| Summary: | 碩士 === 國立陽明大學 === 生物醫學資訊研究所 === 102 === Acinetobacter baumannii is a gram-negative bacillus that is aerobic, pleomorphic, non-motile and known as a major agent in healthcare and nosocomial-associated infections in Taiwan. The ability of A. baumannii to cause diseases in a susceptible host is determined by their virulence factors. The high virulence isolates may have more or different virulence factors than low virulence isolates. Finding the virulence associated factor will be helpful for detecting virulent pathogens, because diagnosis and prevention will then become possible. However, little is known about the virulence of A. baumannii. Two known virulence factors in nosocomial bacteria are lipopolysaccharide (LPS) and capsular polysaccharide (CPS). It is possible that the lipopolysaccharide (LPS) plays an important role in the virulence of A. baumannii, as has been shown for many other gram-negative bacteria. Previous studies describing the heterogeneity of A. baumannii LPS were limited primarily to structural analyses. Although the adhesion of another virulence factor, CPS, is weaker than LPS, and not universal in A. baumannii but does relate to the virulence of some A. baumannii that has no LPS. Therefore, it is interesting to observe the correlation between these surface glycolipids and pathogenesis. The functional domain(s) of those proteins related to LPS synthesis, which were collected by KEGG, were first retrieved by Pfamscan. And do intersection with domains that were found in A. baumannii genomic sequences by using Pfamscan program. One apparent difference in among NTUH isolates is that there are two same domains in most of high virulence isolates, but one in most of the low virulence isolates. The two domains are belonging to two genes, respectively, which eliminates the possibility of domain duplication in one gene. The common gene in most of isolates involves in LPS synthesis. The unique gene in most of high virulence isolates involves in CPS synthesis. There are two possible reasons, which may explain the gain of the enzyme causing the virulence difference among isolates in NTUH. The first one is that the enzyme involves in CPS synthesis may substitute the function of the enzyme in LPS synthesis and increase the amount of LPS product by considering the similar reactions they catalyzed. The other reason is that the high virulence isolates have more antigens as CPS than the low virulence isolates. The pipeline built in this study can be easily applied to identify possible candidate virulence factors among different genomes.
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