Early targeted antibacterial therapy is essential when treating invasive group A streptococcal infection
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Early targeted antibacterial therapy is essential when treating invasive group A streptococcal infection Life-threatening invasive group A streptococcal infections progress rapidly. Effective management depends on early recognition of symptoms and early initiation of antibacterial therapy and aggressive supportive care. The use of intravenous immunoglobulin may be considered in patients with streptococcal toxic shock syndrome.
10 per 100 000 population).[1] Likewise, mean case fatality rates are much higher in middle- and lower-income countries than in affluent countries (25% vs 8–6%).[1] When STSS develops, the case fatality rate is close to 50% in both affluent and lower-income countries.[3]
A highly virulent pathogen
Rare type of infection that can be serious Group A streptococcus (Streptococcus pyogenes or GAS) is a Gram-positive bacterium that causes a range of infections such as pharyngitis, impetigo, acute rheumatic fever and acute glomerulonephritis.[1] Invasive GAS infections are rare, but serious, infections of normally sterile sites, which are associated with high mortality, especially when they lead to streptococcal toxic shock syndrome (STSS). The soft tissues are the site of up to 50% of invasive GAS infections, with necrotizing fasciitis being a particularly severe form. Other clinical syndromes caused by invasion of GAS into sterile sites include pneumonia, osteomyelitis, septic arthritis and meningitis.[1] In »15% of patients with invasive GAS infection, a focus for bacteraemia is not identified. This article summarizes the epidemiology, pathogenesis and management of invasive GAS infection, as reviewed by Steer et al.[1]
Who is at risk? Invasive GAS infection can strike healthy individuals at any age.[1] The risk is increased in those who are young or elderly, are male or injecting drug users, are of White European descent, or have skin lesions, pre-existing diabetes mellitus, heart disease, malignancies or influenza. The risk is also increased during the postpartum period in females.[1] Children with varicella infection are at high risk of developing invasive GAS infections, particularly soft issue infection, including necrotizing fasciitis.[2] Although the mechanism by which varicella predisposes to necrotizing fasciitis is not clear, pox lesions may act as portals of entry to the dermal and fascial layers, and/or varicella infection may cause immunosuppression.[2] The median duration of varicella vesicles before developing symptoms of necrotizing fasciitis is 3–4 days.[1] The incidence of invasive GAS infection is lower in industrialized countries than in developing countries (2–4 vs
It is not yet clear why exposure to GAS leads to invasive infection in some, but not other, individuals.[1] Susceptibility may be due not only to host and environmental factors, but also to acquisition of virulence factors by different types of GAS strains. After invasion, GAS produces exotoxins that act as superantigens that bypass normal immune response pathways, leading to a massive release of proinflammato
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