ABSTRACT: African Horse Sickness lAHSl is an orbiviral viral disease of equids, transmitted by Cuhcoides midges. Mainly seen in Africa, some outbreaks elsewhere have been extensive and the disease has over-wintered in southern Europe. The AHS virus is probably spread by Cuhcoides obsoletus, found in northern Europe AHS causes severe disease, and mortality can be over 90%
At present there is no cure Supportive nursing care should be given and stress minimised. Protecting horses from midges is difficult. The live attenuated polyvalent vaccine used in South Africa is not licensed for use in Europe, but new vaccines are currently being developed
African Horse Sickness (AHS) is a viral disease of equids caused by an orbivirus, related to bluetongue virus (BTV), which causes the disease bluetongue in cattle, sheep, goats and similar species. There are nine serotypes of African horse sickness virus (actually nine closely- related viruses) with a degree of cross-reaction between some of the serotypes.
Transmission
AHS is not contagious – thus it is not passed directly from one horse to another. Rather, it relies on an insect vector to transmit the virus from one host to the next. Like BTV, AHS viruses are transmitted mainly by Culicoides species midges, with Culicoides imicola, the major vector in Africa.
AHS outside Africa
AHS outbreaks outside Africa are associated with the movement of infected equids, or the movement of midges. Midges normally have a flight range of tens of metres to perhaps five kilometres, but under ideal conditions they can be transported hundreds of kilometres on the wind. They may also travel inside trucks and other transport vehicles.
In 1959, an outbreak started in the Middle East and moved eastwards across Asia, reaching India. More than 300,000 equids died and the outbreak stopped only when there were no susceptible equids left to infect – all were dead, vaccinated or had been infected but survived.1
The most recent outbreak in Europe started in 1987 in Spain following the importation of zebras. This was initially controlled within a few months, but the disease over-wintered, reappearing in Spain in 1988, 1989 and 1990, as well as in Portugal and Morocco. The outbreak was finally halted in 1990 by the slaughter of infected horses, movement controls and massive vaccination campaigns.2013
The recent arrival and over-wintering of BTV-8 in northern Europe, with transmission via midges of the Culicoides obsoletus group, which are common in northern Europe, including the UK, has increased concern that AHS also could reach this region and circulate here.'1
Clinical signs
In populations of horses that have never previously encountered the virus, the mortality rate is very high – over 90 percent. In the most severe, peracute form (pulmonary or dunkop), clinical signs are fever with profuse sweating, dyspnoea, depression, coughing and sometimes a frothy nasal discharge (Figure 1); the horse may become recumbent and there is a 95 per cent mortality rate.
Figure 1: Froth may be seen at the nostrils during life or, more commonly, after death las shown here)
In the acute cardiac or dikkop’ form, the main signs are subcutaneous swelling of the head (including the supraorbital fossa) and neck (Figure 2). As swelling increases, the horse may show dyspnoea and cyanosis (50% mortality). Oedema may spread down to the chest but filling of the legs does not occur. Conjunctival oedema and congestion can develop to haemorrhage (Figure 3).
Figure 2: There may be severe oedema of the neck with the cardiac form of AH5, as shown here with finger pressure
Figure 3: Conjunctival haemorrhage is not uncommon
Many cases are a mixture of these two types and this mixed form has a mortality rate of up to 70 per cent. Mild disease (AHS fever) can occur in horses and in donkeys which are partially immune.48*5 Zebras are commonly considered to be the reservoir host for this virus, although infection in them is subclinical. Dogs can become infected by feeding on meat from infected horses and fatalities can follow. Clinical signs are fever and depression, dyspnoea, increased respiratory and heart rates, and froth from the nose.6
Pathology
Post mortem findings include yellow, glossy oedema in the intramuscular fascia of the neck (Figure 4) froth from the nostrils and in the trachea (Figure 1), excessive fluid in the thoracic cavity and between the interlobular septa of the lungs, and froth from the small airways when the lung is cut (Figure 5). In horses with cardiac signs, hydropericardium is present and there may be obvious haemorrhages on the outer (Figure 6) and inner surfaces of the heart.'1 Petechiae may be present on the serosal surfaces of various organs – this is typical of any viraemia or septicaemia, not just AHS.
Figure 4: Yellow, glossy oedema may be seen in the intramuscular fascia of the neck
Figure 5: Froth is visible in the small airways when the lung is incised
Figure 6: Petechiae are visible here on the epicardium
Diagnosis
Diagnosis is based initially on clinical signs and necropsy findings, with infection confirmed by detection of the virus or viral antigens, or by seroconversion.4 It is important to determine the serotype so that the correct vaccine can be used.
Treatment
There is no cure for AHS. Treatment is supportive only – nursing, careful feeding, rest, minimising stress, and normal care for recumbent horses, such as a soft bed and eye protection. Rest and stress minimisation are vital.5 Fluids (including colloids) and NSAIDs can be given, along with furosemide to reduce lung oedema, and antibiotics to prevent secondary infection. Supplemental oxygen may be given to dyspnoeic horses, and tracheotomy performed to improve respiration (Figure 7).
