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SUPPLEMENT ARTICLE
Epidemiology of 2009 Pandemic Influenza A
(H1N1) in the United StatesMichael A. Jhung,
1David Swerdlow,
2Sonja J. Olsen,
3Daniel Jernigan,
1Matthew Biggerstaff,
1Laurie Kamimoto,
1Krista Kniss,
1Carrie Reed, Alicia Fry,
1Lynnette Brammer,
1Jacqueline Gindler, William J. Gregg,
1Joseph Bresee,
1 and Lyn Finelli 1 1Influenza Division;2
National Center for Immunization and Respiratory Diseases, Office of the Director, and 3Division of Emerging Infections and
Surveillance Services, Centers for Disease Control and Prevention, Atlanta, GeorgiaIn 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.
On 15 April 2009, the first case of 2009 pandemic in- fluenza A (H1N1) (pH1N1) virus infection in the United States was identified in a 10-year-old boy in southern California; 2 days later, a second case of in- fection with the same virus was confirmed in a 9-year- old girl in an adjacent county in California [1]. During the subsequent 2 weeks, additional cases of infection with this new virus were detected in Mexico, California,Texas, and other states [2, 3].
The pH1N1 influenza virus contained a combination
(HA) gene, which codes for an important viral surface antigen, was most closely related to the HA found inAmerican swine. The pH1N1 HA had evolved from the
isthoughttohaveenteredhumanandswinepopulationsat about the same time, but to have evolved into distinct
lineages in pigs and in humans [1]. Early serologic data suggested, consistent with the evolutionary origin of the HA, that many older adults had some cross-reactive immunity to the pH1N1 HA due to prior infection with antigenically related strains [4]. Children and most young adults, however, were immunologically naive. The 2009 pandemic virus quickly spread globally, and on 11 June 2009, the World Health Organization (WHO) declared the first influenza pandemic since1968-1969 [5]. As of April 2010, laboratory-confirmed
infections with pH1N1 influenza virus have been iden- tified in 212 countries and overseas territories, and .15,000 laboratory-confirmed deaths have been re- ported to the WHO worldwide [6]. In this report, we summarize the epidemiology of pH1N1 influenza in the United States, including timing of the outbreak, geo- graphic distribution, characteristics of cases, and epi- demiologic parameters, such as attack rates, generation time, and reproductive rate.TEMPORAL AND GEOGRAPHIC
PATTERNS OF DISEASE
In the United States, the pandemic was characterized by2 distinct waves (Figure 1), with lower levels of activity
that persisted between waves and through the end of April 2010. The first wave began in April 2009 with the The findings and conclusions in this report are those of the authors and do not necessarily represent the official position of the Centers for Disease Control andPrevention.
Correspondence: Michael A. Jhung, M.D., 1600 Clifton Rd, MS-A32, Atlanta, GA30333 (mjhung@cdc.gov).
Clinical Infectious Diseases 2011;52(S1):S13-S26
Published by Oxford University Press on behalf of the Infectious DiseasesSociety of America 2011.
