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.     

Bordetella bronchiseptica and toxigenic type D Pasteurella multocida as agents of severe atrophic rhinitis of swine

Bordetella bronchiseptica and toxigenic type-D Pasteurella multocida were cultured from pigs in each of five herds diagnosed as having severe atrophic rhinitis (AR). B. bronchiseptica alone, P. multocida alone, or both organisms isolated from four herds were inoculated intranasally into 1-week-old gnotobiotic pigs which were necropsied 4 weeks post-inoculation (PI). Nasal turbinate atrophy in B. bronchiseptica-inoculated pigs was moderate to severe, while P. multocida-inoculated pigs had slight to severe atrophy. Pigs inoculated with both organisms had moderate to complete turbinate atrophy. P. multocida was reisolated at necropsy from all pigs receiving the organism except those having no turbinate damage. B. bronchiseptica and P. multocida from a fifth herd were simultaneously inoculated into six naturally farrowed 6-day-old SPF pigs. Necropsy performed 4 weeks PI revealed severe to complete turbinate atrophy. Nasal turbinates were normal for control pigs in both experiments.     

Isolation of toxigenic Pasteurella multocida from an outbreak of atrophic rhinitis in pigs

An outbreak of severe atrophic rhinitis is described. A toxigenic strain of P. multocida was isolated from one affected pig. Severe turbinate atrophy was not associated with significantly reduced bodyweight gain in a batch of 34 pigs examined at slaughter. The history of the outbreak suggested that pigs recently introduced from overseas may have been the source of the disease.     

Colonisation by Pasteurella multocida in atrophic rhinitis of pigs and immunity to the osteolytic toxin

Gnotobiotic pig antisera to purified toxoid from a capsule type A or D strain of Pasteurella multocida contained large quantities of antitoxin but comparatively little antibody to a crude lysate of P. multocida. These sera given intraperitoneally to further pigs were almost completely protective against turbinate atrophy after intranasal inoculation of dilute acetic acid and infection with type D toxigenic P. multocida. In contrast, antisera to a crude lysate or bacterin of toxigenic P. multocida which contained large titres of antibody to P. multocida lysate, but no detectable antitoxin, were not protective. Colonisation by toxigenic P. multocida was significantly reduced in protected pigs and was similar to colonisation by nontoxigenic P. multocida in pigs untreated or treated with dilute acetic acid. These results indicated (1) that antitoxin was protective and cross protective between toxins from different capsule types; and (2) that the toxin was the main colonisation factor produced by toxigenic bacteria in the acetic acid model of infection and that immunity to it did not eliminate infection.     

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.     

Long-acting oxytetracycline for control of induced Pasteurella multocida rhinitis in swine

A long-acting oxytetracycline formulation was evaluated for control of rhinitis induced experimentally in pigs with a capsular type A, toxin-negative, low-passage strain of Pasteurella multocida. The pigs were 6 to 7 weeks old and were naturally infected with Haemophilus parasuis. The H parasuis infection was thought to predispose to establishment of P multocida in the nasal cavity. A long-acting oxytetracycline formulation was given IM at the rate of 20 mg/kg, 4 times at 5-day intervals. Medication reduced (P less than 0.05) the severity of turbinate atrophy and the proportion of pigs with P multocida and H parasuis in their nasal cavities. Numbers of colonies of P multocida and H parasuis isolated were also less in medicated pigs.     

Interactions between Bordetella bronchiseptica and toxigenic Pasteurella multocida in atrophic rhinitis of pigs

