Revisiting the host as a growth medium

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Abstract
The ability of a pathogen to cause disease relies on its ability to acquire nutrients in vivo. This Review revisits the concept of the host as a growth medium during infection and outlines the potential of this experimental approach for development of new therapeutics. The carbon source can influence the ability of a pathogen to evade the immune system. Neisseria meningitidis preferentially uses a carbon source which has degradation products that feed directly into the biosynthesis of compounds important for immune evasion. The available carbon source affects site-specific colonization, or tissue tropism, by certain pathogens. Unlike enterohaemorrhagic Escherichia coli (EHEC) strains, uropathogenic E. coli (UPEC) strains can colonize the urinary tract. The ability of UPEC to catabolize D-serine, excreted as a urinary waste product, might help to define this tropism. Carbon resource partitioning is a method used to avoid competition with other organisms. Aggregatibacter actinomycetemcomitans, a slow-growing opportunistic pathogen that is found in the human mouth, uses a non-optimal carbon source that is produced as a waste product by prevalent and fast-growing oral streptococci. Bacteria communicate using diverse chemical signals, and carbon source metabolism can influence production and dissemination of these signals. Pseudomonas aeruginosa responds to aromatic amino acids in cystic fibrosis sputum and increases production of a cell–cell communication signal that is important for interspecies competition and virulence. Many infection sites, as bacterial growth media, remain undefined, and for many pathogens the in vivo carbon source is not known. Much work remains to be done to elucidate bacterial carbon metabolism during infection.