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Update: Influenza Activity -- United States and Worldwide, 1992

During the 1991-92 influenza season, influenza activity was reported at moderate levels in many parts of the world. Influenza A(H1N1), A(H3N2), and influenza B viruses have continued to circulate worldwide. From October 1991 through February 1992, when influenza viruses circulated widely in the Northern Hemisphere, epidemic levels of activity were most commonly associated with the H3N2 subtype of influenza A (1). This report summarizes worldwide influenza activity reported from March through September 1992 and activity in the United States from October 1991 through September 1992.

Asia. During March and April, outbreaks caused by influenza A(H3N2) viruses were reported in Hong Kong and in China. From March through May, India, Singapore, and Thailand reported sporadic isolations of influenza A(H3N2); sporadic isolations of influenza A(H1N1) were reported from China, Hong Kong, Singapore, and Thailand. During March, influenza B outbreaks were reported in China and Indonesia; Hong Kong, Malaysia, Singapore, and Taiwan reported sporadic influenza B activity.

Europe. During March and April, influenza activity declined in reporting countries. No isolates have been reported since May.

North America. Canada reported influenza A isolates through March. In the United States, influenza A outbreaks began in late October. Influenza activity peaked from early December to mid-January, with influenza A(H3N2) viruses predominating, and declined from mid-January through February. Only sporadic isolates were reported during March and April (2), although the number of influenza B isolates increased during this period. During June and early July, nine influenza B isolates were obtained during sporadic activity in Fairbanks, Alaska. Isolates were obtained from sporadic cases in other states through September. Influenza A(H1N1) was isolated from one person in Texas in August 1992.

Central and South America. During June and July, influenza A(H1N1) viruses were isolated during an epidemic in Argentina. Influenza A(H1N1) and A(H3N2) viruses were isolated in Chile during outbreaks peaking in mid-August. During March, Jamaica reported influenza outbreak activity attributed to A(H1N1) viruses. During June, Uruguay reported epidemic influenza activity with the isolation of both influenza A and influenza B viruses. During August and early September, influenza B viruses were isolated during epidemic-level activity in Panama. Sporadic influenza B activity was reported from Brazil in May.

Oceania. Beginning in March, Australia reported influenza activity, caused predominately by influenza A(H3N2) viruses, at a higher level than during the two previous seasons and earlier than is typical. In New Zealand, influenza activity began in April and peaked in June; influenza A(H1N1) was the predominant virus isolated, although influenza A(H3N2) and influenza B viruses also were isolated. Fiji reported one influenza A(H3N2) isolate coincident with outbreaks of influenza-like illness from March to June. Papua New Guinea reported influenza A activity from March to May and detection of influenza B in June.

Africa. From June through August, both influenza A(H3N2) and influenza B viruses were isolated in South Africa, with A(H3N2) viruses predominating. During March and April, influenza A(H3N2) was isolated in Madagascar.

Characterization of influenza virus isolates. During the 1991- 92 worldwide influenza season, 983 isolates were antigenically characterized by the World Health Organization Collaborating Center for Surveillance, Epidemiology, and Control of Influenza at CDC; of these, 550 (56%) were from the United States. Of the 561 influenza A(H3N2) viruses isolated worldwide, 94% resembled the A/Beijing/353/89-like viruses; 5%, the A/Shanghai/24/90-like viruses; and 1%, the A/England/427/88-like viruses (3). A/Taiwan/01/86-like viruses accounted for 61% of the 276 influenza A(H1N1) viruses isolated worldwide, while the antigenically related A/Texas/36/91-like viruses (1) accounted for 39%. Of the 146 influenza B isolates, 5% resembled B/Victoria/02/87; 27%, B/Panama/45/90; and 68%, B/Qingdao/102/91, a minor variant of B/Panama (1).

Reported by: WHO National Influenza Centers. Communicable Diseases Div, World Health Organization, Geneva. WHO Collaborating Center for Surveillance, Epidemiology, and Control of Influenza, Influenza Br, and Epidemiology Activity, Office of the Director, Div of Viral and Rickettsial Diseases, National Center for Infectious Diseases; Div of Immunization, National Center for Prevention Svcs, CDC.

Editorial Note

Editorial Note: Both influenza A and influenza B viruses circulated throughout the world from October 1991 through September 1992, with influenza A(H3N2) viruses predominating. In the United States during the 1991-92 influenza season, influenza A(H1N1) viruses circulated primarily in the mid-Atlantic and South Atlantic regions; during the two previous seasons, influenza A(H1N1) had circulated at very low levels in the United States. This observation, coupled with the detection of influenza B during 1992, suggests that type A(H1N1) and type B viruses may circulate together in the United States during the 1992-93 influenza season.

