Description
CHAPTER ONE
1.0 INTRODUCTION
Since the initial detection or plasmids in streptococci courvalin et al1972 it has become evident that the majority of the genes mediating resistance to antibiotic in this genus are plamid borne.
This type of resistance has spread in recent years among clinical isolate of all streptococcal species studied clewell, 1981 with the remarkable exeption of streptococcus pneumonial.
Multiple antibiotic resistance has emerged in s.pneumoniae since 1977 acquisition of resistance in this species is intriguing because of a novel form of conjugation transfer in the apparent absence of extrachromomal DNA involvement inobatial 1978 BNUHoi shoemaker et al 1980 of this study is to analyses the genetic basic of multiple antibiotic resistance in s. pneumoniae.
1.2 STATEMENT OF THE PROBLEM
The development and spread of antibiotic resistant organisms represent a significant health risk Kath J Kemper M D. 2001 Antibiotic represent an important scientific advance of the 20th Century and a valuable resource in combating serious infectious diseases among infant children adolescents and the adults that limit the effectiveness of antibiotic such as those that promote bacteria resistance to antibiotic jeopadiz current and future pedratric.
1.1 BACKGROUND OF THE STUDY
Antibiotic resistance is an underappreciated threat to public health in nation around the globe, Gold man sachs whith globalization . it is important to understand international patterns of resistance, if countries already experience similar patterns of resistance, it may be too late to worry about international spread, if large countries that are likely to leap ahead in their integration with the rest of the worldChina, Being the standout case have high and distinctive patterns or resistance literature to date provides only limited evidence on these issue.
1.3 PURPOSE/AIM OF THE STUDY
Streptococcus pneumonia continues to be significant in human the worldwide increase in antibiotic resistance in this species has become a serious problem within the last 20 years resistance in S. pneumonia is usually cause by melthylation of A 2058 of the 235. RNA mediated by gene or by an efflux mechanisms mediated by the met gene. In addition other mechanisms of macrolide resistance have been described 4,20,21 ketolides form a new class of semisythetic agent derived form erythromycin A designed to overcome erythromacin A resistance in S. pneumonia Ketolide compounds inhibit bacteria protein synthesis by interacting with the peptidy transferase site on the 50s ribosomal subunite and interact closely with domains II at A752, and V, at A2058 and A2059 of the 235r RNA Ketolides show good activity against grampositive bacteria responsible for respiratory tract infections including penicillin S. pneumonia.
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