Coxiella burnetii is the aetiological agent of Q fever. LPS is a major factor of virulence of the bacterium, and therefore studies of its structure/function relationship studies are of potential interest. In virulent phase I, C. burnetii biosynthesises smooth LPS I with an O-specific chain, whereas in avirulent phase II, it synthesises rough LPS II [¹]. Both LPSs were isolated [¹] from the C. burnetii isolates RSA 493, clone 7, and RSA 439, clone 4, respectively. We investigated an LPS from the C. burnetii clonal derivative RSA 514 named ‘Crazy’ (Cr), which was isolated from the placental tissue of a guinea pig infected with the RSA 493 isolate for 343 days [²]. The major emphasis was put on the lipid A as no data on its structure have been available thus far. It has been recognised recently that variation of the lipid A domain of LPS serves as one strategy utilised [³] by Gram-negative bacteria to promote survival by providing resistance to components of the innate immune system and helping to evade recognition by Toll-like receptor 4. Thus, it was of interest to see if the long-term survival of the microorganism in the host led to modifications in its lipid A in comparison with the known structures for lipid A from the C. burnetii isolate Priscilla [⁴] and also those established most recently in the LPS I and LPS II (P.V. Vadovic and R.T. Toman, unpublished results).