Molecular Mechanisms of Polyhostality in Relation to Emerging Infectious Diseases

The general ecological mechanism that provides species survival and multiplication in a previously unfamiliar environment and is known as pre adaptation appears to be involved in the phenomenon of emerging infections [7]. Living in their natural environment, causative agents of emerging infections might be wild mammal pathogens or be carried asymptomatically by wild animals or be rather microbial community members than true pathogens. Their pre adaptation becomes apparent in the form of polyhostality. The term polyhostality came from descriptions of natural foci of infections where it means that the foci are supported by multiple hosts. Latter, the term polyhostality was widening to describe the capacity of a microbe to colonize several species belonging to different taxa or even to different kingdoms [8]. The Gram-negative bacterium L. pneumophila is a best studied example when adaptation for survival in protozoa provides virulence for humans [9]. The rhizosphere inhabitant Burkholderia cenocepacia was shown to establish chronic infections in immunocompromised patients. Studies of the last years demonstrated that it is a capacity to adapt for a host niche but not host cell or tissue damage that contributes in B. cenocepacia infection in humans [10]. The better known as a food born pathogen, Y. pseudotuberculosis effectively colonizes plants [11]. Another food born pathogen, the Gram-positive bacterium L. monocytogenes, was isolated from a wild spectrum of wildlife including mammals, birds and fish and seems to be a widely spread member of soil ecosystems [12,13].