Functional characterization of toxin-antitoxin system in Mycobacterium tuberculosis.

Toxin-Antitoxin (TA) system is abundant in the microbial genome, especially in bacteria and archaea. Its genetic elements and addiction modules with the role of bacterial persistence and virulence. The TA system consists of a toxin and most unstable antitoxin that could be a protein or non-encoded RNA, TA loci are chromosomally determined and their cellular functions are mostly unknown. Approximately 93 TA systems were demonstrated and more functionally available in M. tuberculosis (Mtb), the organism responsible for tuberculosis (TB). It is an airborne disease, which is causing ill-health to humans. M. tuberculosis possesses higher TA loci than other microbes and non-tubercle bacilli, the following TA types have been identified such as VapBC, MazEF, HigBA, RelBE, ParDE, DarTG, PemIK, MbcTA, and one tripartite type II TAC-Chaperone system. Toxin-antitoxin Database (TADB) brings a detailed update on Toxin-Antitoxin classification in the different pathogens such as staphylococcus aureus, streptococcus pneumonia, Vibrio cholerae, Salmonella typhimurium, Shigella flexneri, and helicobacter pylori, etc. So, this Toxin-Antitoxin system is a master regulator for bacterial growth, and an essential factor in analyzing the properties and function of disease persistence, biofilm formation, and pathogenicity. The TA system is an advanced tool to develop a new therapeutic agent against M. tuberculosis.

Correlation of phenotypic and genotypic virulence markers, antimicrobial susceptibility pattern, and outcome of Pseudomonas aeruginosa sepsis infection.

INTRODUCTION: Pseudomonas aeruginosa (PA) possesses several virulence genes that enable them to evade the immune system and to cause injury in the host tissue. However, the number of studies that characterized the virulence genes profile in PA sepsis is limited. AIM: The main objective of this study was to identify and characterize virulence genes in PA causing sepsis, as well as investigate the relationship between virulence genes, antimicrobial susceptibility patterns, and infection outcomes. METHODOLOGY: A prospective study, conducted between October 2020-October 2021, isolates were recovered from blood samples and identified using standard microbiological procedures. Phenotypic techniques were used to screen for capsule, siderophore production, biofilm formation, serum resistance, hemolysin production, and protease. Molecular techniques were performed to screen for alginate D (alg D), exoenzyme S (Exo S), exotoxin A (tox A), phospholipase H (plc H), phospholipase N (plc N), and elastase B (las B). Kirby-Bauer disc diffusion method was used to determine the antimicrobial susceptibility pattern of isolates, which was then interpreted according to the CLSI 2021 guidelines. RESULTS: Out of the n = 215 Gram-negative bacteria recovered from sepsis patients during our study, n = 20 were Pseudomonas aeruginosa. PA isolates were susceptible to all antibiotics tested except for 3 of the isolates that were resistant to gentamycin, 2 to imipenem, and 1 to ceftazidime, cefepime, meropenem, tobramycin, and amikacin. The most prevalent virulence genes present were capsule (100%), siderophore production (100%), alg D (100%), Las B (100%), and Tox A (100%). CONCLUSION: Our study found that PA causing sepsis harbours a high level of virulence genes. However, the high presence of virulence factors was not statistically associated with antimicrobial susceptibility, as most isolates in our study were susceptible to the antibiotics tested.