In recent years, the Advisory Committee on Immunization Practices (ACIP) has recommended that organized vaccination campaigns be conducted during November. During the 1991-92 season, however, outbreaks occurred in some areas either before vaccination campaigns had been completed or fewer than 2 weeks after vaccination, when vaccine-induced antibody may not be fully developed. As a result, the ACIP reviewed patterns of influenza activity during the previous 10-year period and concluded that mid-October through mid-November is the optimal period for vaccination (4). In addition, beginning each September, persons who are at increased risk for complications from influenza and who visit health-care providers for routine care or are hospitalized should be offered influenza vaccine. Health-care providers should continue to offer vaccine to members of high-risk and other target groups after mid-November and after influenza activity has begun.

Target groups for influenza vaccination include persons who are at high risk for developing serious medical complications following influenza infections, their health-care providers, and household members. Persons at increased risk for complications are

  1. those aged greater than or equal to 65 years; 2) all residents of nursing homes or chronic-care facilities; 3) persons with chronic pulmonary or cardiovascular disorders (including children with asthma); 4) persons requiring medical follow-up during the past year for chronic metabolic diseases, renal dysfunction, hemoglobinopathies, or immunosuppression; and 5) children and teenagers on long-term aspirin therapy who are at increased risk for Reye syndrome if infected with influenza. Based on national estimates, in 1989, only 30% of those aged greater than or equal to 65 years and 12% of those aged less than 65 years who were at increased risk for influenza-related complications received vaccination against influenza (5).

The 1992 influenza vaccine contains virus strains representing the three distinct groups of influenza viruses in worldwide circulation: A/Texas/36/91-like (H1N1), A/Beijing/353/89-like (H3N2), and B/Panama/45/90-like viruses. Most viruses isolated since the beginning of March 1992 are closely related to the 1992- 93 influenza vaccine strains.

Although the vaccine and circulating influenza virus strains appear to be well-matched, the antiviral drug amantadine hydrochloride should be considered as an adjunct to vaccination for prevention and treatment of influenza A infection. Chemoprophylaxis with amantadine is particularly recommended for use in nursing homes and other institutional settings with high-risk persons, for high-risk persons with anaphylactic hypersensitivity to egg protein or other vaccine components, and for immunocompromised persons. Treatment of influenza A infection with amantadine may shorten the duration and reduce the severity of illness when administered within 48 hours after onset of symptoms.

Amantadine is effective against infection with influenza A viruses but not influenza B viruses. When both type A and type B viruses are circulating simultaneously in the United States, laboratory assessment of an influenza-like illness (by obtaining pharyngeal or nasal swab specimens for culture or application of rapid diagnostic techniques) may assist in guiding the choice of influenza-control measures (6).

Local and national reports of influenza surveillance can be used by health-care providers in making clinical decisions. Surveillance information is updated weekly at CDC and is available by telephone (CDC Voice Information System [influenza update] [404] 332-4555) or through the CDC Information Service on the Public Health Network* electronic bulletin board. Periodic updates about influenza activity also may be available from state and local health departments.


  1. World Health Organization. Recommended composition of influenza virus vaccines for use in the 1992-1993 season. Wkly Epidemiol Rec 1992;67:57-60.

  2. CDC. Update: influenza activity -- United States and worldwide, and composition of the 1992-93 influenza vaccine. MMWR 1992;41:315- 7,323.

  3. World Health Organization. Recommended composition of influenza virus vaccines for use in the 1991-1992 season. Wkly Epidemiol Rec 1991;66:57-60.

  4. ACIP. Prevention and control of influenza: recommendations of the Immunization Practices Advisory Committee (ACIP). MMWR 1992;41(no. RR-9).

  5. Rodgers DV, Strikas RA, Martinez B, et al. Influenza vaccination among adults: results of the 1989 National Health Interview Survey [Abstract]. In: Program and abstracts of the CDC Epidemic Intelligence Service 41st annual conference. Atlanta: US Department of Health and Human Services, Public Health Service, CDC, 1992:33-

  6. Waner JI, Todd SJ, Shalaby H, Murphy P, Wall LV. Comparison of Directigen FLU-A with viral isolation and direct immunofluorescence for the rapid detection and identification of influenza A virus. J Clin Microbiol 1990;29:479-82.

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