Enterohemorrhagic Escherichia coli O157: H7 infection

Sumio Shinoda, Shigeo Yamamoto, Ken Ichi Tomochika, Shin-ichi Miyoshi

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

The first recognized outbreaks of hemorrhagic colitis occurred in 1982 in the United States and its etiologic agent was identified to be Escherichia coli O157:H7, a serotype not previously associated with diseases in humans. In Japan, isolates of the serotype O157:H7 from contaminated drinking water were first implicated in an outbreak occurred in 1990 in a kindergarten of the Saitama Prefecture, and at least other 12 such outbreaks have been recorded in 1993-1995. In the year 1996, unprecedentedly large outbreaks and many sporadic cases of disease caused by E. coli O157:H7 occurred in various parts of Japan, affecting more than 9000 people in total (11 deaths). In most cases, however, the ultimate source of the infection could not be traced. Although many different serotypes of E. coli, which are collectively referred to as enterohemorrhagic E. coli (EHEC), were found to cause bloody diarrhea, the serotype O157:H7 has been recognized worldwide as the pathogen associated most frequently with serious complications known as hemolytic colitis and hemolytic uremic syndrome. E. coli O157:H7 is characteristic of a low infectious dose, on the order of a few hundred organisms, which contributes to the spread of the infection in outbreak situations. Cattle are considered to be the major reservoir of EHEC including O157:H7. EHEC strains produce at least two immunologically distinct cytotoxins that closely resemble the Shiga toxin produced by the Shigella dysenteriae type 1 strains. These toxins (called Shiga-like toxins or Vero toxins) appear to be responsible for causing many pathological effects associated with EHEC infections. However, how the toxins move from the intestinal tract lumen to the sites where they damage the kidney remains to be evaluated. Moreover, there are some doubts about the value of antibiotic therapy in such infections because of the observation that some antibiotics can increase the toxin expression in vitro and because of the concern that EHEC which are lysing due to their actions in the gastrointestinal tract lumen may actually release more toxin than do intact bacterial cells. Unique biochemical characteristics of E. coli O157:H7 it ferments sorbitol very slowly and usually does not make, β-glucuronidase are used to differentiate this strain from other enteric E. coli strains. Alternative methods based on the detection of the toxins themselves by enzyme immunoassay are employed in parallel. This review describes the current understanding of the infectious disease caused by E. coli O157:H7, with an emphasis on the main diagnostic tests and epidemiology for this serotype and the role of the toxins in pathogenesis.

Original languageEnglish
Pages (from-to)1-14
Number of pages14
JournalJapanese Journal of Toxicology and Environmental Health
Volume43
Issue number1
Publication statusPublished - 1997

Fingerprint

Enterohemorrhagic Escherichia coli
Escherichia coli O157
Escherichia coli
Disease Outbreaks
Infection
Shiga Toxins
Colitis
Japan
Shigella dysenteriae
Shiga Toxin
Anti-Bacterial Agents
Escherichia coli Infections
Hemolytic-Uremic Syndrome
Sorbitol
Glucuronidase
Cytotoxins
Immunoenzyme Techniques
Routine Diagnostic Tests
Drinking Water
Communicable Diseases

Keywords

  • diagnostic test
  • enterohemorrhagic E. coli
  • epidemiology
  • serotype O157:H7
  • Shiga-like toxin

ASJC Scopus subject areas

  • Toxicology

Cite this

Enterohemorrhagic Escherichia coli O157 : H7 infection. / Shinoda, Sumio; Yamamoto, Shigeo; Tomochika, Ken Ichi; Miyoshi, Shin-ichi.

In: Japanese Journal of Toxicology and Environmental Health, Vol. 43, No. 1, 1997, p. 1-14.

Research output: Contribution to journalArticle

Shinoda, Sumio ; Yamamoto, Shigeo ; Tomochika, Ken Ichi ; Miyoshi, Shin-ichi. / Enterohemorrhagic Escherichia coli O157 : H7 infection. In: Japanese Journal of Toxicology and Environmental Health. 1997 ; Vol. 43, No. 1. pp. 1-14.
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