African Horsesickness (AHS) is a highly fatal, but non-contagious viral disease of equine animals caused by an orbivirus of which there are nine serotypes, all transmitted by Culicoides midges. The disease is associated with an impaired circulatory function resulting in extensive oedema involving the lungs, intermuscular as well as subcutaneous tissues.

The prevalence and distribution of AHS is closely linked to ecological factors such as temperature and rainfall and has a seasonal occurrence. This is due to the fact that the insect vector, Culicoides, which favours damp, moist conditions, plays such an important role in the spread of the disease. Most horses are affected between sunset and sunrise, as this is the time when the midges are most active.

In South Africa, the disease is most prevalent in the northern parts of Mpumalanga and KwaZulu-Natal, but may extend into the other provinces, especially with the altered weather patterns and global warming being a major concern in the world at the moment.

The first cases of AHS usually occur at the beginning of February, with the most serious outbreaks occurring during March and April. Frost is considered to signal the end of the vector season and the decline of clinical cases.

Dogs are the only other animals that may become infected with AHS, but it is doubtful that they play a role in the spread and maintenance of the disease as the Culicoides midges do not readily feed on them. Horses that have recovered from AHS, do not become carriers of the disease.

Pathogenesis

African Horsesickness is closely associated with the erythrocytes (red blood cells) in the blood. The virus has a high affinity for capillary endothelial cells, especially those of the heart and lungs. Endothelial cells of the capillary walls become more permeable with resultant leakage of intravascular fluid volume into the surrounding tissues. This results in oedema. In addition, there are changes in haemostasis, produced by activation of coagulation and fibrinolysis with clotting factor consumption.

Diagnosis

A provisional diagnosis of AHS may be made on the history, clinical signs and macroscopic lesions seen on post mortem. Virus isolation remains the definitive method of diagnosing AHS. Infectious virus may be isolated from whole blood collected in heparin and taken early in the disease.

If a post mortem is conducted on a suspected horsesickness case, samples of the spleen and lung should be collected and forwarded to a laboratory on ice for virus isolation. Various serological tests are available. For these tests a serum sample should be collected and accompanied by the vaccination status of the horse. This sample should be followed by a second sample collected 14 or more days later.

Clinical signs

The disease is characterised by clinical signs and lesions compatible with impaired respiratory and cardiac function. The incubation period is usually from 5-7 days, but could be as short as 48 hours, but not longer than ten days. It is commonly divided into the following four forms:

1. Dunkop form – This form of the disease is seen in fully susceptible horses or foals that have lost their maternal immunity and is also the form seen in dogs, the most characteristic sign being dyspnoea (difficult breathing). Affected horses have a fever for a day or two (41˚C and higher), followed by dyspnoea, coughing and a frothy, serofibrinous nasal discharge. The prognosis for this form of the disease is extremely poor, with < 5% of affected horses surviving.
2. Dikkop form – This is characterised by subcutaneous swelling of the neck (Photo 1) and head, particularly the supraorbital fossae (Photo 3), which usually occurs at the end of the 3-6 day febrile period. As these swellings increase, dyspnoea and cyanosis may become more evident. The lower parts of the legs are not involved. Small haemorrhages are evident in the eyes (Photo 6), eyelids, and on the ventral aspect of the tongue. Their eyes may be swollen shut. Affected horses may develop oesophageal paralysis, babesiosis and colic. This form of AHS occurs in partially immune animals, and has a mortality rate of 50%, with death occurring within four to eight days after the onset of the febrile reaction.
3. Mixed form – This is the most common form of AHS, but is rarely diagnosed clinically. Affected horses may initially present with respiratory distress or oedematous swellings. The mortality rate can be as high as 70% and death follows 3-6 days after the onset of the febrile reaction.
4. Horsesickness – This is the mildest form of AHS and is often not diagnosed clinically. It is characterised by an increase in body temperature lasting from 1-6 days, accompanied by anorexia (failure to eat) and supraorbital oedema (Photo 5). There is no mortality ­associated with this form of the disease.

Differential diagnosis

It is not possible to differentiate the early febrile stage of AHS from the early febrile stages of most infectious diseases occurring in horses. Diseases most often confused with AHS include babesiosis, equine viral arthritis, equine encephalosis and purpura haemorrhagica. However, the mortality rate of AHS is much higher than in any of these diseases.

Treatment

There is no specific therapy for AHS apart from supportive treatment. Generally, affected animals should be carefully nursed, well-fed and stress should be kept to an absolute minimum.

Supportive treatment and procedures performed after admission of a suspected AHS case to the equine clinic of the Onderstepoort Veterinary Academic Hospital, include a thorough clinical examination to assess cardiovascular function (heart rate and respiratory rate), indirect blood pressure measurement and blood collection for haematology (to access the white blood cell and the platelet count) and serum chemistry (to access the total serum proteins – this may provide evidence of whether the animal is losing proteins through the damaged capillary endothelium).

Also, an ultrasound exam (main photo) is performed on the heart and lungs to access the amount of fluid that has accumulated around the heart (Photo 2) and in the lungs. The results of the diagnostic tests are combined with the clinical parameters of the horse, and a basic treatment plan is decided upon.

General treatment may include the ­following: Monitoring of heart rate and respiratory rate/­pattern; intravenous catheterisation and supplementation with polyionic fluid therapy (this is a balanced fluid containing necessary electrolytes); colloids (this helps maintain intravascular fluid volume by plugging the holes in the ­affected ­capillary endothelium); antibiotic therapy to ­control secondary bacterial infections ­(penicillin and gentamicin or sulphonamide); diuretic therapy for lung oedema (furosemide); and non-steroidal anti-inflammatory treatment (DMSO, phenylbutazone and finadyne).

More severely affected horses showing dyspnoea (respiratory discomfort) are placed on oxygen support and may have a tracheostomy tube (Photo 4) placed to facilitate breathing. In horses with ultrasonographic evidence of lung oedema and accumulation of fluid in the thorax, a thoracocentesis will be performed to drain the excessive fluid from the pleural space. Should the cardiac effusion restrict the ability of the heart to function, a pericardiocentesis can be performed to drain excessive fluid from the pericardium.

As babesiosis may be a complication of the disease, we monitor the temperature and perform blood smears of all horses and, if positive, horses should be treated with imidocarb. All horses should be rested for at least 4-6 weeks after recovery before they are returned to normal work.

Control

Immunisation: Prophylactic immunisation is a very effective way of preventing serious losses from the disease, but it cannot be relied upon fully to protect horses against infection or disease. In general, immunisation has no or limited side effects. A two-bottle multivalent vaccine is currently available in South Africa. These should be administered annually between September and December, before exposure to challenge by field virus and at least three weeks apart. Foals should be vaccinated before the age of six months.

In areas where African Horsesickness is expected to occur every year, animals should be vaccinated twice in the first and second year of life, and thereafter annually. A slight rise in body temperature may occur between day 5 and 13 after inoculation, and horses should preferably not be exercised for 21 days after vaccination. Horses that have received three or more courses of immunisation are generally well-protected against the disease.

Insect control: The Culicoides midges are nocturnal and are not inclined to enter barns. Infection can therefore be prevented by stabling horses between dusk and dawn when these midges are most active. The application of insect repellents and the use of insecticides are also recommended. A positive air current should be created within a barn, as these midges are unable to fly against air currents.

AHS is classified as both a notifiable, as well as a controlled disease in South Africa, and immediate notification is required by the national Department of Agriculture.

For more information, contact the authors on e-mail at adrienne.viljoen@up.ac.za or montague.saulez@up.ac.za or write to them at Private Bag X04, Onderstepoort 0110, South Africa.