Bacteria In Chronic Infections Research Articles

Sampling challenges in diagnosis of chronic bacterial infections.

In recent decades there has been an increase in knowledge of the distribution, species diversity and growth patterns of bacteria in human chronic infections. This has challenged standard diagnostic methods, which have undergone a development to both increase the accuracy of testing as well as to decrease the occurrence of contamination. In particular, the introduction of new technologies based on molecular techniques into the clinical diagnostic process has increased detection and identification of infectious pathogens. Sampling is the first step in the diagnostic process, making it crucial for obtaining a successful outcome. However, sampling methods have not developed at the same speed as molecular identification. The heterogeneous distribution and potentially small number of pathogenic bacterial cells in chronic infected tissue makes sampling a complicated task, and samples must be collected judiciously and handled with care. Clinical sampling is a step in the diagnostic process that may benefit from innovative methods based on current knowledge of bacteria present in chronic infections. In the present review, we describe and discuss different aspects that complicate sampling of chronic infections. The purpose is to survey representative scientific work investigating the presence and distribution of bacteria in chronic infections in relation to various clinical sampling methods.

Enhancing the utility of existing antibiotics by targeting bacterial behaviour?

The discovery of novel classes of antibiotics has slowed dramatically. This has occurred during a time when the appearance of resistant strains of bacteria has shown a substantial increase. Concern is therefore mounting over our ability to continue to treat infections in an effective manner using the antibiotics that are currently available. While ongoing efforts to discover new antibiotics are important, these must be coupled with strategies that aim to maintain as far as possible the spectrum of activity of existing antibiotics. In many instances, the resistance to antibiotics exhibited by bacteria in chronic infections is mediated not by direct resistance mechanisms, but by the adoption of modes of growth that confer reduced susceptibility. These include the formation of biofilms and the occurrence of subpopulations of 'persister' cells. As our understanding of these processes has increased, a number of new potential drug targets have been revealed. Here, advances in our ability to disrupt these systems that confer reduced susceptibility, and in turn increase the efficacy of antibiotic therapy, are discussed.

Mechanisms involved in the evasion of the host defence by Pseudomonas aeruginosa

Pseudomonas aeruginosa, an extracellular opportunistic pathogen, utilizes two major mechanisms to evade the host defence system. One of these mechanisms is the production of a large number of extracellular products, such as proteases, toxins, and lipases. The two proteases, alkaline protease and elastase, inhibit the function of the cells of the immune system (phagocytes, NK cells, T cells), inactivate several cytokines (IL-1, IL-2, IFN-r, TNF), cleave immunoglobulins and inactivate complement. Inhibition of the local immune response by bacterial proteases provides an environment for the colonization and establishment of chronic infection. The other mechanism by which P. aeruginosa evades the host defence system is the biofilm mode of growth of the bacteria in chronic infections. The biofilm-grown bacteria induce a low phagocyte response, and provide a barrier for the bacteria against antibodies, complement, and the cells of the immune system. Protection from the host defence system combined with increased antibiotic resistance of the bacteria in the biofilm are the major reasons for the persistence of P. aeruginosa in chronic infections.

Human polymorphonuclear leukocyte response to Pseudomonas aeruginosa grown in biofilms

The interaction of human neutrophils with Pseudomonas aeruginosa biofilms was examined by using a chemiluminescence assay. The biofilms induced an oxidative burst response by polymorphonuclear leukocytes which was slow and only 25% of the response to planktonic bacteria. The reduced response to P. aeruginosa biofilms could play a role in the persistence of bacteria in chronic infections.