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PubMed1976

Effect of biotin deficiency on some properties of Staphylococcus aureus isolates from humans and other animals.

Staphylococcus aureus isolates from humans and other animals were grown in biotin assay medium containing 12 mug of biotin per liter and compared to isolates from the same sources grown concurrently in medium containing adequate biotin. The two cultures were tested for production of coagulase, phosphatase, and fibrinolysin enzymes and for responses to various antimicrobial agents and bacteriophages. Organisms grown in biotin-deficient medium produced less phosphatase; coagulase and fibrinolytic activity was reduced, and they were more susceptible to antimicrobial agents than were normal organisms, but phage susceptibility was not greatly affected.

Animals↗
PubMed1975

Inheritance of low-level resistance to penicillin, tetracycline, and chloramphenicol in Neisseria gonorrhoeae.

The genetics of low-level resistance to penicillin and other antibiotics in a clinical isolate and a multistep laboratory mutant of Neisseria gonorrhoea was studied by transformation. Mutations at three loci affected sensitivity to penicillin. Mutation at penA resulted in an eightfold increase in resistance to penicillin without affecting response to other antimicrobial agents. Mutation at ery resulted in a two- to fourfold increase in resistance to penicillin and similar increases in resistance to many other antibiotics, dyes, and detergents. Mutation at penB resulted in a fourfold increase in resistance to penicillin and tetracycline, the phenotypic expression of which was dependent on the presence of mutation at ery. The cumulative effect of mutations at penA, ery, and penB was an approximate 128-fold increase in penicillin resistance, to a minimum inhibitory concentration of 1.0 mug/ml. Low-level resistance to tetracycline or chloramphenicol was due to similar additive effects between mutations at the nonspecific ery and penB loci and a locus specific for resistance to each drug (tet and chl, respectively). No evidence was found for penicillinases or other drug-inactivating enzymes.

Chloramphenicol↗
PubMed2026

Beyond antibiotics: artificial intelligence-enabled anti-infective ecosystems for next-generation precision therapeutics against antimicrobial resistance.

The rapid global expansion of antimicrobial resistance (AMR) threatens to undermine decades of progress in infectious disease management and highlights the limitations of conventional antibiotic-centered therapeutic strategies. Although emerging technologies-including antimicrobial peptides, bacteriophage therapy, CRISPR-based antimicrobials, microbiome therapeutics, anti-virulence approaches, nanotechnology-enabled drug delivery, and artificial intelligence (AI)-have individually demonstrated considerable promise, they are predominantly being developed as independent interventions rather than as coordinated components of an integrated therapeutic strategy. This Perspective proposes the Intelligent Anti-Infective Ecosystem (IAIE) as a conceptual systems-level framework that computationally integrates multimodal diagnostics, pathogen genomics, microbiome profiling, AI-assisted decision support, programmable precision therapeutics, ecological monitoring, and longitudinal clinical feedback within a continuously learning dynamically optimized workflow. Unlike existing paradigms that primarily optimize individual technologies or therapeutic decisions, IAIE emphasizes closed-loop coordination among complementary antimicrobial approaches to support precision-guided infection management while preserving microbiome integrity and mitigating resistance selection pressure. We further outline the core components, operational principles, translational challenges, and technology readiness of the major therapeutic platforms that could contribute to such an ecosystem, while distinguishing clinically established interventions from emerging experimental strategies. Importantly, IAIE should be interpreted as a prospective conceptual architecture rather than an existing clinical platform. Its proposed clinical value remains to be established through sequential computational, preclinical, and prospective clinical investigations using standardized microbiological, ecological, and patient-centered outcome measures. By framing antimicrobial innovation within an responsive systems perspective, IAIE provides a roadmap for future multidisciplinary research aimed at integrating artificial intelligence and systems microbiology to enable sustainable management of antimicrobial resistance.

Humans↗
PubMed2025

Two decades of resistance surveillance by the British Society for Antimicrobial Chemotherapy: design, development, delivery, deficiencies and future directions.

The British Society for Antimicrobial Chemotherapy Antimicrobial Surveillance Project was established in the United Kingdom (UK) and Ireland in response to dissatisfaction with existing antimicrobial surveillance which, in the 1990s, was fragmented and poorly informative for clinical and public heath purposes. The model developed into an integrated Project that was novel in its management and financing, being a true collaboration between a medical charity, pharmaceutical companies and the laboratories contracted to perform the testing. Separate 'Programmes' within an overall 'Project' collected and tested community- and hospital-acquired respiratory and bloodstream infection isolates. Cooperation with public sector bodies allowed data collection from the Project to be compared to routinely collected data from National Health Service laboratories. Between 1999 and 2019 the Project delivered test results on almost 100 000 isolates, from 17 bacterial genera to 44 antimicrobial agents. The results were made available annually on a specially constructed web site. In this supplement, we summarize the data collected in a series of papers relevant to the two programmes, discussing the Project's strengths and deficiencies. Support for the Project declined in the period after 2010, and collection ceased after 20 years, its demise related to changing priorities within the partner organizations. However, the bacterial collection remains and is to be maintained to assist in future work in combating antimicrobial resistance.

