Magyar T, Chanter N, Lax AJ, Rutter JM and Hall GA (1988)
The pathogenesis of turbinate atrophy in pigs caused by Bordetella bronchiseptica.
Veterinary Microbiology 18:135-146

Agricultural and Food Research Council, Institute for Animal Health, Compton, Berkshire, Gt. Britain.

The pathogenicity of 3 strains of Bordetella bronchiseptica designated B58, PV6 and B65 was compared by intranasal infection of gnotobiotic piglets. Strain B58 was a phase 1 isolate that produced haemolysin, an adhesin for calf erythrocytes, adenylate cyclase, mouse lethal factor, dermonecrotic factor and cytotoxin. B65 was a variant of B58 that produced no detectable haemolysin, adhesin or adenylate cyclase and 10-fold smaller amounts than B58 of mouse lethal factor, dermonecrotic factor and cytotoxin. Strain PV6 was a phase 1 isolate that produced only haemolysin, adhesin and adenylate cyclase. After nasal infection of gnotobiotic pigs, 10(3.2)-10(6.2) colony forming units ml-1 (cfu ml-1) of strains B58 and PV6 were cultured from nasal washings during the next 25 days. In contrast, only 10(1.0)-10(2.8) cfu ml-1 of strain B65 were recovered during the same period. Only pigs infected with strain B58 had turbinate atrophy when they were slaughtered 25 days after infection and neutralising antibody to cytotoxin was detected only in these pigs. These results suggested that the cytotoxin, which may be the same as the mouse lethal and dermonecrotic factors, was the cause of turbinate atrophy. They also support the view that the adhesin for calf erythrocytes is required for colonisation of the nasal cavity in vivo.