Prevention of atrophic rhinitis in piglets by means of intranasal administration of a live non-AR-pathogenic Bordetella bronchiseptica vaccine

The effect of intranasal vaccination of piglets with live non-AR-pathogenic Bordetella bronchiseptica (BB-) against Atrophic Rhinitis (AR) was investigated in a preliminary investigation and in a field trial. In the preliminary investigation 2-day-old SPF piglets (n = 13) were vaccinated. Three weeks after vaccination, challenges were carried out by means of a spray with an AR-pathogenic B (BB+) or an AR-pathogenic Pasteurella multocida (PM+) broth-culture. Four weeks later the piglets were necropsied and examined for atrophy of the ventral conchae (AVC). In contrast with the non-vaccinated SPF piglets, the vaccinated piglets showed a strong and significant reduction of AVC, after both BB+ and PM+ challenge. In the field trial three groups were formed by drawing lots: ten litters (82 piglets) were vaccinated; ten litters (92 piglets) formed the control group and 11 litters (104 piglets) were treated with a placebo. The litters were spread over two units. In unit 1 AR and PM+ were demonstrated incidentally, in unit 2, however, persistently. BB+ was isolated equally frequently in both units. Clinical and bacteriological examinations were done in piglets of 3, 6 and 8 weeks of age. Necropsy examinations was carried out in 41 piglets of 8 weeks of age, chosen randomly by drawing lots. In spite of a second vaccination at the age of 3 weeks, BB- was not well established; this was possibly caused by maternal BB antibodies. In the control and placebo groups PM+ was isolated earlier and more frequently than BB+. It appeared that AVC was correlated more strongly with PM+ than with BB+ infection in the field trial. The percentage of piglets with Brachygnathia superior (BS) at the age of 8 weeks indicated the AR situation in the herd. Although a significant reduction of AVC was determined in unit 2, it was not sufficient to indicate that this method of intranasal vaccination is useful in the prevention of AR in practice.     

Efficacy of Bordetella bronchiseptica bacterin in controlling enzootic atrophic rhinitis in swine.

The efficacy of a Bordetella bronchiseptica bacterin was evaluated in 2 commercial swine herds affected with mild and severe enzootic atrophic rhinitis (AR). In the 1st herd study, (mild AR), the degree of clinical AR, nasal turbinate evaluation, blood serum titer to B bronchiseptica antigen, and adjusted days from birth to 100 kg were determined for individual pigs. Bacterin inoculation reduced the incidence and severity of gross turbinate atrophy 57% and reduced clinical AR over 93%. Inoculated swine had an average blood serum-agglutinating titer greater than 1:2,793 and noninoculated (control) swine had an average titer of 1:112. Increased serum titer significantly (P less than 0.05) correlated with decreased degree of nasal turbinate atrophy. Inoculated and control pigs reached 100 kg in an average of 171 and 178 days after birth, respectively. In the 2nd study (severe enzootic AR), inoculated and control pigs were individually evaluated for clinical AR and total average daily weight gain. Inoculation reduced clinical AR over 90%. The total average daily gain for the inoculated and control pits was 435.84 g and 340.50 g, respectively. Inoculated pigs and control pigs reached 100-kg market weight in 184 and 238 days, respectively.     

Bordetella bronchiseptica isolations from the nasal cavity of pigs in relation to atrophic rhinitis.

The occurrence of Bordetella bronchiseptica and atrophic rhinitis was studied during a one-year period in four Danish sow herds. In three of the heards, the epidemiological studies revealed a relation between the occurrence of B. bronchiseptica in 3--10-week-old pigs and the presence and severity of atrophic rhinitis at slaughter. In the fourth herd no such relation was found.     

Relationship of porcine cytomegalovirus and B bronchiseptica to atrophic rhinitis in gnotobiotic piglets.

Both porcine cytomegalovirus (PCMV) and Bordetella bronchiseptica produced rhinitis and pneumonia when inoculated intranasally into young gnotobiotic pigs. With PCMV the nasal lesions were confirmed to the lamina propria, while Bordetella produced atrophy of the turbinate bones and hyperplasia and degeneration of the nasal epithelium. Some exacerbation of the lesions was observed in the nasal mucosa of pigs given both agents, but the degree of bone atrophy was not increased.     

Protection of piglets against atrophic rhinitis by vaccinating the sow with a vaccine against Pasteurella multocida and Bordetella bronchiseptica

The efficacy of a new vaccine against atrophic rhinitis in pigs was tested in the Netherlands and Denmark. The vaccine contained protein dO (a truncated Pasteurella multocida toxin which is immunogenic and non-toxic), inactivated Bordetella bronchiseptica whole cells, and an adjuvant. The sows were either vaccinated intramuscularly with 2 ml of the vaccine at six to eight and two to four weeks before expected farrowing or left unvaccinated as controls. All the piglets were challenged intranasally with B bronchiseptica when three to seven days old and with P multocida three to four days later. Pigs born to the vaccinated sows performed significantly better than pigs born to the control sows when judged on growth, average daily weight gain and snout scores. The challenge organisms were reisolated more frequently from the control pigs than from the pigs in the vaccinated group. The vaccinated sows and their progeny developed high titres of antibodies against B bronchiseptica and P multocida toxin.     

Development of turbinate lesions and nasal colonization by Bordetella bronchiseptica and Pasteurella multocida during long-term exposure of healthy pigs to pigs affected by atrophic rhinitis.

