Selected content from the Animal Health and Production Compendium (© CAB International 2013). Distributed under license by African Union – Interafrican Bureau for Animal Resources.
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Identity Pathogen/s Overview Distribution Distribution Map for Africa Distribution Table for Africa Hosts/Species Affected Host Animals Systems Affected Epidemiology Impact: Economic Zoonoses and Food Safety Pathology Diagnosis Disease Course Disease Treatment Table Disease Treatment Vaccines Prevention and Control References Links to Websites OIE Reference Experts and Laboratories
Preferred Scientific Name
West Nile viral encephalitis
International Common Names
Near Eastern equine encephalitis, West Nile, West Nile encephalitis, West Nile fever, West Nile infection, West Nile virus encephalomyelitis in horses and sheep - zoonosis, West Nile virus equine encephalomyelitis, West Nile virus in birds, WNV infection
West Nile virus
West Nile virus (WNV) is a mosquito-borne flavivirus that causes West Nile fever (WNF), which is endemic in Africa, the Middle East and south-western Asia. WNV has recently emerged in temperate regions of Europe and North America and presents a threat to public and animal health. The virus was first isolated in the West Nile district of Uganda in 1937 from a native adult human female suffering a mild febrile illness (Smithburn et al., 1940). Subsequently, it was isolated from birds and mosquitoes in Egypt (Taylor et al., 1956) and implicated as a cause of human meningoencephalitis in Israel during the 1950s (Weinberger et al., 2001). A major human epidemic occurred in South Africa during 1974 (McIntosh et al., 1976) and human epidemics have been reported in Romania (Tsai et al., 1998), Southern Russia (L'vov et al., 2000), North-eastern USA (Lanciotti et al., 1999) and Israel. (Chowers et al., 2001).
A major epidemic has occurred in at least 38 States in N America in 2002. There have been 3698 laboratory confirmed cases in humans with 198 deaths. Some 8710 equines have been infected, 3 canines and at least 10 other species. Two thousand six hundred and twelve crows have been killed, together with some 6060 other avian hosts. Canada has also been involved.
Disease among horses caused by WNV was reported in Egypt and France during the early 1960s (Schmidt and El Mansoury, 1963; Hannoun et al., 1969). Cases of WNV equine encephalitis have been reported more recently from countries in North Africa and Europe bordering the Mediterranean Sea and from the Northeastern USA (Ostlund et al., 2000; Murgue et al., 2001; Trock et al., 2001). Mortality among domestic flocks of geese has been reported in Israel (Weinberger et al., 2001).
WNV is a member of the Japanese encephalitis virus sero-complex in the genus Flavivirus of the family Flaviviridae (Heinz et al., 2000). Other members of the group include Japanese encephalitis virus (JEV), St. Louis encephalitis virus (SLEV), Murray Valley encephalitis virus (MVEV) and Kunjin virus (KUNV). They are closely related antigenically and can cross-react, often confusing interpretation when diagnostic serological tests are performed.
Mosquitoes are primarily responsible for vector transmission, with birds acting as the primary reservoir host (Hayes, 1989; Peiris and Amerasinghe, 1994; Hubalek and Halouzka, 1999). Virus has been isolated from many vertebrate species. Humans and equines are normally considered to be accidental or 'dead end' hosts.
Since the mid 1990s three distinct epidemiological trends have emerged, an increase in frequency of outbreaks among humans and equines, an increase in the severity of human disease and high avian death rates accompanying outbreaks (Peterson and Roehrig, 2001). There has been a major increase and extension of WNV activity across much of the United States and Canada in the year 2002, which has involved humans, horses and wild and domestic birds and ruminants.
WNV is the most widely distributed of the flaviviruses, having been isolated in Africa, Asia, Europe, Middle East, Oceania, North America and Russia (Hubalek and Halouzka, 1999).
