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 Table of Contents  
EDITORIAL
Year : 2012  |  Volume : 1  |  Issue : 1  |  Page : 1-2

Latent tuberculosis (TB) bacilli: Yes or no to preventive chemotherapy


1 Mycobacteriology Research Centre, National Research Institute of Tuberculosis and Lung Disease (NRITLD), WHO & UNION Collaborating Centre for TB & Lung Diseases, Shahid Beheshti University (Medical Campus), P.O. 19575/154, Darabad, Tehran 19556, Iran
2 Chronic Respiratory Diseases Research Center, National Research Institute of Tuberculosis & Lung Disease (NRITLD), Shahid Beheshti University of Medical Sciences, Tehran, Iran

Date of Web Publication28-Feb-2017

Correspondence Address:
Parissa Farnia
The Republican Research and Practical Centre for Epidemiology and Microbiology, Filimonova 23, Minsk
Iran
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Source of Support: None, Conflict of Interest: None


DOI: 10.1016/j.ijmyco.2012.01.002

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How to cite this article:
Velayati AA, Farnia P, Masjedi MR. Latent tuberculosis (TB) bacilli: Yes or no to preventive chemotherapy. Int J Mycobacteriol 2012;1:1-2

How to cite this URL:
Velayati AA, Farnia P, Masjedi MR. Latent tuberculosis (TB) bacilli: Yes or no to preventive chemotherapy. Int J Mycobacteriol [serial online] 2012 [cited 2019 Jan 19];1:1-2. Available from: http://www.ijmyco.org/text.asp?2012/1/1/1/201192



Despite extensive investigation over several decades, the mechanism by which Mycobacterium tuberculosis establishes latent infection remains poorly understood. In the latent infection, bacilli typically replicate inside host macrophages until an effective immune response is mounted and the bacilli become restricted to the characteristic tuberculous lesions and the progression of the disease is halted [1]. This remarkable feature may occur after an initial exposure to M. tuberculosis or may happen in tuberculosis (TB) patients who thoroughly followed the antibiotics treatment, but developed late reactivation. To date, investigators have proposed different views regarding the physiological states of latent TB. While the outcome of clinical trials with isoniazid (INH) postulated some metabolic activity for latent TB bacilli [2], the in vitro studies suggested a metabolically inactive state for bacteria [3]. In addition, some evidences suggest bacterial infectivity during latency. In contrast, microscopic examination of these tissues sometimes fails to reveal acid-fast bacilli—the characteristic bacterial forms associated with active, infectious TB [4].

To resolve this paradox, a few investigators proposed the entrance of latent bacilli into an altered developmental state in which they are no longer acid-fast. The others suggested that latent bacilli remain acid-fast, but are present in such low numbers that they defy microscopic detection [5]. Recently, the sequential adaptations of latent TB bacilli using the in vitro gradual oxygen depletion model (Wayne model) were documented [6]. The adaptation was reported from 1 to 48 months post latency using Atomic Force Microscopy (AFM). Overall, two types of latent TB bacilli, i.e., viable culturable, acid-fast cells and viable non-culturable and non-acid-fast bacilli were visible under AFM. As shown in [Figure 1], these filterable and non-acid fast bacilli are too small (150–300μm in size) to be detected by routine techniques. However, their passage into mice model could induce active TB. Therefore, the latent TB bacilli may be considered as a two-phase microorganism which needs effective bactericidal drug(s) against its both metabolic active and inactive states.
Figure 1: The viable, non-culturable, non-acid fast latent bacilli under Atomic Force Microscopy (AFM).

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Today, one third of the world population, i.e., 1.7 billion people have latent TB infection. These individuals constitute a major obstacle for the TB control program, and the efforts to eradicate TB must not solely rely on attacking the actively growing tubercle bacilli, but must also include bacilli in the latent stages. In other words, this research supports preventive chemotherapy.



 
  References Top

1.
Y.C. Manabe, W.R. Bishai, Latent Mycobacterium tuberculosispersistence, patience and winning by waiting, Nat. Med. 16 (2000) 327–1329.  Back to cited text no. 1
    
2.
G.W. Comstock, C. Baum, D.E. Snider, Isoniazid prophylaxis among Alaskan Eskimos: a final report of the bethel isoniazid studies, Am. Rev. Respir. Dis. 119 (1972) 827–830.  Back to cited text no. 2
    
3.
L.G. Wayne, Dormancy of Mycobacterium tuberculosis and latency of disease, Eur. J. Clin. Microbiol. Infect. Dis. 13 (1994) 908–914.  Back to cited text no. 3
    
4.
E.L. Opie, J.D. Aronson, Tubercle bacilli in latent tuberculous lesions and in lung tissue without tuberculous lesions, Arch. Pathol. Lab. Med. 4 (1972) 1–21.  Back to cited text no. 4
    
5.
N.M. Parrish, J.D. Dick, W.R. Bishai, Mechanisms of latency in Mycobacterium tuberculosis, Trends Microbiol. 6 (1998) 107–112.  Back to cited text no. 5
    
6.
A.A. Velayati, P. Farnia, M.R. Masjedi, G.K. Zhavnerko, M.A. Merza, J. Ghanavei, et al, Sequential adaptation in latent tuberculosis bacilli: observation by atomic force microscopy (AFM), Int. J. Clin. Exp. Med. 4 (2011) 193–199.  Back to cited text no. 6
    


    Figures

  [Figure 1]


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