The relationship between equine and human West Nile virus disease occurrence

Cases of human and equine West Nile virus (WNV) disease reported in Texas in 2002 were analyzed to assess their temporal relationship. For each human case with a known residential location, the closest equine case (within a 5 km radius) was selected. A total of 80 human–equine case pairs were identified, 51 (64%) of which were located in urban areas. Dates-of-onset of human and equine cases were positively correlated (r_SP = 0.494, P < 0.001). Although overall there was no significant (P = 0.207) difference between the dates-of-onset of human and equine cases, in urban areas of Texas equine cases were reported significantly (P = 0.011) earlier (August 7) than corresponding human cases (August 19). Monitoring equine populations that are susceptible to WNV disease within close proximity to urban human populations might be useful for predicting disease risk in human populations.     

Environmental risk factors for equine West Nile virus disease cases in Texas

West Nile Virus (WNV) was first detected in the Texas equine population during June 2002. Infection has since spread rapidly across the state and become endemic in the equine population. Environmental risk factors associated with equine WNV attack rates in Texas counties during the period 2002 to 2004 were investigated. Equine WNV attack rates were smoothed using an empirical Bayesian model, because of the variability among county equine populations (range 46−9,517). Risk factors investigated included hydrological features (lakes, rivers, swamps, canals and river basins), land cover (tree, mosaic, shrub, herbaceous, cultivated and artificial), elevation, climate (rainfall and temperature), and reports of WNV-positive mosquito and wild bird samples. Estimated county equine WNV attack rate was best described by the number of lakes, presence of broadleaf deciduous forest, presence of cultivated areas, location within the Brazos River watershed, WNV-positive mosquito status and average temperature. An understanding of environmental factors that increase equine WNV disease risk can be used to design and target disease control programs.     

西尼罗河病毒病的研究进展

西尼罗河病毒病是由西尼罗河病毒(West Nile Virus,WNV)引起的一种人畜共患传染病,病原是一种虫媒病毒,可导致西尼罗河热和致死性的西尼罗河脑炎。自发现以来,西尼罗河病毒病曾在世界上多个国家暴发,给畜牧业和人类生命安全造成了巨大的危害。我国目前尚无该病的发生,但是防治技术储备是必要的。本文对西尼罗河病毒病的流行病学、病原学、致病机制、临床症状和病理剖检变化、诊断方法和候选疗法进行综述,为西尼罗河病毒病的防控提供资料。     

新疆地区蚊类携带西尼罗病毒情况调查研究

为查明新疆地区蚊体内携带西尼罗病毒的情况,从2005年-2007年每年的7月~10月采集新疆不同地区的蚊子共计16000余只,并提取总RNA,通过RT-nest PCR的方法检测样品中西尼罗病毒。结果表明,调查样品中没有检测到西尼罗病毒,但不能就此推测新疆是否存在西尼罗病毒,至少对新疆地区和全国制定针对不同动物和人的积极防御政策有重要的公共卫生学意义。     

West Nile virus infection in horses,Indian ocean

The circulation of West Nile virus (WNV) in horses was investigated in the Southwest Indian ocean. In 2010, blood samples were collected from a total of 303 horses originating from Madagascar, Mauritius, Reunion and the Seychelles and tested for WNV-specific antibodies. An overall seroprevalence of 27.39% was detected in the Indian Ocean with the highest WNV antibody prevalence of 46.22% (95% CI: [37.4–55.2%]) in Madagascar. The age and origin of the horses were found to be associated with the WNV infection risk. This paper presents the first seroprevalence study investigating WN fever in horses in the Southwest Indian Ocean area and indicates a potential risk of infection for humans and animals. In order to gain a better understanding of WN transmission cycles, WNV surveillance needs to be implemented in each of the countries.     