Natural transmission of atrophic rhinitis from pigs from a herd with an endemic atrophic rhinitis problem to pigs from a herd free of atrophic rhinitis was demonstrated. Six replicates each with five pigs from the endemic atrophic rhinitis herd (Group A) and five pigs from the atrophic rhinitis-free herd (Group B) were housed together from 5 wk of age, with each replicate kept in isolation rooms maintained at optimal and controlled environmental conditions. Three replicates each with six pigs/room from the atrophic rhinitis-free herd (Group C), served as nonexposed controls. Group C pigs remained healthy and had no turbinate atrophy at either 10 or 17 wk of study (atrophic rhinitis score = 0 on a 0 to 3 scale). Group A pigs had a mean atrophic rhinitis score of 1.85 +/- 0.84, and group B pigs developed atrophic rhinitis to a mean score of 1.57 +/- 0.70. The isolation rate and quantity of Pasteurella multocida found on nasal swabs was directly related to lesions while those for Bordetella bronchiseptica were inversely related to turbinate atrophy. Of the various types of P. multocida evaluated, nontoxigenic type A and toxigenic type D were both directly related to atrophic rhinitis while nontoxigenic type D strains were not. No toxigenic type A P. multocida strains were isolated.     

Association of growth performance with atrophic rhinitis and pneumonia detected at slaughter in a conventional pig herd in Hungary

The influence of atrophic rhinitis (AR) and pneumonia on growth performance was assessed in a conventional farrow-to-finish pig farm affected by both diseases. All tested pigs (n = 138) were individually weighed at birth, at weaning, at moving to the growing/finishing unit, and at slaughtering. The extent (grade) of turbinate atrophy and lung consolidation attributable to pneumonia was determined in each pig at slaughter. A negative correlation was found between birth weight and the prevalence of nasal lesions at slaughter, suggesting that pigs born with smaller weight may be more susceptible to AR. The growth performance of the pigs also showed a negative correlation with the degree of turbinate atrophy. In the nursery period, the average daily gain (ADG) of pigs with moderate/severe turbinate atrophy was 13.3% lower than that of animals with healthy snouts. In the finishing period, pigs with mild AR lesions had an ADG reduction of 6.2%, while pigs with severe AR lesions had a significant, 9.4% reduction in ADG as compared to the AR-free pigs. The extent of weight gain reduction over the whole life cycle was very similar (approximately 6%) in the pigs having either AR or pneumonia alone. In those pigs where both respiratory diseases were present, their effects seemed to be added up (11.5%); however, nasal lesion scores and percentage of lung consolidation did not show statistically apparent interactive effects on growth performance.     

Experimental atrophic rhinitis in 2 and 4 month old pigs infected sequentially with Bordetella bronchiseptica and toxigenic type D Pasteurella multocida.

Experimental infections with Bordetella bronchiseptica and/or toxigenic type D Pasteurella multocida were studied in 2- and 4-month-old primary specific-pathogen-free pigs. None of the 2-month-old pigs inoculated with B. bronchiseptica or P. multocida alone developed turbinate atrophy. All the pigs inoculated with B. bronchiseptica (10(7) CFU/head) and P. multocida (10(9) CFU/head for 5 consecutive days) together, however, developed clinical and post-mortem signs of atrophic rhinitis (AR) similar to the naturally occurring disease. Slight to severe turbinate atrophy was observed in the 4-month-old pigs inoculated with B. bronchiseptica and P. multocida (at the same concentration as above) at necropsy.     

Investigation into the pathogenesis of atrophic rhinitis in pigs. I. Atrophic rhinitis caused by Bordetella bronchiseptica and Pasteurella multocida and the meaning of a thermolabile toxin of P. multocida

In two groups of swine herds, herds with and without clinical AR the presence of Atrophic Rhinitis (AR) correlated with the presence of toxinogenic Pasteurella multocida (PM) and not with the Bordetella bronchiseptica (BB) infection. Six BB- and eighteen PM-strains have been investigated for AR pathogenicity. Broth cultures were injected intradermally in guinea-pigs (GPST) or intranasally in 3-week-old colostrum deprived specific pathogen free (SPF) piglets. The average atrophy of the ventral conchae (AVC) correlated with the GPST in 4 BB-and 7 PM-strains. One BB- and 2 PM-strains were qualified as doubtful, the others as non-AR pathogenic. With AR pathogenic BB-and PM-strains clinical AR could be induced in 3-and 6-week-old piglets. AVC lesions (gradation greater than 1) could be induced with BB in piglets of 6 and with pathogenic PM in 16-week-old piglets. Six of seven AR pathogenic PM-strains resembled Carter-type D and one resembled type A. No significance was found between AR pathogenicity and somatic serotypes. Intranasal instillations of cell-free broth culture filtrates of AR pathogenic PM-strains also caused AR in piglets. These filtrates also caused lethality in piglets and in mice lethalitytest (MLT) and induced a positive GPST. After heating the pathogenic effects of the filtrates disappeared. The name AR toxin has been introduced for this thermolabile, haemorrhagic dermonecrotic (HDNT) fraction of the AR inducing filtrates. The severity of the AR lesions depended on the amount of the AR toxin intranasally instilled in pigs. Cross protecting antibodies obtained in rabbits against the AR toxins of two PM strains could be demonstrated by a toxin neutralisation test in the MLT and the GPST. Broth cultures were injected intradermally in guinea-pigs (GPST) or intranasally in 3-week-old colostrum deprived specific pathogen free (SPF) piglets.