Dh. Brown et al., GROWTH OF MYCOBACTERIUM-TUBERCULOSIS IN BCG-RESISTANT AND BCG-SUSCEPTIBLE MICE - ESTABLISHMENT OF LATENCY AND REACTIVATION, Infection and immunity, 63(6), 1995, pp. 2243-2247
Growth of mycobacterial species is controlled by a gene, Bcg (candidat
e Nramp). Bcg acts at the macrophage level and is thought to control s
ome aspect of macrophage priming for activation. Infection of Mycobact
erium bovis BCG-susceptible (Bcg(s)) mice with several different mycob
acterial species results in the growth of the microorganisms, while th
e growth of the same organisms is controlled in BCG-resistant (Bcg(r))
mice. The capacity of Bcg to control the growth of M. tuberculosis ha
s not been extensively explored. The purpose of this investigation, th
erefore, was to compare the growth of M. tuberculosis in Bcg(r) and Bc
g(s) mice. We found that the growth of tubercule bacilli was different
in the lungs and spleens of Bcg(r) and Bcg(s) mice when they were ino
culated with fewer then 10(3) CFU of the mycobacterium. The difference
s in growth were more easily distinguished in the lungs then in the sp
leens. 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 initial infection. Activation of the hypothalamic-pituitary
-adrenal axis resulted in reactivation of the growth of M. tuberculosi
s in both Bcg(r) and Bcg(s) mice. Greater numbers of tubercule bacilli
were isolated from lungs than from spleens following reactivation. Th
e utility of this mouse model in the study of the establishment of lat
ency and reactivation of M. tuberculosis is discussed.