Epidemiology of Invasive Group A<i>Streptococcus</i>Disease in the United States, 1995–1999

O’Brien, Katherine L.; Beall, Bernard; Barrett, Nancy L.; Cieslak, Paul R.; Reingold, Arthur; Farley, Monica M.; Danila, Richard; Zell, Elizabeth R.; Facklam, Richard R.; Schwartz, Benjamin; Schuchat, Anne

doi:10.1086/341409

Cited by 318 publications

(323 citation statements)

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“…data), and high rates of GAS skin disease have been found in Pacifi c Islanders in other parts of the world, including in Maoris and other Polynesians in New Zealand (21,22). In most industrialized countries, the annual incidence of invasive GAS disease is 2.5-3.5/100,000 population (8,23), and the case-fatality rate is 7%-15% (6,8,(23)(24)(25)(26). Although some epidemiologic similarities were found between invasive GAS disease in these countries and in Fiji, such as the high rates for elderly persons with coexisting medical conditions, as well as in the clinical spectrum of disease, major differences stand out.…”

Section: Discussionmentioning

confidence: 99%

“…Although >95% of these cases and deaths occur in developing countries, few data exist about the epidemiology of these infections in developing countries. In addition, few data describe the clinical signs and symptoms, case-fatality rate, and risk factors associated with invasive GAS disease or the molecular epidemiology of invasive GAS disease in developing countries because most published reports originate from industrialized countries (4)(5)(6)(7)(8).…”

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Prospective Surveillance of Invasive Group A Streptococcal Disease, Fiji, 2005–2007

Steer¹,

Jenney²,

Kado³

et al. 2009

Emerg. Infect. Dis.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Prospective Surveillance of Invasive Group A Streptococcal Disease, Fiji, 2005–2007

Steer¹,

Jenney²,

Kado³

et al. 2009

Emerg. Infect. Dis.

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“…Serotype M3 strains cause a disproportionate number of invasive disease cases, including necrotizing fasciitis, bacteremia, and streptococcal toxic shock syndrome (5-9). Importantly, serotype M3 strains cause a higher rate of lethal infections than strains of other M types (7)(8)(9). In addition, serotype M3 and other GAS strains can undergo rapid shifts in disease frequency and display epidemic behavior (5).…”

mentioning

confidence: 99%

Molecular genetic anatomy of inter- and intraserotype variation in the human bacterial pathogen group A Streptococcus

Beres

Richter

Nagiec

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

201

177

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In recent years we have studied the relationship between strain genotypes and patient phenotypes in group A Streptococcus (GAS), a model human bacterial pathogen that causes extensive morbidity and mortality worldwide. We have concentrated our efforts on serotype M3 organisms because these strains are common causes of pharyngeal and invasive infections, produce unusually severe invasive infections, and can exhibit epidemic behavior. Our studies have been hindered by the lack of genome-scale phylogenies of multiple GAS strains and whole-genome sequences of multiple serotype M3 strains recovered from individuals with defined clinical phenotypes. To remove some of these impediments, we sequenced to closure the genome of four additional GAS strains and conducted comparative genomic resequencing of 12 contemporary serotype M3 strains representing distinct genotypes and phenotypes. Serotype M3 strains are a single phylogenetic lineage. Strains from asymptomatic throat carriers were significantly less virulent for mice than sterile-site isolates and evolved to a less virulent phenotype by multiple genetic pathways. Strain persistence or extinction between epidemics was strongly associated with presence or absence, respectively, of the prophage encoding streptococcal pyrogenic exotoxin A. A serotype M3 clone significantly underrepresented among necrotizing fasciitis cases has a unique frameshift mutation that truncates MtsR, a transcriptional regulator controlling expression of genes encoding ironacquisition proteins. Expression microarray analysis of this clone confirmed significant alteration in expression of genes encoding iron metabolism proteins. Our analysis provided unprecedented detail about the molecular anatomy of bacterial strain genotypepatient phenotype relationships.carrier ͉ epidemic ͉ genomic resequencing ͉ SNP ͉ phylogeny M icrobial epidemics have repeatedly altered the course of history by decimating human populations, killing domesticated animals, and blighting crops. Despite the impact of these destructive events, we know relatively little about the evolutionary genetic events contributing to bacterial strain emergence and diversification within and between epidemic waves. Also poorly understood is the molecular basis of intraspecies variation in disease phenotype. The recent confluence of genome sequencing and development of high-throughput techniques to interrogate genetic polymorphisms in large samples of strains now permits these topics to be studied at the individual nucleotide level.Group A Streptococcus (GAS) infects humans worldwide and causes an array of diseases ranging from superficial infections such as pharyngitis to fulminant invasive infections characterized by high morbidity and mortality (1, 2). In recent years, we have used serotype M3 GAS strains as model pathogens for studying the molecular processes contributing to clone emergence, epidemic waves, and genotype-phenotype relationships (M protein is a highly polymorphic cell-surface molecule that is antiphagocytic and forms the bas...

