Professor Christopher Dowson
The Infectious Disease Research Group
University of Warwick
Asymptomatic pneumococcal carriage is accompanied by the variable (strain to strain) production of between 0.2-2mM hydrogen peroxide as part of its fermentative, aerobic metabolism. The consequences of this range from killing nasopharyngeal competitors to biochemical and chromosomal self harm. Without a classic SOS repair system and the need to deal with (now quite apparently common) peroxide driven chromosomal deletions, pneumococci have to rely upon their natural transformability and ability to integrate overarching segments of DNA to patch up these lesions by homologous recombination at the lesion junctions. The consequences of all this are interesting as recent genome analysis of globally and locally sampled pneumococcal clones has shed light on previously unmeasurable rates of self v non-self transformation, the frequency of acquiring your siblings' v more distant relatives genes to repair the deletions, and this may explain the rather bipolar nature of pneumococcal chromosomal diversity, which simultaneously displays unusually highly conserved ‘house-keeping’ genes and regions ( most visibly those under an obvious strong selective pressure) which are highly diverse, such as those encoding penicillin resistance.
An account stretching through decades with recent fact, hypotheses and speculation.