The Rapid Identification of Group A Beta-Hemolytic Streptococci in the Upper Respiratory Tract: Current Status

1988 ◽  
Vol 35 (3) ◽  
pp. 535-542 ◽  
Author(s):  
Edward L. Kaplan
Keyword(s):  
Respiratory Tract ◽  
Rapid Identification ◽  
Current Status ◽  
Upper Respiratory Tract ◽  
Group A ◽  
Upper Respiratory

Significance of Quantitative Salivary Cultures for Group A and Non-group A β-Hemolytic Streptococci in Patients with Pharyngitis and in Their Family Contacts

PEDIATRICS ◽  
1979 ◽  
Vol 64 (6) ◽  
pp. 904-912
Author(s):  
Edward L. Kaplan ◽  
Robert Couser ◽  
Barbara Ballard Huwe ◽  
Carolyn Mckay ◽  
Lewis W. Wannamaker
Keyword(s):  
Antibody Response ◽  
Respiratory Tract ◽  
Group A Streptococci ◽  
Upper Respiratory Tract ◽  
C Reactive Protein ◽  
Throat Culture ◽  
Reactive Protein ◽  
Group A ◽  
Bona Fide ◽  
Upper Respiratory

One hundred ninety-six individuals, 86 with clinically overt pharyngotonsillitis and 110 of their clinically negative contacts were studied to evaluate the sensitivity and the specificity of quantitative saliva cultures for group A β-hemolytic streptococci. We also compared this technique with semiquantitative throat cultures as a means of isolating group A streptococci and of differentiating the streptococcal carrier state from patients with bona fide streptococcal upper respiratory tract infection as defmed by the presence of an antibody response. The data indicate that the throat culture is a more reliable means of identifying group A β-hemolytic streptococci in the upper respiratory tract than is the saliva culture. The converse is true for non-group A β-hemolytic streptococci; the saliva culture is a much better means for isolating these organisms. In individuals positive by both techniques we found good correlation between the degree of positivity of the saliva culture and the degree of positivity of the throat culture. Furthermore, while there was a definite trend for individuals with strongly positive cultures to demonstrate more often an antibody rise in either antistreptolysin O and/or antideoxynibonuclease B—indicating bona fide infection—this relationship was not sufficiently constant to provide a clear differentiation. This study also indicates that discordance (one positive, one negative) of simultaneous duplicate semiquantitative throat cultures is much more common among individuals who do not show an antibody response ("carriers") than among those with an antibody response (bona fide infection). This study confirms our previous observations suggesting that the presence of C-reactive protein in the serum of patients with a positive culture for group A streptococci and clinical signs and symptoms of pharyngitis is often an indication of true streptococcal upper respiratory tract infection, and that even with a positive saliva culture at the initial visit, a negative C-reactive protein is only infrequently (25%) associated with an antibody response.

scholarly journals Group A Streptococcus Infection of the Nasopharynx Requires Proinflammatory Signaling Through the Interleukin-1 Receptor

2020 ◽  
Author(s):  
Doris L. LaRock ◽  
Raedeen Russell ◽  
Anders F. Johnson ◽  
Shyra Wilde ◽  
Christopher N. LaRock
Keyword(s):  
Respiratory Tract ◽  
Proinflammatory Cytokine ◽  
Interleukin 1 ◽  
Neutrophil Migration ◽  
High Morbidity ◽  
Invasive Infection ◽  
Upper Respiratory Tract ◽  
Group A ◽  
Upper Respiratory ◽  
Strep Throat

ABSTRACTGroup A Streptococcus (GAS) is the etiologic agent of numerous high morbidity and high mortality diseases which commonly have a highly proinflammatory pathology. One factor contributing to this inflammation is the GAS protease SpeB, which directly activates the proinflammatory cytokine interleukin-1β (IL-1β), independent of the canonical inflammasome pathway. IL-1β drives neutrophil activation and recruitment that limits bacterial growth and invasion during invasive skin and soft tissue infections like necrotizing fasciitis. GAS also causes pharyngitis (strep throat), and the upper respiratory tract is its primary nidus for growth and transmission. Since the fitness selection for the species is likely primarily for this site, we examined the process of IL-1β activation in the murine nasopharynx. SpeB still activated IL-1β, which was required for neutrophil migration, but this inflammation instead increased GAS replication. Inhibiting IL-1β or depleting neutrophils, which both promote invasive infection, prevented GAS infection of the nasopharynx. Prior antibiotic exposure increased GAS growth in the murine nasopharynx, and antibiotics were sufficient to reverse the attenuation previously observed when IL-1β, neutrophils, or SpeB were not present to drive inflammation. Therefore, the same fundamental mechanism has opposing effects on virulence at different body sites. Invasive disease may be limited in part due to specific adaptations for inducing host inflammation that are beneficial for pharyngitis.IMPORTANCEOur previous reports showed that Group A Streptococcus (GAS) protease SpeB directly activates the host proinflammatory cytokine IL-1β and this restricts invasive skin infection. The upper respiratory tract is the primary site of GAS colonization and infection, but the host-pathogen interactions at this site are still largely unknown. We provide the first evidence that IL-1β-mediated inflammation promotes upper respiratory tract infection. This provides experimental evidence that the notable inflammation of strep throat, which presents with significant swelling, pain, and neutrophil influx, is not an ineffectual immune response, but rather is a GAS-directed remodeling of this niche for its pathogenic benefit.

