INTERACTION OF AVIRULENT TRANSPOSITIONAL MUTANTS OF XENORHABDUS NEMATOPHILUS ATCC 19061 (ENTEROBACTERIACEAE) WITH THE ANTIBACTERIAL SYSTEMS OF NON-IMMUNE GALLERIA MELLONELLA (INSECTA) LARVAE

摘要

The interactions of the virulent form of the phase one variant 19061/1 of the bacterial insect pathogen Xenorhabdus nematophilus ATCC 19061/1 (refers to the phase one form) and four avirulent Tn5-insertion mutants with the antibacterial system of non-immune larvae of Galleria mellonella (the greater wax moth) were characterized. There was no discernible relationship between extracellular enzymes of the bacterial strains and bacterial virulence for the insects. Spheroplast formation was negatively correlated with virulence. Bacterial adhesion to the hemocytes varied with the hemocyte type and bacterial strain and was not related to virulence. Changes in the levels of outer membrane proteins with apparent molecular weights of 19 to 40kDa may be associated with bacterial adhesion to hemocytes but not to bacterial virulence. Bacterial hydrophobicity influenced the adhesion of the bacteria to the granulocytes but not to the plasmatocytes. The profiles of the removal of the bacteria from the hemolymph, in vivo, varied with the bacterial strain and was not correlated with virulence. Mutant bacteria possessed leaky outer membranes which released serine proteases that activated the prophenoloxidase system and may have facilitated bacterial adhesion to the hemocytes. Hemocytes were damaged by the lipopolysaccharides isolated from the bacterial strains. The rate of hemocyte damage, however, was less with the bacterial mutants and was due to the slower rates of release of lipopolysaccharides from these strains. The long-term survival of the bacteria in the insects varied with the bacterial strain. Although both the virulent and avirulent strains achieved the same final concentration, the avirulent isolates took longer to achieve the level. This delay may allow the insect to produce antibacterial proteins and/or detoxify virulence-factors (e.g. endotoxin) tipping the balance in favour of the host's survival.