POSTER NO: 519

Comparison of genomes between Staphylococcus epidermidis and Staphylococcus aureus

¹Y.Q. Zhang, ²G. Fu, ²S.X. Ren, ¹D. Qu, ³J. Yang, ³R.S. Chen, ³Y. Shen, ²Z. Chen, ¹Yu-Mei Wen
¹Medical Center of Fudan University, Yi Xue Yuan Road 138#, Shanghai 200032, People's Republic of China, ²Chinese Human Genome center in Shanghai, Shanghai, People's Republic of China, ³Chinese Human Genome center in Beijing, Beijing, People's Republic of China

Microbes represent more than 50% of all living organisms on this planet. Comparison analysis of microbial genomes may reveal undiscovered functions of genetic information and unique genes not present in other organisms. This study reports the comparison of genomes between Staphylococcus epidermidis (SE) and Staphylococcus aureus (SA). SE causes nosocomial infections, while SA is an extraordinary versatile pathogen. In healthy hosts, SE is the normal habitat of skin and mucous membranes, however, in immunocompromised or senescent patients, and most importantly, in patients with foreign bodies, such as indwelling catheters, implanted artificial joints, artificial intraocular lenses etc, SE changes from a commensal organism to a pathogen. By forming biofilms, SE not only is resistant to antibiotics, antibodies and phagocytosis but also can be the reservoir for antibiotic resistant genes which can be transferred to other bacteria. In this study, the complete chromosomal DNA of S. epidermidis strain ATCC 12228, a low or non-pathogenic strain ( Micrococcus pyogenes var. Albus). [WHO 12] was sequenced and compared to that of the reported S. aureus strain N315. The number of predicted ORF was 2332 in SE 12228, and 2595 in SA N315. The genes present in SA but not found in SE were mainly virulent genes, namely, the enterotoxin genes and hemolytic toxin alpha, beta, gamma genes. However, delta toxin, which exhibits activity towards a broad range of cells, was present in SE 12228, suggesting that this toxin is not as potent or pathogenic as the other toxins. There were 640 genes found in SE which were not present in SA, out of which 282 could be annotated, 75 were conserved hypothetical proteins, and 283 were unknown genes or ESTs. More genes encoding adhesive proteins were found in SE than those in SA, which could explain the crucial role of SE in forming biofilm. The reported fbp (fibrinogen binding protein), atlE (autolysin), putative cell-surface adhesion SdrF genes were all found in SE 12228, a streptococcal adhesin gene emb was also present in SE. Furthermore, two new genes predicted with LPXTG motif (binding protein motif) in the translated proteins were also found in SE. However, in SE 12228, the Ica gene (intracellular adhesion gene) which was involved in the production of PIA (polysaccharide intercellular adhesin), was interrupted by an insertion sequence in its regulatory region (icaR), resulting in no expression of PIA. The drug resistance genes in SE 12228 were as abundant as those present in SA N315. Beta-lactamase, oxacillin resistance protein, quinolone resistance proteins, fosfomycin resistance protein, tetracycline resistance protein, lincomycin resistance protein and multidrug resistance proteins were found both in SA N315 and in SE 12228. Less transposons and insertion sequences were found in SE 12228. For instance, eight copies of IS 1181 were found in SA N315, whereas, no IS 1181 was found in SE 12228. These findings suggest that SE is most likely the reservoir for drug resistant genes, while both IS and transposons played important roles in transferring antibiotic resistant genes to SA.