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Louping ill in horses

SIR, – We wish to report seven cases of neuro logical disease in horses in Devon probably caused by louping ill virus (LIV). During the autumn/winter 2006, we experienced unusual cases, in which horses presented with a variety of neurological signs. Horses affected ranged in age from seven months to 20 years, and comprised both sexes among a variety of breeds and types. None was known to have any underlying illness. Common to all cases was ataxia of variable severity, ranging from being almost unable to stand or move to mild incoordination. Affected horses frequently showed muscle tremors of the neck and facial area, altered head carriage, depression and avoidance of bright daylight. Often, there was a form of manic behaviour, such as constant exaggerated chewing. Some presented with pyrexia (up to 40·5°C), which was unresponsive to flunixin. Appetite was depressed in some animals. A potential diagnosis of louping ill was considered, based on clinical signs, exposure to ticks and cases of louping ill in cattle and sheep in the area (Twomey and others 2001). As part of the clinical investigation, serological evidence of LIV was sought, using a LIV haemagglutination inhibition test (HAIT) as described by Reid and Doherty (1971). All cases were found to be seropositive to LIV (Table 1). While one case (horse 2) had a low titre at the time of initial sampling, seroconversion was demonstrated 14 days later. Where follow-up samples have been available to test, all clinical cases have maintained a high antibody titre. Treatment has been limited to supportive non-steroidal anti-inflammatories and broad-spectrum antibiotic cover. In two cases that were deteriorating, a dose of dexamethasone was administered. This dramatically improved one case, and had minimal effect on the other. Five cases have made full recoveries; however, the owners report there to be some subtle changes to the horses’ demeanour and ‘way of going’ in two of the cases. The first case was euthanased after it relapsed, while one case is still in a recovery phase. Of the seven cases so far, six live within one mile of each other and all live on the edge of moorland where there is known to be LIV in the local sheep population, but only in recent years. In response to these recent clinical cases, serum samples from a further 68 apparently healthy horses that live within an approximately two-mile radius of the main cluster of cases have been tested by HAIT for antibody to LIV. This limited survey has identified a further five horses with LIV antibody, two of which are known to have shown neurological signs in the past. No neurological tissue has been available to allow testing for the presence of LIV by standard virus isolation, immunohistochemistry or reverse transcriptase-PCR (Marriott and others 2006). A definitive serological diagnosis is awaited as the sera are being tested against LIV and crossreacting flaviviruses, including West Nile virus, in serum neutralisation assays. These cases are unusual in that they represent a cluster in an area, they occurred late in the year, and constitute a rise in the number of seropositive horses detected by routine diagnostic testing at Moredun, where no equine sera were submitted for LIV testing in 2002, 2003 or 2004. In 2005, six equine sera were tested, with two being seropositive, one from Devon and one from Cumbria, both of which were from horses that also had neurological signs. These findings are not inconsistent with previous reports of louping ill in horses (Timoney 1976, Timoney and others 1976), but the recent cases highlight the need for louping ill be to considered as a potential cause of neurological disease in horses exposed to ticks in a louping ill area.