Loss of 89K Pathogenicity Island in Epidemic Streptococcus suis, China.
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ABSTRACT:
SUBMITTER: Shi X
PROVIDER: S-EPMC4880084 | biostudies-literature | 2016 Jun
REPOSITORIES: biostudies-literature
Publications
Loss of 89K Pathogenicity Island in Epidemic Streptococcus suis, China.
Shi Xiaolu X Ye Huiyan H Wang Jun J Li Zhencui Z Wang Jingzhong J Chen Baoshan B Wen Ronghui R Hu Qinghua Q Feng Youjun Y
Emerging infectious diseases 20160601 6
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Project description:Pathogenicity islands (PAIs), a distinct type of genomic island (GI), play important roles in the rapid adaptation and increased virulence of pathogens. 89K is a newly identified PAI in epidemic Streptococcus suis isolates that are related to the two recent large-scale outbreaks of human infection in China. However, its mechanism of evolution and contribution to the epidemic spread of S. suis 2 remain unknown. In this study, the potential for mobilization of 89K was evaluated, and its putative transfer mechanism was investigated. We report that 89K can spontaneously excise to form an extrachromosomal circular product. The precise excision is mediated by an 89K-borne integrase through site-specific recombination, with help from an excisionase. The 89K excision intermediate acts as a substrate for lateral transfer to non-89K S. suis 2 recipients, where it reintegrates site-specifically into the target site. The conjugal transfer of 89K occurred via a GI type IV secretion system (T4SS) encoded in 89K, at a frequency of 10(-6) transconjugants per donor. This is the first demonstration of horizontal transfer of a Gram-positive PAI mediated by a GI-type T4SS. We propose that these genetic events are important in the emergence, pathogenesis and persistence of epidemic S. suis 2 strains.
| S-EPMC3132442 | biostudies-literature
Project description:BACKGROUND: Streptococcus suis serotype 2 (S. suis 2) has evolved efficient mechanisms to cause streptococcal toxic shock syndrome (STSS), which is a new emerging infectious disease linked to S. suis. We have previously reported that a type IV secretion system (T4SS) harbored by the specific 89K pathogenicity island (PAI) of S. suis 2 contributes to the development of STSS and mediates horizontal transfer of 89K. However, the 89K T4SS machinery assembly in vivo and in vitro is poorly understood, and the component acting directly to digest the bacterial cell wall needs to be identified. RESULTS: The virB1-89K gene product encoded in the 89K PAI is the only one that shows similarity to the Agrobacterium VirB1 component and contains a conserved CHAP domain that may function in peptidoglycan hydrolysis, which makes it a plausible candidate acting as a hydrolase against the peptidoglycan cell wall to allow the assembly of the T4SS apparatus. In the current study, the CHAP domain of VirB1-89K from S. suis 89K PAI was cloned and over-expressed in Escherichia coli, and its peptidoglycan-degrading activity in vitro was determined. The results indicated that the VirB1-89K CHAP domain can degrade the peptidoglycan layer of bacteria. Deletion of virB1-89K reduces significantly, but does not abolish, the virulence of S. suis in a mouse model. CONCLUSIONS: The experimental results presented here suggested that VirB1-89K facilitates the assembly of 89K T4SS apparatus by catalyzing the degradation of the peptidoglycan cell wall, thus contributing to the pathogenesis of S. suis 2 infection.
| S-EPMC3974602 | biostudies-literature
Project description:Streptococcus suis epidemic strains were responsible for two outbreaks in China and possessed increased pathogenicity which was featured prominently by inducing an excessive inflammatory response at the early phase of infection. To discover the critical genes responsible for the pathogenicity increase of S. suis epidemic strains, the genome-wide transcriptional profiles of epidemic strain SC84 were investigated at the early phase of interaction with BV2 cells. The overall low expression levels of 89K pathogenicity island (PAI) and 129 known virulence genes in the SC84 interaction groups indicated that its pathogenicity increase should be attributed to novel mechanisms. Using highly pathogenic strain P1/7 and intermediately pathogenic strain 89-1591 as controls, 11 pathogenicity increase crucial genes (PICGs) and 38 pathogenicity increase-related genes (PIRGs) were identified in the SC84 incubation groups. The PICGs encoded proteins related to the methionine biosynthesis/uptake pathway and played critical roles in the pathogenicity increase of epidemic strains. A high proportion of PIRGs encoded surface proteins related to host cell adherence and immune escape, which may be conducive to the pathogenicity increase of epidemic strains by rapidly initiating infection. The fact that none of PICGs and PIRGs belonged to epidemic strain-specific gene indicated that the pathogenicity increase of epidemic strain may be determined by the expression level of genes, rather than the presence of them. Our results deepened the understanding on the mechanism of the pathogenicity increase of S. suis epidemic strains and provided novel approaches to control the life-threatening infections of S. suis epidemic strains.
| S-EPMC9423846 | biostudies-literature
Project description:Streptococcus suis infection is an emerging zoonosis in Asia. The most common disease manifestation is meningitis, which is often associated with hearing loss and cochleovestibular signs. S. suis infection in humans mainly occurs among risk groups that have frequent exposure to pigs or raw pork. Here, we report a case of S. suis meningitis in a 67-yr-old pig carcass handler, who presented with dizziness and sensorineural hearing loss followed by headaches. Gram-positive diplococci were isolated from cerebrospinal fluid (CSF) and blood cultures and showed gray-white colonies with α-hemolysis. S. suis was identified from CSF and blood cultures by using a Vitek 2 system (bioMérieux, France), API 20 STREP (bioMérieux), and performing 16S rRNA and tuf gene sequencing. Even after receiving antibiotic treatment, patients with S. suis infection frequently show complications such as hearing impairment and vestibular dysfunction. To the best of our knowledge, this is the first case of S. suis meningitis in Korea. Prevention through public health surveillance is recommended, especially for individuals who have occupational exposures to swine and raw pork.
