Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0031350 (pharyngitis)
 2,405 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serum opacity factor (SOF) is a fibronectin-binding protein of group A streptococci that opacifies mammalian sera and is expressed by some strains that cause impetigo, pharyngitis and acute glomerulonephritis. Although SOF is expressed by approximately 35% of known serotypes, its role in the pathogenesis of group A streptococcal infections has not been previously investigated. The sof genes from M types 2, 28 and 49 Streptococcus pyogenes were cloned, sequenced, and their deduced amino acid sequences were compared. The gene for FnBA, a fibronectin-binding protein from Streptococcus dysgalactiae, was also cloned and found to express an opacity factor. The leader sequences, the fibronectin-binding domains, and the membrane anchor regions of these proteins were highly conserved. Short spans of conserved sequences were interspersed throughout the remaining parts of the proteins. The sof2 gene was insertionally inactivated in an M type 2 S. pyogenes strain, T2MR. The resultant SOF-negative mutant (YL3) did not express SOF or opacify serum, and exhibited a 71% reduction in binding fibronectin. Complementation of the SOF-negative defect with sof28 in the recombinant strain YL3(pNZ28) fully restored fibronectin-binding activity and the ability to opacify serum. To determine whether sof plays a role in virulence, mice were challenged intraperitoneally with these strains. None of the 10 mice infected with YL3(pNZ28) survived and only 1 out of 15 mice challenged with T2MR survived, whereas 12 out of 15 mice infected with YL3 survived. These data clearly indicate that SOF is a virulence factor, and they provide the first direct evidence that a fibronectin-binding protein contributes to the pathogenesis of group A streptococcal infections in vivo.
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PMID:Serum opacity factor is a major fibronectin-binding protein and a virulence determinant of M type 2 Streptococcus pyogenes. 1021 62

To analyze bacteriological treatment failure in streptococcal pharyngitis, 40 consecutive Streptococcus pyogenes isolates from 18 patients were characterized. For 17 patients, isolates were indistinguishable with respect to emm type, random amplified polymorphic DNA pattern, and presence of prtF1 encoding the fibronectin-binding protein F1. prtF1 was detected only in the 11 isolates (4 patients) with emm12 and in the single isolate with emm6. Further analysis by vir(mga) regulon typing, sequencing of sic encoding the streptococcal inhibitor of complement from 19 isolates with emm1 (9 patients), and sequencing of drs (distantly related sic) from 11 isolates with emm12 revealed distinct sic alleles with insertions and/or deletions in sic that corresponded to differences in restriction patterns of the vir(mga) regulon only for paired isolates of 2 patients. Among isolates with emm12, 2 novel drs alleles were found. Analysis of these data suggests that neither the presence of prtF1 nor the diversification of sic / drs is required for the persistence of S. pyogenes in pharyngitis.
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PMID:Characterization of consecutive Streptococcus pyogenes isolates from patients with pharyngitis and bacteriological treatment failure: special reference to prtF1 and sic / drs. 1117 Sep 97

In a study assessing genetic diversity, 114 group A streptococcus (GAS) isolates were recovered from pediatric pharyngitis patients in Rome, Italy. These isolates comprised 22 different M protein gene (emm) sequence types, 14 of which were associated with a distinct serum opacity factor/fibronectin binding protein gene (sof) sequence type. Isolates with the same emm gene sequence type generally shared a highly conserved chromosomal macrorestriction profile. In three instances, isolates with dissimilar macrorestriction profiles had identical emm types; in each of these cases multilocus sequence typing revealed that isolates with the same emm type were clones having the same allelic profiles. Ninety-eight percent of the pharyngeal isolates had emm types previously found to be highly associated with mga locus gene patterns commonly found in pharyngeal GAS isolates.
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PMID:Group A streptococcal genotypes from pediatric throat isolates in Rome, Italy. 1132 74

