Escherichia coliO157:H7by Paul D. Fey, Ph.D.Escherichia coli is an importantpathogen which can cause a variety ofdiseases including diarrhea, urinary tractinfections, bacteremia, pneumonia, andmeningitis. Most strains of E. coli arefound surviving as avirulent commensalsin the large bowel of mammals.However, specific virulence traits can beacquired from plasmids and othertransferable elements which allow theorganism to invade or attach to specificcellular types or to produce toxins. Aloose correlation exists between strainsof E. coli that cause specific disease anda serological classification scheme firstdescribed by Kauffman in 1944. Thisscheme is based on two highly variablecellular antigens, the somatic (O) antigenand the flagellar (H) antigen. Strainswith a similar O antigen are of the sameserogroup, while those strains with asimilar O antigen and H antigen are ofthe same serotype. Additionally, strainscan be characterized by the type ofvirulence genes they possess. Strainswhich possess the same virulence factorsare said to be of the same virotype.Using serotyping and virotyping inconjunction, six different groups haveevolved from those strains of E. coli thatcause diarrhea. The first fivegroups include enterotoxigenic E. coli(ETEC), enteroaggregative E. coli(EAEC),enteroinvasive E. coli (EIEC),diffusely adherent E. coli (DAEC), andenteropathogenic E. coli (EPEC).These groups cause diarrheal disease byvarious combinations of virulence traitsand mechanisms including theliberation of enterotoxins (ETEC),adherance to intestinal epithelial cells(EAEC, DAEC, and EPEC) andinvasion of intestinal epithelial cells(EIEC). The sixth group,enterohemorrhagic E. coli or EHEC, isa more serious pathogen which not onlycauses bloody diarrhea but may alsocause other serious diseases such ashemolytic uremic syndrome (HUS).EHEC was first recognized as anemerging pathogen in 1982 when anoutbreak of diarrhea and HUS occuredfollowing ingestion of undercookedhamburgers from a fast-food restaurant.An epidemiological investigation foundthat the etiologic agent causing thedisease was E. coli O157:H7, a serotypenot previously recognized as a humanpathogen. Since that time, largefoodborne outbreaks caused by E. coliO157:H7 have occurred as well assporadic cases of disease. The CDC hasrecently reported E. coli O157:H7 asthe fourth most prevalent bacteriald i a r r h e a l p a t h o g e n b e h i n dCampylobacter sp., Salmonella sp., andShigella sp.E H E C are ingested fromcontaminated water or food and appearto colonize the lower intestine. A smallinfectious dose is required; studies haveshown that as few as 200 bacteria aresufficient to cause disease. The majorvirulence factor of EHEC is abacteriophage-encoded shiga -toxin.This toxin, in part, mediates diarrhealdisease and presumably HC and HUS aswell. There are two different types ofimmunologically distinct shiga-toxinsproduced in EHEC called Stx1 andStx2. Stx1 is identical to the shigatoxinproduced by Shigella dysenteriae.Other virulence factors include an outermembrane protein called intimin, whichis important in colonization of theintestine, and an enterohemolysin,encoded on a 60 Mda plasmid calledpO157. Enterohemolysin maycontribute to virulence by lysing redblood cells and therefore providing asource of iron to the bacterium.Even though E. coli O157:H7 is themajor serotype isolated from patientswith HC and HUS, other serotypes haverecently been isolated which expressS t x 1 , S t x 2 , i n t i m i n a n denterohemolysin. The most commonnon-O157:H7 serotypes isolated fromhumans with diarrheal disease areO26:H11, O103:H2, O111:NM, andO113:H21. Additionally, investigatorshave found Stx-producing Citrobacterfreundii and Enterobacter cloacae frompatients with HUS. Livestock animals,including cattle, sheep, pigs, chickensand goats, are the major reservoir of
Stx-producing E. coli. However, sincethe majority of these isolates are not ofthe O157:H7 serotype and do notcontain other virulence factors such aseae or enterohemolysin, the virulence ofthese isolates is not known.Treatment of patients with HUS is atbest controversial. Some studies havesuggested that EHEC infected patientswho were treated with antibiotics had agreater chance of developing HUS thanthose patients who were not. Therefore,treatment is mostly supportive.However, screening for and detection ofshiga-toxin producing E. coli isnecessary for the detection of outbreaksso that appropriate infection controlmeasures can be administered.Detection of shiga-toxin producing E.coli is difficult in the clinicalmicrobiology laboratory due to thelarge number of avirulent E. colipresent in fecal specimens. However,since E. coli O157:H7 do not fermentsorbitol as strongly as other commensalE. coli, selective and differential mediasuch as sorbitol-MacConkey agar(SMAC) or cefixime-tellurite-sorbitol-MacConkey agar (CT-SMAC) can beused to screen stool samples for thisbacterium. Since other serotypes ofEHEC ferment sorbitol strongly, theywill not be detected using SMAC orCT-SMAC agars. To circumvent thisproblem, investigators have developedELISA and PCR assays that will detectshiga toxin (both Stx1 and Stx2) fromfecal samples. However, due to theexpense of these assays, they are notwidely used in clinical microbiologylaboratories across the country.Therefore, the prevalence of non-E. coliO157:H7 EHEC is not known in mostparts of the United States.If your laboratory is not screeningstool specimens for E. coli O157:H7,the NPHL suggests that you add SMACor CT-SMAC to your routine stoolculture procedure for a period of sixmonths (preferably during the springand summer). We do not suggest thatyou add a SMAC or CT -SMAC plateonly to stools which are visibly bloodysince blood in stools may not bevisually evident. After the six monthperiod, an assessment can be made as towhether continuing to screen for E. coliO157:H7 is appropriate for yourlaboratory. Our opinion is that evenone case of diagnosed E. coli O157:H7infection is worth the cost of the addedSMAC or CT-SMAC agar plate.