This study aimed to conduct a comprehensive phenotypic and genotypic characterization of resistance to MLS antibiotics among Streptococci. The most prevalent resistance mechanism was determined to be the target-site modification of the bacterial 50S ribosomal subunit. Constitutive resistance to MLS emerged as the most predominant phenotype, with the erm genes especially—ermB widely—distributed. The presence of genes encoding MLS inactivating enzymes was detected, notably the ereA gene encoding esterase, while the lnuA gene associated with lincomycin resistance was the least detected. The isolates exhibited varying resistance levels, with higher rates observed for macrolides and lincomycin, representing the MLS or M phenotypes, and the least resistance seen against clindamycin. A significant correlation was established between the reduced susceptibility of isolates to commonly used biocides and their resistance to MLS antibiotics. Notably, both phenotypic and genotypic evidence of increased efflux was observed in the MLS-resistant isolates, indicating a potential link between efflux and resistance to both antibiotics and biocides. However, the most involved mechanism that confers cross-resistance to both biocides and antibiotics is targeting the 50 s sub-ribosomal unit via transferable ermB.