Group C and group G streptococcal infection

INTRODUCTION

Streptococcal infections are extremely common despite the overall susceptibility of these organisms to antibiotics, especially penicillin. While infections caused by the Lancefield group A streptococcus (GAS or Streptococcus pyogenes) have dominated the streptococcal medical literature, Lancefield groups C and G share many microbiologic and clinical characteristics with GAS [1]. (See related topic reviews on GAS).

Work in the early 20th century described S. pyogenes as an exclusively human pathogen and detailed the frequency of carriers and the most characteristic infections [2]. The pioneering work of Rebecca Lancefield led to the identification of a number of groups of streptococci including A, C and G, producing hemolysis on sheep blood agar, exhibiting different biochemical properties and isolated from a variety of animal species [3]. Classification methods based upon the Lancefield methodology were established soon thereafter [4].

Among this diverse group, the group C and group G streptococci have assumed more important clinical roles. For a number of reasons, they can be considered together, separate from other members of the genus Streptococcus. Although less extensively studied, groups C and G streptococci are now appreciated to produce infections quite similar to GAS although they more commonly cause opportunistic and nosocomial infections than GAS.

  • They are widely distributed in the animal kingdom and are also part of the normal human flora.
  • The microbiology is similar to GAS; they are primarily large colony, beta-hemolytic, and produce pyogenic and inflammatory reactions. On plates, colonies often resemble S. pyogenes, especially when susceptible to bacitracin.
  • They cause isolated exudative or common source epidemic pharyngitis and cellulitis indistinguishable clinically from GAS disease.
  • Some strains contain fibrinolysins and streptolysins and infections can stimulate antistreptolysin O titers (ASO), similar to S. pyogenes.

MICROBIOLOGY

Groups C and G streptococci are typical chaining cocci that are Gram positive, facultative anaerobes which produce small or large colonies on sheep blood agar. They are usually, but not exclusively, beta hemolytic. Unlike GAS, which are inhibited by 0.04 units/mL of bacitracin, the group C and G isolates are extremely variable in their bacitracin sensitivity, ranging from as few as 6 to 8 percent [5] to as many as 30 to 67 percent [6]. This variability should discourage the use of bacitracin as a screening step.

                 

