For much of 2009 and into 2010 the attention of the world has been captivated by the emergence and spread of the novel influenza A H1N1 virus. Epidemiologic data indicate that an outbreak of influenza-like respiratory illnesses began in La Gloria, Veracruz, Mexico in mid-February, and the virus quickly spread through this country. The first two pediatric cases were confirmed in independent samples in California in April by the Center For Disease Control and Prevention, and the virus quickly began to spread throughout North America and then from country to country across the globe.1 On June 11, 2009, the World Health Organization raised its pandemic alert status for this virus to the highest level: level 6, as efficient and sustained human-to-human transmission was occurring. As of December 2, 2009, the influenza A (H1N1) pandemic virus has been responsible for 99% of influenza in the United States during the 2009–2010 influenza season.
The influenza A H1N1 virus contains gene segments not previously identified in combination in humans or animals. The genetic composition of this virus demonstrates that it arose from a reassortment of avian/human/swine triple reassortant viruses with Eurasian avian-like swine viruses.2 Monovalent inactivated and live attenuated vaccines to the 2009 H1N1 became available in October. A recent study has reported that a single 15 μg dose of the inactivated vaccine to be immunogenic and well tolerated in infants and children starting at 6 months of age.3 However, these vaccines are not expected to provide protection against seasonal influenza, nor is the seasonal vaccine for the 2009–2010 season expected to protect against 2009 influenza A H1N1.
To date, the vast majority of the 2009 H1N1 tested for drug resistance have been susceptible to the neuraminidase inhibitors oseltamivir and zanamivir, but resistant to the adamantanes amantadine and rimantadine. However, resistance to oseltamivir has been reported.4-6 Treatment with a neuraminidase inhibitor is most effective if started within the first 48 hours of symptoms and should be started empirically as early as possible even before a definitive diagnosis is made.7 In critically ill patients, the use of these agents should not be withheld in those experiencing symptoms for greater than 48 hours as some may still benefit from their use.7 Unfortunately, the rapid diagnosis of 2009 H1N1 has been hampered by the low sensitivity of rapid influenza diagnostic tests to this virus. In addition, false negatives are common, and definitive diagnosis for 2009 H1N1 relies on either viral culture or real-time reverse transcriptase PCR.7
Although most cases of influenza due to 2009 H1N1 have been mild, information on the clinical spectrum and risk factors for more severe disease requiring hospitalization or intensive care are emerging. In a statewide surveillance of California residents, between April 23 and August 11, 2009, who were hospitalized or died with laboratory results indicating infection with 2009 influenza A H1N1 virus, 32% were less than 18 years old.8 The overall hospitalization rate and/or fatality rate was 2.8 per 100,000, but was 11.9 in ...