Delayed Propionibacterium acnes surgical site infections occur only in the presence of an implant.

Whether Propionibacterium acnes (P. acnes) causes surgical-site infections (SSI) after orthopedic surgery is controversial. We previously reported that we frequently find P. acnes in intraoperative specimens, yet none of the patients have clinically apparent infections. Here, we tracked P. acnes for 6 months in a mouse osteomyelitis model. We inoculated P. acnes with an implant into the mouse femur in the implant group; the control group was treated with the bacteria but no implant. We then observed over a 6-month period using optical imaging system. During the first 2 weeks, bacterial signals were detected in the femur in the both groups. The bacterial signal completely disappeared in the control group within 28 days. Interestingly, in the implant group, bacterial signals were still present 6 months after inoculation. Histological and scanning electron-microscope analyses confirmed that P. acnes was absent from the control group 6 months after inoculation, but in the implant group, the bacteria had survived in a biofilm around the implant. PCR analysis also identified P. acnes in the purulent effusion from the infected femurs in the implant group. To our knowledge, this is the first report showing that P. acnes causes SSI only in the presence of an implant.

Vasculitis induced by immunization with Bacillus Calmette-Guérin followed by atypical mycobacterium antigen: a new mouse model for Kawasaki disease.

Kawasaki disease causes systemic vasculitis. The development of skin lesions at the vaccination site with Bacillus Calmette-Guérin (BCG) is an important diagnostic symptom. We hypothesized that infection with ubiquitous microorganisms immunogenically related to BCG might induce an immunopathologic reaction leading to the development of Kawasaki disease. Mice were first inoculated with BCG, and then secondarily inoculated 4 weeks later with crude extract from Mycobacterium intracellulare (cMI), an abundant atypical mycobacterium. Animals inoculated with BCG followed by cMI developed coronary arteritis with infiltration of inflammatory cells, whereas control animals inoculated with only cMI or BCG did not, suggesting that the immune response to the mycobacteria induced autoimmunity to the vascular wall. Intravenous injection with antibodies to peroxiredoxin II, a modulator of vascular remodeling and a suggested target for autoimmune vasculitis, also resulted in coronary arteritis, but only after prior inoculation with BCG. Tumor necrosis factor-alpha, MCP1 and interferon-gamma production were significantly higher in the animals inoculated with BCG than in the control groups (P<0.05). BCG immunization was required for the development of coronary arteritis, suggesting that these cytokines might play important roles. The results indicate that BCG induces primary autoimmunity and stimulates cytokine induction, and that atypical mycobacterial infection boosts the autoimmunity resulting in coronary arteritis.

Syndromic craniosynostosis with elbow joint contracture.

This paper reports a new type of syndromic craniosynostosis that was diagnosed by DNA analysis of the patient's fibroblast growth factor receptor (FGFR) genes. At birth, a male infant had ocular proptosis, a pseudotail, and obstructed respiration. He developed craniosynostosis, craniofacial dysmorphism, hydrocephalus, and bilateral contracture of his elbow joints. His treatment included fronto-orbital advancements and a ventriculoperitoneal shunt. Genetic analysis revealed that he was heterozygous for a missense mutation in exon 9 of the FGFR2 gene that resulted in an amino acid substitution of cysteine for serine at residue 351 (Ser351Cys). Seven cases with this mutation had previously been reported. All had severe craniosynostosis with midface hypoplasia, elbow joint contracture, developmental retardation, and early death.