Bacteria are small single cell organisms, with many bacterial species existing simply as single cells, referred to as planktonic or free-floating bacteria. However, when free-floating bacteria attach themselves to a surface and create a dense, self-sustaining community or colony, biofilm formation occurs.
One of the essential functions of a bacteria cell is to generate energy via either aerobic or anaerobic metabolism, with some bacteria able to adapt their metabolic pathway. However, a singular bacterium lacks sufficient gene volume to adapt to dynamic environmental changes and is therefore generally susceptible to host defences, biocides and antimicrobials3, that is unless individual bacterium come together to form a biofilm.
The ability of the bacteria to establish and maintain an infection is defined by its virulence factors. These include its ability to adhere to surfaces, invade host cells and tissues, secrete or expose toxins that stimulate adverse host responses, secrete enzymes that degrade the host tissue, produce factors that facilitate evasion of the host defences, and finally, the production of biofilms.3
Acute Versus Chronic Bacterial Infections
Acute infections, such as cellulitis, sepsis, and pneumonia, are generally short-duration aggressive infections associated with tissue destruction. Chronic infections in contrast, tend to be focal infections, limited in size, that wax and wane for long durations and are only partially destructive to tissues2. These differences are not necessarily a factor of time or even the type of host immune response, but rather the survival strategies pursued by the infecting microorganisms. The strategies of a single-cell, mobile, free-floating bacterium (planktonic) versus those of a community of bacteria encased in a self-secreted protective matrix (biofilm) are radically different and may define two fundamentally different types of infections: ‘acute’ and ‘chronic’.2
Development of Acute Bacterial Infections
To develop an acute infection, a bacteria or microbe must be pathogenic for a host, or in the case of a non-pathogenic bacteria the host must be immunocompromised. The infectious process begins with attachment or adherence of the pathogenic bacteria in sufficient quantities at a primary site of infection. The bacteria then multiply and further invade the host, both locally and systemically, producing local and/or systemic infections.3 This is referred to as an acute infection and is typically treated with antimicrobials or biocides to assist the host defence systems to eradicate the bacteria. From the physician’s perspective, the diagnosis and clinical management of an acute infection is more straightforward and typically involves a single course of treatment to eradicate the infection.
Treatment of Acute Bacterial Infections and Antimicrobial Resistance
The mainstay treatment strategy for the management of an acute bacterial infection is the administration of antimicrobial drugs. The general mechanism of action of antimicrobials involves targeting essential components of bacterial metabolism, including inhibition of cell wall synthesis, cell membrane function, protein synthesis, RNA synthesis and DNA synthesis. The principal mechanism of action of antimicrobials is to affect a synthesis process during active replication when bacteria are metabolically active. If at any time a bacteria cell becomes quiescent, or metabolically inactive, they become resistant to most antimicrobials.3 An additional complicating factor with regards to antimicrobial susceptibility is that bacteria exhibit both genetic and functional mechanisms that facilitate antimicrobial resistance.
- Genetic mechanisms and gene transfer between bacterium facilitate modification to the antimicrobial target, decreased uptake, efflux pumps, modulation of metabolic pathways and conferred resistance.
- Functional mechanisms involve modifications to the antimicrobial molecule, prevention of target access, bypassing target sites or global cell adaption and resistance.4
Planktonic (free-floating) bacteria