= Present, no further details = Widespread = Localised
= Confined and subject to quarantine = Occasional or few reports
= Evidence of pathogen = Last reported... = Presence unconfirmed
The distribution in this summary table is based on all the information available. When several references are cited, they may give conflicting information on the status. Further information for individual references may be available in the Animal Health and Production Compendium. A table for worldwide distribution can also be found in the Animal Health and Production Compendium.
|Country||Distribution||Last Reported||Origin||First Reported||Invasive||References||Notes|
|Algeria||Disease never reported||OIE, 2012; Le et al., 1996|
|Angola||No information available||OIE, 2009|
|Benin||No information available||OIE, 2009|
|Botswana||Disease never reported||OIE, 2012; Hubalek & Halouzka, 1999|
|Burkina Faso||No information available||OIE, 2009|
|Central African Republic||Present||Hayes, 1989|
|Chad||No information available||OIE, 2009|
|Congo||No information available||OIE, 2009; Hayes, 1989|
|Congo Democratic Republic||Present||Hayes, 1989|
|Côte d'Ivoire||Present||Hubalek & Halouzka, 1999|
|Djibouti||No information available||OIE, 2009|
|Egypt||No information available||NULL||OIE, 2009; Hayes, 1989|
|Eritrea||No information available||OIE, 2009|
|Ethiopia||Disease never reported||OIE, 2012; Hayes, 1989|
|Gabon||No information available||OIE, 2009|
|Gambia||No information available||OIE, 2009|
|Ghana||No information available||OIE, 2009|
|Guinea||No information available||OIE, 2009|
|Guinea-Bissau||No information available||OIE, 2009|
|Kenya||Disease never reported||NULL||OIE, 2009; Hayes, 1989|
|Lesotho||Disease never reported||OIE, 2009|
|Libya||Disease never reported||OIE, 2012|
|Madagascar||Last reported||2010||OIE, 2012; Hayes, 1989|
|Malawi||No information available||OIE, 2009|
|Mali||No information available||OIE, 2009|
|Mauritius||Disease never reported||OIE, 2012|
|Morocco||Last reported||2010||OIE, 2012; Ostlund et al., 2000|
|Mozambique||No information available||NULL||OIE, 2009; Hubalek & Halouzka, 1999|
|Namibia||Disease never reported||OIE, 2012|
|Nigeria||Disease never reported||OIE, 2012; Hayes, 1989|
|Rwanda||Disease never reported||OIE, 2009|
|Senegal||No information available||OIE, 2009; Hubalek & Halouzka, 1999|
|Seychelles||OIE, 2012||Disease suspected|
|South Africa||Last reported||2010||OIE, 2012; Hayes, 1989|
|Sudan||Disease never reported||OIE, 2012; Taylor et al., 1956|
|Swaziland||No information available||OIE, 2009|
|Tanzania||No information available||OIE, 2009|
|Togo||No information available||OIE, 2009|
|Tunisia||Last reported||2008||OIE, 2012; Hubalek & Halouzka, 1999|
|Uganda||No information available||OIE, 2009; Smithburn et al., 1940||First reported 1937|
|Zambia||Disease never reported||OIE, 2012|
|Zimbabwe||Disease never reported||OIE, 2012|
WNV has been isolated most frequently from humans, equines and many different species of wild and domestic birds. Infection by West Nile virus causing acute onset of anorexia and fever has also been recorded in alpacas (Kutzler et al., 2004). The virus has been isolated sporadically from camel, dog and a variety of small mammals (Hayes, 1989; Hubalek and Halouzka, 1999).
|Anser anser (geese)||Domesticated host|
|Equus caballus (horses)||Domesticated host|
|Gallus gallus domesticus (chickens)|
Multisystem - Large Ruminants
Nervous - Poultry
WNV is amplified during periods of adult mosquito blood feeding by a continuous transmission cycle between mosquito vectors, particularly Culex spp. and avian reservoir hosts. Hard and soft ticks may serve as substitute vectors in areas lacking mosquitoes. Two transmission cycles are recognised, a rural or sylvatic cycle comprising wild, usually wetland birds and bird feeding mosquitoes, and an urban cycle involving birds and mosquitoes, which feed upon birds and humans. The significance of the urban cycle was apparent during the recent human epidemics in Bucharest, Volvograd and New York City. Environmental factors, including water management, sanitation and substandard housing contribute to mosquito breeding, virus amplification and disease transmission in urban areas.
A sufficient number of vectors must feed on an infectious host to ensure that some survive the viral incubation period of approximately two weeks allowing them to feed again and transmit to a susceptible host. (Komar, 2000). Peak virus activity in birds, occurs during seasons of high temperature and rainfall that coincide with high vector density and increased vector feeding capacity. Other modes of transmission are not confirmed, although direct bird to bird transmission has been suggested (Komar, 2000).
