues of the head and a variable distance down the neck. With remarkable swelling the horse may develop dyspnea (difficult breathing) and cyanosis. Ventral edema and limb edema does not occur. Swelling of the esophagus can lead to dysphagia (difficult swallowing) and aspiration pneumonia. Colic may also develop. Death occurs in over 50% of the cases and usually occurs 4 to 8 days after the fever first develops.

Mixed Form

Although the most common form of AHS it is often not diagnosed before death. Fever and mild respiratory disease, most often dyspnea (difficult breathing), are first seen. This is followed by edematous swelling around the head. Death then occurs do to cardiac failure usually 3 to 6 days after the febrile reaction begins.

Horsesickness Fever

This is the mildest form of AHS and most often seen in donkeys, zebras, and horses with some amount of immunity do to prior infection or vaccination. Incubation is 4 to 9 days which is followed by fever that rises over a 4 day period to as high as 104 degrees F (40 degrees C). In most cases other clinical signs do not develop but there may be mild respiratory or cardiac symptoms.

Diagnosis

Presumptive diagnosis can be made from the clinical signs described above and supporting blood work:

leukopenia (decreased WBC count)
thrombocytopenia (decreased platelets)
increased hematocrit and erthrocyte count (increased RBC's)
increased clotting times and fibrinogen degradation products

However the cardiac form of AHS cannot be differentiated clinically from equine encephalosis which is not as fatal as AHS. Virus isolation is necessary to differentiate these two disease in the living animal. On necropsy the lesions are usually enough to differentiate the two diseases.

The petechial hemmorages in AHS can be similar to that caused by purpura hemmoragica (PH) or Equine Viral Arteritis (EVA). In both these diseases the swelling tends to be more ventrally oriented than in AHS. The hemmorages in PH tend to be larger and more widely spread than in AHS. The early stages of piroplasmosis can be confused with AHS and is further complicated that horses suffering from AHS may also have piroplasmosis and in these horses ventral edema may be prominent.

PCR has experimentally provided a way of positively diagnosing AHS in an little as 3 hours. When this test becomes available routinely it should help in making early decisions on treatment and management of horses that have clinical disease:

More Information on Real Time PCR

Res Vet Sci. 2008 Sep 7.
Rapid and sensitive detection of African horse sickness virus by real-time PCR.

Fernández-Pinero J, Fernández-Pacheco P, Rodríguez B, Sotelo E, Robles A, Arias M, Sánchez-Vizcaíno JM.
Centro de Investigación en Sanidad Animal (CISA-INIA), Valdeolmos, 28130 Madrid, Spain.

A highly sensitive and specific TaqMan-MGB real-time RT-PCR assay has been developed and standardised for the detection of African horse sickness virus (AHSV). Primers and MGB probe specific for AHSV were selected within a highly conserved region of genome segment 7. The robustness and general application of the diagnostic method were verified by the detection of 12 AHSV isolates from all of the nine serotypes. The analytical sensitivity ranged from 0.001 to 0.15TCID(50) per reaction, depending on the viral serotype. Real-time PCR performance was preliminarily assessed by analysing a panel of field equine samples. The same primer pair was used to standardise a conventional RT-PCR as an affordable, useful and simple alternative method in laboratories without access to real-time PCR instruments. The two techniques present novel tools to improve the molecular diagnosis of African horse sickness (AHS).

Virus insolation can be performed but may require between as long as 2 weeks for an answer.

AHS can be detected through antibody detection in the serum of horses infected longer than 3 weeks. There are a number of tests available including complement fixation (CF), agar gel immunodiffusion (AGID), enzyme linked immunosorbent assay (ELISA) or serum neutralizing tests (SN). Whereas the antibodies detected by CF are relatively short lived, ELISA and SN can detect antibody for years after infection.

Treatment

There are currently no specific antiviral treatments that have been tested and shown to be useful against AHS. Treatment is supportive and NSAID's along with good nursing care may help reduce the severity of some of the symptoms. Rest is essential. For those that recover they should continue to be rested for at least a month at which time very light work can be attempted. Monitoring for complications like piroplasmosis should also be instituted.

Prevention

In endemic areas annual vaccination in late winter to early summer is a effective way of control. Horses that receive a primary series of 3 or more vaccinations 3 weeks apart of a polyvalent vaccine and then are annually boostered are usually well protected though occasional vaccine failures are reported. Onderstepoort Biological Products produces both a trivalent (serotypes 1,3 and 4) and quadrivalent (2,6,7,and 8) vaccine. It is believed that the quadrivalent vaccine induces cross protection to serotypes 5 and 9.

Immunization usually has few side effects. A slight fever may occur between days 5 and 13 post vaccination. Occasionally horses receiving the vaccine for the first time will exhibit signs of AHS. Failure rate of the vaccine is thought to be less than 10%.

Foals receiving colostrum from immune mares will have passive immunity to the disease than can inactivate the vaccine. This immunity wanes by a few days after birth to 6 months of age. For that reason it has been recommended that these foals should begin vaccine at 6 months. However for those who's immunity wanes early they will be susceptible to infection before 6 months.

The risk of infection in susceptible horses can be greatly reduced by stabling between dusk and dawn as the vector, Culicoides, is nocturnal. Strong fans and screening the stalls will further reduce exposure.

Importation from Endemic Areas

There are guidelines for importing horses out of AHS endemic areas which usually center around quarantining in a vector proof area for at least 40 days and demonstrating a negative or stable AHS antibody titer.