Silversides JA, Lappin E, Ferguson AJ. Staphylococcal toxic shock syndrome: mechanisms and management. Curr Infect Dis Rep. 2010 Sep;12(5):392-400.
Staphylococcal toxic shock syndrome is a rare complication of Staphylococcus aureus infection in which bacterial toxins act as superantigens, activating very large numbers of T cells and generating an overwhelming immune-mediated cytokine avalanche that manifests clinically as fever, rash, shock, and rapidly progressive multiple organ failure, often in young, previously healthy patients. The syndrome can occur with any site of S. aureus infection, and so clinicians of all medical specialties should have a firm grasp of the presentation and management. In this article, we review the literature on the pathophysiology, clinical features, and treatment of this serious condition with emphasis on recent insights into pathophysiology and on information of relevance to the practicing clinician.
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Lappin E, Ferguson AJ. Gram-positive toxic shock syndromes. Lancet Infect Dis. 2009 May;9(5):281-90.
Toxic shock syndrome (TSS) is an acute, multi-system, toxin-mediated illness, often resulting in multi-organ failure. It represents the most fulminant expression of a spectrum of diseases caused by toxin-producing strains of Staphylococcus aureus and Streptococcus pyogenes (group A streptococcus). The importance of Gram-positive organisms as pathogens is increasing, and TSS is likely to be underdiagnosed in patients with staphylococcal or group A streptococcal infection who present with shock. TSS results from the ability of bacterial toxins to act as superantigens, stimulating immune-cell expansion and rampant cytokine expression in a manner that bypasses normal MHC-restricted antigen processing. A repetitive cycle of cell stimulation and cytokine release results in a cytokine avalanche that causes tissue damage, disseminated intravascular coagulation, and organ dysfunction. Specific therapy focuses on early identification of the illness, source control, and administration on antimicrobial agents including drugs capable of suppressing toxin production (eg, clindamycin, linezolid). Intravenous immunoglobulin has the potential to neutralise superantigen and to mitigate subsequent tissue damage.
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Murray RJ. Recognition and management of Staphylococcus aureus toxin-mediated disease. Intern Med J. 2005 Dec;35 Suppl 2:S106-19.
The ubiquitous human pathogen Staphylococcus aureus is capable of producing a formidable range of extracellular toxins that can have significant deleterious effects on the host. Toxic shock syndrome (TSS) results from infection or colonization with a strain of S. aureus that produces staphylococcal enterotoxin(s). The key features of TSS are widespread erythroderma occurring in association with profound hypotension and multiple organ dysfunction. As morbidity and mortality from TSS are appreciable, early recognition of TSS combined with intensive supportive management is critical. Staphylococcal foodborne disease (SFD) is caused by contamination of food during preparation or serving by preformed S. aureus enterotoxin(s). Symptom-onset is abrupt and the disease may be severe enough to warrant hospitalization, but it is usually self-limiting and does not require specific antistaphylococcal therapy. Staphylococcal scalded skin syndrome (SSSS) results from colonization or infection with a strain of S. aureus that produces epidermolytic toxin(s). SSSS ranges in severity from trivial focal skin blistering to extensive, life-threatening exfoliation. This review discusses the epidemiology, pathogenesis, diagnosis, and management of TSS, SFD and SSSS.
Chuang YY, Huang YC, Lin TY. Toxic shock syndrome in children: epidemiology, pathogenesis, and management. Paediatr Drugs. 2005;7(1):11-25.
Toxic shock syndrome (TSS) is an acute, toxin-mediated illness, like endotoxic shock, and is characterized by fever, rash, hypotension, multiorgan involvement, and desquamation. TSS reflects the most severe form of the disease caused by Staphylococcus aureus and Streptococcus pyogenes. A case definition for staphylococcal TSS was well established in the early 1980s and helped in defining the epidemiology. Since the late 1980s, a resurgence of highly invasive streptococcal infections, including a toxic shock-like syndrome, was noted worldwide and a consensus case definition for streptococcal TSS was subsequently proposed in 1993. Both TSS and the toxic shock-like syndrome occur at a lower incidence in children than in adults. Changes in the manufacturing and use of tampons led to a decline in staphylococcal TSS over the past decade, while the incidence of nonmenstrual staphylococcal TSS increased. Nonmenstrual TSS and menstrual TSS are now reported with almost equal frequency. The incidence of streptococcal TSS remains constant after its resurgence, but varies with geographic location. Streptococcal TSS occurs most commonly following varicella or during the use of NSAIDs. Sites of infection in streptococcal TSS are much deeper than in staphylococcal TSS, such as infection caused by blunt trauma, and necrotizing fasciitis. Bacteremia is more common in streptococcal TSS than in staphylococcal TSS. Mortality associated with streptococcal TSS is 5-10% in children, much lower than in adults (30-80%), and is 3-5% for staphylococcal TSS in children.TSS is thought to be a superantigen-mediated disease. Toxins produced by staphylococci and streptococci act as superantigens that can activate the immune system by bypassing the usual antigen-mediated immune-response sequence. The host-pathogen interaction, virulence factors, and the absence or presence of host immunity determines the epidemiology, clinical syndrome, and outcome. Early recognition of this disease is important, because the clinical course is fulminant and the outcome depends on the prompt institution of therapy. Management of a child with TSS includes hemodynamic stabilization and appropriate antimicrobial therapy to eradicate the bacteria. Supportive therapy, aggressive fluid resuscitation, and vasopressors remain the main elements. An adjuvant therapeutic strategy may include agents that can block superantigens, such as intravenous immunoglobulin that contains superantigen neutralizing antibodies.
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