Marion K. Cooney

The following findings were made from observations of adenovirus (AV) infections in Seattle VW families, 1965-1969, which extended the 1961-1965 New York VW studies: That infections are predominantly enteric, may be abortive or invasive and followed by persistent intermittent excretion was confirmed. That such excretion is most characteristic of types 1, 2, 3 and 5 viruses may explain why these types were usually endemic. However, since observed duration of excretion was not increased despite a longer average observation period, persistent excretion appears not to continue indefinitely and generation-to-generation transmission now seems improbable. Unilike New York, alternate cycling of types 1 and 2 viruses was not seen. Among homotypic susceptibles, infection rates for the endemic types were highest in infants (greater than 90% for types 1 and 2), decreased with age in older children but increased in parents, perhaps because of closer contact with infants. Development of serum neutralizing antibody was most frequent (about 90%) after types 1 and 2 infection; in all cases, titers decayed over time. While delayed virus spread related to persistent intermittent excretion did occur, spread closely following new or renewed (after larger than or equal to 3 months) excretion was more important. Sibling introducers were more effective spreaders than infants, and duration of excretion was more important than mode. These data indicate that homotypic immunity is 85% protective against infection. A protective effect of heterotypic immunity could not be shown. Illness (chiefly respiratory and often febrile) was associated with 49% of infections in susceptibles and with 65% when respiratory shedding occurred. The contribution of AV to all infectious illness, based on virus-positive infections only, was 5% in infants and 3% in the 2-4-year age group; for febrile illness, the corresponding contributions were about 10% and 5%. Inclusion of infections discovered only be serology (49% of all infections) would greatly increase the contribution of AV to illness.

Pneumonia due to Mycoplasma pneumoniae was monitored in a large prepaid medical-care group in Seattle, Washington, between 1963 and 1975. The disease was diagnosed by isolation of M. pneumoniae and/or significant rises in titer of complement-fixing (antilipid) antibody in paired sera. Infection was endemic without significant seasonal fluctuations. Two epidemics occurred: the first peaked in January 1967, the second late in the summer of 1974. Total rates of pneumonia infection in children increased during M. pneumoniae epidemics, but epidemics of infection with respiratory syncytial virus had a greater effect. Age-specific attack rates for M. pneumoniae pneumonia among children aged five to nine years (about six per 1,000) were about twice the rates for younger children and four times those for adults. Serologic study of healthy schoolchildren showed annual rates of infection that paralleled but greatly exceeded rates of recognized M. pneumoniae pneumonia. Infection rates varied from 2% in endemic years to 35% in epidemic periods. A higher proportion of infections among children aged five to nine years than among adolescents aged 15-19 years resulted in pneumonia.

Intensive surveillance of Seattle, Washington, families with school-age children for influenzavirus infections during 1975-1979 encompassed 639 family- and 2732 person-seasons of observation, covering four influenzavirus epidemic seasons: type B (1975-1979), type A/H3N2 (1975-1976 and 1977-1978) and type A/H1N1 (1978-1979). Late spring "herald" waves of infection occurred in 1977 (A/H3N2), 1978 (A/H1N1) and 1979 (type B), the latter presaging an epidemic in 1979-1980. Out-of-season infections, recognized by serology only, included type B and A/H3N2 viruses in each summer and A/H1N1 virus in 1978. In epidemic seasons, infection rates were highest in children aged 5-9 years (A/H3N2) or in teenagers (A/H1N1 and type B). A/H1N1 virus caused the sharpest epidemic, with 31% of the population (but only 2% of adults) infected and 72% of households invaded in 1978-1979. These compare with infection rates of 17-24% overall and 6-13% of adults and the invasion of 38-53% of households observed in the type B and two A/H3N2 epidemics. Extended observation (largely serologic) of a cohort of 1965-1969 Virus Watch families for up to 14 years (including one three-year gap) indicated overall infection rates of 13.7 and 16.4 per 100 person-years with types B and A/H3N2 viruses, respectively, and rates of first and second reinfections of about 3 and 1 per 100 person-years, respectively, with each virus. Close surveillance in 1975-1979 revealed second family episodes of infection with each prevalent virus, 37 with A/H3N2, 15 with type B and 13 with A/H1N1 virus. Risk of infection in these episodes was related more to current hemagglutination-inhibiting titers than to experience (infected or not) in the initial episodes, with 67-100% reinfection when titers were low. Among younger (less than 20 years old) members, related illness was as frequent with reinfection as with initial infection.

<p>24 February 2017</p>\n<p>A foray into the rich exchanges between the Düsseldorf and London art scenes in the early 1970s. Otherwise inaccessible films by the Düsseldorf Film Group will be shown as will a newly digitized anarchic tape slide work by Achim Duchow, <em>Buick Adventure</em> (1974), featuring Sigmar Polke and Gallery House’s director Sigi Krauss.</p>\n

Journal Article INFLUENZAVIRUS INFECTIONS IN SEATTLE FAMILIES, 1975–1979: II. PATTERN OF INFECTION IN INVADED HOUSEHOLDS AND RELATION OF AGE AND PRIOR ANTIBODY TO OCCURRENCE OF INFECTION AND RELATED ILLNESS Get access JOHN P. FOX, JOHN P. FOX 1Dept. of Epidemiology, School of Public Health and Community Medicine, U. of WashingtonSeattle, WA 98195 (reprint requests to Dr. Fox at this address) reprint requests to Dr. Fox at this address Search for other works by this author on: Oxford Academic PubMed Google Scholar MARION K. COONEY, MARION K. COONEY 2Dept. of Pathobiology, School of Public Health and Community Medicine, U. of WashingtonSeattle, WA Search for other works by this author on: Oxford Academic PubMed Google Scholar CARRIE E. HALL, CARRIE E. HALL 1Dept. of Epidemiology, School of Public Health and Community Medicine, U. of WashingtonSeattle, WA 98195 (reprint requests to Dr. Fox at this address) Search for other works by this author on: Oxford Academic PubMed Google Scholar HJORDIS M. FOY HJORDIS M. FOY 1Dept. of Epidemiology, School of Public Health and Community Medicine, U. of WashingtonSeattle, WA 98195 (reprint requests to Dr. Fox at this address) Search for other works by this author on: Oxford Academic PubMed Google Scholar American Journal of Epidemiology, Volume 116, Issue 2, August 1982, Pages 228–242, https://doi.org/10.1093/oxfordjournals.aje.a113408 Published: 01 August 1982 Article history Received: 16 November 1981 Revision received: 01 March 1982 Published: 01 August 1982