Survey of Genes Encoding Staphylococcal Enterotoxins, Toxic Shock Syndrome Toxin 1, and Exfoliative Toxins in Members of the
            <i>Staphylococcus sciuri</i>
            Group

Dakić, Ivana; Vuković, Dragana; Stepanović, Srdjan; Hauschild, Tomasz; Ježek, Petr; Petřáš, Petr; Morrison, Donald A.

doi:10.1128/jcm.43.9.4875-4876.2005

“…YPM may be associated with the particular scarlatinoid fever syndromes because it mediates an uncontrolled host immune system activation [20,54]. This is analogous to the role of superantigens in staphylococcal and streptococcal toxic shock syndromes [18,19]. The similarities in the clinical presentation of scarlet and scarlet-like fever suggest a direct role of YPM in the pathogenesis and the distinct clinical manifestation of Y.…”

Section: Resultsmentioning

confidence: 99%

“…In 1959, an epidemic of Y. pseudotuberculosis infections on the Pacific coast of Russia was called Far East scarlet-like fever (FESLF), or scarlatinoid fever [10–17] for its clinical similarities to scarlet fever caused by group A streptococci [18,19] . Such atypical infections in Far East Asia are severe, and the clinical presentation includes erythematous skin rash, skin desquamation, exanthema, hyperhemic tongue, and toxic shock syndrome [10,11,18,19].…”

Section: Introductionmentioning

confidence: 99%

The Complete Genome Sequence of Yersinia pseudotuberculosis IP31758, the Causative Agent of Far East Scarlet-Like Fever

Eppinger

¹

,

Rosovitz

²

,

Fricke

³

et al. 2007

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The first reported Far East scarlet-like fever (FESLF) epidemic swept the Pacific coastal region of Russia in the late 1950s. Symptoms of the severe infection included erythematous skin rash and desquamation, exanthema, hyperhemic tongue, and a toxic shock syndrome. The term FESLF was coined for the infection because it shares clinical presentations with scarlet fever caused by group A streptococci. The causative agent was later identified as Yersinia pseudotuberculosis, although the range of morbidities was vastly different from classical pseudotuberculosis symptoms. To understand the origin and emergence of the peculiar clinical features of FESLF, we have sequenced the genome of the FESLF-causing strain Y. pseudotuberculosis IP31758 and compared it with that of another Y. pseudotuberculosis strain, IP32953, which causes classical gastrointestinal symptoms. The unique gene pool of Y pseudotuberculosis IP31758 accounts for more than 260 strain-specific genes and introduces individual physiological capabilities and virulence determinants, with a significant proportion horizontally acquired that likely originated from Enterobacteriaceae and other soil-dwelling bacteria that persist in the same ecological niche. The mobile genome pool includes two novel plasmids phylogenetically unrelated to all currently reported Yersinia plasmids. An icm/dot type IVB secretion system, shared only with the intracellular persisting pathogens of the order Legionellales, was found on the larger plasmid and could contribute to scarlatinoid fever symptoms in patients due to the introduction of immunomodulatory and immunosuppressive capabilities. We determined the common and unique traits resulting from genome evolution and speciation within the genus Yersinia and drew a more accurate species border between Y. pseudotuberculosis and Y. pestis. In contrast to the lack of genetic diversity observed in the evolutionary young descending Y. pestis lineage, the population genetics of Y. pseudotuberculosis is more heterogenous. Both Y. pseudotuberculosis strains IP31758 and the previously sequenced Y. pseudotuberculosis strain IP32953 have evolved by the acquisition of specific plasmids and by the horizontal acquisition and incorporation of different genetic information into the chromosome, which all together or independently seems to potentially impact the phenotypic adaptation of these two strains.

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“…The typical features of S. sciuri are coagulase negative, oxidase positive and novobiocin-resistant[33]–[35]. The isolate HBXX06 met these requirements.…”

Section: Discussionmentioning

confidence: 90%

“…It was also reported that one or more exfoliative toxins produced by isolates of S. hyicus from different countries could be detected [6]. Dakic and his colleagues examined the genes encoding staphylococcal enterotoxins (sea to see, seg, and seh), toxic shock syndrome toxin 1 (tst), and exfoliative toxins (eta and etb) in a panel of 48 Staphylococcus sciuri group isolates from animals and did not find any these genes [41]. In Another study, one hundred and twenty-one isolates from human and animals were examined for biofilm formation, hemagglutination, presence of clumping factor, production of spreading factors and exotoxins, cytotoxicity and capacity to stimulate nitric oxide production, and it was found that a wide spectrum of possible virulence determinants of S. sciuri existed [42], however their exact contribution to virulence of this bacterium in vivo remains to be determined.…”

Section: Discussionmentioning

confidence: 99%

A Highly Pathogenic Strain of Staphylococcus sciuri Caused Fatal Exudative Epidermitis in Piglets