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“…Menos frecuentemente produce lo que se denominan infecciones invasivas definidas por la presencia de bacteriemia, neumonía o cualquier otra infección asociada con el aislamiento de EGA en un medio habitualmente estéril, incluyendo entre ellas la fascitis necrotizante y la miositis gangrenosa espontá-nea. La prevalencia de estas infecciones invasivas según estudios prospectivos poblacionales se establece entre 1-5 casos por cada 100.000 habitantes (1,2). Un tercio de ellas se complican con el llamado Síndrome de Shock Tóxico Estreptocóci-co (SSTE) definido por la presencia de una infección invasiva por Estreptococo Pyogenes asociada a shock y fallo multiorgá-nico, presentando una tasa de mortalidad que oscila entre el 30 y el 70% de los casos según las series publicadas (2,3).…”

Section: Discussionunclassified

Fallo renal agudo en varón joven con celulitis en extremidad inferior

Lorenzo¹,

Villar

2008

An. Med. Interna (Madrid)

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INTRODUCCIÓNNo existe ningún dato patognomónico de la fascitis necrotizante producida por Estreptococo del Grupo A, no obstante diferentes datos locales y sistémicos nos orientan a su diagnóstico (5,6). Quizás el síntoma más precoz sea el dolor desproporcionado a la apariencia de la infección cutánea, habitualmente secundaria a una pequeña herida o traumatismo previo. La presencia de un edema indurado extendiéndose más allá del área de eritema es otro signo local habitual, siendo infrecuente la presencia de linfangitis. La presencia de cambios cutáneos debidos a trombosis de vasos subcutáneos, suelen producirse posteriormente, yendo de una piel brillante y tensa inicialmente a purpuracea y grisácea, frecuentemente asociado a la formación de bullas rellenas de líquido serosanguinolento. Las pruebas de imagen pueden revelar un aumento de partes blandas y la presencia de gas en los tejidos sugiren una etiología diferente como infección por clostridium, celulitis anaeróbico no-clostridium o fascitis necrotizante tipo 1. Entre las manifestaciones sistémicas la fiebre es hallazgo consistente asociada a una elevada leucocitosis con desviación izquierda y la presencia de valores elevados de CPK sugieren una infección profunda de tejidos blandos, no obstante en ocasiones puede existir leucopenia. La progresión de CPK es un dato orientativo correlacionado con la progresión de la infección. Bisno y Stevens (7) establecen tres fases clíni-cas del SSTE. En la fase 1, se detectan síntomas precoces de SSTE que incluyen mialgia, escalofríos, fiebre, náuseas, vómitos y diarrea, acompañados por dolor el el sitio de trauma menor. En la fase 2, taquicardia, fiebre y taquipnea y aumento del dolor en el sitio de la infección. En la fase 3, la presencia de fiebre persistente, dolor incoercible en el lugar de la infección y evidencia de shock y fallo multiorgánico. La hipotensión está presente en el 40-50% de los pacientes en el momento del ingreso hospitalario y el resto la desarrollan en las siguientes 4-8 horas de evolución. Frecuentemente, la insuficiencia renal precede a la hipotensión, como se refleja en el presente caso clínico aportado. Presentamos un caso clínico de paciente joven que desarrolló una fascitis necrotizante fulminante por Estreptococo pyogenes, cuyo debut clínico fue un [0212-7199 (2008) RESUMENLa fascitis necrotizante producida por el Streptococo pyogenes presenta una mortalidad elevada. Habitualmente el reto supone detectar la infección antes de que el cuadro progrese al denominado síndrome de shock tóxico posestreptocócico, ya que entonces las medidas terapéuticas resultan frecuentemente ineficaces. En la secuencia de eventos en la progresion de la infección a shock es frecuente la presencia de insuficiencia renal previa a la hipotensión. Presentamos un caso clínico de un paciente de 38 años que desarrolló una fascitis necrotizante fulminante por Streptococo pyogenes cuya sintomatología al ingreso hospitalario fue la presencia de celulitis en extremidad inferior asociada a fallo renal.

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Epidemiology of Invasive Group AStreptococcusDisease in the United States, 1995–1999

Cited by 318 publications

References 55 publications

Prospective Surveillance of Invasive Group A Streptococcal Disease, Fiji, 2005–2007

Prospective Surveillance of Invasive Group A Streptococcal Disease, Fiji, 2005–2007

Molecular genetic anatomy of inter- and intraserotype variation in the human bacterial pathogen group A Streptococcus

Fallo renal agudo en varón joven con celulitis en extremidad inferior

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