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Salmonella enterica serovar Pullorum (S. Pullorum) is an important pathogen specific to avian species, which poses a serious threat to the poultry industry. The transmission of S. Pullorum occurs both horizontally and vertically but the airborne transmission of S. Pullorum has been neglected historically. In this study, the effects of aerosolized S. Pullorum on young chickens were investigated. The results showed that the colonization and morbidity induced by bioaerosol infection are dose dependent. The bacteria colonized in chicken lung for more than 14 days following the exposure to ≥ 1.25 × 106 CFU/m3 of aerosolized S. Pullorum. Tachypnoea and depression were present in all the chickens between 5 and 7 days after infection, and some died, following the exposure to ≥1.25 × 108 CFU/m3 of aerosolized S. Pullorum. RT–PCR results showed that significant expressions of inflammatory cytokines, including tumour necrosis factor α, interleukin 1β (IL-1β), IL-6, and IL-8 were noted in the lung and spleen. Histopathological examination showed lung swelling, with obvious lesions, including inflammatory cell infiltration, tissue injury, and acute haemorrhage. These results suggest that uncontrolled and detrimental inflammation is caused by a high dose of aerosolized S. Pullorum. These results further extend our understanding of the pathogenicity of air-transmitted S. Pullorum on chickens. RESEARCH HIGHLIGHTS Aerosolized S. Pullorum caused tachypnoea, depression, and lung swelling in chickens. The colonization and morbidity caused by aerosolized S. Pullorum are dose dependent. Detrimental inflammation is caused by high doses of aerosolized S. Pullorum in lung. [ABSTRACT FROM AUTHOR]

Abstract We report that Clostridium perfringens was present in 23.1% (130/562) of broiler chickens and 15.1% (38/252) of retail chicken meat samples in central China. Among 168 isolates, type A was the preponderant genotype, and 3% of isolates were positive C. perfringens enterotoxin (cpe). Among different sources, the prevalence was higher in free-range chickens compared to chickens from intensive poultry farms, but with lower proportions of antimicrobial resistance. Highlights • C. perfringens was found in 23.1%of broiler chickens and 15.1% of retail chicken meat. • Type A C. perfringens was the predominant genotype in broiler chickens and chicken meat. • 3% (5/168) of C. perfringens isolates were positive for CP enterotoxin. • The prevalence in free-range farms was high, but with lower antimicrobial resistance rate. [ABSTRACT FROM AUTHOR]

Salmonella Pullorum is a pathogen specific to birds that can cause Pullorum disease in young chickens and lead to considerable economic losses in the poultry industry. During transmission and infection, S. Pullorum will encounter various environmental stresses and host defenses. The stringent response is an important adaptation response induced by (p)ppGpp, and in Salmonella , (p)ppGpp is synthesized by two (p)ppGpp synthetases, RelA and SpoT. To investigate the role of (p)ppGpp synthetases in the adaptation and pathogenicity of S. Pullorum, a (p)ppGpp synthetases mutant (Δ relA Δ spoT) was constructed, and its physiological phenotypes and pathogenicity, as well as transcription profiling, were compared with the parent strain. The Δ relA Δ spoT mutant showed decreased ability to form biofilms, and reduced resistance to acidic, alkaline, high osmolarity and H 2 O 2 conditions. The internalization of the Δ relA Δ spoT mutant into host cells in vitro and its lethality and colonization abilities within young chickens were also significantly reduced. RNA sequencing showed that the (p)ppGpp synthetases did not only affect the classic stringent response, such as inhibition of DNA replication and protein synthesis, but also controlled the expression of many virulence factors, in particular, the Salmonella pathogenicity island 1 (SPI-1) and SPI-2 type III secretion systems (T3SSs), and adhesion factors. These results suggest that the (p)ppGpp synthetases are required for the pathogenicity of S. Pullorum by affecting its stress response and the expression of the virulence factors. [ABSTRACT FROM AUTHOR]