Two patients with toxic shock-like syndrome are presented. Both patients had necrotizing cellulitis due to Streptococcus pyogenes, and both patients required extensive surgical debridement. The association of Streptococcus pyogenes infection and toxic shock-like syndrome is discussed

Connolly, Thomas J.

Connolly, Thomas L.

Lanspa, Eugene F.

Pavelka, Donald J.

English

Henry Ford Health System Scholarly Commons

Henry Ford Hospital Medical Journal Volume 37 Number 2 Article 5 6-1989 Toxic Shock-like Syndrome Associated with Necrotizing Streptococcus Pyogenes Infection Thomas J. Connolly Donald J. Pavelka Eugene F. Lanspa Thomas L. Connolly Follow this and additional works at: https://scholarlycommons.henryford.com/hfhmedjournal  Part of the Life Sciences Commons, Medical Specialties Commons, and the Public Health Commons Recommended Citation Connolly, Thomas J.; Pavelka, Donald J.; Lanspa, Eugene F.; and Connolly, Thomas L. (1989) "Toxic Shock-like Syndrome Associated with Necrotizing Streptococcus Pyogenes Infection," Henry Ford Hospital Medical Journal : Vol. 37 : No. 2 , 69-72. Available at: https://scholarlycommons.henryford.com/hfhmedjournal/vol37/iss2/5 This Article is brought to you for free and open access by Henry Ford Health System Scholarly Commons. It has been accepted for inclusion in Henry Ford Hospital Medical Journal by an authorized editor of Henry Ford Health System Scholarly Commons. Toxic Shock-like Syndrome Associated with Necrotizing Streptococcus Pyogenes Infection Thomas J. Connolly,* Donald J. Pavelka, MD,^  Eugene F. Lanspa, MD, and Thomas L . Connolly, MD' Two patients with toxic shock-like syndrome are presented. Bolh patients had necrotizing cellulitis due to Streptococcus pyogenes, and both patients required extensive surgical debridement. The association of Streptococcus pyogenes infection and toxic shock-like syndrome is discussed. (Henry Ford Hosp MedJ 1989:37:69-72) S ince 1978, toxin-producing strains of Staphylococcus aureus have been implicated as the cause of the toxic shock syndrome (TSS), which is characterized by fever and rash and followed by desquamation, hypotension, and multisystem in-volvement (1). Most cases subsequently reported have occurred in menstruadng women in association with tampon use (2-6). However, TSS associated with Staphylococcus aureus infection has been described in numerous other clinical illnesses includ-ing use of contraceptive sponges (7), nasal packing (8,9), sur-gical wound infection (10), and nonsurgical infections at various sites including skin and subcutaneous tissue (11,12). Cone et al (13) recently described a toxic shock-like illness in two patients with cellulitis due to group A beta-hemolytic strep-tococci (Streptococcus pyogenes). Several other reports have im-plicated Streptococcus pyogenes in TSS (14-16). Two patients with necrotizing Streptococcus pyogenes infec-tions associated with a toxic shock-like syndrome have been ob-served at our hospital in the past three years. These padents were admitted with streptococcal cellulitis with prominent necrosis of skin and subcutaneous tissue which required extensive surgical debridement to control the illness. One ofthe patients was also bacteremic with Streptococcus pyogenes. We report these cases to increase the awareness that Streptococcus pyogenes may pro-duce a toxic shoek-like syndrome and that aggressive surgical treatment may be necessary to obtain an optimal result. brought to the emergency room where a physical examination revealed a temperature of 40.9°C (I05.6°F), blood pressure of 98/72 mm Hg, respiration of 36 breaths/min, and a pulse of 72 beats/min. The skin showed a bright sunburn-type rash, most prominent over the trunk and face, but present over the entire body. Desquamation of skin ofthe up-per and lower extremities, particularly the hands and feet, occurred later A strawberry tongue was present, and there was prominent infec-tion of both bulbar and palpebral conjunctivae. A 3 x 3 cm abrasion was noted over the right elbow. The surrounding skin was indurated, erythematous, and