We describe 2 cases of fatal necrotizing fasciitis and toxic shock syndrome caused by Streptococcus agalactiae-a rare entity that has been reported in only 9 patients-in 2 nonpregnant adults.published_or_final_versio

Ho, PL

Tang, WM

Wong, JW

Yau, WP

Yip, DK

Clinical Infectious Diseases

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Title Report of 2 fatal cases of adult necrotizing fasciitis and toxicshock syndrome caused by Streptococcus agalactiae.Author(s) Tang, WM; Ho, PL; Yau, WP; Wong, JW; Yip, DKCitationClinical Infectious Diseases : An Official Publication Of TheInfectious Diseases Society Of America, 2000, v. 31 n. 4, p. E15-17Issued Date 2000URL http://hdl.handle.net/10722/42164Rights Creative Commons: Attribution 3.0 Hong Kong Licensee15Report of 2 Fatal Cases of Adult Necrotizing Fasciitis and Toxic ShockSyndrome Caused by Streptococcus agalactiaeW. M. Tang,1 P. L. Ho,2 W. P. Yau,1 J. W. K. Wong,1and D. K. H. Yip11Department of Orthopaedic Surgery and 2Departmentof Microbiology (Division of Infectious Diseases), the Universityof Hong Kong, Hong Kong, ChinaWe describe 2 cases of fatal necrotizing fasciitis and toxic shock syndrome caused by Strep-tococcus agalactiae—a rare entity that has been reported in only 9 patients—in 2 nonpregnantadults.Necrotizing fasciitis is a severe soft-tissue infection associatedwith rapidly progressive necrosis of the subcutaneous tissue andsuperficial fascia [1]. The disease is also characterized by earlydevelopment of systemic toxicity [2]. The dreadful disease isusually caused by invasive Streptococcus, of which Streptococ-cus pyogenes is the most often encountered species [3–5]. Delayin diagnosing necrotizing fasciitis is common because differ-entiating the evolving necrotizing fasciitis from cellulitis can bevery difficult [6]. Treatments include rapid radical debridementand administration of appropriate antibiotics. However, evenwith proper treatment, the mortality rate remains as high as53% [3].We describe 2 adults with fatal necrotizing fasciitis associatedwith toxic shock–like syndrome due to Streptococcus agalactiae.Only 9 similar cases have been reported previously.Case ReportsCase 1. A 75-year-old hypertensive woman was referredto our teaching hospital by her family physician because ofshock and left-leg swelling; the overlying skin had a duskyappearance. Severe left-leg pain had begun 2 days prior toadmission. The diagnosis on the referral letter was “deep-veinthrombosis.”She was in a comatose state on admission. Her blood pressurewas 95/55 mm Hg, and her pulse rate was 120 beats/min. Theskin of her left leg was inflamed up to the knee, with somepatchy areas having a dusky appearance. The dorsum of herleft foot was grossly swollen. The second and third toes of herleft foot had pressure sores at the tips, with claw-toe deformitiesthat were probably due to peripheral vascular disease secondaryto her long-term, poorly controlled hypertension. We believedthat the ulcers were the entry sites of the bacteria. AlthoughReceived 16 November 1999; revised 28 February 2000; electronicallypublished 17 October 2000.Reprints or correspondence: W. M. Tang, Dept. of Orthopaedic Surgery,University of Hong Kong, Pokfulam, Hong Kong SAR, China (wmtanga@hkucc.hku.hk).Clinical Infectious Diseases 2000;31:e15–7q 2000 by the Infectious Diseases Society of America. All rights reserved.1058-4838/2000/3104-00E2$03.00there was no effusion on the left knee, there was a positivepatellar tap in the opposite knee. Subcutaneous aspiration ofthe left-leg lesion and intra-articular aspiration of the right kneewere performed, and gram-positive organisms were present inthe specimens from both sites. Penicillin G and clindamycinwere given intravenously. The gram-positive organisms werelater confirmed to be a pure growth of S. agalactiae that issusceptible to penicillin G and clindamycin.The initial blood investigation revealed leukopenia, with aWBC count