Implant Related Infections - Biomedical Technology - page 167

P. aeruginosa in these lungs while P. aeruginosa is often found without a B. cepacia
co-infection. The reason for this dependence is that B. cepacia reacts to the specific
homoserine lactones produced by P. aeruginosa ,but P. aeruginosa does not respond
to the homoserine lactones produced by B. cepacia [ 25 ]. In this way these two
pathogens manage to communicate and as a consequence to increase their resistances
against antibiotics. For the role of species in asymptomatic biofilm communities
one may even speculate that some of these bacteria may be useful for controlling
aggressive pathogens or reduce their pathogenicity. Currently, such ideas are mere
speculations because we have no clue on the functions of these non-pathogens but
our understanding of mechanisms in microbial ecology has advanced considerably
and the methods for the assessment of microbial interactions have been developed
which will allow us the elucidation of the roles of these non-pathogenic bacteria.
Unfortunately, the situation is even more complicated because not only the inter-
actions between the different bacterial species have to be deciphered but also their
interaction with the host. That there are a multitude of interactions between the host
and his bacteria has been shown in a number of impressive studies. This has also been
underlined simply by the fact that individuals, even monozygotic twins, have their
own characteristic microbial consortia [ 26 ]. It becomes more and more apparent that
there are a huge number of interactions between our body and our microbiome and
it can be predicted that unravelling the various interactions in pathogenic biofilm
communities will be a slow process. But from the results already reported some
conclusions for improved control of biofilm infections can be drawn.
4 Conclusion
Biofilm infections are difficult to treat due to their antibiotic resistances and a deeper
understanding of the risk factors for their formation is urgently needed. To achieve
this, bacterial biofilm communities of rhythm management devices from asymp-
tomatic patients were assessed and compared with those found on symptomatic ones.
From 108 devices in asymptomatic patients 47% had bacterial DNA and remained
asymptomatic. The identified bacterial taxa were untypical for clinical device infec-
tions. No correlations were found between known risk factors for device infections
and the bacteria detected. The results were compared with rhythm management
devices explanted due to acute infections revealing very different biofilm communi-
ties between these two types. Symptomatic biofilms were dominated by Staphylo-
coccus spp. and had a much higher bacterial diversity. The results suggest that it is
not essential to suppress any biofilm formation but only pathogenic bacteria species
characteristic for symptomatic biofilms. Such an approach would be different to the
current one where any bacterium attaching to an implant is fought independently of
its pathogenicity. While all attempts to find a surface bactericidal to all pathogens
turned up empty handed attempts for control of specific pathogens may be more
successful.