Effect of streptomycin antibiotic on gram-positive bacteria

[EmmaLou90]

Hi! Can anyone help me? I'm currently doing my biology coursework and we had to test the effects of two antibiotics (penicillin G and streptomycin) on a gram positive bacteria (bacillus subtilis). I found that the strep. antibiotic was more effective than the penicillin as it produced a larger clear zone but I'm finding it extremely hard to explain why!!

I found it easy to explain why penicillin affected the bacteria as it affects the cell wall but strep. affects cell membranes and ribosomes, and as gram+ve bacteria have a thick cell wall in the way of these two things, how does it get past it? Is the wall permeable to strep.? If it is, then I think I could explain it.. but even then, it seems that penicillin should have been more effective as the cell wall is easier to target what with it being on the outside and all..!

Many thanks to anyone who can help!

Emma

[snowcapk]

I'm not qualified to answer but I found a thread on soc.bio.microbiology (here) that can help.

Basically, that guy had a result opposite yours (i.e. penicillin more effective against streptomycin for his g+ bacteria, Staph. albus). There is a lot of speculation on that thread, but the gist is that the wall of g+ bacteria is permeable to streptomycin (something about porins?) and that strep is effective against "wt" g+ bacteria. The effectiveness of streptomycin on g+ bacteria might depend on species-specific things like the rRNA sequences of the streptomycin binding site on the 16S ribosomal subunit. A quick search of RCSB reveals a structure (1fjg) of steptomycin bound to the 16S subunit and interfering with tRNA binding to the 30S subunit, if you are interested in binding mechanism.

Anyways, you might not find that your steptomycin > penicillin result holds for all gram-positive bacteria, so your explanation might speculate that (a) the 16S subunit of B. subtilis is highly susceptible to streptomycin binding, (b) B subtilis are "metabolically weak" and interfering with their translation machinery has a larger effect than on other g+ bacteria, or (c) your strain of B. subtilis is less susceptible to penicillin G (possibly due to mutations in Penicillin Binding Proteins affecting the penicillin binding site, or upregulation of PBPs so that more antibiotic is required for dysfunction) than other strains or other gram-positive species. All of those explanations are species-specific.