Czynniki wirulencji Staphylococcus aureus zależne od bakteriofagów

Phage-related virulence factors of Staphylococcus aureus
W. M. Helbin, K. Polakowska, J. Międzobrodzki

1. Wprowadzenie. 2. Wpływ bakteriofagów na wirulencję gatunku Staphylococcus aureus. 3. Gronkowcowe wyspy patogenności SaPIs (staphylococcal pathogenicity islands). 4. Wpływ antybiotyków na odpowiedź SOS i indukcję bakteriofagów. 5. Podsumowanie

Abstract: Mobile genetic elements play fundamental role in the emergence of new pathogens and in the adaptation of all bacteria species to the enviromnent. It is believed that the horizontal gene transfer has a major impact on genome structure of Staphylococcus aureus which of both commensal and major pathogen of humans and warm-blooded animals. Bacteriophages via lysogenic conversion are source of the major staphylococcal virulence factors, contribute to strain diversity and enable rapid changes in host specificity. Bacteriophages have also close connection to other kind of mobile genetic elements, known as staphylococcal pathogenicity islands, SaPIs. SaPIs excision from chromosome and replication is possible only after infection of a particular phage and the islands are able to leave the host cell inside hijacked capsids. Horizontal transfer of SaPIs which occurs through a modified transduction may be responsible for spread of toxic-shock syndrome toxin TSST-1, and other superantigenes among S. aureus
strains, and possibly from S. aureus to other species. Recently it has been reported that β-lactam and fluorochinolone antibiotic in subinhibitory concentration promote SOS-mediated prophage induction, replication of SaPIs in its host cells and consequently the further spread of SaPIs, and lysogenic conversion genes in pathogenic bacteria. Further understanding of phage and phage-dependent mobile genetic elements can provide insight into staphylococcal virulence and help in the development of efficient treatment of S. aureus infections.
1. Introduction. 2. Effect of bacteriophages on the virulence of Staphylococcus aureus. 3. Staphylococcal pathogenicity islands SaPIs. 4. Antibiotic dependent SOS response and the induction of prophages. 5. Summary