SummaryGetah virus is an arbovirus that was first isolatedfrom mosquitoes in Malaysia in 1955. Outbreaks ofinfection by Getah virus have been recorded in horsesin Japan and India. Infection can occur in a wide rangeof vertebrates, and the virus is probably maintainedin a mosquito-pig-mosquito cycle. Clinical disease inhorses is generally mild, characterised by pyrexia,oedema of the limbs, urticaria and a stiff gait. Aninactivated whole-virus vaccine is available in Japan.

IntroductionGetah virus is an arbovirus that was first isolated frommosquitoes (Culex gelidus) in Malaysia in 1955 (Berge1975). However, it was not until 1978 that the viruswas shown to be responsible for a mild disease amongracehorses in Japan (Kamada et al. 1980; Sentsui andKono 1980a; Timoney 2004). Subsequent outbreaks ofGetah virus infection have been documented inracehorses in Japan in the 1970s and 1980s (Sentsuiand Kono 1985) and among breeding horses in Indiain 1990 (Brown and Timoney 1998). Infection with thevirus also occurs in other domestic animals, includingpigs where it has been associated with illness anddeath in young piglets aged up to 18 days. Serologicalevidence of infection has been found in a large numberof vertebrate species (mammals, birds and reptiles) inwhich the infection appears to be subclinical (Dohertyet al. 1966). There is no evidence that the virus caninfect man (Fukunaga et al. 2000).

AetiologyGetah virus is a positive-stranded RNA virusbelonging to the genus Alphavirus of the familyTogaviridae (Calisher et al. 1980; Timoney 2004). It

GETAH VIRUS INFECTION T. S. Mair* and P. J. Timoney†

Bell Equine Veterinary Clinic, Mereworth, Maidstone, Kent ME18 5GS; and †Gluck Equine ResearchCenter, University of Kentucky, Lexington, Kentucky 40546-0099, USA.

Keywords: horse; Getah virus; arbovirus; Semliki Forest viruses

*Author to whom correspondence should be addressed.

is classified in the Semliki Forest complex along withSemliki Forest, Bebaru, Ross River, Chikungunya,O’nyong-nyong, Una and Mayaro viruses (vanRegenmortel et al. 2000). Several subtypes of Getahvirus are recognised, including Sagiyama, Ross Riverand Bebaru viruses (Calisher and Walton 1996).

Getah virus possesses haemagglutinating andcomplement fixing antigens, which have been used todevelop diagnostic tests for the virus. These tests inaddition to the neutralisation test have been used toinvestigate antigenic relationships between differentstrains and subtypes of virus (Fukunaga et al. 2000).

EpidemiologyGetah virus is transmitted by mosquitoes, and iswidely distributed in southeast Australasia andsurrounding countries, including Australia, Borneo,Cambodia, China, Indonesia, Japan, Korea,Malaysia, Mongolia, the Philippines, Russia,Thailand, Sarawak, Siberia, Sri Lanka and Vietnam(Calisher and Walton 1996; Fukunaga et al. 2000;Timoney 2004). Natural infection in wildlife isbelieved to be subclinical (Fukunaga et al. 2000). Intropical areas of Asia, pigs appear to be important inmaintaining a reservoir of infection via a mosquito-pig-mosquito cycle (Chanas et al. 1977). Pigs, andpossibly other vertebrates, may play an importantrole as amplifying hosts for the virus (Fukunaga et al. 2000).

Serological surveys of horses in Japan have shownthat the virus is widespread in this country, withseropositive rates up to 93% (Imagawa et al. 1981;Sentsui and Kono 1980b; Brown and Timoney 1998;Sugiura and Shimada 1999). The highest rates ofseropositivity occurred in older horses in the coolerregions of northern Japan. Seroprevalence wasreported as 17% in India and 25% in Hong Kong(Kamada et al. 1991; Shortridge et al. 1994). Many

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cases of Getah virus infection in horses are subclinical(Fukunaga et al. 2000).

The principal vectors for the transmission ofGetah virus to horses are mosquitoes (species of Culexor Aedes) (Calisher and Walton 1996; Fukunaga et al. 2000), although horse to horse transmissioncould also occur (Sentsui and Kono 1980a). Highlevels of virus can be found in nasal secretions ofhorses experimentally infected by Getah virus by thenasal route (Kamada et al. 1991), thereby permittinghorse to horse spread in animals in close contact. Nonvector spread of the virus was believed to havecontributed to the outbreak of Getah virus in India in1990 (Brown and Timoney 1998).

