Virulence ranking of some Mycobacterium tuberculosis and Mycobacterium bovis strains according to their ability to multiply in the lungs, induce lung pathology, and cause mortality in mice

Abstract

Three virulent strains of Mycobacterium tuberculosis (H37Rv, Erdman, and NYH-27) and two virulent strains of M. bovis (Ravenel and Branch) were compared in terms of their growth rates in the livers and the lungs of mice, their ability to cause lung pathology, and the time taken for them to cause death. In immunocompetent mice, all strains caused an infection that progressed for 20 days or more and then underwent resolution in the liver but not in the lungs. In the lungs, infection persisted and induced progressive pathology. According to host survival time, Ravenel was the most virulent strain, followed, in decreasing order of virulence, by Branch, H37Rv, Erdman, and NYH-27. The much longer survival times of mice infected with M. tuberculosis strains allowed time for lung histopathology to change from a histiocytic alveolitis to a chronic fibroblastic fibrosis that eventually obliterated most of the lung architecture. By contrast, in mice infected with M. bovis strains, the alveolitis that developed during early infection was rapid and expansive enough to cause death before chronic lung pathology became evident. In mice depleted of CD4 ؉ T cells, increased growth of all virulent strains induced necrotic exudative lung lesions that rapidly filled most of the alveolar sacs with inflammatory cells. These mice died much earlier than infected control mice did. Attenuated strains had longer population doubling times in vivo and failed to cause progressive disease or pathology in the lungs or livers of immunocompetent mice. MATERIALS AND METHODS Mice. Male B6D2F1 (C57BL/6 ϫ DBA/2) mice were obtained from the Trudeau Institute Animal Breeding Facility, Saranac Lake, N.Y., and used in experiments at 7 to 9 weeks of age. CD2F1 (BALB/c ϫ DBA/2) mice were used for the production of hybridoma ascites. All mice were known to be free of common viral pathogens according to routine serological screening performed by the

Airway macrophages as the guardians of tissue repair in the lung

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Infection intensity and infectivity of the tick‐borne pathogen Borrelia afzelii

“…Different isolates of a given pathogen species often differ considerably in within-host growth (e.g. Dunn & North, 1995;Pennington et al, 1997;Mackinnon & Read, 1999;De Roode & Altizer, 2010), implying the presence of genetic variation for exploitation and harm of the host. How does natural selection act on such variation and shape the level of exploitation?…”

Tumour necrosis factor receptors and apoptosis of alveolar macrophages during early infection with attenuated and virulent Mycobacterium bovis

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