Three strains of Bordetella bronchiseptica were compared for their ability to assist colonisation of the nasal cavity of gnotobiotic pigs by toxigenic Pasteurella multocida. Toxigenic P multocida (counted in nasal washings) colonised the cavity in large numbers in pigs previously infected with a cytotoxic phase I strain of B bronchiseptica (B58), whereas it colonised only in small numbers in those previously infected with B65, a phenotypic phase III variant of B58. Toxigenic P multocida colonised pigs infected with a non-cytotoxic phase I strain of B bronchiseptica (PV6) in fewer numbers than were seen in pigs infected with the cytotoxic phase I strain but in greater numbers than in pigs infected with the phase III strain. The turbinates of pigs infected with the cytotoxic phase I strain of B bronchiseptica and toxigenic P multocida were most severely affected and those in pigs infected with the non-cytotoxic phase I strain and toxigenic P multocida were moderately reduced in size. The turbinates of pigs infected with the phase III strain and toxigenic P multocida were slightly reduced in size except for one piglet whose turbinates were severely affected. Pigs infected with the non-cytotoxic phase I strain of B bronchiseptica alone showed no signs of atrophy and their turbinates were used to calculate reductions (per cent) in those infected with P multocida. The reduction (per cent) in size of turbinates and total numbers of P multocida isolated from the nasal washings of each pig were linearly related.(ABSTRACT TRUNCATED AT 250 WORDS)     

Expression of the dermonecrotic toxin by Bordetella bronchiseptica is not necessary for predisposing to infection with toxigenic Pasteurella multocida

This experiment was designed to determine whether a Bordetella bronchiseptica mutant that does not produce dermonecrotic toxin (DNT) is still capable of predisposing pigs to infection with toxigenic Pasteurella multocida. Three groups of pigs were initially inoculated intranasally with a wild type B. bronchiseptica that produces DNT, an isogenic mutant of B. bronchiseptica that does not produce DNT, or PBS. All pigs were then challenged intranasally with a toxigenic strain of P. multocida 4 days later. P. multocida was recovered infrequently and in low numbers from pigs initially inoculated with PBS, and no turbinate atrophy was present in these pigs. P. multocida was isolated in similar numbers from the pigs initially inoculated with either the wild type or the DNT mutant of B. bronchiseptica, and turbinate atrophy of a similar magnitude was also seen in pigs from both of these groups. Thus, although the DNT has been shown to be responsible for much of the pathology seen during infection with B. bronchiseptica by itself, infection with non-DNT-producing strains can still predispose to secondary respiratory infections with P. multocida.     

Turbinate atrophy in gnotobiotic pigs intranasally inoculated with protein toxin isolated from type D Pasteurella multocida

Three doses (75 micrograms, 25 micrograms, and 25 micrograms) of purified toxin isolated from a toxigenic strain of type D Pasteurella multocida were given (by atomizer) into the right nasal cavities of each of 10 gnotobiotic pigs on the 21st, 24th, and 27th days of age, respectively. Inoculated pigs (usually 2) and 1 noninoculated control pig each were necropsied on 3, 6, 9, 12, and 15 days after inoculations were given. Severe bilateral atrophy of turbinates occurred in all toxin challenge-exposed pigs. Atrophy was more severe in the inoculated nasal cavity than that in the noninoculated side in 2 of the 10 pigs. Microscopic changes in turbinates of toxin challenge-exposed pigs were more severe in pigs killed at later dates. Dominant changes included degeneration and necrosis of osteoblasts, markedly accelerated osteoclastic osteolysis, replacement of the osseous core by a highly cellular mesenchymal stroma, and multifocal atrophy of submucosal glands. Seemingly, a protein toxin isolated from toxigenic type D strains of P multocida produced rapid atrophy of turbinates and may be a contributing factor in development of clinical progressive atrophic rhinitis in swine.     

Screening pig herds for toxigenic Pasteurella multocida and turbinate damage in a health scheme for atrophic rhinitis

The Pig Health Control Association launched a health scheme for atrophic rhinitis in 1978. For several years pig herds were monitored by scoring the degree of turbinate damage and by clinical inspections. When laboratory facilities became available for detecting toxigenic Pasteurella multocida, nasal swabs were taken from pigs in Association herds during 1988 and 1989 to determine whether the organism was present. Sows were screened routinely and in the worst affected herds, sucklers and weaners were also swabbed. In 12 of 19 herds with consistently low snout scores toxigenic P multocida were not isolated, and in 15 herds which developed higher snout scores with time toxigenic P multocida were also not found. Eleven herds had never been listed by the Association, either because their snout scores were consistently high or because they had received importations of stock from herds with high snout scores; of six of these herds with the most persistently high snout scores five showed varying degrees of the clinical signs of atrophic rhinitis, but none of the six showed evidence of infection with toxigenic P multocida, and the organism was not found in the other five herds in the group. There seems to be an overlap between the clinical and gross pathological signs of atrophic rhinitis seen in some herds not infected with toxigenic P multocida and the mild and spasmodic signs of atrophic rhinitis seen in some herds which are substantially infected with the organism.     

