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Workshop Overview1

THE DOMESTIC AND INTERNATIONAL IMPACTS OF THE 2009-H1N1 INFLUENZA A PANDEMIC: GLOBAL CHALLENGES, GLOBAL SOLUTIONS

In March and early April 2009, a new, swine-origin 2009-H1N1 influenza A virus (S-OIV)2 emerged in Mexico and the United States. During the first few weeks of surveillance, the virus spread by human-to-human transmission worldwide to over 30 countries, causing the World Heath Organization (WHO) to raise its pandemic alert level to Phase 5 of 6. On June 11, 2009, the WHO raised the worldwide pandemic alert level to Phase 6 in response to the sustained global spread of the 2009-H1N1 influenza A virus. President Obama, on October 24, 2009, signed an official proclamation declaring the 2009-H1N1 influenza A swine flu outbreak a national emergency in the United States (The White House, 2009). This declaration does “hereby find and proclaim that, given that the rapid increase in illness across the Nation may overburden health care resources and that the temporary waiver of certain standard Federal requirements may be warranted in order to enable U.S. health care facilities to implement emergency operations plans, the 2009 H1N1 influenza pandemic in the United States constitutes a national emergency.”

1

The Forum’s role was limited to planning the workshop, and this workshop summary has been prepared by the workshop rapporteurs as a factual summary of what occurred at the workshop.

2

While this pandemic H1N1 strain of influenza A virus has gone by many, many names—including “swine flu”—since it was first recognized and characterized in April 2009, for the purposes of this document we refer to it using the nomenclature found in the Report to the President on the U.S. Preparations for 2009-H1N1 Influenza (PCAST, 2009).



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Workshop Overview1 THE DOMESTIC AND INTERNATIONAL IMPACTS OF THE 2009-H1N1 INFLUENZA A PANDEMIC: GLOBAL CHALLENGES, GLOBAL SOLUTIONS In March and early April 2009, a new, swine-origin 2009-H1N1 influenza A virus (S-OIV)2 emerged in Mexico and the United States. During the first few weeks of surveillance, the virus spread by human-to-human transmission world- wide to over 30 countries, causing the World Heath Organization (WHO) to raise its pandemic alert level to Phase 5 of 6. On June 11, 2009, the WHO raised the worldwide pandemic alert level to Phase 6 in response to the sustained global spread of the 2009-H1N1 influenza A virus. President Obama, on October 24, 2009, signed an official proclamation declaring the 2009-H1N1 influenza A swine flu outbreak a national emergency in the United States (The White House, 2009). This declaration does “hereby find and proclaim that, given that the rapid increase in illness across the Nation may overburden health care resources and that the temporary waiver of certain standard Federal requirements may be warranted in order to enable U.S. health care facilities to implement emergency operations plans, the 2009 H1N1 influenza pandemic in the United States constitutes a national emergency.” 1 The Forum’s role was limited to planning the workshop, and this workshop summary has been prepared by the workshop rapporteurs as a factual summary of what occurred at the workshop. 2 While this pandemic H1N1 strain of influenza A virus has gone by many, many names—including “swine flu”—since it was first recognized and characterized in April 2009, for the purposes of this document we refer to it using the nomenclature found in the Report to the President on the U.S. Preparations for 2009-H1N1 Influenza (PCAST, 2009). 1