A total of 66 clinical isolates of group A streptococci (GAS) were obtained from 66 Japanese children with pharyngitis. The prtF1 gene (encoding fibronectin-binding protein F1) and the sic gene (encoding the streptococcal inhibitor of complement) were present in 51 (77.3%) and 48 (72.7%) of the 66 isolates, respectively. These results indicated that a high prevalence of two virulence genes, prtF1 and sic, is characteristic of GAS in Japan.
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PMID:Association of the prtF1 gene (encoding fibronectin-binding protein F1) and the sic gene (encoding the streptococcal inhibitor of complement) with emm types of group A streptococci isolated from Japanese children with pharyngitis. 1235 93

Sixty-two strains of Streptococcus pyogenes isolated from 30 asymptomatic school children and 32 children with pharyngitis were characterized to analyze the involvement of 2 fibronectin-binding proteins (F/SfbI and PrtF2/PfbpI) in S. pyogenes colonizing asymptomatic carriers and to determine the possible association between these proteins and the genes associated with macrolide resistance. In this study, we demonstrated that the proportion of S. pyogenes strains carrying the pfbpI gene was significantly higher among asymptomatic carriers (80%) than among children with pharyngitis (53%; P<.05). With regard to the proportion of prtF1-positive strains, no significant differences were found between the 2 groups (70% vs. 69%, for asymptomatic carriers and children with pharyngitis, respectively). Another important finding is the significant association between macrolide resistance and protein F/SfbI (P<.001) in both groups. These results suggest that the presence of the pfbpI gene can be linked to the ability of S. pyogenes to persist in the throat of asymptomatic carriers.
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PMID:Internalization-associated proteins among Streptococcus pyogenes isolated from asymptomatic carriers and children with pharyngitis. 1285 8

The group A streptococcus (GAS), or Streptococcus pyogenes, is a strict human pathogen of medical significance, causing infections ranging from pharyngitis (strep throat) to necrotizing fasciitis (flesh-eating disease). Several virulence genes that encode factors important for colonization, internalization, and immune evasion are under the control of the multiple gene regulator of the GAS, or Mga. Mga functions as a DNA-binding protein that interacts with sites both proximal (Pemm and PscpA) and distal (PsclA) to the start of transcription for the genes that it regulates. The genes encoding serum opacity factor, sof, and a novel fibronectin-binding protein, sfbX, are cotranscribed and represent two uncharacterized Mga-regulated virulence genes in the GAS. Analysis of the promoter region of sof-sfbX identified a putative Mga-binding site 278 bp upstream of the regulated start of transcription as determined by primer extension. Electrophoretic mobility shift assays demonstrated that Mga is able to bind specifically to the single distal site in a fashion similar to the previously characterized PsclA. In order to better understand the events that take place at this and other Mga-regulated promoters, an in vitro transcription assay was established. Using this assay, we showed that Mga is sufficient to activate transcription in vitro for Mga-regulated promoters containing both proximal (Pemm) and distal (PsclA and Psof-sfbX) binding sites. These results indicate that additional factors are not required for Mga-specific activation at diverse promoters in vitro, although they do not rule out the potential influence of other components on the Mga virulence regulon in vivo.
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PMID:Mga is sufficient to activate transcription in vitro of sof-sfbX and other Mga-regulated virulence genes in the group A Streptococcus. 1651 33

Streptococcus pyogenes is a major cause of pharyngitis in humans and encodes several fibronectin-binding proteins. M protein and protein F1 (PrtF1/SfbI) are differentially regulated by CO(2) and O(2), respectively, and both mediate the invasion of epithelial cells. This study examined whether PrtF1/SfbI shares other properties with M protein. Expression of the PrtF1/SfbI protein by an M-negative mutant conferred resistance to phagocytosis and partial inhibition of C3 deposition on the S. pyogenes surface.
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PMID:Protein F1 and Streptococcus pyogenes resistance to phagocytosis. 1737 55

