Abstract
Members of the genus Campylobacter are frequently responsible for human enteric disease, often through consumption of contaminated poultry products. Bacteriophages are viruses that have the potential to control pathogenic bacteria, but understanding their complex life cycles is key to their successful exploitation. Treatment of Campylobacter jejuni biofilms with bacteriophages led to the discovery that phages had established a relationship with their hosts typical of the carrier state life cycle (CSLC), where bacteria and bacteriophages remain associated in equilibrium. Significant phenotypic changes include improved aerotolerance under nutrient-limited conditions that would confer an advantage to survive in extra-intestinal environments, but a lack in motility eliminated their ability to colonize chickens. Under these circumstances, phages can remain associated with a compatible host and continue to produce free virions to prospect for new hosts. Moreover, we demonstrate that CSLC host bacteria can act as expendable vehicles for the delivery of bacteriophages to new host bacteria within pre-colonized chickens. The CSLC represents an important phase in the ecology of Campylobacter bacteriophage.
Highlights
Human enteric disease caused by members of the genus Campylobacter is widespread throughout the world
We have previously examined the effect of bacteriophage treatments of Campylobacter biofilms using two lytic group III bacteriophages, CP8 and CP30A, and demonstrated that these bacteriophages can reduce the numbers of viable bacteria and disperse the matrix [22]
All were sensitive to superinfection by other phages. The ability of these isolates to form plaques could not be removed by repeated washing, centrifugation 4 and resuspension of the cells, and was stably maintained through five successive subcultures from single colonies on blood agar (BA) plates. These features typify the phage carrier state life cycle (CSLC) where bacteria and bacteriophages remain associated in equilibrium
Summary
Human enteric disease caused by members of the genus Campylobacter is widespread throughout the world. Various strategies to reduce contamination have been suggested and evaluated [1]. Among these is the novel approach of using Campylobacter-specific bacteriophages, which are natural predators of the pathogen, but this requires an understanding of their complex life cycles to enable successful exploitation [2]. Bacteriophage life cycles are generally ascribed as being either lytic or lysogenic [3]. Bacteriophage infection redirects host metabolism towards the replication of the phage nucleic acid and assembly of new phage particles, which are released upon cell lysis. In the lysogenic life cycle, injected phage nucleic acid either integrates into the host genome or remains as a stable episome, replicating along with the host.
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