Piglets infected intranasally with Bordetella bronchiseptica were injected with two fluorochrome markers. Transverse sections of undecalcified nasal conchae (cut between the third incisor and the third premolar teeth) were examined by microradiography and fluorescence microscopy; surface-stained sections were evaluated by light microscopy. The fluorescent surface of the nasal ventral conchae from the infected piglets was increased as compared with the controls. This was due to an increased amount of fluorescent mineralization fronts as well as to the presence of abnormal fluorescent areas within trabeculae. Trabecular mineral content of the microradiographs was irregular and varied from hypo- to hypermineralized. When compared with the corresponding surface-stained sections, no correlation could be made between the mineral content and the type of tissue. These findings suggest that an increased number of osteoblasts which secrete prebone matrix but are modified so that mineralization does not occur normally.

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. This would account for the presence of high concentrations of PGH in the plasma and a functionally competent hypophysis cerebri, which responded to GHRH injection that have retarded growth in pigs affected with AR.