Annual Report

26. Comparison of Respiratory Lesions in C3H and C3H-Scid Mice Experimentally Infected with CAR Bacillus

Akihiro Kawano, Satoru Matsushita, and Hiromi Takahashi-Omoe

Keywords: CAR bacillus, respiratory lesion, Scid mice

Cilia-associated respiratory (CAR) bacillus is an unclassified, gram-negative, filamentous bacterium that was tentatively designated in 1985 as one of the agents that cause chronic respiratory diseases in laboratory rodents. CAR bacillus infection is characterized by histological lesions consisting of attachment of the organisms on the ciliated epithelium of the respiratory tract and peribronchial cuffing with round cells such as lymphocytes and plasma cells, accompanied by mucopurulent exudate filling the bronchial lumen and leukocytic infiltration in the lamina propria.

To understand the mechanisms of anti-CAR bacillus host defenses, we infected C3H/He (C3H) mice and C3H/He-scid/scid (Scid) mice, which lack functional T and B lymphocytes and consequently show severe combined immunodeficiency, with the SMR strain of CAR bacillus. 18 mice of each strain were inoculated intranasally with a lung homogenate containing the SMR strain, and 18 mice of each strain were inoculated with sterile PBS. Three inoculated mice and three control mice of each group were euthanatized on days 4, 7, 14, 21, 28 and 56 postinoculation (PI). The body weight of C3H mice inoculated with the SMR strain decreased from day 28 PI as compared with that of control mice. However, the body weight of inoculated Scid mice from day 21 PI was less than that of the Scid mice on day 0 PI. Histologically, CAR bacilli were observed on the ciliated epithelial cells of trachea from day 7 PI and those of bronchi from day 14 PI in each group. Although CAR bacilli increased with time after inoculation, the number of CAR bacilli was not different between the groups throughout the experimental period. In the trachea, round cell infiltration was observed in the tracheal lamina propria of C3H mice from day 7 PI and the lesions progressed with time. Mucopururent exudate was mild in the tracheal lumen throughout the period. In Scid mice, however, mucopururent exudate became severe with time and round cell infiltration was slight. In the lungs, peribronchitis with peripheral lymphoid follicles was observed in C3H mice from day 21 PI and these lesions developed extensive mucopurulent bronchopneumonia and atelectasis with time. In Scid mice, peribronchitis was mild and peripheral lymphoid follicles were not shown. Neutrophilic exudate in the bronchial lumen was more severe than that of C3H mice, but mucopurulent bronchopneumonia and atelectasis were intensive as compared with those of C3H mice. It is suggested that Scid mice may be affected more severely than C3H mice in CAR bacillus infection, because the body weight of Scid mice decreased markedly. The respiratory lesions of Scid mice are characterized by the following findings as compared with those of C3H mice: (i) milder peribronchitis with poor round cell infiltration, (ii) more severe neutrophilic exudate in the lamina of affected airways, and (iii) more intensive mucopurulent bronchopneumonia.

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