Skip directly to site content Skip directly to page options Skip directly to A-Z link Skip directly to A-Z link Skip directly to A-Z link
Volume 5, Number 2—April 1999
Letter

Shiga Toxin–Producing Escherichia coli O157:H7 in Japan

On This Page
Article Metrics
9
citations of this article
EID Journal Metrics on Scopus

Cite This Article

To the Editor: Shiga toxin-producing Escherichia coli (STEC) O157:H7 infection, which can cause hemolytic uremic syndrome and death, is a global public health concern. Patients younger than 5 years of age are at high risk for hemolytic uremic syndrome (1) and shed the organism longer than adults (2). The public health importance of this symptomatic shedding in transmission among preschool children is well established (3); however, that of symptom-free shedding in adults is unknown. We report here that the rate of symptom-free STEC O157:H7 shedding is higher in adults 30 to 49 years of age than in others.

STEC infections have been notifiable in Japan since August 1996. When STEC is found in the feces of patients in schools, families, and hospitals, local health centers and public health institutes must test (generally using MacConkey sorbitol agar with cefixime-potassium tellurite medium) for the pathogen in stool specimens of contacts of the patients. The pathogen is also sought twice a month in the stool specimens of food-handlers. All isolates from culture-positive patients are collected by Japan's National Institute of Infectious Diseases.

In 1997, 1,412 STEC O157:H7 human isolates were examined for subtyping of Shiga toxin genes stx1 and stx2 by polymerase chain reaction, for genotyping by XbaI-digested pulsed-field gel electrophoresis (PFGE) (4,5), and for their relationship with symptoms; 1,381 isolates (from culture-positive persons with well-characterized clinical status) were further analyzed. The rates by age group among STEC O157:H7-shedding persons reporting one or more symptoms (vs. culture-positive persons without symptoms) were as follows: 82% (475 of 576) younger than 10 years old; 81% (145 of 178), 10 to 19 years; 63% (98 of 156), 20 to 29 years; 25% (32 of 128), 30 to 39 years; 34% (34 of 100), 40 to 49 years; 54% (57 of 106), 50 to 59 years; 56% (38 of 68), 60 to 69 years; 68% (47 of 69), older than 70 years. Culture-positive persons under 20 years of age, especially children under 10 years of age, were more likely to have symptoms than other age groups. Intermediate rates of symptom-free persons with positive stool cultures occurred in young adults (20 to 29 years of age) and the elderly (70 years of age), while the highest rates of stool-positive, symptom-free persons were adults, especially those between 30 and 49 years of age. In terms of pathogen virulence, we did not find significant differences in the distribution of stx subtypes and PFGE genotypes between strains shed by symptomatic and asymptomatic persons. These results suggest that the rate of symptom-free STEC O157:H7 shedding may be associated with age rather than organism-related factors. Possible age-related host factors that could influence the presence of STEC O157:H7 in the stools of symptom-free persons include qualitative and quantitative differences in intestinal cross-reactive antibodies against STEC O157:H7, intestinal bacterial flora, or the sensitivity to Stx toxins between children and adults. Further investigations will be required to determine the relative importance of these and other host factors. Our finding of a high rate of asymptomatic shedding in adults may suggest the potential for secondary transmission of the bacteria from symptom-free STEC O157:H7-shedding adults to healthy children.

Top

Acknowledgments

We thank investigators of prefectural and municipal public health institutes for their collaboration.

This work was supported by a grant from the Ministry of Health and Welfare of Japan.

Top

Jun Terajima, Hidemasa Izumiya, Akihito Wada, Kazumichi Tamura, and Haruo Watanabe
Author affiliations: National Institute of Infectious Diseases, Tokyo, Japan

Top

References

  1. Tarr  PI. Escherichia coli O157:H7: clinical, diagnostic, and epidemiological aspects of human infection. Clin Infect Dis. 1995;20:18.PubMedGoogle Scholar
  2. Belongia  EA, Osterholm  MT, Soler  JT, Ammend  DA, Braun  JE, MacDonald  KL. Transmission of Escherichia coli O157:H7 infection in Minnesota child day-care facilities. JAMA. 1993;269:8838. DOIPubMedGoogle Scholar
  3. Karch  H, Russman  H, Schmidt  H, Schwarzkopf  A, Heesmann  J. Long-term shedding and clonal turnover of enterohemorrhagic Escherichia coli O157:H7 in diarrheal diseases. J Clin Microbiol. 1995;33:16025.PubMedGoogle Scholar
  4. Watanabe  H, Wada  A, Inagaki  Y, Itoh  K, Tamura  K. Outbreaks of enterohaemorrhagic Escherichia coli O157:H7 infection by two different genotype strains in Japan. Lancet. 1996;348:8312. DOIPubMedGoogle Scholar
  5. Izumiya  H, Terajima  J, Wada  A, Inagaki  Y, Itoh  K, Tamura  K, Molecular typing of enterohemorrhagic Escherichia coli O157:H7 isolates in Japan by using pulsed-field gel electrophoresis. J Clin Microbiol. 1997;35:167580.PubMedGoogle Scholar

Top

Cite This Article

DOI: 10.3201/eid0502.990222

Related Links

Top

Table of Contents – Volume 5, Number 2—April 1999

EID Search Options
presentation_01 Advanced Article Search – Search articles by author and/or keyword.
presentation_01 Articles by Country Search – Search articles by the topic country.
presentation_01 Article Type Search – Search articles by article type and issue.

Top

Page created: December 10, 2010
Page updated: December 10, 2010
Page reviewed: December 10, 2010
The conclusions, findings, and opinions expressed by authors contributing to this journal do not necessarily reflect the official position of the U.S. Department of Health and Human Services, the Public Health Service, the Centers for Disease Control and Prevention, or the authors' affiliated institutions. Use of trade names is for identification only and does not imply endorsement by any of the groups named above.
file_external