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Chapter 7 : The Reemergence of Severe Group A Streptococcal Disease: an Evolutionary Perspective

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Abstract:

This chapter reviews changes in the epidemiology of group A streptococcal infections and describes factors associated with the fitness and virulence of the pathogen. It also highlights the genetic diversity of group A streptococci, which, acted on by host factors, may account for periodic changes in disease severity. Childbed fever was one of the most frequent causes of death among postpartum women. A number of characteristics of group A streptococci may contribute to their fitness. These determinants can be categorized into three functional classes: adherence and colonization, invasion and replication, and avoidance of host defenses. Activation of the alternate complement pathway produces C5a, which is one of the primary mediators of chemotaxis in human tissue, attracting neutrophils to sites of infection. Horizontal gene transfer has resulted in -like genes and regulons with mosaic structures. Such an ability to recombine, in conjunction with strong selective pressures, can accelerate the evolution of functional diversity. The current increase in severe disease, particularly streptococcal toxic shock syndrome (STSS) and necrotizing fasciitis, is most likely related to changes in serotype distribution, production of toxins, and/or other factors. As immunity to these virulence factors increases, virulence will be lost. The author believes that this resurgence of more severe group A streptococcal disease does not represent the natural selection of a more virulent clone that will predominate but rather that as population immunity increases one will once again return to periods of waxing and waning of group A streptococcal disease severity.

Citation: Low D, McGeer A, Schwartz B. 1998. The Reemergence of Severe Group A Streptococcal Disease: an Evolutionary Perspective, p 93-123. In Scheld W, Armstrong D, Hughes J (ed), Emerging Infections 1. ASM Press, Washington, DC. doi: 10.1128/9781555816940.ch7

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Tumor Necrosis Factor alpha
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Restriction Fragment Length Polymorphism
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Toxic Shock Syndrome
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Figures

Image of Figure 1.
Figure 1.

The •like genes of group A streptococci are located adjacent to each other at a chromosomal locus called the regulon, where they are flanked by a regulatory gene called and the gene. which encodes a C5a peptidase. (Reprinted from [123] with permission from M. A. Kehoe and Elsevier Science.)

Citation: Low D, McGeer A, Schwartz B. 1998. The Reemergence of Severe Group A Streptococcal Disease: an Evolutionary Perspective, p 93-123. In Scheld W, Armstrong D, Hughes J (ed), Emerging Infections 1. ASM Press, Washington, DC. doi: 10.1128/9781555816940.ch7
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Image of Figure 2.
Figure 2.

Bridging of T cells and antigen-presenting cell s. A schematic model of a superantigen (SAg) interaction with a TCR and an MHC class II molecule is shown. APC. antigen-presenting cell; Ag. antigen. (Reprinted from Clinical Microbiology Reviews 125) with permission from M. Kotb and the American Society for Microbiology.)

Citation: Low D, McGeer A, Schwartz B. 1998. The Reemergence of Severe Group A Streptococcal Disease: an Evolutionary Perspective, p 93-123. In Scheld W, Armstrong D, Hughes J (ed), Emerging Infections 1. ASM Press, Washington, DC. doi: 10.1128/9781555816940.ch7
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Image of Figure 3.
Figure 3.

Interplay between T-cell• and antigen-presenting cell (APC)-derived cytokines and induction of an inflammatory cytokine cascade by superantigens. IFN, interferon; Sag, Superantigen; TNF, tumor necrosis factor. (Reprinted (from ( ) with permission from M. Kotb and the American Society), for Microbiology.)

Citation: Low D, McGeer A, Schwartz B. 1998. The Reemergence of Severe Group A Streptococcal Disease: an Evolutionary Perspective, p 93-123. In Scheld W, Armstrong D, Hughes J (ed), Emerging Infections 1. ASM Press, Washington, DC. doi: 10.1128/9781555816940.ch7
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Image of Figure 4.
Figure 4.

Reported cases of scarlet fever per 100.000 persons and scarlet fever case fatality rates in Oslo, Norway, from 1863 to 1878. (Reprinted from the [ ] with permission from R. M. Krause and the University of Chicago Press.)

Citation: Low D, McGeer A, Schwartz B. 1998. The Reemergence of Severe Group A Streptococcal Disease: an Evolutionary Perspective, p 93-123. In Scheld W, Armstrong D, Hughes J (ed), Emerging Infections 1. ASM Press, Washington, DC. doi: 10.1128/9781555816940.ch7
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Image of Figure 5.
Figure 5.

Monthly incidences of group A streptococcal bacteremia in Sweden. 1987 10 1989. (Reprinted from the [ ] with permission from A. Strömberg and the University of Chicago Press.)

Citation: Low D, McGeer A, Schwartz B. 1998. The Reemergence of Severe Group A Streptococcal Disease: an Evolutionary Perspective, p 93-123. In Scheld W, Armstrong D, Hughes J (ed), Emerging Infections 1. ASM Press, Washington, DC. doi: 10.1128/9781555816940.ch7
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Image of Figure 6.
Figure 6.

(A) Temporal distribution of New Zealand M type 1 and 12 isolates as percentages or all M typeable isolates by year. (B) Years in which each RFLP type was found among New Zealand isolates. (Reprinted from the [346] with permission from D. R. Martin and the University of Chicago Press.,

Citation: Low D, McGeer A, Schwartz B. 1998. The Reemergence of Severe Group A Streptococcal Disease: an Evolutionary Perspective, p 93-123. In Scheld W, Armstrong D, Hughes J (ed), Emerging Infections 1. ASM Press, Washington, DC. doi: 10.1128/9781555816940.ch7
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Tables

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Table 1.

Possible virulence and transmissibility determinants of group A streptococci: adherence and colonization

Citation: Low D, McGeer A, Schwartz B. 1998. The Reemergence of Severe Group A Streptococcal Disease: an Evolutionary Perspective, p 93-123. In Scheld W, Armstrong D, Hughes J (ed), Emerging Infections 1. ASM Press, Washington, DC. doi: 10.1128/9781555816940.ch7