In addition to the severity of cognitive and motor sequelae, mild cases of executive function loss, motor skills abnormalities, and tremor were seen (Levinson, 2006). The intensive effort in discovering effective clinical treatment and in producing efficient laboratory diagnosis have made for further discovery of WNV infection clinical features such as histologic lesions similar to poliomyelitis, flaccid paralysis, chorioretinitis, and fever with neurologic disorder symptoms (Levinson, 2006). As well, Immunosuppressed individuals are inclined to the development of central nervous system infection and fulminant courses (Levinson, 2006).
Nonetheless, WNV transmission through organ donation and transplantation including blood transfusion led for organ and blood donors screening by means of nucleic-acid-based clinical tests (Levinson, 2006). The West Nile Virus Epidemics The New York City encephalitis outbreak in 1999 was ascribed to the virulence of the WNV. In that tragic event, more than 50 cases of infections were reported including the death of five patients as well as the death of crows and other avian species (Levinson, 2006).
By the year 2000, the epidemic reoccurred, which caused 19 cases of viral infections including the death of one patient (Levinson, 2006). It was estimated that in July 2001 that the WNV would have reached New Hampshire, Florida and even Louisiana. In the same year, more than 50 WNV cases were noted including the death of five infected individuals (Levinson, 2006). In the following year, there was a great increase in the number of infected patients, with higher than 4,000 observed cases and 274 deaths as the epidemic invaded Colorado (Levinson, 2006).
The trend continued in 2003 with 7,700 WNV cases including 166 deaths as the virulence found its way toward California (Levinson, 2006). The cases mentioned earlier were considered as the most historical tragic events in the United States brought by a mosquito-borne virus. As estimated, WNV incubation period is around 3–14 days, however, most human WNV contagions were not clinically documented (Loeb et al. , 2008). In fact, the 1999 survey on New York City outbreak revealed that only 20% of the infected individuals were diagnosed by physicians (Gottfried, Quinn, and Jones, 2005).
Likewise, the surveillance prioritized the neurologic disease complications rather than the symptoms of WNV infections. In the previously mentioned outbreaks, the patients’ conditions were described as febrile condition with headache, lymphadenophaty, eye pain, nausea, myalgia, malaise, rashes, vomiting, and anorexia that can last within a week (Loeb et al. , 2008). Similarly, in the New York City 1999 outbreak, the serosurvey showed that headache, myalgia, arthralgia, and fatigue on infected individuals along with flaccid paralysis on 10% of the cases (Gottfried, Quinn, and Jones, 2005).
While the 1999–2000 New York City survey showed a single case of encephalitis or meningitis in 150 infected individuals, the serosurvey in Romania reported that in 140–320 contagions, one infection led to encephalitis or meningitis (Gottfried, Quinn, and Jones, 2005). Moreover, infected individuals with ages of 50 or more years have high risk of neurologic disease severity (Jean, Honarmand, Louie, and Glaser, 2007). It was noted that this observation cannot solely be ascribed to mosquito exposure difference which was in concordance with the 1996 WNV outbreak in Romania (Jean, Honarmand, Louie, and Glaser, 2007).
In the most recent WNV outbreak, anemia, elevation of peripheral leukocyte, hyponatremia, and lymphocytopenia were reported. Pleocytosis was detected through cerebrospinal fluid showing lymphocytes predominance in 0–1782 cells per cubic millimeter of leukocytes (Martin et al. , 2002). Elevated protein concentrations within the range of 51–899 milligram per deciliter were generally noted for all WNV cases as the blood glucose remained normal (Martin et al. , 2002).