tender Vesicles were present (Figure). The abraded area oozed serous drainage. The patient became more hypotensive, and a Swan-Ganz catheter was inserted for hemodynamic monitoring. In-travenous crystaloid infusions, albumin, and dopamine were admin-istered to maintain adequate blood pressure. He received 2 g of nafcillin intravenously every six hours for 48 hours and subsequently 6 mU of penicillin intravenously every 24 hours for 19 days. He also received 500 mg of inctronidazole intravenously every six hours from days 3 through 16 and I g of cefoperazone intravenously every 12 hours from days 3 through 13. He developed a rapidly rising creatinine (424 ixmol/ L [4.8 mg/dL] on admission), abnormal liver function, renal failure, and acute respiratory distress syndrome. Hemodialysis and ventilatory support were given. Blood cultures and cultures of drainage from the elbow area revealed Streptococcus pyogenes. The organism produced pyrogenic streptococcal type B toxin but not toxins A and C.§ His con-dition was further complicated by colonic distention, gastrointestinal bleeding due to gastritis, and cardiac arrhythmias. He developed rapidly progressive necrotic changes of the skin and subcutaneous tissue of the right arm and forearm, accompanied by hemorrhagic Case Reports Casel A 76-year-old man suffered a superficial abrasion of his right elbow two days prior to admission. He was being treated with chlorthalidone and metropolol for hypertension but otherwise had been in good health. He was not diabetic. Over a two-day period the elbow area became pro-gressively more erythematous, tender, and swollen. He was visited at home by a nurse who noted that he was confused and severely il l . He was noted to have a bright erythroderma over most of his body. He was Submitted for publication: March 19. 1989. Accepted for publication; August I , 1989. *Creighton University School of Medicine. Omaha. tCreighton University School of Medicine. Bergan Mercy Hospital. Omaha. ^Formerly Department of Internal Medicine. Henry Ford Hospital. Currently Creighton University School of Medicine. Bergan Mercy Hospital, Omaha. Address correspondence to Dr Thomas L. Connolly. 7710 Mercy Road. Ste 601. Omaha. NE68I24. ijToxin determinations performed by Patrick M. Schlieverl. PhD. University of Min-nesota. Minneapolis. MN. Henry Ford Hosp Med J—Vol 37, No 2. 1989 S. Pyogenes and Toxic Shock—Connolly et al 69 Table Laboratory Values in Two Patients with Streptococcal Necrotizing Cellulitis and Toxic Shock Syndrome Case 1 Case 2 12/15/87 12/18/87 4/29/86 5/1/86 WBC count (per |xL) 11.0 14.6 21.4 14.6 Hemoglobin (g/dL) 17.6 12.8 11.8 10.4 Hematocrit (%) 53.7 36.2 35.4 30.8 Platelet count (per JJLL) 193 48 248 170 Creatinine |j.mol/L (mg/dL) 424 (4.8) 813(9.2) 566 (6.4) 194(2.2) BUN mmol/L (mg/dL) 15.7(44) 38.2(107) 24.9 (70) 17.9 (50) Bilirubin IJtmol/L (mg/dL) 27(1.6) 72 (4.2) 67 (3.9) 123 (7.2) Alkaline phosphatase M-kat/L (U/L) 0.4 (22) 0.8 (45) 4.4 (261) 2.6(153) SCOT* |xkat/L (U/L) 1.40 (84) 13.94(836) 0.63 (38) 0.62 (37) CPKt 2,417 2.386 319 509 Albumin g/L (g/dL) 29(2.9) 32(3.2) 30 (3.0) 30 (3.0) Calcium mmol/L (g/dL) 2.20(8.8) 1.60(6.4) 1.87 (7.5) 1.77 (7.1) *SGOT denotes aspartate aminotransferase. tCPK denotes creatinine phosphokinase. Figure—Dorsum of forearm with cellulitis with bleb formation. bullae. These changes required repeated extensive surgical debride-ment over a three-week period following admission. The infection was ultimately controlled, and skin grafting was performed prior to the patient's discharge from the hospital. Laboratory data are listed in the Table. Case 2 A 22-year-old nulliparous woman noted erythema and tenderness of the right breast 72 hours prior to admission. She was obese but other-wise had been in excellent health. She was not diabetic. Her breast had not been injured. She had completed a normal menstrual period one week previously. She had not used tampons and had not been sexually active. She had not had any vaginal irritation or discharge. Twenty-four hours after her initial symptoms, she