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Pathogenic investigations of Streptococcus pasteurianus, an underreported zoonotic pathogen, isolated from a diseased piglet with meningitis.

Shuoyue WangMiaohang MaZijing LiangXinchi ZhuHuochun YaoLiping WangZongfu Wu
Published in: Transboundary and emerging diseases (2021)
Streptococcus pasteurianus, an underreported opportunistic pathogen, is considered an increasingly recognized cause of meningitis and bacteremia in many animals and humans worldwide. However, except for some epidemiological studies, there is no report about the gene-deletion mutagenesis, virulence factors, reservoir niches, or animal infection models for this pathogen. In this study, we first isolated an S. pasteurianus strain from a newly weaned piglet's brain with meningitis. The genomic sequence of this swine isolate WUSP067 shared high homology with that of two human strains. The comparative genome analysis showed that strain WUSP067 contained a fucose utilization cluster absent in human strains, and it shared 91% identity with that of an integrative and conjugative element (ICE) ICEssuZJ20091101-2 from Streptococcus suis, another important swine bacterial pathogen. Strain WUSP067 was resistant to erythromycin, tulathromycin, lincomycin, clindamycin, doxycycline, and gentamycin, and ICEs are vehicles for harboring antimicrobial resistance genes. The infection model was established using the three-week-old newly weaned ICR mice. The 50% lethal dose value of strain WUSP067 was 4.0×107 colony-forming units per mouse. The infected mice showed severe signs of meningitis and pathological changes in brains. Furthermore, the capsule-deficient mutant was generated using natural transformation, and we showed that capsule was an essential virulence factor for S. pasteurianus. In addition, we found that tonsils and hilar lymph nodes of healthy pigs may be reservoir niches for this bacterium. Thus, our study provided valuable information about the pathogenetic characteristics and antimicrobial resistance of S. pasteurianus and paved the way for studying its pathogenesis. This article is protected by copyright. All rights reserved.
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