The 1986-87 influenza epidemic was caused by influenza A(H1N1) viruses resembling A/Taiwan/1/86(H1N1), a variant first isolated in China, Malaysia, Japan, and Singapore during January-April 1986 (1). The 1986-87 season was the third season during which influenza A(H1N1) strains predominated in the United States since this subtype reappeared in 1977 (2).

National data on influenza activity were obtained from four major sources:

1. State morbidity reports. Each week, state and territorial epidemio- ogists estimated the extent of influenza-like activity indicated by surveillance systems in their state or territory by using the following categories: no cases, sporadically occurring cases, regional outbreaks (occurring in counties collectively constitutingless than 50% of the state's population), or widespread outbreaks (occurring in counties collectively constituting greater than or equal to50% of the state's population).

2. Sentinel physician surveillance network. CDC received weekly reports from 138 physician members of the American Academy of Family Physicians who recorded the number of patient visits for influenza-like illnesses. Reports were based on a clinical case definition, but some physicians submitted specimens to a central laboratory for diagnosis by rapid culture confirmation of influenza virus (3).

3. Mortality in 121 cities. Death certificate data listing pneumonia or influenza (P&I) as a cause of death were reported from 121 cities weeklyy and analyzed to determine if the percentage of deaths attributed to P&I was higher than would be expected in the absence of an influenza epidemic. This index has historically reflected seasonal influenza- attributable mortality (4).

4. World Health Organization (WHO) collaborating laboratories. Sixty-four WHO collaborating laboratories provided weekly reports of the number of respiratory specimens submitted for virus isolation and the number and types of influenza isolates identified. The WHO collaborating laboratories included state public health laboratories in 47 states and the District of Columbia as well as several county, city, and university laboratories.

In addition to the methods described above, CDC received reports from military laboratories and Veterans Administration hospitals and reports of outbreaks and unusual influenza cases from a variety of sources.

Most of the outbreaks reported to CDC during the 1986-87 season occurred among children and young adults. Only one nursing home outbreakk was reported, suggesting that outbreaks among the elderly were uncommon (5). This observation is consistent with other recent A(H1N1) epidemics . However, this was the first A(H1N1) epidemic since this subtype reappeared that was associated with excess P&I deaths reported through the 121 cities.

Sporadic cases of influenza A(H1N1) occurred in Hawaii in June and August 1986 but were not identified in the contiguous United States until late September (6). The first reported U.S. outbreak occurred in October at a military facility in Florida (7). Communitywide activity also involved other regions of the United States in late 1986. Sentinel physicians reported a peak in outpatient visits for influenza-like illness (Figure 1) from mid-December 1986 through January 1987. State epidemiologists in 42 states and the District of Columbia reported regional or widespread outbreaks, primarily in the northeast, west northh central, mountain, and Pacific regions (Figure 2). Influenza activity reported by state epidemiologists also increased during December and peaked during January (Figure 1).

P&I deaths slightly exceeded the epidemic threshold for 4 weeks fromm mid-January to mid-February and again during the first 2 weeks of March 1987 (Figure 3). Approximately 80% of these deaths occurred in persons 65 years of age or older.

Influenza A(H1N1) strains were reported from all 50 states and the District of Columbia. WHO collaborating laboratories in the United States reported 2222 influenza virus isolates. Influenza A(H1N1) virusess accounted for 2206 (99.3%) of the isolates. Sentinel physicians reportedd an additional 33 A(H1N1) isolates. Ninety-five percent of virus isolateds from WHO collaborating laboratories were reported during a 13-week period between November 30, 1986, and February 28, 1987 (Figure 1). Reports of virus isolation were most frequent from mid-December through January. Influenza type A(H3N2) and type B strains were rarely isolated .

Age group of patients was available for 1918 A(H1N1) isolates reported by WHO collaborating laboratories. Of these isolates, 1874 (97.7%) were obtained from persons under 65 years of age (Table 1). Moree detailed information regarding ages of patients with laboratory diagnosis is available for 261 of the specimens submitted to the WHO Collaborating Center for Influenza (WHOCCI). Of these, 235 (90%) were obtained from persons less than 36 years of age.

WHOCCI did antigenic analysis on 315 influenza A(H1N1) isolates collected in 42 states. Most were closely related to the reference strain A/Taiwan/1/86(H1N1). Of the nine influenza A(H3N2) isolates submitted to WHOCCI for antigenic analysis, four resembled A/Leningrad/360/86(H3N2), a newly recognized minor variant; the remaining five resembled previously identified strains. Four influenza B isolates were submitted for antigenic analysis; one resembled B/Ann Arbor/1/86, and the other was a related variant.

