Fig. 2.—

Alterations in sequences of genes associated with resistance. (A) The whole genome maximum-likelihood phylogeny is displayed as in figure 1. (B) Each column corresponds to a codon alignment of a gene whose sequence influences the antibiotic resistance profile of the host bacterium, with the width of the column representing the length of the alignment. The sequences are arranged according to the class of antibiotics to which they cause resistance: pbp1a, pbp2x, and pbp2b determine resistance to β-lactams, whereas the sequences dyr and folP determine resistance to trimethoprim and sulphonamides. Each of these alignments were independently analyzed using BRATNextGen, which clusters the sequences into alleles and identifies recombinations. The background color of each row represents the “recipient” cluster to which the overall sequence belongs, with changes in color indicating recombination breakpoints resulting from import of sequence from “donor” clusters. The specific sites of changes within the folP and dyr genes that are associated with resistance are indicated by the downwards-pointing arrows at the top of the columns. Sulphamethoxazole resistance arises through insertions shortly after S61 in folP. The ancestral form of the sequence (S61S–YV) is found in isolates with a grey box to the right of the gene sequence analysis; different colors indicate the distribution of five different alleles encoding insertions in this region of the protein. In the case of dyr, trimethoprim resistance is associated with the substitution of isoleucine with leucine at position 100; the amino acid present at this site in each gene is indicated by the black and grey boxes adjacent to the analysis of gene sequences.