Live Streptococcus suis type 5 strain XS045 provides cross-protection against infection by strains of types 2 and 9

Jiang, Xiaowu; Yang, Yunkai; Zhu, Lexin; Gu, Yunqing; Shen, Hongxia; Shan, Ying; Li, Xiaoliang; Wu, Jiusheng; Fang, Weihuan

doi:10.1016/j.vaccine.2016.05.003

Cited by 14 publications

(8 citation statements)

References 49 publications

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“…Cell cytotoxicity of PrsA was conducted as previously described (Jiang et al, 2016). The mouse brain microvascular endothelial cell line bEND3.0 cultured in DMEM supplemented with 10% FBS (Gibco, USA) were stimulated with purified PrsA at different concentrations and incubated for 1 or 2 h at 37°C with 5% CO 2 .…”

Section: Methodsmentioning

confidence: 99%

Roles of the Putative Type IV-like Secretion System Key Component VirD4 and PrsA in Pathogenesis of Streptococcus suis Type 2

Jiang

Yang

Zhou

et al. 2016

Front. Cell. Infect. Microbiol.

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Streptococcus suis type 2 (SS2) is a zoonotic pathogen causing septic infection, meningitis and pneumonia in pigs and humans. SS2 may cause streptococcal toxic shock syndrome (STSS) probably due to excessive release of inflammatory cytokines. A previous study indicated that the virD4 gene in the putative type IV-like secretion system (T4SS) within the 89K pathogenicity island specific for recent epidemic strains contributed to the development of STSS. However, the functional basis of VirD4 in STSS remains unclear. Here we show that deletion of virD4 led to reduced virulence as shown by about 65% higher LD50, lower bacterial load in liver and brain, and lower level of expression of inflammatory cytokines in mice and cell lines than its parent strain. The ΔVirD4 mutant was more easily phagocytosed, suggesting its role as an anti-phagocytic factor. Oxidative stress that mimic bacterial exposure to respiratory burst of phagocytes upregulated expression of virD4. Proteomic analysis identified 10 secreted proteins of significant differences between the parent and mutant strains under oxidative stress, including PrsA, a peptidyl-prolyl isomerase. The SS2 PrsA expressed in E. coli caused a dose-dependent cell death and increased expression of proinflammatory IL-1β, IL-6 and TNF-α in murine macrophage cells. Our data provide novel insights into the contribution of the VirD4 factor to STSS pathogenesis, possibly via its anti-phagocytic activity, upregulation of its expression upon oxidative stress and its involvement in increased secretion of PrsA as a cell death inducer and proinflammatory effector.

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Section: Methodsmentioning

confidence: 99%

Roles of the Putative Type IV-like Secretion System Key Component VirD4 and PrsA in Pathogenesis of Streptococcus suis Type 2

Jiang

Yang

Zhou

et al. 2016

Front. Cell. Infect. Microbiol.

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“…The task is not easy because of the great diversity among S. suis strains. Nevertheless, the research aimed at obtaining such vaccine is being undertaken by many prominent scientists worldwide, some of whom have recently published promising results in this area [55,95,96,97]. We appeal to the governmental and international organizations, such as UNESCO, WHO, FAO, the European Union, and others, for a significant financial support of such research that would hopefully result in obtaining an effective, universal and licensed vaccine within the next 5-10 years.…”

Section: Resultsmentioning

confidence: 99%

Streptococcus suis: a re-emerging pathogen associated with occupational exposure to pigs or pork products. Part II – Pathogenesis

Dutkiewicz

Zając

Sroka

et al. 2018

Ann Agric Environ Med.

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Streptococcus suis is a re-emerging zoonotic pathogen that may cause severe disease, mostly meningitis, in pigs and in humans having occupational contact with pigs and pork, such as farmers, slaughterhose workers and butchers. The first stage of the pathogenic process, similar in pigs and humans, is adherence to and colonisation of mucosal and/or epithelial surface(s) of the host. The second stage is invasion into deeper tissue and extracellular translocation of bacterium in the bloodstream, either free in circulation or attached to the surface of monocytes. If S. suis present in blood fails to cause fatal septicaemia, it is able to progress into the third stage comprising penetration into host's organs, mostly by crossing the blood-brain barrier and/or blood-cerebrospinal fluid barrier to gain access to the central nervous system (CNS) and cause meningitis. The fourth stage is inflammation that plays a key role in the pathogen esis of both systemic and CNS infections caused by S. suis. The pathogen may induce the overproduction of pro-inflammatory cytokines that cause septic shock and/or the recruitment and activation of different leukocyte populations, causing acute inflammation of the CNS. Streptococcus suis can also evoke - through activation of microglial cells, astrocytes and possibly other cell types - a fulminant inflammatory reaction of the brain which leads to intracranial complications, including brain oedema, increased intracranial pressure, cerebrovascular insults, and deafness, as a result of cochlear sepsis. In all stages of the pathogenic process, S. suis interacts with many types of immunocompetent host's cells, such as polymorphonuclear leukocytes, mononuclear macrophages, lymphocytes, dendritic cells and microglia, using a range of versatile virulence factors for evasion of the innate and adaptive immune defence of the host, and for overcoming environmental stress. It is estimated that S. suis produces more than 100 different virulence factors that could be classified into 4 groups: surface components or secreted elements, enzymes, transcription factors or regulatory systems and transporter factors or secretion systems. A major virulence factor is capsular polysaccharide (CPS) that protects bacteria from phagocytosis. However, it hampers adhesion to and invasion of host's cells, release of inflammatory cytokines and formation of the resistant biofilm which, in many cases, is vital for the persistence of bacteria. It has been demonstrated that the arising by mutation unencapsulated S. suis clones, which are more successful in penetration to and propagation within the host's cells, may coexist in the organism of a single host together with those that are encapsulated. Both 'complementary' clones assist each other in the successful colonization of host's tissues and persistence therein. S. suis has an open pan-genome characterized by a frequent gene transfer and a large diversity. Of the genetic determinants of S. suis pathogenicity, t...

