Abstract
Much of the fundamental understanding of microbial physiology is based on
laboratory studies of freely suspended cells. While these studies have been essential
for our foundational understanding of the genetics, physiology and behavior of
microbes, it is now recognized that a majority of bacterial cells in nature exist in
biofilms [1] associated with surfaces or as floating cell aggregates. In fact, it has
recently been proposed that microbial communities originally developed on surfaces,
including the first bacterial and archael cells, and that the planktonic cell phenotype
evolved as a dispersal mechanism [2]. Hallmarks of cells residing in biofilm
communities are increased metabolic efficiency [3] as well as increased resistance
to environmental stresses such as desiccation, ultraviolet radiation and oxidative
stress [4–6]. This correlation has dramatic consequences as residing in aggregates
has been shown to confer increased resistance of bacterial cells also to biocides such
as antibiotics, disinfectants and detergents [7–9]. In addition, once established, these
biofilms are able to resist invasion by other organisms and predation by protozoans in
nature or host immune cells in the human body [5,6,10]. This is especially problematic
as it is also recognized that the majority of bacterial infections involve biofilms
[11]. The recent explosion of research in the field of biofilm biology has led to an
enhanced appreciation for the multicellular aspects of microbiology and has resulted
in the general acceptance of a model of the biofilm mode of life.
Pseudomonas aeruginosa has become a model organism for the study of biofilms
due to its metabolic versatility and variability in its response to environmental signals,
which promotes successful colonization of different habitats and growth under
varying environmental conditions [12,13]. This ability is likely a reflection of its large
genome, allowing for metabolic plasticity and quick responses to varying stimuli.
P. aeruginosa is also a human pathogen that causes infection in burn patients, and is
the predominant cause of lung infections and mortality in patients with cystic fibrosis (CF) [14,15]. This chapter will address various aspects of biofilm development,
dispersal and resistance, and its role in the infection process.