Subscribers log in here

To continue reading this article you must have access through your hospital or your group practice, log in to your personal subscription, or purchase a personal subscription. For more information, click below.
Literature review current through: Apr 2013. | This topic last updated: May 25, 2010.
The content on the UpToDate website is not intended nor recommended as a substitute for medical advice, diagnosis, or treatment. Always seek the advice of your own physician or other qualified health care professional regarding any medical questions or conditions. The use of this website is governed by the UpToDate Terms of Use ©2013 UpToDate, Inc.
References
Top
  1. Broyles LN, Van Beneden C, Beall B, et al. Population-based study of invasive disease due to beta-hemolytic streptococci of groups other than A and B. Clin Infect Dis 2009; 48:706.
  2. Rammelkamp CH Jr. Epidemiology of streptococcal infections. Harvey Lect 1955- 1956; 51:113.
  3. Lancefield RC. A SEROLOGICAL DIFFERENTIATION OF HUMAN AND OTHER GROUPS OF HEMOLYTIC STREPTOCOCCI. J Exp Med 1933; 57:571.
  4. Sherman JM. THE STREPTOCOCCI. Bacteriol Rev 1937; 1:3.
  5. Pollock HM, Dahlgren BJ. Distribution of streptococcal groups in clinical specimens with evaluation of bacitracin screening. Appl Microbiol 1974; 27:141.
  6. Stoner RA. Bacitracin and coagglutination for grouping of beta-hemolytic streptococci. J Clin Microbiol 1978; 7:463.
  7. Facklam, RR, Washington, JA II. Streptococcus and related catalase-negative gram- positive cocci. In: Manual of Clinical Microbiology, 5th ed, Ballows, A, Hausler, WJ Jr, Hermann, KL et al (Eds), American Society for Microbiology, Washington, DC, 1991, p. 238.
  8. Freney J, Bland S, Etienne J, et al. Description and evaluation of the semiautomated 4-hour rapid ID 32 Strep method for identification of streptococci and members of related genera. J Clin Microbiol 1992; 30:2657.
  9. Kirby R, Ruoff KL. Cost-effective, clinically relevant method for rapid identification of beta-hemolytic streptococci and enterococci. J Clin Microbiol 1995; 33:1154.
  10. Vandamme P, Pot B, Falsen E, et al. Taxonomic study of lancefield streptococcal groups C, G, and L (Streptococcus dysgalactiae) and proposal of S. dysgalactiae subsp. equisimilis subsp. nov. Int J Syst Bacteriol 1996; 46:774.
  11. Kaufhold A, Ferrieri P. The microbiologic aspects, including diagnosis, of beta-hemolytic streptococcal and enterococcal infections. Infect Dis Clin North Am 1993; 7:235.
  12. Humar D, Datta V, Bast DJ, et al. Streptolysin S and necrotising infections produced by group G streptococcus. Lancet 2002; 359:124.
  13. Brandt CM, Spellerberg B. Human infections due to Streptococcus dysgalactiae subspecies equisimilis. Clin Infect Dis 2009; 49:766.
  14. Brandt CM, Haase G, Schnitzler N, et al. Characterization of blood culture isolates of Streptococcus dysgalactiae subsp. equisimilis possessing Lancefield's group A antigen. J Clin Microbiol 1999; 37:4194.
  15. Davies MR, McMillan DJ, Beiko RG, et al. Virulence profiling of Streptococcus dysgalactiae subspecies equisimilis isolated from infected humans reveals 2 distinct genetic lineages that do not segregate with their phenotypes or propensity to cause diseases. Clin Infect Dis 2007; 44:1442.
  16. Gerber MA, Randolph MF, Martin NJ, et al. Community-wide outbreak of group G streptococcal pharyngitis. Pediatrics 1991; 87:598.
  17. Turner JC, Hayden FG, Lobo MC, et al. Epidemiologic evidence for Lancefield group C beta-hemolytic streptococci as a cause of exudative pharyngitis in college students. J Clin Microbiol 1997; 35:1.
  18. Barnham M, Thornton TJ, Lange K. Nephritis caused by Streptococcus zooepidemicus (Lancefield group C). Lancet 1983; 1:945.
  19. Gnann JW Jr, Gray BM, Griffin FM Jr, Dismukes WE. Acute glomerulonephritis following group G streptococcal infection. J Infect Dis 1987; 156:411.
  20. Schnitzler N, Podbielski A, Baumgarten G, et al. M or M-like protein gene polymorphisms in human group G streptococci. J Clin Microbiol 1995; 33:356.
  21. Sriprakash KS, Hartas J. Lateral genetic transfers between group A and G streptococci for M-like genes are ongoing. Microb Pathog 1996; 20:275.
  22. Bradley SF, Gordon JJ, Baumgartner DD, et al. Group C streptococcal bacteremia: analysis of 88 cases. Rev Infect Dis 1991; 13:270.
  23. Hare, R. Sources of hemolytic streptococcal infections of wounds in war and in civil life. Lancet 1940; 1:109.
  24. Rolston KV. Group G streptococcal infections. Arch Intern Med 1986; 146:857.
  25. Gossling J. Occurrence and pathogenicity of the Streptococcus milleri group. Rev Infect Dis 1988; 10:257.
  26. Vartian C, Lerner PI, Shlaes DM, Gopalakrishna KV. Infections due to Lancefield group G streptococci. Medicine (Baltimore) 1985; 64:75.
  27. Skogberg K, Simonen H, Renkonen OV, Valtonen VV. Beta-haemolytic group A, B, C and G streptococcal septicaemia: a clinical study. Scand J Infect Dis 1988; 20:119.
  28. Rantz, LA, Kirby, WMM. Hemolytic streptococcus bacteremia. N Engl J Med 1942; 227:730.
  29. Feingold DS, Stagg NL, Kunz LJ. Extrarespiratory streptococcal infections. Importance of the various serologic groups. N Engl J Med 1966; 275:356.
  30. Duma, RJ, Weinberg, AN, Medrek, JF, Kunz, LJ. Streptococcal Infections. Medicine 1969; 48:87.
  31. Salata RA, Lerner PI, Shlaes DM, et al. Infections due to Lancefield group C streptococci. Medicine (Baltimore) 1989; 68:225.
  32. Sylvetsky N, Raveh D, Schlesinger Y, et al. Bacteremia due to beta-hemolytic Streptococcus group G: increasing incidence and clinical characteristics of patients. Am J Med 2002; 112:622.
