JOURNAL OF THE LOUISIANA STATE MEDICAL SOCIETY
CLINICAL PRESENTATION
5. Lancefield RC and Hare R. The serological differentiation of pathogenic and non-pathogenic streptococci from parturient women. J Exp Med 1935; 61: 335-349 as read in Smyth EG, Pallett AP, and Davidson RN. Group G Streptococcal endocarditis: two case reports, a review of the literature and recommendations for treatment. J Infect Dis . 1988 16:169-176. 6. Bennett, JE, Dolin, R, and Blaser, MJ. Viridans Streptococci and Groups C and G Streptococci. Mandell, Douglas and Bennett’s Principles and Practice of Infectious Diseases. 8th edition 2173-2177. 7. Farrow, J. A. E., and M. D. Collins. 1984. Taxonomic studies on streptococci of serological groups C, G, and L, and possibly related taxa. Sys Appl Microbiol. 5:483–493. 8. Kilpper-Balz, R., and K. H. Schleifer. 1984. Nucleic acid hybridization and cell wall composition studies of pyogenic streptococci. FEMS Microbiol. Lett. 24:355–364 9. Facklam, R. What happened to the streptococci: overview of the taxonomic and nomenclature changes. Clin Microbiol Rev. 2002; 15: 613-30. 10. Lo HH, Cheng WS. Distribution of virulence factors and association with emm polymorphism or isolation site among beta-hemolytic group G Streptococcus dysgalactiae subspecies equisimilis. APMIS. 2015 Jan; 123(1):45-52. doi: 10.1111/apm.12305. 11. Liao CH, Liu LC, Huang YT, Teng LJ, Hsueh PR. Bacteremia caused by group G Streptococci, Taiwan. Emerg Infect Dis. 2008 May; 14(5):837-40. doi: 10.3201/eid1405.070130. 12. Brandt CM, Spellerberg B. Human infections due to Streptococcus dysgalactiae subspecies equisimilis. Clin Infect Dis. 2009 Sep 1;49(5):766- 72. doi: 10.1086/605085. 13. Jorgensen, JH and Pfaller, MA (Eds.) Chapter 20: Streptococcus. Manual of Clinical Microbiology. 11th ed. 14. Vieira VV, Teixeira LM, Zahner V, Momen H, Facklam RR, Steigerwalt AG, Brenner DJ, Castro AC. Genetic relationships among the different phenotypes of Streptococcus dysgalactiae strains. Int J Syst Bacteriol . 1998 Oct;48 Pt 4:1231-43. 15. Gherardi G, Imperi M, Palmieri C, Magi G, Facinelli B, Baldassarri L, Pataracchia M, Creti R. Genetic diversity and virulence properties of Streptococcus dysgalactiae subsp. equisimilis from different sources. J Med Microbiol. 2014 Jan;63(Pt 1):90-8. doi: 10.1099/jmm.0.062109-0. Epub 2013 16. Rantala S, Vahakuopus S, Vuopio-Varkila J, Vuento R, Syrjanen J. Streptococcus dysgalactiae subsp. equisimilis Bacteremia, Finland, 1995-2004. Emerg Infect Dis . 2010 May;16(5):843-6. doi: 10.3201/ eid1605.080803. 17. Vandamme P, Pot B, Falsen E, Kersters K, Devriese LA.Taxonomic study of Lancefield streptococcal groups C, G, and L (Streptococcus dysgalactiae) and proposal of S. dysgalactiae subsp. equisimilis subsp. Int J Syst Bacteriol. 1996 Jul; 46(3):774-81. Erratum in: Int J Syst Bacteriol 1997 Apr;47(2):605. 18. Jensen A, Kilian M. Delineation of Streptococcus dysgalactiae, its subspecies, and its clinical and phylogenetic relationship to Streptococcus pyogenes. J Clin Microbiol. 2012 Jan;50(1):113-26. doi: 10.1128/JCM.05900- 11. Epub 2011 Nov 9. 19. Rantala S. Streptococcus dysgalactiae subsp. equisimilis bacteremia: an emerging infection. Eur J Clin Microbiol Infect Dis. 2014 Aug; 33(8):1303- 10. doi: 10.1007/s10096-014-2092-0. Epub 2014 Mar 29. Review. 20. Koh, TH et al. 2009. Streptoccoccal cellulitis following preparation of fresh raw seafood. Zoonoses Public Health 56:206-208. 21. Hule GP, Karmarkar MG, Cameron A, Hase N, Khopkar U, Mehta PR, McNeilly CL, McMillan D, Sriprakash KS.Seropositivity for Antibodies to DRS-G, a Virulence Factor from Streptococcus dysgalactiae subsp. equisimilis, Is an Independent Risk Factor for Poststreptococcus Glomerulonephritis and Chronic Kidney Disease in Mumbai, India. Clin Vaccine Immunol. 2015 Aug;22(8):938-42. doi: 10.1128/CVI.00275-15. Epub 2015 Jun 17. 22. Fernández-Aceñero MJ, Fernández-López P. Cutaneous lesions associated with bacteremia by Streptococcus dysgalactiae. J Am Acad Dermatol. 