摘要
In order to study erythromycin resistance of Streptococcus suis under high or low concentration of selective drug pressure, Streptococcus suis strain LN was isolated from a diseased pig in 2005 and showed to be susceptible to erythromycin as determined by disc diffusion and tube dilution tests. In this study, clean level rabbits were divided into three groups of six rabbits each, including a prevention dosage group, a treatment dosage group, and a control group. After injection with S. suis strain LN, erythromycin （20 μg mL^-1） was taken orally in the prevention dosage group, erythromycin （5 mg kg^-1） was injected intramuscularly in the treatment dosage group, and no treatment was given in the control group. S. suis with intermediate resistance to erythromycin was isolated on the 5th day after infection from the prevention dosage group （5th PDG） and on the 7th day after infection from the treatment dosage group （7th TDG）. Both isolates were determined to be the constitutive macrolide-lincosamide-streptogramin B （cMLSB） resistance phenotype. The resistance gene ermB was detected in all of the isolates. The results suggested that both the 5th PDG and 7th TDG isolates had a mutation （A2372T） in the 23S rRNA gene. In addition, the 5th PDG isolates had a mutation in ribosomal protein L4 （detected as G268A） and a mutation in ribosomal protein L22 （A345C）; and the 7th TDG isolates had a C insertion at site 564. Each of these mutations is considered as a possible mechanism of erythromycin resistance in S. suis strain LN. This study demonstrated that erythromycin resistance was readily induced in S. suis at a low erythromycin dose creating selective pressure in vivo. Resistance appeared to be mediated by ribosome methylation, encoded by the ermB gene.
In order to study erythromycin resistance of Streptococcus suis under high or low concentration of selective drug pressure, Streptococcus suis strain LN was isolated from a diseased pig in 2005 and showed to be susceptible to erythromycin as determined by disc diffusion and tube dilution tests. In this study, clean level rabbits were divided into three groups of six rabbits each, including a prevention dosage group, a treatment dosage group, and a control group. After injection with S. suis strain LN, erythromycin （20 μg mL^-1） was taken orally in the prevention dosage group, erythromycin （5 mg kg^-1） was injected intramuscularly in the treatment dosage group, and no treatment was given in the control group. S. suis with intermediate resistance to erythromycin was isolated on the 5th day after infection from the prevention dosage group （5th PDG） and on the 7th day after infection from the treatment dosage group （7th TDG）. Both isolates were determined to be the constitutive macrolide-lincosamide-streptogramin B （cMLSB） resistance phenotype. The resistance gene ermB was detected in all of the isolates. The results suggested that both the 5th PDG and 7th TDG isolates had a mutation （A2372T） in the 23S rRNA gene. In addition, the 5th PDG isolates had a mutation in ribosomal protein L4 （detected as G268A） and a mutation in ribosomal protein L22 （A345C）; and the 7th TDG isolates had a C insertion at site 564. Each of these mutations is considered as a possible mechanism of erythromycin resistance in S. suis strain LN. This study demonstrated that erythromycin resistance was readily induced in S. suis at a low erythromycin dose creating selective pressure in vivo. Resistance appeared to be mediated by ribosome methylation, encoded by the ermB gene.
基金
funded by the National Basic Research Program of China (973 Program,2006CB504400)
the National Key Techology R&D Program of China(2004BA519A60)
