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Many pathogens have evolved the ability to alter surface-exposed molecules, most often in response to selective pressures associated with the host immune system (1). Pathogenic bacteria exhibit numerous examples of this adaptive strategy, and a range of molecular mechanisms has evolved in these bacteria for generating genetic variation at individual loci termed “contingency loci” (2). Many contingency genes are controlled by simple sequence DNA repeats that accumulate reversible, rec-independent mutations at high frequency. A striking feature of the complete genome sequences of the human pathogens Haemophilus influenzae and Neisseria meningitidis is the abundance of loci containing simple sequences (3, 4). Intriguingly, both of these bacteria are obligate commensals of the upper respiratory tract of humans but can, in some hosts, cause life-threatening invasive disease. In this Perspective we provide a synthesis of our current understanding of how polymorphisms in simple sequence contingency loci produce phenotypic variation. We also evaluate the role of this variation in pathogenesis and the evolution of virulent bacterial strains.

The simple sequence contingency loci of Haemophilus influenzae and Neisseria meningitidis