Acute serogroup A streptococcal shock: A porcine model.

To elucidate the pathophysiology of acute shock caused by serogroup A streptococci (GAS), GAS were given intravenously to 25 pigs. Short-time infusions of GAS (n=11) caused variable and unpredictable responses. A continuous infusion of 5x108 cfu/kg/h (n=8) caused pulmonary hypertension, arterial hypotension, and reduced cardiac output and liver perfusion, progressing to circulatory shock within 2-4 h. Halving the infusion rate (n=6) induced a more gradual development of shock and doubled the mean survival time from 2.1 to 4.0 h. Mean tumor necrosis factor-alpha levels (+/-SE) increased from 25+/-1 to 40+/-3 pg/mL. Only slight signs of organ dysfunction were observed, which indicates that this is primarily a model of acute septic shock. Light microscopy revealed moderate inflammatory reactions in lung, liver, and gut biopsy samples, although high numbers of viable, M-typeable GAS were recovered from tissues. The present model may be useful to study mechanisms involved in acute septic shock as well as therapeutic interventions.