In addition, some patients have an increase in periventricular areas and leptomeninges as observed in their magnetic resonance image, while their computed brain tomography scan failed to detect any contagion sign (Martin et al. , 2002). In the above-mentioned outbreaks, meningoencephalitis was the most common clinical diagnosis among the patients as compared to meningitis. Also, over 90% of the infected individuals had changes in their mental disturbances, fever, headache, and weakness (Patnaik, Juliusson, and Vogt, 2007).
Skin rashes on legs, neck, arms, and trunk such as popular, erythematous, macular, and morbilliform eruption were observed on some patients (Jean, Honarmand, Louie, and Glaser, 2007). Furthermore, fulminant hepatitis, ataxia, polyradiculitis, pancreatitis, myelitis, extrapyramidal signs, optic neuritis, myocarditis, cranial nerve abnormalities, and seizures rarely appear during the 1990 New York City outbreak (Jean, Honarmand, Louie, and Glaser, 2007).
Nevertheless, in the 1999 New York outbreak, the series of autopsies done on the infected individuals revealed mononuclear inflammation of the roots of the cranial nerves as well as mononuclear inflammation that resulted to the formation of the perivascular cluster and microglial nodules in both the gray and white matter of the brain (Martin et al. , 2002). The mortality rates at 12% and 14% were reported respectively in 1999 in New York City and in Israel in 2000 (Jean, Honarmand, Louie, and Glaser, 2007).
While Romania in 1996 has only 4% fatality rate, the rate remained the same for the reoccurrence of WNV pestilence in 2000–2001 in the United States (Jean, Honarmand, Louie, and Glaser, 2007). Furthermore, the rate of mortality was higher in infected individuals of ages greater than 70 years (Patnaik, Juliusson, and Vogt, 2007). The observed mortality rates for these high risk patients were 29% and 15%, respectively, in Israel and Romania (Jean, Honarmand, Louie, and Glaser, 2007).
Likewise, as observed in New York cases, patients with ages higher than 70 years had about nine times more fatality than patients of younger age (Patnaik, Juliusson, and Vogt, 2007). In relation with this, changes in consciousness level and muscle weakness severity of patient with encephalitis were also a strong predictor of fatality (Patnaik, Juliusson, and Vogt, 2007).
In the 1999 New York outbreak, the Department of Health of the New York City reported the persistence of muscle weakness, walking difficulty, fatigue, depression, and memory loss among the patients in their post-hospitalization period (Jean, Honarmand, Louie, and Glaser, 2007). However, insufficient data on the co-occurrence of WNV contagion with immunosuppression and diabetes mellitus were available to be considered as determinant of death (Jean, Honarmand, Louie, and Glaser, 2007).
Also, in 2000, about one-third among New Jersey and New York patients failed to report for follow up medications after hospital discharge (Jean, Honarmand, Louie, and Glaser, 2007). Thus, limited data on post-hospitalization morbidity of WNV patients were available for a longitudinal analysis. Based on WNV patients admitted in New Jersey and New York hospitals in 2000, mechanical ventilation was employed in two infected individuals while five patients were confined in intensive care units (Jean, Honarmand, Louie, and Glaser, 2007). The West Nile virus, WNV, has a single RNA strand (Botha et al. , 2008).
This viral strain was classified under Flavivirus of the Flaviviridae family. It is transmitted to humans by the Culex mosquito vector through a wild bird reservoir (Khairallah et al. , 2007). In line with this, both humans and avian species were infected to death in Israel and the United States by WNV (Botha et al. , 2008). In addition, WNV was identified in line with the virus serocomplex of the Japanese encephalitis similar with the Kunjin virus and the Saint Louis and Murray valley viral encephalitis (Botha et al. , 2008). This antigenic tie among these flaviviruses determined the observed serologic cross reactions in diagnostic studies.
The WNV viral hemagglutinin, E-glycoprotein, has an important role in the human cell intrusion (Botha et al. , 2008). E-glycoprotein is an important viral protein that generates antibodies for the virus. Genetically, WNV can be categorized into two groups wherein only one of which is contagious to humans. As such, the 1999 WNV outbreak in New York City and the 1997–2000 Israel WNV outbreak were attributed to lineage 1 (Botha et al. , 2008). These phylogenetic lineages were categorized into two based on the place or continental origin (Botha et al. , 2008).
Whereas the strains of WNV or Kunjin virus originating from Australia, Europe, North Africa, North and South America, and Asia belong to the lineage 1, WNV lineage 2 is a strain of Madagascar and of Southern African origins (Botha et al. , 2008). Even though lineage 1 strain was observed to cause greater cases of death and infection than lineage 2, studies have shown that the latter has severe virulence capability (Botha et al. , 2008). Also, the strain of lineage 2 has been isolated from a goshawk in Hungary which died on encephalitis, denoting the transmission of this WVN strain by means of migratory birds (Botha et al. , 2008).