DEMONSTRATION THAT AUSTRALIAN PASTEURELLA-MULTOCIDA ISOLATES FROM SPORADIC OUTBREAKS OF PORCINE PNEUMONIA ARE NONTOXIGENIC (TOXA(-)) AND DISPLAY HETEROGENEOUS DNA RESTRICTION-ENDONUCLEASE PROFILES COMPARED WITH TOXIGENIC ISOLATES FROM HERDS WITH PROGRESSIVE ATROPHIC RHINITIS
Sp. Djordjevic et al., DEMONSTRATION THAT AUSTRALIAN PASTEURELLA-MULTOCIDA ISOLATES FROM SPORADIC OUTBREAKS OF PORCINE PNEUMONIA ARE NONTOXIGENIC (TOXA(-)) AND DISPLAY HETEROGENEOUS DNA RESTRICTION-ENDONUCLEASE PROFILES COMPARED WITH TOXIGENIC ISOLATES FROM HERDS WITH PROGRESSIVE ATROPHIC RHINITIS, Journal of Medical Microbiology, 47(8), 1998, pp. 679-688
Capsular types A and D of Pasteurella multocida cause economic losses
in swine because of their association with progressive atrophic rhinit
is (PAR) and enzootic pneumonia, There have been no studies comparing
whole-cell DNA profiles of isolates associated with these two porcine
respiratory diseases. Twenty-two isolates of P. multocida from disease
d pigs in different geographic localities within Australia were charac
terised genotypically by restriction endonuclease analysis (REA) with
the enzyme CfoI, Seven of 12 P. multocida isolates from nasal swabs fr
om pigs in herds where PAR was either present or suspected displayed a
capsular type D phenotype, These were shown to possess the toxA gene
by polymerase chain reaction (PCR) and Southern hybridisation, and fur
ther substantiated by production of cytotoxin in vitro. The CfoI profi
le of one of these seven isolates, which was from the initial outbreak
of PAR in Australia (in Western Australia, WA), was identical with pr
ofiles of all six other toxigenic isolates from sporadic episodes in N
ew South Wales (NSW), The evidence suggests that the strain involved i
n the initial outbreak was responsible for the spread of PAR to the ea
stern states of Australia. Another 10 isolates, representing both caps
ular types A and D, were isolated exclusively from porcine lung lesion
s after sporadic outbreaks of enzootic pneumonia in NSW and WA. CfoI r
estriction endonuclease profiles of these isolates revealed considerab
le genomic heterogeneity. Furthermore, none of these possessed the tox
A gene. This suggests that P. multocida strains with the toxA gene do
not have a competitive survival advantage in the lower respiratory tra
ct or that toxin production does not play a role in the pathology of p
neumonic lesions, or both. REA with polyacrylamide gel electrophoresis
and silver staining was found to be a practical and discriminatory to
ol for epidemiological tracing of P. multocida outbreaks associated wi
th PAR or pneumonia in pigs.