Chen

¹

,

Wang

²

,

Chen

³

et al. 2007

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Staphylococcus sciuri are important human pathogens responsible for endocarditis, peritonitis, septic shock, urinary tract infection, pelvic inflammatory disease and wound infections. However, little information is known regarding the pathogenicity of S. sciuri to animals. From the pericardial fluid of a diseased piglet with exudative epidermitis (EE), we isolated a strain of Staphylococcus in pure culture. Surprisingly, this isolate was a member of S. sciuri rather than S. hyicus as identified by its biochemical traits and also by analysis of 23S ribosomal DNA using Internal Transcribed Spacer PCR. In addition, inoculation of newborn piglets with 1×1010 CFU of the isolate by oral feeding or intra-muscular injection successfully reproduced EE in piglets, which suggested that the oral intake of the pathogen by the animals is one of the major routes of exposure. These unexpected findings prioritized S. sciuri as important zoonotic agents, which may have ramifications for human medicine.

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“…Often, Y. pseudotuberculosis isolates from environmental and clinical sources harbor various plasmids ranging in size from 3-125 kb [7], some of which have been linked to pathogenicity [8,9]. In 1959, an epidemic of Y. pseudotuberculosis infections on the Pacific coast of Russia was called Far East scarlet-like fever (FESLF), or scarlatinoid fever [10][11][12][13][14][15][16][17] for its clinical similarities to scarlet fever caused by group A streptococci [18,19]. Such atypical infections in Far East Asia are severe, and the clinical presentation includes erythematous skin rash, skin desquamation, exanthema, hyperhemic tongue, and toxic shock syndrome [10,11,18,19].…”

Section: Introductionmentioning

confidence: 99%

Genome Sequence of Y. pseudotuberculosis IP31758, the Causative Agent of Far East Scarlet Like Fever: Linking Genomic Plasticity to Pathogenicity

Eppinger¹,

Rosovitz²,

Fricke³

et al. 2005

PLoS Genet

0

View full text Add to dashboard Cite

The first reported Far East scarlet-like fever (FESLF) epidemic swept the Pacific coastal region of Russia in the late 1950s. Symptoms of the severe infection included erythematous skin rash and desquamation, exanthema, hyperhemic tongue, and a toxic shock syndrome. The term FESLF was coined for the infection because it shares clinical presentations with scarlet fever caused by group A streptococci. The causative agent was later identified as Yersinia pseudotuberculosis, although the range of morbidities was vastly different from classical pseudotuberculosis symptoms. To understand the origin and emergence of the peculiar clinical features of FESLF, we have sequenced the genome of the FESLF-causing strain Y. pseudotuberculosis IP31758 and compared it with that of another Y. pseudotuberculosis strain, IP32953, which causes classical gastrointestinal symptoms. The unique gene pool of Y pseudotuberculosis IP31758 accounts for more than 260 strain-specific genes and introduces individual physiological capabilities and virulence determinants, with a significant proportion horizontally acquired that likely originated from Enterobacteriaceae and other soil-dwelling bacteria that persist in the same ecological niche. The mobile genome pool includes two novel plasmids phylogenetically unrelated to all currently reported Yersinia plasmids. An icm/dot type IVB secretion system, shared only with the intracellular persisting pathogens of the order Legionellales, was found on the larger plasmid and could contribute to scarlatinoid fever symptoms in patients due to the introduction of immunomodulatory and immunosuppressive capabilities. We determined the common and unique traits resulting from genome evolution and speciation within the genus Yersinia and drew a more accurate species border between Y. pseudotuberculosis and Y. pestis. In contrast to the lack of genetic diversity observed in the evolutionary young descending Y. pestis lineage, the population genetics of Y. pseudotuberculosis is more heterogenous. Both Y. pseudotuberculosis strains IP31758 and the previously sequenced Y. pseudotuberculosis strain IP32953 have evolved by the acquisition of specific plasmids and by the horizontal acquisition and incorporation of different genetic information into the chromosome, which all together or independently seems to potentially impact the phenotypic adaptation of these two strains.

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Survey of Genes Encoding Staphylococcal Enterotoxins, Toxic Shock Syndrome Toxin 1, and Exfoliative Toxins in Members of the Staphylococcus sciuri Group

Cited by 12 publications

References 17 publications

The Complete Genome Sequence of Yersinia pseudotuberculosis IP31758, the Causative Agent of Far East Scarlet-Like Fever

The Complete Genome Sequence of Yersinia pseudotuberculosis IP31758, the Causative Agent of Far East Scarlet-Like Fever

A Highly Pathogenic Strain of Staphylococcus sciuri Caused Fatal Exudative Epidermitis in Piglets

Genome Sequence of Y. pseudotuberculosis IP31758, the Causative Agent of Far East Scarlet Like Fever: Linking Genomic Plasticity to Pathogenicity

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