A total of 1,838 subjects from the community and 393 subjects from health care-related facilities in Taiwan were evaluated for the prevalence of nasal Staphylococcus aureus colonization and to identify risk factors associated with S. aureus and methicillin-resistant S. aureus (MRSA) colonization. Among the community subjects, 3.5% had nasal MRSA colonization. Subjects from health care-related facilities had a lower S. aureus colonization rate (19.1%) than community subjects (25.2%) but had a significantly higher rate of colonization with MRSA (7.63%). Age (P < 0.001) was a significant risk factor for S. aureus colonization, with subjects under age 20 years or between 71 and 80 years showing higher rates of colonization. Recent gastrointestinal disease (P ‫؍‬ 0.011) and hospital admission (P ‫؍‬ 0.026) were risk factors for nasal MRSA colonization. Comparison of hospital MRSA isolates with the colonization strains by staphylococcal cassette chromosome mec (SCCmec) gene typing and pulsed-field gel electrophoresis (PFGE) typing revealed that most MRSA strains carried in the community were SCCmec type IV and that most clinical hospital isolates were type III, while health care facility-related carriage isolates were mainly SCCmec type III and type IV. Two new variant SCCmec types were identified. Six clusters of PFGE patterns were distinguished: two mainly comprised health care facility-related MRSA strains, three mainly comprised community MRSA strains, and one comprised mixed community and health care facility-related MRSA strains. In conclusion, a high prevalence of MRSA colonization was observed among people with no relationship to the hospital setting. The high level of multiple-drug resistance among community MRSA strains in association with the previously reported excessive use of antibiotics in Taiwan highlights the importance of the problem of antibiotic selective pressure. Our results indicate that both the clonal spread of MRSA and the transmission of hospital isolates contribute to the high MRSA burden in the community.

Although diverse mechanisms were identified, production of OXA-72 carbapenemase was the most common mechanism of carbapenem resistance in A. baumannii from this Taiwanese hospital. The plasmidic location of the gene had facilitated its spread to multiple strains.

Recently, a putative tumor suppressor gene, PTEN/MMAC1, has been identified at chromosome 10q23.3, which encodes a 403 amino acid dual-specificity phosphatase containing a region of homology to tensin and auxillin. Somatic mutations of the PTEN/MMAC1 gene have been identified in a number of cancer cell lines and primary cancers. Mutations in PTEN/MMAC1 are most frequently found in advanced cancers. To evaluate the role of the PTEN/MMAC1 gene in leukemia, bone marrow and/or peripheral blood from 62 acute myeloid leukemia (AML) patients, 5 hemopoietic cell lines (HL60, U937, Raji, KG-1, K562), and 30 normal controls were analyzed. The results showed aberrant PTEN/MMAC1 transcripts in 15 of the 62 (24%) AML patients, 4 of the 5 cell lines (80%), and 4 of the 30 (13%) normal controls. As in our previous study of TSG101, the abnormal transcripts may result from aberrant RNA splicing as evidenced by the presence of both these aberrant transcripts and normal full length transcripts in all specimens examined. Loss of heterozygosity (LOH) analysis and PCR-SSCP of the entire coding region showed that none of the AML cases had LOH or mutation. Only one frameshift mutation at codon 130 (insertion of CCCG) with premature termination of coding sequence was observed in the U937 cell line. Our results indicate that the PTEN/MMAC1 gene may play a role in a small percentage of AML, but its significance needs to be further evaluated.