Strains of containing different combinations of the transmissible plasmids governing production of α-haemolysin (Hly), enterotoxin (Ent) and K88 antigen (K88) were prepared by the selective addition or removal of these plasmids and tested for ability to produce diarrhoea when given orally to naturally reared piglets and to recently weaned pigs.

The removal of the K88 plasmid from an O141:K85ab,88ab strain was accompanied by the loss of its diarrhoea-producing capacity. It was restored by introducing a K88 plasmid from another strain of . The removal of the Hly plasmid had no observable effect. Neither did its removal from another wild enteropathogenic strain of antigenic formula O141:K85ac; the Hly form of this strain, like the Hly form, produced oedema disease in addition to diarrhoea.

As a consequence of receiving an Ent plasmid, a non-haemolytic O8:K40, 88ab:H9 strain produced diarrhoea more frequently and more severely in piglets than hitherto; after the removal of the K88 plasmid it became non-enteropathogenic.

A non-pathogenic O9:K36:H19 strain was rendered enteropathogenic by the introduction of plasmids. The K88 Ent form produced moderately severe diarrhoea in piglets. A smaller proportion of those given the K88 Ent form developed a milder diarrhoea. The K88 Ent and the K88 Ent forms had no observable ill-effect.

Bacteriological examinations on the animals given the different forms of the O141:K85ab,88ab, the O8:K40,88ab:H9 and the O9:K36:H19 strains revealed that it was the K88 antigen that enabled the organisms to proliferate high up in the small intestine, an essential prerequisite in the pathogenesis of diarrhoea. The Ent plasmid appeared to play no part in this proliferation, only in the diarrhoea that followed.

The introduction of Hly into strains of was usually accompanied by an increase in virulence for mice challenged intraperitoneally, the extent of the increase varying according to the particular Hly plasmid introduced. Virulence was not related directly to haemolytic activity.

K88 forms of strains of were less virulent for mice on intraperitoneal injection than were the corresponding K88 forms. So were K88 forms of and after intraperitoneal and oral infection; the K88 organisms were less able to survive in the alimentary tract and in the tissues than were the K88 ones. A K88 form of was also less virulent for pigs than was the corresponding K88 form.


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