Studys On Mechanism Of Streptococcus Suis Against Macrolides

Streptococcus suis was a well-recognized worldwide swine pathogen of emerging clinical significance in most countries with intensive swine industry. In addition to its significant sanitary and economic impact in the swine industry, S. suis was a zoonoses and communicable diseases , especially type 2 S.suis which could cause septicemia and meningitis in humans , even to die. S.suis was associated with different clinical conditions such as meningitis, arthritis, endocarditis, and septicemia. Moreover, clinically healthy pigs could carry S. suis in their nasal cavities, tonsils and upper respiratory tracts, contributing to the dissemination and transmission of this pathogen.Macrolides was a kind antibiotic of similar structure and action against bacterium. They had a common structure formed by a large from 12 to 20 lactone rings. They included 14 lactone ring erythromycin,clarithromycin and roxithromycin; 15 lactone ring azithromycin; 16 lactone ring midecamycin,spiramycin and jossamycin. Erythromycin and tylosin were widely used in veterinary. Because antibiotic was abused, resistance rate of S.suis against macrolides was more than 30%. The resistance could lead to the failure in treatment of S.suis. Resistance gene could transmit at different strain bacterium. So it must be attached important to us.Resistance mechanism of streptococcal against erythromycin was three points. The predominant mechanisms of resistance to erythromycin and the other macrolides in Streptococcal were through target site modification by methylation that prevented the binding of the antibiotic to its ribosomal target, encoded by the erm gene, or through efflux of the antibiotic, mediated by the mef(A) gene, or by mutation of ribosome protein.Methylation of the ribosomal target of the antibiotics leaded to cross-resistance to macrolides (M), lincosamides (L), and streptogramin B (SB), the so-called MLSB phenotype. Methylation was thought to induce a conformational change in the 50S ribosomal subunit, leading to reduce binding of and coresistance to macrolide, lincosamide, and streptogramin B (MLS) antibiotics, whose binding sites probably overlapped. This resistance was either inducible (strains are resistant to 14- and 15-membered ring macrolides and susceptible to 16-membered ring, iMLSB) or constitutive (resistance includes 14-,15- and 16-membered ring, cMLSB).Only recently have a macrolide efflux mechanism been described for streptococci, in which it was associated with a new resistance pattern (M phenotype) characterized by resistance to 14- and 15-membered macrolides and susceptibility to 16-membered macrolides, lincosamides, and streptogramin B. Efflux protein coded by mef gene was membrane protein with energy, which was composed by 405 amino acid, included 12 crossed membrane film. Mef pumped out 14- and 15-membered ring macrolides by proton motility. Alterations in ribosomal proteins L4 and L22 or 23S rRNA have been reported to cause resistance in S.pneumoniae.1500 pathological tissues were collected from countrywide, which included lung, liver,...