Peptidoglycan is an important component of bacterial cell wall, which plays an important role in maintaining the integrity of bacterial cell structure, stimulating immune response, and anti-infection. Peptidoglycan recycling is an indispensable process for bacterial cell growth and reproduction. In recent years, it has been reported that the peptidoglycan recycling is closely related to the occurrence and development of bacterial resistance, especially with the antibacterial activity of β-lactam antibiotics. In this paper, the relationship between peptidoglycan recycling and resistance is described by combining relevant reports and taking Mycobacterium tuberculosis and Pseudomonas aeruginosa as examples, so as to promote the understanding of bacterial resistance mechanisms and provide potential targets for the development of new antimicrobial drugs.
Protein post-translational modifications (PTMs) are critical for modulating protein structure and function. Among these, lysine lactylation (Kla) has garnered significant attention in recent years as a newly discovered PTM. Although Kla has been thoroughly investigated in eukaryotic systems, its study in prokaryotes, especially bacteria, remains comparatively limited. Emerging research highlights that bacterial Kla, operating through dynamic modification mechanisms, is pivotal in processes such as growth and metabolism, virulence control, pathogenicity, and host-pathogen interactions. This article provides a comprehensive overview of the latest progress in bacterial Kla research, emphasizing its historical discovery, distinct modification features, and underlying molecular regulatory mechanisms. We further explore the regulatory roles of this modification in bacterial physiological processes and pathogenesis, concluding with a discussion of current research challenges and prospective future developments.
Objective To analyze the clinical pathogenic characteristics of children with co-infected pneumonia, and to provide reference for clinical diagnosis and treatment. Methods Children with co-infected pneumonia treated in the pediatrics department of the First Affiliated Hospital of Chengdu Medical College between June 2023 and May 2024 were selected. According to age, the children were divided into infants, toddlers, preschoolers, school-aged children, and adolescentsg roup. The clinical pathogenic characteristics of children with pneumonia would be analyzed. ResultsA total of 358 pediatric patients were included. Among them, there were 189 males (52.79%) and 169 females (47.21%). There was no statistically significant difference in the composition of males and females in different age groups, types of pneumonia(P>0.05). The bacteria infecting the child are mainly Haemophilus influenzae, Staphylococcus aureus, Moraxella catarrh and Streptococcus pneumoniae. Viruses in the pathogen mainly include adenovirus, influenza A, B stream, human rhinovirus and respiratory syncytial virus. Except for typical pathogens (P>0.05), the detection rates of bacteria and viruses in different age groups showed statistically significant differences (P<0.05). The detection rates of bacterial co-infections, viral co-infections, bacterial+viral infections, and co-infections involving atypical pathogens were compared among different age groups, and the differences were statistically significant (P<0.001). The detection rate of different types of pathogens is highest in winter. Conclusions Children with co-infected pneumonia are mainly aged 0-7 years old. The incidence of pneumonia in children with co-infected is highest in winter. Mycoplasma is the main pathogen in dual infections or co-infections. Co-infections in early childhood are mainly caused by bacterial infections, and the incidence of viral infections increases with age.
ObjectiveTo explore the relationship between imipenem-resistant Pseudomonas aeruginosa (IRPA) and outer membrane porin protein OprD2 gene mutation.MethodsIRPA strains (n=30) and imipenem-sensitive Pseudomonas aeruginosa strains (n=30) isolated from the clinical specimens in the First Affiliated Hospital of Chengdu Medical College from December 2018 to December 2019 were collected. Bacteria identification and drug sensitivity experiments were performed by VITEK-2 Compact combined with Kirby-Bauer method. Quantitative real-time polymerase chain reaction was used to detect the expression levels of OprD2 gene in the imipenem-resistant group and the imipenem-sensitive group, and then the strains with decreased expression were sequenced.ResultsThe expression level of OprD2 gene in the imipenem-resistant group was significantly lower than that in the imipenem-sensitive group (P=0.048). Compared with the X63152 sequence, all the 11 Pseudomonas aeruginosa strains with significantly decreased OprD2 expression carried genetic variation, which occurred in coding regions. The variation sites presented diversity. The missense mutation of c.308C→G, c.344A→C, c.379G→C, c.471G→C, c.508T→C, c.553G→C, c.556-558CCG→GGC and c.565-566TG→AC caused amino acid change in the loop L2 and L3 of OprD2 porin, which affected the binding to imipenem. In addition, the mutations at 127, 169-171, 175, 177, 604, 628-630, 688, 719, 785, 826, 828, 842-843, 886, 901, 928-930, 934, 936, 944-945, 1039, 1041 and 1274 all resulted in the changes of amino acid. We also detected a deletion (c.1114-1115delAT) and other nonsense mutations. Large fragment deletion of OprD2 gene occurred in Strain 12. ConclusionsThe mutation and deletion of OprD2 gene can reduce the expression lever of OprD2 gene, leading to the resistance to imipenem of Pseudomonas aeruginosa. The variation of OprD2 gene of IRPA from clinical strains is diverse.
ObjectiveTo study the antibacterial activity of ceftazidime/avibactam against carbapenem-resistant Klebaiella pneumoniae (CRKP) in vitro and detect the resistance genes of CRKP, so as to provide reference for the treatment of patients with CRKP infection.MethodsA total of 120 CRKP strains isolated from clinical specimens from May 2014 to November 2017 were collected. The activitis of 11 antimicrobial agents against those CRKP strains were detected by broth microdilution method, and the genes related to resistance to ceftazidime/avibactam were detected by polymerase chain reaction in the 120 CRKP isolates.ResultsThe resistance rate of the 120 CRKP isolates against ceftazidime/avibactam was 16.67% (20/120), which was significantly lower than that against cefotaxime (100.00%), aztreonam (98.33%), ceftazidime (95.83%), cefoperazone/sulbactam (95.83%), meropenem (95.83%), imipenem (95.00%), levofloxacin(92.50%), amikacin (54.17%), minocycline (39.17%), and tegacycline (23.33%). Among the 20 CRKP strains resistant to ceftazidime/avibactam, there were 12 Klebsiella pneumoniae carbapenemase (KPC)-2-producing strains, 3 KPC-3-producing strains, 1 New Delhi metallo-β-lactamase-1 (NDM-1)-producing strain, and 1 oxacillin β-lactamase-48-producing strain; none of the 20 strains had KPC mutation.ConclusionsCeftazidime/avibactam is an effective agent agianst CRKP, and its resistance rate is significantly lower than that of other commonly used antimicrobial agents, especially other β-lactam antibiotics. In terms of resistance genes, except for one isolate producing NDM-1, no other known gene resistant to ceftazidime/avibactam has been found.