Apr 1, 2010
West Nile virus at low levels but endemic in US
The incidence of the most serious cases of West Nile virus (WNV) in the United States has fallen to one fourth of what it was in the virus's peak years and one half of what it was just 3 years ago, the Centers for Disease Control and Prevention (CDC) report today in a 10-year summary of surveillance for the disease. WNV, which arrived in the United States in 1999, is a nationally notifiable disease, and the surveillance data included reports from 47 states and Washington, D.C., between 1998 and 2008. (Alaska, Hawaii, and Maine reported no cases in that period.) Overall, there were 28,961 confirmed or probable cases of WNV disease in that decade, and 41% of them, or 11,822, were the invasive form that can cause meningitis, encephalitis, and paralysis. In the disease's worst year, 2002, the rate of neuroinvasive WNV was 1.02 per 100,000 members of the population; that fell to 0.5 in 2006 and 0.23 in 2008. Almost all WNV cases occurred between July and September, and the majority occurred in Plains states and the Rocky Mountains. The low rate of disease in 2008 was surprising to CDC researchers, who had assumed WNV had sunk to an endemic level at around 0.5/100,000 and would remain there. Transmission via blood transfusion remains a rare but consistent risk, despite the development of tests to detect the virus. In 2008, there were 10 cases of WNV transmission via donated blood in which the virus was below detectable levels.
Apr 2 MMWR report
Experimental flu treatment does not increase pneumonia
A recombinant protein being examined for prevention and treatment of influenza appears to protect against secondary bacterial infections despite concerns it might increase lung vulnerability to pneumonia. In a preclinical study published in the Journal of Infectious Diseases, mice experimentally infected with flu virus and pneumococcus and then given the compound DAS181 (Fludase) did not develop pneumococcal pneumonia. In addition, tissues tested in vitro did not show increased colonization by pneumococcus. DAS181 works by inactivating the sialic-acid receptors in lung epithelium to which influenza virus adheres. Its desialylation activity had previously raised concerns that it would render lung epithelium more vulnerable to pneumococcal colonization and thus to the secondary bacterial pneumonias known to occur after flu.
Apr 1 J Infect Dis abstract