Early-onset GBS disease (EOD) with presence of pulmonary edema and septic shock has the pathophysiologic characteristics of a toxemic shock syndrome. A polysaccharide exotoxin (GBS toxin) has been isolated from culture media of bacteria obtained from GBS infected neonates (Pediatr Res 15:892, 1981), which induces a complement activated cytokine driven inflammatory response in other systems (AACR proceedings 36:1334, 1995). GBS toxin has previously not been demonstrated in patients with GBS sepsis.

Using a newly developed technique, 3 neonates with culture proven GBS sepsis of varying severity were studied during the first 2d after birth. One infant required ECMO, the 2nd high frequency ventilation and nitric oxide and the 3rd with mild disease only increased FiO2 for 7h with maixmum of 0.4. Plasma TNF levels in the 3 patients were 116, 38 and 23 pg/ml and IL8 level were 159, 73 and 0.1 ng/ml, respectively. Presence of GBS toxin in blood and urine of all 3 patients was demonstrated by a sandwich ELISA assay using both anti-C3 and anti-GBS toxin MoAb for detection. Urine concentrations ranged from 6 to 9 μg/ml. No GBS toxin was identified in 18 control infants. Decreasing urine concentrations were observed in the 2nd infant from 6 to 36 h after birth, during which time 2.03 mg was excreted. A compound, isolated from the urine of the 2nd infant cochromatographed with and had the same sugar composition as GBS toxin. It was given to a young lamb in a dose of 8 μg/kg i.v. and elicited a pathophysiologic response similar to the symptomatology of neonates with EOD and comparable to that observed from GBS toxin isolated from GBS culture media (Pediatr Res 35:571, 1994).

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