The role of migrating birds in the transmission of WNV, particularly to temperate zones, has received considerable attention following the epidemics in Europe and North America (Rappole et al., 2000). Northward spring migrations from Africa across the Middle East, Turkey and the Black Sea provide a route to introduce WNV to southern Europe and Russia. Possible mechanisms for overwintering of WNV in temperate zones include prolonged infection in hibernating mosquitoes and low level trans-ovarial transmission (Hubalek and Halouzka, 1999). Molecular and antigenic studies of isolates from around the world have provided clues as to the source and migration of WNV; the virus isolated from cases in New York has a close homology to virus isolated from domestic geese in Israel in 1998 (Lanciotti et al., 2000).
Initial accounts of the disease in endemic areas of Africa (Taylor ,1956) indicated that infection among humans occurred during early childhood and was asymptommatic or resulted in only mild disease. The epidemics during the 1990s in Europe, Southern Russia, North America and the Middle East have involved increased fatality associated with encephalitic infection among adults. Mortality among horses has been reported recently in France, Italy, USA, and North Africa and among a variety of wild, domesticated and exotic bird species in Israel and the USA. An estimate of public expenditure attributed to the outbreak in New York State during 1999 exceeded US $15 million (Komar, 2000). Restrictions on the export of horses from affected states in the USA were imposed temporarily by several countries including the European Union during 1999 and 2000. Several major national and international equestrian competitions due to be held in the northeastern USA during 2000 were cancelled.
Affected individuals develop a flu-like illness characterized by acute fever, headache, sore throat, chills, generalised lymphadenopathy, nausea and myalgia. The incubation period ranges from 5-15 days with rapid onset of signs and a convalescent period of 1-2 weeks. There have also been occasional reports of hepatitis, pancreatitis and myocarditis. More severe illness has been reported during recent epidemics, involving acute aseptic meningitis or encephalitis particularly among elderly patients, leading in a small percentage of cases to coma and death. Signs in these patients include fever, headache, vomiting, confusion, rash, stiff neck and profound muscle weakness requiring respiratory support.
Cantile et al. (1999) and Ostlund et al. (2000) described gross and histological lesions in horses that have died from WNV infection. Postmortem examination revealed little or no gross lesions. External injuries were observed as a result of trauma during recumbency. Lesions if present were limited to the central nervous system. The dura was thickened and adherent and sub-meningeal oedema with petechial or diffuse haemorrhages was observed.
Histological lesions in the brain were similar to those observed for other equine encephalitic viruses, a nonsuppurative mild to moderate encephalitis and vasculitis with perivascular cuffing and monocytic cellular infiltration. During the outbreak in Italy reported by Cantile et al. (1998) the predominant lesions were in the lower brainstem and ventral horns of the thorax and lumbar spinal cord with focal gliosis and haemorrhage occasionally observed. Lesions are consistent with an ascending neurological dysfunction but not specific for WNV infection.
Steele et al. (2000) has described the pathology of WNV infection among native and exotic birds in the USA. Haemorrhages of the brain, splenomegaly, meningeoencephalitis and myocarditis were the most prominent lesions. Gross and histological lesions were common in the cerebellum including haemorrhages, Purkinje cell necrosis, gliosis and inflammatory infiltrates. Changes were less severe in other portions of the brain. Crows did not exhibit the extensive lesions of the brain observed in other birds. Lesions observed in other tissues included lymphocytic myocarditis, focal necrosis of the liver and spleen, pancreatitis, pulmonary haemorrhage and inflammation of the adrenal glands. Viral antigen was detected in a wide range of avian tissues and cells confirming the pantropic nature of the invading strain of WNV.
Targeting of the Purkinje cells of the cerebellum observed in WNV infection of mammals and birds is considered unique to the flaviviruses (Komar, 2000).
Laboratory tests are essential for establishing diagnosis of WNV infection. Case definitions for WNV infection in humans and equines including clinical signs and confirmatory laboratory evidence are available in 'Epidemic/Epizootic West Nile Virus in the United States: Revised Guidelines for Surveillance, Prevention and Control' (Centers for Disease Control and Prevention, 2001).
