Correspondence
Invasive Group A Streptococcal Infections
N Engl J Med 1997; 336:513-515February 13, 1997
- Article
To the Editor:
Davies et al. (Aug. 22 issue)1 identify an annual incidence of 1.5 cases of invasive group A streptococcal disease in Ontario, Canada, in 1992 and 1993. The mortality rate was 15 percent. This prospective study relies on identifications from hospital microbiology laboratories and from Ontario's largest private laboratory service. These statistics may be misleading; the real incidence is probably much higher and the mortality rate much lower. The problem is that most patients with invasive streptococcal infection will present to the family practitioner or community pediatrician with uncomplicated superficial cellulitis, erysipelas,2 or perianal cellulitis.3 Occasionally, blood cultures will be taken, but more often than not empirical treatment with antibiotics will be undertaken, resulting in an uncomplicated resolution of the infection. It would not be surprising if a substantial number of uncomplicated invasive group A streptococcal infections escape detection.
3 ReferencesRichard Couper, M.B., Ch.B.
University of Adelaide, North Adelaide, SA 5006, Australia1
Davies HD ,McGeer A ,Schwartz B , et al. Invasive group A streptococcal infections in Ontario, Canada. N Engl J Med 1996;335:547-554
Full Text | Web of Science | Medline2
Stevens DL . Invasive group A streptococcus infections. Clin Infect Dis 1992;14:2-11
CrossRef | Web of Science | Medline3
Kokx NP ,Comstock JA ,Facklam RR . Streptococcal perianal disease in children. Pediatrics 1987;80:659-663
Web of Science | Medline
To the Editor:
Holm (Aug. 22 issue)1 states that “there is no invasive clone” of Streptococcus pyogenes, serotype M1, and that “the same organism can produce necrotizing fasciitis, impetigo, or pharyngitis.” He argues that the risk of transmission of invasive disease to household contacts of patients with invasive streptococcal disease is no greater than if the patient had streptococcal pharyngitis and suggests that the call by Davies et al. for antibiotic prophylaxis in those contacts2 is unwarranted.
One need not, however, assume the presence of an invasive clone of M1 streptococcus in order to justify chemoprophylaxis for invasive disease. As Holm notes, the M antigen is itself partly responsible for the virulence of the different streptococcal strains, and people who lack antibodies to the M protein may lack protection from invasive infection.1 One might therefore expect to find that some serotypes are more prone to cause invasive disease than others. Indeed, there is ample evidence that the M1 serotype is disproportionately associated with severe infections.2-5 In one study, whereas only 11.7 percent of pharyngeal infections were associated with M1 isolates, 26.3 percent of the isolates from blood and 33.3 percent of those from spinal fluid were M1.4 In another, the M1 serotype accounted for only 18.2 percent of pharyngeal infections but for 25.7 percent of serious streptococcal infections.3 Finally, Schwartz et al. found that serotypes M1 and M3 were more invasive than other M-typable strains.5
Despite the lack of compelling evidence of an invasive clone of M1 streptococci, it is clear that patients with invasive streptococcal disease are substantially more likely to be infected with the invasive strain, the M1 serotype, than patients with pharyngitis. Contrary to Holm's view, the infectivity of the former group ought to be markedly higher than that of the latter, and it is not surprising that Davies et al. found that invasive disease was nearly 200 times as likely to develop in the household contacts of people with invasive streptococcal disease as in the general population.2 In this light, their call for antibiotic prophylaxis in patients' close contacts appears to be well grounded.