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2 IMPACTS OF THE 2009-H1N1 INFLUENZA A PANDEMIC This novel, swine-origin, influenza A virus has now become the first pan- demic of the twenty-first century. The international scientific, public health, secu- rity, and policy communities quickly mobilized to characterize the novel virus (hereinafter 2009-H1N1 influenza A) and address its potential effects. Within six months of the discovery of the 2009-H1N1 influenza A virus, researchers had gained considerable knowledge about the latest pandemic influenza virus and produced a vaccine against it, but many scientific and policy questions raised by the 2009-H1N1 influenza A virus remained to be answered. The arrival of an influenza pandemic in 2009 was both anticipated and unexpected. That a novel, readily transmissible, influenza virus would spread widely and rapidly along with its globe-trotting hosts seemed inevitable; that this pandemic strain emerged in the Americas, rather than Asia, surprised many infectious disease experts. “We have all been preparing for a pandemic,” veteran flu researcher Robert Webster of St. Jude Children’s Research Hospital remarked recently (Webster, 2009). “H5N1 [Avian influenza] has been at the top of our list and surprise, surprise, 2009-H1N1 influenza A came out of left field.” In the months since the initial identification of the 2009-H1N1 influenza A virus, the disease has now spread to over 213 countries and territories while scientists, healthcare providers, policy makers, the media, and the general public attempted to anticipate, and mitigate, the myriad potential consequences of the evolving pandemic. Studies of the evolution of influenza viruses attest to their essential unpredictability, but knowledge gathered during the recent influenza season in the Southern Hemisphere can inform strategies to address the expected resurgence of 2009-H1N1 influenza A with winter’s return to the Northern Hemi- sphere. This effort will also be advanced by the ongoing evaluations of public health capacities to address current and future challenges presented by this pan- demic, its economic repercussions, and its sociopolitical effects. In the recent past, the Institute of Medicine’s (IOM’s) Forum on Microbial Threats has convened several workshops focused on pandemic disease emer- gence, spread, and response. The first followed the emergence of severe acute respiratory syndrome (SARS) in 2003 (IOM, 2004); others considered the poten- tial global threat posed by H5N1 influenza virus (IOM, 2004, 2005, 2007a,b) and the dynamics of infectious disease transmission in a highly interconnected world (IOM, 2010). Within months of its declaration as the first pandemic of the twenty-first century, the Forum convened a 2-day public workshop, on Sep- tember 15th and 16th, 2009, to discuss the domestic and international impacts of, and responses to, the 2009-H1N1 influenza A pandemic. Through invited presentations and discussions, participants explored the origins, evolution, and epidemiology of the 2009-H1N1 influenza A virus; potential lessons learned from 2009-H1N1 influenza A infection patterns in the Southern Hemisphere; the role of disease detection, surveillance, and reporting in mapping and anticipating disease spread and evaluating the effects of mitigation measures; progress toward and prospects for vaccine and drug development and availability; considerations

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3 WORKSHOP OVERVIEW for the use of nonpharmaceutical interventions to reduce 2009-H1N1 influenza A transmission; and the global public health responses to the pandemic as it continues to unfold. Organization of the Workshop Summary This workshop summary was prepared by the rapporteurs for the Forum’s members and includes a collection of individually authored papers and com- mentary. Sections of the workshop summary not specifically attributed to an individual reflect the views of the rapporteurs and not those of the Forum on Microbial Threats, its sponsors, or the IOM. The contents of the unattributed sections are based on the presentations and discussions at the workshop. The workshop summary is organized into sections as a topic-by-topic description of the presentations and discussions that took place at the workshop. Its purpose is to present lessons from relevant experience, to delineate a range of pivotal issues and their respective problems, and to offer potential responses as discussed and described by the workshop participants. Manuscripts and reprinted articles, submitted by some but not all of the workshop’s participants, may be found in Appendixes A1 through A14. Although this workshop summary provides an account of the individual presentations, it also reflects an important aspect of the Forum’s philosophy. The workshop functions as a dialogue among representatives from different sectors of the infectious disease communities and allows them to present their beliefs about which areas may merit further attention. These proceedings summarize only the statements of participants in the workshop and are not intended to be an exhaus- tive exploration of the subject matter or represent the findings, conclusions, or recommendations of a consensus committee process. 2009-H1N1 Influenza A in Context This workshop took place amid broad-based, global efforts to characterize the 2009-H1N1 influenza A virus, determine its evolutionary origins, and evaluate its potential public health and socioeconomic consequences, while monitoring and mitigating the impact of a fast-moving pandemic. The presentations summarized in this report, and the original contributions by the speakers collected in Appendix A, offer a snapshot of these activities taken in the late summer of 2009, as the Northern Hemisphere’s flu season approached and as the United States prepared to undertake a campaign of mass immunization against 2009-H1N1 influenza A. What Is Influenza? The influenza viruses are members of the family Orthomyxoviridae and include influenza virus types A, B, and C (see Box WO-1). Influenza is typically

