E. coli O157:H7 bacteria and other pathogenic E. coli mostly live in the intestines of cattle, but E. coli bacteria have also been found in the intestines of chickens, deer, sheep, and pigs. A 2003 study on the prevalence of E. coli O157:H7 in livestock at 29 county and three large state agricultural fairs in the United States found that E. coli O157:H7 could be isolated from 13.8% of beef cattle, 5.9% of dairy cattle, 3.6% of pigs, 5.2% of sheep, and 2.8% of goats. Over 7% of pest fly pools also tested positive for E. coli O157:H7. Shiga toxin-producing E. coli does not make the animals that carry it ill. The animals are merely the reservoir for the bacteria.
According to a study published in 2011, an estimated 93,094 illnesses are due to domestically acquired E. coli O157:H7 each year in the United States. Estimates of foodborne-acquired O157:H7 cases result in 2,138 hospitalizations and 20 deaths annually.
What makes E. coli O157:H7 remarkably dangerous is its very low infectious dose, and how relatively difficult it is to kill these bacteria. “E. coli O157:H7 in ground beef that is only slightly undercooked can result in infection.” As few as 20 organisms may be sufficient to infect a person and, as a result, possibly kill them. And unlike generic E. coli, the O157:H7 serotype multiplies at temperatures up to 44° Fahrenheit, survives freezing and thawing, is heat-resistant, grows at temperatures up to 111 F, resists drying, and can survive exposure to acidic environments. And, finally, to make it even more of a threat, E. coli O157:H7 bacteria are easily transmitted by person-to-person contact.
The colitis caused by E. coli O157:H7 is characterized by severe abdominal cramps, diarrhea that typically turns bloody within 24 hours, and sometimes fever. The incubation period—that is, the time from exposure to the onset of symptoms—in outbreaks is usually reported as 3 to 4 days but may be as short as 1 day or as long as 10 days. Infection can occur in people of all ages but is most common in children.
After ingestion, E. coli bacteria rapidly multiply in the large intestine and then bind tightly to cells in the intestinal lining. This snug attachment facilitates absorption of the toxins into the small capillaries within the bowel wall. Once in the systemic circulation, Shiga toxin becomes attached to weak receptors on white blood cells, thus allowing the toxin to “ride piggyback” to the kidneys where it is transferred to numerous avid (strong) Gb3 receptors that grasp and hold on to the toxin.
Inflammation caused by the toxins is believed to be the cause of hemorrhagic colitis, the first symptom of E. coli infection, which is characterized by the sudden onset of abdominal pain and severe cramps. Such symptoms are typically followed within 24 hours by diarrhea, sometimes fever. As the infection progresses, diarrhea becomes watery and then may become grossly bloody; that is, bloody to the naked eye. E. coli symptoms also may include vomiting and fever, although fever is an uncommon symptom.
On rare occasions, E. coli infection can cause bowel necrosis (tissue death) and perforation without progressing to hemolytic uremic syndrome (HUS)—a complication of E. coli infection that is now recognized as the most common cause of acute kidney failure in infants and young children and at times death.