(Applied Biosystems, Foster City, CA, USA). This allowed detection of mutations at nucleotide position 913, and also confirmed PCR-RFLP results. PCR-RFLP analysis discriminated the blaTEM genes into three restriction linkage groups (according to polymorphic sequence variations) (Table 1): the ‘TEM-1A type’ (n = 1), the ‘TEM-1B type’ (n = 14) and the ‘TEM-1C type’ (n = 2). Nucleotide sequencing of blaTEM genes representative of each group confirmed this classification. The linkage groups of these blaTEM genes from animal sources were identical to those of the corresponding parental blaTEM genes from human specimens. 1 – 3 All linkage groups had C32 in the promoter region, indicating a weak promoter. However, some of the strains presented resistance phenotypes (with MICs of amoxicillin 1024–>2048 mg/L, cefalothin 16–>32 mg/L and mecillinam 0.5–>256 mg/L, data not shown). This may be due to enzyme hyperproduction as a result of the gene being on multicopy plasmids, tandem-genes in a single plasmid and/or reduced permeability of outer cell membrane to antibiotics. Analysis of the molecular diversity of blaTEM genes encoding b-lactamases contributes to our understanding of this mechanism of resistance in Enterobacteriaceae isolated from humans, or animals (this study). We demonstrated the genetic relatedness between blaTEM genes in pathogenic E. coli strains isolated from humans, and animal species (this study). This genetic proximity is in agreement with the known zoonotic potential of uropathogenic E. coli strains: these strains display PapA subunit diversity and share the same papG alleles coding for the Pap fimbriae adhesin, both of which are virulence factors.