Coronavirus Disease 2019 (COVID-19), during the second wave in early 2021, has caused devastating chaos in India. As daily infection rates rise alarmingly, the number of severe cases has increased dramatically. The country has encountered health infrastructure inadequacy and excessive demand for hospital beds, drugs, vaccines, and oxygen. Adding more burden to such a challenging situation, mucormycosis, an invasive fungal infection, has seen a sudden surge in patients with COVID-19. The rhino-orbital-cerebral form is the most common type observed. In particular, approximately three-fourths of them had diabetes as predisposing comorbidity and received corticosteroids to treat COVID-19. Possible mechanisms may involve immune and inflammatory processes. Diabetes, when coupled with COVID-19–induced systemic immune change, tends to cause decreased immunity and an increased risk of secondary infections. Since comprehensive data on this fatal opportunistic infection are evolving against the backdrop of a major pandemic, prevention strategies primarily involve managing comorbid conditions in high-risk groups. The recommended treatment strategies primarily included surgical debridement and antifungal therapy using Amphotericin B and selected azoles. Several India-centric clinical guidelines have emerged to rightly diagnose the infection, characterise the clinical presentation, understand the pathogenesis involved, and track the disease course. Code Mucor is the most comprehensive one, which proposes a simple but reliable staging system for the rhino-orbital-cerebral form. A staging system has recently been proposed, and a dedicated registry has been started. In this critical review, we extensively analyse recent evidence and guidance on COVID-19–associated mucormycosis in India.

The emergence of Pseudomonas aeruginosa as a potential threat in persistent infections can be attributed to the plethora of virulence factors expressed by it. This review discusses the various viru... Graphical abstract

Biginelli dihydropyrimidinone derivatives as structural analogs of monastrol, a known human kinesin Eg5 inhibitor, were synthesized. IC50 values of the synthesized compounds against the proliferation of human hepatocellular carcinoma and human epithelial carcinoma cell lines were determined through MTT assay. Molecular docking study gave a clear insight into the structural activity relationship of the compounds in comparison with monastrol.

Antimicrobial resistance renders conventional therapy, demanding the need for alternative therapeutic techniques. A potential strategy for treating infections caused by multi-drug-resistant bacteria is using bacteriophages, viruses that only multiply and infect specific bacteria. This review aims to evaluate the findings of clinical studies on phage therapy for bacterial illnesses. A comprehensive search method was utilized to identify 11 appropriate trials, which were then assessed for safety, efficacy, and treatment outcomes. The Joann-Briggs-Institute checklist and PRISMA criteria were used to evaluate these studies thoroughly. The results were summarized by extracting and analyzing data on trial design, treatment outcomes, safety profiles, and therapeutic effectiveness. Phage treatment had a strong safety profile, with few side effects recorded across many routes, including oral, intravenous, and topical. Clinical studies demonstrated its effectiveness in lowering bacterial loads, resolving infections, and destroying biofilms. However, diversity in trial designs hampered the generalizability of the findings. This study emphasizes the promise of phage therapy as a safe and efficient treatment for bacterial-illnesses. Despite its potential, there are still significant gaps in clinical application, long-term efficacy assessment, and trial standardization. Addressing these issues is critical to developing phage therapy as an effective alternative treatment for multidrug-resistant-illnesses.

Bacteria and bacteriophages are in a co-evolutionary arms race, developing intricate bacterial defense mechanisms that enable phage resistance and counterstrategies. Bacteria evolve diverse defense mechanisms to inhibit each stage of the phage infection cycle.Surface-based defenses prevent phage adsorption and infection, including receptor modifications, capsule production, and biofilm formation. Intracellular systems such as restriction-modification (R-M) and abortive infection (Abi) mechanisms degrade phage DNA or sacrifice infected cells to protect the population. Adaptive immunity, particularly through CRISPR-Cas systems, enables bacteria to recognize and neutralize recurring phage attacks. Phages counter these defenses through anti-CRISPR proteins, receptor mimicry, and depolymerization, which degrade capsules and biofilm matrices. These dynamic interactions shape microbial ecosystems, offering insights for the development of novel antimicrobial strategies. Emerging approaches, including engineered phages and combination therapies, hold promise for addressing bacterial resistance. Understanding these bacterial-phage dynamics is critical for advancing phage therapy as a powerful tool against multidrug-resistant bacterial infections. This review aims to systematically examine and integrate current knowledge on bacterial antiphage defense systems and the evolutionary adaptations employed by bacteriophages to overcome these barriers.

Acinetobacter baumannii is a Gram-negative opportunistic pathogen and a major cause of healthcare-associated infections, including ventilator-associated pneumonia, bacteraemia, meningitis, and urinary tract infections. Its persistence in hospital environments is due to its ability to survive desiccation, resist disinfectants, and colonize both biotic and abiotic surfaces. Virulence in A. baumannii is largely associated with structures such as Csu pili, biofilm-associated protein (Bap), and outer membrane protein A (OmpA), which enable surface attachment, biofilm formation, and host cell damage. The production of extracellular polysaccharides and quorum sensing further enhance biofilm development. Iron uptake systems support bacterial growth even under iron-limited conditions within the host. Resistance to polymyxins often results from lipid A modifications regulated by the PmrCAB operon and LpxL -related genes, which also reduce immune recognition via the TLR4 pathway. Phase variation allows phenotypic changes that aid immune evasion. The highly adaptable genome of A. baumannii enables rapid acquisition of multiple resistance determinants, including OXA-type carbapenemases, efflux pumps, and aminoglycoside-modifying enzymes. Due to its extensive multidrug resistance, the World Health Organization lists A. baumannii as a critical-priority pathogen. This review aims to comprehensively examine the molecular mechanisms driving its virulence and resistance, highlighting potential therapeutic targets and strategies to combat this formidable pathogen.