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Understanding the immunological mechanisms of protection and the viral proteins involved in the induction of a protective immune response to the African swine fever virus (ASFV) is still limited. In the last years, the CD2v protein (gp110-140) of the ASFV has been proven to be a serotype-specific protein. Current work is devoted to the investigation of the possibility of creating protection against virulent ASFV strain Mozambique-78 (seroimmunotype III) in pigs previously vaccinated with vaccine strain FK-32/135 (seroimmunotype IV) and then immunized with the pUBB76A_CD2v plasmid, containing a chimeric nucleotide sequence from the CD2v protein gene (EP402R, nucleotides from 49 to 651) from the MK-200 strain (seroimmunotype III). Vaccination with the ASFV vaccine strain FK-32/135 protects pigs from the disease caused by the strain with homologous seroimmunotype—France-32 (seroimmunotype IV). Our attempt to create balanced protection against virulent strain Mozambique-78 (seroimmunotype III) by induction of both humoral factors of immunity (by vaccination with strain FK-32/135 of seroimmunotype IV) and serotype-specific cellular immunity (by immunization with the plasmid pUBB76A_CD2v of seroimmunotype III) was unsuccessful.

African swine fever virus (ASFV) is an extremely genetically and phenotypically heterogeneous pathogen. Previously, we have demonstrated that experimental inoculation of pigs with an attenuated strain, Katanga-350 (genotype I, seroimmunotype I) (ASFV-Katanga-350), can induce protective immunity in 80% of European domestic pigs against the homologous virulent European strain Lisbon-57. At least 50% of the surviving pigs received protection from subsequent intramuscular infection with a heterologous virulent strain, Stavropol 01/08 (genotype II, seroimmunotype VIII) (ASFV-Stavropol 01/08). In this study, we assessed clinical signs, the levels of viremia, viral DNA, anti-ASFV antibodies and post-mortem changes caused by subsequent intramuscular injection with ASFV-Katanga-350 and heterologous ASFV-Stavropol 01/08. Inoculation of pigs with the ASFV-Katanga-350 did not protect animals from the disease in the case of the subsequent challenged ASFV-Stavropol 01/08. However, 40% of pigs were protected from death. Moreover, the surviving animals showed no pathomorphological changes or the presence of an infectious virus in the organs after euthanasia at 35 days post challenging. The ability/inability of attenuated strains to form a certain level of protection against heterologous isolates needs a theoretical background and experimental confirmation.

The African swine fever virus (ASFV) is the cause of a recent pandemic that is threatening the global pig industry. The virus infects domestic and wild pigs and manifests with a variety of clinical symptoms, depending on the strain. No commercial vaccine is currently available to protect animals from this virus, but some attenuated and recombinant live vaccine candidates might be effective against the disease. This article describes the immunobiological characteristics of one such candidate—the laboratory-attenuated ASFV strain, Katanga-350—which belongs to genotype I. In this study, we assessed clinical signs and post-mortem changes, the levels of viremia and the presence of viral DNA caused by injection of ASF virus strains Katanga-350, Lisbon-57, and Stavropol 08/01. Intramuscular injection of this strain protected 80% of pigs from a virulent strain of the same genotype and seroimmunotype (Lisbon-57). At least 50% of the surviving pigs received protection from subsequent intramuscular infection with a heterologous (genotype II, seroimmunotype VIII) virulent strain (Stavropol 08/01). Virus-specific antibodies were detectable in serum and saliva samples between 8–78 days after the first inoculation of the Katanga-350 strain (the observational period). The results suggested that this strain could serve as a basis for the development of a recombinant vaccine against ASF viruses belonging to seroimmunotype I.

Elizabethkingia anophelis is an emerging multidrug-resistant pathogen that causes severe nosocomial and community-acquired infections worldwide. We report the first case of E. anophelis isolation in Russia and the first isolation from raw cow’s milk. The ML-44 demonstrated resistance to 28 antimicrobials of 33 tested in the disk-diffusion test. Whole genome-based phylogeny showed ML-44 strain clustered together with the F3201 strain isolated from a human patient in Kuwait in 1982. Both strains were a part of the “endophytica” clade. Another clade was formed by subsp. anophelis strains. Each of the E. anophelis compared genomes carried 18 to 21 antibiotic resistance determinants. The ML-44 chromosome harbored nine efflux system genes and three beta-lactamase genes, along with six other antimicrobial resistance genes. In total, 72 virulence genes were revealed. The set of virulence factors was quite similar between different E. anophelis strains and included LPS and capsule encoded genes, type IV pili, oxidative stress response genes, and genes encoding TIVSS and TVISS effectors. The particular interest caused the mip and zmp1 gene homologs, which can be essential for intracellular survival. In sum, our findings suggest that raw milk might be a source of E. anophelis harboring a set of virulence factors and a broad resistance to generally used antimicrobials.