of 2.9 cells/mm3; anemia, with a hemoglobin levelof 11.5 g/dL; and thrombocytopenia, with a platelet count ofcells/L. The prothrombin time (14.4 s), activated par-967 3 10tial thromboplastin time (45.9 s), and international normalizedratio (1.4) were all prolonged. The fibrinogen level was 6.32 g/L. Her random blood glucose level was 9.5 mmol/L. Otherlevels were as follows: urea, 24.0 mmol/L; creatinine, 372 mmol/L; and spot glucose, 5.1 mmol/L.Four hours after admission, an emergency above-knee am-putation of her left lower limb was performed, and an openarthrotomy was done on her right knee to ensure thoroughirrigation of the joint. Intraoperative findings, including loss ofresistance of the subcutaneous planes, fat and fascia necrosis,and edema of the fascial layer, were typical of that of necrotizingfasciitis. The diagnosis was finally confirmed by histologic ex-amination of the surgical specimens.She was treated in the intensive care unit after surgery, withventilator and ionotropic supports. She died of disseminatedintravascular coagulopathy 48 hours after surgery.Case 2. A 64-year-old man with a known history of livercirrhosis was admitted to our service because of right-calf swell-ing of 1 day’s duration. He had no history of injury to theaffected limb. He was at the end stage of liver cirrhosis withascites and had had previous episodes of bleeding esophagealvarices.His blood pressure on admission was 90/60 mm Hg, and hisoral temperature was 407C. His right calf was tender. The skinwas dusky up to the knee, with bullae formation (figure 1). Hehad pancytopenia with a leukocyte count of cells/L,91.4 3 10a hemoglobin level of 10.5 g/dL, and a platelet count ofcells/L. Prothrombin time was 29.6 s, and activated960 3 10partial thromboplastin time was 110.0 s. Other laboratory val-e16 Tang et al. CID 2000;31 (October)Figure 1. The right calf of a 64-year-old man, showing signs typicalof necrotizing fasciitis: dusky skin and hemorrhagic bullae.ues were as follows: spot glucose, 17.6 mmol/L; creatinine, 216mmol/L; urea, 18.4 mmol/L; and total bilirubin, 59 mmol/L.We obtained a pure growth of S. agalactiae from the 2 con-secutive sets of blood cultures done prior to the commencementof antibiotic treatment. The organism was susceptible to peni-cillin G and clindamycin; iv cefuroxime was given empirically,but this was switched to iv penicillin G and clindamycin afterwe obtained the blood-culture results.An above-knee amputation of his right lower limb was per-formed 4 h after admission. The intraoperative findings weretypical of necrotizing fasciitis, including loss of tissue-planeresistance and necrosis of the subcutaneous fat. He was trans-ferred to the intensive care unit after surgery because of res-piratory and renal failure, disseminated intravascular coagu-lation, and persistent septic shock. He required dopamine andadrenaline to maintain a systolic blood pressure 1100 mm Hg.He died 6 days after the operation.Histologic examination of the amputated specimens con-firmed the diagnosis of necrotizing fasciitis. However, bacte-riologic studies of the amputated specimens and the peritonealfluid were negative.DiscussionThe ability of S. agalactiae to cause invasive infections inadults is well documented [7–10]. Nevertheless, necrotizing fas-ciitis caused by S. agalactiae, which is probably the most severeand fatal form of invasive streptococcal infection, has been onlyrarely described in the literature. To the best of our knowledge,only 9 cases have been previously reported in the English-lan-guage literature [11–16]; these involved 3 neonates, 1 boy (10years old), and 5 adults (table 1). S. agalactiae caused necro-tizing fasciitis in 3 children born prematurely [11, 13] and 1otherwise healthy child after operative treatment for a fracture[16]. Among reported adult infections, Sutton et al. [15] de-scribed a case of necrotizing fasciitis that complicated an epi-siotomy , and Riefler et