ABSTRACT
West Nile virus (WNV) infection is mosquito-borne zoonoses involving birds, horses, humans and other species of animals. This study was designed to determine the seroprevalence and risk factors of WNV infection in horses and to detect for the viral antigen in mosquitoes in Kaduna State, Nigeria. A total of 368 horses and 31 pools of Culex species of mosquitoes were tested for anti WNV IgG antibodies and antigen using Competitive Enzyme-Linked Immonosorbent Assay and Vector test® respectively in four selected Local Government Areas (LGAs) of Kaduna State. A structured interviewer administered questionnaire was used to determine presence of factors in the stables that are associated with WNV infection in horses. Out of the 368 horses tested, 331(89.9%) were seropositive for WNV infection. Based on the LGA, a statistically significant higher seroprevalence (P=0.003) was found in Kaduna North LGA (98.9%) followed by Zaria, Igabi and Sabon Gari with prevalence of 88.7%, 86.0% and 78.3% respectively. There was no significant association of WNV seropositivity with age and sex of horses. Only 1(3.2%) pool from Zaria LGA out of the 31 mosquito pools, tested positive for WNV antigen. There was low level of awareness on WNV infection and its transmission among horse attendants and presence of wild birds, stagnant water, grasses, trees and waste bins around the stables. This study has identified high seroprevalence of WNV in apparently healthy horses in Kaduna State and Culex species of mosquito in stables at the time of study are carrying WNV. Conditions suitable for transmission of WNV infection are abundant in horse stable environments in the state. There is the need for dedicated surveillance for WNV infection in Nigeria. The inclusion of WNV in the differential diagnosis of fevers of unknown origin in medical hospitals, along-side public health education of the population on the disease is necessary.
CHAPTER ONE
INTRODUCTION
1.1 Background of the study
West Nile virus (WNV) is a re-emerging mosquito-transmitted disease causing WNV disease in humans and animals (Cantile et al., 2000; Durand et al., 2002; Murgue et al., 2001a; Autorino et al., 2002; Charrel et al., 2003 Castillo-Olivares and Wood, 2004). WNV was first isolated in 1937 from the blood of a febrile adult human in the West Nile District of Uganda (Smithburn et al., 1940). The virus (WNV) is a member of the Japanese encephalitis virus complex which includes, Japanese encephalitis virus (JEV), Saint Louis encephalitis virus (SLEV), and Murray Valley encephalitis virus within the genus Flavivirus and family Flaviviridae (Heinz et al., 2000). The genetic material of the WNV isa positive-sense, single stranded RNA that is between 11,000 and 12,000 nucleotides long, which encode seven non-structural proteins and three structural proteins. The RNA strand is held within a nucleocapsid formed from 12-kDa protein blocks, the capsid is contained within a host-derived membrane altered by two viral glycoproteins (Galli et al., 2004).
The virus is transmitted in natural cycles mainly between mosquitoes and birds, with humans and horses serving as incidental hosts as well as dead-end host (Burke and Monath, 2001). In humans and equines, WNV infection is usually asymptomatic or characterized by a mild febrile illness to encephalitis with fatal outcome (Petersen and Reohrig, 2001; Bunning et al., 2002; Garcia-Bocanegra et al., 2011). There is no specific treatment for WNV disease and clinical management is supportive. Diagnosis is based on serology, viral isolation and characterization (CDC, 2015a).
WNV has since been reported in Africa, the Middle East, Asia, Southern Europe, Australia and North America (Campbell et al., 2002; Roehrig et al., 2002; Zeller and Schuffenecker, 2004; MacKenzie and Williams, 2009). The initial outbreak of the virus in North America was recognized in the fall of 1999 in New York City with reported death in humans, horses, and numerous species of birds, since then, there has been an increase in geographic distribution of WNV in North America (CDC, 2002a; Brien et al,2008).
WNV disease is considered a re-emerging pathogen affecting both humans and animals (Morens et al., 2004). Multiple factors contributing to the emergence of the virus include human susceptibility to infections, climate and weather, breakdown of public health measures, economic development and land use, human demographics and behaviour, along with international travel and commerce, contribute to the emergence and re-emergence of the disease (Morse, 1995; Felissa, 2006).
WNV is globally distributed and the first case was reported in Western Hemisphere in 1999 in New York City (Nash et al., 2001). The virus has also spread to Europe, beyond the Mediterranean basin, and a new strain of the virus was reported in Italy in 2012 (Barzon et al., 2012). WNV is considered to be an endemic pathogen in Africa, Asia, Australia, Middle East, Europe and United States, of which there was an experience of one of its worst epidemics in the year 2012 resulting in death of 286 people in the United States of which Texas being mostly affected with the disease outbreak (Murray et al., 2013), making the year (2012) the worst record for WNV disease outbreak in the United States (Fox, 2013).
WNV can occur in horses as West Nile encephalitis virus, resulting from mild febrile illness to encephalitis, the incubation period for equine West Nile encephalitis following mosquito transmission is estimated to be 3–15 days (OIE, 2013). A transient viraemia of low virus load anticipate clinical onset of WNV infection (Schmidt and El Mansoury, 1963; Bunning et al., 2002). In humans and equine, most WNV infections are asymptomatic; approximately 20 to 30% of infected individuals develop flu-like clinical manifestation characterized as West Nile fever (Perelygin et al., 2002; Wang et al, 2004a). In a subpopulation of individuals, at least 1 out of 150 develops a neuroinvasive or encephalitis disease caused by WNV. (Petersen et al., 2001; Perelygin et al., 2002; Pestka et al., 2004).