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4 IMPACTS OF THE 2009-H1N1 INFLUENZA A PANDEMIC transmitted from infected mammals through the air by coughs or sneezes, creat- ing aerosols containing the virus, and from infected birds through their drop- pings. Influenza can also be transmitted by saliva, nasal secretions, and feces. Infections occur through contact with these bodily fluids or with contaminated surfaces. Influenza viruses can remain infectious for about one week at human body temperature, for more than 30 days at 0°C (32°F), and indefinitely at very low temperatures (such as lakes in northeast Siberia). They can be inactivated easily by disinfectants and detergents. Box WO-1 provides a general overview of influenza virus classification, structure, and life cycle. For a complete overview on this topic and an extensive reference list please see Treanor (2010). The scientific and public health response to the 2009-H1N1 influenza A pandemic was both informed and influenced by observations of past pandemics and seasonal influenza epidemics, by the response to an abortive pandemic threat from H1N1 swine influenza in 1976, and from ongoing efforts to address the pandemic threat posed by the highly pathogenic H5N1 avian influenza, follow- ing its emergence in humans in 1997. In this section, we review these events in order to establish the 2009-H1N1 influenza A pandemic within a historic and scientific context. Ten apparent influenza pandemics, five of which occurred during the nine- teenth century, have been recorded over the past 300 years. The three twentieth- century pandemics—presented in Table WO-1—which began in 1918, 1957, and 1968, respectively, are known to have been caused by three different anti- genic subtypes3 of the influenza A virus, denoted H1N1, H2N2, and H3N2 in order of their emergence (Morens et al., 2009). While these pandemics varied widely in terms of their geographic origins and epidemiological characteristics, all gave warnings of their arrival, featured significant increases in mortality among younger age groups (a phenomenon known as “pandemic age shift”), and continued to cause morbidity and mortality months to years beyond their peaks (Simonsen et al., 2005) as will be discussed in greater detail, below. 1918–1919: “Mother of All Pandemics” Beginning in the spring of 1918, the H1N1 influenza virus that infected approximately one-third of the world’s population was exceptionally virulent (IOM, 2005; Taubenberger and Morens, 2006). It caused an estimated 50–100 million deaths, with a case-fatality rate of greater than 2.5 percent (compared with less 3 Every influenza A virus has a gene coding for 1 of 16 possible hemagglutinin (HA) surface proteins and another gene coding for 1 of 9 possible neuraminidase (NA) surface proteins. HA facilitates viral attachment to host tissues; NA is involved in the release of viral progeny from the host. Of the 144 possible combinations of H and N genes, only 3 (H1N1, H2N2, and H3N2) have ever been found in truly human-adapted viruses (Morens et al., 2009).

