Epidemiological analysis methods such as plasmid profiles, pulse-field gel electrophoresis, randomly amplified polymorphic DNA, and multilocus sequence typing have been proposed for H. cinaedi isolates

[24], [28] and [57]. We have developed a nested PCR system, as mentioned above [37], to directly catch the bacterial DNA (antigen GKT137831 clinical trial detecting system) in the clinical specimens, and have established an immunological diagnosis method (antibody detecting test) with high specificity to detect the exposure history of H. cinaedi [94]. Using these methods, we have analyzed many healthy subjects working in a hospital (doctors, nurses, staff members, etc.) and found some healthy individuals infected with H. cinaedi [37]. This finding suggests asymptomatic carriers exist, and may be related to nosocomial infections. Further investigations are needed to clarify the complete infection route and the nosocomial transmission route of H. cinaedi infection. It appears that, because H. cinaedi is thought not to cause acute severe disease, little importance has been placed on this organism. However, we now know that it likely causes nosocomial infections, is difficult to eradicate, and has a high incidence of recurrence. Furthermore, an association with chronic illnesses such as arrhythmia and arteriosclerosis has been pointed out in recent years. Therefore,

there is a need to rapidly establish guidelines for the use of antimicrobial agents, susceptibility http://www.selleckchem.com/products/pifithrin-alpha.html testing, and the treatment regimen in diagnosed H. cinaedi infection cases. In addition, it is important to elucidate PLEKHM2 the infection route.

To our knowledge, no medical center or clinic that has detected recurrent H. cinaedi infection has successfully eradicated it. Taking into account the variety of environmental or animal vector routes, both the route and the mechanism of infection by this microorganism should be clarified. Furthermore, we need to carefully monitor and understand the trends in H. cinaedi infections. Authors declare no conflict of interest. We thank the following persons for their helpful discussions and cooperation in medical, genetic, or biochemical analysis; Takatsugu Goto, Gifu University; Hideki Hirakawa, Kazusa DNA Research Institute; Tetsuro Matsunaga, Tohoku University Graduate School of Medicine; Masaru Baba, Toranomon Hospital. We are grateful to the following individuals for providing the H. cinaedi isolates used in this study: Shunji Takahashi, Sapporo City General Hospital; Masashi Narita, Ohta-nishinouchi Hospital; Ayako Oumi, Social Insurance Chuo General Hospital; Ken Kikuchi, Juntendo University; Yoshihito Otsuka, Kameda Medical Center; Haruki Sawamura and Hiroshige Mikamo, Aichi Medical University; Yoko Kawakami, National Hospital Organization Kyushu Cancer Center; Toshio Kitamura, Shuichi Higashi, Keita Yamakawa, and Itsuo Honda, Kumamoto Orthopedic Hospital.