Contaminated drinking water in one town manifesting as an outbreak of cryptosporidiosis in another.

In early 1992 we identified an outbreak of cryptosporidiosis in Oregon and sought to identify and control its source. We used a series of studies to identify risk factors for illness: (i) a case-control study among employees of a long-term-care facility (LTCF); (ii) a matched case-control study of the general community; (iii) a cohort study of wedding attendees; and (iv) a cross-sectional survey of the general community. Drinking Talent water was associated with illness in the LTCF (OR = 22.7, 95 % CI = 2.7-1009.0), and in the community (matched OR = 9.5, 95% CI 2.3-84.1). Drinking Talent water was associated with illness only among non-Talent residents who attended the wedding (P < 0.001) and in the community (RR = 6.5, 95 % CI 3.3-12.9). The outbreak was caused by contaminated municipal water from Talent in the absence of a discernible outbreak among Talent residents, suggesting persons exposed to contaminated water may develop immunity to cryptosporidiosis.

Epidemic serogroup B meningococcal disease in Oregon: the evolving epidemiology of the ET-5 strain.

CONTEXT: In 1993, Oregon's incidence of serogroup B meningococcal disease began to rise because of a highly clonal group of strains designated enzyme type 5 (ET-5), the first such increase observed in the United States. OBJECTIVE: To evaluate the impact that the ET-5 strain has had on the epidemiology of meningococcal disease in Oregon. DESIGN AND SETTING: Epidemiologic analysis of surveillance data on Oregon meningococcal disease cases from 1987 through 1996 and multilocus enzyme electrophoresis typing of serogroup B isolates from June 1993 through April 1995 and from April through June 1996. PATIENTS: A total of 836 persons with invasive meningococcal disease. MAIN OUTCOME MEASURES: Disease frequency and clonality of strains. RESULTS: Serogroup B disease incidence rates more than doubled from the preepidemic period in 1987-1992 (1.0 case per 100000 population) to the recent epidemic period in 1995-1996 (2.2 cases per 100000). The age-specific incidence rate of serogroup B disease among those 15 through 19 years old increased 13-fold between the preepidemic period (0.5 case per 100000) and 1995-1996 (6.4 cases per 100000). However, the proportion of cases with meningococcemia and the case-fatality rate did not change. Of 99 Neisseria meningitidis isolates obtained from 1993-1995, 88 (89%) belonged to the ET-5 complex. Of these, 69 (78%) were a single clone, designated 301. Of 20 serogroup B isolates from 1996, 18 (90%) belonged to the ET-5 complex; 17 (94%) were the 301 clone. CONCLUSION: Serogroup B meningococcal disease incidence continues at high levels in Oregon with increasing predominance of the ET-5 clonal strains.

Tobacco smoke as a risk factor for meningococcal disease.

BACKGROUND: Since 1992 the US Pacific Northwest has experienced a substantial increase in the incidence of serogroup B meningococcal disease. The current meningococcal polysaccharide vaccine is poorly immunogenic in young children and does not protect against N. meningitidis serogroup B. Defining alternative approaches to the prevention and control of meningococcal disease is of considerable public health importance. METHODS: We performed a case-control study comparing 129 patients in Oregon and southwest Washington with 274 age- and area-matched controls. We used conditional logistic regression analysis to determine which exposures remained associated with disease after adjusting for other risk factors and confounders and calculated the proportion of disease attributable to modifiable exposures. RESULTS: After adjustment for all other significant exposures identified, having a mother who smokes was the strongest independent risk factor for invasive meningococcal disease in children < 18 years of age [odds ratio (OR), 3.8; 95% confidence interval (CI) 1.6 to 8.9)], with 37% (CI 15 to 65) of all cases in this age group potentially attributable to maternal smoking. Adult patients were more likely than controls to have a chronic underlying illness (OR 10.8, CI 2.7 to 43.3), passive tobacco smoke exposure (OR 2.5, CI 0.9 to 6.9) and to smoke tobacco (OR 2.4, CI 0.9 to 6.6). Dose-response effects were seen for passive smoke exposure and risk of disease in all age groups. CONCLUSION: Tobacco smoke exposure independently increases the risk of developing meningococcal disease.