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5 WORKSHOP OVERVIEW than 0.1 percent for other pandemic strains). As Morens et al. (2009) point out, all influenza pandemics since that time, and indeed most cases of influenza A world- wide (other than human infections from avian viruses such as H5N1 and H7N7), have been caused by descendants of the 1918 virus, as illustrated in Figure WO-2. These include the H2N2 (1957) and H3N2 (1968) viruses, which possessed key genes from the 1918 virus along with additional avian influenza genes. Hence, the 1918 H1N1 virus is truly the “mother” of all influenza pandemics. In the spring of 1918, a “herald wave” of relatively mild influenza cases occurred in New York City. That fall, a second wave of severe disease (and in many places, a subsequent wave in early 1919) produced significantly higher rates of mortality among people between the ages of 20 and 34, and particu- larly among pregnant women, than is typical of seasonal influenza epidemics (Simonsen et al., 2005). Two conditions tended to occur (both individually and in combination) in these fatal H1N1 cases: bronchopneumonia, likely caused by a secondary bacterial infection, and severe acute respiratory distress, often leading to cyanosis (CIDRAP, 2009). Despite its depiction as the “Spanish flu,”4 the geographic origin of the 1918 H1N1 strain of the influenza virus remains a mystery (CIDRAP, 2009). It is likely that the virus, which had previously infected birds, emerged as a human pathogen in the Midwestern United States and accompanied American troops to Europe during World War I. Some investigators believe that the avian virus jumped into swine at approximately the same time it began to infect humans (Morens et al., 2009; Zimmer and Burke, 2009). Others contend, based on viral phylogeny, that genetic components of the 1918 pandemic strain circulated among swine and humans as early as 1911, which in turn suggests that the pandemic virus was generated by reassortment over a period of years and not introduced directly from birds into humans (Smith et al., 2009). Swine are believed to act as a “mixing vessel” for the reassortment of avian and human viruses (Salomon and Webster, 2009). As noted earlier, such events in doubly infected pigs generated the 1957 and 1968 pandemic influenza strains. 1957: A Model for 2009? Between 1957 and 1958, an estimated 25 percent of the U.S. population was infected with pandemic H2N2 influenza, resulting in nearly 70,000 fatalities out of an estimated 1 million deaths worldwide (CIDRAP, 2009; Henderson et 4 “America in 1918 was a nation at war. Draft call-ups, bond drives, troop shipments were all in high gear when the flu epidemic appeared. American soldiers from Fort Riley carried the disease to the trenches of Europe, where it mutated into a killer virus. The disease would later be dubbed, inac- curately, Spanish influenza. Spain had suffered from a devastating outbreak of influenza in May and June of 1918. The country, being a non-combatant in the war, did not censor news of the epidemic that was cutting through its population and was therefore incorrectly identified as its place of origin” (PBS, 2009).

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6 IMPACTS OF THE 2009-H1N1 INFLUENZA A PANDEMIC BOX WO-1 The Influenza Life Cyclea The Orthomyxoviridae are a family of single-stranded RNA viruses that i ncludes five genera: Influenza virus A, Influenza virus B, Influenza virus C, savirus, I and Thogotovirus. A sixth has recently been described (Presti et al., 2009). The first genus contains viruses that cause influenza in vertebrates, including birds, humans, and other mammals. Influenza B and C viruses circulate in humans. Isaviruses infect salmon; thogotoviruses infect both vertebrates and invertebrates such as ticks (Ely, 1999; Jones and Nuttall, 1989; Raynard et al., 2001). Viral Replication Viruses can only replicate in living cells. Influenza infection and replication is a multistep process: the virus must first bind to and enter the cell, then deliver its genome to a site where it can produce new copies of viral proteins and RNA, as- semble these components into new viral particles, and finally exit the host cell. Influenza viruses infect epithelial cells of the respiratory tract by attaching to sialic acid receptors. The virus particle contains a genome consisting of eight single stranded, negative sense RNA genes surrounded by viral proteins and a host-derived lipid membrane. The surface of the virus particle contains spikes of hemagglutinin (HA) that are responsible for attachment of virions to the cell surface. The HA binds to sialic acid receptors located at the tip of glycan chains conjugated to host cell membrane proteins and lipids (stage 1 in Figure WO-1)— typically in the nose, throat, and lungs of mammals and in the intestines of birds. Multivalent binding of the virus particle to the cell triggers uptake by endocytosis and subsequent fusion of the viral envelope to the endosome membrane, deliver- ing the genome into the host cell cytoplasm. Once inside the cell, the acidic conditions in the endosome cause two events to happen: first part of the HA protein fuses the viral envelope with the vacuole’s membrane, then the M2 ion channel allows protons to move through the viral envelope and acidify the core of the virus, which causes the core to disassemble and release the viral RNA and core proteins. The viral RNA (vRNA) molecules, accessory proteins, and RNA-dependent RNA polymerase are then released into the cytoplasm (stage 2). The M2 ion channel is blocked by amantadine drugs, preventing infection. These core proteins and vRNA form a complex that is transported into the cell nucleus, where the RNA-dependent RNA polymerase begins transcribing complementary positive-sense vRNA (stages 3a and 3b). The vRNA is either exported into the cytoplasm and translated (stage 4) or remains in the nucleus. Newly synthesised viral proteins are either secreted through the Golgi apparatus onto the cell surface (in the case of neuraminidase and hemagglutinin, stage 5b) or transported back into the nucleus to bind vRNA and form new viral genome particles (stage 5a). Other viral proteins have multiple actions in the host cell, a or a complete overview on this topic and an extensive reference list please see Treanor F (2010) and Wikipedia (2009).

