These virulence genes, frequently assembled in operons, may be part of large mobile elements (plasmids, prophages, pathogenicity islands, transposons, integrons) or generated by gene duplications. According to the ‘pan-genome' concept for bacterial species (Tettelin et al., Rasko et al., Bentley, Lapierre & Gogarten, ), the genes encoding virulence factors, which enable the pathogens to occupy specific habitats in their hosts and to survive in these often hostile infected environments, belong to the ‘character genes'. These events as well as the integration of newly acquired genes into pre-existing regulatory circuits may add new or re-shape established virulence properties (for recent reviews see Ambur et al., Juhas et al., Wagner, Dobrindt et al., ). The genes for the specific virulence factors of pathogenic bacteria are mainly obtained by lateral DNA transfer and/or mutations of existing genes that are established by selection. Thus, in general, it is not the bacterial species that defines the virulence potential, but rather the special set of pathogenicity/fitness factors acquired by the bacterium (defining the ‘pathotype') and the fitness of the host. By comparison, facultative pathogens, being less well equipped with such factors, require special host opportunities to cause infectious diseases. For this goal, obligate pathogens are equipped with indispensible basic sets of pathogenicity and fitness (including metabolic) factors that allow optimal adaptation to the cellular, immunological and metabolic properties of their infected host niches. The infection strategy of obligate pathogenic bacteria aims to efficiently proliferate in the infected host and to spread into new hosts.
These bacteria are able to breach body barriers, to escape even a competent innate immune system or to gain control over the physiological function of the mucosal interfaces (e.g. The third group, the obligate pathogenic bacteria, do not belong naturally to the human microbiome. These latter bacteria use the respective host habitat more or less as culture medium, and some of them can survive and proliferate in natural environments as well. These members are termed facultative pathogenic bacteria to distinguish them from the other group of the indigenous microbiota, the nonpathogenic bacteria. In the case of defects of the innate immunity, caused by injuries, genetic or physiological disorders, certain members of the microbiota may, however, breach this barrier, replicate and eventually disseminate into deeper tissue and cause infections.
Sketchy micro listeria professional#
mucus/mucosal epithelium), microbicidal (poly)peptides and professional phagocytes, controls the containment of the microbiota and prevents the bacteria from crossing the border. In these hosts, the innate immune system, comprised of physical barriers (e.g. In humans and other mammals, bacteria mainly colonize the outer surface (skin/cutis) and the pharyngeal-gastro-intestinal tract forming highly diversified indigenous microbiota. Many bacteria are able to interact with higher organisms in different ways and the outcome of these interactions can be either advantageous (commensal and mutualistic bacteria) or disadvantageous (pathogenic bacteria) for the host. Human bacterial pathogens, nonpathogenic relatives, extra- and intracellular replication, carbon metabolism, virulence gene expression Introduction Furthermore, we discuss – whenever relevant data for the pathogenic representatives are available – the possible effect of the metabolism on the expression of virulence genes.
The question therefore arises whether there are specific metabolic requirements that support stable intracellular replication. However, their ability to replicate intracellularly differs significantly. All bacteria selected have the potential to reach the interior of mammalian host cells.
The focus of this review is on the metabolic potentials and adaptations of three different groups of human extra- and intracellular bacterial pathogens and their nonpathogenic relatives. The knowledge of how these bacteria adapt their metabolism to the preferred habitats is critical for our understanding of pathogenesis, commensalism and symbiosis, and – in the case of bacterial pathogens – could help to identify targets for new antimicrobial agents. Most bacteria pathogenic for humans have closely related nonpathogenic counterparts that live as saprophytes, commensals or even symbionts (mutualists) in similar or different habitats.