Infecciones por estreptococos del grupo S. anginosus en pediatría / S. anginosus group streptococcal infections in children

Los estreptococos del grupo Streptococcus anginosus (EGA), también llamados "Streptococcus milleri", fueron reconocidos como parte de los estreptococos del grupo viridans (EGV) desde principios del siglo XX. Su rol como patógenos humanos, sin embargo comenzó a destacarse recién en la década de 1970. En esta actualización se describen aspectos microbiológicos y clínicos de los EGA. Los métodos fenotípicos de identificacón e incluso algunos genotípicos carecen de precisión para reconocer las tres especies del grupo (Streptococcus anginosus, Streptococcus constellatus y Streptococcus intermedius) e incluso pueden fallar en su clasificación a nivel de grupo. La mayoría de ellos son sensibles a los antibióticos beta-lactámicos pero son considerables los porcentajes de resistencia a macrólidos, lincosamidas y tetraciclinas. Los EGA son colonizantes habituales de las mucosas orofaríngea, intestinal y genitourinaria, pero, cada vez más frecuentemente, son reconocidos como patógenos humanos. Es ampliamente conocida su capacidad de formar abscesos en órganos sólidos, especialmente abscesos cerebrales, pulmonares y hepáticos. También producen sinusitis, empiemas y colecciones en piel y tejidos blandos, hueso, articulaciones, etc. Se han encontrado asociados con exacerbaciones pulmonares en pacientes con fibrosis quística y con enfermedad pulmonar obstructiva crónica. Producen también infecciones posteriores a mordeduras humanas, infecciones diseminadas, bacteriemia sin foco aparente y, en menor medida, endocarditis infecciosa (AU)

Streptococci from the Streptococcus anginosus group (SAG), also termed "Streptococcus milleri", were recognized as members of the viridans group streptococci (VGS) in the early 20th century. Nevertheless, their role as human pathogens only became evident in the 1970s. In this update, microbiological and clinical aspects of the SAG are described. Phenotypic and even some genotypic identification methods lack accuracy in recognizing the three species of the group (Streptococcus anginosus, Streptococcus constellatus, and Streptococcus intermedius) and may fail to classify them at the group level. Most of them are sensitive to beta-lactam antibiotics but rates of resistance to macrolides, lincosamides, and tetracyclines are significant. SAGs are common colonizers of the oropharyngeal, intestinal, and genitourinary mucosa, but are increasingly recognized as human pathogens. Their ability to form abscesses in solid organs, especially brain, lung and liver, is widely known. They may produce sinusitis, empyemas, and collections in skin and soft tissues, bone, joints, etc. They have also been associated with pulmonary exacerbations in patients with cystic fibrosis and chronic obstructive pulmonary disease. In addition, they may cause infections following human bites, disseminated infections, bacteremia without apparent focus, and, to a lesser extent, infective endocarditis (AU)

Host cytokine responses distinguish invasive from airway isolates of the Streptococcus milleri/anginosis group.

BACKGROUND: The Streptococcus Milleri/Anginosus Group (SMG) colonize mucosal surfaces, especially the airways, and are considered to be normal mucosal microbiota; however, they are a major cause of abscesses, pneumonia and pleural empyema. The production of exoenzymes and virulence factors do not correlate with SMG pathogenicity. Since SMG infections are associated with robust inflammatory responses, we hypothesized that host immune responses might distinguish strains associated with asymptomatic carriage and those associated with fulminant disease. METHODS: We measured IL1ß, TNF, IL10, IL12, IL23, IL17, and IL4 production from human peripheral blood mononuclear cells (PBMCs) stimulated with a panel of clinical isolates from the airways and infections and measured the ability of these isolates to stimulate TLR2. RESULTS: Isolates were categorized based on the levels of cytokines they induced from PBMCs (high, intermediate, low). Airway isolates predominantly induced low levels of cytokines and isolates from invasive disease induced higher levels, although about 10% of the strains produced divergent cytokine responses between donors. Interestingly, the donors were most divergent in their production of IL17, IL12 and IL23. CONCLUSIONS: We propose that the ability to inhibit or avoid an inflammatory response is associated with carriage in the airways and variability in responses between isolates and donors might contribute to susceptibility to disease.

The Streptococcus milleri population of a cystic fibrosis clinic reveals patient specificity and intraspecies diversity.

The genetic relatedness of Streptococcus milleri group isolates from the airways of cystic fibrosis patients was determined by using pulsed-field gel electrophoresis. This study reveals no evidence for patient-to-patient transmission in our patient population; however, within individual patients, complex inter- and intraspecies diversity and dynamics can be observed.

Characterization of Streptococcus milleri group isolates from expectorated sputum of adult patients with cystic fibrosis.

With the recent insights into the Streptococcus milleri group (SMG) as pulmonary pathogens in patients with cystic fibrosis (CF), we sought to characterize 128 isolates from the sputum of adults with CF, along with 45 isolates from patients with invasive diseases for comparison. The tests performed included Lancefield grouping; tests for hemolysis; tests for the production of hyaluronidase, chondroitin sulfatase, DNase, proteases, and hydrogen peroxide; and PCR for the detection of the intermedilysin gene (ily). We also generated biochemical profiles with the Rapid ID Strep 32 API system and tested cell-free supernatants for the presence of the signal molecule autoinducer-2 (AI-2) using a Vibrio harveyi bioassay with a subset of CF strains. The S. intermedius isolates from both strain collections were similar, while the S. constellatus and S. anginosus isolates yielded several biotypes that differed in prevalence between the two strain collections. Beta-hemolytic, Lancefield group C S. constellatus comprised 74.4% of the S. constellatus isolates from patients with CF but only 13.3% of the corresponding isolates from patients with invasive infections. This was the only S. constellatus biotype associated with pulmonary exacerbations. Hyaluronidase-positive S. anginosus was detected only among the isolates from patients with CF. Strain-to-strain variability in AI-2 expression was evident, with the mean values being the highest for S. anginosus, followed by S. constellatus and then S. intermedius. Cluster analysis and 16S rRNA sequencing revealed that the species of SMG could be accurately determined with a minimum of three phenotypic tests: tests for the Lancefield group, hyaluronidase production, and chondroitin sulfatase production. Furthermore, isolates from patients with invasive infections clustered with isolates from the sputum of patients with CF, suggesting that the respiratory tract isolates were equally pathogenic.

Species-level molecular identification of invasive "Streptococcus milleri" group clinical isolates by nucleic acid sequencing in a centralized regional microbiology laboratory.

Organisms belonging to the "Streptococcus milleri" group are important invasive human pathogens. A detailed understanding of their pathogenesis in human infection has only recently been facilitated by the use of molecular methods to study this group of organisms.