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7 WORKSHOP OVERVIEW including degrading cellular mRNA and using the released nucleotides for vRNA synthesis and also inhibiting translation of host cell mRNAs. Negative-sense vRNAs that form the genomes of future viruses, RNA- d ependent RNA polymerase, and other viral proteins are assembled into a virion. HA and neuraminidase molecules cluster into a bulge in the cell membrane. The vRNA and viral core proteins leave the nucleus and enter this membrane protrusion (stage 6). The mature virus buds off from the cell in a sphere of host phospholipid membrane, acquiring HA and neuraminidase with this membrane coat (stage 7). As before, the viruses adhere to the cell through hemagglutinin; the mature viruses detach once their neuraminidase has cleaved sialic acid residues from the host cell. Drugs that inhibit neuraminidase, such as oseltamivir, therefore prevent the release of new infectious viruses and halt viral replication. After the release of new influenza viruses, the host cell dies (Figure WO-1). Virion Nucleus Transcription Translation Splicing mRNAs Ribosomes RNA Golgi Replication Apparatus Cell Figure WO-1 FIGURE WO-1 Host cell invasion and replication by the influenza virus. The R01627 steps in this process are discussed in the text. bitmapped image SOURCE: Wikipedia (2007 [figure], 2009 [text]). type replaced

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8 IMPACTS OF THE 2009-H1N1 INFLUENZA A PANDEMIC TABLE WO-1 Mortality Associated with Influenza Pandemics and Selected Seasonal Epidemic Events, 1918-2009a Excess Deaths from Any Cause (no. per Years Circulating Virus (genetic mechanism) 100,000 persons/yr) 1918-1919 H1N1 (viral introduction), pandemic 598.0 1928-1929 H1N1 (drift) 96.7 1934-1936 H1N1 (drift) 52.0 1947-1948 H1N1 A′ (intrasubtypic reassortment) 8.9 1951-1953 H1N1 (intrasubtypic reassortment) 34.1 1957-1958 H2N2 (antigenic shift), pandemic 40.6 1968-1969 H3N2 (antigenic shift), pandemic 16.9 1972-1973 H3N2 A Port Chalmers (drift) 11.8 1975-1976 H3N2 (drift) and H1N1 (“swine flu” outbreak) 12.4 1977-1978 H3N2 (drift) and H1N1 (viral return) 21.0 1997-1999 H3N2 A Sydney (intrasubtypic reassortment) and 49.5 H1N1 (drift) 2003-2004 H3N2 A Fujian (intrasubtypic reassortment) and 17.1 H1N1 (drift) 2009 H3N2 and H1N1 (drift) and swine-origin H1N1 ? (viral introduction), pandemic aMortality data include deaths associated with all influenza A and B viruses combined. Many of these data have been calculated with the use of differing methods and may not be strictly comparable (Noble, 1982; Thompson et al., 2003). The 1934, 1951, and 1997 data span 2 years. SOURCE: Reprinted with permission from Morens et al. (2009). Copyright © 2009 Massachusetts Medical Society. All rights reserved. al., 2009). Once again, influenza morbidity and mortality were skewed toward younger people (ages 5 to 35) compared with nonpandemic years. The first U.S. cases of what became known as the “Asian flu,” reported in June 1957, followed outbreaks on military bases in Korea and Japan in April and May of that year (Henderson et al., 2009). Throughout the summer of 1957, outbreaks of mild ill- ness occurred throughout the United States in conference centers, summer camps, migrant workers’ barracks, and other such institutional settings. Although these local outbreaks were characterized by attack rates that in some cases exceeded 50 percent, little community-wide transmission appeared until schools reopened in the Fall. Beginning in mid-September, an epidemic wave of influenza swept U.S. communities (Henderson et al., 2009). Vaccine (which was no more than 60 per- cent effective against the virus) became available in limited supply in October, but