| S-EPMC3129354 | biostudies-literature
Project description: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.
| S-EPMC3291228 | biostudies-literature
Project description:Streptococcus suis sequence type (ST) 7 has been spreading throughout China. To determine events associated with its emergence, we tested 114 isolates. In all 106 ST7 strains responsible for human outbreaks and sporadic infections, the tetracycline-resistance gene, tetM, was detected on the conjugative transposon Tn916. Horizontal transmission of tetM is suspected.
| S-EPMC2600270 | biostudies-literature
Project description:To determine if the 2005 Chinese outbreak strain of Streptococcus suis is circulating in the United States, three different PCR primer-pairs derived from the nucleotide sequences surrounding and internal to the unique pathogenicity island -like DNA segment of the Chinese outbreak strain (strain 05ZYH33) were used to screen 290 swine isolates of S. suis obtained from different locations. The first primer pair amplified an approximately 1000-bp fragment from 47 (16%) of the United States isolates and the second amplified an 1800-bp fragment from 23 (8%) of the isolates. Nucleotide sequences of the amplicons shared identity with those of strain 05ZYH33. The third primer pair amplified a 716-bp amplicon from the DNA of strain 05ZYH33 only. These observations demonstrated that the PAI homologue of strain 05ZYH33 is absent in the United States isolates tested and suggested that the PCR method may be useful for active surveillance to monitor possible spread of the highly invasive strain.
| S-EPMC3077239 | biostudies-literature
Project description:The bacterial species Vibrio cholerae includes harmless aquatic strains as well as strains capable of causing epidemics and global pandemics of cholera. While investigating the relationship between pathogenic and nonpathogenic strains, we identified a chromosomal pathogenicity island (PAI) that is present in epidemic and pandemic strains but absent from nonpathogenic strains. Initially, two ToxR-regulated genes (aldA and tagA) were studied and were found to be associated with epidemic and pandemic strains but absent in nontoxigenic strains. The region containing aldA and tagA comprises 13 kb of previously unidentified DNA and is part of a PAI that contains a regulator of virulence genes (ToxT) and a gene cluster encoding an essential colonization factor and the cholera toxin phage receptor (toxin-coregulated pilus; TCP). The PAI is 39.5 kb in size, has low %G+C (35%), contains putative integrase and transposase genes, is flanked by att sites, and inserts near a 10Sa RNA gene (ssrA), suggesting it may be of bacteriophage origin. We found this PAI in two clinical non-O1/non-O139 cholera toxin-positive strains, suggesting that it can be transferred within V. cholerae. The sequence within this PAI includes an ORF with homology to a gene associated with the type IV pilus gene cluster of enteropathogenic Escherichia coli, a transposase from Vibrio anguillarum, and several ORFs with no known homology. As the PAI contains the CTXPhi receptor, it may represent the initial genetic factor required for the emergence of epidemic and pandemic cholera. We propose to call this island VPI (V. cholerae pathogenicity island).
| S-EPMC19707 | biostudies-literature
Project description:Streptococcus suis, a Gram-positive pathogen, is widely recognized as an important agent of swine infection, and it is also known to cause a variety of zoonoses, such as meningitis, polyarthritis and pneumonia. Suilysin (SLY), an extracellular pore-forming toxin that belongs to the cholesterol-dependent cytolysin family, is an essential virulence factor of S. suis capsular type 2 (SS2). Here, we found that morin hydrate (morin), a natural flavonoid that lacks anti-SS2 activity, inhibits the hemolytic activity of SLY, protects J774 cells from SS2-induced injury and protects mice from SS2 infection. Further, by molecular modeling and mutational analysis, we found that morin binds to the "stem" domain 2 in SLY and hinders its transformation from the monomer form to the oligomer form, which causes the loss of SLY activity. Our study demonstrates that morin hinders the cell lysis activity of SLY through a novel mechanism of interrupting the heptamer formation. These findings may lead to the development of promising therapeutic candidates for the treatment of SS2 infections.
| S-EPMC5357624 | biostudies-literature
Project description:BACKGROUND:Streptococcus suis is a zoonotic pathogen that causes serious systemic infections in pigs and occupation-related infections in humans who contact with pigs or pork products. In China, it has caused two outbreaks of human infection and surveillance for S.suis has been ongoing since last time. CASE PRESENTATION:Two cases of meningitis and sepsis caused by S. suis were reported in this study. Both patients work in relation to the pork trade, a risk factor for S. suis infection. The outcome was favorable after a prolonged ceftriaxone therapy but one patient was left with mild hearing loss. Two isolates were identified as sequencing type (ST) 7, S. suis serotype 2 (SS2), which is one the most prevalent and cause two outbreaks in China. Whole-genome sequencing (WGS) revealed that a high degree identity was noted in the genome organizations and sequences between two sporadic ST7 SS2 isolates in this study and representative epidemic virulent isolates. Major differences among them are two sporadic ST7 SS2 isolates lacked a virulence factor called agglutinin receptor and an 89?K pathogenicity island (PAI), which plays important role in the pathogenesis of streptococcal toxic shock syndrome (STSS). A summary about STs of human infection with S. suis in China was completed. The result showed ST1 and ST7 were still the major STs and several novel STs were successfully discovered in different provinces. CONCLUSIONS:Our results enhanced the understanding of the ability to cause life-threatening infections in humans and the distribution and evolution of the S. suis in China.
| S-EPMC7071708 | biostudies-literature