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Getah virus infection

Getah virus infection

Getah virus infection

Previous authors: P J TIMONEY

Current authors:
H BANNAI - Fellow, PhD, DVM, 1400-4 Shiba, Shimotsuke, Tochigi, 329-0412, Japan
T KONDO - Chief of Research Planning & Coordination Division, DVM, PhD, Equine Research Institute, Japan Racing Association, 1400-4, Shiba, Shimotsuke, Tochigi, 329-0412, Japan
P J TIMONEY - Professor, MVB (Hons), MS, PhD, FRCVS, Maxwell H. Gluck Equine Research Center, Department of Veterinary Science, University of Kentucky, Lexington, Kentucky, 40546 - 0099, USA

GENERAL INTRODUCTION: TOGAVIRIDAE

Introduction

Getah virus is an arbovirus that was first isolated from Culex gelidus mosquitoes collected near Kuala Lumpur, Malaysia, in 1955.4 The name of the virus is thought to be derived from the Malaysian word for rubber, ‘getah’. This relates to the fact that mosquitoes from which the original isolation of Getah virus was made were collected under a mature rubber tree canopy on a rubber plantation.22 For many years following its initial isolation there was no evidence that the virus was pathogenic for humans or animals. It was not until 1978, following an epidemic of a mild, self-limiting illness among racehorses in Japan that Getah virus was shown to be capable of causing disease.18, 33 Since then, the virus has been shown to be pathogenic for other species of livestock. It has been infrequently identified with foetal infection in pregnant sows as well as illness and death in new-born piglets.37, 43

Additional outbreaks of Getah virus infection in horses occurred at racetracks and training facilities in Japan in 1979 and 1983.36 For more than three decades, no outbreaks of the infection were recorded among Japanese horses. However the disease reoccurred in 2014 with an outbreak among racehorses at a training facility in Japan.30 This was followed by outbreaks at the same facility in 2015 and 2016.3, 29 With the exception of an extensive outbreak on a Thoroughbred breeding farm in India in 1990,5 there have been no reported occurrences of Getah virus infection outside Japan.  To date, there is no evidence to indicate that Getah virus is a human pathogen.11

Aetiology

Getah virus is an enveloped, positive-stranded RNA virus belonging to the genus Alphavirus of the family Togaviridae.7 Based on amino acid sequence analysis of the E1 viral structural protein,39 it has been classified in the Semliki Forest complex together with Semliki Forest, Bebaru, Ross River, Chikungunya, O’nyong-nyong, Una and Mayaro viruses.41

Getah virus is a relatively small virus, with a particle diameter of 66 to 70 nm18 and comprising two envelope proteins, E1 and E2, together with a core protein.34 Like many other RNA viruses that replicate as quasi-species, Getah virus can undergo frequent mutations in nature and when passaged both in vivo and in vitro.8, 28, 38 The virus possesses haemagglutinating and complement-fixing antigens which have been used to develop diagnostic tests for this infection and, together with the neutralization test, to investigate antigenic relationships between different strains and subtypes of the virus.11

Apart from horses and pigs, serological evidence of Getah virus infection has been found in a large number of vertebrate species (mammals, birds and reptiles) in nature.12, 26, 27 Experimentally, the virus has been transmitted to mice, hamsters, guinea pigs and rabbits.1, 24 Transplacental infection can occur in pregnant mice and hamsters.1, 35

In vitro, Getah virus can replicate in a range of equine and non-equine cell culture systems, e.g. Vero, BHK-21, RK- 13, MA-104, MDBK, LLC-MK2 and MDCK,19 including certain mosquito cell lines, e.g. C6/36.14

The infectivity of Getah virus is readily destroyed by exposure to lipid solvents19 and to dry, hot, acidic or alkaline conditions (pH <5 or >10).31 However, the virus can remain viable for years in a lyophilized state.6

Epidemiology

Getah virus is mosquito-borne and is widely distributed throughout Southeast Asia and surrounding areas, including Australia, Borneo, Cambodia, China, India, Indonesia, Japan, Korea, Malaysia, Mongolia, the Philippines, Russia, Thailand, Sarawak, Siberia, Sri Lanka and Vietnam.6, 11 While most Getah virus isolations from mosquitoes have been from Culex spp., the virus has also been frequently isolated from Aedes spp., especially in Japan.11

With the exception of infrequently encountered outbreaks or cases of clinical disease in horses and pigs,5, 18, 34, 36, 37, 43 natural infection in other domestic or wildlife species is believed to be subclinical.11

In tropical areas of Asia, Getah virus is thought to be maintained year-round in a mosquito–pig–mosquito cycle.6 Based on levels and duration of viraemia, pigs appear to play an important role as amplifying hosts in endemic regions.11 The role of other vertebrates such as rodents or birds as amplification or reservoir hosts of Getah virus is currently undetermined. Whether there is transtadial or transovarial transmission of the virus in mosquitoes is also not known.6

