Objective To use the technique of ribotyping to investigate the genetic diversity of Australian isolates of Pasteurella multocida associated with outbreaks of clinical disease in Australian pigs. Design One hundred and seven porcine P multocida isolates were analysed by ribotyping using the restriction enzymes HpaII and HindIII. The genetic population structure of the Australian porcine P multocida isolates was determined through statistical analysis of the joint ribotype patterns, and this was then compared with biochemical and epidemiological data available for the population. Results A total of 25 combined ribotypes were recognised, which were grouped into five ribotype clusters. Despite the deliberate selection of diverse isolates, the study revealed only a limited degree of genetic diversity. Fourteen of the ribotypes contained multiple isolates, and 12 of these ribotypes were present on more than one farm. Three of the seven biovars analysed in the study showed very limited diversity. All fifteen biovar 2 isolates (subsp multocida) were found in a single cluster (III), while all four biovar 8 isolates, which correspond to P multocida subsp gallicida, were allocated by themselves to a single cluster (IV). All nine of the biovar 12 isolates (lactose‐positive subsp multocida) were assigned to a single cluster (I), together with the single biovar 14 isolate, which was the only other lactose‐positive isolate in the population (ODC‐negative). Conclusion A limited number of ribotypes of P multocida are associated with Australian pigs. The majority of these ribotypes are widely distributed across multiple farms, and across multiple states. Individual farms can possess multiple ribotypes of P multocida. Some of the unusual biochemical variants of P multocida present in Australian pigs have a very limited genetic diversity. The nature of pig production in Australia, primarily involving continuous flow systems with few closed herds, has possibly contributed to the widespread distribution of a limited number ribotypes.
Objectives To clarify the serological identity of the proto type strain of a group of Actinobacillus pleuropneumoniae isolates that could not be serotyped in previous studies and to establish the serovar of 378 isolates of A pleuropneumoniae obtained from pigs in Australia over the period 1993 to 1996.Design After initial validation, QGD and IHA tests were used to characterise the prototype isolate (HS143) selected to represent the cross‐reacting isolates that were found in a previous study. Next, 378 recent field isolates of A pleurop‐neumoniae were characterised using the existing gel diffusion serotyping technique and/or the IHA or QGD tests.Results The indirect haemagglutination test was shown to be capable of correctly recognising the reference strain for all serovars except serovar 11. While the quantitative gel diffu sion test was not as effective as indirect haemagglutination, it could recognise serovar 11. When the two tests were used to examine the prototype strain (HS143) of the cross‐reactive isolates, the results indicated that HS143 is serologically distinct from all 12 of the recognised serovars of A pleurop‐neumoniae. However, as HS143 was subsequently identified as serovar 12 by one of the leading international reference laboratories, the antiserum to isolate HS143 was used as the serovar 12 antiserum. A total of 346 of the 378 A pleuropneumoniae field isolates examined could be confidently serotyped with almost 90% of the isolates being either serovar 1 (104 isolates); serovar 7 (83 isolates) or serovar 12 (142 isolates). A range of other serovars and some cross‐reactive isolates made up the remainder of the isolates.Conclusion The serovar 12 antiserum produced against the international reference strain (1096) does not recognise Australian serovar 12 isolates. The antiserum raised against isolate HS143 does recognise the Australian serovar 12 isolates. The dominant serovars of A pleuropneumoniae infecting Australian pigs are (in decreasing order) serovars 12, 1 and 7.
utero or during the early postnatal life (total body or head alone) produced a supp?.ession of the development of hembarbital metahlising enzyme system in liver. A k @ inhibition of the hepatic enzyme system after x-irradiation was also noted in adult male rats, but with higher radiation doses, suggesting that the central nervous system plays but also in the maintenance of optimal level of 81 rn ' l . --. S P . -* -,Ben m *-a regulatory role not only in the development n . ** I . " 01 enzyme activity in liver. M Y S FIG. 3. The response of the h e x o k b k d metablising enzyme system in adult male rat liver to a) 1,OOo R head x-irradaaticm, b) 2,000 R head x-irradi-a4ion and d) hypophysectoany are compared. has to suppress the nd tance with the radiation plrocedure. Grateful xkmledgemerrt is made to the University of Chiqo canceT ~~~w and the Deprtment of Radiology fm use of the radiation facilities arbd Mr. James Bland for his assisdevelopmental increase of enzyme activity s e n in male rats ( 8). I t is shown in 4. he present studies (Fig. 3) that hypophysectomy in a d d t rats (65 days old) also results in an inhibiation of the hepatic enzyme system. Although the mechanisms underlying Ithe a -effects of head irradiation on liver enzyme activity cannot be outlined yet, collateral evidence suggests that radiation impairment af the hypophysea,l regulation may be responsible for the distamt effects observed. It is also apparent from our results that the central nervous system exerts a regulatory role not only in the development but also in the maintenance Olf an optimal level of enzyme activity in liver. Summary. Exposure to m5rradiation in 1. Gillette, J. R., Progress in Drug Resead, edit.Types A and B botulinal toxins and antitoxins appear to be quite specific as determined by animal neutralization tests(1). Multiple precipitin bands and crossreactions have been observed, h m v e r , in gel-diffusion tests. Lamanna and Lowenthal (2) showed that type A crystalline botulinal toxin f m e d two precipitin bands with type A antitoxin in the Ouch geldiffusion test and one band with type B antitoxin. They demonstrated that one of the homologous bands and the cross-reacting band were attributable to the hemagglutinin in type A toxin and its antibody present in the homologous and heterologous antitoxins. Gendon( 3 ) demonstrated numerous bands between crude type A toxin at GEORGETOWN UNIV MED CTR on July 13, 2015 ebm.sagepub.com Downloaded from
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