25 Jul 2016
Horses are second only to humans as the most travelled creatures on the planet, with global competitions and international movement for breeding now commonplace. With such large-scale travel comes the potential for infections and disease to spread. Philip Ivens reviews three diseases of equines – west Nile disease, equine infectious anaemia and equine herpes myeloencephalopathy.
Figure 1. Map showing the distribution of west Nile disease lineage 1 and lineage 2 reported to the OIE in 2011. Numbers in orange boxes show the number of west Nile cases occurring in humans in the period 26 July and 24 November, 2011. Not shown on map: Israel [33]. (Source: World Organization for Animal Health, 2011; European Centre of Disease Prevention and Control).
Horses are the most travelled animals after humans, including temporary and permanent movements as well as intercontinental movements for competition and breeding.
In this article the author outlines three examples of topical, new or emerging threats to the UK’s equine population.
West Nile virus (WNV) belongs to the Flaviviridae family of viruses and is vector-borne, as it is transmitted by mosquitoes (Culex species). The primary amplifying non-vector hosts are birds, for instance, house sparrows (passerines), crows and birds of prey. Horses and humans are dead-end hosts and do not contribute to the propagation of disease – acting, instead, as sentinels for the virus.
WNV is a seasonal virus, with cases occurring during peak mosquito activity. In northern, temperate climates, peak activity occurs in the summer, particularly July and August. WNV encephalitis has been one of the leading causes of neurological disease in horses in the US since the disease’s introduction in 1999.
WNV is an important zoonosis and causes neurological disease in humans. However, disease is spread because the bird reservoir maintains the virus in an endemic life cycle, allowing transmission by mosquitoes to humans. Little risk of disease by direct contact with an infected horse exists, except during postmortem examination whenever infected tissues are inappropriately handled.
The majority of WNV infections in horses are subclinical. It is estimated only 10% of infected horses go on to develop clinical signs. The virus causes a wide variety of clinical signs symptomatic of the encephalomyelitis (diffuse inflammation of the brain and spinal cord):
Two lineages are circulating in mainland Europe (Figure 1):
The UK has been found to have the correct species of mosquitoes to act as the bridge vector and an abundance of bird wildlife to act as the amplifying host.
It obviously also has large populations of dead-end hosts – horses and humans. Therefore, many infectious disease experts believe it is a question of when, not if, WNV comes to the UK.
After lobbying by members of the equine veterinary profession, rules about testing for WNV were changed. WNV is a notifiable disease so, previously, if a clinician wanted to rule it out from a differential diagnosis list, testing triggered immediate Defra restrictions on the horse and the premises it was housed in. It was argued the effect of this was counterproductive, leading to reduced surveillance and early detection. This was potentially based on the misconception of the human zoonosis risk from horses.
Now, though, clinicians can request WNV serology in suspected cases, or to rule out from a differential diagnosis list, without triggering a premises restriction. This will now only come into force if the results come back consistent with WNV infection.
Vaccination against WNV is available in the UK and owners of horses travelling to or through Europe should be advised to vaccinate ahead of time. Vaccination can be performed with Proteq West Nile (from five months) or Equip WNV (from six months). A primary course of two vaccinations (four-to-six or three-to-five weeks apart) is followed by an annual booster and immunity is established four weeks after the first dose of the primary vaccination. To achieve full protection the full primary course must be given.
Equine infectious anaemia (EIA), also known as “swamp fever”, is caused by an equid-specific Lentivirus related to Maedi-visna virus, feline immunodeficiency virus and HIV-1, among others. All Lentivirus types cause persistent infections and most cause slowly progressive disease that frequently results in death.
In contrast, EIA virus infection results in an acute phase, followed by recurrent clinical disease episodes that eventually subside in most horses. These horses become persistently infected, lifelong, inapparent carriers.
The virus is transmitted by mechanical transmission on the proboscis on blood-feeding insects such as horseflies and deer flies. Iatrogenic transmission with needles, syringes and veterinary instruments is also possible. Aerosol transmission over short distances can occur.
The following list is in descending order of occurrence frequency:
Clinicopathology often reveals an anaemia and thrombocytopenia. After the initial disease episode, the majority of infected horses experience recurrent episodes of viraemia, fever, lethargy, inappetence, thrombocytopenia
and anaemia.
The disease is endemic in certain European states, including Romania and Italy, with periodic sporadic outbreaks in western Europe, including France, Germany and Poland in 2015.
In 2006, Ireland suffered a high-profile outbreak caused by use of equine plasma imported from Italy, without a licence, to treat foals. In 2010, EIA was reported in the UK in two out of six horses shipped from Romania via Belgium. Later that year a horse that had come to the UK from the Netherlands tested positive.
The conclusion is movement of horses and equine biological products is a significant risk to equine health. Pre-export testing and certification is a vital prevention tool. Adequate border controls and enforcement are in place with the added value of post-import surveillance and testing.
Equine herpesvirus-1 (EHV-1) and EHV-4 are associated with three clinical disease syndromes:
EHM is not restricted by pregnancy, age or gender and occurs in foals, yearlings, geldings, stallions and both barren and pregnant mares. Transmission is assumed to be through the respiratory route and contagious transmission occurs from clinical cases, so it produces potential for large outbreaks of the disease to occur. Neurological clinical signs appear during or towards the end of the viraemic phase of infection. The interval between infection and subsequent onset of neurological disease is usually between 6 and 10 days, but may be as short as a day.
Invariably, no premonitory clinical signs of respiratory disease are seen, and pyrexia is likely to be the only warning clinical sign. The presentation and severity of clinical signs are highly variable and depend on the extent and location of the neurological lesions. The spinal outflow to the caudal and sacral plexus is affected most often:
In early 2016, a case of EHM was diagnosed in a four-year-old maiden filly that had not long arrived to stud from overseas. The mare was placed in isolation, as was routine on this stud, before clinical signs occurred that included ataxia and bladder dysfunction.
Appropriate measures were implemented in accordance with the Horserace Betting Levy Board’s (HBLB) codes of practice (www.hblb.org.uk) and continued until a clear status was achieved. The case highlights the use of isolation and active screening for disease in preventing the ubiquitous virus EHV-1 from causing EHM cases in more than one animal – and effectively preventing an outbreak to occur.
EHV-1 disease control programmes have three goals, as outlined in the HBLB codes of practice
Equine infectious disease is a constant threat and one can argue more so now than ever.
A clear understanding of the diseases involved and up-to-date knowledge of the local, national and international disease states can greatly aid recognition of diseases, and mean prompt diagnosis and the implementation of control measures.