Clinical signsClinical infection caused by Getah virus has beenobserved almost exclusively in the horse. Outbreaksof the disease in horses have been sporadic, and havenot been associated with any mortality (Fukunaga et al. 2000). The morbidity rate in one outbreak ofinfection in racehorses was 38% (Kamada et al. 1980;Sentsui and Kono 1980a), with slow and irregularspread of infection.

The clinical signs associated with Getah virusinfection in horses vary depending on the strain ofvirus and viral dose (Timoney 2004). Some infectionsonly produce a febrile response with associatedinappetence and depression (Sentsui and Kono1980a). The febrile stage lasts 1–4 days. Other signsseen in infected horses include lower limb oedema(Fig 1), swelling of the submandibular lymph nodes (Fig 2), urticaria (especially on the neck, shouldersand hind quarters) (Fig 3) and a stiff gait (Kamadaet al. 1980; Sentsui and Kono 1980a; Fukunaga et al.1981a; Brown and Timoney 1998). Mild colic, icterusand scrotal oedema have also been reported (Timoney2004). Limb oedema and urticaria usually appearseveral days after the onset of pyrexia. Mild anaemiaand a transient lymphopenia may be present(Fukunaga et al. 2000). Serum alkaline phosphatasecan be elevated during the acute phase of theinfection, whereas serum lactic dehydrogenase andglutamine pyruvic transaminase rise duringconvalescence (Calisher and Walton 1996). Mostaffected horses make a full clinical recovery withinone week, although a small number may require upto 2 weeks to recover (Timoney 2004). Abortion is nota feature of the disease, and foals born to mares that

FIGURE 1: Lower limb oedema due to Getah virus infection.

FIGURE 2: Submandibular lymphadenopathy associated withGetah virus infection. FIGURE 3: Urticaria due to Getah virus infection.

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have had the disease during gestation are normal(Brown and Timoney 1998). In experimentalinfections, the clinical signs are similar, but infectedhorses also commonly develop a serous nasaldischarge (Kamada et al. 1991).

DiagnosisIn view of its clinical similarity to a range of otherinfectious and noninfectious equine diseases, aprovisional clinical diagnosis must be confirmedthrough laboratory examination. Included in adifferential diagnosis of Getah virus infection areequine viral arteritis, equine rhinopneumonitis,equine encephalosis, equine influenza, equineinfectious anaemia, African horse sickness fever,purpura haemorrhagica and hoary alyssum toxicosis.Virus isolation or demonstration of viral nucleic acidby reverse-transcription polymerase chain reactionmay be performed on nasal swabs, unclotted blood orsaliva of acutely infected animals (Kamada et al.1980; Sentsui et al. 1980; Fukunaga et al. 1981a). Thevirus can be cultivated in a range of equine and nonequine cell culture systems, especially Vero andRK-13 cell lines, as well as in suckling miceinoculated by the intracerebral route. Highest ratesof virus isolation have been achieved from plasma(Fukunaga et al. 1981b). Detection of Getah virus isoptimal where specimens are collected as early aspossible after the onset of fever.

Serum antibodies to Getah virus can be detectedby haemagglutination inhibition, complementfixation, enzyme-linked immunosorbent assay(ELISA) and neutralisation tests (Kamada et al.1980; Sentsui and Kono 1980; Sentsui and Kono1985; Brown and Timoney 1998). If possible, pairedsamples taken during the acute and convalescentstages of the disease should be assayed. Theneutralisation test is considered the most specifictest at differentiating Getah virus infection fromother antigenically related alphaviruses (Chanas et al. 1977).

ControlControl of Getah virus in endemic areas relies oncontrol of the mosquito vector (Fukunaga et al. 2000;Timoney 2004). This can be achieved by eliminatingor reducing mosquito breeding sites, and use oflarvicides and adulticides. The risk of exposure of

horses to virus-infected mosquitoes can be reduced byhousing them during dusk and at night.

An inactivated whole-virus vaccine is available inJapan. Horses receive an annual booster dose of thevaccine in May or June, prior to the onset of themosquito season. No epidemics of Getah virusinfection have been recorded in horses in Japan sincethe current vaccination programme was implementedin 1979 (Timoney 2004).

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