Various serological surveys on the distribution and prevalence of Getah virus infection in horses in Japan have shown that the virus is widespread in the country, with seropositivity rates of neutralizing antibodies ranging from 3 to 72 per cent.16, 34 It appears that many cases of Getah virus infection in horses are subclinical.11

Transmission of Getah virus is primarily by mosquitoes.4, 31 Depending on the region of the world in which the virus is present, the principal vector may be different species of Culex or Aedes mosquitoes.6, 11 While horses are considered most often exposed to Getah virus through the bite of infected mosquitoes, there is the potential for direct horse-to-horse transmission.33 Although virus has been demonstrated in the nasal secretions of horses experimentally infected by the intramuscular or intranasal route, virus titres are believed insufficient to infect other horses by direct contact.20, 21 Accordingly, transmission of Getah virus via animal to animal contact with nasal secretions is not considered to play a significant role in virus spread during field outbreaks. However, the potential for indirect transmission of infection via virus contaminated fomites/personnel should not be overlooked in the course of outbreaks at training facilities where horses come into close contact with one another. Non-vector transmission may have been a possible explanation for rapid spread of the virus as observed during an outbreak on a breeding farm in India in 1990.5

While outbreaks of the disease may be extensive, so far they have been sporadic in occurrence and associated with a zero case-fatality rate.11 The morbidity rate observed in one epidemic among non-vaccinated racehorses was 37.9 per cent.10, 18, 33 That occurrence was characterized by the slow and irregular spread of the virus.

Clinical signs

Clinical disease due to Getah virus has been observed almost exclusively in horses. There is evidence to indicate that clinical expression of infection is influenced by the particular strain of Getah virus, viral dose, and passage history in cell culture in the case of experimentally induced infections. Some viral strains only produce a febrile response in infected horses.33

The principal clinical signs of Getah virus infection in horses include a fever of up to 41 °C, lower hind limb oedema, swelling of the submaxillary lymph nodes, urticarial rash on various parts of the body, especially on the neck, shoulders and hind quarters, and stiffness in gait.5, 10, 18, 33 Mild colic, icterus and scrotal oedema have been observed in some affected animals. The range and severity of clinical signs vary among individual horses. When present, the limb oedema and skin rash usually appear a few days after the onset of fever and are symmetrical in distribution.11

A mild anaemia has been reported in horses during the acute and convalescent stages of the disease; it is more pronounced in febrile horses with limb oedema and skin rash than in those that only experience fever. A transient lymphopenia can occur early in the clinical course of the disease.5, 11 Biochemically, serum alkaline phosphatase may be elevated during the acute stage of illness, and serum lactic dehydrogenase and glutamic pyruvic transaminase levels increase during convalescence.6

The vast majority of affected horses make complete clinical recoveries within a week.5, 10, 18, 33 A very small percentage may require up to two weeks to achieve full recovery from the disease. Neither abortions nor birth defects were reported in a group of 16 pregnant mares infected between the second and sixth months of gestation.5

The clinical response in horses experimentally infected with low cell passaged strains of Getah virus is essentially similar to that observed in natural cases of the disease. However, such animals usually also develop a serous nasal discharge.20, 21

Aside from horses, clinical disease associated with Getah virus infection has been reported very uncommonly in pigs.37, 43 In one outbreak the virus was implicated in a peracute illness in new-born piglets38 that was fatal within 24 to 48 hours of the onset of clinical signs. Affected piglets exhibited depression, tremors and a yellowish-brown diarrhoea two to three days after birth. The litter mates that survived experienced a temporary loss in condition. No clinical signs were observed in the sow of the affected litter. On another occasion, Getah virus was isolated from several dead foetuses removed by caesarean section from a clinically healthy sow at 114 days’ gestation.37 While three out of five affected foetuses were normal in appearance, two had congestion and discoloration of the skin.

Experimental Getah virus infection of pigs has not consistently resulted in a clinical response.17, 23, 25, 32 No signs of disease were reported in two studies in which young piglets, pigs two to five months of age, and pregnant sows were challenged parentally with various strains of the virus.17, 32 In contrast, clinical responses were produced in two other studies involving conventionally reared or gnotobiotic pigs and different strains of Getah virus.23, 25 Additional to fever and anorexia noted in older pigs inoculated with the MIP-99 or MI-110 virus strains, depression, diarrhoea and a transient lymphopenia were observed in young piglets.25 The most pronounced clinical response was reported in a study in which 5- to 18-day-old piglets were infected with the Kanagawa strain of Getah virus.23 Affected piglets exhibited anorexia, depression, skin discoloration, tremors of the tongue and body, and posterior incoordination. They became moribund and died two to three days after inoculation.

