We can see differences in drug susceptibility in the same bacterial species and by even greater force of logic we can assume that can be different also the susceptibility of species belonging to the same genus. The best approach is test the single strain.

Anyway, it is probable that the drug "find" the same target  in bacteria belonging to the same genus.

The degree of susceptibility of bacteria depends on the genus and species for a given drug. It might also depend on the availability of the target which will be the same in all species of that genus.

I agree with L. Bano. It is strain specific than genus or species. I had Vibrio colorea strains with different antibiotic susceptibility. Also it depends on how long the strains are exposed to the drugs. Example, one strain might be sensitive a particular drug, when you grow them repeatedly with the same drug it will develop resistance in 4 or 5th generation. Also when you repeatedly grow the resistant strain for long time without the drug, it might lose that resistance. Resistance can be induced by other chemicals to, example, pesticides can induce antibiotic resistance. Example, we isolated few bacterial strains from a remote agri-land, which was possibly never exposed to any antibiotics, but to pesticides. The surprise is 70% of the strains isolated were resistant to penicillin. Finally as I mentioned above, it is strain specific than genus or species.

To some extent there is similarity in sensitivity pattern because of the common target in a given species, but there are variations due to the source or environment where the bacteria has been isolated from. The best option is to treat each strain differently, i.e. perform AST in each individual isolate.

I agree very well with Thavasi, but I work on protozoan parasites and drug resistance/drug development rather than bacterial, but the issues are surprisingly similar. In short, you can get any variation: some dugs are highly specific for a subspecies. For instance pentamidine is a drug with EC50 value of 2-3 nanomolar against Trypanosoma brucei brucei but is 100-fold less active against Trypanosoma congolense. The reason is unique transport proteins expressed in brucei but not congolense species, or the also closely related Leishmania species. On the other hand some driugs have good activity against a large number of species, for instance nito-heterocycles such as metronidazole. In that case the activity is often related to a more general cellular toxicity, however, less specific.

Finally, I agree with the earlier posters that resistance to many drugs can be induced very quickly. But yet again there is no universality here. For instance, we were unable to induce any level of resistance to curcumin in trypanosomes, even after a year of culturing with exposure, using protocols that worked rapidly with several other drugs.