Equine encephalomyelitis outbreak caused by a genetic lineage 2 West Nile virus in Hungary

Background: The spread of lineage 2 West Nile virus (WNV) from sub‐Saharan regions to Europe and the unpredictable change in pathogenicity indicate a potential public and veterinary health threat and requires scientific awareness. Objectives: To describe the results of clinical and virological investigations of the 1st outbreak of a genetic lineage 2 WNV encephalomyelitis in horses. Animals: Seventeen horses with neurologic signs. Methods: Information regarding signalment, clinical signs, and outcome was obtained for each animal. Serology was performed in 15 cases, clinicopathological examination in 7 cases, and cerebrospinal fluid was collected from 2 horses. Histopathology was carried out in 4 horses, 2 of which were assessed for the presence of WNV in their nervous system. Results: WNV neutralizing antibody titers were between 10 and 270 (median, 90) and the results of other serological assays were in agreement with those of the plaque reduction neutralization test. Common signs included ataxia, weakness, asymmetric gait, muscle tremors, hypersensitivity, cranial nerve deficits, and recumbency. Twelve animals survived. Amplicons derived from the infection‐positive specimens allowed molecular characterization of the viral strain. Conclusions and Clinical Importance: From our results, we conclude that this outbreak was caused by a lineage 2 WNV strain, even though such strains often are considered nonpathogenic. Neurological signs and survival rates were similar to those reported for lineage 1 virus infections. The disease occurrence was not geographically limited as had been the typical case during European outbreaks; this report describes a substantial northwestern spread of the pathogen.     

Serologic Responses of West Nile Virus Seronegative Mature Horses to West Nile Virus Vaccines

A 42-day study was conducted to assess the impact of three West Nile virus vaccines given either as separate injections or incorporated with their counterpart equine encephalitis and tetanus vaccines on serological responses under field use conditions. Two hundred forty mature, West Nile virus seronegative (<4) horses were followed serologically pre- and postprimary and secondary vaccination with six different vaccination programs, all including West Nile virus antigens. Forty horses were unvaccinated sentinel horses. All vaccines stimulated both a primary and secondary (booster) response to vaccination that was significantly higher than that of seronegative controls. However, inclusion of West Nile virus with equine encephalitis viruses and tetanus toxoid in vaccines had a significant detrimental impact on West Nile virus serum neutralization antibody production to both the primary and secondary vaccinations.     

西尼罗病毒套式RT-PCR检测方法的建立

从GenBank上调取西尼罗病毒的基因序列,经过分析,设计并合成2套套式RT-PCR引物,分别对西尼罗病毒灭活苗进行扩增,结果扩增出与目的片段大小一致的条带,将其克隆入pMD18-T-Vector中,进行序列测定,证实为WNV的基因。建立了套式RT-PCR检测方法,经各反应条件的优化后,发现2套nest-PCR引物能分别扩增出85个拷贝和62个拷贝的双链DNA,对乙型脑炎病毒、黄热病毒等11种病毒核酸进行扩增,发现具有良好的特异性,显示建立套式RT-PCR具有高效、快速、特异、灵敏的特点,可用于口岸WNV的检测和监测。     

The economic impact of West Nile virus infection in horses in the North Dakota equine industry in 2002

This study estimated economic impacts associated with the West Nile virus (WNV) outbreak in horses for North Dakota in 2002.The 2002 epidemic in the United States was the largest meningoencephalitis epidemic reported in the Western Hemisphere. Over 15,257 horse cases were reported in 43 states with most cases occurring in central United States. North Dakota reported over 569 horse cases, with a mortality rate of 22%. The total costs incurred by the state were approximately US$1.9 million. The costs incurred by horse owners were about US$1.5 million. Of the US$1.5 million, about US$781,203 and US$802,790 were spent on medical costs and losses due to inability to use animals because of the disease, respectively. Medical costs included the cost of vaccinating 152 horses, and the treatment costs for 345 horses which were US$4,803 and US$524,400 respectively. Costs associated with mortality were US$252,000 for the 126 horses which died of WNV. The state government spent US*$400,000 on WNV monitoring, control, and surveillance under the WNV-control program in 2002. Despite these conservative estimates, the data suggest that economic costs attributable to WNV epidemic to horse owners in North Dakota were substantial.     

