Keeping Their Options Open: Acute versus Persistent Infections
Open Access
- 15 February 2006
- journal article
- review article
- Published by American Society for Microbiology in Journal of Bacteriology
- Vol. 188 (4) , 1211-1217
- https://doi.org/10.1128/jb.188.4.1211-1217.2006
Abstract
Among the reasons for the growing interest in studying bio- film formation is the role of these microbial communities in chronic infections (24, 38). Such biofilm-like chronic infections include the respiratory infections caused by Pseudomonas aeruginosa in the cystic fibrosis (CF) lung (7), relapsing otitis media primarily caused by Haemophilus influenzae (41), and staphylococcal lesions in endocarditis (17). It is also important to note, however, that all of these microbes can also contribute to acute infections in human patients and, in fact, are among the most feared nosocomial pathogens (48). So, how do these organisms cause acute infections in some settings and chronic infections in others? A series of recent papers suggests that bacteria can choose which strategy they employ, either causing an acute infection, growing and spreading rapidly in the host, or, alternatively, adopting a chronic, biofilm infection strategy. While replication in the context of the chronic infection is likely less rapid, bacteria involved in these long-term infections can persist for extended periods of time and continue to shed planktonic (e.g., free-swimming) bacteria, as well as biologi- cally active molecules, into the host during the course of the persistent infection (69). Establishing that acute and chronic infections are distinct processes requires we demonstrate that these are really two different strategies employed by microbes when interacting with a host. That is, do organisms differ in the molecular mechanisms utilized to cause acute versus chronic infections? Furthermore, a single microbe must presumably have the ca- pability to cause both acute and persistent infections.Keywords
This publication has 83 references indexed in Scilit:
- Role of the Type III Secreted Exoenzymes S, T, and Y in Systemic Spread of Pseudomonas aeruginosa PAO1 In VivoInfection and Immunity, 2005
- Pathogenicity ofgacAmutant ofPseudomonas aeruginosaPA01 in the silkworm,Bombyx moriFEMS Microbiology Letters, 2005
- The galU Gene of Pseudomonas aeruginosa Is Required for Corneal Infection and Efficient Systemic Spread following Pneumonia but Not for Infection Confined to the LungInfection and Immunity, 2004
- An Adenylate Cyclase-Controlled Signaling Network Regulates Pseudomonas aeruginosa Virulence in a Mouse Model of Acute PneumoniaInfection and Immunity, 2004
- Bacterial biofilms: from the Natural environment to infectious diseasesNature Reviews Microbiology, 2004
- Role of bacterial proteases in pseudomonal and serratial keratitisBiological Chemistry, 2004
- Effects of reduced mucus oxygen concentration in airway Pseudomonas infections of cystic fibrosis patientsJournal of Clinical Investigation, 2002
- Impact of theagrQuorum‐Sensing System on Adherence to Polystyrene inStaphylococcus aureusThe Journal of Infectious Diseases, 2000
- Global Climate and Infectious Disease: The Cholera ParadigmScience, 1996
- Pseudomonas aeruginosa elastase and elastolysis revisited: recent developmentsMolecular Microbiology, 1991