Title
Clinical cystic fibrosis (CF) isolates of Burkholderia cepacia have been found to have several properties: secreted iron chelators and high antibiotic resistance. The laboratory strain 249-2, produces the iron chelator salicylic acid (SA), but has lost the ability to secrete it. This strain is also susceptible to many antibiotics. The general consensus on antibiotic resistance is that increased exposure to antibiotics promotes resistance. We are proposing an alternative theory wherein B. cepacia becomes antibiotic resistant, even in the absence of antibiotics. Increased mucin production inherent in the CF lung creates a low iron condition which induces B. cepacia to secrete SA, which in turn has been shown to regulate antibiotic resistance. We will test a genomic library from K61-3, a CF clinical isolate of B. cepacia for the ability to confer on B. cepacia 249-2, growth under low iron conditions. We will then test the transformed 249-2 for the ability to secrete SA as well as for antibiotic resistance. The resulting information, along with sequence information, will enable us to validate our theory, potentially leading to new avenues of treating CF lung infections.
