Case report: Intraabdominal infection of Mycobacterium syngnathidarum in an immunocompetent patient confirmed by whole-genome sequencing.

Background: The taxonomic group of non-tuberculous mycobacteria (NTM) encompasses more than 190 species and subspecies, some of which can cause pulmonary and extrapulmonary diseases across various age groups in humans. However, different subspecies exhibit differential drug sensitivities, and traditional detection techniques struggle to accurately classify NTM. Therefore, clinicians need more effective detection methods to identify NTM subtypes, thus providing personalized medication for patients. Case presentation: We present the case of a 47-year-old female patient diagnosed with an intraabdominal infection caused by Mycobacterium syngnathidarum. Despite computed tomography of the chest suggesting potential tuberculosis, tuberculosis infection was ruled out due to negative TB-DNA results for ascites fluid and sputum and limited improvement of lung lesions after treatment. Additionally, acid-fast staining and Lowenstein-Jensen culture results revealed the presence of mycobacterium in ascites fluid. Subsequent whole-genome sequencing (WGS) confirmed the DNA sequences of Mycobacterium syngnathidarum in colonies isolated from the ascites fluid, which was further corroborated by polymerase chain reaction and Sanger sequencing. Ultimately, the patient achieved a complete recovery following the treatment regimen targeting Mycobacterium syngnathidarum, which involved clarithromycin, ethambutol hydrochloride, pyrazinamide, rifampicin, and isoniazid. Conclusion: This is the first reported case of Mycobacterium syngnathidarum infection in humans. Mycobacterium syngnathidarum was detected by WGS in this case, suggesting that WGS may serve as a high-resolution assay for the diagnosis of different subtypes of mycobacterium infection.

Regulation of maltocin synthesis in Stenotrophomonas maltophilia by positive and negative regulators.

Maltocin P28, produced by Stenotrophomonas maltophilia P28, is an R-type phage tail-like bacteriocin (PTLB). Its gene cluster consists of 23 putative genes, including nine nonstructural genes and fourteen structural genes. In this work, three nonstructural genes, mpsA, mpsH and mpsR, were found to encode transcriptional regulators to control maltocin P28 synthesis. MpsA activated the transcription of mpsH and lysis genes. MpsH activated the transcription of structural genes. Under normal growth conditions, MpsR repressed the transcription of mpsA and the structural genes, as well as its own. When S. maltophilia P28 was treated with mitomycin C, an immediate and significant decrease in the amount of MpsR was observed, followed by derepressed expression of mpsA, mpsR and structural genes, a marked rise in the expression of all regulatory and structural genes, and finally a clear increase in the maltocin P28 production. Neither the recA gene nor the lexA gene was found to be involved in the induced synthesis of maltocin P28. Our study indicated that a unique mechanism regulates the expression of maltocin genes in S. maltophilia, representing a novel strategy for balancing the expression of PTLB genes in bacteria.

Tracing membrane biofouling to the microbial community structure and its metabolic products: An investigation on the three-stage MBR combined with worm reactor process.

The biofouling characteristics of an MBR (S-MBR) combined with the worm reactor and a conventional MBR (C-MBR) were analyzed, respectively, over the three-stage (fast-slow-fast) process. Whether it was in the C-MBR or the S-MBR, the species of the active sludge (AS) were similar to that of the cake sludge (CS) in stage 1 (before day 1), the bacterial adsorption and the metabolites attachment contributed to this transmembrane pressure (TMP) rise. In the stage 2, the TMP increasing rate of the C-MBR was eight times more than that of the S-MBR. During this period, a characteristic community colonized the AS and CS of the S-MBR with the microbes, ie Flavobacteria, Firmicutes and Chloroflexi which were responsible for the degradation of extracellular polymeric substances (EPS) and soluble microbial products (SMP). These dominant species caused the slower accumulation of biofouling metabolites in the CS, resulting in the slow rise-related in TMP. Meanwhile, the enrichment of ß-proteobacterium and the absence of Mycobacterium and Propionibacterium in AS and CS of the C-MBR were deemed as the main biological factors bringing about the rise-associated in TMP. In the stage 3, the biofilm was matured, and the cake layer was more compacted, which resulted in an abrupt rise in TMP and severe membrane fouling. Additionally, the statistical analysis revealed that a highly correlation between the TMP increasing rate and the content of carbonhydrates in SMP (SMPc). When the SMPc content increased slowly, there was a relatively slow biofouling. But, when the SMPc increasing rate was greater, it led to a more serious membrane fouling with the sudden TMP jump. Additionally, there was also a highly significant correlation coefficient for the TMP rise and the content of carbonhydrates in EPS (EPSc) and the protein in SMP (SMPp), rather than the protein in EPS (EPSp). The cluster analysis showed that the microbes contributing to membrane fouling were more abundant in the C-MBR, while the microbes related to organic compounds degradation were more abundant in the S-MBR. There was significant correlation between the microbes and their metabolites. The SMPc in conjunction with EPSc and SMPp were the main factors accelerating the membrane fouling. It was concluded that a quick rise in SMPc triggered an abrupt increase in TMP, while the EPSc and SMPp caused the sustained increase in TMP.