Totally, 45 L. monocytogenes strains isolated from meat, poultry, dairy, and fish products in the Central European part of Russia in 2001–2005 and 2019–2020 were typed using a combined MLST and internalin profile (IP) scheme. Strains belonged to 14 clonal complexes (CCs) of the phylogenetic lineages I and II. Almost half of the strains (20 of 45) belonged to six CCs previously recognized as epidemic clones (ECs). ECI and ECV strains were isolated during both studied periods, and ECII, ECIV, ECVI, and ECVII strains were isolated in 2001–2005, but not in 2019–2020. ECI, ECIV, ECV, and ECVII strains were isolated from products of animal origin. ECII and ECVI were isolated from fish. Testing of invasion efficiencies of 10 strains isolated in different years and from different sources and belonging to distinct CCs revealed a statistically significant difference between phylogenetic lineage I and II strains but not between ECs and non-EC CCs or strains differing by year and source of isolation. Strains isolated in 2001–2005 were characterized by higher phylogenetic diversity and greater presentation of ECs and CCs non-typical for natural and anthropogenic environments of the European part of Russia comparatively to isolates obtained in 2019–2020.Closing of the Russian market in 2019–2020 for imported food might be responsible for these differences.

Susceptibility of 117 L. monocytogenes strains isolated during three time periods (1950–1980; 2000–2005, and 2018–2021) to 23 antibiotics was tested by the disk diffusion method. All strains were sensitive to aminoglycosides (gentamicin, kanamycin, neomycin, streptomycin), glycopeptides (vancomycin and teicoplanin), clarithromycin, levofloxacin, amoxicillin/clavulanic acid, and trimethoprim/sulfamethoxazole. Resistance to clindamycin was observed in 35.5% of strains. Resistance to carbapenems, imipenem and meropenem was found in 4% and 5% of strains, respectively. Resistance to erythromycin, penicillin G, trimethoprim, and ciprofloxacin was found in 4%, 3%, 3%, and 2.5% of strains, respectively. Resistance to tylosin, ampicillin, enrofloxacin, linezolid, chloramphenicol, and tetracycline was found in less than 2%. Three strains with multiple antibiotic resistance and 12 strains with resistance to two antibiotics were revealed. Comparison of strains isolated in different time periods showed that the percentage of resistant strains was the lowest among strains isolated before 1980, and no strains with multiple antibiotic resistance were found among them. Statistical analysis demonstrated that the temporal evolution of resistance in L. monocytogenes has an antibiotic-specific character. While resistance to some antibiotics such as ampicillin and penicillin G has gradually decreased in the population, resistance to other antibiotics acquired by particular strains in recent years has not been accompanied by changes in resistance of other strains.

This article summarizes the study results on the generation of attenuated strains of African swine fever virus (ASFV) of seroimmunotypes I–VIII and the creation of live vaccines for temporary protection of pigs during a period of epizootics in the surveillance zone (a zone adjacent to the area of outbreak). These studies were initiated at the Federal Research Center for Virology and Microbiology (FRCVM, formerly VNIIVViM) at the time of introduction of the pathogen to the Iberian Peninsula in the middle of the 20th century. The developed experimental vaccines against ASFV seroimmunotypes I–V provided protection against virulent strains of homologous seroimmunotypes by day 14 after vaccination, lasting at least four months.

Listeriosis is one of the most significant humans and animals foodborne infectious diseases. Here, we characterized 48 Listeria monocytogenes strains isolated in the territory of inner Eurasia during the second half of the 20th century. A total of 23 strains (52.3%) were susceptible to the nine antibiotics tested, 30.43%, 15.22%, and 8.7% were resistant penicillin G, ampicillin, and enrofloxacin, respectively. We applied the multilocus sequence typing (MLST) scheme to determine the phylogenetic positions of the strains. All but one strain belonged to the II phylogenetic lineage, and the majority of the strains belonged to one of the previously described clonal complexes (CCs). More than 60% of the strains belonged to the clonal complex CC7 that prevailed among all sources, including cattle (58%), small ruminants (64%), rodents (71%), and humans (50%). Further, CC7, CC101, and CC124 were found among human isolates. The MLST scheme was supplemented with virulence gene analysis. In total, eight inlA, six inlB, and six inlC allelic variants were found, and all but one strain carried one of the two inlE alleles. Most strains (62.5%) belonged to the same multivirulence locus sequence typing (MvLST) type, which includes CC7, inlA allele 4, inlB allele 14, inlC allele 6, and inlE allele 8.