Streptococcus suis outbreak was associated with exposure to sick or dead pigs.

No abstract

Intermediately pathogenic strain ST25 has evolved to become highly pathogenic strain ST1, which, in turn, has more recently evolved to become epidemic strain ST7. ST7 has the ability to stimulate the production of massive amounts of proinflammatory cytokines, leading to STSLS.

An outbreak of Streptococcus suis serotype 2 emerged in the summer of 2005 in Sichuan Province, and sporadic infections occurred in 4 additional provinces of China. In total, 99 S. suis strains were isolated and analyzed in this study: 88 isolates from human patients and 11 from diseased pigs. We defined 98 of 99 isolates as pulse type I by using pulsed-field gel electrophoresis analysis of SmaI-digested chromosomal DNA. Furthermore, multilocus sequence typing classified 97 of 98 members of the pulse type I in the same sequence type (ST), ST-7. Isolates of ST-7 were more toxic to peripheral blood mononuclear cells than ST-1 strains. S. suis ST-7, the causative agent, was a single-locus variant of ST-1 with increased virulence. These findings strongly suggest that ST-7 is an emerging, highly virulent S. suis clone that caused the largest S. suis outbreak ever described.

Bacterial pathogens impose a heavy health burden worldwide. In the new era of high-throughput sequencing and online bioinformatics, real-time genome typing of infecting agents, and in particular those with potential severe clinical outcomes, holds promise for guiding clinical care to limit the detrimental effects of infections and to prevent potential local or global outbreaks. Here, we sequenced and compared 85 isolates of Streptococcus suis, a zoonotic human and swine pathogen, wherein we analyzed 32 recognized serotypes and 75 sequence types representing the diversity of the species and the human clinical isolates with high public health significance. We found that 1,077 of the 2,469 genes are shared by all isolates. Excluding 201 common but mobile genes, 876 genes were defined as the minimum core genome (MCG) of the species. Of 190,894 single-nucleotide polymorphisms (SNPs) identified, 58,501 were located in the MCG genes and were referred to as MCG SNPs. A population structure analysis of these MCG SNPs classified the 85 isolates into seven MCG groups, of which MCG group 1 includes all isolates from human infections and outbreaks. Our MCG typing system for S. suis provided a clear separation of groups containing human-associated isolates from those containing animal-associated isolates. It also separated the group containing outbreak isolates, including those causing life-threatening streptococcal toxic shock-like syndrome, from sporadic or less severe meningitis or bacteremia-only isolates. The typing system facilitates the application of genome data to the fields of clinical medicine and epidemiology and to the surveillance of S. suis. The MCG groups may also be used as the taxonomical units of S. suis to define bacterial subpopulations with the potential to cause severe clinical infections and large-scale outbreaks.

We report the identification of HGA in China and likely nosocomial transmission of HGA from direct contact with blood or respiratory secretions.

, 1a, 2a, 2b, 3a, 4a, 5b, X, and Y, found that all belong to a new sequence type (ST), ST91. Pulsed-field gel electrophoresis revealed 154 pulse types with 655 S. flexneri isolates analyzed and identified 57 serotype switching events. The data suggest that S. flexneri epidemics in China have been caused by a single epidemic clone, ST91, with frequent serotype switching to evade infection-induced immunity to serotypes to which the population was exposed previously. The clone has also acquired resistance to multiple antibiotics. These findings underscore the challenges to the current vaccine development and control strategies for shigellosis.

Phylogenetic analyses have provided strong evidence that amino acid changes in spike (S) protein of animal and human SARS coronaviruses (SARS-CoVs) during and between two zoonotic transfers (2002/03 and 2003/04) are the result of positive selection. While several studies support that some amino acid changes between animal and human viruses are the result of inter-species adaptation, the role of neutralizing antibodies (nAbs) in driving SARS-CoV evolution, particularly during intra-species transmission, is unknown. A detailed examination of SARS-CoV infected animal and human convalescent sera could provide evidence of nAb pressure which, if found, may lead to strategies to effectively block virus evolution pathways by broadening the activity of nAbs. Here we show, by focusing on a dominant neutralization epitope, that contemporaneous- and cross-strain nAb responses against SARS-CoV spike protein exist during natural infection. In vitro immune pressure on this epitope using 2002/03 strain-specific nAb 80R recapitulated a dominant escape mutation that was present in all 2003/04 animal and human viruses. Strategies to block this nAb escape/naturally occurring evolution pathway by generating broad nAbs (BnAbs) with activity against 80R escape mutants and both 2002/03 and 2003/04 strains were explored. Structure-based amino acid changes in an activation-induced cytidine deaminase (AID) “hot spot” in a light chain CDR (complementarity determining region) alone, introduced through shuffling of naturally occurring non-immune human VL chain repertoire or by targeted mutagenesis, were successful in generating these BnAbs. These results demonstrate that nAb-mediated immune pressure is likely a driving force for positive selection during intra-species transmission of SARS-CoV. Somatic hypermutation (SHM) of a single VL CDR can markedly broaden the activity of a strain-specific nAb. The strategies investigated in this study, in particular the use of structural information in combination of chain-shuffling as well as hot-spot CDR mutagenesis, can be exploited to broaden neutralization activity, to improve anti-viral nAb therapies, and directly manipulate virus evolution.