Streptococcus pyogenes: Difference between revisions
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Streptococcus pyogenes
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== Classification of Invasive Disease == |
== Classification of Invasive Disease == |
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* As per the Public Health Agency of Canada [https://www.canada.ca/en/public-health/services/diseases/group-a-streptococcal-diseases/health-professionals/national-case-definition.html National case definition: Invasive group A streptococcal disease] |
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=== Confirmed case === |
=== Confirmed case === |
Revision as of 01:19, 12 September 2019
- Also commonly referred to as Group A Streptococcus
Microbiology
- Gram-positive coccus, typically in short chains
- Non-motile, non–spore forming, catalase-negative, and facultatively anaerobic
- β hemolytic on blood agar (complete hemolysis)
Pathophysiology
Virulence factors
- Capsular hyaluronic acid is similar to human
- M protein is the main factor imparting virulence
- M protein differences given S. pyogenes its serotypes
- Confers resistance to phagocytosis by modulating host immune response
Clinical Presentation
- Skin and soft tissue infections, including necrotizing fasciitis
- Upper and lower respiratory tract infections
- Bacteremia without a focus
- Septic arthritis and osteomyelitis
- Pelvic infections, including postpartum endometritis
- Many other foci
Classification of Invasive Disease
- As per the Public Health Agency of Canada National case definition: Invasive group A streptococcal disease
Confirmed case
- Laboratory confirmation of infection with or without clinical evidence of invasive disease, requiring isolation of group A streptococcus (Streptococcus pyogenes) from a normally sterile site
- Blood, CSF, pleural fluid, pericardial fluid, peritoneal fluid, deep tissue specimen taken during surgery (e.g. muscle collected during debridement for necrotizing fasciitis), bone or joint fluid excluding the middle ear and superficial wound aspirates (e.g. skin and soft tissue abscesses).
Probable case
- Clinical evidence of invasive disease in the absence of another identified aetiology and with non-confirmatory laboratory evidence of infection:
- Isolation of group A streptococcus from a non-sterile site
- or
- Positive group A streptococcus antigen detection
Clinical evidence
- Streptococcal toxic shock syndrome, which is characterized by hypotension (systolic blood pressure ≤ 90 mm Hg in an adult and < 5 percentile for age for children) and at least two of the following signs:
- Renal impairment (creatinine level ≥ 177 μmol/L for adults)
- Coagulopathy (platelet count ≤ 100,000/mm3 or disseminated intravascular coagulation)
- Liver function abnormality (SGOT, SGPT, or total bilirubin ≥ 2x upper limit of normal)
- Adult respiratory distress syndrome
- Generalized erythematous macular rash that may desquamate
- Soft-tissue necrosis, including necrotizing fasciitis, myositis or gangrene
- Meningitis
Prognosis
- Highest risk of streptococcal toxic shock syndrome (TSS) or death
- Necrotizing fasciitis (50% and 50%)
- Pneumonia (30% and 30%)
- Bacteremia (15% and 25%)
References
- ^ Athanasios G. Michos, Chrysanthi G. Bakoula, Maria Braoudaki, Foteini I. Koutouzi, Eleftheria S. Roma, Anastasia Pangalis, Georgia Nikolopoulou, Elena Kirikou, Vassiliki P. Syriopoulou. Macrolide resistance in Streptococcus pyogenes: prevalence, resistance determinants, and emm types. Diagnostic Microbiology and Infectious Disease. 2009;64(3):295-299. doi:10.1016/j.diagmicrobio.2009.03.004.
- ^ Walter H. Traub, Birgit Leonhard. Comparative Susceptibility of Clinical Group A, B, C, F, and G β-Hemolytic Streptococcal Isolates to 24 Antimicrobial Drugs. Chemotherapy. 1997;43(1):10-20. doi:10.1159/000239529.
- a b Matthias Imöhl, Mark van der Linden. Jose Melo-Cristino. Antimicrobial Susceptibility of Invasive Streptococcus pyogenes Isolates in Germany during 2003-2013. PLOS ONE. 2015;10(9):e0137313. doi:10.1371/journal.pone.0137313.
- ^ A. C. Bowen, R. A. Lilliebridge, S. Y. C. Tong, R. W. Baird, P. Ward, M. I. McDonald, B. J. Currie, J. R. Carapetis. Is Streptococcus pyogenes Resistant or Susceptible to Trimethoprim-Sulfamethoxazole?. Journal of Clinical Microbiology. 2012;50(12):4067-4072. doi:10.1128/jcm.02195-12.