multocida strains representing various somatic types [24, 58–63]. Since endotoxin (LPS) is a key virulence factor in P. multocida, we examined each gene involved in LPS biosynthesis in
the X73 and P1059 strains and compared with the Pm70 strain. All three strains BMN-673 produced two glycoforms simultaneously, termed glycoforms A and B. Both X73 and P1059 contained the inner core biosynthetic complement of genes, including kdtA (P1059-01455; X73- 01363), hptA (opsX; P1059-02017; X73- 01921), kdkA (P1059-01451; X73-01359), hptC (rfaF; P1059-02018 ; X73-01922), hptD (P1059-01443; X73-01351 ) and gctA (P1059-01456; X73-01364). The gene that encodes for the enzyme which catalyzes the attachment of phosphoethanolamine to L-α-D Heptose −11 (Pm70-pm0223) was present only in strains P1059 and Pm70. There appeared to be some variation in the hptD gene between Pm70 and the X73 and P1059 strains although it was generally conserved between strains. Linking the inner core to the outer core is the hptE gene, present in both X73 and P1059 (X73-01185; P1059-01293). The outer core structure expressed by X73,
P1059 and Pm70 strains are structurally distinct and distal part of the molecule because in all three strains a polymeric O antigen was absent. The X73 strain but not P1059 and Pm70 express an outer core oligosaccharide that contains two terminal galactose residues, with phosphocholine (PCho). Present in X73 but absent from Pm70 and P1059 were the outer core biosynthetic genes involved in phosphocholine (PCho) biosynthesis LCZ696 order genes for somatic type 1. As reported previously , these genes include pcgA (X73-01180), pcgB (X73-01182), pcgC (X73-01181), and pcgD (X73-01183) as well as gatA (X73-01184). X73 attaches Sunitinib a phosphoethanolamine (PEtn) residue to the terminal galactose. Studies have shown  that PCho on the LPS is important for virulence of X73 strain to chickens. However, a clear role for PEtn has not been defined. Present in the outer core of Pm70 and P1059,
but absent in X73, were the biosynthetic genes for somatic type 3. These genes include losA (Pm70-Pm1143; P1059-01292); (Pm70-Pm1138; P1059-01287); (Pm70-Pm1139; P1059-01288); (Pm70-Pm1140; P1059-01289); and (Pm70- Pm1141; P1059-01290). In summary, comparative analyses of highly virulent versus avirulent P. multocida identified a number of genomic differences that may shed light on the ability of highly virulent strains to cause disease in the avian host. Most of the differences observed involved the presence of additional systems in virulent avian-source strains P1059 and/or X73 that appear to play metabolic roles. Such systems might enhance the fitness of these strains in the avian extraintestinal compartment, but without experimental evidence this is purely a speculative observation.