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Toxic shock syndrome

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Streptococcal Toxic-Shock Syndrome: Spectrum of Disease, Pathogenesis, and New Concepts in Treatment

Dennis L. Stevens, Ph.D., M.D.

Professor of Medicine, University of Washington School of Medicine, Seattle,Washington
Chief, Infectious Disease Section, Veterans Affairs Medical Center, Boise, Idaho, USA

Since the 1980s there has been a marked increase in the recognition and reporting of highly invasive group A streptococcal infections with or without necrotizing fasciitis associated with shock and organ failure. Such dramatic cases have been defined as streptococcal toxic-shock syndrome. Strains of group A streptococci isolated from patients with invasive disease have been predominantly M types 1 and 3 that produce pyrogenic exotoxin A or B or both. In this paper, the clinical and demographic features of streptococcal bacteremia, myositis, and necrotizing fasciitis are presented and compared to those of streptococcal toxic-shock syndrome. Current concepts in the pathogenesis of invasive streptococcal infection are also presented, with emphasis on the interaction between group A Streptococcus virulence factors and host defense mechanisms. Finally, new concepts in the treatment of streptococcal toxic-shock syndrome are discussed.

An emerging pathogen can be one that is totally new (e.g., human immunodeficiency virus), one that was known but has only recently been identified (e.g., Helicobacter pylori), or one that is old but has learned new tricks. The last type is, as Dr. Stanley Falkow contends, merely trying to "make a living" in a changing environment. Regardless of environmental pressures, many old pathogens have become major clinical problems because of increased virulence or antibiotic resistance (e.g., penicillin-resistant pneumococcus, multidrug-resistant Mycobacterium tuberculosis, methicillin-resistant Staphylococcus aureus, and vancomycin-resistant Enterococcus faecium).

Arguably, group A Streptococcus (GAS) is the quintessence of an old organism that has become more virulent. In this manuscript, the epidemiology, clinical spectrum, and pathogenesis of GAS infection are discussed in relation to the streptococcal toxic-shock syndrome (TSS).

Current and Historical Perspectives on the Prevalence and Severity of Streptococcal Infections

The British tabloids have recently coined the term "flesh-eating bacteria" to describe invasive necrotizing infections caused by GAS and have suggested that epidemics of streptococcal infection are imminent. Such aggrandizement is unfounded, yet it has served to heighten public awareness of this sporadic, but serious, infectious disease. Strictly speaking, an epidemic is defined as an increase in the prevalence of disease over a baseline endemic rate. In this context, we are, in fact, experiencing an epidemic of severe invasive GAS infections; however, few concrete prospective population-based data support this notion. Estimates suggest that the incidence of these infections is 10 to 20 cases/ 100,000 population. Thus, the stimulus for such public interest has not been the incidence of the syndrome, but more likely, the dramatic nature of these infections.

Whether these types of group A streptococcal infections will decline, stay the same, or increase is not known. History is replete with descriptions of epidemics of GAS infections and their nonsuppurative sequelae. In the 1600s, epidemics of scarlet fever spread from Italy and Spain to Northern Europe (1), and in 1736, an outbreak occurred in the American colonies, killing 4,000 people (2). Major epidemics of rheumatic fever occurred in World War II in the U.S. military (3). Soon afterward post-streptococcal glomerulonephritis struck several regions of the United States (4,5).

Many of these epidemics waxed and waned before the advent of antibiotics, suggesting that either changes in socioeconomic conditions or variations in the expression of virulence factors by the pathogen were responsible. This concept is best exemplified by the extraordinary mortality rate of scarlet fever documented in the latter part of the 1880s in New York, Chicago, and Norway; 25% to 30% of children with scarlet fever died during that period (5,6). By 1900, the mortality rate had dropped to under 2% in all three locations. Since socioeconomic conditions likely did not change markedly during that time and antibiotics were not yet available, the decrease in mortality rates must have been caused by reduced expression of a streptococcal virulence factor or by the slow acquisition of herd immunity to that factor.

The epidemiology of GAS infection is complex. More than 80 different M types of S. pyogenes exist, and five separate and distinct scarlatina toxins, streptococcal pyrogenic exotoxins (SPEs) (5) have also been described; some of these can be transmitted to different M types by bacteriophage. Minor drifts in the antigenic or virulence properties of GAS could account for the 5- to 6-year cycles of scarlet fever documented by Kohler (9). In the same way as antigenic shifts in influenza virus cause pandemics, major alterations in GAS virulence properties could cause major changes in clinical disease. The recent increases in severe GAS infections, following a 50- to 60-year span of relatively benign clinical disease, support this notion.

Toxic shock syndrome > 1 > 2 > 3 > 4

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