al. [14] described another, involving awoman with diabetes mellitus. Both patients survived the in-fections despite significant morbidity. The first fatal case ofnecrotizing fasciitis due to S. agalactiae was reported by Gar-dam et al. [12], which involved a 67-year-old patient withchronic leukemia who developed necrotizing fasciitis and toxicshock syndrome. All the cases documented until now occurredin continental North America.The significance of the concurrent septic arthritis in case 1is 2-fold: it further demonstrated the invasiveness of the or-ganism, and, more important, it illustrated the presence of mul-tiple septic foci in necrotizing fasciitis. Although septic arthritisis a well-documented complication of bacteremia, its presencetogether with necrotizing fasciitis is underreported [17]. In ourcase 1, the effusion of the septic arthritis could have easily beenmasked by the alarming signs and symptoms of necrotizingfasciitis. Therefore, in managing a life-threatening infectionsuch as necrotizing fasciitis, a clinician should maintain a highindex of suspicion of multiple septic foci.Toxic shock syndrome is a rapidly deteriorating clinical sit-uation including shock, multiorgan failure, and destructive soft-tissue infection. While it is well-known that group A strepto-cocci induce this systemic problem, group B streptococci haveonly recently been described as a cause. Only 2 cases of S.agalactiae–related toxic shock–like syndrome have been pre-viously reported in the English-language literature; these in-volved a 27-year-old woman with streptococcal toxic shocksyndrome caused by S. agalactiae that was probably due tovaginal colonization [18], and a 67-year-old woman withchronic leukemia with coexisting necrotizing fasciitis [12].CID 2000;31 (October) S. agalactiae Necrotizing Fasciitis e17Table 1. Summary of documented cases of necrotizing fasciitis caused by group B streptococci.ReferencePatient’sage/sexUnderlying disease and/orpredisposing condition Site(s) affected Antibiotic(s) given Outcome[13] 7 w/M Premature birth at 28 w Right thigh Penicillin Survival with debridement[13] 11 w/M Premature birth at 32 w Scalp, meninges (meningitis) Penicillin, gentamicin Survival with debridement[11] 5 w/F 1150-g Firstborn twin Right mandible Methicillin, gentamicin Survival with debridement[16] 10 y/M Supracondylar fracture of righthumerus; open reductionand internal fixation doneDistal third of the rightarm, postoperative day 2Penicillin G Survival with debridement[14] 51 y/F Diabetes mellitus, leftfemoropopliteal bypass doneLeft calf and leg, 1 mopostoperativePenicillin G Survival after above-kneeamputation[15] 26 y/F Episiotomy for a spontaneousdeliveryLower abdominal wall,perineum, and buttockon postoperative day 4Penicillin, clindamycin,tobramycinSurvival with extensivedebridement[12] 67 y/F Chronic lymphocytic leukemia Both legs Penicillin G, clindamycin,ceftriaxone, ampicillinDeath, despite above-kneeamputation of left leg[12] 51 y/M Diabetes mellitus, alcohol abuse Scrotum Ciprofloxacin, cephazolin,gentamicin, metronidazole,penicillin GSurvival with extensivedebridement[12] 34 y/M Diabetes mellitus Right calf Ciprofloxacin, penicillin G,clindamycinSurvival with extensivedebridementPR 75 y/F Hypertension Left leg (and right-kneeseptic arthritis)Penicillin G, clindamycin Death, despite above-kneeamputation of left legPR 64 y/M End-stage liver cirrhosis,diabetes mellitusRight calf Penicillin G, clindamycin Death, despite above-kneeamputation of right legNOTE. F, female; M, male; PR, present report.The 2 cases described in the present report fulfilled the def-initions of streptococcal toxic shock syndrome introduced bythe Working Group on Severe Streptococcal Infections [2].Therefore, all 3 patients who did not survive were 160 yearsold, and all had both necrotizing fasciitis and toxic shock–likesyndrome concomitantly. It is not clear why some patients withinvasive S. agalactiae infection