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Review
. 2006 Feb;188(4):1211-7.
doi: 10.1128/JB.188.4.1211-1217.2006.

Keeping their options open: acute versus persistent infections

S Furukawa  1 , S L Kuchma, G A O'Toole
Affiliations
Review

Keeping their options open: acute versus persistent infections

S Furukawa et al. J Bacteriol. 2006 Feb.
No abstract available

PubMed Disclaimer

Figures

FIG. 1.
FIG. 1.
Acute versus persistent infections. In response to uncharacterized signals, bacteria either initiate an acute infection utilizing factors like TTSS and various toxins or establish a chronic, biofilm-like infection, wherein bacterial cells (green) are surrounded by a matrix (gray), displaying properties, like antibiotic resistance, typically associated with biofilms.
FIG. 2.
FIG. 2.
A model for the coordinate regulation of factors required for acute infection and chronic persistence. The model shown here is based largely on genetic and in vivo regulatory studies performed with P. aeruginosa strains PA14, PAO1, PAK, and PA103. The functions boxed in green are involved primarily in biofilm formation and/or chronic persistence. The factors in the red boxes play a role in acute infection. Arrows indicate experimentally demonstrated genetic interactions. Abbreviations: EPS, exopolysaccharide; Cup, cupB and cupC genes; ToxA, endotoxin A; QS, quorum-sensing systems.
See this image and copyright information in PMC

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