United Kingdom↗
PubMed1975

Antimicrobial activity of human peritoneal fluid.

Cell free peritoneal fluids from 23 normal women had antimicrobial activity which was directed against gram-positive and gram-negative bacteria and also against yeasts. The activity was bacteriostatic or bactericidal and seemed to be due to the presence of a variety of factors which varied in their heat stability and dependence on complement. Lysozyme was present in the fluids but was not responsible for all the antimicrobial activity.

Ascitic Fluid↗
PubMed2025

The small bacterial membrane protein YohP induces nucleoid condensation in E. coli and inhibits oligomerization of antimicrobial peptides.

Prokaryotic organisms execute multiple stress response mechanisms in order to cope with rapidly changing environments. Some mechanisms respond to specific cues, such as the OxyR-dependent response to hydrogen peroxide or the SOS-response that is induced upon DNA-damage. These specific responses complement general mechanisms that respond to multiple and diverse stressors. One example is nucleoid condensation, which is a rapid and effective mechanism for genome protection and observed in response to various stresses, including entry into stationary phase. Recently, the upregulation of small membrane proteins (SMPs) in response to stress was observed, but details on how this emerging class of proteins modulate the stress response is largely unknown. Here, we demonstrate that the production of two SMPs, YohP and YncL, cause nucleoid condensation in Escherichia coli. Nucleoid condensation is the result of YohP-/YncL-induced sublethal membrane depolarization, which induces the phage-shock response and leads to a reduction of global protein synthesis. YohP production also prevents the oligomerization of the antimicrobial peptide magainin-2 in the E. coli membrane and reduces the metabolic activity of E. coli cells. Thus, the synthesis of YohP and likely of other SMPs potentially protects bacterial cells against some unfavorable conditions by shifting them into a metabolically silent state.

YncL↗
PubMed1979

Anaerobic bacterial pneumonitis.

Clinical features of 46 patients with anaerobic bacterial pneumonitis were compared with those of patients with pneumococcal pneumonia. The presenting features in these 2 groups were comparable in terms of fever, leukocyte count, and radiographic abnormalities. In only 2 patients with anaerobic bacterial pneumonitis was putrid sputum noted on initial evaluation. None of the patients with anaerobic bacterial pneumonitis had shaking chills, although this was reported by nearly one half of those with pneumococcal pneumonia. The response to treatment with antimicrobial drugs was comparable in the 2 groups, except that 20% of patients with anaerobic bacterial pneumonitis subsequently developed pulmonary abscesses, despite the use of antimicrobial agents presumed to be active against the infecting flora. There was also a high incidence of bronchogenic neoplasms among patients who had anaerobic bacterial pneumonitis in the absence of an associated condition that would predispose to aspiration. The findings of this review suggest that anaerobic bacterial pneumonitis may be difficult to distinguish from pneumococcal pneumonia on the basis of clinical presentation.

Bacteria↗
PubMed1979

[Lipoid A, a factor in the pathogenesis of chronic pyelonephritis. Experimental and clinical studies of a lipoid A dependent pathological immune reaction].

Lipid A injected into the temporarily occluded renal pelvis of adult dogs, persisted in the kidney tissue and induced an abacterial interstitial nephritis with positive anti-lipid A titers. This reaction was increased by a single dose of lipid A vaccine, reduced by four consecutive immunisations prior to the lipid A injection and absent in puppies. The presence of IgG, IgM and complement complexes in the kidney was demonstrated by immunofluoroscopy. Lipid A antibody titers were measured by the passive hemolysis test in 349 humans. In two out of 20 healthy adults and 16 out of 18 children with recurrent urinary tract infection anti-lipid A antibodies were present. In contrast, no titers were found in 23 newborn babies. In a group of 156 patients with acute urinary tract infection, 28% revealed positive titers, whereas in a group of 132 patients with recurrent urinary tract infection titers occurred in 81%. Selected from this group of 132 patients 61 suffered from an acute infection of the upper tract. 59 oft these (96%) showed definite titers. There was no difference in the development of anti-lipid A antibodies between men and women and the height of the titers did not correlate with the clinical picture of the disease (acute or chronic). The combination of proteinuria and anti-lipid A antibodies indicates the pressure of reccurrent urinary tract infection or chronic pyelonephritis with about 90% accuracy. The titers are caused by immunogenically active lipid A in the body. Since lipid A has the ability to remain in the renal tissue for a long period of time and thereby to maintain the inflammatory response, long-term antimicrobial prophylaxis (six months) should be given to patients with a high risk of recurrent urinary tract infection.

