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Background.— To determine the natural history of eosinophilia-myalgia syndrome, we followed up all patients with eosinophilia-myalgia syndrome reported to the Oregon Health Division, Portland, during the recent epidemic caused by contaminated tryptophan. Methods.— Patients were interviewed by telephone from 1 to 5 months after illness onset and again at least 12 months after onset. Symptoms (type, onset, and duration), overall disability, treatment, and tryptophan lot and dose were assessed for each patient. Results.— Information was obtained for 55 (96%) of 57 case-patients: 53 patients completed interviews and two patients had died. For the 53 patients who were interviewed, symptoms with onset more commonly during the first 3 months of illness included severe myalgias, fatigue, generalized weakness, edema, and rash. Symptoms with later onset included paresthesias, muscle cramps, extremity weakness, and alopecia. At 12 months, 41 patients (77%) continued to report fatigue, 36 (68%) weakness, and 34 (64%) myalgias; 26 patients (49%) had difficulty climbing stairs, 23 (43%) had difficulty getting up from a chair, and 15 (28%) had difficulty holding a cup. Higher doses of tryptophan were correlated with more severe disability, both initially ( r s =.33) and at follow-up ( r s =.42). Although most patients reported improvement in symptoms at 12 months, only 14 (26%) patients reported that they were able to perform all normal daily activities. Conclusions.— Most patients with eosinophilia-myalgia syndrome in this population-based cohort are still symptomatic 1 year after onset, primarily with the complaints reported early in the illness. The association between degree of disability and daily tryptophan dose suggests that ingestion of varying amounts of contaminant may be responsible, in part, for the severity of symptoms experienced by individual patients. ( Arch Intern Med. 1992;152:1889-1892)

Background Pertussis incidence has increased in the United States since 1980, punctuated by outbreaks that involve adults and adolescents. We investigated a community-wide outbreak and studied risk factors among adults to identify prevention and control opportunities. Methods We analyzed surveillance data, interviewed patients, visited outbreak sites, and conducted a case-control study of risk factors for first-in-household adult infection during a Jackson County, Oregon, outbreak in 2003. Results In Jackson County, 135 pertussis cases were reported; the incidence was 71 per 100 000 population compared with 0 to 1 per 100 000 population from 1995 through 2001. Case investigations identified 2658 close contacts (19.7 per case); 1050 (40%) received antibiotic prophylaxis. Older children and adolescents (aged 10-17 years) and adults (aged ≥18 years) accounted for 67% of cases. Five infants were hospitalized (192 hospitalizations per 100 000 infants) compared with 18 in the remainder of the state (33 per 100 000 infants). Many cases occurred among epidemiologically linked clusters of varied composition, such as jail inmates and employees, methamphetamine users, low-income housing residents, school students and employees, and employees in certain work settings. Adult patients were more likely than controls to live with children aged 6 to 10 years (odds ratio, 6.4; 95% confidence interval, 1.8-23.4) and less likely to report a complete childhood vaccination history (odds ratio, 0.1; 95% confidence interval, 0.003-0.9). Conclusion The predominance of adolescent and adult cases, appearance of new clusters despite aggressive control efforts, clustering of cases in hard-to-reach populations, and absence of modifiable risk factors for adult disease in this outbreak all suggest that universal booster vaccination of adolescents and adults might offer the only effective means to prevent such events in the future.

In Reply.— We thank Drs Ford and Rothman for their interest in our article and their comments regarding statistical analysis of the pulmonary function data. In our analysis, we used a Mann-Whitney U rank-sum test to compare the median values of observed lung-function parameters between the two hockey teams and the comparison group. We also analyzed the data using a multiple logistic regression model that controlled for height, weight, and age. No statistically significant differences in pulmonary function were found between the two exposure groups and thecontrol group initially or at follow-up testing by either method of analysis. These tests were used because they allowed us to compare the distributions of lung-function parameters between the groups, rather than the proportions of each group performing below an arbitrary threshold value. Also, we did not combine the players with single and multiple (chronic) exposures in the analysis because we believe that

ContextIn December 1995, reported Salmonella enterica serotype Newport (SN) infections increased sharply in Oregon and British Columbia but not elsewhere in North America. Similar unexplained increases had been noted in 6 other states in the fall of 1995.ObjectiveTo determine the source of the outbreak(s).DesignCase-control studies, environmental investigations, bacterial subtyping, and surveillance information review.SettingsOregon and British Columbia communities (winter 1995-1996) and Georgia, Oklahoma, Pennsylvania, Vermont, Virginia, and West Virginia (fall 1995).ParticipantsOregon and British Columbia residents with culture-confirmed SN infections and onset from December 1, 1995, through February 29, 1996, and healthy community controls.Main Outcome MeasuresOdds ratio (OR) of illness associated with exposures; distribution patterns and culture of alfalfa seeds and sprouts; subtyping of SN isolates.ResultsWe identified 133 cases in Oregon and British Columbia; 124 (93%) occurred in patients older than 18 years; 87 (65%) were female. Case patients were more likely than community control subjects to report having eaten alfalfa sprouts in the 5 days preceding illness (41% [17/41] vs 4% [3/75]; OR, 17.0; 95% confidence interval, 4.3-96.0). Case isolates shared a distinctive pulsed-field gel electrophoresis (PFGE) pattern. The SN was grown from seeds and alfalfa sprouts. The distribution of 1 seed lot to multiple growers corresponded to the distribution of cases. Distribution of a second seed lot from the same European wholesaler corresponded to the location of the fall outbreak, which was characterized by a similar demographic profile. The PFGE pattern of fall outbreak isolates and confiscated sprouts and seeds was indistinguishable from the Oregon and British Columbia outbreak and differed from background isolates.ConclusionsThe SN-contaminated alfalfa seeds were distributed to multiple growers across North America in 1995 and resulted in a protracted international outbreak scattered over many months. Current sprouting methods are inadequate to protect consumers from such events. Alfalfa sprouts may be an elusive but important vehicle for salmonellosis and other enteric infections.

During February 1987 an outbreak of nitrogen dioxide-induced respiratory illness occurred among players and spectators of two high school hockey games played at an indoor ice arena in Minnesota. The source of the nitrogen dioxide was the malfunctioning engine of the ice resurfacer. Case patients experienced acute onset of cough, hemoptysis, and/or dyspnea during, or within 48 hours of attending, a hockey game. One hundred sixteen cases were identified among hockey players, cheerleaders, and band members who attended the two games. Members of two hockey teams had spirometry performed at 10 days and 2 months after exposure; no significant compromise in lung function was documented. Nitrogen dioxide exposure in indoor ice arenas may be more common than currently is recognized; only three states require routine monitoring of air quality in ice arenas, and the respiratory symptoms caused by exposure to nitrogen dioxide are nonspecific and easily misdiagnosed.