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Proxy Clinical Markers for Shiga Toxin Disease Identified


 

WASHINGTON — The severity of disease caused by Shiga toxin-producing bacteria may be tracked with a new scale in development that uses clinical markers of disease rather than direct measurement of toxin load, Dr. Martin M. Bitzan reported at a biodefense research meeting sponsored by the American Society for Microbiology.

“While the clinical diagnosis of hemolytic uremic syndrome appears straightforward, there are no defined criteria to describe and grade the severity of hemolytic uremic syndrome or of the preceding gastrointestinal disease,” Dr. Bitzan of the department of nephrology, Montreal Children's Hospital, said in a poster.

Measurement of Shiga toxin in body fluids or tissue is currently not feasible, which makes it necessary to develop proxy markers of Shiga toxinemia, he and his colleague noted.

Sporadic cases or outbreaks of infections involving Shiga toxin-producing bacteria mostly occur in children in community settings. The majority of these infections in North America are caused by Escherichia coli serotype O157:H7.

The researchers developed a disease severity scale comprising four distinct facets of Shiga toxin-producing E. coli infections: enteropathy, inflammation and vasculopathy, thrombotic microangiopathy, and nephropathy.

They tested the scale on a database of 146 consecutive patients aged 1–16 years with Shiga toxin-producing E. coli who had bloody (85%) or nonbloody (15%) diarrhea that resulted in partial (5%) or complete (13%) hemolytic uremic syndrome (HUS). The scores of patients with HUS on all of the scale's components except enteropathy became significantly worse 3–5 days after disease onset than those without the syndrome. The scale is being validated in another study.

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