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9 WORKSHOP OVERVIEW FIGURE WO-2 Genetic relationships among human and relevant swine influenza viruses, 1918–2009. Yellow arrows reflect exportation of one or more genes from the avian influ- enza A virus gene pool. The dashed red arrow indicates a period without circulation. Solid red arrows indicate the evolutionary paths of human influenza virus lineages; solid blue arrows, of swine influenza virus lineages; andWO-2 Figure the blue-to-red arrow, of a swine-origin R01627 human influenza virus. All influenza A viruses contain eight genes that encode the follow- ing proteins (shown from top to bottom within each virus): polymerase PB2, polymerase uneditable bitmapped image neuraminidase (NA), PB1, polymerase PA, hemagglutinin (HA), nuclear protein (NP), matrix proteins (M), and nonstructural proteins (NS). The genes of the 1918 human and swine H1N1 and the 1979 H1N1 influenza A viruses were all recently descended from avian influenza A genes, and some have been “donated” to the pandemic human H1N1 strain. SOURCE: Reprinted with permission from Morens et al. (2009). Copyright © 2009 Massachusetts Medical Society. All rights reserved.

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10 IMPACTS OF THE 2009-H1N1 INFLUENZA A PANDEMIC it was too little, too late to slow the progression of the epidemic across the United States. By mid-November, numbers of new cases and deaths from influenza and pneumonia had leveled off and begun to decline. Following a return to normal levels in December, a second wave of excess mortality due to respiratory illness began in January 1958 and peaked the following month. Henderson et al. (2009) note several similarities in epidemiologic behavior between the 1957 H2N2 pandemic and the 2009 H1N1 pandemic: both arose early in the year and spread widely during the spring, both abated over the early summer months in the Northern Hemisphere while major epidemics developed in the Southern Hemisphere (as is also typical of seasonal influenza), and both (to date) were marked by relatively mild illness with low case-fatality rates. 1968 (United States) and 1969 (Europe) Pandemic H3N2 emerged in Hong Kong in 1968 and spread rapidly across the globe. During the winter of 1968-1969, the virus caused an estimated 40,000 deaths in the United States, but in Europe, it inexplicably smoldered until the following winter before causing significant morbidity and mortality (Simonsen et al., 2005). That this pandemic was the least deadly of the three twentieth-century pandemics may be due to the fact that only the H antigen in H3N2 had “shifted” with respect to the previous pandemic H2N2 strain. In people born before 1891, the presence of H3 antibodies may have also afforded this otherwise vulnerable population some degree of protective immunity against the H3N2 influenza A virus. In the United States, people between the ages of 45 to 64 were shown to have a threefold higher risk of death from pandemic H3N2 than from epidemic influenza during the years prior to and following the pandemic (Simonsen et al., 2005). 1976 Swine Flu: The Pandemic that Wasn’t Early in 1976, an outbreak of swine-origin influenza among military personnel at Fort Dix, New Jersey, resulted in 13 confirmed cases, including one death (CIDRAP, 2009). Serologic studies suggested that more than 200 soldiers had been infected with an H1N1 virus and that person-to-person transmission had occurred (Sencer and Millar, 2006). The outbreak, however, never spread beyond Fort Dix. Its origin remains unknown (CIDRAP, 2009). The major events in the swine flu vaccination campaign, adapted from Neustadt and Feinberg (1978), are presented in Box WO-2. Similarities between the 1976 H1N1 virus and the 1918 H1N1 pandemic strain prompted concern that a similarly devastating pandemic was imminent, recalled keynote speaker David Sencer, who in 1976 was the director of the Centers for Disease Control (CDC). He reviewed the process by which the decision was made to start a mass vaccination program to protect the American public from