Pathology

The pathological changes in horses infected with Getah virus are based on a single experimental study in which a small group of animals were inoculated intramuscularly or intranasally with the virus.42 On gross examination, there was moderate enlargement of the lymph nodes throughout the body, especially the splenic and inguinal nodes. Splenomegaly with lymphoid follicular hyperplasia was present in some and hepatomegaly in other infected horses. Moderate congestion of the renal glomeruli and the piamater was observed in individual animals. In horses with a skin rash there was moderate subcutaneous oedema and scattered maculae in the dermis.

Histopathologically, the most consistent lesion present was moderate lymphoid hyperplasia of the spleen and lymph nodes. Where skin lesions were present, these were characterized by perivascular infiltration of lymphocytes, histiocytes and in some cases, eosinophils, with oedematous thickening of blood vessel walls and occasional focal haemorrhages. In some of the infected horses, there was perivascular mononuclear cell cuffing in the cerebrum and sporadic small haemorrhagic foci in the spinal cord.42

Diagnosis

A provisional clinical diagnosis of Getah virus infection must always be corroborated by laboratory testing to confirm the presence of the virus or viral nucleic acid in appropriate specimens or to demonstrate seroconversion or a significant (fourfold or greater) rise in antibody titres between acute and convalescent sera.11

Appropriate specimens for virus isolation or detection by reverse-transcription polymerase chain reaction from the acutely infected horse include nasal swabs and unclotted blood.10, 18, 33 To optimise the chances of virus detection, specimens should be collected as early as possible after the onset of fever. Swabs should be placed in a suitable vial containing viral transport medium and these and other specimens kept refrigerated during transit to the laboratory.

Isolation of Getah virus can be readily achieved in a range of cell cultures, especially Vero or RK-13 cells,10, 18 as well as in suckling mice inoculated by the intracerebral route.33 Highest isolation rates from natural cases of the infection were 29.7 per cent from plasma and 11.8 per cent from nasal swabs.10

Serum antibodies to Getah virus can be detected using the complement fixation, enzyme-linked immunosorbent assay (ELISA) and neutralization tests, preferably on paired blood samples collected early in the acute stage and three to four weeks later during the convalescent phase of the disease.5, 18, 33, 36 The neutralization test is the most specific test for differentiating infection due to Getah virus from that caused by other antigenically closely related alphaviruses.8

Differential diagnosis

The clinical features of Getah virus infection in horses bear similarity to a number of other equine infectious and noninfectious diseases, especially equine viral arteritis and equine encephalosis.40 Other diseases that should be considered in a differential diagnosis include purpura haemorrhagica, equine infectious anaemia, dourine, equine influenza, equid herpesvirus 1 and 4 infections and toxicosis caused by ingestion of the hoary alyssum plant (Berteroa incana).

Control

In view of the fact that Getah virus is a mosquito-borne infection, measures should be taken to control the appropriate vector populations in regions where the virus is known to be endemic.11 Concerted efforts should be made to eliminate or reduce mosquito breeding sites such as old receptacles, tyres and containers or areas of standing water on farms or at racetracks where horses are congregated together. Additionally, measures should be taken to control mosquito populations through the selective use of larvicides and, if indicated and where permissible, adulticides. The risk of potential exposure to the virus can be reduced by housing horses during dusk and night-time hours.

In Japan surveillance of Getah virus infection in domestic species, especially pigs, is considered important in controlling spread of the disease. Vaccination with an inactivated, whole-virus vaccine was introduced in that country over 35 years ago to prevent Getah virus infection in horses.11 A challenge study indicated that vaccinated horses were protected against clinical disease and development of viraemia.15 Horses receive a course of two doses of vaccine in the first year generally in May and June, prior to the onset of the mosquito season. From the second year onwards, they receive an annual booster dose. The vaccine was believed to be highly effective in the field, because no epidemics of Getah virus infection had been recorded in Japan for more than 30 years after the implementation of current vaccination programme in 1979. However, Japan experienced outbreaks among vaccinated horses in three consecutive years from 2014.30  Prevalence analysis of these occurrences revealed that horses that received only one dose of vaccine before the outbreak were more susceptible to clinical signs of infection than those vaccinated twice or more often.2

A comparison between the outbreaks in 1978 and 2014 at the same training facility in Japan underscored the significance of herd-effect by vaccination. During the outbreak in 1978, none of the horses had been vaccinated and 571 (30.0 per cent) of 1903 horses developed fevers.18 In contrast, during the 2014 outbreak when all horses had been routinely vaccinated, only 64 (3.3 per cent) of 1950 horses became pyretic.2 Subclinical infection among horses during the 2014 outbreak (7.1 per cent) was also much less (34.2 per cent) than that observed in 1978.2, 18 Therefore, ensuring that all horses are kept fully vaccinated is highly recommended not only to protect individual animals, but also to minimize disease spread among the at-risk horse population.

References

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