The nasal septa of fetal rabbits at 26？days of gestation were harvested by cesarean section of the does while under anesthesia and then exposed to Bordetella bronchiseptica or its lipopolysaccharide (LPS) for periods of 2 and 4？hours. A total of 240 explants were used. The tissues were examined using the Hematoxylin & Eosin technique. Then, semithin sections (0.5？ m) were stained with toluidine blue and examined with indirect immunoperoxidase (IPI) and lectin histochemistry. The most frequent and statistically significant findings were as follows: (1) cell death and increased goblet cell activity when exposed to bacteria and (2) cell death, cytoplasmic vacuolation and infiltration of polymorphonuclear leukocytes when exposed to LPS. The lesions induced by the bacterium were more severe than with LPS alone, except for the cytoplasmic vacuolation in epithelial cells. IPI stained the ciliated border of the epithelium with the bacterium more intensely, while LPS lectin histochemistry preferentially labeled the cytoplasm of goblet cell. These data indicate that B. bronchiseptica and its LPS may have an affinity for specific glycoproteins that would act as adhesion receptors in both locations. 1. Introduction Bordetella bronchiseptica is a Gram-negative bacterium capable of colonizing the respiratory tract of a large range of mammalian hosts, including mice, rats, guinea pigs, rabbits, cats, dogs, pigs, sheep, horses, and bears [1]. B. bronchiseptica is responsible for a wide spectrum of overt respiratory diseases such as kennel cough in dogs, atrophic rhinitis in pigs, and snuffles and pneumonia in rabbits [2–4]. B. bronchiseptica can also lead to permanent asymptomatic colonization of the respiratory tract [1, 5]. In dogs, B. bronchiseptica causes tracheobronchitis with two patterns of histological lesions. One pattern consists of focal areas of epithelial degeneration, necrosis, and cellular disorganization with vacuolation and pyknosis represented by congestion in the lamina propria, infiltrated with macrophages and lymphocytes. The second pattern consists of mucopurulent exudates that accumulate in the lumen of the airway with edema in the lamina propria, marked infiltration of polymorphonuclear leukocytes and clumps of bacteria located between the cilia of the tracheobronchial epithelium [10]. In piglets, B. bronchiseptica can cause upper respiratory illness, leading to nonprogressive atrophic rhinitis; histologically, other common lesions include hyperplasia of the epithelium with metaplasia and deciliated cells. In rabbits, B. bronchiseptica causes a
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