Vaccine efficacy for reducing turbinate atrophy and improving growth rate in piggeries with endemic atrophic rhinitis

Two vaccines, based on formalin-killed whole cells of toxigenic Pasteurella multocida type D and Bordetella bronchiseptica combined with a partially toxoided cell extract of P multocida, were prepared with Freund's incomplete adjuvant (vaccine 1) or by alum precipitation (vaccine 2). Each was tested for safety and efficacy in reducing the severity of nasal turbinate atrophy and improving the growth rate of pigs in three Western Australian commercial piggeries with endemic atrophic rhinitis. In safety experiments with vaccine 1, no adverse clinical effects were observed in vaccinated sows or their progeny. Piglets receiving vaccine 2 showed no injection site abnormalities, pyrexia or turbinate atrophy. In field trials, vaccine 1 significantly reduced the prevalence of moderate to severe nasal turbinate atrophy (Done score 3 to 5) when used in two piggeries (A and B). Progeny from vaccinated sows in piggery B also grew significantly faster than controls. When vaccine 2 was used in piggery A at a later date and in another piggery (C), growth rate was not improved in either piggery and the prevalence of moderate to severe turbinate atrophy was reduced only in piggery C.     

Toxigenic type D Pasteurella multocida in New South Wales pig herds—prevalence and factors associated with infection

Between March and July 1987, a study was undertaken to determine the prevalence of and factors associated with toxigenic type D Pasteurella multocida infection in New South Wales pig herds. Toxigenic type D P. multocida was isolated from the nasal cavities of pigs in one (2%) of 50 randomly selected herds. Toxigenic isolates were also recovered from 2 (8%) of a separate group of 25 herds that had purchased pigs from a known infected piggery in South Australia (herd SA). Snout abnormalities were present in 9.4%, 3.2% and 1.8% of grower pigs in the 3 affected herds. Isolation of toxigenic P. multocida was significantly associated (p less than 0.0001) with the occurrence of clinically affected pigs in the herd. Purchase of at least 5 pigs from herd SA was associated with an elevated risk (p less than 0.05) of isolation of toxigenic P. multocida.     

Effects of purified Pasteurella multocida dermonecrotoxin on the nasal ventral turbinates of fattening pigs: histological observations.

Fattening specific pathogen-free derived pigs were injected intramuscularly with dermonecrotoxin of Pasteurella multocida, capsular type D. Ten days later, the nasal ventral turbinates and liver were examined histologically. A moderate turbinate atrophy was observed due to an increased number of osteoclasts and the absence of intramembranous bone apposition. Liver lesions were limited to some hepatocyte necrosis, sinusoid neutrophil infiltration and Kupffer cell hypertrophy. This study demonstrated that adult pigs are sensitive to P. multocida dermonecrotoxin.     

The pathogenesis of persistent turbinate atrophy induced by toxigenic Pasteurella multocida in pigs

Six one-week-old piglets were pretreated with a 1% acetic acid solution for two days in one or both nostrils. Three piglets were not treated with acetic acid. Three days after treatment all nine piglets were inoculated in both nostrils with a toxigenic type D strain of Pasteurella multocida. Three piglets were killed seven days after inoculation; one died spontaneously 13 days after inoculation and the remaining pigs were killed at approximately 90 kg body weight, i.e., five to six months of age. All acetic acid-treated animals developed severe atrophy of the turbinates in the treated nostrils. Untreated nostrils were normal. The present results showed that toxigenic P. multocida can induce turbinate atrophy that persisted until 90 kg body weight when the lesions were similar to spontaneous atrophic rhinitis in pigs. The turbinate atrophy was not accompanied by inflammatory reaction, atrophy of other bone structures, or lesions in other organs. The experiment showed furthermore that toxigenic P. multocida may be present in the tonsils of control animals without causing turbinate atrophy. A pathogenesis for atrophic rhinitis in pigs is proposed.     

