This study was to characterize and determine the classification of the novel strain TM49^T, isolated from a blood culture of a patient who developed bacteremia while receiving high-dose cytarabine chemotherapy for acute myeloid leukemia. The novel strain TM49^T was characterized at the species level through a polyphasic taxonomic analysis, incorporating morphological, physiological, biochemical, phylogenetic, and genome sequence analyses. 16S rRNA gene sequence analysis revealed that the strain belonged to the genus Lachnoanaerobaculum. The 16S rRNA gene sequence of strain TM49^T was observed to be most similar to that of "Lachnoanaerobaculum gingivalis" strain ChDC B114^T (99.2%). Strain TM49^T formed circular, glossy, slightly milky colonies with an undulate margin on BD™ Columbia Agar containing 5% sheep blood after 48 h at 37 °C, exhibiting less spreading compared to species of the genus Lachnoanaerobaculum. The major fatty acids of strain TM49^T were C_16:0, C_14:0, C_18:1 ω9c DMA, and C_18:1 ω7c DMA. The draft genome sequence of strain TM49^T was 2,821,554 bp in length, with a G+C content of 36.4. Digital DNA-DNA hybridization values between strain TM49^T and "L. gingivalis" ChDC B114^T, L. umeaense CD3: 22^T, L. orale N1^T, and L. saburreum CCUG 28089^T were 52.2%, 29.7%, 26.2%, and 24.5%, respectively. The Orthologous Average Nucleotide Identity values between strain TM49^T and "L. gingivalis" ChDC B114^T, L. umeaense CD3: 22^T, L. orale N1^T, and L. saburreum CCUG 28089^T were 93.1%, 84.9%, 83.2%, and 81.5%, respectively. Strain TM49^T (JCM 36186^T = DSM 116945^T) was found to be distinct from previously described species of the genus Lachnoanaerobaculum. Therefore, it is proposed as a new species, Lachnoanaerobaculum sanguinis sp. nov., with strain TM49^T as the type strain (= JCM 36186^T = DSM 116945^T).

Pseudomonas aeruginosa infection is considered a high-risk nosocomial infection and is very difficult to eradicate because of its tolerance to antibiotic treatment. A new compound, autoinducer analog-1 (AIA-1), has been demonstrated to reduce antibiotic tolerance, but its mechanisms remain unknown. This study aimed to investigate the mechanisms of AIA-1 in the antibiotic tolerance of P. aeruginosa. A transposon mutant library was constructed using miniTn5pro, and screening was performed to isolate high tolerant mutants upon exposure to biapenem and AIA-1. We constructed a deletion mutant and complementation strain of the genes detected in transposon insertion site determination, pruR and PA0066-65-64, and performed killing assays with antibiotics and AIA-1. Gene expression upon exposure to biapenem and AIA-1 and their relationship to stress response genes were analyzed. High antibiotic tolerance was observed in Tn5-pruR and Tn5-PA0065 transposon mutants and their deletion mutants, ΔpruR and ΔPA0066-65-64. Complemented strains of pruR and PA0066-65-64 with their respective deletion mutants exhibited suppressed antibiotic tolerance. It was determined that deletion of PA0066-65-64 increased rpoS expression, and PA0066-65-64 affects antibiotic tolerance via the rpoS pathway. Additionally, antibiotics and AIA-1 were found to inhibit pruR and PA0066-65-64. This study proposed that pruR and PA0066-65-64 are members of the antibiotic tolerance suppressors.

Odontogenic infection is the most common infection of the orofacial area. It can cause sepsis, activate host inflammatory response, and progress to organ failure and death. Patients presenting critical symptoms of sepsis need prompt diagnosis, monitoring, and risk stratification. Therefore, a biomarker specific to bacterial infection is essential for rapid diagnosis, immediate treatment, and saving lives. Procalcitonin is an elevated biomarker in response to bacterial infection; however, its use in oral and maxillofacial surgery is still limited. This review aimed to evaluate the role of procalcitonin as a biomarker in odontogenic infection. Procalcitonin was useful in managing odontogenic maxillofacial infections leading to sepsis, odontogenic deep neck infections, and abscesses. Procalcitonin can also direct antibiotic therapy initiation, escalation, and cessation, reflecting its usefulness in antibiotic stewardship. Future studies should elucidate the optimum cut-off value of procalcitonin in odontogenic infection management and its potential to be combined with other markers.

The threat of antibiotic resistance has been a global public health issue. This problem is often aggravated by inappropriate antibiotic administration, including those after the third molar surgery. Thus, systemic antibiotic use in third molar surgery should be considered strictly. The use of antiseptics after third molar surgery, such as chlorhexidine, may help prevent postoperative complications; therefore, its use should be encouraged. This study aimed to determine whether chlorhexidine is beneficial in preventing alveolar osteitis without systemic antibiotics. This review was conducted to determine whether chlorhexidine is beneficial in preventing alveolar osteitis (AO) and was designed according to the PICO model. Alternating combinations of keywords were used, including "third molar surgery," "chlorhexidine," "mouthwash," "wound dressing," and "irrigation" to search PubMed, Cochrane Library, and Scopus. Clinical studies of third molar surgery that reported clinical outcomes after postoperative chlorhexidine supplementation without systemic antibiotic prescription were included. Twelve studies were included in the meta-analysis. The incidence of alveolar osteitis (AO) in the chlorhexidine group was significantly lower than that in the control group (9.58% vs. 16.8%, P < 0.0001). Chlorhexidine reduced the risk of AO by 42.9%. The use of chlorhexidine can effectively prevent AO and should be considered good clinical practice to mitigate antimicrobial resistance.