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Outbreaks of influenza A (H3N2, A/Shanghai/11/87-like) occurred in two partially (60% and 79%) vaccinated nursing home populations in January 1988. A retrospective cohort study using chart review was designed to assess the effectiveness of influenza vaccination and amantadine prophylaxis (100 mg per day) in controlling the outbreaks and to determine the amantadine susceptibility of influenza viruses isolated from case-patients. The point estimate of vaccine efficacy in preventing influenza-like illness was -33% (95% confidence interval -115% to 18%). However, 9% of vaccinated case-patients died within 14 days after onset of influenza-like illness compared with 26% of unvaccinated case-patients (relative risk = 0.4, 95% confidence interval 0.1-1.0). There was no significant difference in illness severity among case-patients who became ill before amantadine prophylaxis was started (n = 84) compared with those who became ill while taking amantadine (n = 34). Four virus isolates obtained before amantadine prophylaxis was started demonstrated 52-68% inhibition by 1 microgram/ml of amantadine; by comparison, six isolates (resistant viruses) obtained from residents who became ill while taking amantadine demonstrated 1-18% inhibition. The resistant viruses had four different RNA sequences in the gene coding for the M2 protein transmembrane region. Three resistant viruses with identical RNA sequences were isolated from residents living in contiguous rooms who had onset of signs and symptoms during a 6-day interval. Further studies are needed to determine how frequently and under what circumstances resistant viruses occur when antiviral agents are used to control institutional influenza A outbreaks. Strategies for antiviral agent administration that limit the emergence and transmission of resistant virus strains may be needed.

Influenza A (H3N2) viruses were isolated from outbreaks and epidemics of disease during the period December 1977 to March 1978. For the last two months of this period, H1N1 strains of influenza A were also responsible for epidemics. In some regions (e.g., Hawaii) co-circulation of H1N1 AND H3N2 strains occurred, whereas in other regions (e.g., Wisconsin) isolation of H3N2 strains had almost ceased prior to isolation of H1N1 strains. Few influenza B isolates were reported. Analysis of the ages of patients from whom specimens were submitted for influenza virus isolation confirmed that, whereas H3N2 strains were isolated from persons of all ages, greater than 97 per cent of H1N1 isolates in six states analyzed were recovered from patients less than 26 years old, although specimens were tested from older persons who were ill during the period of prevalence of H1N1 influenza. The majority of H3N2 isolates tested by hemagglutinin-inhibition reaction were similar to A/Texas/1/77, and the majority of H1N1 isolates were similar to A/USSR/90/77. Antigenic analysis of isolates, however, identified a small number of variants of H3N2 and H1N1 strains.

At a time when outbreaks and sporadic cases of influenza caused a A/Victoria/3/75-like and A/Texas/1/77-like H3N2 strain of influenza were occurring in the Rocky Mountain region of the USA, about 60% of the students of a high school in Cheyenne, Wyoming, were involved in an outbreak of influenza-like illness. Six influenza A(H1N1) virus isolates were obtained from throat swabs collected from 12 of these students. Virus isolated from a seventh student, however, contained a mixture of H1 and H3 (A/Victoria/3/75-like) hemagglutinins and N1 and N2 neuraminidases, as shown by the ability to clone from the mixture viruses with antigenic components H1N1, H3N1, and H3N2. An antigenic hybrid virus with H3N1 composition was re-isolated from the original throat swab. The results show that one student was shedding a mixture of A/Victoria/3/75(H3N2)-like and A/USSR/90/77(H1N1)-like viruses at the time his throat swab was taken.

To determine risk factors for outbreaks of influenza virus infections in chronic-care facilities for the elderly, the authors compared the characteristics of two groups of nursing homes in Genesee County, Michigan, in 1982-1983, following a community-wide epidemic caused by A/Bangkok/1/79-like (H3N2) viruses: seven homes in which an outbreak occurred (case homes) and six homes with sporadic illnesses only (control homes). The two groups were similar in many respects, including the physical characteristics of the facilities, visitation and staffing patterns, infection control practices, and demographic and clinical profiles of residents. Case homes, however, had larger resident populations than control homes (median 160 vs. 92, respectively; p = 0.028) and a lower proportion of residents who had been vaccinated with A/Bangkok antigen the previous autumn (median 51% vs. 81%, respectively; p = 0.047). Based on a retrospectively determined estimate of the efficacy of influenza vaccine in preventing illness (43%), the number of residents presumed to be susceptible to the epidemic strain was higher in case homes than in control homes (median 102 vs. 61, respectively; p = 0.0047) and was the most important factor selected by a stepwise, multivariate logistic regression model (p less than 0.0005). These findings are consistent with mathematical models of vaccine-induced herd immunity in closed populations and suggest that high rates of vaccination can reduce the risk of influenza outbreaks in this setting.