Animals↗
PubMed1977

Perinephric abscess: an unusual presentation of perforation of the colon.

Perinephric abscess caused by spread of infection from an adjacent extrarenal focus is rare. Prior to diagnosis, several features of this case suggested such a pathogenesis: absence of an associated upper urinary tract infection or a distant focus for hematogenous seeding, and late recurrence of the abscess despite prompt clinical response following drainage and antimicrobial therapy. Specifically, the large bowel was suspected early on and subsequently documented as the source of infection because of the unusual finding of a polymicrobial perinephric abscess.

Abscess↗
PubMed1978

Ascorbic acid, neutrophil function, and the immune response.

The role of ascorbic acid is reviewed with regard to antimicrobial activity, interferon production, and humoral and cellular immune responses. Ascorbic acid appears to play a role in a number of neutrophil functions including increased chemotaxis, increased particulate ingestion, enhanced lysozyme-mediated non-oxidative killing, protection against the toxic effects of superoxide anion radical, inhibition of the halide-peroxide-myeloperoxidase system without a pronounced bactericidal effect, and stimulation of the hexose monophosphate shunt.

Animals↗
PubMed2026

Identification of essential genes for conjugative transfer in antimicrobial resistance-associated pELF-type linear plasmids of opportunistic pathogen Enterococcus faecium.

The pELF-type linear plasmid is a critical mobile genetic element responsible for the dissemination of various antimicrobial resistance (AMR) genes, most notably vancomycin resistance in Enterococcus faecium, which is a leading cause of hospital outbreaks worldwide. Despite their crucial role in the expansion of AMR, the molecular mechanisms underlying the conjugative transfer of these linear plasmids remain poorly understood. In this study, the transfer (tra) region of pELF2, a representative vanA-harboring linear plasmid was characterized. Transcriptomic data suggested that the FtsK/VirD4-type adenosine triphosphatase is encoded within a multi-gene operon. By developing a genetic manipulation framework for E. faecium, an extensive mutational analysis of the tra region was performed and the following three essential genes were identified: traCB4 (a putative VirB4 analog), traDD4 (a VirD4-like coupling protein), and traGB6 (a putative VirB6 analog). These genes are indispensable for conjugative transfer. Reporter assays experimentally confirmed the presence of a functional promoter upstream of the identified tra genes. We confirmed that these genes are highly conserved among pELF-type plasmid sequences deposited in public database. The study findings revealed that pELF-type plasmids utilize highly minimized conjugation machinery, which is similar to unusual systems previously identified in other gram-positive bacteria, such as Streptomyces. This study provides the first molecular insights into the transmission of these clinically important linear plasmids in enterococci and lays a foundation for understanding the dissemination of resistance determinants mediated by atypical mobile genetic elements.

Enterococcus faecium↗
PubMed1978

Cellular antimicrobial immunity.

Acquired resistance to infectious disease may be expressed by a predominantly humoral or a cellular mechanism or, more frequently, by a combination of the two. The cellular interactions which are responsible for the induction of the immune response in the skin, lung, intestinal mucosa, genitourinary tract, conjunctiva, and peritoneal cavity are discussed and the role of living or dead vaccines in the induction of acquired resistance is outlined. The host response involves three different cell types: the phagocytic cell (polymorphs or macrophages), the thymus-dependent (T) lymphocyte, and the thymus-independent (B) lymphocyte-plasma cell line. The normal unstimulated phagocytic cell is capable of killing most nonpathogenic bacteria that gain entry to the tissues. However, the presence of opsonic antibodies and activated macrophages is required to eliminate the pathogenic intracellular parasites. Such immunological activation involves the presence of sensitized T-lymphocytes in the lesion. The cellular response is also characterized by the simultaneous development of a state of delayed-type hypersensitivity (DTH), along with the antimicrobial CMI response. A rising humoral response normally develops subsequently. Killed bacterial cells (except when incorporated into Freund's complete adjuvant) induce the humoral response without the CMI reaction so that such vaccines are not able to fully protect the host against the naturally acquired disease. With the development of cell fractionation methods as well as the identification of distinctive cell surface markers, suspensions of B- and T-cells and macrophages can now be prepared for use in increasingly sophisticated transfer and reconstitution studies. The role of the different cell types in the expression of humoral and cellular immunity has been determined, and the effect of various immunopotentiating and immunosuppressive regimens on the immune system as a whole has been evaluated quantitatively. These studies have led to an appreciation of the role played by suppressor B- and T-cells in the interplay of both humoral and cellular components of the host defense system during the development of immune tolerance, desensitization, anergy, autoimmunity, and the expression of an anamnestic immune response following reinfection.

