By now readers of this site are well versed in Marler Clark’s ongoing efforts to have non-O157 shiga toxin-producing strains of E. coli (STECs) declared “adulterants” by the United States Department of Agriculture (USDA). These currently unregulated strains are highly dangerous to humans—severely sickening tens of thousands of people per year and killing many others. Just this past August Cargill recalled 8,500 pounds of ground beef products due to E. coli O26; three are sick in Maine and New York.  Two years prior, in August 2008, an outbreak of E. coli O111 at an Oklahoma restaurant sickened 300 and killed one.  A May 2010 outbreak of E. coli O145 in lettuce sickened 26.

Beyond non-O157 STEC detection in product, an article in the latest of issue of the CDC’s publication, Emerging Infectious Diseases, titled “Hemolytic-Uremic Syndrome in a Grandmother,” underscores the other key component to effectively confront the non-O157 shiga toxin-producing E. coli problem—proper human detection. The authors focus right in on why human detection is so invaluable: “Failure to test for these serotypes leads to underdiagnosis and underreporting of STEC infection, to the detriment of patient care and public health surveillance, respectively.” 

The article’s primary author, Lane C. Crawford, is a fourth-year medical student at Vanderbilt University whose own grandmother became seriously ill from Hemolytic Uremic Syndrome (HUS), resulting in an 11 day hospitalization with another 18 days in rehabilitation. Her illness course was terrible with both renal and neurological involvement, and removal of all but the distal 12 inches of her colon. Thankfully, her HUS experience, unlike many others we have encountered, resulted in a remarkable recovery.

The difficulties underlying the accurate diagnosis of the source of her HUS are complex and thus I encourage you to read the full article for a complete understanding. Essentially, because the leading cause of HUS is STEC infection, a stool sample was collected and tested for the presence of E. coli. The results were negative. In actuality, however, she was very likely suffering from an undetected non-O157 E. coli infection. Her E. coli-negative test result set into motion a series of decisions that likely had a significant impact on her illness course. 

My father learned that stool culture on commonly used culture media is quite effective for identification of Salmonella spp. and other bacteria not normally found in human bowel. However, because E. coli is part of normal bowel flora, a separate strategy is needed to distinguish diarrheagenic E. coli serotypes from their nonpathogenic brethren. To do this, most laboratories use a selective medium called sorbitol-MacConkey agar (SMAC) to identify the pathogenic serotype E. coli O157:H7. Whereas most other E. coli serotypes ferment sorbitol and grow as pink colonies, this serotype does not ferment sorbitol and grows as colorless colonies. When my father asked how often stool culture results from patients with actual bacterial colitis were negative, the technician assured him, "almost never." Thus, when my grandmother’s stool culture came back negative, my father did not question it.

This, however, was far from conclusive evidence of her lack of an E. coli infection:

One recent article stated that 20%–50% of all STEC infections in the United States are caused by non-O157 STEC serotypes, some of which can cause HUS (2). A second article explained that non-O157 STEC is not detected by SMAC because, like nonpathogenic E. coli, it ferments sorbitol. Instead, both O157 and non-O157 STEC could be detected by enzyme immunoassay for Shiga toxin (3). My grandmother’s negative stool culture now seemed less conclusive.

In other words, labs relying only on SMAC for STEC detection are getting but a fraction of the full picture. 

As illustrated by this case report, STEC infection may be difficult to recognize clinically, so appropriate laboratory testing is crucial for accurate and timely diagnosis. Up to 20%–50% of STEC infections in the United States, or ≈37,000 cases per year, are caused by non-O157 E. coli serotypes (2,5), some of which have been associated with severe disease and HUS (6,7). Failure to test for these serotypes leads to underdiagnosis and underreporting of STEC infection, to the detriment of patient care and public health surveillance, respectively. A 2006 report strongly urges clinical diagnostic laboratories to assay all stool specimens for Shiga toxin, to simultaneously culture the specimens on SMAC for organism isolation, and to forward positive specimens to a public health laboratory (8).

As the article highlights, the ramifications of misdiagnosed STEC infections are very serious. Until all laboratories follow the CDC’s best practice recommendations for full STEC detection, the true breadth of harm from these nasty pathogens with remain unknown.