BackgroundPresence of Mycobacterium fortuitum in respiratory tracts usually indicates mere colonization or transient infection, whereas true pulmonary infection occurs in patients with gastroesophageal disease. However, little is known about the diagnostic indications for true M. fortuitum pulmonary infection and the natural history of the disease.Case presentationA 59-year-old man was referred to our hospital for treatment against M. fortuitum pulmonary infection. Fifteen years before the referral, he underwent total gastrectomy, after which he experienced esophageal reflux symptoms. After the referral, the patient was closely monitored without antimicrobial therapy because of mild symptoms and no pathological evidence of M. fortuitum pulmonary infection. During the observation, chest imaging showed migratory infiltrates. Two years after the referral, his lung biopsy specimen revealed foamy macrophages and multinucleated giant cells, indicating lipoid pneumonia. However, he was continually monitored without any treatment because there was no evidence of nontuberculous mycobacterial infection. Four years after the referral, he developed refractory pneumonia despite receiving adequate antibiotic therapy. After confirmation of granulomatous lesions, multiple antimicrobial therapy for M. fortuitum resulted in a remarkable improvement with no exacerbation for over 5 years. Random amplified polymorphic DNA polymerase chain reaction analysis revealed identical M. fortuitum strains in seven isolates from six sputum and one intestinal fluid specimens obtained during the course of the disease.ConclusionsWe have described a patient with M. fortuitum pulmonary infection who presented with migratory infiltrates. The pathological evidence and microbiological analysis suggested that M. fortuitum pulmonary infection was associated with lipoid pneumonia and chronic exposure to gastrointestinal fluid. Therefore, physicians should carefully monitor patients with M. fortuitum detected from lower respiratory tract specimens and consider antimicrobial therapy for M. fortuitum infection when the patient does not respond to adequate antibiotic therapy against common pneumonia pathogens.

The acidogenic phase of a continuous stirred tank reactor (CSTR) inoculated with well acclimated sludge will produce a substantial amount of hydrogen gas and steady state microbial biomass. Hydrogen production of more than 65% was observed at high dilution rate and 71% at low dilution rate. Gas production rate of more than 10 1/day was also observed from the chemostat reactors. The true yield (Yt) value was 0.625 g.VSS/g.COD-utilized and the kd value was 0.41 hr-1. Sample sludge (cell) from chemostat reactors was then collected at steady state and small amount was inoculated into small vials. Many sets of vials were prepared and all were filled up by different concentrations of glucose and growth medium with the same proportion. The vials were treated as batch culture of the mixed microorganisms, incubated at 30°C and put on a rotating shaker with 130 osc.min.-1. The VSS values analyzed on the vials sample at predetermined time intervals will provide the data for the inhibitory constants determinations. From the available kinetics parameters and inhibitory model equation, graph fittings computations were done. The inhibitory model fits to some degree on the experimental data. These findings confirmed the inhibitory effects of glucose concentrations and the ability to recover hydrogen gas from organic substances at certain predetermined concentrations.

Mycobacterium ulcerans subsp. shinshuense produces mycolactone and causes Buruli ulcer. Here, we report the complete sequence of its genome, which comprises a 5.9-Mb chromosome and a 166-kb plasmid (pShT-P). The sequence will represent the essential data for future phylogenetic and comparative genome studies of mycolactone-producing mycobacteria.

Background The clinical impact of infection with Mycobacterium ( M. ) abscessus complex (MABC), a group of emerging non-tuberculosis mycobacteria (NTM), is increasing. M. abscessus subsp. abscessus / bolletii frequently shows natural resistance to macrolide antibiotics, whereas M. abscessus subsp. massiliense is generally susceptible. Therefore, rapid and accurate discrimination of macrolide-susceptible MABC subgroups is required for effective clinical decisions about macrolide treatments for MABC infection. We aimed to develop a simple and rapid diagnostic that can identify MABC isolates showing macrolide susceptibility. Methods Whole genome sequencing (WGS) was performed for 148 clinical or environmental MABC isolates from Japan to identify genetic markers that can discriminate three MABC subspecies and the macrolide-susceptible erm (41) T28C sequevar. Using the identified genetic markers, we established PCR based- or DNA chromatography-based assays. Validation testing was performed using MABC isolates from Taiwan. Finding We identified unique sequence regions that could be used to differentiate the three subspecies. Our WGS-based phylogenetic analysis indicated that M. abscessus carrying the macrolide-susceptible erm (41) T28C sequevar were tightly clustered, and identified 11 genes that were significantly associated with the lineage for use as genetic markers. To detect these genetic markers and the erm (41) locus, we developed a DNA chromatography method that identified three subspecies, the erm (41) T28C sequevar and intact erm (41) for MABC in a single assay within one hour. The agreement rate between the DNA chromatography-based and WGS-based identification was 99·7%. Interpretation We developed a novel, rapid and simple DNA chromatography method for identification of MABC macrolide susceptibility with high accuracy. Funding AMED, JSPS KAKENHI

Mycobacterium pseudoshottsii is a fish pathogen that produces mycolactone. Here, we report the complete chromosome sequence of a type strain of M. pseudoshottsii (JCM 15466). The sequence will represent essential data for future phylogenetic and comparative genome studies of mycolactone-producing mycobacteria.