Bacterial fibers may contribute to avian, human infection
While Escherichia coli is typically a friendly and ubiquitous bacterial resident in the guts of humans and other animals, the bacteria can occasionally colonize other regions of the body, resulting in serious health consequences. Researchers at Arizona State University's Biodesign Institute and the University of Florida at Gainesville examined avian pathogenic E. coli and how they infect other parts of the body.
E. coli form threadlike fibers known as E. coli common pilus which can be found on the surface of bacteria cells. The researchers studied how ECPs contribute to APEC's ability to cause infection and form biofilms. Biofilms provide reservoirs for pathogenic organisms to persist in the body and can express increased resistance to antibiotics.
The researchers found that ecpA, a gene coding for a structural subunit of ECP previously associated with human pathogenic E. coli, was present in 76 percent of tested samples of APEC strains derived from turkeys and chickens afflicted with coliobacillosis. Coliobacillosis is a collective term for infections that cause significant economic losses to the poultry industry due to treatment costs, lowered egg production and mortality.
The authors said the results confirm that APEC and human pathogenic E. coli, which can cause diarrheal diseases, pneumonia and urinary tract infections, share virulence traits. The researchers further speculate that ecpA may allow E. coli to persist in the intestine before migrating to extra-intestinal sites and becoming pathogenic.
When the researchers deleted ECP-related genes from bacteria, they found a reduction in biofilm production. The researchers suggest that ECP could be a target for future therapeutics aimed at serious infections in humans and animals.
"Our study has clearly shown that although the gene of ECP was found in a large number of APEC, these bacteria express this gene differently when they are in contact with cells or in biofilm," Melha Mellata, an assistant professor at Arizona State, said. "Elucidating how the expression of some genes is turned on or off by different factors will help us understand how these bacteria cause disease."