Figure 7: A tracheostomy tube has been placed to assist in respiration Note also the intravenous line for giving fluids
Thoracocentesis and ultrasound-guided pericardiocentesis can be used to remove excess fluid, but such treatments must be balanced against the stress caused by carrying out these procedures. Because AHS is not contagious, there is no need to take an affected horse away from its stable mates – an action which would increase stress.
Preventive husbandry
Vector-borne diseases usually are controlled at least in part by controlling the vector(s). However, the size (at only 1.5 mm long) and natural history of Culicoides midges makes them difficult to control.4 Their breeding habitats include muck heaps, cowpats and any area of damp soil enriched with organic matter; when these are spread out, it makes them practically impossible to eliminate.
Midges are mainly active dusk to dawn. Equids can be housed at night in buildings with all windows and other openings covered with fine mesh screens (holes less than 1.6 mm), preferably dipped in, or sprayed with, a residual insecticide such as a synthetic pyrethrin.7 If appropriate mesh is not available, gauze can be used. Fans inside the building can increase air movement, making the interior less attractive to midges.
However, even housing horses in such stables from before dusk to after dawn will not give complete protection and the midges also fly and feed on overcast days. No insecticides are totally effective against midges and even the strong insect repellent DEF.T, which is very effective at repelling mosquitoes, is only effective against midges for about four hours after it is applied.
Vaccination
AHS can be prevented by vaccination, and in South Africa horses are routinely protected by this method. The standard vaccination regimen involves two vials (produced by Onderstepoort Biological Products |OBP|), each containing several serotypes of live attenuated virus, given 21 days apart – serotypes 1, 3 and 4 in the first vial and serotypes 2, 6, 7 and 8 in the second. Serotypes 5 and 9 are not included, but protection against these is provided by cross-reaction between serotypes 5 and 9 and between 6 and 8.
Individual horses, however, may respond better to some of the serotypes than to others, resulting in reduced or inadequate protection against some serotypes. Foals may not be fully protected while maternally derived antibodies are waning; and owners may not vaccinate their horses in time, before the onset of midge activity.
If the vaccines are not maintained at the proper temperature prior to use then they will be ineffective. Also, not all horse owners vaccinate, and infected horses, donkeys and zebras can act as a source of virus from which further midges can be infected, thereby increasing the risk of infection for all equids.
With any live vaccine there is a theoretical risk of the virus reverting to virulence and actually causing the disease; this is a major reason why veterinary authorities in areas where AHS is non-endemic are reluctant to allow the use of such vaccines (although they were used extensively in Spain, Portugal and Morocco in the 1987-1990 outbreak). A recent paper, thankfully, did not show any such reversion of the AHS live vaccine.8
Another objection to the vaccine is that it is not possible to tell whether the antibodies detected in a horse are in response to the vaccine, or to infection, which might complicate epidemiological studies.
There would be less concern over the use of a killed vaccine, because if manufactured to appropriate standards there is no live virus present in the vaccine, so absolutely 110 risk of reversion. During the Spanish and Portuguese outbreak, a killed vaccine was produced against serotype 4, the type involved in the outbreak. However, this is no longer available and there are only very limited data 011 its efficacy.
For Europe, rules 011 control of AHS have been laid down in EU Council Directive 92/35/EEC. They include slaughter of affected equids, movement restrictions, vector control measures and vaccination. The OBP vaccine is not licensed for use in Europe. However, in 2008 the EU decided that it would be advantageous to stockpile monovalent live attenuated vaccine for each of the AHS serotypes in the OBP vaccine. While the live vaccine is not licensed by the Veterinary Medicines Directorate for use in Great Britain, the chief veterinary officer could allow its use in an emergency situation.
Future
Work is under way to develop new AHS vaccines. Using technology which allowed development of a recombinant canary pox-vectored vaccine against West Nile Virus, Merial Animal I lealth has developed a recombinant vaccine against serotype 4 of AHS, and this has been tested successfully: vaccinated horses were protected against challenge with live AHS virus.9
Defra has funded work by the Institute of Animal Health, Pirbright, the Animal Health Trust, Newmarket, and the Cambridge Infectious Diseases Consortium on another vaccine, with AHS surface proteins expressed by a recombinant modified Vaccinia Ankara virus. This has been shown to result in production of neutralising antibodies against AHS (which should be protective).
Author
Debra Bourne MA VetMB PhD MRCVS
Debra completed her PhD on toxoplasmosis and other diseases in the Bennett's wallabies at Whipsnade Zoo in 1997. Since then she has worked for Wildlife Information Network IWIN), now part of Twycross Zoo – East Midland Zoological Society Limited, as a veterinary editor, producing Wildpro electronic encyclopaedia volumes on wild animal health and management, and emerging infectious diseases.
To cite this article use either
DOI: 10.1111/j.2045-0648.2011.00067.x or Veterinary Nursing Journal Vol 26 pp 315-318
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Veterinary Nursing Journal • Vol 26 • September 2011