Age, Genetics Determine E. coli Virulence

Not all E. coli bacteria are created equal. This bacteria is commonly isolated from pigs, and may or may not be the primary cause of disease, depending on the age of the pig and the genetic makeup of the pig and the E. coli.

At the University of Minnesota Veterinary Diagnostic Laboratory, we test the genetic makeup of the E. coli bacteria using polymerase chain reaction (PCR) tests for specific genes that are associated with virulence, or the ability to cause disease. A list of the genes we test for is listed below.

In order for an E. coli bacteria to cause disease, it first must attach to the intestinal lining of the pig. The E. coli have genes that encode for fimbria or adhesion factors that allow the bacteria to adhere to the gut. For example, if the E. coli has the gene for the F18 fimbria, the bacteria can adhere to the F18 receptor in the gut of the pig and can potentially cause disease.

The pig receptors for the E. coli are also controlled by genetics. For example, the F18 receptor in pigs don’t develop until approximately weaning age, so the E. coli bacteria with the F18 fimbria won’t adhere to the gut in younger pigs. The receptor for the F18 fimbria has been bred out of some lines of pigs, so that even in older pigs, the E. coli can’t adhere to the gut and cause disease. The same is true for other fimbrial receptors that have been bred out of genetic lines of pigs.

After the E. coli has adhered to the gut, the bacteria must have toxin genes in order to release the toxins that cause disease. A list of toxins is also included in the table below.

The distribution of the fimbrial, adhesion and toxin genes we test for is shown in the graphs below. It’s interesting to note that the fimbrial genes we detect are predominantly the F4 (also known as K88) for the first several weeks, as would be expected for this bacteria primarily associated with neonatal diarrhea. The F18 increases and predominates postweaning, in keeping with the lack of receptors in younger pigs. The toxin genes are dominated by heat stable enteroxin 1 and heat stable enterotoxin B. The shigatoxin 2e gene that is associated with postweaning edema disease is relatively low in comparison.

Click to view graphs.

Jerry Torrison, DVM, Kurt Rossow, DVM, Simone Oliveira, DVM
University of Minnesota Veterinary Diagnostic Laboratory