Here is another one used for uncomplicated bloodstream infection events:

Infections due to these species of streptococci are usually rapidly responsive to appropriate antibiotic therapy which can be of short duration with no minimum IV requirement as endocarditis is not a usual consideration.  Penicillin resistance has not been documented and flucloxacillin is just as active (see this discussion).

Less commonly, Streptococcus pyogenes (group A strep) causes invasive disease such as necrotizing infection of the skin and fascia, gangrenous myositis or pneumonia, and these types of infection are complicated by a toxic shock syndrome (below)  in approximately one-third of cases.

Hunter region data (2008-2013) on bacteraemic infections document 487 community-acquired events due to these species, of which 42% were due to a skin or soft tissue source and 34% due to sepsis with no primary focus. A significant minority (7%) presented as community acquired pneumonia. In this case series, the proportions due to species groups A,  B, and C or G were 36%, 32% and 32% respectively.  Pharyngitis or other ENT infection was a rare source of bacteraemic infection, occurring in 6 cases only. Endocarditis occurred in 10 cases.  Over the same period, there were 51 healthcare-associated bacteraemic cases, a majority due to Streptococcus agalactiae (group B strep).

Toxic shock syndrome (TSS) should be considered in patients presenting with shock in the absence of a clear aetiology. There are a number of infectious causes aside from Group A streptococci.  Other important findings include a history of recent trauma, severe pain, and fever.  The current CDC case definition is detailed here and includes presence of multi-organ involvement with two or more systems including kidney, coagulation, liver, lungs (ARDS), skin (typically an erythematous macular rash that may desquamate) and soft tissue necrosis ( including necrotizing fasciitis or myositis, or gangrene).

Additional treatment considerations in TSS include surgical debridement, addition of clindamycin to reduce toxin production (and other putative effects) and administration of intravenous immunoglobulin (toxin neutralisation). These patients frequently require intensive care management and mortality is high.