The rise and spread of a new pathogen: Seroresistant Moraxella catarrhalis

  1. Thierry Wirth1,2,6,7,
  2. Giovanna Morelli3,6,
  3. Barica Kusecek3,
  4. Alex van Belkum4,
  5. Cindy van der Schee4,
  6. Axel Meyer1, and
  7. Mark Achtman3,5,7
  1. 1 Department of Biology, University Konstanz, D-78457 Konstanz, Germany;
  2. 2 Department of Systematics and Evolution, Muséum National d’Histoire Naturelle, Ecole Pratique des Hautes Etudes, F-75231 Paris cedex 05, France;
  3. 3 Department of Molecular Biology, Max-Planck Institut für Infektionsbiologie, D-10117 Berlin, Germany;
  4. 4 Department of Medical Microbiology and Infectious Diseases, Erasmus MC University Medical Centre Rotterdam, 3015 GD Rotterdam, The Netherlands;
  5. 5 Department of Microbiology, University College Cork, Cork, Ireland
  1. 6 These authors contributed equally to this work.

Abstract

The nosocomial human pathogen Moraxella catarrhalis is one the most important agents of human respiratory tract infections. This species is composed of two distinct lineages, one of only moderate virulence, the so-called serosensitive subpopulation, and a second, the seroresistant one, which is enriched among strains that harbor two major virulence traits: complement resistance and adherence to epithelial cells. Using a suite of population genetics tools, we show that the seroresistant lineage is also characterized by higher homologous recombination and mutation rates at housekeeping genes relative to its less pathogenic counterpart. Thus, sex and virulence have evolved in tandem in M. catarrhalis. Moreover, phylogenetic and Bayesian analyses that take into account recombination between the two clades show that the ancestral group was avirulent, is possibly 70 million years old, and must have infected mammals prior to the evolution of humans, which occurred later. The younger seroresistant isolates went through an important population expansion some 5 million years ago, coincident with the hominid expansion. This rise and spread was possibly coupled with a host shift and the acquisition of virulence genes.

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