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11 WORKSHOP OVERVIEW BOX WO-2 The 1976 Swine Flu Campaign: Chronology of Major Events 1976 • id-January: Large number of cases of respiratory disease are reported M among Army recruits at Fort Dix, New Jersey; Walter Reed Army Laboratory identifies adenovirus as cause of earlier outbreak of respiratory disease at Fort Meade, Maryland. • ebruary 13: Scientists at CDC confirm that the isolates are indeed swine-type F influenza A viruses; at Sencer’s request, Dr. Walter Dowdle, head of CDC’s labs, notifies scientists and health officials across the country of the A swine discovery, and invites them to a meeting at CDC the next day. • arch 24: President goes before television cameras to announce that he is M recommending a mass vaccination program for all Americans and urges that Congress immediately pass a special $135 million appropriation. • October 1: First swine flu shots given. • November 12: Case of Guillain-Barré Syndrome in Minnesota vaccinee. • ecember 16: Sencer conducts morning conference call, his third in four D days, with 20 experts from NIAID, BoB [Bureau of Biologics] and the states, conferees agree on recommendation of a one month suspension to allow for investigation of link; Sencer calls Cooper with the recommendation; Coo- per confers with Mathews and Cavanaugh; telephones Salk; President okays suspension. 1977 • anuary 14: ACIP meets in Atlanta and concludes that the moratorium on all J influenza vaccine ought to be lifted; observes that flu shots do appear to entail some slight additional risk of contracting Guillain-Barré (estimated at one case for every 100,000 to 200,000 vaccinations); recommends that main focus of resumed program should be on high risk group. SOURCE: Adapted with permission from Neustadt and Fineberg (1978). this apparent threat, and then—amid political wrangling and media scrutiny—to suspend that program less than three months later in order to investigate a pos- sible serious side-effect of the vaccine (see Sencer and Millar in Appendix A11). Sencer said that the intention of his remarks was to highlight “what went right” in this series of events that is often referred to as a “fiasco” or “debacle” (Neustadt and Fineberg, 1978).

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84 IMPACTS OF THE 2009-H1N1 INFLUENZA A PANDEMIC between the hospitals and the public health department, he said. “We were at least able to help the hospitals manage their scarce resources by loaning to one another, and they were coordinated with the public health response,” Duchin concluded. He also described Tamiflu® clinics and a call center as particularly useful ele- ments of the public health response. In New York City, Fine reported that, based on their experience during the spring, the public health department modified several aspects of their surge strat- egy in order to better manage the anticipated return of 2009-H1N1 influenza A in the fall of 2009. The New York City Department of Health and Mental Hygiene (NYCDOH) would not conduct case-based surveillance but would, instead, con- tinue syndromic surveillance; monitor trends in overall incidence, clinical and epidemiological risk factors, and pathogens; conduct monthly population surveys by telephone; use sentinel hospitals and a primary care network for limited inten- sive in-patient surveillance; and match laboratory-confirmed cases with registered deaths to determine the number of confirmed influenza deaths. After hospitals coped with a series of problems not anticipated in their surge plans, her department instituted a series of changes, Fine said. They have reviewed all hospital surge plans and have provided hospitals with guidance on suggested practices in addressing the resurgence of 2009-H1N1 influenza A. After localized shortages occurred during the spring wave, antiviral medications have been made more accessible. Hospitals were requested to activate their incident command systems in mid-September, as schools returned to session. Protocols for using Medical Reserve Corps volunteers remained under consideration but could involve training and preselecting volunteers to work if needed. To ease pressure on EDs, New York City has established about 100 flu diag- nostic and treatment centers that will treat all patients, regardless of their usual source of care or insurance status, Fine said. The clinics will be open evenings and weekends, and will offer seasonal and pandemic vaccines as well as anti- virals, should they become unavailable through the commercial sector. Local physicians and health care workers will also receive guidance encouraging them to discuss and prescribe antivirals early for their high-risk patients, in order to ensure access. Based on his experience during the spring wave of the H1N1 influenza pandemic Duchin called for more vigorous efforts to get antivirals to high-risk individuals. “With the sudden rise and the rapid transmission you can’t expect patients to get to their physicians, get diagnosed, get to the pharmacy, and get their drug in the time frame that you really want that to happen,” he asserted. Moreover, he stated, pharmacies do not maintain their stocks, so even if in theory there is no shortage, there are times when antivirals are locally unavailable. “I think we have to be very aggressive about getting the message out that high-risk patients, pregnant women for example, should have Tamiflu® . . . now, not wait until they need it when the outbreak is hitting in the community,” he concluded, adding that he would extend that recommendation to other high-risk people.