Adjuvants, Immunologic↗
PubMed2026

Time-resolved proteomic adaptation of multidrug-resistant Acinetobacter baumannii to antimicrobial stress induced by partially purified fraction from Caesalpinia pulcherrima flower using DEqMS.

UNLABELLED: The global prevalence of multidrug-resistant (MDR) bacteria represents an urgent public health challenge, emphasizing the critical need for novel antimicrobial agents. MDR Acinetobacter baumannii, a nosocomial pathogen of critical global concern owing to its capacity to acquire and disseminate antimicrobial resistance, was employed as a bacterial model to investigate the antimicrobial potential of natural products derived from Caesalpinia pulcherrima (L.) Sw. (Fabaceae). This medicinal plant represents a promising reservoir of novel bioactive compounds; however, its molecular effects on the A. baumannii proteome had not previously been characterized. The partially purified ethyl acetate fraction of C. pulcherrima flowers (CPF4) exhibited potent bactericidal activity against susceptible A. baumannii (minimum inhibitory concentration and minimum bactericidal concentration = 31.25 µg/mL), and time-resolved label-free quantitative LC-MS/MS proteomics was subsequently performed on MDR A. baumannii cultures treated with CPF4 at 24 h, 48 h, and 72 h post-treatment alongside untreated controls in biological triplicate, with differential protein expression assessed using differential expression of quantified mass spectrometry data. No significantly differentially expressed proteins were detected at 24 h or 48 h relative to the control, indicating that the proteomic effects of CPF4 manifest predominantly at the late treatment stage. In contrast, a robust late-phase response was identified at 72 h, comprising the coordinated induction of proteins associated with DNA damage repair, transcriptional regulation, and cell surface glycosylation remodeling. The sensor histidine kinase PmrB was significantly upregulated at 72 h vs 48 h (adjusted P = 0.029), implicating the PmrA/PmrB two-component system in late-phase colistin tolerance acquisition under sustained CPF4 exposure. IMPORTANCE: These findings provide mechanistic insight into the adaptive survival strategies employed by multidrug-resistant Acinetobacter baumannii in response to plant-derived antimicrobial challenge and support the further development of Caesalpinia pulcherrima-derived natural products as candidate antimicrobial agents.

Acinetobacter baumannii↗
PubMed2026

Comparative Genomics of Paenibacillus Secondary Metabolism: Unveiling the Putative Biosynthetic Gene Cluster for Paenialvins in Paenibacillus Alvei Strain 32.

In this study, we used comparative genomics and culture-based methods to investigate Biosynthetic Gene Clusters (BGCs) responsible for the production of antimicrobial peptides. Paenibacillus alvei strain 32 was isolated from a cystic fibrosis sputum. Its genome was sequenced using Illumina, showing a size of 6,584,590 bp with 239 contigs assembled in 26 scaffolds, an average coverage of 243X, and 6,832 coding sequences. ANI analysis and in silico DNA-DNA hybridization showed its affiliation inside Paenibacillus alvei, with a clear separation from other related strains, leading us to propose a distinct species-level genomic clade (genomospecies) within this group. AntiSMASH analysis predicted 22 putative BGCs in the genome of strain 32. Its culture supernatant exhibited inhibitory activity against Gram-positive pathogens, including methicillin-resistant Staphylococcus aureus (MRSA), Bacillus cereus, and Enterococcus faecalis. By comparing in silico BGC predictions with activities described in the literature, we propose that strain 32 harbours a specific 110-kb cluster (cluster 6.2) with five non-ribosomal peptide synthetase (NRPS) genes. These synthetases are predicted to direct the assembly of a 16-amino acid backbone that correlates with the structure of paenialvins, which are known anti-MRSA molecules. This study describes the putative biosynthetic pathway of the paenialvins and explains structural variations, bringing useful data on Paenibacillus secondary metabolism for future antibiotic development.

Paenibacillus alvei↗
PubMed1977

Infective endocarditis: a current review.

