In the United States, children are reported to have died of community-acquired methycillin-resistant Staphylococcus aureus (CA-MRSA) infection between 1997 and 1999. During The same period, CA-MRSA was also isolated and reported in Europe and Australia. The characteristics of the pathogen were clarified, and CA-MRSA infection became the focus of global attention as a global infection. CA-MRSA differs from conventional MRSA (hospital-acquired MRSA, HA-MRSA) in origin. It produces a leukocidin, PVL, and in many cases, has a type IV methycillin-resistance region (type IV SCCmec). Genetically, CA-MRSA consists of several different continentspecific clones. Analysies such as multi-locus sequence typing (MLST), spa typing, agr allele analysis, and toxin gene pattern analysis are used. One clone has thus far been confirmed in Europe, several in the United States, 2 in Oceania, and 2 prevalent in Asia. Drug sensitivity depends on the type of prevalent clone, and some strains of CA-MRSA are susceptible to many antimicrobial agents other than penicillin/cephems. In many cases, such CAMRSA is associated with skin/soft tissue infection, and is frequently detected in children. Fatal necrotizing pneumonia and bacteremia appear to be increasing. CA-MRSA in Japan differs from European and North American cases in that; the proportion of PVL-negative strains is relatively high and genetic features vary. PVLpositive CA-MRSA, which is rarely isolated, is common to Oceania CA-MRSA in many respects, although not identical, rather than to European and North American CA-MRSA. PVL-positive CA-MRSA infection is spreading even among young, healthy individuals. A survey on the worldwide distribution, identification of populations and areas at high risk for colonization and infection, and analysis of the detailed infectious mechanism are curently under way.

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During the 6 months between April and September 2003, we monitored the frequencyof Candida spp. isolation and resistance at 6 facilities in Yamanashi.
Samples numbered 8, 496, and Candida spp. was predominantly isolated from 608 isolates (7.2%). By species, Candida albicans was most frequently isolated, accounting for 67.3% of all Candida isolates. The second and third most frequent isolates were Candida glabrata (16.0%; 97 isolates) and Candida tropicalis (14.0%; 85 isolates). Candida parapsilosis accounted for 1.6%(10 isolates).
Frequently isolated C. albicans, C. glabrata, and C. tropicalis, numbering 420 isolates, were subjected to susceptibility testing, and 1μg/mL of amphotericin B and 0.13μg/mL of micafungin inhibited the growth of all isolates tested. The MIC of fluconazole distributed from 0.13μg/mL to≥128μg/mL, and 2.6% of isolates were susceptible dose-dependently, while 2.1% were resistant.
Analysis of multicenter survey results may thus help in selecting therapeutic agents for deep mycosis, which is difficult to diagnose and treat.

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Vancomycin-resistant enterococci (VRE) was first isolated in our hospital from a sputum specimen from an inpatient in August 2002. Subsequently, VRE was also isolated from a fecal specimen in another patient in February 2003. The former strain exhibited an MIC of 8μg/mL for vancomycin (VCM), and the latter strain exhibited an MIC of 16μg/mL. Another strain with an MIC of 4μg/mL was isolated from the latter patient after the cessation of VCM treatment. All three strains grew in a VRE-selection medium and were demonstrated to have the van B gene. The MIC increased when the strain with an MIC of 4μg/mL was cultured in VCMsupplemented medium, indicating the induction of VCM resistance. These results suggest that routine laboratory tests might not detect the presence of VRE with the van B gene, which has a MIC.

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Since vancomycin-resistant enterococci (VRE) was first isolated in our hospital, we have studied a total of 459 fecal specimens from 250 inpatients to elucidate the relationship between the detection of vancomycin (VCM)-resistant bacteria and the use of VCM in our hospital. To detect VCM-resistant bacteria, we used 4μg/mL VCM supplemented broth and 8μg/mL VCM supplemented culture agar. VCM-resistant bacteria was detected in 12 out of 23 patients (52%) who were treated with VCM. On the other hand, VCM-resistant bacteria was detected in 48 out of 182 patients (26%) who were not treated with VCM. The VCM-resistant bacteria positive rate was significantly higher in patients who were treated with VCM (p<0.05). These results suggest a relationship between the detection of VCM-resistant bacteria and the use of VCM. Therefore, careful use of VCM is recommended.

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