Whole genome sequencing of meticillin-resistant Staphylococcus aureus

Kuroda, Makoto; Ohta, Toshiko; Uchiyama, Ikuo; Baba, Tadashi; Yuzawa, Hiroko; Kobayashi, Ichizo; Cui, Longzhu; Oguchi, Akio; Aoki, Kenichi; Nagai, Yoshimi; Lian, JianQi; Ito, Teruyo; Kanamori, Mutsumi; Matsumaru, Hiroyuki; Maruyama, Atsushi; Murakami, Hiroyuki; Hosoyama, Akira; Mizutani-Ui, Yoko; Takahashi, Noriko; Sawano, Toshihiko; Inoue, Ryotaro; Kaito, Chikara; Sekimizu, Kazuhisa; Hirakawa, Hideki; Kuhara, Satoru; Goto, Susumu; Yabuzaki, Junko; Kanehisa, Minoru; Yamashita, Atsushi; Oshima, Koichiro; Furuya, Keiko; Yoshino, Chie; Shiba, Tadayoshi; Hattori, Masahira; Ogasawara, Nagahisa; Hayashi, Hideo; Hiramatsu, Kazumasa

doi:10.1016/s0140-6736(00)04403-2

Cited by 1,768 publications

(1,349 citation statements)

References 39 publications

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“…In addition, SAgs are highly expressed by the methicillin-resistant S. aureus strains associated with community and hospital settings. 9,[20][21][22] In addition to their clinical significance, SAgs are also important from a biodefense initiative. One of the SAg exotoxins released by S. aureus, staphylococcal enterotoxin B (SEB), is a designated biological weapon.…”

mentioning

confidence: 99%

Human Leukocyte Antigen Class II Transgenic Mouse Model Unmasks the Significant Extrahepatic Pathology in Toxic Shock Syndrome

Tilahun

Marietta

et al. 2011

The American Journal of Pathology

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Among the exotoxins produced by Staphylococcus aureus and Streptococcus pyogenes, the superantigens (SAgs) are the most potent T-cell activators known to date. SAgs are implicated in several serious diseases including toxic shock syndrome (TSS), Kawasaki disease, and sepsis. However, the immunopathogenesis of TSS and other diseases involving SAgs are still not completely understood. The commonly used conventional laboratory mouse strains do not respond robustly to SAgs in vivo. Therefore, they must be artificially rendered susceptible to TSS by using sensitizing agents such as D-galactosamine (D-galN), which skews the disease exclusively to the liver and, hence, is not representative of the disease in humans. SAg-induced TSS was characterized using transgenic mice expressing HLA class II molecules that are extremely susceptible to TSS without D-galN. HLA-DR3 transgenic mice recapitulated TSS in humans with extensive multiple-organ inflammation affecting the lung, liver, kidneys, heart, and small intestines. Heavy infiltration with T lymphocytes (both CD4 ؉ and CD8؉), neutrophils, and macrophages was noted. In particular, the pathologic changes in the small intestines were extensive and accompanied by significantly altered absorptive functions of the enterocytes. In contrast to massive liver failure alone in the D-galN sensitization model of TSS, findings of the present study suggest that gut dysfunction might be a key pathogenic event that leads to high morbidity and mortality in humans with

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mentioning

confidence: 99%

Human Leukocyte Antigen Class II Transgenic Mouse Model Unmasks the Significant Extrahepatic Pathology in Toxic Shock Syndrome

Tilahun

Marietta

et al. 2011

The American Journal of Pathology

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“…All experiments were conducted with MRSA strain NRS70, a clinical respiratory isolate [16]. The minimal inhibitory concentration for vancomycin against NRS70 was determined by the clinical microbiology laboratory at the Buffalo VA Hospital to be 0.5 lg/mL.…”

Section: Bacteriamentioning

confidence: 99%

Cathodic Voltage-controlled Electrical Stimulation Plus Prolonged Vancomycin Reduce Bacterial Burden of a Titanium Implant-associated Infection in a Rodent Model