In contrast to most years, two influenza vaccines were manufactured for use during the 1986-87 season. The new A/Taiwan/1/86-like variants were detected relatively early, and viruses were submitted promptly fromm national influenza centers in Asia to the WHOCCIs in Atlanta and London ; thus, July 1986 data supported the need to manufacture a monovalent A/Taiwan/1/86 vaccine (8). This vaccine was specifically recommended forr high-risk persons less than 35 years of age to supplement the standard trivalent influenza vaccine (9). Approximately seven million doses of the monovalent vaccine were manufactured and distributed before the epidemic peaked in early 1987. Reported by: Participating State and Territorial Epidemiologists and State Laboratory Directors. Sentinel Physicians of the American Academy of Family Physicians. WHO Collaborating Laboratories. Participating Veterans Administration Hospitals. Letterman Army Medical Center, San Francisco, California. Hackensack Hospital, Hackensack, New Jersey. Strong Memorial Hospital, Rochester, New York. Vanderbilt Univ, Nashville, Tennessee. Influenza Research Center, Baylor College of Medicine, Houston; 5th Army Medical Laboratory, Fort Sam Houston; USAF School of Aerospace Medicine, Epidemiology Div, Brooks AFB, Texas. Statistical Svcs Br, Div of Surveillance and Epidemiologic Studies, Epidemiology Program Office; Div of Immunization, Center for Prevention Svcs; WHO Collaborating Center for Influenza, Influenza Br, Div of Viral Diseases, Center for Infectious Diseases, CDC.

Editorial Note

Editorial Note: The 1986-87 influenza season illustrated the ability of a new strain of influenza to rapidly spread after appearing in Asia. In January 1986, influenza A(H1N1) variants related to A/Taiwan/1/86 first appeared in Northern China. During April and May, unusually high levels of epidemic activity were reported from Malaysia and Singapore. At the same time, similar viruses were isolated in Japan and Taiwan, where the 1985-86 winter epidemic was ending. Outbreaks were reported in some Pacific Island nations during June and July. In the United States, activity peaked rapidly during December and January and declinedd in February.

Despite the high transmissibility of the new variant, countries suchh as Australia and New Zealand were virtually unaffected by the virus. Some of these countries had experienced severe epidemics of the previouss A(H1N1) variant (related to A/Chile/1/83). This observation suggests that cross-protection from prior natural infection with the A/Chile-likee viruses may have attenuated the spread of A/Taiwan- like viruses in somee regions or countries. However, laboratory data suggest that inactivated A/Chile influenza vaccine showed poor cross-protection to A/Taiwan in one U.S. outbreak (7,8).

Preliminary analysis of death certificates suggests that the A/Taiwan-like viruses may have been responsible for mortality during thee winter. However, this finding contradicts the limited number of outbreaks reported in the elderly, the population generally at greatest risk in influenza epidemics. Analysis of hospital discharge diagnosis records and mortality data from the National Center for Health Statistics may clarify the impact of type A(H1N1) influenza in all age groups.

References

1. CDC. Antigenic variation of recent influenza A(H1N1) viruses. MMWR 1986;35:510-2.

2. Gregg MB, Hinman AR, Craven RB. The Russian flu: its history and implications for this year's influenza season. JAMA 1978;240:2260-3.

3. Reichelderfer PS, Kappus KD, Kendal AP. Economical laboratory supportt system for influenza virus surveillance. J Clin Microbiol 1987;25:947-8 .

4. Baron RC, Dicker RC, Bussell KE, Herndon TL. Assessing trends in mortality in 121 U.S. cities, 1970-79, from all causes and from pneumonia and influenza. Public Health Rep 1988;103:120-8.

5. CDC. Influenza A(H1N1) associated with mild illness in a nursing home--Maine. MMWR 1987;36:57-9.

6. CDC. Update: influenza activity--Micronesia, United States. MMWR 1986;35:685-7.

7. CDC. Influenza activity in civilian and military populations and key points for the use of influenza vaccines. MMWR 1986;35:729-31.

8. CDC. Antibody response to A/Taiwan/86(H1N1) virus in young adults receiving supplemental monovalent A/Taiwan/86 influenza vaccine following trivalent influenza vaccine. MMWR 1986;35:818-9.

9. Immunization Practices Advisory Committee. Monovalent influenza A(H1N1) vaccine, 1986-1987. MMWR 1986;35:517-21.

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