5 ReferencesDavid Charytan, M.A.
New York University School of Medicine, New York, NY 100161
Holm SE . Invasive group A streptococcal infections. N Engl J Med 1996;335:590-591
Full Text | Web of Science | Medline2
Davies HD ,McGeer A ,Schwartz B , et al. Invasive group A streptococcal infections in Ontario, Canada. N Engl J Med 1996;335:547-554
Full Text | Web of Science | Medline3
Johnson DR ,Stevens DL ,Kaplan EL . Epidemiologic analysis of group A streptococcal serotypes associated with severe systemic infections, rheumatic fever, or uncomplicated pharyngitis. J Infect Dis 1992;166:374-382
CrossRef | Web of Science | Medline4
Colman G ,Tanna A ,Efstratiou A ,Gaworzewska ET . The serotypes of Streptococcus pyogenes present in Britain during 1980-1990 and their association with disease. J Med Microbiol 1993;39:165-178
CrossRef | Web of Science | Medline5
Schwartz B ,Facklam RR ,Breiman RF . Changing epidemiology of group A streptococcal infection in the USA. Lancet 1990;336:1167-1171
CrossRef | Web of Science | Medline
To the Editor:
In his editorial, Holm describes the early signs of necrotizing fasciitis as high fever plus swelling and marked tenderness of an affected extremity and concludes that “early treatment with antibiotics still seems to be the best way to prevent death.”
The perivascular inflammation and occlusion of fascia-perforating small-muscle vessels is the initial process in necrotizing fasciitis. Fascia necrosis follows. In later phases the necrosis spreads to subcutaneous tissue, so that swelling can be observed before the characteristic cutaneous signs appear. Ultrasonography typically shows a hypoechoic area between the subcutaneous and muscle tissue.1 The diagnosis of necrotizing fasciitis is first a clinical one. Administering antibiotics alone is — even in early cases — a fatal error. If necrotizing fasciitis is suspected, a deep incision to the fascia is indicated. After verification of necrotizing fasciitis, early and radical débridement of all necrotic tissue is the only way to resolve the focus, remove the toxic bacterial products, and preserve the patient's limb and life.2 Inefficient or delayed surgical therapy increases mortality. The time of the first surgical intervention correlates with the survival rate.3 As Thibault observed, “There are times when the internist's most important job is to know when to ask for help and where to go to get that help.” 4
4 ReferencesPeter Kujath, M.D.
Christian Eckmann, M.D.
Medical University Luebeck, D-23538 Luebeck, Germany1
Kujath P ,Eckmann C ,Benecke P . Diagnose und Therapie der nekrotisierenden Fasziitis. Dtsch Med Wochenschr 1995;120:965-968
CrossRef | Web of Science | Medline2
Bisno AL ,Stevens DL . Streptococcal infections of skin and soft tissues. N Engl J Med 1996;334:240-245
Full Text | Web of Science | Medline3
Voros D ,Pissiotis D ,Georgantas D ,Katsaragakis S ,Antoniou S ,Papadimitriou J . Role of early and extensive surgery in the treatment of severe necrotizing soft tissue infection. Br J Surg 1993;80:1190-1191
CrossRef | Web of Science | Medline4
Thibault GE . Desperate appliance. N Engl J Med 1994;330:623-626
Full Text | Web of Science | Medline
Author/Editor Response
The authors reply:
To the Editor: Dr. Couper points out that our definition of invasive disease (that associated with a positive sterile-site culture) excludes cases in which patients had bacteremia but for whom cultures were not done, as well as the many cases of moderately severe disease with tissue invasion in which sterile-site cultures were negative. Our surveillance system is designed not to assess the burden of illness due to group A streptococcus but rather to monitor trends in the epidemiology of severe disease. There are many similar valuable surveillance systems for bacterial disease.1,2
Charytan presents a rationale in support of chemoprophylaxis for close contacts. Indeed, some jurisdictions — including Ontario, Quebec, Alberta, and Manitoba in Canada — have issued guidelines in support of chemoprophylaxis for household contacts of patients with invasive disease. However, many questions are still unanswered, and there remains considerable disagreement among experts about the magnitude of the risk of disease in household contacts and about whether chemoprophylaxis will be effective. One of these unanswered questions is whether the severity of the infection in the index patient is predictive of the severity of the illness in the exposed contacts. Of 11 household pairs with invasive group A streptococcal infection that were reported to the Centers for Disease Control and Prevention, 6 index patients had the streptococcal toxic shock syndrome (STSS) and 5 had invasive disease alone. In the 6 households with an index case of STSS, 4 of the subsequent cases were associated with STSS. In contrast, none of the 5 cases subsequent to uncomplicated invasive disease were associated with STSS (P = 0.06). These data suggest that close contacts who become infected are likely to have disease similar in severity to that of the index patient. Recent evidence that there is substantial genetic diversity within common M serotypes might explain why strains of the same serotype may be associated with different severities of disease.3,4
4 ReferencesAllison McGeer, M.D.
Donald E. Low, M.D.
