Tag Archives: Staphylococcal toxic shock syndrome

Nosocomial Staphylococcal Toxic Shock. Case Report

DOI: 10.1515/jccm-2016-0020

Staphylococcal toxic shock syndrome (STSS) is a rare, potentially lethal infection, with a clinical picture of multiple organ dysfunction and shock. The etiology is Staphylococcus aureus exotoxin, while enterotoxins act as superantigens. Most cases are identified in women using a vaginal tampon.  A 51-year-old female, with a past medical history of biliary dyskinesia, presented in the emergency room complaining of sudden onset of abdominal pain, vomiting, headache, myalgia, and chills. The initial diagnosis was biliary colic and was treated parenterally with Amoxi-clavulanate and fluid replacement. Initially, progress was unsatisfactory. Four days after admission she developed a systemic inflammatory syndrome, diffuse rash, jaundice, oliguria, confusion, persistent hypotension and biological evidence of thrombocytopenia, nitrogen retention, and cholestasis. She was admitted to the intensive care unit. A gluteal phlegmon induced after intramuscular injections was identified and surgically treated. Blood bacteriological cultures were negative, though MRSA was isolated in phlegmon pus. A diagnosis of STSS was based on CDC criteria.
The risks of similar infections could be prevented by limiting intramuscular treatments and monitoring invasive procedures.

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The Management of Staphylococcal Toxic Shock Syndrome. A Case Report

DOI: 10.1515/jccm-2016-0011

Staphylococcal toxic shock syndrome (TSS) is most frequently produced by TSS toxin-1 (TSST-1) and Staphylococcal enterotoxin B (SEB), and only rarely by enterotoxins A, C, D, E, and H. Various clinical pictures can occur depending on severity, patient age and immune status of the host. Severe forms, complicated by sepsis, are associated with a death rate of 50-60%. The case of a Caucasian female infant, aged seven weeks, hospitalized with a diffuse skin rash, characterized as allergodermia, who initially developed TSS with axillary intertrigo, is reported. TSS was confirmed according to 2011 CDC criteria, and blood cultures positive for Methicillin-sensitive Staphylococcus aureus (MSSA). Severe development occurred initial, including acidosis, consumption coagulopathy, multiple organ failures (MOF), including impaired liver and kidney function. Central nervous system damage was manifest by seizures. Clinical management included medical supervision by a multidisciplinary team of infectious diseases specialist and intensive care specialist, as well as the initiation of a complex treatment plan to correct hydro electrolytic imbalances and acidosis. This treatment included antibiotic and antifungal therapy, diuretic therapy, immunoglobulins, and local treatment similar to a patient with burns to prevent superinfection of skin and mucous membranes lesions. There was a favourable response to the treatment with resolution of the illness.

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