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Abstract

Introduction: Streptococcal toxic-shock syndrome (STSS) carries a high mortality of 39%(1,2) and is defined by a criteria of isolation of Group A Streptococcus (GAS) from a sterile site with hypotension as well as clinical or laboratory evidence of two or more of the following: renal impairment, coagulopathy, liver abnormalities, acute respiratory distress syndrome, extensive tissue necrosis or erythematous rash(3). Almost half the sources of infection are not found. The mechanism of action is similar to that of Staphylococcal toxic syndrome via exotoxin (super antigens) triggering the immune similar to that of an allergic reaction leading widespread vessel dilation and shock with multi-organ failure. A 54 year old male with no significant past medical history comes to the emergency room with complaints of sudden fatigue, nausea, vomiting, fever and shortness of breath for the last few hours. In the emergency room, he was noted to be hypotensive despite adequate fluid resuscitation and tachypnic, which ultimately required intubation. His physical exam revealed a temperature over 102°F, requiring mechanical ventilation with 100% FiO2 with an oxygen saturation of 90%, 80/50 mmHg and a heart rate of 120 beats per minute. Skin was warm to touch without any evidence of rash, awake on the ventilator able to follow commands, clear breath sounds, tachycardic without evidence of murmur, soft abdomen with no evidence of guarding or rigidity. No bowel sounds were heard. Radiological pan scan was negative. Notable lab investigations yielded leukopenia, lactic acid of 9mg/dl, coagulopathy, deranged hepatic profile and renal dysfunction. Blood cultures yielded Streptococcus pyogenes; other cultures including lumbar, sputum and urine culture were negative. Empiric antibiotics including a beta-lactam had been started on arrival and the patient continued to deteriorate. When the blood cultures returned clindamycin was added to supplement penicillin therapy. Patient stabilized over one week and was transferred out of the intensive care unit. Streptococcal toxic shock syndrome is distinctly different from Staphylococcal toxic shock syndrome, besides different bacterial genus, in that it is always associated with a desquamating rash as the prevalent feature and essential for diagnosis. Rash is not required for STSS. It is essential to remember that both Streptococcal and Staphylococcal toxic shock syndrome carry a high mortality rate and that suspicion clinically should warrant a thorough check for source (foreign body, radiology, cultures) as well as antibiotic therapy with beta lactams as well as clindamycin. Studies report that a high concentration of GAS leads to a loss of beta lactam binding sites, thus decreasing its efficacy(4). This highlights the importance of adding clindamycin, as it is not affected by the concentration of GAS, suppresses the exotoxin production, increases host phagocytosis and has been shown retrospectively to be associated with better outcomes(5).