Nontoxigenic C. diphtheria, fermenting starch, of convertible phage types ABCDFCH, ABCDFG, ABCDF, ABCD, ABD, ACDf, CDf, AF and A, and also strains of nonconvertible bacteriophage types I, H and K proved to be noncoricynogenic in the corycine test and weakly sensitive to bacteriocin of the No. 3463 test strain (a study was made of a total of 502 strains). Strains (383) isolated from 354 patients and carriers--starch-fermenting and toxigenic to the gravis type--were toxigenic were lysed by a combination of bacteriophages O, P, Q, R, S, T produced an active bacteriocine against the test strains No. 23 BC, and were insensitive to bacteriocine of the strain No. 3453. Strains of phage type G(g) were noncorycinogenic. Only one strain of phage type G, which produced corycine, active against the test strain No. 23 BC served as an exception. With the aid of phages A, B, C, D, F, G, H, I, K it was possible to separate 244 strains of the phage type G(g) into 3 phage types--bc, ABfGH and Abg. Strains of phage type ABfGH were noncorycinogenic; the only strain of phage type bG available produced bacteriocine.
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Pf bacteriophages, lysogenic viruses that infect are implicated in the pathogenesis of chronic infections; phage-infected (Pf+) strains are known to predominate in people with cystic fibrosis (pwCF) who are older and have more severe disease. However, the transmission patterns of Pf underlying the progressive dominance of Pf+ strains are unclear. In particular, it is unknown whether phage transmission commonly occurs horizontally between bacteria within the airway via viral particles or if Pf+ bacteria are mostly acquired via new infections.
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January 2025
Laboratory of Molecular Microbiology, Institute of Chemical Biology and Fundamental Medicine, Siberian Branch of Russian Academy of Sciences, 630090 Novosibirsk, Russia.
is an important opportunistic pathogen often resistant to antibiotics. Specific phages can be useful in eliminating infection caused by . phage vB_KlebPS_265 (KlebP_265) and its host strain were isolated from the sputum of a patient with infection.
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January 2025
State Research Center for Applied Microbiology and Biotechnology, City District Serpukhov, Moscow Region, 142279 Obolensk, Russia.
is a widely distributed nosocomial pathogen that causes various acute and chronic infections, particularly in immunocompromised patients. In this study, the activities of the K9-specific virulent phage AM24 and phage-encoded depolymerase DepAPK09 were assessed using in vivo mouse sepsis and burn skin infection models. In the mouse sepsis model, in the case of prevention or early treatment, a single K9-specific phage or recombinant depolymerase injection was able to protect 100% of the mice after parenteral infection with a lethal dose of of the K9-type, with complete eradication of the pathogen.
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January 2025
Department of Biology and Toxicology, Ashland University, Ashland, OH 44805, USA.
Until recently, the only methods for finding out if a particular strain or species of bacteria could be a host for a particular bacteriophage was to see if the bacteriophage could infect that bacterium and kill it, releasing progeny phages. Establishing the host range of a bacteriophage thus meant infecting many different bacteria and seeing if the phage could kill each one. Detection of bacterial killing can be achieved on solid media (plaques, spots) or broth (culture clearing).
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January 2025
Intensive Care Unit, Sismanogleio General Hospital, 37 Sismanogleiou Str., 15126 Marousi, Greece.
Metabolic disorders, including type 2 diabetes mellitus (T2DM), obesity, and metabolic syndrome, are systemic conditions that profoundly impact the skin microbiota, a dynamic community of bacteria, fungi, viruses, and mites essential for cutaneous health. Dysbiosis caused by metabolic dysfunction contributes to skin barrier disruption, immune dysregulation, and increased susceptibility to inflammatory skin diseases, including psoriasis, atopic dermatitis, and acne. For instance, hyperglycemia in T2DM leads to the formation of advanced glycation end products (AGEs), which bind to the receptor for AGEs (RAGE) on keratinocytes and immune cells, promoting oxidative stress and inflammation while facilitating Staphylococcus aureus colonization in atopic dermatitis.
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