Acute rheumatic fever (ARF) is an autoimmune disease occurring in individuals following untreated group A streptococcal infection believed to be triggered by antibodies to bacterial components that cross-react with human tissues. We developed a multiplexed immunoassay for the simultaneous quantitation of antibodies to nine streptococcal-related antigens including streptolysin O (SLO), DNase B, collagen I and IV, fibronectin, myosin, group A carbohydrate, M6 protein and streptococcal C5a peptidase. Utilizing this method, we examined serum from 49 ARF, 58 pharyngitis patients and age- and sex-matched controls in samples collected at initial disease onset, and at 4 weeks, 6 months and 1 year after diagnosis. Antibody responses were significantly higher for SLO, DNase B, M6 protein, group A carbohydrate and the cross-reactive antigens collagen I and myosin in ARF compared with pharyngitis patients (P <or= 0.05). Moreover, we found significantly elevated antibody responses in the ARF patients with rheumatic heart disease to fibronectin and collagen I compared with ARF patients without heart disease. The major differences between the ARF patients with and without carditis appear to be in the immune response to the putative heart valve components, collagen I and fibronectin.
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PMID:Comprehensive analysis of antibody responses to streptococcal and tissue antigens in patients with acute rheumatic fever. 1824 83

In 2002, the Romanian National Reference Laboratory was invited to join the Strep-EURO project to study invasive Streptococcus pyogenes infections. During 2003 and 2004, a total of 33 isolates recovered from invasive disease were received from eight Romanian counties. For comparison, 102 isolates from non-invasive disease, as well as a collection of 12 old invasive strains (isolated between 1967 and 1980) were included. All isolates were characterized by several methods: T and emm typing, presence of the fibronectin-binding protein F1 gene (prtF1), serum opacity factor (sof), and superantigen (SAg) genes (speA, speB, speC, speF, speG, speH, ssa and smeZ). The recent invasive isolates exhibited 19 emm-types, of which emm1, emm81, emm76, emm49 and emm78 covered 57 % of the strains. Furthermore, multilocus sequence typing analysis revealed nine new sequence types, corresponding to emm types 1, 12, 49, 81, 92, 100, 106 and 119. The non-invasive isolates comprised 24 different emm types with a predominance of emm1 and 12; the old invasive strains were of eight emm types, of which four were unique for this group. All isolates harboured speB and speF; smeZ was detected in all invasive strains, except for the emm49 and emm81 isolates. The majority of isolates from carriers, and patients with pharyngitis were prtF1 positive, most of these (14 strains) being emm12. High tetracycline resistance rates were noted among both invasive and control isolates (54 % and 35 %, respectively), whereas macrolide resistance rates were low (3 % and 5 %, respectively). Active and continuing surveillance is required to provide an accurate assessment of the disease burden and to provide epidemiological data on the character of isolates in Romania.
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PMID:Molecular characterization of invasive and non-invasive Streptococcus pyogenes isolates from Romania. 1892 12

Group A Streptococcus (GAS, Streptococcus pyogenes) is a gram-positive human pathogen responsible for a diverse variety of diseases, including pharyngitis, skin infections, invasive necrotizing fasciitis and autoimmune sequelae. We have recently shown that GAS cell adhesion and biofilm formation is associated with the presence of pili on the surface of these bacteria. GAS pilus proteins are encoded in the FCT (Fibronectin-Collagen-T antigen) genomic region, of which nine different variants have been identified so far. In the present study we undertook a global analysis of GAS isolates representing the majority of FCT-variants to investigate the effect of environmental growth conditions on their capacity to form multicellular communities. For FCT-types 2, 3, 5 and 6 and a subset of FCT-4 strains, we observed that acidification resulting from fermentative sugar metabolism leads to an increased ability of the bacteria to form biofilm on abiotic surfaces and microcolonies on epithelial cells. The higher biofilm forming capacity at low environmental pH was directly associated with an enhanced expression of the genes encoding the pilus components and of their transcription regulators. The data indicate that environmental pH affects the expression of most pilus types and thereby the formation of multicellular cell-adhering communities that assist the initial steps of GAS infection.
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PMID:Environmental acidification drives S. pyogenes pilus expression and microcolony formation on epithelial cells in a FCT-dependent manner. 2107 80


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