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85 WORKSHOP OVERVIEW The tireless efforts demonstrated by Duchin, Fine, and their departments in the face of this pandemic should not obscure the fact that “local public health capacity to respond to H1N1 and other large-scale health emergencies is tenuous and unstable,” as Duchin has observed. Indeed, perhaps the most important lesson learned from the domestic and international public health community’s experi- ences with the 2009-H1N1 influenza A pandemic is, in his words, that “inadequate long-term sustainable funding for both core public health and health emergency preparedness undermines the ability of local communities to adequately prepare for and respond to large scale health emergencies of any type.” WORKSHOP OVERVIEW REFERENCES Andreasen, V., C. Viboud, and L. Simonsen. 2008. Epidemiologic characterization of the 1918 in- fluenza pandemic summer wave in Copenhagen: implications for pandemic control strategies. Journal of Infectious Diseases 197(2):270-278. Australian Government, Department of Health and Aging. 2010. Australian influenza surveillance 2010—latest report, http://www.healthemergency.gov.au/internet/healthemergency/publishing. nsf/Content/ozflucurrent.htm (accessed January 14, 2010). Bertozzi, S., A. Kelso, M. Tashiro, V. Savy, J. Farrar, M. Osterholm, S. Jameel, and C. P. Muller. 2009. Pandemic flu: from the front lines. Nature 461(7260):20-21. Bridges, C. B., W. Lim, J. Hu-Primmer, L. Sims, K. Fukuda, K. H. Mak, T. Rowe, W. W. Thompson, L. Conn, X. Lu, N. J. Cox, and J. M. Katz. 2002. Risk of influenza A (H5N1) infection among poultry workers, Hong Kong, 1997-1998. Journal of Infectious Diseases 185(8):1005-1010. Brownstein, J. S., C. C. Freifeld, and L. C. Madoff. 2009. Digital disease detection—harnessing the Web for public health surveillance. New England Journal of Medicine 360(21):2153-2155, 2157. Buenos Aires Herald. 2009. Nationwide alert: Argentina declares health emergency, flu found in pigs, http://www.buenosairesherald.com/BreakingNews/View/6666 (accessed August 21, 2009). Bustamante, J. 2009. Argentina confirms first H1N1 flu case, http://www.reuters.com/article/ latestCrisis/idUSN07423083 (accessed August 21, 2009). Cauchemez, S., N. M. Ferguson, C. Wachtel, A. Tegnell, G. Saour, B. Duncan, and A. Nicoll. 2009. Closure of schools during an influenza pandemic. Lancet Infectious Diseases 9(8):473-481. CDC (Centers for Disease Control and Prevention). 2009a. CDC guidance for state and local public health officials and school administrators for school (K-12) responses to influenza during the 2009-2010 school year, http://www.cdc.gov/h1n1flu/schools/schoolguidance.htm (accessed November 3, 2009). ———. 2009b. Novel H1N1 flu: facts and figures, http://www.cdc.gov/h1n1flu/surveillanceqa.htm (accessed November 3, 2009). ———. 2009c. Oseltamivir-resistant 2009 pandemic influenza A (H1N1) virus infection in two summer campers receiving prophylaxis—North Carolina, 2009. Morbidity and Mortality Weekly Report 58(35):969-972. ———. 2009d. Serum cross-reactive antibody response to a novel influenza A (H1N1) virus after vaccination with seasonal influenza vaccine. Morbidity and Mortality Weekly Report 58(19):521-524. ———. 2009e. Swine influenza A (H1N1) infection in two children—Southern California, March- April 2009. Morbidity and Mortality Weekly Report 58(15):400-402. ———. 2009f. Update: novel influenza A (H1N1) virus infection—Mexico, March-May, 2009. Morbidity and Mortality Weekly Report 58(21):585-589.

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