Nodzo

Tobias

Ahn

et al. 2016

Clinical Orthopaedics &Amp; Related Research

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Background Cathodic voltage-controlled electrical stimulation (CVCES) of titanium implants, either alone or combined with a short course of vancomycin, has previously been shown to reduce the bone and implant bacterial burden in a rodent model of methicillin-resistant Staphylococcus aureus (MRSA) implant-associated infection (IAI). Clinically, the goal is to achieve complete eradication of the IAI; therefore, the rationale for the present study was to evaluate the antimicrobial effects of combining CVCES with prolonged antibiotic therapy with the goal of decreasing the colony-forming units (CFUs) to undetectable levels.Questions/purposes (1) In an animal MRSA IAI model, does combining CVCES with prolonged vancomycin therapy decrease bacteria burden on the implant and surrounding bone to undetectable levels? (2) When used with prolonged vancomycin therapy, are two CVCES treatments more effective than one? (3) What are the longer term histologic effects (inflammation and granulation tissue) of CVCES on the surrounding tissue? Methods Twenty adult male Long-Evans rats with surgically placed shoulder titanium implants were infected with a clinical strain of MRSA (NRS70). One week after infection, the rats were randomly divided into four groups of five: (1) VANCO: only vancomycin treatment (150 mg/ kg, subcutaneous, twice daily for 5 weeks); (2) VANCO + 1STIM: vancomycin treatment (same as the VANCO group) coupled with one CVCES treatment (À1.8 V for 1 hour on postoperative day [POD] 7); (3) VANCO + 2STIM: vancomycin treatment (same as the VANCO group) coupled with two CVCES treatments (À1.8 V for 1 hour on POD 7 and POD 21); or (4) CONT: no treatment. On POD 42, the implant, bone, and peripheral blood were collected for CFU enumeration and histological analysis, where we compared CFU/mL on the implants and bone among the groups. A pathologist, blinded to the experimental conditions, performed a semiquantitative analysis Clinical Orthopaedics and Related Research ®A Publication of The Association of Bone and Joint Surgeons® of inflammation and granulation tissue present in serial sections of the humeral head for animals in each experimental group. Results The VANCO + 1STIM decreased the implant bacterial burden (median = 0, range = 0-10 CFU/mL) when compared with CONT (median = 5.7 9 10 4 , range = 4.0 9 10 3 À8.0 9 10 5 CFU/mL; difference of medians = À5.6 9 10 4 ; p \ 0.001) and VANCO (median = 4.9 9 10 3 , range = 9.0 9 10 2 À2.1 9 10 4 CFU/mL; difference of medians = À4.9 9 10 3 ; p \ 0.001). The VANCO + 1STIM decreased the bone bacterial burden (median = 0, range = 0-0 CFU/mL) when compared with CONT (median = 1.3 9 10 2 , range = 0-9.4 9 10 2 CFU/ mL; difference of medians = À1.3 9 10 2 ; p \ 0.001) but was not different from VANCO (median = 0, range = 0-1.3 9 10 2 CFU/mL; difference of medians = 0; p = 0.210). The VANCO + 2STIM group had implant CFU (median = 0, range = 0-8.0 9 10 1 CFU/mL) and bone CFU (median = 0, range = 0-2.0 9 10 1 CFU/mL) that were not different from the VANCO + 1STIM treatment ...

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“…However, until data from genome sequencing became available, the mutual distances between genetic markers within each PFGE fragment were unknown. (11,139). Half of all predicted proteins of strain N315 were similar to those of Bacillus subtilis or Bacillus halodurans, and these proteins mostly coded for essential functions such as DNA replication, protein synthesis, and carbohydrate metabolism.…”

Section: Genomementioning

confidence: 99%

“…Recent sequencing of two S. aureus strains revealed three new classes of pathogenicity islands: TSST family islands, exotoxin islands, and enterotoxin islands. A considerable number of new putative virulence genes were also identified (139).…”

Section: Virulence Factorsmentioning

confidence: 99%

Molecular Epidemiology of Methicillin-Resistant Staphylococcus aureus in Finland

Salmenlinna¹,

Lyytikäinen

Kotilainen

et al. 2000

European Journal of Clinical Microbiology & Infectious Dise

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Whole genome sequencing of meticillin-resistant Staphylococcus aureus

Cited by 1,768 publications

References 39 publications

Human Leukocyte Antigen Class II Transgenic Mouse Model Unmasks the Significant Extrahepatic Pathology in Toxic Shock Syndrome

Human Leukocyte Antigen Class II Transgenic Mouse Model Unmasks the Significant Extrahepatic Pathology in Toxic Shock Syndrome

Cathodic Voltage-controlled Electrical Stimulation Plus Prolonged Vancomycin Reduce Bacterial Burden of a Titanium Implant-associated Infection in a Rodent Model

Molecular Epidemiology of Methicillin-Resistant Staphylococcus aureus in Finland

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