developed some vesiculation of the skin. She was seen by her physician who prescribed 500 mg of cephalexin every six hours. She developed some nausea and diarrhea the following day. Two days after antibiotics were started, she devel-oped rapidly increasing erythema, swelling and induration ofthe breast, with necrosis ofthe skin and subcutaneous tissue with extensive eschar formation. She was noted to be confused and was brought to the hospital. Physical examination revealed an acutely ill woman. Her tem-perature was 38.9°C (I02°F), blood pressure 90/70 mm Hg, and pulse 100 beats/min. She was confused. There was diffuse erythroderma of the skin of the trunk and extremities resembling a sunburn. There was considerable erythema, induration, and necrosis of the skin of the right breast. Extensive blister formation was also present. Desquamation of skin ofthe hands occurred later Bulbar and palpebral conjunctival in-fection and a strawberry tongue were present. Muscles of the upper and lower extremities were markedly tender to palpation. She received 2 g of nafcillin intravenously every four hours for nine days and 900 mg of clindamycin intravenously every eight hours for three days. She was given an initial dose of 2 mg/kg of tobramycin intravenously with sub-sequent doses being adjusted for dysfunction. She received tobramycin for nine days. Although her .serum creatinine initially was 566 pimol/L (6.4 mg/dL), dialysis was not necessary. Cultures from several areas of the inflamed breast grew Streptococcus pyogenes. Streptococcal pyrogenic toxin determinations were not performed, and the strep-tococcal isolate is not available. Cultures of the breast also revealed Pseudomonas aeruginosa and Enterobacter cloacae. Vaginal cultures K\e.n\c(i Escherichia coh, Pseudomonas aeruginosa, and Candida al-bicans. Blood and urine cultures were negative. Extensive surgical debridement of skin and subcutaneous tissue of the breast was performed, with skin grafting to the breast accomplished later Laboratory data are noted in the Table. Discussion Streptococcus pyogenes may cause numerous infections in-cluding pharyngitis, cellulitis, impedgo, erysipelas, puerperal fever, and bacteremia, as well as necrotizing cellulitis, fasciids, or myosins. It may also be responsible for noninfectious i l l -nesses including rheumatic fever, glomerulonephritis, and erythema nodosa. While Streptococcus pyogenes may produce toxins A, B, and C, recently type A toxin has been produced by far fewer strains than in previous years (17). Streptococcal tox-ins have diverse toxic properdes that include pyrogenicity, en-hancement of lethal endotoxin effects, and increased vascular permeability and skin reactivity, as seen in scariet fever (18-21). Willoughby and Greenberg (22) noted that Streptococcus pyogenes produced toxins with biologic features in common with toxins associated with staphylococcal TSS and suggested that these streptococcal toxins might also cause a toxic shock-like syndrome. Toxic shock syndrome toxin-I (TSST-1) (23-26), 70 Henry Ford Hosp Med J—Vol 37. No 2. 1989 S. Pyogenes and Toxic Shock—Connolly et al previously termed staphylococcal enterotoxin F or pyrogenic exotoxin C, and staphylococcal enterotoxin B (27,28) are considered to be the staphylococcal products responsible for staphylococcal TSS. It has been noted that streptococcal toxin A and staphylococ-cal toxin B are related structurally (29). Both of our patients manifested symptoms characteristic of staphylococcal toxic shock. These features included diffuse erythroderma, conjunctival infecdon, strawberry tongue, hypo-tension, both hepatic and renal dysfunction, and desquamation of the skin. The patient in Case 1 was bacteremic with Streptococcus pyogenes. His rash was that of a bright erythroderma and not the typical sandpaper rash of scarlet fever Prominent conjunctival infection, strawberry tongue, and hepatic dysfunction were present. These features and the severe renal dysfunction requir-ing dialysis that occurred with mild hypotension strongly sug-gested a toxic shock-like