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Query: UMLS:C0031350 (pharyngitis)
 2,405 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cultures of Streptococcus equisimilis (Lancefield group C) from three outbreaks of illness were found to carry the T-protein antigen 204. Strains of this type were not otherwise represented in a collection of 743 cultures of these 'pyogenes-like' streptococci isolated from other outbreaks of infection or as random isolates. Two of the three outbreaks were of pharyngitis. The third arose in a maternity unit where the organism was isolated from mothers with puerperal fever, from staff and also from the environment. Representative strains were found to carry M-protein antigens as judged by their ability to survive and multiply in fresh normal human blood. Comparison of absorbed rabbit antiserum to the M antigens in opsonic and precipitin tests showed that a distinct M antigen was present on isolates from one outbreak of sore throat and that all cultures from the other two incidents shared a common M antigen. Samples of serum were also available from patients in the outbreak of puerperal sepsis. Most patients developed antibodies to one or more streptococcal antigens including the M protein, streptolysin O, streptokinase and the hyaluronidase specific for strains of group C and group G streptococci.
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PMID:The presence of M proteins in outbreak strains of Streptococcus equisimilis T-type 204. 280 34

We studied 15 strains of group C (Streptococcus equi subsp. equisimilis) [corrected] isolated from the throats of college students with acute pharyngitis and 5 strains isolated from patients with noninfectious problems. Nineteen of the 20 strains resisted phagocytic killing during incubation in normal human blood, suggesting that they might express M proteins. Genomic DNA from all 20 strains hybridized with a probe corresponding to the carboxyterminal one-third of the group A M-protein gene emm24, a region that is highly conserved among M proteins of group A and group G streptococci. The DNA sequences of the N-terminal (variable) regions of the M-protein-encoding genes from two disease-associated group C isolates and one control isolate were determined. The predicted amino acid sequences of the two pharyngitis strains were identical and were 88% homologous to the amino acid sequence of a group G M-protein gene. The predicted terminal amino acid sequence of the control strain does not correspond to any such sequences in the GenBank database. All three strains studied possess the conserved region domain common to class I group A M-protein types epidemiologically associated with rheumatic fever. These studies demonstrate the presence of M proteins in strains of S. equi subsp. equisimilis [corrected] isolated in cases of endemically occurring acute pharyngitis. Certain of these proteins are similar to those of group G streptococci, while others may represent new M types. The similarity in structure and function between M proteins of nonrheumatogenic serogroups and those of rheumatogenic group A streptococci suggests that factors other than or in addition to M protein per se are likely involved in the pathogenesis of rheumatic fever.
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PMID:M proteins of group C streptococci isolated from patients with acute pharyngitis. 888 May 11

In the latter half of the 20th century, the clinical importance of variation in the virulence of strains of GAS has been clearly demonstrated. Although still obscure, the pathogenesis of ARF requires immunologically significant infection of the throat by virulent GAS strains. These strains contain large hyaluronate capsules and large M-protein molecules. The latter contain epitopes cross-reactive with host tissues, and also contain superantigenic toxic moieties. In areas where ARF has become rare, GAS pharyngitis continues to be common but is caused predominantly by GAS strains of relatively low virulence. These, however, may colonize the throat avidly and stubbornly. Molecularly distinct pyoderma strains may cause acute glomerulonephritis, but they are not rheumatogenic even though they may secondarily infect the throat. In developing countries with a very high incidence of rheumatic heart disease, identification of the prevalent rheumatogenic GAS strains and development of a multivalent vaccine against them is currently an interesting strategy. Pending vaccine development, intense primary and secondary penicillin prophylaxis should continue to be sharply focused on populations with the highest prevalence of RHD as such measures may often succeed in driving away the most virulent rheumatogenic clones of GAS from their midst.
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PMID:Can we eradicate rheumatic fever in the 21st century? 1142 92

Variation in strain virulence helps to account for the wide spectrum of group A streptococcal diseases and for their striking epidemiological variation. Recent studies of the genetic control of the expression of the virulence factors of group A streptococci (GAS) are beginning to illuminate such variation. Although still obscure, the pathogenesis of acute rheumatic fever (RF) requires primary infection of the throat by highly virulent GAS strains. Those that have clearly caused RF contain large hyaluronate capsules and extended M-protein molecules. The M molecule contains some epitopes cross-reactive with host tissues, and also has superantigenic properties like the secreted GAS erythrogenic toxins. In settings where ARF has become rare, GAS pharyngitis continues to be quite common but is most often caused by relatively attenuated strains. These, however, may colonize the throat avidly, and often stubbornly. GAS "skin strains" that cause pyoderma (impetigo) are molecularly distinct from "throat strains". Although they may secondarily colonize and infect the throat, the pyoderma strains are generally less virulent and are not rheumatogenic. Some skin strains, however, may cause acute glomerulonephritis. The diagnosis, treatment and prevention of GAS pharyngitis is reviewed in relation to the varying prevalence of RF in different geographical and social settings.
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PMID:Current issues in the prevention of rheumatic fever. 1241 Jan 70

