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Chapter 15 : Staphylococcal Phages

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Abstract:

The staphylococci are highly lysogenic; it is a rare strain that harbors no prophage. This chapter details the relationships between lysogeny and pathogenicity in the staphylococci. An infecting bacteriophage may either immediately replicate itself, causing lysis of the host bacterium, or integrate its DNA into the bacterial chromosome, leading to a state of lysogeny. Staphylokinase (SAK) is only one of several virulence factors that may be carried by beta-hemolysin-converting phages. Several prophages that are integrated into and carry different alleles of putative enterotoxin genes have been found in sequenced genomes. The positioning of enterotoxin genes on prophages may allow for the diversification of toxins that are capable of both attacking and evading the ever-evolving mammalian immune system. The very first reported association between lysogeny and toxigenicity in involved alpha-hemolysin, but it has not been confirmed, nor has conversion to delta-hemolysin production. Staphylococcal phages in other families exist, but none have been linked to virulence. Several broad generalizations can be made about the medically important staphylococcal phages. These generalizations will certainly be refuted as more staphylococcal phages are discovered, given the propensity of bacteriophages to recombine. A chromosomal gene that is adjacent to an integrated prophage can be mobilized by aberrant prophage excision. The simultaneous diversification and circulation of pathogenicity factors by prophages and other mobile elements contribute mightily to the pathogenic versatility of the staphylococci.

Citation: Matthews A, Novick R. 2005. Staphylococcal Phages, p 297-318. In Waldor M, Friedman D, Adhya S (ed), Phages. ASM Press, Washington, DC. doi: 10.1128/9781555816506.ch15
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FIGURE 1

Alignment of putative GEH catalytic domains, with key residues indicated with asterisks. The area corresponding to the 18-kb core site is shown in a box ( ). In strain COL, there is a prophage inserted in immediately downstream of this core.

Citation: Matthews A, Novick R. 2005. Staphylococcal Phages, p 297-318. In Waldor M, Friedman D, Adhya S (ed), Phages. ASM Press, Washington, DC. doi: 10.1128/9781555816506.ch15
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Image of FIGURE 2
FIGURE 2

ϕETA. Bar, 100 nm. Reprinted from with permission of the publisher.

Citation: Matthews A, Novick R. 2005. Staphylococcal Phages, p 297-318. In Waldor M, Friedman D, Adhya S (ed), Phages. ASM Press, Washington, DC. doi: 10.1128/9781555816506.ch15
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Image of FIGURE 3
FIGURE 3

ϕSTL. Bar, 100 nm. Reprinted from with permission of the publisher.

Citation: Matthews A, Novick R. 2005. Staphylococcal Phages, p 297-318. In Waldor M, Friedman D, Adhya S (ed), Phages. ASM Press, Washington, DC. doi: 10.1128/9781555816506.ch15
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Tables

Generic image for table
TABLE 1

Indirect evidence of recombination and modularity in staphylococcal phages

Negative conversion of beta-hemolysin is caused by integration of the prophage into . The specificity of the phage integrase determines the site of insertion. The serotype is determined by the phage particle proteins.

Citation: Matthews A, Novick R. 2005. Staphylococcal Phages, p 297-318. In Waldor M, Friedman D, Adhya S (ed), Phages. ASM Press, Washington, DC. doi: 10.1128/9781555816506.ch15
Generic image for table
TABLE 2

Medically important bacteriophages of the staphylococci

Citation: Matthews A, Novick R. 2005. Staphylococcal Phages, p 297-318. In Waldor M, Friedman D, Adhya S (ed), Phages. ASM Press, Washington, DC. doi: 10.1128/9781555816506.ch15

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