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Nutrition: infecting the starved cell
- Phage-Host Interaction: an Ecological Perspective

Scientists in the laboratory generally work with media maintaining optimal growth of their bacteria. Bacteria in the marine environment have to live with much less nutrients.

Consequently, in situ burst size (the number of phages produced per infected cell) is generally smaller in the marine environment than in the laboratory, where bacteria grow to larger sizes. It was predicted that the normal state of a marine bacterium corresponds to the nutritional state of a laboratory bacterium under stationary phase. In the laboratory, bacteria cannot be productively infected with phages in the stationary phase. In general, infected stationary-phase cells release progeny phage only after resumption of cell growth. This observation could explain the persistence of virulent phages within populations of nongrowing cells. However, there are reports of Pseudomonas phages that productively infect host cells maintained under starvation conditions (57). In this case, the latent period was lengthened and the burst size greatly reduced when compared to those of logarithmic-phase infection (71). In fact, mycobacteriophages have found a way to replicate in slow-growing cells (51).

The nutritional considerations are also relevant for applied phage research like the therapeutic use of phages against pathogenic bacteria. Empirical phage therapy was conducted in the United States during the 1930s and in the Soviet Union until quite recently, where substantial success against bacterial diarrhea and skin infections was reported (59). Notably, oral T4-like phages survived the gastrointestinal passage in mice (19) and humans (unpublished results). However, the presence of a host cell and a corresponding phage is not sufficient to lead to a phage infection in the intestine. The host cell must be in an appropriate physiological state to allow productive infection, and the cell must be in an accessible anatomical location for the phage. Mouse experiments demonstrated that the resident E. coli flora was protected against oral phage exposure, although the majority of the fecally excreted E. coli strains were infected by the same phage in vitro (19). At first glance, one would expect that the gut is a nutritionally privileged anatomical site. However, E. coli within the lumen of the colon is nutritionally deprived and nonreplicating (53) and is thus a poor target for phages. The metabolically active intestinal E. coli cells are found in microcolonies associated with the mucus layer of the gut mucosa (37, 52), where they are probably physically shielded from luminal phages. In contrast, E. coli strains freshly introduced into the mouse infection model were fully susceptible to oral phage exposure (19). Apparently, these new E. coli cells were actively replicating but not yet associated with the mucus layer of the gut mucosa. This example illustrates that we need a detailed knowledge of the ecology of target bacteria and the therapeutic phages in the gut of the mammalian host if phage therapy is to be successful (38). Similar considerations apply for the application of phages to other body sites, e.g., the skin. The Soviet experience suggested the use of phages for the treatment of wound infections (59), and food microbiologists explore the use of phages to decontaminate the skin of slaughtered chicken from Salmonella and Campylobacter spp. (30) and E. coli O157 for beef (38). The potential medical and food safety applications of phages are favored by the availability of broad-host-range Myoviridae for Staphylococcus aureus (50) and Listeria monocytogenes (41).

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