Capsular polysaccharide is the principal virulence factor for the nosocomial pathogen, Acinetobacter baumannii, which was recently listed by the World Health Organisation as the most critical pathogen of global concern due to resistance to almost all therapeutically suitable antibiotics. We have shown that the genetic content at the capsule biosynthesis locus (K locus) varies extensively between isolates, which allows the species to generate different capsule structures on the cell surface. This indicates that capsule variation may be providing a crucial fitness advantage for survival and persistence. Our analysis of the K locus has revealed more than 100 different clusters of genes, including KL12 and KL73 that each contain a module of 10 genes, 6 of which are required for synthesis of 5,7-di-N-acetyllegionaminic acid (Leg5Ac7Ac), a non-2-ulosonic acid associated with virulence properties in other bacteria. Three of the remaining four genes were novel but shared by both clusters, while the remaining gene was unique. The chemical composition and structure of the capsule purified from strains carrying KL12 and KL73 were determined using Nuclear Magnetic Resonance (NMR). The K12 capsule contained a 5,7-acetylated form of a novel non-2-ulosonic acid, which has never previously been found before in nature. We named this sugar acinetaminic acid (Aci) after the species it was discovered in. The K73 capsule similarly contained a 5,7-acetylated form of a different non-2-ulosonic acid, which was found to be the 8-epimer of Aci, and we named this sugar 8-epi-acinetaminic acid (8eAci). Both these new sugars are 7/8-epimers of Leg5Ac7Ac, and a biosynthetic pathway for Aci from Leg5Ac7Ac was proposed. Examination of the genetics and chemical structures of these major antigenic structures is the first step towards understanding the role of capsule variation in the success of A. baumannii clones in the hospital environment.