2006 Nov; 55(5 Suppl):S91-2. 23. Mylvaganam H, Bruun T, Vindenes HA, Langeland N, Skrede S. Molecular epidemiological investigation of an outbreak of invasive beta-haemolytic streptococcal infection in western Norway. Clin Microbiol Infect. 2009 Mar; 15(3):245-52. doi: 10.1111/j.1469-0691.2008.02664.x. 24. Loubinoux J, Plainvert C, Collobert G, Touak G, Bouvet A, Poyart C; CNR-Strep Network. Adult invasive and noninvasive infections due to Streptococcus dysgalactiae subsp. equisimilis in France from 2006 to 2010. J ClinMicrobiol . 2013 Aug; 51(8):2724-7. doi: 10.1128/JCM.01262-13. 25. Gavira, JM and Bisno L. 2000. Group C and G streptocci. P238-254. In DL Stevens and EL Kaplan (Eds.) Streptococcal infections: clinical aspects, microbiology and molecular pathogenesis. Oxford University Press, New York, NY as cited in Lopardo HA, Vidal P, Sparo M, Jeric P, Centron D, Facklam
Group A streptococci and Group G streptococci can cause similar types of infections. Like Group A streptococci, Group G streptococci can cause skin and soft tissue infections, such as wound infections, erysipelas, cellulitis, 19 bacteremia, endocarditis, 25 acute rheumatic fever, acute glomerulonephritis, and toxic shock-like syndrome 22 associated with necrotizing fasciitis. 10 The most common portal of entry in patients with GGS bacteremia is the skin. 16,19,26,27,28 This further highlights the importance of dermatologic disease in the elderly populations as a predisposing factor to infection. This includes lower leg cellulitis and decubitis ulcers, 27 and skin malignancies including squamous cell cancer and mycosis fungoides. 26 In patients with Group G Streptococcal bacteremia, the mortality rate varies between 2-18 percent. 19
TREATMENT
Group G streptococcal bacteremia are susceptible responsive to β-lactam antibiotic therapy. Improvement in clinical course can be seen within 24-48 hours of antibiotic therapy initiation. 27 The drug of choice for GGS bacteremia is intravenous penicillin G. 19,26,28,30,31 Other effective treatment options include second and third generation cephalosporins, vancomycin, and fluoroquinolones. 26,32 The resistance tomacrolide antibiotics, like erythromycin, varies; with some regions such as North American reporting macrolide resistance as high as 19%. 12 Thus, these antibiotics may not serve as reliable empiric treatment options. In cases of toxic shock-like syndrome with necrotizing fasciitis, clindamycin is often added to β-lactam antibiotic therapy for toxin inhibition by facilitating phagocytosis of streptococci by inhibiting M protein and suppressing both penicillin binding proteins needed for cell wall synthesis and tumor necrosis factor production. 33
CONCLUSION
Group G streptoccocus is a pathogen which should be considered in the setting of burn wound infections. Infections with this organism are typically seen in patients with chronic underlying illness such as alcohol abuse, cardiovascular disease, diabetes mellitus, and malignancy. REFERENCES 1. National Hospital Ambulatory Medical Care Survey: 2011 Emergency Department Summary Tables (accessed on March 1, 2016 at http://www. cdc.gov/nchs/data/ahcd/nhamcs_emergency/2011_ed_web_tables.pdf 2. Mayhall CG. The epidemiology of burn wound infections: then and now. Clin Infect Dis. 2003 Aug 15;37(4):543-50. Epub 2003 Jul 30. 3. Bang RL, Gang RK, Sanyal SC, Mokaddas E, Ebrahim MK. Burn septicaemia: an analysis of 79 patients. Burns 1998 Jun;24(4):354-61. 4. Shimomura Y, Okumura K, Murayama SY, Yagi J, Ubukata K, Kirikae T, Miyoshi-Akiyama T. Complete genome sequencing and analysis of a Lancefield group G Streptococcus dysgalactiae subsp. equisimilis strain causing streptococcal toxic shock syndrome (STSS). BMC Genomics. 2011 Jan 11; 12:17. doi: 10.1186/1471-2164-12-17.
22 J La State Med Soc VOL 169 JANUARY/FEBRUARY 2017
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