Care is required when handling virus because of the zoonotic potential of WNV. Laboratories working with known WNV isolates should adhere to established containment requirements. Caution should be exercised when collecting material from live or dead specimens, particularly when central nervous tissue is examined. Precautions should include wearing two layers of waterproof gloves and a facemask.
A definitive diagnosis is possible by detection of viral RNA using polymerase chain reaction (PCR) or by isolation in tissue culture; for example, Vero cells or neonatal mouse inoculation. Preferred tissues from equines are brain or spinal cord, although isolation of WNV from brain tissue can be difficult. Equine blood and cerebrospinal fluid (CSF) from clinically sick animals is not a reliable source for the determination of the presence of virus by PCR or virus isolation because viraemia occurs before clinical signs are observed (Johnson et al., 2001). Multiple unfixed specimens from the cerebrum, brainstem and representative segments of the spinal cord should be obtained for analysis. Multiple tissue samples from other mammals should include samples of brain and kidney. Specimens from dead birds should include kidney, brain and heart tissue. Material should be chilled during transit and sent by overnight delivery service. Additional specimens from brain and spinal cord should be fixed in formalin and submitted for histological examination.
Isolates are identified using WNV-specific monoclonal antibodies, virus neutralisation assays or reverse transcriptase-polymerase chain reaction (RT-PCR). An RT-nested PCR (RT-nPCR) has proved to be a reliable and rapid method for detecting WNV in both equine and avian tissues (Johnson et al., 2001). WNV antigen can be detected in fixed tissues using immunohistochemical (IHC) techniques with WNV-specific antisera. In situ hybridisation detection of WNV nucleic acid in avian tissue has been reported (Steele et al., 2000). Species-specific antigen capture ELISA is available to detect antigen in avian tissues and mosquito pools (Centers for Disease Control Workshop, 2001).
Serological evidence of recent WNV infection is confirmed by a 4-fold or greater rise in plaque-reduction neutralising (PRNT) antibody in paired sera. The first serum should be drawn as soon as possible after the onset of clinical signs and the second between 14 and 21 after the first. Neutralising antibody may not be present until 2 weeks or more after exposure to WNV; so it is possible that clinical signs will be observed before a serum is PRNT positive. Other tests include detection of specific immunoglobulin M (IgM) to WNV by IgM-capture enzyme-linked immunosorbent assay (MAC-ELISA) in sera or CSF, haemagglutination inhibition (HI) and complement fixation (CF). PRNT can be applied to sera and CSF from all species and adapted to reflect antibody activity to currently circulating strains. However, it does require the use of live virus.
IgM antibody induced during the acute phase of WNV infection is short lived; approximately 3 months in horses (Ostlund et al., 2000). IgM-capture ELISA is a valuable tool for the detection of recent infection in all species. It is species-specific and must be modified for each new species to be tested. Whilst HI and ELISA are used extensively for diagnosis and serological prevalence studies they do cross react with other flaviviruses and should be used only as a screening test. Positive samples should be confirmed by neutralisation and serological samples should be screened against a panel of arboviral antigens, depending on the geographic distribution of known pathogens in the area.
Among horses, signs range from inapparent infections to fatal encephalitis with mortality of 30-45% in clinical cases. The most common signs reported by Ostlund et al. (2000) include marked abnormalities of gait, primarily of the hind limbs, with varying degrees of ataxia and muscular weakness, progressing on occasion to recumbency. Other neuromuscular signs include circling, head-tilt and tremors of the face, limbs, trunk and shoulder. Sick horses continue to eat and drink but behavioural changes such as depression or anxiety and nervousness are observed.
