To calculate the burden of 2009 pandemic influenza A (pH1N1) in the United States, we extrapolated from the Centers for Disease Control and Prevention's Emerging Infections Program laboratory-confirmed hospitalizations across the entire United States, and then corrected for underreporting. From 12 April 2009 to 10 April 2010, we estimate that approximately 60.8 million cases (range: 43.3-89.3 million), 274,304 hospitalizations (195,086-402,719), and 12,469 deaths (8868-18,306) occurred in the United States due to pH1N1. Eighty-seven percent of deaths occurred in those under 65 years of age with children and working adults having risks of hospitalization and death 4 to 7 times and 8 to 12 times greater, respectively, than estimates of impact due to seasonal influenza covering the years 1976-2001. In our study, adults 65 years of age or older were found to have rates of hospitalization and death that were up to 75% and 81%, respectively, lower than seasonal influenza. These results confirm the necessity of a concerted public health response to pH1N1.
Clostridium diffi cile is a recognized pathogen in neonatal pigs and may contribute to enteritis in calves. Toxinotype V strains have been rare causes of human C. diffi cileassociated disease (CDAD). We examined toxinotype V in human disease, the genetic relationship of animal and human toxinotype V strains, and in vitro toxin production of these strains. From 2001 through 2006, 8 (1.3%) of 620 patient isolates were identifi ed as toxinotype V; before 2001, 7 (<0.02%) of ≈6,000 isolates were identifi ed as toxinotype V. Six (46.2%) of 13 case-patients for whom information was available had community-associated CDAD. Molecular characterization showed a high degree of similarity between human and animal toxinotype V isolates; all contained a 39-bp tcdC deletion and most produced binary toxin. Further study is needed to understand the epidemiology of CDAD caused by toxinotype V C. diffi cile, including the potential of foodborne transmission to humans. R ecent evidence suggests that the epidemiology of Clostridium diffi cile-associated disease (CDAD) is increasing in incidence and severity (1-3). These changes are due, at least in part, to the emergence of a more virulent C. diffi cile strain, designated NAP1 (based on its pulsed-fi eld gel electrophoresis [PFGE] pattern), BI (by restriction endonuclease analysis [REA]), toxinotype III (by PCR characterization of the pathogenicity locus), and 027 (by PCR ribotyping) (4). However, the emergence of BI/NAP1/027 may not be solely responsible for changes in CDAD epidemiology, and the origin of this and other virulent strains is still largely unknown. C. diffi cile has also recently emerged as a pathogen or commensal in food animals such as neonatal pigs and beef and dairy calves (5-7); most of these animal isolates are toxigenic. Although several ribotypes have been identifi ed in calves, the predominant ribotype in both calves and pigs is a toxinotype V strain (8,9). Moreover, recent reports suggest that C. diffi cile strains recognized as causes of human disease may contaminate retail meats (10).To better understand whether food sources could be a source of infection for humans, we investigated recent and past human CDAD caused by toxinotype V C. diffi cile and compared isolates from these cases with those recovered from neonatal pigs and calves. We documented apparent changes in the frequency with which these toxinotype V strains cause human CDAD and compared the molecular characterization and toxin production of these strains with those of recent epidemic (i.e., BI/NAP1/027) and nonepidemic isolates. Materials and Methods Human Case Finding and Defi nitionsCase fi nding was performed by reviewing recent and past human isolates of interest from 2 sources. Cases were defi ned as patients with clinical isolates identifi ed as toxinotype V by analysis of restriction fragment length polymorphisms (RFLPs) of toxin-encoding genes. First, we reviewed 620 C. diffi cile human isolates sent to the Centers for Disease Control and Prevention (CDC) from healthcare facilities and ...
In April 2009, the Centers for Disease Control and Prevention confirmed 2 cases of 2009 pandemic influenza A (H1N1) virus infection in children from southern California, marking the beginning of what would be the first influenza pandemic of the twenty-first century. This report describes the epidemiology of the 2009 H1N1 pandemic in the United States, including characterization of cases, fluctuations of disease burden over the course of a year, the age distribution of illness and severe outcomes, and estimation of the overall burden of disease.
Background Variant influenza virus infections are rare but may have pandemic potential if person-to-person transmission is efficient. We describe the epidemiology of a multistate outbreak of an influenza A(H3N2) variant virus (H3N2v) first identified in 2011. Methods We identified laboratory-confirmed cases of H3N2v and used a standard case report form to characterize illness and exposures. We considered illness to result from person-to-person H3N2v transmission if swine contact was not identified within 4 days prior to illness onset. Results From 9 July to 7 September 2012, we identified 306 cases of H3N2v in 10 states. The median age of all patients was 7 years. Commonly reported signs and symptoms included fever (98%), cough (85%), and fatigue (83%). Sixteen patients (5.2%) were hospitalized, and 1 fatal case was identified. The majority of those infected reported agricultural fair attendance (93%) and/or contact with swine (95%) prior to illness. We identified 15 cases of possible person-to-person transmission of H3N2v. Viruses recovered from patients were 93%–100% identical and similar to viruses recovered from previous cases of H3N2v. All H3N2v viruses examined were susceptible to oseltamivir and zanamivir and resistant to adamantane antiviral medications. Conclusions In a large outbreak of variant influenza, the majority of infected persons reported exposures, suggesting that swine contact at an agricultural fair was a risk for H3N2v infection. We identified limited person-to-person H3N2v virus transmission, but found no evidence of efficient or sustained person-to-person transmission. Fair managers and attendees should be aware of the risk of swine-to-human transmission of influenza viruses in these settings.
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