| First Author | Brown DH | Year | 1995 |
| Journal | Infect Immun | Volume | 63 |
| Issue | 6 | Pages | 2243-7 |
| PubMed ID | 7768604 | Mgi Jnum | J:25685 |
| Mgi Id | MGI:73397 | Doi | 10.1128/iai.63.6.2243-2247.1995 |
| Citation | Brown DH, et al. (1995) Growth of Mycobacterium tuberculosis in BCG-resistant and -susceptible mice: establishment of latency and reactivation. Infect Immun 63(6):2243-7 |
| abstractText | Growth of mycobacterial species is controlled by a gene, Bcg (candidate Nramp). Bcg acts at the macrophage level and is thought to control some aspect of macrophage priming for activation. Infection of Mycobacterium bovis BCG-susceptible (Bcgs) mice with several different mycobacterial species results in the growth of the microorganisms, while the growth of the same organisms is controlled in BCG-resistant (Bcgr) mice. The capacity of Bcg to control the growth of M. tuberculosis has not been extensively explored. The purpose of this investigation, therefore, was to compare the growth of M. tuberculosis in Bcgr and Bcgs mice. We found that the growth of tubercule bacilli was different in the lungs and spleens of Bcgr and Bcgs mice when they were inoculated with fewer then 10(3) CFU of the mycobacterium. The differences in growth were more easily distinguished in the lungs then in the spleens. The growth of the microorganisms in both strains of mice peaked between 35 and 43 days, and a latent infection was established by 65 days after infection. Activation of the hypothalamic-pituitary-adrenal axis resulted in reactivation of the growth of M. tuberculosis in both Bcgr and Bcgs mice. Greater numbers of tubercule bacilli were isolated from lungs than from spleens following reactivation. The utility of this mouse model in the study of the establishment of latency and reactivation of M. tuberculosis is discussed. |