Infective endocarditis is a dynamic disease for which various infective organisms may be responsible in different patient populations. Antimicrobial therapy should be directed against the specific organism after it has been identified by blood culture. An agent with a spectrum that includes the enterococci should be given in the meantime. Prophylactic use of a bactericidal agent is necessary for patients with valvular or congenital heart disease. Recent advances in microbiologic and cardiac diagnostic procedures offer the clinician various methods of following the activity of the disease, and immunobiology has provided new insights into its pathogenesis.

Endocarditis, Bacterial↗
PubMed2025

A genome-wide survey reveals a diverse array of enhancers coordinate the Drosophila innate immune response.

To defend against microbes, animals regulate a complex immune response. The Drosophila innate immune system deploys a large transcriptional induction of signaling proteins, antimicrobial effectors, and other critical immune factors. This transcriptional response is encoded in enhancers, cis-regulatory sequences that modulate gene expression by binding transcription factors (TFs). While enhancers and transcription factor binding sites (TFBS) have been identified for several immune responsive genes in Drosophila, most enhancers that regulate immune-induced genes are unknown. By identifying enhancers, we can understand how their composition controls expression and contributes to infection outcome. We employed STARR-seq (Self Transcribing Active Regulatory-Region sequencing) in a hemocyte-like cell line to identify immune-specific enhancers across the D. melanogaster genome and performed ATAC-seq in hemocytes extracted from adult flies to assess the chromatin state of these enhancers before and after immune stimulus. We identified thousands of enhancers responsive to IMD stimulation, one of the two primary immune signaling pathways in Drosophila. As expected, immune enhancers are enriched for motifs of Relish, an NF-κB factor, and Kay/Jra, a bZip heterodimer pair, involved in the Imd and JNK pathways respectively, compared to enhancers active in unstimulated cells. However, when grouping enhancers by their target gene's expression timing or functional role or by the enhancers' chromatin accessibility pre- or post-stimulus, different groups of TFBS motifs are enriched, suggesting distinct regulatory logic for different parts of the immune response. Identification and characterization of the diverse array of enhancers that regulate the innate immune response expands our understanding of how animals fight infections.

Drosophila immunity↗
PubMed2025

Reflecting on Fleming's caveat: the impact of stakeholder decision-making on antimicrobial resistance evolution.

Antimicrobial resistance poses one of the greatest and most imminent threats to global health, environment and food security, for which an urgent response is mandated. Evolutionary approaches to tackling the crisis tend to focus on proximate issues including the mechanisms and pathways to resistance, with associated calls to action for infection control and antimicrobial stewardship. This is of clear benefit but overlooks the fundamental influence of policy and stakeholder decision-making on resistance evolution. In 1945, Fleming issued a stark warning on the irresponsible use of penicillin and its potential to cause death due to penicillin-resistant infections. Attention to resistance evolution theory and heeding Fleming's advice could have allowed for a vastly different reality. Embedding evolutionary theory within policy, industry and regulatory bodies is not only essential but is now a race against time. Hence, critical appraisal of historical behaviour and attitudes at a global scale can inform a paradigm of anticipatory and adaptive policy. To undertake this exercise, we focused on the largest group of antibiotics with the greatest clinical and economic footprint, the beta-lactams. We examined historical case studies that affected how beta-lactams were developed, produced, approved and utilized, in order to relate stakeholder decision-making to resistance evolution. We derive lessons from these observations and propose sustainable approaches to curb resistance evolution. We set a position that actively incorporates an evolutionary theory of antimicrobial resistance into decision-making within antimicrobial development, production and stewardship.

Anti-Bacterial Agents↗
PubMed1978

Antibiotic-induced lethal enterocolitis in hamsters: studies with eleven agents and evidence to support the pathogenic role of toxin-producing Clostridia.

Clindamycin-induced enterocolitis in hamsters was studied, using a tissue culture assay to detect clostridial toxin. It was found that animals with lethal enterocolitis had a cytopathogenic substance in cecal contents and blood that was neutralized by clostridial antitoxins. Cultures of the cecal flora yielded numerous species of clostridia, but only 1 organism was detected which produced a toxin which was cytopathic in tissue culture. This organism, Clostridium difficile, was consistently present in high concentrations, and the cell-free supernate of these strains caused enterocolitis if injected intracecally into hamsters. Ten additional antimicrobials were tested ih hamsters. Ampicillin, vancomycin, erythromycin, cephalosporins, and oral gentamicin caused lethal enterocolitis in most recipients, and all animals which died had evidence of clostridia toxin in cecal contents at necropsy. Tetracycline and metronidazole were well tolerated, and the animals given these antimicrobials had no evidence of the toxin. We conclude that toxin-producing clostridia are responsible for lethal enterocolitis due to a variety of antimicrobials in hamsters.

Ampicillin↗