Princess Margaret and Mount Sinai Hospitals, Toronto, ON M5G 1X5, CanadaH. Dele Davies, M.D.
Alberta Children's Hospital, Calgary, AB T2N 1N4, CanadaBenjamin Schwartz, M.D.
Centers for Disease Control and Prevention, Atlanta, GA 303331
Hofmann J ,Cetron MS ,Farley MM , et al. The prevalence of drug-resistant Streptococcus pneumoniae in Atlanta. N Engl J Med 1995;333:481-486
Full Text | Web of Science | Medline2
Farley MM ,Harvey RC ,Stull T , et al. A population-based assessment of invasive disease due to group B streptococcus in nonpregnant adults. N Engl J Med 1993;328:1807-1811
Full Text | Web of Science | Medline3
Musser JM ,Kapur V ,Szeto J ,Pan X ,Swanson DS ,Martin DR . Genetic diversity and relationships among Streptococcus pyogenes strains expressing serotype M1 protein: recent intercontinental spread of a subclone causing episodes of invasive disease. Infect Immun 1995;63:994-1003
Web of Science | Medline4
Stanley J ,Desai M ,Xerry J ,Tanna A ,Efstratiou A ,George R . High resolution genotyping elucidates the epidemiology of group A streptococcus outbreaks. J Infect Dis 1996;174:500-506
CrossRef | Web of Science | Medline
Author/Editor Response
With respect to Charytan's comments: It is well known that the risk of spreading streptococci from infected persons is much higher within a household. If we assume that the epidemiologic situation over time is rather similar among family members and thus that the lack of immunity to a new microbial agent is also similar, it is logical to give all members of a family antibiotic prophylaxis when there is a serious streptococcal infection in one family member. That holds true whether the streptococci belong to an “invasive clone” or not. As I pointed out in the editorial, the mechanism behind this spread of severe streptococcal infection within a family is not different from that of the streptococci associated with routine throat infections. So far, there is no clear evidence that some M types are more virulent than others, although it may seem so from epidemiologic points of view.
The start of necrotizing fasciitis is insidious, and often antibiotic treatment is not given early enough to hinder its development. Once established, necrotizing fasciitis can usually be treated only with very extensive surgical intervention. A delay would be disastrous for the patient. The approach outlined by Drs. Kujath and Eckmann seems quite reasonable.
Stig E. Holm, M.D., Ph.D.
University of Umeå, 90185 Umeå, Sweden- Citing Articles (6)
Citing Articles
1
R.E. Horch. (2008) Fournier-Gangrän. Der Chirurg 79:11, 1080-1081
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Takuma Tajiri, Genshu Tate, Hidetaka Akita, Nobuyuki Ohike, Atsuko Masunaga, Toshiaki Kunimura, Toshiyuki Mitsuya, Toshio Morohoshi. (2008) Autopsy cases of fulminant-type bacterial infection with necrotizing fasciitis: Group A (beta) hemolytic Streptococcus pyogenes versus Vibrio vulnificus infection. Pathology International 58:3, 196-202
CrossRef3
Takuma Tajiri, Genshu Tate, Tetsuji Enosawa, Hidetaka Akita, Nobuyuki Ohike, Atsuko Masunaga, Toshiaki Kunimura, Toshiyuki Mitsuya, Toshio Morohoshi. (2007) Clinicopathological findings in fulminant-type pneumococcal infection: Report of three autopsy cases. Pathology International 57:9, 606-612
CrossRef4
Tara C Smith, Darren D Sledjeski, Michael D.P Boyle. (2003) Regulation of protein H expression in M1 serotype isolates of Streptococcus pyogenes. FEMS Microbiology Letters 219:1, 9-15
CrossRef5
Johann Auer, Robert Berent, Michael Porodko, Bernd Eber. (2001) Streptococcus infection and splenectomy. The Lancet 357:9262, 1130
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G. N. Rutty, A. Busuttil. (2000) Necrotizing Fasciitis. The American Journal of Forensic Medicine and Pathology 21:2, 151-154
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