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In contrast to the lytic cycle, phages infecting bacteria via the lysogenic cycle do not immediately kill their host cell. Instead, they combine their genome with the host genome, allowing the bacteria to replicate the phage DNA along with the bacterial genome. The incorporated copy of the phage genome is called the prophage. Some prophages can re-activate and enter the lytic cycle. This often occurs in response to a perturbation, such as DNA damage, but can also transpire in the absence of...
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Invasion of Human Cells by a Bacterial Pathogen
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Pathogenic conversion of coagulase-negative staphylococci.

Wenqi Yu1, Hwan Keun Kim1, Sabine Rauch1

  • 1Department of Microbiology, University of Chicago, Chicago, IL, USA.

Microbes and Infection
|December 26, 2016
PubMed
Summary

The acquisition of specific Staphylococcus aureus genes enables commensal staphylococci to become invasive pathogens. These genes facilitate bacterial agglutination in blood, promoting survival and dissemination in hosts.

Keywords:
AbscessAgglutinationClumpingCoagulationStaphylococcusVirulence

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Area of Science:

  • Microbiology
  • Pathogenesis
  • Bacterial Genetics

Background:

  • Staphylococci colonize humans and animals, but only some species cause invasive disease.
  • The genetic mechanisms underlying the transition from commensal to pathogenic staphylococci remain unclear.

Purpose of the Study:

  • To investigate the role of Staphylococcus aureus genes (coa, vwb, clfA) in the pathogenic conversion of commensal staphylococci.
  • To determine if these genes are sufficient to confer invasive capabilities.

Main Methods:

  • Genetically engineered coagulase-negative staphylococci (Staphylococcus epidermidis, Staphylococcus simulans) to express S. aureus genes (coa, vwb, clfA).
  • Assessed coagulase activity, bacterial agglutination in plasma, survival in human whole blood, and pathogenicity in a mouse bloodstream infection model.

Main Results:

  • Expression of coa and vwb alone conferred a coagulase-positive phenotype but did not lead to disease in mice.
  • Simultaneous expression of coa, vwb, and clfA enabled bacterial agglutination in plasma and enhanced survival in human blood.
  • Agglutination facilitated dissemination and replication in distal organs in a mouse infection model.

Conclusions:

  • Acquisition of genes for bacterial agglutination with fibrin is sufficient for converting commensal staphylococci into invasive pathogens.
  • Specific virulence factors can transform harmless bacteria into disease-causing agents.