Antibiotic Resistance: Relationship to Persistence of Group A Streptococci in the Upper Respiratory Tract

PEDIATRICS ◽  
1996 ◽  
Vol 97 (6) ◽  
pp. 971-975
Author(s):  
Michael A. Gerber
Keyword(s):  
Respiratory Tract ◽  
Upper Respiratory Tract ◽  
Beta Lactam ◽  
Erythromycin Resistance ◽  
In Vitro Susceptibility ◽  
Beta Lactam Antibiotics ◽  
Group A ◽  
Resistant Strains ◽  
Upper Respiratory

Despite the use of penicillin for more than 40 years in treating GABHS infections, there has been no significant change in the in vitro susceptibility of GABHS to penicillin. Reported failures to eradicate GABHS from the upper respiratory tracts of patients with pharyngitis and the apparent resurgence of serious Group A streptococcal infections and their sequelae probably are not related to the emergence of penicillin resistance. Although erythromycin resistance in GABHS had been a major problem in Japan and continues to be a major problem in Finland, it has not been a problem in this country. The susceptibility of GABHS to the newer macrolide antibiotics appears to be similar to that of erythromycin. Comprehensive, community-wide programs to continuously monitor for erythromycin resistance in GABHS would be difficult to justify. However, because little is known about how erythromycin resistance in GABHS is acquired or spread, it would be reasonable to periodically monitor isolates of GABHS for erythromycin resistance. A substantial proportion of GABHS are currently resistant to tetracyclines and these agents are inappropriate for treating GABHS infections. Although little recent information is available about the susceptibility of GABHS to sulfonamides, these agents have been shown to be ineffective in eradicating GABHS from the upper respiratory tract regardless of the in vitro sensitivities. GABHS have not been shown to be resistant to any of the commonly used oral cephalosporins; however, there is a great deal of variability among these agents in their activity against GABHS. Clindamycin resistance in GABHS has remained unusual. This agent is an alternative for treating GABHS infections due to macrolide-resistant strains in patients who cannot be treated with beta-lactam antibiotics. There is no reason, based on the in vitro susceptibilities of GABHS, to change the current recommendations for treating GABHS infections with penicillin and for using erythromycin for patients who are allergic to penicillin.

Comparison of Erythromycin Ethyl Succinate, Stearate and Estolate Treatments of Group A Streptococcal Infections of the Upper Respiratory Tract

1975 ◽  
Vol 14 (12) ◽  
pp. 1098-1110 ◽  
Author(s):  
R. S. Janicki ◽  
J. C. Garnham ◽  
M. C. Worland ◽  
W. E. Grundy ◽  
J. R. Thomas
Keyword(s):  
Respiratory Tract ◽  
Oral Treatment ◽  
Upper Respiratory Tract ◽  
Streptococcal Infections ◽  
Acute Group ◽  
Clinical Responses ◽  
Group A ◽  
Upper Respiratory ◽  
Initiation Of Therapy

The microbiologic and clinical responses of acute Group A beta-hemolytic streptococcal infections of the upper respiratory tract to oral treatment with erythromycin ethyl succinate, stearate, and estolate were studied in 303 patients. Streptococcal M and T typing was done on all positive cultures. The overall cure rate was 95.4 per cent, with no statistically significant differences in clearing organisms from the pharynx. Of the 285 cured patients who completed the prescribed follow-up period, 11 had recurrences between the 12th and 31st day after initiation of therapy, and five developed new infections. No cases of rheumatic fever or glomerulonephritis were encountered during a follow-up study. Eight gastrointestinal reactions and one transient rash occurred. Results with these forms of erythromycin compare favorably with published results for similar infections treated with oral penicillins.

scholarly journals The 4.5S RNA component of the signal recognition particle is required for group A Streptococcus virulence

Microbiology ◽  
2010 ◽  
Vol 156 (5) ◽  
pp. 1342-1350 ◽  
Author(s):  
Jeanette Treviño ◽  
Nataly Perez ◽  
Paul Sumby
Keyword(s):  
Respiratory Tract ◽  
Signal Recognition Particle ◽  
Infection Model ◽  
Signal Recognition ◽  
Upper Respiratory Tract ◽  
Streptolysin O ◽  
Group A ◽  
Upper Respiratory ◽  
Tract Infections ◽  
4.5S Rna

The signal recognition particle (SRP) is a ribonucleoprotein complex that targets proteins for secretion in a co-translational manner. While originally thought to be essential in all bacteria, recent data show that the SRP is dispensable in at least some streptococcal species. The SRP from the human pathogen group A Streptococcus (GAS, Streptococcus pyogenes) is predicted to be composed of protein Ffh and 4.5S RNA. Deletion of ffh alters the secretion of several GAS proteins, and leads to a severe reduction in virulence. Here, we report that mutation of the gene encoding 4.5S RNA results in phenotypes both similar to and distinct from that observed following ffh mutation. Similarities include a reduction in secretion of the haemolysin streptolysin O, and attenuation of virulence as assessed by a murine soft tissue infection model. Differences include a reduction in transcript levels for the genes encoding streptolysin O and NAD-glycohydrolase, and the reduced secretion of the SpeB protease. Several differences in transcript abundance between the parental and mutant strain were shown to be dependent on the sensor-kinase-encoding gene covS. Using growth in human saliva as an ex vivo model of upper respiratory tract infection we identified that 4.5S RNA mutation leads to a 10-fold reduction in colony-forming units over time, consistent with the 4.5S RNA contributing to GAS growth and persistence during upper respiratory tract infections. Finally, we determined that the 4.5S RNA was essential for GAS to cause lethal infections in a murine bacteraemia model of infection. The data presented extend our knowledge of the contribution of the SRP to the virulence of an important Gram-positive pathogen.

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