西尼罗病毒的基因进化分析

为更好的了解西尼罗病毒在世界各地的流行特征,从GenBank中随机选取45株西尼罗病毒的全基因或部分基因序列,进行同源性分析构建了基因进化树.发现西尼罗病毒可以分为两个谱系,1系病毒广泛分布在非洲西部、中东、东欧、印度、美国和澳大利亚等地,2系病毒分布在非洲亚撒哈拉、马达加斯加等地.1系的西尼罗病毒可进一步分为3个分支.对其中的22株西尼罗病毒部分基因序列进行同源性比较,发现1系病毒之间核苷酸同源在76.8%以上,氨基酸同源性在78.3%以上,而2系病毒与1系病毒核苷酸同源性约为64.7%～76.2%,氨基酸同源性约为64.7%～93.0%.     

West Nile virus: North American experience

West Nile virus, a mosquito‐vectored flavivirus of the Japanese encephalitis serogroup, was first detected in North America following an epizootic in the New York City area in 1999. In the intervening 11 years since the arrival of the virus in North America, it has crossed the contiguous USA, entered the Canadian provinces bordering the USA, and has been reported in the Caribbean islands, Mexico, Central America and, more recently, South America. West Nile virus has been reported in over 300 species of birds in the USA and has caused the deaths of thousands of birds, local population declines of some avian species, the clinical illness and deaths of thousands of domestic horses, and the clinical disease in over 30 000 Americans and the deaths of over 1000. Prior to the emergence of West Nile virus in North America, St. Louis encephalitis virus and Dengue virus were the only other known mosquito‐transmitted flaviviruses in North America capable of causing human disease. This review will discuss the North American experience with mosquito‐borne flavivirus prior to the arrival of West Nile virus, the entry and spread of West Nile virus in North America, effects on wild bird populations, genetic changes in the virus, and the current state of West Nile virus transmission.     

Epidemic West Nile virus encephalomyelitis: a temperature-dependent, spatial model of disease dynamics

Since first being detected in New York in 1999, West Nile virus (WNV) has spread throughout the United States and more than 20,000 cases of equine WNV encephalomyelitis have been reported. A spatial model of disease occurrence was developed, using data from an outbreak of serologically confirmed disease in an unvaccinated population of horses at 108 locations in northern Indiana between 3 August and 17 October 2002. Daily maximum temperature data were recorded at meteorological stations surrounding the study area. The distribution of the total number of degree-days elapsing between July 4 and the date of diagnosis of each case was best described by a normal distribution (mean = 5243 °F, S.D. = 1047). The days on which the average risk was >25, >50 and >75% were predicted (versus observed) to occur on August 23 (August 9), August 31 (September 2) and September 9 (September 9). The epidemic was predicted to occur 3 days earlier, or 4 days later, than observed if temperatures in the study area were uniformly increased, or decreased, by 5 °F, respectively. Maps indicated that WNV encephalomyelitis risk always remained greater in the northwest quadrant of the study area. Since WNV might exist at a hypoendemic level of infection, and occasionally re-emerge as a cause of epidemics in equine populations, by identifying factors that contributed to this epidemic, the potential impact of future epidemics can be reduced. Such studies rely on a GIS framework, availability of meteorological and possibly remotely sensed data and information on host and landscape factors. An early-warning system for WNV transmission in equine populations could be developed.     

Clinical screening of horses and early warning for West Nile virus

Clinical presentation of West Nile disease in horses is variable, but ataxia, weakness and muscle fasciculations are often observed, sometimes with abnormal behaviour, teeth grinding and bruxism. Practitioners should be aware that horses are more sensitive to infection than man and serve as sentinels for an early warning of West Nile virus circulation in a given area. This early warning allows the implementation of preventive and control measures such as vaccination of horses and mosquito control.     

