Heme, an iron supply for vibrios pathogenic for fish

One of the main mechanisms present in gram-negative bacterial pathogens to obtain iron is the utilization of free heme or heme proteins from the host tissues. Vibrio anguillarum, the etiological agent of vibriosis in fish, and Photobacterium damselae subsp. piscicida, the causative agent of fish pasteurellosis, can acquire iron from free heme or heme-containing proteins present in the host tissues by a siderophore-independent mechanism. Similarly to other animal and human pathogens, the general mechanism for heme uptake in these two species consists in the presence of an outer membrane receptor that transport the heme molecule into the periplasm via a TonB-dependent process, and additional proteins that complete the transport of heme from the periplasm into the cell cytoplasm. Expression of heme uptake genes is iron-regulated at the transcriptional level by the repressor protein Fur. The heme uptake mechanisms are believed to contribute to virulence for fish. The existence of variability in the distribution of heme transport genes among strains suggests that gene inactivation and/or horizontal transfer might play a significant role in generating intraespecific genetic diversity.