Short-sequence DNA repeat (SSR) loci can be identified in all eukaryot
ic and many prokaryotic genomes. These loci harbor short or long stret
ches of repented nucleotide sequence motifs. DNA sequence motifs in a
single locus can be identical and/or heterogeneous, SSRs are encounter
ed in many different branches of the prokaryote kingdom. They are foun
d in genes encoding products as diverse as microbial surface component
s recognizing adhesive matrix molecules and specific bacterial virulen
ce factors such as lipopolysaccharide-modifying enzymes or adhesins. S
SRs enable genetic and consequently phenotypic flexibility. SSRs funct
ion at various levels of gene expression regulation. Variations in the
number of repeat units per locus or changes in the nature of the indi
vidual repeat sequences may result from recombination processes or pol
ymerase inadequacy such as slipped-strand mispairing (SSM), either alo
ne or in combination with DNA repair deficiencies. These rather comple
x phenomena can occur with relative ease, with SSM approaching a frequ
ency of 10(-4) per bacterial cell division and allowing high-frequency
genetic switching. Bacteria use this random strategy to adapt their g
enetic repertoire in response to selective environmental pressure. SSR
-mediated variation has important implications for bacterial pathogene
sis and evolutionary fitness. Molecular analysis of changes in SSRs al
lows epidemiological studies on the spread of pathogenic bacteria. The
occurrence, evolution and function of SSRs, and the molecular methods
used to analyze them are discussed in the context of responsiveness t
o environmental factors, bacterial pathogenicity, epidemiology, and th
e availability of full-genome sequences for increasing numbers of micr
o-organisms, especially those that are medically relevant.