West Nile virus and its emergence in the United States of America

Zoonotic West Nile virus (WNV) circulates in natural transmission cycles involving certain mosquitoes and birds, horses, humans, and a range of other vertebrates are incidental hosts. Clinical infections in humans can range in severity from uncomplicated WNV fever to fatal meningoencephalitis. Since its introduction to the Western Hemisphere in 1999, WNV had spread across North America, Central and South America and the Caribbean, although the vast majority of severe human cases have occurred in the United States of America (USA) and Canada. By 2002-2003, the WNV outbreaks have involved thousands of patients causing severe neurologic disease (meningoencephalitis and poliomyelitis-like syndrome) and hundreds of associated fatalities in USA. The purpose of this review is to present recent information on the epidemiology and pathogenicity of WNV since its emergence in North America.     

Characterization of West Nile virus (WNV) isolates from Assam,India: Insights into the circulating WNV in northeastern India

West Nile virus (WNV) is a mosquito-borne flavivirus that causes subclinical symptoms, febrile illness with possible kidney infarction and encephalitis. Since WNV was first serologically detected in Assam during 2006, it has become recognized as an important etiological agent that causes acute encephalitis syndrome (AES) in addition to endemic Japanese encephalitis virus (JEV). Therefore, isolating and characterizing the currently circulating strain of WNV is important. The virus was isolated from the cerebrospinal fluid (CSF) of two patients that presented with AES. The genotyping of the isolates HQ246154 (WNIRGC07) and JQ037832 (WNIRTC08) based on the partial sequencing of 921 nucleotides (C-prM-E) of the genome placed them within lineage 5 along with other Indian strains isolated prior to 1982, but the present circulating virus formed a distinct subclade. The derived amino acid sequence alignment indicated substitution in A₈₁T and A₈₄P of the capsid region in HQ246154. A cross-neutralization assay suggested substantial antigenic variation between isolates. The pathogenesis in mice that suggested the circulating WNV was neuroinvasive and comparatively more pathogenic than previous strains from India.     

First serological evidence of West Nile virus infection in wild birds in Northern Algeria

While the epidemiology of Flaviviruses has been extensively studied in most of the Mediterranean basin, little is known about the current situation in Algeria. In order to detect the circulation of West Nile (WNV) and Usutu viruses (USUV) in Kabylia, 165 sera were collected from two wild birds species, namely the long distance migrant Turdus philomelos (song thrush) (n = 92) and the resident Passer domesticus (house sparrow) (n = 73). A total of 154 sera were first analyzed by commercial competition ELISA. WNV and USUV micro-neutralization tests were performed on all c-ELISA positive sera and all samples with poor volume. Overall, 7.8 % (CI95 %: 3.5–11.9) were positive by c-ELISA. Positive results were detected in 12.5 % (CI95 %:5.6–19.4) of song thrushes and 1.5 % (CI95 %: 0.0–4.5) for sparrow.Micro-neutralization tests revealed an overall seroprevalence of 6.7 % for WNV (CI95 %: 2.9–10.3), Neutralizing antibodies were found in 8.7 % (CI95 %: 3.0–14.4) for song thrushes and in 4.1 % (CI95 %: 0.0–8.7) of sparrows. The current study demonstrates significant seroprevalence of WNV antibodies in wild birds in Algeria.     

A metapopulation model to simulate West Nile virus circulation in Western Africa, Southern Europe and the Mediterranean basin

In Europe, virological and epidemiological data collected in wild birds and horses suggest that a recurrent circulation of West Nile virus (WNV) could exist in some areas. Whether this circulation is permanent (due to overwintering mechanisms) or not remains unknown. The current conception of WNV epidemiology suggests that it is not: this conception combines an enzootic WNV circulation in tropical Africa with seasonal introductions of the virus in Europe by migratory birds. The objectives of this work were to (i) model this conception of WNV global circulation; and (ii) evaluate whether the model could reproduce data and patterns observed in Europe and Africa in vectors, horses, and birds. The model was calibrated using published seroprevalence data obtained from African (Senegal) and European (Spain) wild birds, and validated using independent, published data: seroprevalence rates in migratory and resident wild birds, minimal infection rates in vectors, as well as seroprevalence and incidence rates in horses. According to this model, overwintering mechanisms are not needed to reproduce the observed data. However, the existence of such mechanisms cannot be ruled out.