Research on Group A streptococci (GAS) before 1950 paved the way for successful clinical trials to prevent acute rheumatic fever (ARF) by treating the prior streptococcal infection with penicillin. Prevention of ARF has led to almost complete disappearance of rheumatic heart disease in the industrialized world, but has yet to be accomplished in developing countries, where most of the world's populations reside. Twenty years of research beginning in 1918 by Lancefield and others delineated the modern classification of haemolytic streptococci and led to the recognition that only Group A is responsible for the pharyngitis that causes ARF. M-protein, identified as a major virulence factor, is a powerful inhibitor of phagocytosis, and antibodies to it promote type-specific phagocytosis and therefore type-specific immunity. Other virulent properties of GAS include a bulky capsule, as well as extracellular toxins such as streptolysins S and O and streptococcal proteinase. McCarty and others pursued the cell biology of GAS and identified the cellular localization of various antigenic components. The discovery of purified M-protein as a helical coiled-coiled fibrillar protein has sparked development of M-protein vaccine. US, UK, and Trinidad scientists described differences between streptococcal infections of the throat and skin and noted particularly that many of the GAS M-types that cause impetigo are less likely to cause pharyngitis. GAS impetigo may cause acute glomerulonephritis, but such infections do not result in ARF. The changing manifestations of disease over time and the evolution of microbes are common themes in medicine today. These themes are relevant to GAS pharyngitis and ARF, especially the decline in the incidence of severe ARF and the decrease in severity of GAS pharyngitis. Research on GAS bacteriophages led to the discovery of a relationship between lysogenic GAS and production of erythrogenic toxin and has broadened approaches to the molecular epidemiology of GAS virulence. The 21st century begins with determination of the complete genome sequence of M-1, M-18, and M-3 strains of GAS. These studies provide evidence for phage-encoded toxins, high-virulence phenotypes, and clone emergence. This research will reveal genetic processes at the molecular level that control the emergence and decline of streptococcal diseases in different places and times and the shifting patterns in clinical manifestations.
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PMID:A half-century of streptococcal research: then & now. 1244 Jan 94

Group A streptococcus (GAS) is the most common pathogen causing bacterial pharyngitis. We isolated streptococcal strains from tonsils removed from patients with tonsillar disease (n=202) and studied their ability to bind the complement regulators factor H (FH) and C4b binding protein (C4BP) using 125 I-labeled proteins. Blood isolates of GAS (n=10) were obtained from patients with bacteraemia. Streptococci were isolated from 21% of the tonsillitis patients. The emm and T types of the GAS strains were determined. Of the 26 GAS strains studied, only six could bind FH and/or C4BP above the threshold levels. The fraction of the offered radioactive protein bound ranged between 6-12% for FH and 19-56% for C4BP. The clinical course of the tonsillar disease was not related to the binding of FH or C4BP by GAS. The binding strains were mostly of the T4M4 or T28M28 type. From the invasive strains (n=10), three bound FH (binding level: 8-11%) and two C4BP (36-39%). The binding correlated only partially to M-protein (emm) type suggesting that the binding was not exclusively due to M-protein. The results indicate that complement regulator binding by GAS is only partially related to pathogenicity and not a universal property of all group A streptococci.
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PMID:Binding of complement regulators factor H and C4b binding protein to group A streptococcal strains isolated from tonsillar tissue and blood. 1853 13

Streptococcus pyogenes is a major human pathogen. It is a common cause of pharyngitis, cellulitis and wound infections. Late complications like rheumatoid arthritis and glomerulonephritis are associated with certain M proteins on the surface of the bacteria. In 1987 an increase was noted in the incidence of serious infections caused by this bacterium. The increase has been associated with protein type M 1. Typing with antibodies against T proteins is simpler to perform than M typing and can give as good epidemiological information. Culture results from January 11986 to December 31 1993, from the Department of Microbiology at the National University Hospital in Reykjavik, were reviewed. T protein type of some of the strains, that had been preserved by freezing, was determined by agglutination after culture in Todd Hewitt broth as described by Efstratiou. T-protein type of 384 strains from 1991-1993 was determined and the results compared to unpublished results from 1988 and 1989. T-protein type was also determined on all S. pyogenes strains that were isolated from blood in 1989 to 1993. The following T-types were most common: 1988-1989 Tl vas 30%; 1991, T4 and T28 70% and 62% in 1992; in 1993 Tl and T3 were 59%. Thirty one strains were sent to the Streptococcal Reference Laboratory, Central Public Health Laboratory, London, for determination of M-proteins. All strains but one, that were sent to Britain for M-protein typing, had corresponding T-proteins (Mx=Tx; My=Ty and so on). Big fluctuations in the number of isolations of S. pyogenes strains was observed during the study period: Fewest in 1989 or 629, but the number was highest in 1993 or 2057. The changes in incidence seemed to correlate with certain serotypes.
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PMID:[Results of cultures and serotyping of S. pyogenes 1986-1993.]. 2006 64

Macrolide resistance (MR) in group A Streptococcus (GAS) has been well documented in several countries and has become clinically significant since the large increases in macrolide usage during the 1970s. Macrolides are recommended as an alternative therapy for GAS pharyngitis, the most common cause of bacterial pharyngitis. Macrolide resistance has been associated with certain emm types, a sequence-based typing system of the hypervariable region of the GAS M-protein gene. Clinical failure of macrolide treatment of GAS infections can be associated with complications including acute rheumatic fever and rheumatic heart disease, the leading cause of acquired heart disease in children worldwide. Here we report 2 pediatric cases of MR and/or treatment failure in the treatment of GAS pharyngitis with the subsequent development of acute rheumatic fever. We also review the literature on worldwide MR rates, molecular classifications, and emm types, primarily associated with GAS pharyngeal isolates between the years of 2000 and 2010. The use of macrolides in the management of GAS pharyngitis should be limited to patients with significant penicillin allergy.
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PMID:Macrolide treatment failure in streptococcal pharyngitis resulting in acute rheumatic fever. 2231 96