syndrome rather than effects of strep-tococcal bacteremia. Both padents rapidly developed extensive necrotic changes of skin and subcutaneous dssue. Extensive sur-gical debridement was performed early in the course of both pa-tients; repeated surgical debridement was required in Case 1. For this patient in pardcular, the effectiveness of debridement ap-peared to be correlated with clinical improvement, with clinical deterioration occurring when further necrosis of tissue developed. The degree of skin involvement, mucous membrane man-ifestations, and deg ree of tissue destruction in this syndrome have been quite varied. Hribalova (15) reported a case of peri-tonids with rash but no mucous membrane involvement. Two of the three cases described by Bartter et al (14) had erythroderma, but mucous membrane involvement and tissue destrucdon were not noted. Desquamation was noted in one patient. Both cases described by Cone et al (13) had erythema of the face and con-junctivids, but a strawberry tongue was not noted. Desquama-tion did not occur, and tissue destruction was not noted. Tissue destruction was a prominent feature of the 20 cases described by Stevens et al (16), but generalized erythema was not noted. Two of their cases had a petechial rash, and two had maculopapular rash. Four of their patients had desquamadon. These authors emphasized the role of erythrogenic toxin type A in their cases. Eight of the ten strains of Streptococcus pyogenes produced pyrogenic exotoxin A, three produced toxins A and B, one pro-duced toxins A, B, and C, and one produced only toxin B. Both of our cases had prominent erythroderma followed by desquamadon, conjunctivids, and strawberry tongue. Both also had prominent tissue destruction requiring extensive debride-ment. In Case 1 where tissue destruction was most marked, toxin analysis revealed the presence of exotoxin B but not toxins A or C. In a recent editorial, Stollerman (30) noted that all three erythrogenic toxins, types A, B, and C, of Streptococcus pyogenes possessed potent toxin properties with type A being the most potent. It is thus not surprising that TSS due to Strep-tococcus pyogenes may be associated with both toxins A and B and possibly toxin C as well, although type A appears to be the most prevalent. It is important to recognize that TSS may be associated with various Streptococcus pyogenes infections, some clinically ob-vious and some occult, and that patients with prominent tissue destruction requiring extensive debridement comprise an impor-tant group of these infections. References 1. Todd J, Fishaut M, Kapral F, Welch T. Toxic-shock syndrome associated wilh phage-group-1 staphylococci. Lancet 1978;2:1116-8. 2. Davis JP, Chesney PJ. Wand PJ, La Venture M. Toxic-shock syndrome: Epidemiologic features, recurrence, risk factors, and prevention. N Engl J Med 1980:303:1429-35. 3. Shands KN. Schmid GP, Dan BB, et al. Toxic-shock syndrome in men-struating women: Association with tampon use and Staphylococcus aureus and clinical features in 52 cases. N Engl J Med 1980;303:1436-42. 4. Osterholm MT, Davis JP, Gibson RW, Mandel JS, Wintermyer LA, Helms NT. Tri-state toxic-shock syndrome study. I . Epidemiologic findings. J Infect Dis 1982;145:431-40. 5. Schlech WF III . Shands KN, Reingold AL, Dan BB, Schmid GP. Hargrett NT. Risk factors for development of toxic shock syndrome: Association with a tampon brand. JAMA 1982;248:835-9. 6. Kehrberg MW, Latham RH. Haslam BT, Hightower A, Tanner M, Jacob-son JA. Risk factors for staphylococcal toxic-shock syndrome. Am J Epidemiol 1981;114:873-9. 7. Faich G, Pearson K, Fleming D, Sobel S, AnelloC. Toxic shock syndrome and the vaginal contracepfive sponge. JAMA 1986;255:216-8. 8. Barbour SD, Shlaes DM, Guertin SR. Toxic-shock syndrome associated with nasal packing: Analogy to tampon-associated illness. Pediatrics 1984; 73:163-5. 9. Hull HF, Mann JM, Sands CJ, Gregg SH, Kaufman PW. Toxic shock syn-drome related to nasal packing. Arch Otolaryngol Head Neck Surg 1983; 109:624-6. 