<p><i>Streptococcus dysgalactiae</i> subsp. e<i>quisimilis</i> (SDSE) is an emerging bacterial pathogen of pigs, presenting with septicemia and acute death. Here, we explored the sequential development of pathogenesis of porcine isolate of SDSE in mouse model. Forty Swiss albino mice of either sex, aged 3–4 weeks (Group I) were intravenously inoculated with 0.1&#xa0;ml of bacterial inoculum containing 2.1 × 10<sup>7</sup> CFU, while 24 (Group II) received sterile PBS at the same volume via the same route and observed daily for clinical signs and mortality up to 15 days. The mice (6 infected and 4 control mice at each time point) were sacrificed at 1, 3, 5,7,10 and 15 days post-inoculation for the estimation of hematobiochemical parameters, bacterial load, pro-inflammatory cytokines, pathological changes with demonstration of bacterial antigens, and apoptosis. The infected group of mice showed anaemia, leucopenia, higher levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), blood urea nitrogen (BUN) and creatinine, higher lipid peroxidation (LPO) levels, and lower levels of antioxidant enzymes (superoxide dismutase, reduced glutathione, and catalase), and higher amounts of pro-inflammatory cytokines as compared to control mice. Microscopically, infected group of mice showed septicemic lesions with predominant lesions of myocarditis. The immunolocalization of SDSE antigens was observed in the lungs and spleen of the inoculated mice. The immunodetection of caspase-3 in the splenocytes confirmed the presence of apoptosis due to bacterial toxin. The clinical signs, hematobiochemical parameters, bacterial load, oxidative stress parameters, pathological lesions, and apoptosis were higher during 3rd -5th DPI and reduced thereafter. Understanding the pathogenesis during progressive stages of infection by SDSE will pave the way for its effective control.</p>

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Sequential development of pathological changes in relation to bacterial loads, apoptosis, and immune responses in experimental infection of Streptococcus dysgalactiae subsp. equisimilis (SDSE) in Swiss albino mice

  • Sagar Patel,
  • Monalisa Sahoo,
  • Jigarji Chaturji Thakor,
  • Rajendra Singh,
  • Karampal Singh,
  • Salauddin Qureshi,
  • Shailesh Kumar Patel,
  • Varsha Jayakumar,
  • Akash Balasaheb Mote,
  • Susen Kumar Panda,
  • Aditya Prasad Acharya,
  • Ritun Patra,
  • Prabin Kumar Sahoo,
  • Ramakant Acharya,
  • Mamata Pasayat,
  • Nihar Ranjan Sahoo

摘要

Streptococcus dysgalactiae subsp. equisimilis (SDSE) is an emerging bacterial pathogen of pigs, presenting with septicemia and acute death. Here, we explored the sequential development of pathogenesis of porcine isolate of SDSE in mouse model. Forty Swiss albino mice of either sex, aged 3–4 weeks (Group I) were intravenously inoculated with 0.1 ml of bacterial inoculum containing 2.1 × 107 CFU, while 24 (Group II) received sterile PBS at the same volume via the same route and observed daily for clinical signs and mortality up to 15 days. The mice (6 infected and 4 control mice at each time point) were sacrificed at 1, 3, 5,7,10 and 15 days post-inoculation for the estimation of hematobiochemical parameters, bacterial load, pro-inflammatory cytokines, pathological changes with demonstration of bacterial antigens, and apoptosis. The infected group of mice showed anaemia, leucopenia, higher levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), blood urea nitrogen (BUN) and creatinine, higher lipid peroxidation (LPO) levels, and lower levels of antioxidant enzymes (superoxide dismutase, reduced glutathione, and catalase), and higher amounts of pro-inflammatory cytokines as compared to control mice. Microscopically, infected group of mice showed septicemic lesions with predominant lesions of myocarditis. The immunolocalization of SDSE antigens was observed in the lungs and spleen of the inoculated mice. The immunodetection of caspase-3 in the splenocytes confirmed the presence of apoptosis due to bacterial toxin. The clinical signs, hematobiochemical parameters, bacterial load, oxidative stress parameters, pathological lesions, and apoptosis were higher during 3rd -5th DPI and reduced thereafter. Understanding the pathogenesis during progressive stages of infection by SDSE will pave the way for its effective control.