- 著者
- Hidemasa Nakaminami Hinako Kawasaki Shunsuke Takadama Hiroshi Kaneko Yoshiko Suzuki Hiroshi Maruyama Norihisa Noguchi
- 出版者
- National Institute of Infectious Diseases, Japanese Journal of Infectious Diseases Editorial Committee
- 雑誌
- Japanese Journal of Infectious Diseases (ISSN:13446304)
- 巻号頁・発行日
- vol.74, no.1, pp.82-84, 2021-01-29 (Released:2021-01-22)
- 参考文献数
- 15
- 被引用文献数
- 8
In the last decade, methicillin-resistant Staphylococcus aureus (MRSA) has been identified in livestock animals, such as swine, poultry, and veal calves, and has been termed livestock-associated MRSA (LA-MRSA). LA-MRSA sequence type (ST) 398 strains can effectively infect and colonize humans, with subsequent human-to-human transmission in both community and hospital settings. Unlike other countries, LA-MRSA had not been reported in Japanese patients until 2019. However, we recently reported a case of intractable arthritis caused by an LA-MRSA CC398 (ST1232) clone, which is a single-locus variant of ST398, in a patient in Tokyo, Japan, with no animal contact (Nakaminami H, et al. Emerg Infect Dis. 2020; 26: 795-7.). Uniquely, the strain was positive for Panton-Valentine leukocidin. Here, we report the second such case in Japan. To prevent the dissemination of LA-MRSA in the Japanese community, the prevalence of the CC398 MRSA clone should be closely monitored in the future.
- 著者
- Nanako Takeda-Hirokawa Lian-Pin Neoh Hiroaki Akimoto Hiroshi Kaneko Takashi Hishikawa Iwao Sekigawa Hiroshi Hashimoto Shun-ichi Hirose Tsutomu Murakami Naoki Yamamoto Tohru Mimura Yutaro Kaneko
- 出版者
- Center For Academic Publications Japan
- 雑誌
- MICROBIOLOGY and IMMUNOLOGY (ISSN:03855600)
- 巻号頁・発行日
- vol.41, no.9, pp.741-745, 1997 (Released:2008-03-17)
- 参考文献数
- 25
To clarify the mechanism by which curdlan sulfate (CRDS) inhibits human immunodeficiency virus (HIV)-1 infection, we examined its influence on the binding of gp120 to CD4 molecules on T cells and macrophages, as well as on the production of TNF-α by gp120-stimulated macrophages (which promotes HIV-1 replication). CRDS treatment of cells not only inhibited the binding of HIV-1 gp120 to CD4+ cells, but also inhibited TNF-α production induced by gp120. Inhibition of HIV-1 infection by CRDS may be related to these two actions.