develop streptococcal septicshock–like syndrome and others develop necrotizing fasciitis orboth. Although McGeer et al. [19] have recently shown thatthe risk factors for developing group A streptococcal toxicshock–like syndrome included patient age and toxin A geno-type, an M-protein serotype and the presence of diabetes mel-litus favor the development of necrotizing fasciitis. Such as-sociations are not clear in S. agalactiae infections, however.References1. Green RJ, Dafoe DC, Raffin TA. Necrotizing fasciitis. Chest 1996;110:219–29.2. The Working Group on Severe Streptococcal Infections. Defining the groupA streptococcal toxic shock syndrome: rationale and consensus definition.JAMA 1993;269:390–1.3. Jarrett P, Rademaker M, Duffill M. The clinical spectrum of necrotisingfasciitis: a review of 15 cases. Aust N Z J Med 1997;27:29–34.4. Kiska DL, Thiede B, Caracciolo J, et al. Invasive group A streptococcalinfections in North Carolina: epidemiology, clinical features, and geneticand serotype analysis of causative organisms. J Infect Dis 1997;176:992–1000.5. Weiss KA, Laverdiere M. Group A Streptococcus invasive infections: a review.Can J Surg 1997;40:18–25.6. Meltzer DL, Kabongo M. Necrotizing fasciitis: a diagnostic challenge. AmFam Physician 1997;56:145–9.7. Farley MM, Harvey RC, Stull T, et al. A population-based assessment ofinvasive disease due to group B Streptococcus in nonpregnant adults. NEngl J Med 1993;328:1807–11.8. Jackson LA, Hilsdon R, Farley MM, et al. Risk factors for group B strep-tococcal disease in adults. Ann Intern Med 1995;123:415–20.9. Schwartz B, Schuchat A, Oxtoby MJ, et al. Invasive group B streptococcaldisease in adults: a population-based study in metropolitan Atlanta.JAMA 1991;266:1112–4.10. Zangwill KM, Schuchat A, Wenger JD. Group B streptococcal disease in theUnited States, 1990: report from a multistate active surveillance system.Morb Mortal Wkly Rep CDC Surveill Summ 1992;41:25–32.11. Bomar WE Jr, Ferlauto JJ, Wells DH. An unusual presentation of a b he-molytic group B streptococcal infection. J Pediatr Surg 1980;15:683–5.12. Gardam MA, Low DE, Saginur R, et al. Group B streptococcal necrotizingfasciitis and streptococcal toxic shock–like syndrome in adults. Arch In-tern Med 1998;158:1704–8.13. Ramamurthy RS, Srinivasan G, Jacobs NM. Necrotizing fasciitis and nec-rotizing cellulitis due to group B streptococcus. Am J Dis Child 1977;131:1169–70.14. Riefler J III, Molavi A, Schwartz D, et al. Necrotizing fasciitis in adults dueto group B streptococcus: report of a case and review of the literature.Arch Intern Med 1988;148:727–9.15. Sutton GP, Smirz LR, Clark DH, et al. Group B streptococcal necrotizingfasciitis arising from an episiotomy. Obstet Gynecol 1985;66:733–6.16. Viani RM, Lewis A, Bradley JS. Postoperative group B streptococcal nec-rotizing fasciitis in a previously healthy child. Pediatr Infect Dis J 1997;16:630–1.17. Gonzalez Ruiz A, Ridgway GL, Cohen SL, et al. Varicella gangrenosa withtoxic shock–like syndrome due to group A streptococcus infection in anadult: case report. Clin Infect Dis 1995;20:1058–60.18. Schlievert PM, Gocke JE, Deringer JR. Group B streptococcal toxicshock–like syndrome: report of a case and purification of an associatedpyrogenic toxin. Clin Infect Dis 1993;17:26–31.19. McGeer A, Green K, Schwartz B, et al. Is necrotizing fasciitis a componentof streptococcal toxic shock syndrome or a separate disease entity? [ab-stract K-156]. In: Program and abstracts of the 37th Interscience Con-ference on Antimicrobial Agents and Chemotherapy. Washington, DC:American Society for Microbiology, 1997.

Report of 2 fatal cases of adult necrotizing fasciitis and toxic shock syndrome caused by Streptococcus agalactiae.

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Report of 2 fatal cases of adult necrotizing fasciitis and toxic shock syndrome caused by Streptococcus agalactiae.

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