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“…suis infection in pigs is reported worldwide, from the United States and Canada to South America (Brazil), Europe (United Kingdom, The Netherlands, France, Denmark, Norway, Spain, Poland and Germany), Asia (China, Thailand, Vietnam, and Japan), Australia, and New Zealand [28,40,48]. Of the 35 known S. suis serotypes, types 2, 1/2, 3, 4, 5, 7, 9 and 14 have been reported to cause infections in pigs [25,49]. Among 4,711 cases of S. suis infections identified worldwide in pigs between 2002-2013, the most common was serotype 2 (27.9%), followed by serotype 9 (19.4%) and serotype 3 (15.9%).…”

Section: Transmission Among Pigs and Predisposing Factorsmentioning

confidence: 99%

“…Positive examples of such studies are the results obtained recently by Chinese scientists. Jiang et al [49] identified a natural low-virulence S. suis type 5 strain XS045 as a live vaccine candidate, and demonstrated its safety and effectiveness by providing cross-protection against challenges by type 2 and type 9 S. suis strains. In another study, Wang et al [31] detected significant genomic differences between the avirulent S. suis strain 05HAS68 and the highly virulent strain 05ZYH33.…”

Section: • As a Vaccine For Use In Humans Is Still Unavailable Contimentioning

confidence: 99%

Streptococcus suis: a re-emerging pathogen associated with occupational exposure to pigs or pork products. Part I – Epidemiology

Dutkiewicz

Sroka²,

Zając³

et al. 2017

Ann Agric Environ Med.

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Streptococcus suis (ex Elliot 1966, Kilpper-Bälz & Schleifer 1987) is a facultatively anaerobic Gram-positive ovoid or coccal bacterium surrounded by a polysaccharide capsule. Based on the antigenic diversity of the capsule, S. suis strains are classified serologically into 35 serotypes. Streptococcus suis is a commensal of pigs, commonly colonizing their tonsils and nasal cavities, mostly in weaning piglets between 4-10 weeks of age. This species occurs also in cattle and other mammals, in birds and in humans. Some strains, mostly those belonging to serotype 2, are also pathogenic for pigs, as well as for other animals and humans. Meningitis is the primary disease syndrome caused by S. suis, both in pigs and in humans. It is estimated that meningitis accounted for 68.0% of all cases of human disease reported until the end of 2012, followed by septicaemia (including life-threatening condition described as 'streptococcal toxic shock-like syndrome' - STSLS), arthritis, endocarditis, and endophthalmitis. Hearing loss and/or ves tibular dysfunction are the most common sequelae after recovery from meningitis caused by S. suis, occurring in more than 50% of patients. In the last two decades, the number of reported human cases due to S. suis has dramatically increased, mostly due to epidemics recorded in China in 1998 and 2005, and the fulminant increase in morbidity in the countries of south-eastern Asia, mostly Vietnam and Thailand. Out of 1,642 cases of S. suis infections identified between 2002-2013 worldwide in humans, 90.2% occurred in Asia, 8.5% in Europe and 1.3% in other parts of the globe. The human disease has mostly a zoonotic and occupational origin and occurs in pig breeders, abattoir workers, butchers and workers of meat processing facilities, veterinarians and meat inspectors. Bacteria are transmitted to workers by close contact with pigs or pig products, usually through contamination of minor cuts or abrasions on skin of hands and/or arms, or by pig bite. A different epidemiologic situation occurs in the Southeast Asian countries where most people become infected by habitual consumption of raw or undercooked pork, blood and offal products in the form of traditional dishes. Prevention of S. suis infections in pigs includes vaccination, improvement in pig-raising conditions, disinfection and/or fumigation of animal houses, and isolation of sick animals at the outbreak of disease. Prevention of human infections comprises: protection of skin from pig bite or injury with sharp tools by people occupationally exposed to pigs and pig products, prompt disinfection and dressing of wounds and abrasions at work, protection of the respiratory tract by wearing appropriate masks or repirators, consulting a doctor in the case of febrile illness after exposure to pigs or pork meat, avoidance of occupations associated with exposure to pigs and pork by immunocompomised people, avoidance of consumption of raw pork or pig blood, adequate cooking of pork, and health edu...

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Live Streptococcus suis type 5 strain XS045 provides cross-protection against infection by strains of types 2 and 9

Cited by 14 publications

References 49 publications

Roles of the Putative Type IV-like Secretion System Key Component VirD4 and PrsA in Pathogenesis of Streptococcus suis Type 2

Roles of the Putative Type IV-like Secretion System Key Component VirD4 and PrsA in Pathogenesis of Streptococcus suis Type 2

Streptococcus suis: a re-emerging pathogen associated with occupational exposure to pigs or pork products. Part II – Pathogenesis

Streptococcus suis: a re-emerging pathogen associated with occupational exposure to pigs or pork products. Part I – Epidemiology

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