At a time when outbreaks and sporadic cases of influenza caused a A/Victoria/3/75-like and A/Texas/1/77-like H3N2 strain of influenza were occurring in the Rocky Mountain region of the USA, about 60% of the students of a high school in Cheyenne, Wyoming, were involved in an outbreak of influenza-like illness. Six influenza A(H1N1) virus isolates were obtained from throat swabs collected from 12 of these students. Virus isolated from a seventh student, however, contained a mixture of H1 and H3 (A/Victoria/3/75-like) hemagglutinins and N1 and N2 neuraminidases, as shown by the ability to clone from the mixture viruses with antigenic components H1N1, H3N1, and H3N2. An antigenic hybrid virus with H3N1 composition was re-isolated from the original throat swab. The results show that one student was shedding a mixture of A/Victoria/3/75(H3N2)-like and A/USSR/90/77(H1N1)-like viruses at the time his throat swab was taken.

In February 1982, a four-year-old Nevada girl with acute lymphoblastic leukemia in remission was hospitalized with fulminant pneumonia and died eight days later at a hospital in California. An influenza virus was the only pathogen detected, and was present in both antemortem and postmortem specimens. The virus was closely related antigenically to A/New Jersey/8/76 (H1N1) and had a genome very similar to a contemporary enzootic swine influenza virus. The patient had had no known contact with swine, and the source of infection could not be determined. Only five possible secondary cases could be detected by retrospective investigation of 62 contacts, and there was no evidence of spread to the general community. Swine influenza viruses circulate among pigs in the United States annually, and it is likely that sporadic transmissions to humans will continue to be detected. Nevertheless, person-to-person spread under these circumstances appears to be limited.

A jet airliner with 54 persons aboard was delayed on the ground for three hours because of engine failure during a takeoff attempt. Most passengers stayed on the airplane during the delay. Within 72 hours, 72 per cent of the passengers became ill with symptoms of cough, fever, fatigue, headache, sore throat and myalgia. One passenger, the apparent index case, was ill on the airplane, and the clinical attack rate among the others varied with the amount of time spent aboard. Virus antigenically similar to A/Texas/1/77(H3N2) was isolated from 8 of 31 passengers cultured, and 20 of 22 ill persons tested had serologic evidence of infection with this virus. The airplane ventilation system was inoperative during the delay and this may account for the high attack rate.

Influenza A (H3N2) viruses were isolated from outbreaks and epidemics of disease during the period December 1977 to March 1978. For the last two months of this period, H1N1 strains of influenza A were also responsible for epidemics. In some regions (e.g., Hawaii) co-circulation of H1N1 AND H3N2 strains occurred, whereas in other regions (e.g., Wisconsin) isolation of H3N2 strains had almost ceased prior to isolation of H1N1 strains. Few influenza B isolates were reported. Analysis of the ages of patients from whom specimens were submitted for influenza virus isolation confirmed that, whereas H3N2 strains were isolated from persons of all ages, greater than 97 per cent of H1N1 isolates in six states analyzed were recovered from patients less than 26 years old, although specimens were tested from older persons who were ill during the period of prevalence of H1N1 influenza. The majority of H3N2 isolates tested by hemagglutinin-inhibition reaction were similar to A/Texas/1/77, and the majority of H1N1 isolates were similar to A/USSR/90/77. Antigenic analysis of isolates, however, identified a small number of variants of H3N2 and H1N1 strains.

In late October 1986, an outbreak of influenza-like illness was detected at the Naval Air Station in Key West, Florida. Between October 10 and November 7, 1986, 60 active duty personnel reported experiencing a respiratory illness characterized by fever, cough, sore throat, and myalgia. Influenza A/Taiwan/1/86 (H1N1) virus was recovered from three symptomatic patients. Forty-one (68%) of 60 case-patients belonged to a 114-person squadron that had traveled to Puerto Rico for a temporary assignment from October 17-28, 1986. Among squadron members, the attack rate for persons previously vaccinated with the 1986-1987 trivalent influenza vaccine and for those unvaccinated was the same (37%). Transmission of infection among squadron personnel appeared to have commenced in Key West and continued in a barracks in Puerto Rico and aboard two DC-9 aircraft that transported the squadron back to Key West on October 28. There was no evidence that the outbreak spread to the surrounding civilian communities in Puerto Rico or Key West. This was the first reported outbreak of respiratory illness due to influenza A/Taiwan/1/86 (H1N1) in the continental United States in the 1986-1987 influenza season.