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Biology Articles » Ecology » Phage-Host Interaction: an Ecological Perspective » Lysogeny: a survival strategy for both phage and bacteria

Lysogeny: a survival strategy for both phage and bacteria
- Phage-Host Interaction: an Ecological Perspective

Theory predicts that lysogeny becomes the preferred strategy when the cell density falls below the lower limit necessary for maintenance of the phage density by repeated cycles of lytic infections. The argument is that the production of temperate phages is independent of host cell density. Indeed, two marine surveys revealed 40% mitomycin C-inducible cells, and similar proportions of lysogens were identified in Pseudomonas colonies from lakes. In contrast, UV or sunlight was not a good inducer of prophages in water samples. The surveys showed a trend for lysogeny to be more prevalent in oligotrophic environments (35). This observation fits with theory, since this setting is dominated by the low density of slow-growing bacteria. Other data contradict this interpretation. Surveys in estuarine waters showed a seasonal development of lysogeny with highs in the summer months when eutrophic conditions were prevalent and lows in the winter months when cells were at their minimum (20, 44). There are further contradictions with expectations. First, spontaneous induction of prophages is generally low (10–2 to 10–5 phage per bacterium per generation). This release can only account for far less than 1% of the phage concentrations in the ocean (35). Second, large phage surveys in the North Sea revealed that only 10% of the phage isolates are temperate. In contrast, the genome maps of the major virulent S. thermophilus phages isolated from dairies still betray their origin from temperate parental phages. The preponderance of virulent phages in dairy collections might therefore represent a secondary character and an adaptation to the abundance of host cells in the dairy environment. In fact, serial passage of a temperate S. thermophilus phage resulted in its replacement by a virulent derivative deletion mutant after only a few days.

However, lysogeny is a survival strategy for phage as well as for bacteria (17). Lysogens frequently outcompete the nonlysogenic congeners, possibly due to the selective advantage conferred by lysogenic conversion genes of the prophages. Some of them are relatively universal, such as immunity functions and superinfection exclusion genes. Other prophages contribute genes that make the lysogen competitive under special ecological situations (serum resistance conferred to the lysogen by the phage lambda bor gene during blood growth of E. coli [3]). This phenomenon seems to be widespread in bacterial pathogens where many virulence factors are encoded by prophages. However, even the laboratory phages P1, P2, lambda, and Mu confer to the E. coli lysogen a higher metabolic activity and faster and longer growth than the nonlysogens (25, 39).

Shiga-toxin producing E. coli (STEC) strains represent a spectacular case of lysogeny. These strains are commonly found in the intestines of asymptomatic cattle, while in humans the STEC O157:H7 strains are dangerous food pathogens. The available evidence suggests that they are derived over the last 50 years from the enteropathogenic E. coli strain O55:H7 by the acquisition of two prophages encoding the Shiga toxins Stx1 and Stx2, the major pathogenicity factor of STEC (58). In fact, the two sequenced O157:H7 isolates contained 16 to 18 prophages, including many closely related lambda-like prophages. Whole-genome PCR scanning of eight distinct O157 strains revealed a high degree of genomic diversity, mainly due to extensive structural and positional diversity of the prophages, implying that prophages are the major factor in generating genomic diversity in the O157 lineage (49).

Toxin production differed in human and bovine STEC isolates (54). The lysogen expresses Stx in case of low iron concentration (a typical growth-limiting factor for intestinal bacteria) (64), leading to intestinal hemorrhage (liberating iron from red blood cells leading to resumed bacterial growth and Stx downregulation). Notably, stx is under the control of the Fur repressor and thus part of a large bacterial iron-controlled regulon. Similarly, the diphtheria toxin encoded by a corynephage is under the control of the DTxR, the master repressor of an iron regulon in this gram-positive bacterium. Stx has no physiological secretion pathway and is only released by lysing cells. As antibiotics induce the prophage, chemotherapy can result in an aggravation of the clinical condition. In a fascinating illustration of the selfish gene concept, STEC recruits bystander intestinal E. coli cells via infection with the released Stx phage for an amplification of the suicidal Stx production (29). Experiments with mice demonstrated that the resistance or susceptibility pattern of the intestinal flora towards the released Stx phage exerts either a protective or an enhancing effect on the severity of STEC infections. Clinically, this observation could explain the variability of the disease symptoms in different O157-infected patients.

The observation that pathogenic bacteria convert environmental and commensal bystander bacteria via lysogenization into toxin-producing bacteria is not restricted to STEC (55) but was also found in Vibrio spp. (26) and Streptococcus pyogenes (11).


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