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We describe 8 cases of POWV encephalitis in Massachusetts and New Hampshire in 2013-2015. Prior to this, there had been only 2 cases of POWV encephalitis identified in Massachusetts. These cases may represent emergence of this virus in a region where its vector, I. scapularis, is known to be prevalent or may represent the emerging diagnosis of an underappreciated pathogen. We recommend testing for POWV in patients who present with encephalitis in the spring to fall in New England.

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Although the toxicity of streptolysin O (SLO) and streptolysin S (SLS) in purified group A streptococci (GAS) has been established, the effect of these molecules in natural infection is not well understood. To identify whether biologically relevant concentrations of SLO and SLS were cytotoxic to epithelial and phagocytic cells that the bacteria would typically encounter during human infection and to characterize the influence of cell injury on bacterial pathogenesis, we derived GAS strains deficient in SLO or SLS in the background of an invasive GAS M3 isolate and determined their virulence in in vitro and in vivo models of human disease. Whereas bacterial production of SLO resulted in lysis of both human keratinocytes and polymorphonuclear leukocytes, GAS expression of SLS was associated only with keratinocyte injury. Expression of SLO but not SLS impaired polymorphonuclear leukocyte killing of GAS in vitro, but this effect could only be demonstrated in the background of acapsular organisms. In mouse invasive soft-tissue infection, neither SLO or SLS expression significantly influenced mouse survival. By contrast, in a mouse model of bacterial sepsis after intraperitoneal inoculation of GAS, SLO expression enhanced the virulence of both encapsulated and acapsular GAS, whereas SLS expression increased the virulence only of acapsular GAS. We conclude that the cytotoxic effects of SLO protect GAS from phagocytic killing and enhance bacterial virulence, particularly of strains that may be relatively deficient in hyaluronic acid capsule. Compared to SLO, SLS in this strain background has a more modest influence on GAS pathogenicity and the effect does not appear to involve bacterial resistance to phagocytosis.Group A streptococci (GAS) are important human pathogens. Millions of children each year develop GAS pharyngitis. Although throat infection is typically benign, it can be complicated by the development of acute and chronic rheumatic heart disease. Invasive GAS infection occurs less frequently than pharyngitis but causes significantly more morbidity. The incidence of severe invasive GAS disease associated with shock and organ failure appears to be increasing (14,38,40).GAS produce two hemolysins that may contribute to pathogenesis. Streptolysin O (SLO) is a well-characterized oxygenlabile prototype of a cholesterol-binding bacterial exotoxin. When cultured in broth, GAS express SLO during exponentialphase and early stationary-phase growth (1). Streptolysin S (SLS) is an oxygen-stable oligopeptide primarily responsible for the characteristic zone of beta-hemolysis surrounding GAS colonies grown on blood-agar medium (17). SLS production occurs when cells are in stationary-phase growth conditions in broth culture (9).Early studies of purified SLO and SLS demonstrated that these hemolysins were toxic to a variety of human cells in vitro and in vivo (3,10,16,19,20). In rabbits, injection of SLO caused blood vessel contraction, increased capillary permeability, massive intravascular thrombosis, dermal necrosis, cardio...

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