West Nile virus: 2004 season

March 2004

---Richard F. Jacobs, MD

The 2002 and 2003 seasons of West Nile virus (WNV) neuroinvasive disease and West Nile fever produced a spreading wave of cases in an outbreak distribution across the United States (see map 1).

“There have never been back-to-back domestic flavivirus epidemics in North America. Then, in 2002 and 2003, we have the two largest West Nile encephalitis outbreaks to ever occur … anywhere. We are very concerned that this is going to be an annual event rather than a periodic event,” said Tony Marfin, MD, MPH, acting deputy director of the division of vector-borne infectious diseases at the CDC at a presentation at the 4th Pediatric Infectious Diseases Conference in 2003.

Never before in the United States have we experienced back-to-back years of a confirmed flavivirus outbreak. In 2002, the final number of reported WNV cases was 4,103. This was followed in 2003 by a current estimate of more than 8,717 cases. Not since the outbreak of St. Louis encephalitis in 1975, when 2,000 cases were reported, has the United States seen this number of cases of encephalitis due to a flavivirus. Interestingly, in 1974 (one year prior) and 1976 (one year after the outbreak), there were no cases of St. Louis encephalitis. There was no evidence to indicate a continued outbreak or spread. Over the past 70 years, St. Louis encephalitis has occurred in periodic waves of every 10 to 15 years.

So why is WNV different from other flavivirus infections in the United States?

The beginning of West Nile virus neuroinvasive disease and West Nile fever began on the East Coast in 1999 and spread during the next two years to the Southeast and in 2002 and 2003 through the upper Midwest to include Colorado, Nebraska, the Dakotas and finally to New Mexico and Arizona (see map 2).

At the very end of the 2003 season, Imperial Valley in California identified cases. Although the Northeast has had cases of West Nile virus neuroinvasive disease for each of the past five years, the recent outbreak spread of WNV has now impacted the blood product pool, organ donation programs, and raised questions about breast-feeding and perinatal acquisition. The primary cycle of WNV is in birds and ornithophilic mosquitoes. Humans and mammals are “dead-end” hosts and the cycle persists without humans.

The clinical expression of WNV infections include about 1% of cases as West Nile virus neuroinvasive disease (WNND), about 20% of cases as West Nile fever and about 80% as asymptomatic cases.

Although the 2003 data indicate that the mean age for West Nile virus neuroinvasive disease is 45 years with a range of 15 to 83 years, the inclusion of West Nile virus neuroinvasive disease in the differential diagnosis of cases of meningoencephalitis has already impacted the diagnostic approach of pediatric cases in the summer.

Even though children represented only 7.3% of reported cases of West Nile virus neuroinvasive disease as of Dec. 7, 2003 (1999-2003; 192/2617 total cases of West Nile virus neuroinvasive disease), it emphasized the need to evaluate children with compatible clinical presentations. The age breakdown for these 192 West Nile virus neuroinvasive disease cases from 1999 to 2003 is interesting: age <1 year: 8 (4%), age 1 to 4 years: 18 (9%), age 5 to 13 years: 83 (43%), and age 14 to 17 years: 83 (43%).

There have been no deaths attributable to West Nile neuroinvasive disease in these age groups. However, follow-up information on neurological morbidity is lacking at this time. The neurological presentation has continued to evolve with patients manifesting meningoencephalitis, encephalitis, acute flaccid paralysis, optic neuritis, and/or a parkinsonian-like presentation.

Peak season

For 2002 and 2003, the peak seasonal attack rates have occurred in the summer months with late July to early September accounting for more than 75% of reported cases (see graph). The presentation, death rates and spread of WNV have dramatically increased since 1999 and have manifested in 2002 and 2003 with the presentations listed in the table.

Another significant impact of the WNV outbreaks has been concerns over our blood product pool and organ donation programs. In 2002, there were 233 cases of transfusion-acquired WNV, four cases of organ-acquired WNV, one case linked to breast-feeding, and one transplacental case of WNV. Blood donor surveillance in 2002 identified 16 infectious donors with red blood cells, plasma, stored plasma and platelets confirmed as infected. In 2003, more than 1,000 viremic blood donors were identified. At an FDA meeting in December 2003, regarding blood product safety, Marfin provided these data and the conclusions rendered from that meeting reflected the tremendous advances in screening blood and organ donor products but gave the continued warning that the risk is not yet 0.

Vectors

The transmission of WNV in the western USA has been primarily by the Culex tarsalis mosquito, which is considered the primary vector in 10 states. The Culex pipiens mosquito is considered the primary vector in four states with other Culex species predominant in two other states. The spread to rural areas with a higher burden of disease has been identified through the irrigated lands of the arid west. Culex tarsalis has many attributes that make the concern for ongoing outbreaks significant. It is an important mosquito in irrigated lands, a very efficient transmitter of WNV in the laboratory, a long-distance flyer, feeds equally on birds and humans, and is very hard to control.

With constant irrigation patterns from year to year and the variable climate conditions, the stage is set to make the prediction of ongoing WNV outbreaks.

“Much of the increase may be due to the fact that Culex tarsalis, a mosquito associated with irrigated western lands, is an excellent vector for West Nile virus. It is a species that amplifies the virus well and readily bites humans. The West Nile virus, which had previously been found in Africa, Asia and the Middle East, may have found an excellent niche in the high plains and western states of the United States,” Marfin said.

To project this information on the prospect of WNV for the coming summer season, Marfin offered the following sage advice: “It is never good to be fed on by a blood-sucking insect. People must not be accepting of mosquito bites and should be using personal precautions and behaviors to reduce mosquito bites.”

I am indebted to Dr. Marfin for his time and expertise in preparing this editorial. The summer months are coming and in preparation, mosquito-eradication efforts and education are paramount for what will surely be an interesting meningoencephalitis season. The formula is potentially ominous: many potential bridging mosquitos and many potential amplifying avian species plus an increased role of Culex tarsalis in irrigated lands equals another WNV season.