Lack of effect of aerial ammonia on atrophic rhinitis and pneumonia induced by Mycoplasma hyopneumoniae and toxigenic Pasteurella multocida

The objective of this experimental study was to determine the effects of aerial ammonia on disease development and bacterial colonization in weaned pigs inoculated with toxigenic Pasteurella multocida and Mycoplasma hyopneumoniae. Two groups of 10 pigs each were continuously exposed to 50 and 100 p.p.m. ammonia, respectively, and compared to a non-exposed control group of 20 pigs. Following aerosol inoculation with M. hyopneumoniae at day 9, all pigs were aerosol-inoculated with toxigenic P. multocida type A at days 28, 42 and 56. At day 63 they were euthanized. Clinical signs including coughing and respiratory distress were present in all groups following inoculation. No significant differences could be established in the extent or frequency of pneumonia between ammonia-exposed pigs and controls, or in the extent of conchal atrophy, the frequency of isolation of toxigenic P. multocida from conchae, tonsils, lungs and kidneys, or the average daily weight gain. The recovery of toxigenic P. multocida from nasal swabs following inoculation was significantly greater in pigs exposed to 50 p.p.m. ammonia or more as compared to the control group. In conclusion, high levels of ammonia combined with inoculations with M. hyopneumoniae and toxigenic P. multocida had no significant effect on disease development, but may have enhanced colonization by toxigenic P. multocida on the nasal turbinates.     

Pasteurella multocida and Bordetella bronchiseptica in atrophic rhinitis and pneumonia in swine.

A total of 163 pigs from nine farrow-to-finish herds representing various levels of atrophic rhinitis (AR) were selected for postslaughter examination of AR and pneumonia. Nasal swabs and lungs were cultured for detection of Bordetella bronchiseptica and Pasteurella multocida. Seventy-three pigs were examined at eight weeks of age and 90 contemporaries at six months of age. Mean AR scores were 1.21 and 1.11 for the eight week and six month old pigs, respectively (0 = normal, 3 = severe). In individual pigs increasing AR score was related to increasing pneumonia score in eight week old pigs but not in six month old hogs. In eight week old pigs, B. bronchiseptica and P. multocida were isolated more frequently from pigs with higher AR scores. From nasal swabs of six month old hogs, Bordetella was almost never recovered while Pasteurella was frequently isolated score. Toxigenic type DP. multocida was isolated from nasal cultures of only seven (4%) pigs and from lung cultures of only one pig. Pasteurella was never isolated from lungs of the eight week old pigs and Bordetella never from the six month old hogs. The isolation rate of P. multocida, predominantly type A, from lungs of six month old pigs increased from 11% in grossly normal lungs to 86% in lungs with severe pneumonia. Pigs from one herd free from lesions of AR and pneumonia were also examined; type AP. multocida was isolated from nasal cultures of one of six eight week old pigs. Somatic antigens of P. multocida were determined for 94 nasal and 20 lung isolates. Somatic serovar 3 was found in 93% of the nasal isolates and in all lung isolates.(ABSTRACT TRUNCATED AT 250 WORDS)     

Detection and distribution of toxigenic Pasteurella multocida in pig herds with different degrees of atrophic rhinitis

Four herds of pigs were selected which had different degrees of clinical atrophic rhinitis and used different specific counter-measures. In two of them, the clinical signs occurred spasmodically and were slight. The sows, suckling pigs and growing pigs in all the herds were sampled for toxigenic Pasteurella multocida. In one of the slightly affected herds (herd D), the weaners were moved to a second farm for finishing. No toxigenic P multocida were found at the breeding farm, but 50 per cent of the large growing pigs were positive. It seemed that the organism had entered only at the finishing farm and that the mild clinical signs were due to the infection starting in older pigs than usual. In the second mildly affected herd, 47 per cent of the sows and 42 per cent of the growers were infected. Three toxigenic isolates from this herd produced as severe turbinate damage experimentally in specific-pathogen-free pigs as a stock pathogenic strain. Except in herd D, toxigenic P multocida were found in all the age groups of pigs sampled. However, the pattern of distribution of the organism within the herds was not obviously correlated with the severity of the disease. In a fifth herd there were obvious cases of clinical atrophic rhinitis, with marked turbinate atrophy, from which toxi-genic P multocida were recovered in abundance. Subsequently, the clinical disease disappeared and, despite extensive and repeated sampling, the organism was not found again.     