1058-4838/2011/52S1-0001$37.00
DOI: 10.1093/cid/ciq0082009 Pandemic H1N1 EpidemiologydCID 2011:52 (Suppl 1)dS13Downloaded from https://academic.oup.com/cid/article/52/suppl_1/S13/498323 by guest on 18 May 2023
identification of the first US cases. Within 1 week, 10 cases had been confirmed in 3 states, and investigations of probable cases were underway in 6 additional states [2]. This first wave peaked during June 2009, and by August influenza activity levels had decreased substantially in most states, although activity was sustained throughout the summer months at levels substantially above what is normally seen during the summer for seasonal influenza [8]. Although pH1N1 infections were observed in all US statesduring the first wave, the largest numbers of cases were reported from California, Connecticut, Florida, Hawaii, Illinois, Texas, New Jersey, New York, Pennsylvania, and Wisconsin (Figure 2a) and were largely confined to major cities within states(differences in the number ofcasesreportedtothe Centers for Disease Control and Prevention (CDC) among states were partly due to differences in state testing and reporting practices). Alaska, Connecticut, Delaware, Hawaii, Illinois, Massachusetts, Texas, Utah, Wisconsin, and Wyoming reported the highest rates of infection during the first wave (Figure 2b). In addition, outbreaks of disease among children attending summer camps were widely reported [9], and many camps that primarily served children with chronic medical conditions were cancelled. The second pandemic wave began in the Southeastern United States as children returned to school in mid-August and early Sep- tember. Over the following 2 months, disease became geo- graphically widespread throughout the United States. Illness occurring during this fall wave ultimately accounted for the majority of US cases seen during the pandemic. The fallwave peaked in late October, and since that time, althoughcirculation of pH1N1 virus has continued, influenza activity has
decreased and remained below what is expected in the winter months [8]. The geographic spread of pH1N1 virus and the timing of the 2 pandemic waves can be visualized using national out- patient illness data. The US Outpatient Influenza-Like-Illness (ILI) Surveillance Network (ILINet) is a system of.3000 sentinel health care providers who report the weekly per- centage of outpatient visits for ILI to CDC [10]. ILI is defined as temperature.37.8?C accompanied by cough or sore throat in the absence of other known causes. ILI surveillance correlates well with the number of weekly positive influenza test results and has historically been used to monitorinfluenza activity (CDC, unpublished data). To facilitate smaller scale visualization of national ILINet data, the CDC and colleagues at the Johns Hopkins AppliedPhysics Lab (Baltimore, MD) derived threshold statistics describing influenza activity at a core-based statistical area (CBSA) geographic level. This meth- odology allowed assessment of CBSA-specific influenza activity, measured by the number of standard deviations (SDs) above a weighted mean baseline of ILINet provider ratios within each CBSA (CDC, unpublished data). During the peak of the spring wave, ILI activity was predominately focal (Figure 3, Map 1), and this focal pattern continued throughout the summer and the beginning of the fall wave (Figure 3, Map 2). By mid- September, activity was widespread throughout the Southeastern United States, and by October 2009, during the peak of the second wave, ILI activity was widespread throughout the UnitedFigure 1.Number of pH1N1 viral isolates tested by week and overall percent positive for all influenza, reported to the Centers for Disease Control and
Prevention by World Health Organization/National Respiratory and Enteric Virus Surveillance System laboratories from April 2009 through March 2010 in
the United States [7].S14dCID 2011:52 (Suppl 1)dJhung et al.Downloaded from https://academic.oup.com/cid/article/52/suppl_1/S13/498323 by guest on 18 May 2023
States (Figure 3, Map 3). By February 2010, ILI activity had once again become focal (Figure 3, Map 4). By March 2010, influenzaactivity had decreased to the lowest levels measured during thepandemic in most states; however, elevated activity persisted
briefly in the Southeastern United States before also decreasing by April 2010 in that region [11].Figure 2. a)pH1N1 influenza infections, number of cases by state-United States, 15 April-23 July 2009.b)pH1N1 influenza infections, rate of cases
by state-United States, 15 April-23 July 2009.2009 Pandemic H1N1 EpidemiologydCID 2011:52 (Suppl 1)dS15Downloaded from https://academic.oup.com/cid/article/52/suppl_1/S13/498323 by guest on 18 May 2023
CHARACTERISTICS OF pH1N1 INFLUENZA
CASES When the pH1N1 outbreak was first detected in April 2009, the CDC worked with state and local health departments to collect and analyze information describing early cases. From 15 April through 16 June 2009, individual laboratory-confirmed cases were reported [12, 13], and from 17 June through 23 July 2009, aggregate data on cases, hospitalizations, and deaths in 5 age groups (0-4 years, 5-24 years, 25-49 years, 50-64 years, and >65 years) were collected [14, 15]. From 15 April through 23 July 2009, there were a total of 43,771 laboratory-confirmed cases reported. Case reports accelerated quickly in the early weeks of the pandemic, peaked at.6000 cases per week in late June and early July, and decreased to 3000 cases per weekin late July, after which time individual case reportingwas discontinued and aggregate reporting was initiated for
laboratory-confirmed hospitalizations and deaths only (Figure