Growth hormone concentrations in plasma of healthy pigs and pigs with atrophic rhinitis.

Plasma concentrations of porcine growth hormone (PGH) were similar in healthy pigs and those with atrophic rhinitis (AR), therefore, observed reduced growth rates and feed efficiency in naturally infected pigs with AR were not attributed to low concentrations of plasma PGH. Also, pituitary glands in both groups of pigs were responsive to growth hormone-releasing hormone (GHRH) challenge by increasing PGH secretion. Administration of clonidine hydrochloride to pigs naturally infected with AR failed to elicit any significant change (5.3 +/- 1.4 ng/ml) in the plasma concentration of PGH within a 45-minute bleeding interval. The pretreatment concentrations of PGH were similar in specific-pathogen-free toxin-treated and specific-pathogen-free control groups, but they increased significantly in toxin-treated pigs (20.7 +/- 8.2 ng/ml) within 15 minutes after GHRH injection. Porcine growth hormone release in toxin-treated pigs was variable; however, all pigs did not respond to GHRH administration: 3 responded with an increase in PGH release (35.6 +/- 10.6 ng/ml), 2 did not respond (6.7 +/- 0.5 ng/ml), and 1 had a decrease in PGH release (3.9 ng/ml). Therefore, the observed reduced growth rates reported in the literature may be attributed to factors at the target level of PGH action, such as insufficient or down-regulation of PGH receptors, changes or impaired ability in the PGH receptor-binding characteristics, and inability of PGH receptor complex to transduce signal. Toxins are known to modulate signal transduction pathways. It has been speculated that serotype-D Pasteurella multocida toxin may influence growth by its effect on signal transduction from PGH receptor complex on the cell membrane to the interior of the cell.(ABSTRACT TRUNCATED AT 250 WORDS)     

Prevention and treatment of atrophic rhinitis in pigs with Getroxel, chlorquinaldol and oxytetracycline.

The sensitivity of ten Bordetella bronchiseptica and ten Pasteurella multocida strains, each isolated from cases of atrophic rhinitis (AR), was examined in tube dilution test. Getroxel, chlorquinaldol and oxytetracycline and the former two ones combined with trimethoprim inhibited the growth of both species in vitro. The minimum inhibitory and the minimum bactericidal concentration was less than 0.5 microgram/ml. When efficacy was tested in SPF in the group fed a combination of Getroxel, chlorquinaldol and oxytetracycline (60 mg, 240 mg and 360 mg/kg of feed, respectively), P. multocida disappeared from the nasal cavity by the end of a 30-day treatment. B. bronchiseptica was reisolated in low numbers from 2 out of 9 piglets. The daily body mass gain was by 7.9% higher and the feed conversion rate was by 19% better than in the control group. After slaughter, only mild signs of AR were seen in 3 out of 9 piglets treated with the above-mentioned drug combination, while in the control group severe lesions were observed in 8 out of 9 pigs. In treated commercial herds P. multocida disappeared from the nasal cavity of the piglets by the end of the treatment (42nd day of life), but the B. bronchiseptica strains could not be completely eliminated. Due to the treatment, mortality between 2 and 6 weeks of age decreased by 0.8-7.6%. Daily body mass gain was, on the average, 16.4% higher, the amount of feed needed for 1 kg body mass gain was by 15.3% lower and the duration of fattening was by 30.8 days shorter than in the control groups.     

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.     

The quantitation of turbinate atrophy in pigs to measure the severity of induced atrophic rhinitis.

The two-fold purpose of this study was to establish a useful image analysis technique for quantitation of turbinate atrophy and to determine an optimum bacterial dose for inducing atrophic rhinitis (AR). Two morphometric analysis methods were compared to determine a turbinate area ratio (TAR) and a turbinate perimeter ratio (TPR); the ratios of turbinate area to total nostril area and of turbinate perimeter to total nostril perimeter, respectively. Our first image analysis method differed from Collins et al (1) in that we used direct image capture (digitalization) via a video camera and a Macintosh microcomputer, rather than photographs and a digitizer tablet. The tracing techniques were the same as those used by Collins et al. The second morphometric method was modified from the first by exclusion of dorsal turbinate when tracing the nostril area and directly tracing only the ventral turbinate to get a turbinate measurement without subtracting. Area and perimeter ratios, for both methods, were compared to conventional visual snout scores, ventral measurements, and to each other. The results of the two image analysis methods correlated well, both with each other and with the visual scores. Doses of Pasteurella multocida (Pm) at a constant level, and Bordetella bronchiseptica (Bb) at various concentrations, were administered to 36 Hampshire-Duroc F1 SPF pigs to determine the best dose and frequency for inducing AR. Although the dose selection may have been somewhat affected by the pre-existing presence of Bb, the optimal dose per naris in this study was 2 mL Bb at 10(7) cfu/mL combined with 2 mL Pm at 10(9) cfu/mL inoculum. The frequency of administration (1 x or 2 x) did not greatly affect results. Turbinate area ratio was the best tool for quantitating gross morphological turbinate changes associated with atrophic rhinitis in this study. Our simplified modification of Collins et al image analysis method (exclusion of dorsal turbinates and direct measurement of ventral turbinates) correlated well with visual scores, and, when compared to Collins et al method, required less data manipulation and labour.     

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.     

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)     

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.     

Cell culture assay for toxigenic Pasteurella multocida from atrophic rhinitis of pigs

A toxin produced by strains of Pasteurella multocida isolated from pigs with atrophic rhinitis caused a cytopathic effect in cell cultures derived from embryonic bovine lung. The toxin was produced during the late logarithmic phase of bacterial growth and inactivated by heating for 30 minutes at 56 degrees C. The cell culture assay was reproducible and 10(3) to 10(4) times more sensitive than a lethal assay in BALB/c mice. There was complete agreement between results in the two tests with 76 isolates of P multocida. Neutralising activity was demonstrated in both assays with sera from infected gnotobiotic piglets. It was concluded that embryonic bovine lung cell cultures provided a sensitive in vitro test for the differentiation of toxigenic from non toxigenic isolates of P multocida. The assay could be used in diagnostic laboratories and for characterisation of the toxin.