Effect of aerial ammonia on porcine infection of the respiratory tract with toxigenic Pasteurella multocida

The objective of the experimental study was to examine whether aerial ammonia alone could predispose the respiratory system of pigs to infection with toxigenic Pasteurella multocida type A. Two groups of 5 pigs each were continuously exposed to 50 ppm ammonia and less than 5 ppm ammonia, respectively, for a 59-day period (from 37 kg to 90 kg bodyweight) followed by necropsy. In an aerosol chamber all pigs were exposed to an aerosol of toxigenic P. multocida type A (mean bacterial concentration in the aerosol-exposure chamber: 10(5) colony forming units/m3; exposure period: 25 min) at day 10, 21, 35 and 49 after the onset of ammonia exposure. During the experiment none of the pigs showed clinical signs of pneumonia nor did they develop visible distortion of the snout. None of the pigs had gross lesions in the lungs at necropsy and toxigenic P. multocida was not detected by culture from the lungs from any of the pigs. The chance of recovering toxigenic P. multocida from nasal swabs (collected during experiment) was 2-4 times greater in the test group compared to the control group. The average daily weight gain was lower for the ammonia exposed pigs compared to the control group. In conclusion the results from this study suggest that ammonia in concentrations of 50 ppm is unlikely to predispose growing pigs to pulmonary infection with toxigenic P. multocida.     

Pasteurella multocida (type D and A) and atrophic rhinitis of swine--hemagglutination, fimbriae and adhesion in vitro in the nasal mucosa of swine fetuses

79 strains of P. multocida were investigated, mostly isolated from porcine nasal cavities, and a mannose-resistant hemagglutination with guinea pig and human group 0, but not with porcine erythrocytes was found. Fimbriae as adhesins were demonstrated only on 2 strains. A correlation between capsular type, hemagglutination, fimbriation and toxigenicity on the examined P. multocida strains was not observed. Three strains were investigated for the adherence to the nasal mucosa of neonatal pigs; aggregates shown by scanning electron microscopy indicate colonization; a correlation of adherence with surface proteins and slime production of P. multocida is discussed.     

Colonization of the pharyngeal tonsil and respiratory tract of the gnotobiotic pig by a toxigenic strain of Pasteurella multocida type D

Seven-day-old gnotobiotic pigs were inoculated intranasally with Pasteurella multocida and euthanatized 2, 5, 9, and 14 days after inoculation. Tissues from the oropharynx and respiratory tract of pigs were cultured quantitatively and analyzed microscopically. Pigs remained afebrile and alert, except one that died of acute fibrinopurulent pneumonia. Pasteurella multocida was isolated in greatest numbers from the pharyngeal tonsils, but only in low numbers from turbinate, trachea, lung, spleen, and liver. Significant histologic changes were limited to the tonsil. Infected pigs developed mild tonsillitis with lymphocytic hyperplasia, and accumulation of cell debris and bacteria in crypts. Capsular antigens of P. multocida, identified on tissue sections with rabbit anti-capsular polysaccharide antibody and immunocytochemical reagents, were confined to the crypt lumen. Ultrastructurally, bacteria were free within crypt material or within phagosomes of macrophages or neutrophils. In a second experiment, 5-day-old pigs were infected with Streptococcus suis type 2, followed by toxigenic Pasteurella multocida at 7 days of age; one pig died of streptococcal septicemia. Pigs developed a mild tonsillitis, and both bacteria were cultured from the tonsillar crypts for up to 14 days after infection. These studies show that a toxigenic strain of Pasteurella multocida, which is a causative agent of atrophic rhinitis, can colonize the tonsil and respiratory tract of gnotobiotic pigs for up to 14 days. In addition, colonization can occur concurrently with Streptococcus suis type 2.