The spread of antibiotic resistance is regarded as one of the most important factors affecting healthcare. Historically the spread of antibiotic resistance genes has been considered to be due to the spread of plasmids from one bacterial cell to another via conjugation. The possibility of inter-specific conjugation events, together with possible transmission through transformation by environmental DNA, has made this an even greater concern. However, it is becoming clear that it is also possible for antibiotic resistance genes to be found in bacteriophage, suggesting that transduction may also provide a route for their spread.

In the current work we investigate the putative origins of all antibiotic resistance genes which are reported in the GenBank database as having been isolated from bacteriophages. All candidate sequences including examples of resistance genes for tetracycline [tetO], macrolides [mefA], and aminoglycoside [aadE]) were downloaded from the database and compared to other sequences within the database to identify related sequences from both the bacterium infected by the relevant phage, and also from other species harbouring a related resistance gene. Based on this information dendrograms were constructed to examine the relationship between these sequences. In addition, codon usage patterns were compared between the antibiotic resistance genes from the phages, any other genes present in the phages and the genes from the other organisms identified for dendrogram construction, to assay the level of any codon amelioration patterns which have taken place.

Most phage antibiotic resistance genes were most similar to genes previously described in the genus Streptococcus, although the position of these genes within the phylogenetic trees suggested that there had been multiple acquisition events.