Role of ISAba1 and ISAba125 in governing the expression of blaADC in clinically relevant Acinetobacter baumannii strains resistant to cephalosporins.

Acinetobacter baumannii is a multi-resistant opportunistic nosocomial pathogen responsible for several outbreaks worldwide. It can cause several infections at various sites of the body. One of the main infections caused by this bacterium is ventilator-associated pneumonia in patients in intensive care units. Treating these infections is becoming difficult because of the high resistance to antimicrobial agents. This study compared the expression of the chromosomally encoded bla(ADC) gene in isolates having ISAba1, ISAba125 and no insertion upstream of the bla(ADC) gene in A. baumannii clinical isolates. It showed that the expression of bla(ADC) was six times greater when ISAba125 was present upstream of the gene in comparison with the constitutively expressed bla(ADC) gene with no insertion present upstream. The study indicated that ISAba125 has better promoters than ISAba1 and this is responsible for the overexpression of the bla(ADC) gene as they share considerable homology to the well-established Escherichia coli promoters. The -10 box of ISAba125 formed a fusion promoter with the -35 box of the bla(ADC) gene causing the bla(ADC) gene to be significantly overexpressed. The ability to upregulate the expression of bla(ADC) with the assistance of different insertion elements such as ISAba1 and ISAba125 has become an important factor in A. baumannii resistance to cephalosporins.