“…Antibodies against capsule, lipopolysaccharides and outer membrane proteins serve as opsonins, thereby enabling phagocytosis by neutrophils (Thwaits and Kadis, 1991; Byrd and Kadis, 1992), but do not destroy A. pleuropneumoniae cells by complement binding (Rycroft and Cullen, 1990). Although these antibodies provide only partial protection against challenge by homologous A. pleuropneumoniae serotypes and, particularly, by heterologous serotypes (Inzana et al, 1988, 1991, 1993; Jansen, 1994; Beaudet et al, 1994), respective antigens contribute to typical lesion formation (Fenwick and Osburn, 1986; Paradis et al, 1994; Fenwick, 1994). Non‐capsulated A. pleuropneumoniae mutants are not virulent, but are useful as vaccines in protecting against swine pleuropneumonia (Inzana, 1996).…”