A swimming-associated outbreak of hemorrhagic colitis caused by Escherichia coli O157:H7 and Shigella sonnei.

BACKGROUND: In the summer of 1991, simultaneous outbreaks of bloody diarrhea and hemolytic-uremic syndrome caused by Escherichia coli O157:H7 and of bloody diarrhea caused by Shigella sonnei were traced to a lakeside park near Portland, Oregon. METHODS: We identified cases primarily from routine surveillance reports. In case-control studies, the activities of persons with park-associated E. coli O157:H7 or S. sonnei infections were compared independently with those of three sets of controls. We also evaluated environmental conditions at the park and subtyped the bacterial isolates. RESULTS: We identified 21 persons with park-associated E. coli O157:H7 infections (all of them children; median age, six years) and 38 persons with S. sonnei infections (most of them children). These 59 people had visited the park over a 24-day period. Their illnesses were not associated with food or beverage consumption. All the case patients reported swimming, however, and in case-control studies swimming was strongly associated with both types of infection (P = 0.015 or less). The case patients were more likely than the controls to report having swallowed lake water, and they had spent more time in the lake. Numbers of enterococci indicative of substantial fecal contamination (geometric mean, > 50 per deciliter) were detected in the swimming area during some but not all of the outbreak period. Park-associated E. coli O157:H7 isolates were identical by pulsed-field gel electrophoresis and were distinguishable from other isolates in the Portland area. CONCLUSIONS: Lake water that was fecally contaminated by bathers was the most likely vehicle for the transmission of both the E. coli O157:H7 and the S. sonnei infections. The unusually prolonged outbreak suggests both the survival of these enteric organisms in lake water and a low infectious dose.

Evaluation of a method for detecting outbreaks of diseases in six states.

A new statistical method, developed for detection of changes in reporting, has proved useful in analysis of provisional data reported by state health departments to the National Notifiable Diseases Surveillance System (NNDSS). In this system, data from the current four-week period can be compared with data from the previous, same, and subsequent four-week periods from each of the preceding five years, and reports exceeding historical limits are highlighted in a horizontal bar graph. To evaluate the usefulness of this method at the state level, we applied it to weekly reports of seven notifiable diseases in six states over a four-month period. Participating state health departments investigated all events exceeding historical limits and reported known outbreaks that were not identified by the method. During the four-month period, the method identified 27 episodes of disease reports exceeding historical limits. Of these, 14 (52%) represented outbreaks. None was detectable by analysis of aggregate national surveillance data. Five outbreaks known to state health department officials were not identified by the method, because of increased disease activity during the baseline period or lack of timely provisional reporting of outbreak-related cases. Methods for detection of increases in reporting at the state level may identify events of public health importance that are obscured in aggregate national data and may supplement other local sources of information available to state health departments in the recognition of significant public health events.

Eosinophilia-myalgia syndrome associated with exposure to tryptophan from a single manufacturer.

Although eosinophilia-myalgia syndrome has been linked to use of tryptophan, it has been unclear whether tryptophan itself or a contaminant causes illness. In Oregon, we compared the brand and source of tryptophan used by 58 patients with eosinophilia-myalgia syndrome with the brand and source of tryptophan used by 30 asymptomatic controls identified through a random telephone survey and 63 asymptomatic controls who contacted the Oregon Health Division voluntarily. Although a single brand/retail lot of tryptophan was statistically associated with the development of eosinophilia-myalgia syndrome, there was no common importer, wholesaler, tablet maker, encapsulator, or distributor. However, 45 (98%) of 46 cases had taken a product made by one manufacturer, compared with three (30%) of 10 telephone survey controls and 15 (48%) of 31 volunteer controls. Retail lots of tryptophan from this manufacturer that were associated with cases were significantly more likely to have been produced from January through June 1989 than lots from this manufacturer that were taken by controls. These findings indicate that the recent epidemic of eosinophilia-myalgia syndrome was caused by a contaminant or an alteration in a subset of tryptophan manufactured by a single company in Japan shortly before the outbreak began.