The effect of dermonecrotic toxin (DNT) expression of Bordetella bronchisep
tica was studied in mice by comparing the pathology induced by a wild type
strain with that induced by an isogenic DNT- strain in which part of the st
ructural gene has been replaced by an antibiotic resistance cassette. While
extracts of strain B58 proved toxic in intravenously inoculated mice, simi
lar extracts from strain B58GP had lost toxic activity. The parent (B58) an
d the mutant (B58GP) strains of B. bronchiseptica each possessed comparable
virulence for mice. These findings confirmed that DNT production was succe
ssfully abolished in strain B58GP while other virulence characteristics req
uired for pathogenicity in mice remained intact, at a comparable level to t
he parent strain. Turbinate atrophy was observed in mice infected with the
DNT+ strain, but not in those infected with the DNT- strain. This indicates
that DNT is the cause of turbinate atrophy in the mice and not other facto
rs produced by phase I strains of B. bronchiseptica. B. bronchiseptica DNT
showed a lienotoxic effect (lymphocyte depletion and a reduction in the int
ensity of extramedullar haemocytopoieis) that is considered to adversely al
ter the immune function of the host animal. In mice infected with strain B5
8GP, catarrhal pneumonia with characteristic lympho-histiocytic peribronchi
al and perivascular infiltration was noticed. In mice infected with strain
B58, large necrotic areas were seen surrounded by an inflammatory reaction.
The DNT appears to directly damage lung tissues, at least in mice. DNT pro
duction seems to enhance the establishment of B. bronchiseptica in the lung
s, presumably by reducing the local resistance and causing severe local dam
age to the lung tissues.