Symptoms of E. coli infection
What happens after the Shiga toxin-producing E. coli are ingested?
E. coli infection occurs when a person ingests Shiga toxin (Stx)-producing E. coli (e.g., E. coli O157:H7) after exposure to contaminated food, beverages, water, animals, or other persons. After ingestion, E. coli bacteria rapidly multiply in the large intestine and bind tightly to cells in the intestinal lining. This snug attachment facilitates absorption of the toxin into the small capillaries within the bowel wall, where it attaches to globotriaosylceramide (Gb3) receptors.
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, followed within 24 hours by diarrhea (Boyce, Swerdlow, & Griffin, 1995; Tarr, 1995). Hemorrhagic colitis typically occurs within 2 to 5 days of ingestion of E. coli, but the incubation period, or time between the ingestion of E. coli bacteria and the onset of illness, may be as broad as 1 to 10 days.
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. In about 10 percent of E. coli cases, the Shiga toxin attachment to Gb3 receptors results in HUS.
HUS had been recognized in the medical community since at least the mid-1950’s; however, the syndrome first caught the public’s attention in 1993 following a large E. coli outbreak in Washington State that was linked to the consumption of contaminated hamburgers served at a fast-food chain. A total of 501 E. coli cases were reported; 151 were hospitalized (31 percent), 45 persons (mostly children) developed HUS (9 percent), and three died (Bell, et al., 1994).
During HUS, the majority of the toxin gains access to the systemic circulation where it becomes attached to weak receptors on white blood cells (WBC) thus allowing the toxin to “ride piggyback” to the kidneys where it is transferred to numerous strong Gb3 receptors that grasp and hold on to the toxin.
Organ injury is primarily a function of Gb3 receptor location and density. These receptors are probably always in the gut wall and kidneys, but heterogeneously distributed in the other major body organs. This may be the reason that some patients develop injury in other vital organs (e.g., brain, etc). Once Stx attaches to receptors, it moves into the cells’ cytoplasm where it shuts down the cells’ protein machinery resulting in cellular injury or death, and subsequent damage to vital organs such as the kidney, pancreas, and brain.