Resistance to glyphosate does not result in resistance to other antibiotic agents. Antibiotics used in medicine today operate by very specifically blocking one or more steps in microbial metabolism. Glyphosate inhibits a specific biochemical pathway involved in the production of protein precursors (aromatic amino acids). Susceptible microbes cannot grow without this pathway unless they have access to an alternative source of these amino acids. Specifically, glyphosate inhibits an enzyme, EPSPS, (enol-phosphate-shikimate-3-phosphate-synthase). Resistance to glyphosate in microbes is due to the existence of variants of EPSPS which are not inhibited by glyphosate. None of the antibiotics we use today act on the specific metabolic step (EPSPS) inhibited by glyphosate, so glyphosate resistance does not confer resistance to other antibiotics.
Multiple antibiotic resistance in bacteria is sometimes due to a collection of antibiotic resistance genes grouped together on an inheritable ring of DNA called a plasmid. When multiple antibiotic resistance genes travel together, the use of one antibiotic can select for resistance to multiple antibiotics. The gene affected by glyphosate is not carried on such a plasmid, so use of glyphosate does not select for multiple resistant organisms.
At one time, scientists were interested in the possibility of using glyphosate as an antibiotic for exactly this reason- it has a unique mechanism and thus might help manage bacteria resistant to other antibiotics. Glyphosate is not well absorbed orally and is very rapidly excreted, levels needed to kill microbes are relatively high, and resistance can develop readily, so it has never proven to be a clinically useful antibiotic.