Chapter 28 : Virulence Plasmids of Nonsporulating Gram-Positive Pathogens

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Infection with can result in a wide variety of diseases, including wound infections, toxic shock, food poisoning, endocarditis, pneumonia, and septicemia ( ). Virulence and drug resistance often occur together, as recent outbreak strains of methicillin-resistant also produce a number of different virulence factors ( ). It is perhaps not surprising that a bacterium capable of causing such a wide array of diseases possesses a diverse repertoire of virulence factors. A consequence of this versatility is that the pathogenesis of is usually multifactorial ( ).

Citation: Van Tyne D, Gilmore M. 2015. Virulence Plasmids of Nonsporulating Gram-Positive Pathogens, p 559-576. In Tolmasky M, Alonso J (ed), Plasmids: Biology and Impact in Biotechnology and Discovery. ASM Press, Washington, DC. doi: 10.1128/microbiolspec.PLAS-0002-2013
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Image of Figure 1
Figure 1

Plasmid map of pIB485, encoding staphylococcal enterotoxins SED () and SEJ (). Toxin genes are colored red. Genes encoding resistance to cadmium sulfate () as well as resistance to beta-lactams () are colored dark blue.

Citation: Van Tyne D, Gilmore M. 2015. Virulence Plasmids of Nonsporulating Gram-Positive Pathogens, p 559-576. In Tolmasky M, Alonso J (ed), Plasmids: Biology and Impact in Biotechnology and Discovery. ASM Press, Washington, DC. doi: 10.1128/microbiolspec.PLAS-0002-2013
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Image of Figure 2
Figure 2

Plasmid map of a representative staphylococcal enterotoxin B (ETB)-expressing plasmid, TY825 pETB. The outer circle shows genes that are transcribed clockwise; genes in the inner circle are transcribed counterclockwise. Genes in red are pathogenic factors; genes in green encode antibiotic resistances; genes in blue are involved in DNA replication, recombination, and repair; genes in light blue are transcriptional regulators; genes in purple are transposases; genes in yellow are involved in conjugal transfer; genes in orange encode the BacR1/C55 lantibiotic operon; and genes in gray are conserved ORFs. Structural comparison of TY4 pETB and TY825 pETB plasmids of . Shading indicates homologous regions. Figure is adapted from reference .

Citation: Van Tyne D, Gilmore M. 2015. Virulence Plasmids of Nonsporulating Gram-Positive Pathogens, p 559-576. In Tolmasky M, Alonso J (ed), Plasmids: Biology and Impact in Biotechnology and Discovery. ASM Press, Washington, DC. doi: 10.1128/microbiolspec.PLAS-0002-2013
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Figure 3

Schematic showing the principal events during pheromone-responsive plasmid transfer between cells.

Citation: Van Tyne D, Gilmore M. 2015. Virulence Plasmids of Nonsporulating Gram-Positive Pathogens, p 559-576. In Tolmasky M, Alonso J (ed), Plasmids: Biology and Impact in Biotechnology and Discovery. ASM Press, Washington, DC. doi: 10.1128/microbiolspec.PLAS-0002-2013
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Image of Figure 4
Figure 4

Pheromone-response regulation and virulence factors encoded on plasmid pAD1 Genes encoded by pAD1 that are involved in plasmid transfer and pheromone sensing. Blue genes are involved in replication and maintenance, red genes are negative regulators of pheromone response, and green genes are positive regulators of pheromone response. Detail of the postsegregation killing (PSK) locus of pAD1, which encodes the Fst toxin. Detailed schematic of individual genes within the cytolysin operon.

Citation: Van Tyne D, Gilmore M. 2015. Virulence Plasmids of Nonsporulating Gram-Positive Pathogens, p 559-576. In Tolmasky M, Alonso J (ed), Plasmids: Biology and Impact in Biotechnology and Discovery. ASM Press, Washington, DC. doi: 10.1128/microbiolspec.PLAS-0002-2013
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Figure 5

Regulation of pheromone sensing and plasmid transfer by the enterococcal Tra regulon. Genes encoding surface exclusion protein () and aggregation substance () are shown in dark blue. Positive regulators are shown in green, and negative regulators are shown in red. Straight arrows below the genes indicate transcripts detected in the uninduced and induced states, and arrow thickness indicates relative transcript abundance. (Adapted in part from , 9–12, 1993, with permission from Elsevier [ ], and from the , 3816–3825, 2000, with permission from ASM [ ].)

Citation: Van Tyne D, Gilmore M. 2015. Virulence Plasmids of Nonsporulating Gram-Positive Pathogens, p 559-576. In Tolmasky M, Alonso J (ed), Plasmids: Biology and Impact in Biotechnology and Discovery. ASM Press, Washington, DC. doi: 10.1128/microbiolspec.PLAS-0002-2013
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Figure 6

Schematic of cytolysin expression, posttranslational modification, processing, and export. CylL and CylL precursor peptides are synthesized and are intracellularly modified by CylM to create CylL* and CylL*. CylL* and CylL* are secreted and further modified by CylB, resulting in CylL′ and CylL′, which are cleaved extracellularly by CylA to form the active cytolysin components CylL″ and CylL″. CylL″ and CylL″ are capable of forming aggregates and are prevented from lysing cytolysin-expressing cells via CylI .

Citation: Van Tyne D, Gilmore M. 2015. Virulence Plasmids of Nonsporulating Gram-Positive Pathogens, p 559-576. In Tolmasky M, Alonso J (ed), Plasmids: Biology and Impact in Biotechnology and Discovery. ASM Press, Washington, DC. doi: 10.1128/microbiolspec.PLAS-0002-2013
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Figure 7

Plasmid map of the virulence plasmid p33701 of . Genes believed to be involved in plasmid maintenance and conjugation are shown in red, genes encoding Vaps are shown in blue, and putative genes within the proposed pathogenicity island are depicted in yellow. Figure is adapted from reference .

Citation: Van Tyne D, Gilmore M. 2015. Virulence Plasmids of Nonsporulating Gram-Positive Pathogens, p 559-576. In Tolmasky M, Alonso J (ed), Plasmids: Biology and Impact in Biotechnology and Discovery. ASM Press, Washington, DC. doi: 10.1128/microbiolspec.PLAS-0002-2013
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