Sodium polyanethole sulphonate (SPS) under the trade name Liquoid is a constituent in culture media used for growth of bacteria from blood samples from patients suspected of bacteraemia. SPS prevents killing of bacteria by innate cellular and humoral factors. We analyzed the effect of SPS on the three complement activation pathways, the classical, the alternative, and the lectin pathway, respectively. Inhibition of complement activity by SPS is caused by a blocking of complement activation and is not a result of complement consumption. The classical pathway is inhibited at SPS concentrations higher than 0.1mg/ml, and complete inhibition is seen at 0.4mg/ml. An SPS concentration of 0.5mg/ml completely inhibits binding of C1q, and subsequent incorporation of C3, C4, and C9. The same was observed for the alternative pathway with an inhibition at SPS concentrations from 0.1mg/ml and a complete inhibition from 0.4mg/ml. Here properdin binding was completely absent and no incorporation of C3 and C9 was observed. In contrast, the lectin complement pathway remains unaffected at these SPS concentrations and inhibition is first observed from 0.7mg/ml. A complete inhibition required concentrations higher than 1mg/ml. SPS is used in growth media (e.g BACTEC(TM) and BacT/Alert(R)) in concentrations from 0.3-0.5mg/ml. The well-known finding that certain bacteria are growth-inhibited by blood factors could therefore be a consequence of the lectin pathway, which is not inhibited at these concentrations. Additionally our findings also open up for a new assay for the assessment of the functional capacity of the lectin complement pathway.