  33. Hill HR, Caldwell GG, Wilson E, et al. Epidemic of pharyngitis due to streptococci of Lancefield group G. Lancet 1969; 2:371.
  34. Cohen D, Ferne M, Rouach T, Bergner-Rabinowitz S. Food-borne outbreak of group G streptococcal sore throat in an Israeli military base. Epidemiol Infect 1987; 99:249.
  35. Turner JC, Fox A, Fox K, et al. Role of group C beta-hemolytic streptococci in pharyngitis: epidemiologic study of clinical features associated with isolation of group C streptococci. J Clin Microbiol 1993; 31:808.
  36. Bert F, Bariou-Lancelin M, Lambert-Zechovsky N. Clinical significance of bacteremia involving the "Streptococcus milleri" group: 51 cases and review. Clin Infect Dis 1998; 27:385.
  37. Smyth EG, Pallett AP, Davidson RN. Group G streptococcal endocarditis: two case reports, a review of the literature and recommendations for treatment. J Infect 1988; 16:169.
  38. McCue JD. Group G streptococcal pharyngitis. Analysis of an outbreak at a college. JAMA 1982; 248:1333.
  39. Liu CE, Jang TN, Wang FD, et al. Invasive group G streptococcal infections: a review of 37 cases. Zhonghua Yi Xue Za Zhi (Taipei) 1995; 56:173.
  40. Cohen-Poradosu R, Jaffe J, Lavi D, et al. Group G streptococcal bacteremia in Jerusalem. Emerg Infect Dis 2004; 10:1455.
  41. Eriksson BK. Anal colonization of group G beta-hemolytic streptococci in relapsing erysipelas of the lower extremity. Clin Infect Dis 1999; 29:1319.
  42. Schattner A, Vosti KL. Bacterial arthritis due to beta-hemolytic streptococci of serogroups A, B, C, F, and G. Analysis of 23 cases and a review of the literature. Medicine (Baltimore) 1998; 77:122.
  43. Ike RW. Septic arthritis due to group C streptococcus: report and review of the literature. J Rheumatol 1990; 17:1230.
  44. Gaunt PN, Seal DV. Group G streptococcal infection of joints and joint prostheses. J Infect 1986; 13:115.
  45. Burkert T, Watanakunakorn C. Group G streptococcus septic arthritis and osteomyelitis: report and literature review. J Rheumatol 1991; 18:904.
  46. Nielsen SV, Kolmos HJ. Bacteraemia due to different groups of beta-haemolytic streptococci: a two-year survey and presentation of a case of recurring infection due to Streptococcus "equisimilis". Infection 1993; 21:358.
  47. Bisno AL, Gaviria JM. Murine model of recurrent group G streptococcal cellulitis: no evidence of protective immunity. Infect Immun 1997; 65:4926.
  48. Stein DS, Panwalker AP. Group C streptococcal endocarditis: case report and review of the literature. Infection 1985; 13:282.
  49. Sandre RM, Shafran SD. Infective endocarditis: review of 135 cases over 9 years. Clin Infect Dis 1996; 22:276.
  50. Baddour LM. Infective endocarditis caused by beta-hemolytic streptococci. The Infectious Diseases Society of America's Emerging Infections Network. Clin Infect Dis 1998; 26:66.
  51. Raizes EG, Livingston MB, Farrar WE. Fatal cardiac tamponade in a young man with group C streptococcal endocarditis. Am J Med Sci 1987; 294:353.
  52. Pollack BD, Belkin RN, Rubin DA, Moggio RA. Aortic annular abscess complicating prosthetic valve endocarditis with group G streptococcus: detection during life with transesophageal echocardiography. J Heart Valve Dis 1993; 2:558.
  53. Dolinski SY, Jones PG, Zabransky RJ, Rasansky M. Group C streptococcal pleurisy and pneumonia: a fulminant case and review of the literature. Infection 1990; 18:239.
  54. Keiser P, Campbell W. 'Toxic strep syndrome' associated with group C Streptococcus. Arch Intern Med 1992; 152:882, 884.
  55. Wagner JG, Schlievert PM, Assimacopoulos AP, et al. Acute group G streptococcal myositis associated with streptococcal toxic shock syndrome: case report and review. Clin Infect Dis 1996; 23:1159.
  56. Maniglia RJ, Roth T, Blumberg EA. Polymicrobial brain abscess in a patient infected with human immunodeficiency virus. Clin Infect Dis 1997; 24:449.
  57. Ruoff KL, Kunz LJ, Ferraro MJ. Occurrence of Streptococcus milleri among beta-hemolytic streptococci isolated from clinical specimens. J Clin Microbiol 1985; 22:149.
  58. Wong CA, Donald F, Macfarlane JT. Streptococcus milleri pulmonary disease: a review and clinical description of 25 patients. Thorax 1995; 50:1093.
  59. Ahmed RA, Marrie TJ, Huang JQ. Thoracic empyema in patients with community-acquired pneumonia. Am J Med 2006; 119:877.
  60. Gerber MA, Baltimore RS, Eaton CB, et al. Prevention of rheumatic fever and diagnosis and treatment of acute Streptococcal pharyngitis: a scientific statement from the American Heart Association Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee of the Council on Cardiovascular Disease in the Young, the Interdisciplinary Council on Functional Genomics and Translational Biology, and the Interdisciplinary Council on Quality of Care and Outcomes Research: endorsed by the American Academy of Pediatrics. Circulation 2009; 119:1541.
  61. Petersen K, Phillips RS, Soukup J, et al. The effect of erythromycin on resolution of symptoms among adults with pharyngitis not caused by group A streptococcus. J Gen Intern Med 1997; 12:95.
  62. Carroll KC, Monroe P, Cohen S, et al. Susceptibility of beta-hemolytic streptococci to nine antimicrobial agents among four medical centers in Salt Lake City, Utah, USA. Diagn Microbiol Infect Dis 1997; 27:123.
  63. Seppälä H, Klaukka T, Vuopio-Varkila J, et al. The effect of changes in the consumption of macrolide antibiotics on erythromycin resistance in group A streptococci in Finland. Finnish Study Group for Antimicrobial Resistance. N Engl J Med 1997; 337:441.
  64. Jacobs JA, de Krom MC, Kellens JT, Stobberingh EE. Meningitis and sepsis due to group G streptococcus. Eur J Clin Microbiol Infect Dis 1993; 12:224.