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aureus , group B streptococcus, and Gram negative enteric organisms. Combination therapy is normally provided while culture results are pending and consists of a semisynthetic penicillin , such as oxacillin and gentamicin . Patients allergic to penicillin can be treated with a first generation cephalosporin. Group A Streptococcal Toxic Shock Syndrome (StrepTSS) StrepTSS usually occurs secondary to soft tissue infections, particularly as a secondary infection of varicella lesions or as a complication of necrotizing fasciitis, myositis, pneumonia, or post-partum infection.

M-type l GAS has been the predominant serotype associated with StrepTSS, but types 3, 12, and 28 have been implicated as well (7,80,87).

Recent interest in the pathophysiology of this disorder has focused on the role of streptococcal pyrogenic exotoxins (SPEs), extracellular products of group A streptococci that mediate not only scarlatiniform-like rashes but also multi-organ damage and shock.

These toxins were rarely associated with GAS strains in the United States until the recent increase in the number of cases of StrepTSS amoxicillin for walking pneumonia (7,87). SPEA is the most common exotoxin found in the United States and has been shown to be both a superantigen and a potent inducer of tumor necrosis factor (7).

SPEB has also been implicated but more commonly occurs in episodes of StrepTSS in European countries (7,80,87).

Recently, nicotine adenine glycohydrolase (NADase) has been linked with the resurgence of severe invasive group A streptococcal infections (86).

The patient with StrepTSS requires intensive management of hemodynamic abnormalities and vital functions. Patients with a soft tissue focus of infection may require surgical intervention.

Broad spectrum antibiotic coverage should be instituted until the presence of group A streptococcus has been confirmed. Therapy may then consist of parenterally administered clindamycin . In StrepTSS, tissue destruction continues despite high concentrations of penicillin .

Penicillin is known to be relatively ineffective in the treatment of soft tissue infections with a high concentration of organisms (the Eagle effect) (83,85).

This is thought to be due to the slow rate of replication of group A streptococci, decreased expression of penicillin-binding proteins, and the fact that penicillin acts by interfering with cell wall synthesis (83,85).

Clindamycin inhibits protein synthesis, decreases the production of M proteins and toxins, and is unaffected by slow growing toxin-producing streptococci (83,85).

showed that by the 4th day of therapy, the frequency of capsular expression by GAS was significantly lower in patients treated with clindamycin than in patients treated with penicillin (9). A mouse model of a soft tissue infection with GAS showed clindamycin to be more effective than penicillin (83).

Erythromycin and ceftriaxone may also be more effective than penicillin in such cases.

Accompanying the increase in number and severity of invasive group A streptococcal infections is an increase in the incidence of group A streptococcal bacteremia. There have been a number of cases associated with intravenous drug abuse as well as nosocomial outbreaks in nursing homes.

Intravenous drug use has become the leading cause of GAS bacteremia in individuals between the ages of 14 and 40 years (78).

Bacteremia usually follows a cutaneous focus of infection but may follow an upper respiratory infection. In addition, the number of children with varicella who develop GAS bacteremia has increased (26).

reported an increased incidence of GAS bacteremia in patients with varicella from 7% to 50% at their institution (26).

GAS bacteremia in varicella is thought to occur secondary to a superinfected cutaneous lesion.

Serotypes M1 and M3 have been most commonly isolated in patients with GAS bacteremia. Serotypes M1, M3, and M18 are more invasive and are associated with higher morbidity and mortality rates than M4 and M12, which are generally considered less virulent.

M type 1 strains produce pyrogenic exotoxins A and B, and the latter toxin also has associated proteinase activity (7). Therapy for GAS bacteremia consists of parenterally administered penicillin . Patients allergic to penicillin can be treated with clindamycin , vancomycin, or a first generation cephalosporin.

Pneumonia secondary to group A streptococcus is frequently associated with preceding or concurrent viral infections such as measles, varicella, or influenza. Since the mid 1980s, the number of reports describing this association has increased.

Up to 30% of patients with GAS pneumonia have a history of group A streptococcal upper respiratory tract infection (8). Empyema develops in 40% of patients, and bacteremia in 15%. Other complications include mediastinitis, pericarditis, pneumothorax, and bronchiectasis. Therapy consists of surgical drainage of an empyema and parenteral penicillin .

Adequate drainage of pleural infection may be difficult and frequently requires prolonged chest amoxicillin throwing up tube drainage, thoracoscopy or pleural surgery. P eritonsillar Abscess (AQuinsy@): Peritonsillar abscess results from direct extension of group A streptococcus from an acute pharyngitis.