Phenotype M was determined in 46 isolates; 45 had the mefA gene. An additional three isolates expressed the inducible phenotype (iMLSB), and one expressed the ermB gene.
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Alternative hypotheses are proposed such as the genetics of mefenoxam resistance inP. erythroseptica is probably under the control of more than one major gene and perhaps some minor genes of additive effect.
Researchers are also investigating whether changes in additional genes, particularly genes on the X chromosome, contribute to the development of signs and symptoms.