Serratia & GBS single isolate seq

1. Using the assembled genes compare clinical samples of interest (S21, S22, S23) to controls. We couldn't get stats for S24 (being only 1 sample), just a count difference. S21–23 are non-CRE (carbapenem resistance element) isolates; S24 is an ESBL (extended spectrum beta-lacatamase)

2.Consider further plasmid analysis. It depends what you want from the plasmid analysis – are we just trying to detect known plasmids? In that case srst2 is a good tool to use. If you want to have more info like %coverage and %genes present relative to known plasmid reference sequences then we'd need a different approach (something like PlasmidSeeker)

3.Some of the isolates do not harbour carbapenemases or ESBL genes, but are carbapenem resistant. One of the other mechanisms of resistance are porin changes which prevent entry of the drug into the cell. These are typically mutations to outer membrane proteins like ompC and ompF, which were highlighted in a recent paper. I suspect they were identified using the presence/absence analysis and then investigated further. Would you be able to extract the gene sequences for these genes for us to inspect manually for SNPs which may be causing the observed resistance (do multisequence alignment including reference sequence)? (Note: We did something similar for the Strep pneumoniae project if I remember correctly, so I can modify those scripts to do alignments). The gene list so far is: . AcrB/AcrD/EmrA/Mdt/OmpK36/CpxA/EnvZ/RpoE.