African Horse Sickness: Introduction - The Merck Veterinary Manual

African Horse Sickness: Introduction

African horse sickness (AHS) is an acute or subacute, insectborne, viral disease of Equidae that is endemic to Africa. It is characterized by clinical signs and lesions associated with respiratory and circulatory impairment.

Etiology and Epidemiology:

AHS is caused by an orbivirus, 55-70 nm in diameter, of the family Reoviridae. There are 9 immunologically distinct types. Extracts of mouse brain infected with AHS virus hemagglutinate horse RBC. The virus is inactivated at a pH of <6 or ≥12, or by formalin, β-propiolactone, acetylethyleneimine derivatives, or radiation.

Appearance of AHS is preceded by seasons of heavy rain that alternate with hot and dry climatic conditions. Outbreaks in central and east Africa have extended to Egypt, the Middle East, and southern Arabia. In 1950-1960, a major epidemic extended from India to the Near Eastern countries; an estimated 300,000 Equidae were destroyed. A second epidemic in 1966 occurred in northeast Africa and southern Spain. In 1987, the disease entered Spain via imported zebra from Namibia. These 2 outbreaks in Spain were controlled, but another occurred in 1988, and sporadic cases occurred through early 1989. Recent AHS outbreaks (through 2001) have been reported only in Botswana and Namibia. In Botswana there were fewer cases in 2000 than in 1999. The disease was reported in horses and donkeys in the western regions. In 2001, 11 outbreaks were reported in Botswana. Two outbreaks were reported in Namibia in 2000, and 7 outbreaks in 2001. In a survey in Egypt, antibodies to AHS virus were detected in sheep, goats, camels, buffalo, and dogs.

Transmission:

Culicoides spp are the principal vectors of transmission. AHS is seen during warm, rainy, seasons, which favor propagation of the vectors, and disappears after frost. The virus was isolated from blood of clinically healthy street dogs, the dog tick Rhipicephalus sanguineus sanguineus , and the camel tick Hyalomma dromedarii during winter in the Aswan region of southern Egypt where the disease is endemic. AHS has been experimentally transmitted by infected mosquitos. Limited studies in Egypt using dogs that had recovered from experimental infection revealed that 3 successive daily attacks by groups of Culex pipiens activated latent AHS virus and initiated viremia and fever. It has been suggested that the virus may overwinter in dogs with persistent infection. However, the full role of arthropods in transmission of the disease is unclear.

Clinical Findings and Lesions:

African horse sickness, swelling of supraorbital fossa

Mortality depends on virulence of the viral strain and susceptibility of the host. It may reach 90% in epidemics. The acute respiratory form is characterized by an incubation period of 3-5 days, interlobular edema, and hydropericardium; death occurs in ~1 wk. A fever of 40-40.5°C (104-105°F) for 1-2 days is followed by dyspnea, spasmodic coughing, and dilated nostrils; the animal stands with its legs apart and head extended. The conjunctiva is congested and the supraorbital fossa may be swollen. Recovery is rare, and the animal dies of anoxia. At necropsy, pulmonary edema is especially visible in the intralobular spaces. The lungs are distended and heavy, and frothy fluid may be found in the trachea, bronchi, and bronchioles. There may be pleural effusion. Thoracic lymph nodes may be edematous, and the gastric fundus may be congested. Petechiae are found in the pericardium, and there is an increase in pericardial fluid; however, cardiac lesions usually are not outstanding. The abdominal viscera may be congested. A frothy exudate may ooze from the nostrils. The pulmonary form is the usual form in dogs.

The cardiac form is subacute with an incubation period of 1-2 wk. A fever of <1 wk is followed by swelling of the supraorbital fossa, which is pathognomonic. Swelling usually extends to the eyelids, facial tissues, neck, thorax, brisket, and shoulders. Death usually occurs within 1 wk and may be preceded by colic. The mortality rate is ~50%. Petechiae and ecchymoses on the epicardium and endocardium are prominent. The lungs are usually flaccid or slightly edematous. There are yellow, gelatinous infiltrations of the subcutaneous and intramuscular tissues, especially along the jugular veins and ligamentum nuchae. Other lesions include hydropericardium, myocarditis, hemorrhagic gastritis, and petechiae on the ventral surface of the tongue and peritoneum. A mixed pulmonary and cardiac form is usually found in outbreaks, with signs and lesions of one type predominating.

Diagnosis:

In endemic areas, clinical signs and lesions may lead to a provisional diagnosis. However, laboratory confirmation is essential for definitive diagnosis and determination of the serotype; the latter is important for control measures. Blood specimens should be obtained at the peak of fever, preserved in OCG solution (50% glycerol, 0.5% potassium oxalate, 0.5% phenol), and transported (at 4°C) to the laboratory. Spleen samples collected from freshly dead animals should be preserved in 10% buffered glycerin. For virus isolation, infant mice or cell cultures are used. Infected mice may develop nervous and paralytic signs and should be observed for 3 wk. To obtain a high-titered antigen from mouse brains for the complement fixation test, 2 or 3 passages may be necessary. Brains from paralyzed mice only are harvested for antigen preparation. The complement fixation test is useful for disease diagnosis; virus neutralization and/or hemagglutination-inhibition tests are used for serotyping.

Prevention and Control:

Surviving Equidae develop solid immunity to the homologous serotype but remain susceptible to other serotypes. There are vaccines for all 9 serotypes. These are either cell-culture adapted or mouse-brain attenuated and provide long-lasting protection. Inactivated vaccines are available; 2 doses are required to provide adequate immunity. These vaccines induce local reaction at the site of inoculation and a short protection period.

When the disease first appears in an area, affected horses should be eliminated immediately, and noninfected Equidae should be vaccinated with polyvalent vaccine and rested for 2 wk. When the virus isolate has been typed, animals that received polyvalent vaccine should be revaccinated with the homologous vaccine. Vector control is also initiated by using insecticides and repellents. Vaccinated horses should be kept in insect-proof housing because vaccine failure may occur. Aircraft flying from endemic areas to countries free of the disease should be sprayed with insecticides on arrival. In the USA, equids from African countries are quarantined for 2 mo and then tested for the virus. Presence of antibodies does not interfere with importation of Equidae into countries free of the disease.