10. BartleU P, Reingold AL, Graham DR, Dan BB, Selinger DS, Tank GW. Toxic shock syndrome associated with surgical wound infections. JAMA 1982;247:1448-50. 11. Reingold AL, Dan BB, Shands KN, Broome CV, Toxic-shock syndrome not associated with menstruation: A review of 54 cases. Lancet 1982;1:1-4. 12. Reingold AL, HargreU NT, Dan BB, Shands KN, Strickland BY, Broome CV. Nonmenstrual toxic shock syndrome: A review of 130 cases. Ann Intem Med 1982;96:871-4. 13. Cone LA, Woodard DR, Schlievert PM, Tomory GS. Clinical and bac-teriologic observations of a toxic shock-like syndrome due to Streptococcus pyogenes. N Engl J Med 1987;317:146-9. 14. Bartter T, Dascal A, Carroll K, Curiey FJ. "Toxic strep syndrome": A manifestation of group A streptococcal infection. Arch Intern Med 1988; 148:1421-4. 15. Hribalova V. Streptococcus pyogenes and the toxic shock syndrome (Let-ter). Ann Intem Med 1988;108:772. 16. Stevens DL, Tanner MH, Winship J, et al. Severe group A streptococcal infections associated with a toxic shock-like syndrome and scarlet fever toxin A. N Engl J Med 1989;321:1-7. 17. Schlievert PM, Betrin KM, Watson DW. Production of pyrogenic exotoxin by groups of streptococci: Association with group A. J Infect Dis 1979;140:676-81. 18. Watson DW. Characterization and pathobiological properties of group A streptococcal pyrogenic exotoxins. In: Parker MT, ed. Pathogenic sUeptococci. Proceedings of the Seventh Intemational Symposium on Streptococci and Strep-tococcal Diseases. Chertsey, England: Reedbooks, 1979:62-3. 19. Schlievert PM, Bettin KM, Watson DW. Purification and characterization of group A streptococcal pyrogenic exotoxin type C. Infect Immun 1977; 16:673-9. 20. Barsumian EL, Cunningham CM, Schlievert PM, Watson DW. Hetero-geneity of group A streptococcal pyrogenic exotoxin type B. Infect Immun 1978;20:512-8. 21. Kim YB, Watson DW. Streptococcal exotoxins; biological and patholog-ical properties. In: Wannamaker LW, Matsen JM, eds. Streptococci and strep-tococcal diseases: Recognition, understanding and management. New York: Henry Ford Hosp Med J—Vol 37, No 2, 1989 S. Pyogenes and Toxic Shock—Connolly et al 71 Academic Press, 1972:33-50. 22. Willoughby R, Greenberg RN. The toxic shock syndrome and strep-tococcal pyrogenic exotoxins. Ann Intern Med I983;98:559. 23. Bergdoll MS, Crass BA. Reiser RF, Robbins RN. Davis JP. A new staphylococcal enterotoxin, enterotoxin F, associated with toxic-shock-syn-drome Sto/j/iy/ococcui aureus isolates. Lancet 1981;1:1017-21. 24. Schlievert PM. Shands KN, Dan BB, Schmid GR NishimuraRD. Identi-fication and characterization of an exotoxin from Staphylococcus aureus associ-ated with toxic-shock syndrome. J Infect Dis 1981;143:509-16. 25. Bonventre PF, Weckbach L, Staneck J. Schlievert PM, Thompson M. Production of staphylococcal enterotoxin F and pyrogenic exotoxin C by Staphylococcus aureus isolates from toxic shock syndrome-associated sources. Infect Immun 1983;40:1023-9. 26. Schlievert PM. Biological properties of toxic shock syndrome exotoxin. Surv Synth Pathol Res 1984;3:54-62. 27. Garbe PL, Arko RJ, Reingold AL, Graves LM, Hayes PS, Hightower AW. Staphylococcus aureus isolates from patients with nonmenstrual toxic shock syndrome: Evidence foradditional toxins. JAMA 1985;253:2538-42. 28. Schlievert PM. Staphylococcal enterotoxin B and toxic-shock syndrome toxin-I are significantly associated with non-menstrual TSS. Lancet 1986; 1:1149-50. 29. Johnson LP, LTtalien JJ, Schlievert PM. Streptococcal pyrogenic ex-otoxin type A (scarlet fever toxin) is related to Staphylococcus aureus entero-toxin B. Moi Gen Genet 1986;203:354-6. 30. Stollerman GH. Changing group A streptococci: The reappearance of streptococcal "toxic shock" (Editorial). Arch Intem Med 1988:148:1268-70. 72 Henry Ford Hosp Med J—Vol 37. No 2. 1989 S. Pyogenes and Toxic Shock—Connolly et al 

Toxic Shock-like Syndrome Associated with Necrotizing Streptococcus Pyogenes Infection

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Toxic Shock-like Syndrome Associated with Necrotizing Streptococcus Pyogenes Infection

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