West Nile virus (WNV) was not important in Europe for a very long time, as there was no evidence that the virus circulated in domestic birds or Austrian horses until 2002 (Weissböck et al., 2003). However, WNV lineage 2 was first registered in southeastern Hungary in early 2004 (Bakonyi et al., 2006) and spread to neighboring countries over several years (Bakonyi et al., 2013; Wodak et al., 2011). This notifiable disease has been detected in horses in Europe in Austria, Bulgaria, France, Germany, Greece, Hungary, Italy, Portugal, Slovenia, and Spain (Young, Coulombier, Domanovic, Zeller & Gossner, 2019).
Retrospective serological investigations revealed that three humans had already tested positive in Austria in 2009 and 2010 (Stiasny, Aberle, & Heinzl, 2013).
WNV lineage 2 infection can be asymptomatic, cause non-specific flu-like symptoms or neurological symptoms in humans (Danis et al., 2011; Papa, Danis, Tsergouli, Tsioka & Gavana, 2011), horses and some avian species (Bakonyi et al., 2013, Wodak et al., 2011, Ziegler et al., 2013). The assumption that "lineage 2" is non-pathogenic or of low pathogenicity was thus refuted. In humans, 1% of infections with WNV lineage 2 result in death, whereas mortality in diseased horses is 8%-10% (Bunning et al. 2002; Sejvar, 2014).
The authors (University of Veterinary Medicine Vienna, AGES, Academy of Sciences Brno) collected and analyzed relevant data from seven horses from Austria affected by the neuroinvasive form of West Nile fever. These were neurological symptoms, blood values, and virological, serological, molecular biological, and, if available, neuropathological findings.
Two cases were from 2016, three from 2017, and two from 2018. Four geldings and three mares were involved; none of these horses had ever been vaccinated against WNV. It was known that five horses were born in Austria and never left the country. There was no information about travel activity from the other two animals examined.
All infected horses showed abnormalities in their gait (ataxia, bradykinesia (slowed movements), hind limb lameness). Similarly, involuntary muscle tremors (fasciculation and tremor) in the neck and triceps region occurred in six of seven horses. In four cases, the animals exhibited elevated temperature, five horses showed agitation, and two animals were lethargic at hospitalization. Three horses had additional gastrointestinal symptoms such as colic. These symptoms were probably caused by a lesion of the autonomic nervous system (Bielefeldt-Ohmann et al., 2017; Carod-Artal, 2018; Tewari et al., 2004). One horse showed signs of palpitations (tachycardia) and immobility (stupor) and lapsed into a comatose state. Blood chemistry including liver values also showed elevated values (creatinine kinase, leukocytosis and neutrophilia, glutamate dehydrogenase and gamma-glutamyltransferase) in three horses examined. Because of the severe symptomatology, four horses were euthanized and the brain was examined neuropathologically. Characteristic lesions consisted of predominantly truncal, nonpurulent brain and meningitis (leptomeningoencephalitis non purulenta). Viral RNA could be detected by molecular biology in five of seven horses, immunoglobulin M (IgM) or immunoglobulin G (IgG) could be detected in six and seven cases, respectively, while specific neutralizing antibodies against WNV were present in all animals.
In addition to the patient data collection, six mosquito species were collected in the horse stall of the first case. Several individuals of the common mosquito (Culex pipiens) were sometimes caught, which showed a high WNV viral load in a pool sample. This species is the primary vector in Europe and North America (Hubálek & Halouzka ,1999). In addition, neutralizing antibodies against WNV without further signs of disease were found in two more of a total of 14 contact horses to the first case.
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