Until recently, reports of birds showing clinical disease during epizootics of WNV infection have been rare. Fatal neurological disease was a feature among wild and exotic birds during outbreaks in the USA (Steele et al., 2000) and among domestic flocks of geese in Israel (Weinberger et al., 2001). In the USA, mortality was high amongst corvids (crows and jays) but many other native bird species were also affected. Sick birds showed weakness often lie in sternal recumbency. Neurological signs were the principal manifestation however, including tremors, abnormal head position, ataxia, wobbly gait and circling.
|Drug||Dosage, administration and withdrawal times||Life stages||Adverse affects||Drug resistance||Type|
|equine West Nile vaccine (Fort Dodge)||For horses. Two doses given intramuscularly, one month apart.||All Stages||No||Vaccine|
There is no specific treatment for clinical WNV infection in humans or animals. Therapies may be applied to reduce pain, inflammation, to provide supportive care, prevent injury and minimise the adverse consequences associated with recumbency. Nonsteroidal anti-inflammatory medications assist in reducing inflammation of the central nervous system and alleviating pain. Slings, plus nutrient and fluid support are also of value.
|Vaccine||Dosage, Administration and Withdrawal Times||Life Stages||Adverse Affects|
|equine West Nile vaccine (Fort Dodge)||For horses. Two doses given intramuscularly, one month apart.||-Other: All Stages|
The control and prevention of arboviral disease may be accomplished through an integrated management program undertaken by trained and experienced personnel (Rose, 2001). Components include surveillance, source reduction, larvicide and biological control, resistance monitoring, public relations and education. The emergence of WNV infection causing human encephalitis, particularly in non-endemic areas, has prompted increased surveillance. A sophisticated monitoring system has been developed in the USA with the collaboration of medical, public health and veterinary resources at federal, state and local level (Centres for Disease Control Workshop, 2001). It involves active and passive surveillance for human cases of viral encephalitis, veterinary surveillance for disease in horses and other mammals and surveillance in populations of wild and sentinel birds and mosquitoes. Surveillance in the vector populations determines the minimum infection rate (MIR) expressed as the number infected per 1000 specimens examined, and provides warning of a probable disease outbreak. Such a program requires specialised laboratory diagnostic procedures, detailed epidemiological monitoring, data recording and analysis supported by trained personnel. Not all countries have the resources available, or have more urgent medical priorities and rely on passive medical and veterinary surveillance during the summer months when the incidence of disease is highest.
Source reduction to eliminate mosquito larval habitats and prevent mosquito breeding is achieved by improved sanitation such as the elimination of standing pools of water, management of irrigation projects, swamp and marshlands and public education. The most commonly used biological controls are the mosquito fish, Gambusia affinis and G. holbrooki. If the above are not feasible or have failed then 'larviciding', the application of chemicals to kill larva and pupae by ground or aerial treatment can be tried. Larvicidal chemicals may be applied in various formulations and include temephos, methoprene, oils and bacterial larvicides. Application of 'adulticides' to kill adult mosquitoes by ground or aerial spraying is the least effective control method but may be used as one of last resort during an outbreak. Adulticides include organophosphates, malathion and naled, natural and synthetic pyrethrums such as pyrethrins, permethrin, resmethrin and sumithrin. They can be applied as an ultra low volume (ULV) spray from truck-mounted equipment, fixed wing or rotary aircraft. The use of chemical insecticides has aroused considerable public controversy with respect to their potential human and environmental toxic effects. Education, particularly via local television and radio can overcome public apprehension and may be used to explain preventive measures prior to and during an outbreak.
Exposure of horses to mosquito vectors can be minimised by stabling in vector-proofed buildings plus the use of repellants such as N, N-diethyl-metatoluamide (DEET).
In August 2001 the United States Department of Agriculture (USDA) issued a conditional license for the use of an inactivated adjuvant equine WNV vaccine manufactured by Fort Dodge Animal Health. Commercial flocks of geese in Israel received an attenuated vaccine derived from Israel turkey meningoencephalitis (ITM) virus during 1999 (Komar, 2000). ITM, a flavivirus is administered to young goslings to provide cross protection to WNV infection. Studies are underway to develop vaccines for humans and horses that examine the safety and efficacy of DNA and live attenuated WNV vaccines.
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Dr Rossella Lelli
Istituto Zooprofilattico Sperimentale dell'Abruzzo e del Molise "G. Caporale"
Via Campo Boario
Tel: +39 0861 33.22.05 Fax: +39 0861 33.22.51
Dr Eileen Ostlund
National Veterinary Services Laboratories
USDA, APHIS, Veterinary Services
P.O. Box 844
Ames, Iowa 50010
UNITED STATES OF AMERICA
Tel: +1-515 337 75 51 Fax: +1-515 337 73 48
Date of report: 03/06/2013
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