A murine pneumonia model to study pathogenesis of Stenotrophomonas maltophilia

Early attempts to develop an animal model of infection appeared to support the hypothesis that Stenotrophomonas maltophilia does not cause serious sepsis when bacteria are intravenously administered to mice. This species has also been implicated in an increasing number of infections such as, bacteremia, endocarditis, ophthalmological syndromes, skin lesions, urinary, respiratory tract and gastrointestinal infections. Despite this clinical importance, the mechanisms involved in the pathogenesis of S. maltophilia infections have not been elucidated and the virulence factors of importance in the pathogenesis of S. maltophilia associated pulmonary infection remain to be characterized. The purpose of this study was to establish an infection model using 5 clinical isolates of S. maltophilia in a mouse pneumonia model. All strains were able to establish themselves in respiratory tract with peak of infection occurring at 24 h post infection. The strains were able to cause neutrophil influx, were taken up and intracellularly killed by alveolar macrophages except Sm2 that persisted for a slightly longer time in the macrophages. All strains were resistant to lytic action of serum and survived in blood confirming their ability to cause bacteremia. The strains were cleared from spleen and liver by 7th and 4th day but caused tissue damage that was measured in terms of lipid peroxidation, lactate dehydrogenase activity and histopathological examination of lung tissue homogenate. All strains caused interstitial pneumonitis in lungs of mice.