Endoparasites of rabbits (Oryctolagus cuniculus domesticus) in Southern Ukraine

One of the main tasks of ecological parasitology at the present stage is to establish patterns of spread of invasive diseases of animals in the environment through a thorough epidemiological examination, as well as to determine the main directions and factors of spread of parasites in Ukraine. Among the many pathogens, endoparasites play a major role in a number of diseases in rabbits with increased morbidity and mortality. In the body of both wild and domestic rabbits several species of parasites that form a parasitocenosis can be localized. The latter have a pathogenic effect on organs and tissues, leading to reduced weight gain, premature slaughter and even mortality. The prevalence of endoparasitoses was studied in weaned rabbits 60 days of age, 120 days of age at fattening, 180 days of age – mating age and adults of 320 days of age to determine the extensiveness and intensity of the dominant invasion. A total of 720 head was studied, 180 animals from each age group. Three species of nematodes were recorded in the rabbits: Trichostrongylus retortaeformis (Zeder, 1800), Nematodirus leporis (Ransom, 1907) and Passalurus ambiguus (Rudolphi, 1819); the cestode Taenia pisiformis (Bloch, 1780); three species of Emeria: Eimeria stiedae (Lindermann, 1865), which parasitizes in the bile ducts of the liver and gallbladder, E. magna (Perard, 1925) and E. media (Kessel, 1929) – in the epithelial cells of the intestine. The prevalence of the infestation depends on the age of the animals. According to the data obtained, eimeriosis was one of the main parasitic diseases of the rabbits. Dominant invasions of Eimeria in the intestines of 60-day-old rabbits were found in the studied animals, their extensiveness reached 19.4%, while the spread of hepatic Eimeria was registered in 13.3% of the examined rabbits. The total infestation of weaned rabbits with helminths was 22.2%, in rabbits for fattening – 26.7%, and in rabbits of mating age and adults – 20.0% and 20.6%, respectively. Global climate change will change the distribution and dynamics of soil-borne helminthiases, but host immunity may also affect host-parasite interactions. Subsequent studies will be aimed at elucidating the effect of mono and mixed invasions on the body of rabbits. Updated data on helminthiasis will expand the screening strategy to maintain rabbit health and reduce economic losses

Neutrophils Are Resistant to Yersinia YopJ/P-Induced Apoptosis and Are Protected from ROS-Mediated Cell Death by the Type III Secretion System

The human innate immune system relies on the coordinated activity of macrophages and polymorphonuclear leukocytes (neutrophils or PMNs) for defense against bacterial pathogens. Yersinia spp. subvert the innate immune response to cause disease in humans. In particular, the Yersinia outer protein YopJ (Y. pestis and Y. pseudotuberculosis) and YopP (Y. enterocolitica) rapidly induce apoptosis in murine macrophages and dendritic cells. However, the effects of Yersinia Yop J/P on neutrophil fate are not clearly defined.In this study, we utilized wild-type and mutant strains of Yersinia to test the contribution of YopJ and YopP on induction of apoptosis in human monocyte-derived macrophages (HMDM) and neutrophils. Whereas YopJ and YopP similarly induced apoptosis in HMDMs, interaction of human neutrophils with virulence plasmid-containing Yersinia did not result in PMN caspase activation, release of LDH, or loss of membrane integrity greater than PMN controls. In contrast, interaction of human PMNs with the virulence plasmid-deficient Y. pestis strain KIM6 resulted in increased surface exposure of phosphatidylserine (PS) and cell death. PMN reactive oxygen species (ROS) production was inhibited in a virulence plasmid-dependent but YopJ/YopP-independent manner. Following phagocytic interaction with Y. pestis strain KIM6, inhibition of PMN ROS production with diphenyleneiodonium chloride resulted in a reduction of PMN cell death similar to that induced by the virulence plasmid-containing strain Y. pestis KIM5.Our findings showed that Yersinia YopJ and/or YopP did not induce pronounced apoptosis in human neutrophils. Furthermore, robust PMN ROS production in response to virulence plasmid-deficient Yersinia was associated with increased PMN cell death, suggesting that Yersinia inhibition of PMN ROS production plays a role in evasion of the human innate immune response in part by limiting PMN apoptosis

A Novel Core Genome-Encoded Superantigen Contributes to Lethality of Community-Associated MRSA Necrotizing Pneumonia

Bacterial superantigens (SAg) stimulate T-cell hyper-activation resulting in immune modulation and severe systemic illnesses such as Staphylococcus aureus toxic shock syndrome. However, all known S. aureus SAgs are encoded by mobile genetic elements and are made by only a proportion of strains. Here, we report the discovery of a novel SAg staphylococcal enterotoxin-like toxin X (SElX) encoded in the core genome of 95% of phylogenetically diverse S. aureus strains from human and animal infections, including the epidemic community-associated methicillin-resistant S. aureus (CA-MRSA) USA300 clone. SElX has a unique predicted structure characterized by a truncated SAg B-domain, but exhibits the characteristic biological activities of a SAg including Vβ-specific T-cell mitogenicity, pyrogenicity and endotoxin enhancement. In addition, SElX is expressed by clinical isolates in vitro, and during human, bovine, and ovine infections, consistent with a broad role in S. aureus infections of multiple host species. Phylogenetic analysis suggests that the selx gene was acquired horizontally by a progenitor of the S. aureus species, followed by allelic diversification by point mutation and assortative recombination resulting in at least 17 different alleles among the major pathogenic clones. Of note, SElX variants made by human- or ruminant-specific S. aureus clones demonstrated overlapping but distinct Vβ activation profiles for human and bovine lymphocytes, indicating functional diversification of SElX in different host species. Importantly, SElX made by CA-MRSA USA300 contributed to lethality in a rabbit model of necrotizing pneumonia revealing a novel virulence determinant of CA-MRSA disease pathogenesis. Taken together, we report the discovery and characterization of a unique core genome-encoded superantigen, providing new insights into the evolution of pathogenic S. aureus and the molecular basis for severe infections caused by the CA-MRSA USA300 epidemic clone

Characterization of a Staphylococcus aureus surface virulence factor that promotes resistance to oxidative killing and infectious endocarditis

Staphylococcus aureus is a prominent human pathogen and a leading cause of community- and hospital-acquired bacterial infections worldwide. Herein, we describe the identification and characterization of the S. aureus 67.6-kDa hypothetical protein, named for the surface factor promoting resistance to oxidative killing (SOK) in this study. Sequence analysis showed that the SOK gene is conserved in all sequenced S. aureus strains and homologous to the myosin cross-reactive antigen of Streptococcus pyogenes. Immunoblotting and immunofluorescence analysis showed that SOK was copurified with membrane fractions and was exposed on the surface of S. aureus Newman and RN4220. Comparative analysis of wild-type S. aureus and an isogenic deletion strain indicated that SOK contributes to both resistance to killing by human neutrophils and to oxidative stress. In addition, the S. aureus sok deletion strain showed dramatically reduced aortic valve vegetation and bacterial cell number in a rabbit endocarditis model. These results, plus the suspected role of the streptococcal homologue in certain diseases such as acute rheumatic fever, suggest that SOK plays an important role in cardiovascular and other staphylococcal infections