Frey J, Kuhn R, Nicolet J
Institute for Veterinary Bacteriology, University of Berne, Switzerland.
FEMS Microbiol Lett. 1994 Dec 1;124(2):245-51. doi: 10.1111/j.1574-6968.1994.tb07291.x.
A non-hemolytic mutant of Actinobacillus pleuropneumoniae serotype 5 has a deletion spanning the entire apxI operon. Therefore it does not produce ApxI and is unable to secrete ApxII. This mutant also has lost the co-hemolytic CAMP effect which is characteristic of the species A. pleuropneumoniae. The CAMP effect is restored when the mutant is complemented in trans by the apxIBD genes cloned in a broad host range vector, thus permitting secretion of ApxII, or when the entire apxI operon is cloned in the mutant, thus restoring the original toxin phenotype ApxI+ ApxII+. When the toxins ApxI, ApxII or ApxIII individually are expressed and secreted from E. coli harboring recombinant plasmids containing the genes apxICA and apxIBD or apxIICA and apxIBD or apxIIICABD, respectively, the distinct CAMP phenomenon is produced by the recombinant strains. The CAMP phenomenon is strongest by the recombinant E. coli strain expressing the non-hemolytic ApxIII, somewhat less when ApxI is expressed, and weak when ApxII is expressed. In A. pleuropneumoniae the CAMP phenomenon is also strongest in those serotypes which express ApxIII. The CAMP phenomenon of A. pleuropneumoniae is assumed to be directly caused by any of the RTX-toxins ApxI, ApxII or ApxIII. A previously reported gene from A. pleuropneumoniae, named cfp or hlyX, which provides E. coli strains with a hemolytic character and a CAMP phenomenon, shows high similarity to the E. coli global regulation gene fnr, and which is able to complement a delta fnr mutant.(ABSTRACT TRUNCATED AT 250 WORDS)
