APPLICATION OF MOLECULAR TYPING TO THE EPIDEMIOLOGY OF STREPTOCOCCUS-PNEUMONIAE

Authors
Citation
Lmc. Hall, APPLICATION OF MOLECULAR TYPING TO THE EPIDEMIOLOGY OF STREPTOCOCCUS-PNEUMONIAE, Journal of Clinical Pathology, 51(4), 1998, pp. 270-274
Citations number
45
Categorie Soggetti
Pathology
ISSN journal
00219746
Volume
51
Issue
4
Year of publication
1998
Pages
270 - 274
Database
ISI
SICI code
0021-9746(1998)51:4<270:AOMTTT>2.0.ZU;2-4
Abstract
The spread of antibiotic resistance and the development of new vaccine s have focused attention on the epidemiology of Streptococcus pneumoni ae over recent years. While serotyping and the determination of antibi otic resistance remain primary methods for characterising pneumococci, molecular typing can add greater discrimination and complementary inf ormation. Methods based on restriction fragment length polymorphism wi thin total DNA or non-specific polymerase chain reaction provide infor mation representative of the whole genome and can be used to recognise closely related isolates from different sources, whether in the inves tigation of possible cross infection at the local level or in the inve stigation of national or international spread of antibiotic resistant strains. Fingerprinting of penicillin binding protein genes adds furth er information in the analysis of penicillin resistant isolates. The u se of a combination of typing methods to analyse both the genome as a whole and specific loci has led to the realisation that pneumococci un dergo horizontal gene transfer much more often than most other bacteri al species. In particular the spread of penicillin resistance has been characterised by a combination of the spread of epidemic strains, tra nsfer of chromosomal resistance genes from such strains into other gen etic backgrounds, and transfer of capsule genes resulting in the switc h of serotypes within strains. In the future molecular typing will hav e an important role in discovering whether widespread vaccination lead s to genetic modification of the pneumococcal population causing invas ive disease.