[A case of endobronchial noncartilaginous hamartoma removed by high-frequency electrosurgical snaring and semiconductor laser].

A 55-year-old woman presented with wheezing and difficulty breathing. Chest computed tomography demonstrated a tumor in the left main bronchus. Flexible fiber-optic bronchoscopy revealed a polypoid mass obstructing the orifice of the left main bronchus. Biopsy specimens were consistent with hamartoma; therefore endoscopic resection was selected as treatment. High-frequency electrosurgical snaring and a semiconductor laser with electrocautery therapy were used to completely excise the tumor. Histologic sections of the resected tissue revealed a rare case of noncartilaginous hamartoma. This case demonstrates that endoscopic resection can be used for the non-surgical management of endobronchial hamartoma.

[A case of community-acquired pneumonia caused by Corynebacterium propinquum].

Corynebacterium propinquum, which is classified as Corynebacterium ANF-3, has not yet been described as a cause of the respiratory infections. In this paper, we reported a case of 67-year-old immunocompetent male with community-acquired pneumonia caused by C. propinquum. Our study suggested that Gram staining of the pulurent sputum was the most important diagnostic tool to determine the pathogenecity of this organism.

Molecular characteristics of outbreaks of nosocomial infection with influenza A/H3N2 virus variants.

OBJECTIVE: To describe outbreaks of nosocomial influenza infection with molecular methods and to elucidate the viral linkages among outbreak case patients including both inpatients and healthcare workers (HCWs). SETTING: A 180-bed acute and long-term care hospital in Japan. METHODS: Retrospective observational study of nosocomial outbreaks of infection with influenza A/H3N2. Together with information about onset dates and vaccination history, we obtained nasopharyngeal swab samples from individuals with cases of influenza or influenza-like illness (ILI). The hemagglutinin genes of the recovered viruses were sequenced and compared, along with those of community-circulating strains, for similarity by phylogenetic tree analysis. RESULTS: The outbreaks occurred from February 26 through April 3, 2007, during the 2006-2007 epidemic season, and they involved 11 patients and 13 HCWs. The 2 outbreaks involved 2 different genotypes of influenza A/H3N2 viruses. These virus variants were closely related to the influenza strains that were circulating in the community during the same epidemic season. CONCLUSION: This study showed the dissemination of highly homologous influenza virus variants among inpatients and HCWs within a short period, as a result of nosocomial transmission. These strains were also similar to influenza strains that were circulating in the community.

High prevalence of amantadine-resistance influenza a (H3N2) in six prefectures, Japan, in the 2005-2006 season.

Substantial increase in amantadine-resistant influenza A (H3N2) was reported in Asia and North America in 2005. In this study the frequency and genetic characteristics of amantadine-resistant influenza A, circulated in Japan in 2005-2006 season, were investigated. Isolates were tested by amantadine susceptibility test (TCID(50)/0.2 ml method), and sequencing of the M2 gene to identify mutations that confer resistance. Additionally, the hemagglutinin (HA) and neuraminidase (NA) genes of the viruses were examined. In total, 415 influenza A isolates from six prefectures were screened, and 231 (65.3%) of 354 influenza A (H3N2) were amantadine-resistant, with a serine to asparagine (S31N) change in the M2 gene. However, none of 61 A (H1N1) isolates were resistant. In addition, genetic analyses of the HA gene showed all amantadine-resistant viruses clustered in one (named clade N), possessing specific double mutations at 193, serine to phenylalanine (S193F), and at 225, asparatic acid to asparagine (D225N), and sensitive viruses belonged to another group (clade S). The clinical presentations at the clinical visit did not differ between patients shedding clade N virus and those shedding clade S virus. None of the patients had received previous treatment with amantadine. The results indicate an unusually high prevalence and wide circulation of the amantadine-resistance influenza A (H3N2) in Japan in the 2005-2006 season. These strains had the characteristic double mutations in the HA, in addition to the M2 mutation responsive for resistance. Antiviral resistance monitoring should be intensified and maintained for rapid feedback into treatment strategies, and selection of alternative therapeutic agents.