Streptococcus pyogenes, a group A Streptococcus (GAS) species, is the most important human pathogen within the Streptococcus genus. The most common diseases caused by S. pyogenes are pharyngitis and skin conditions, with possible sequelae of poststreptococcal glomerulonephritis and acute rheumatic fever. Streptococci also have the ability to invade tissues and cause bacteremia. Recently an increase in Streptococcus group B infections has been observed.
Presentation
Many species belong to the Streptococcus genus, which are Gram-positive, nonmotile cocci. They can be classified according to more than one scheme [1]. Their hemolytic capabilities on sheep blood agar define their division into three groups (β-, α-, and γ-hemolytic streptococci). Further classification subdivides these groups according to cell wall carbohydrate antigens into A, B, C, and other groups. The most important representative is S. pyogenes, which is a group A (beta-hemolytic) streptococcus (GABHS).
S. pyogenes causes a variety of diseases, the most common being pharyngitis and skin infections. The manifestations of pharyngitis are variable, from mild discomfort at swallowing to exudative pharyngitis with high fever [2]. In addition to throat pain, the manifestations may include chills, headache, and, in young children, abdominal pain, and vomiting. The possibility of local suppurative complications, such as peritonsillar abscess, should be checked if there is an intense pain [2]. Rarely, the pharyngitis is associated with scarlet fever.
Scarlet fever used to be a serious complication of streptococcal pharyngitis, but with the use of antibiotics, it is not considered an important threat today. However, serious conditions can develop following streptococcal infections. One is acute poststreptococcal glomerulonephritis [3], which presents with edema, hypertension, hematuria, and other urinary abnormalities. The disease is on the decline. Another sequel is rheumatic fever, an autoimmune disease initiated by S. pyogenes but dependent on the host’s immune responses. The development of the disease is associated with certain serotypes of the M protein, a cell wall component of S. pyogenes. Rheumatic fever can present as an inflammation of the joints, heart, central nervous system, or skin [3]. A large proportion of acquired heart disease cases in children originates from rheumatic fever [4]. Neuropsychiatric disorders can also follow streptococcal infections.
Superficial manifestations of streptococcal infection, other than pharyngitis, are skin conditions, such as impetigo, and erysipelas.
The most serious consequences of streptococcal infections stem from their ability to cause invasive diseases. These include sepsis, bacteremic pneumonia, necrotizing fasciitis and streptococcal toxic shock syndrome. Most of the mortality from streptococcal infections is associated with invasive disease and rheumatic fever [5]. The characteristics of an invasive streptococcal disease include systemic toxicity, hypotension, shock, multiple organ failure, rapid necrosis, and gangrene [3]. Several bacterial factors (for example pyrogenic exotoxins and nucleases) are thought to contribute to the pathogenesis of an invasive disease. [3].
Group B Streptococcus infections, caused by Streptococcus agalactiae, were thought to occur mainly in women after childbirth and in newborn babies. However, recently, the infection has appeared in nonpregnant adults, usually associated with comorbidities.
Workup
Early diagnosis of streptococcal infections is important not just for the treatment of the acute disease, but also to prevent complications [6], such as rheumatic fever [7]. Therefore, while culture is regarded as the most reliable method for the identification of Streptococcus species [3], decisions regarding treatment sometimes have to be made before the results are available because of the time required for growth of the bacterial cultures [7].
Several quick assays have been developed based on the immunological detection of the group-specific cell wall carbohydrate of GAS organisms. These assays use latex agglutination, enzyme immunoassay, and optical immunoassay; DNA is detected by PCR methods and chemiluminescent DNA probes [8]. These methods are very specific, but of variable sensitivity, although this has been reported to be high in some assays [6] [7] [8] [9]. Recommendations by the Infectious Diseases Society of America advocate the use of rapid antigen detection tests and/or cultures for the diagnosis of streptococcal pharyngitis, with negative immunological tests to be followed up by culturing the organism in populations at high risk for acute rheumatic fever (children and adolescents) [10].
Assaying for antistreptococcal antibodies in serum is most valuable for the diagnosis of rheumatic fever and other poststreptococcal diseases. In cases of necrotizing fasciitis, a frozen section biopsy can be used to identify or confirm the presence of the organism.
Treatment
Prognosis
Etiology
Epidemiology
Pathophysiology
Prevention
References
- Hamada S, Kawabata S, Nakagawa I. Molecular and genomic characterization of pathogenic traits of group A Streptococcus pyogenes. Proc Jpn Acad Ser B Phys Biol Sci. 2015;91(10):539-559.
- Wessels MR. Streptococcal pharyngitis. N Engl J Med.2011;364(7):648-655.
- Cunningham MW. Pathogenesis of group A streptococcal infections. Clin Microbiol Rev. 2000;13(3):470-511.
- Pavone P, Parano E, Rizzo R, Trifiletti RR. Autoimmune neuropsychiatric disorders associated with streptococcal infection: Sydenham chorea, PANDAS, and PANDAS variants. J Child Neurol. 2006;21(9):727-736.
- O’Loughlin RE, Roberson A, Cieslak PR, et al. The epidemiology of invasive group A streptococcal infection and potential vaccine implications: United States, 2000-2004. Clin Infect Dis. 2007;45(7):853-862
- Smith JM, Bauman MC, Fuchs PC. An OIA for the direct detection of group A strep antigen. Lab. Med. 1995;26: 408–410.
- Orda U, Gunnarsson R, Orda S, Fitzgerald M, Rofe G, Dargan A. Etiologic predictive value of a rapid immunoassay for the detection of group A Streptococcus antigen from throat swabs in patients presenting with a sore throat. Int J Infect Dis. 2016;45:32-35.
- Leung AK, Newman R, Kumar A, Davies HD. Rapid antigen detection testing in diagnosing group A beta-hemolytic streptococcal pharyngitis. Expert Rev Mol Diagn. 2006 Sep;6(5):761-766.
- Lasseter GM, McNulty CAM, Hobbs FDR, Mant D, Little P. In vitro evaluation of five rapid antigen detection tests for group A beta-haemolytic streptococcal sore throat infections. Family Practice. 2009; 26: 437–444.
- Shulman ST, Bisno AL, Clegg HW, et al. Clinical practice guideline for the diagnosis and management of group a streptococcal pharyngitis: 2012 update by the Infectious Diseases Society of America. Clin Infect Dis. 2012;55(10):e86-e102.