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INTRODUCTION

Tuberculosis (TB) has been an affliction of humankind since before recorded history. TB inspired the writer John Bunyan to aptly describe this deadly and mysterious disease in 1660 as “the captain of all these men of death that came against him to take him away, was the consumption for it was that brought him down to the grave.”1 As with classic works of literature, tuberculosis endures. In spite of the heralded medicinal cures developed in the 1940s and 1950s, tuberculosis still devastates populations throughout the world. Aspects of the pathogenesis of this disease still remain shrouded in mystery. Even more disturbing, Mycobacterium tuberculosis, the etiologic agent of TB, has become increasingly resistant to antimycobacterial medications and travels with, and has been especially virulent among those suffering from acquired immunodeficiency syndrome (AIDS). These trends keep tuberculosis at the forefront among the deadly infections of humankind.

THE MICROBIOLOGY OF M. TUBERCULOSIS

M. tuberculosis is classified within a group nearly genetically identical organisms and is thus referred to as the M. tuberculosis complex. The members of the M. tuberculosis complex include Mycobacterium bovis, and several uncommon and very rare human pathogens: M. pinnipedii, M. microti, M. cannettii, M. orygis, M. caprae, and M. africanum.2 M. tuberculosis and M. bovis along with Mycobacterium leprae cause communicable disease, which set these species apart from the more than 170 other species of Mycobacteria, which are generally found within the environment and referred to as nontuberculous mycobacteria (NTM). In contrast, M. tuberculosis is not found within the environment.3

M. tuberculosis organisms exhibit a bacillary morphology and produce an impervious waxy cell wall. The cell wall, composed mostly of a beta-hydroxy fatty acid, mycolic acid, excludes most antimicrobial agents and is resistant to alkali and acid. The latter property is taken advantage of by the acid-fast stains (e.g., Ziehl-Neelsen, Kinyoun, fluorochrome). M. tuberculosis organisms can be killed relatively easily by ultraviolet (UV) light at 254-nm wavelength, sunlight, heat, and specific disinfectants such as tricresol and phenol. Modern molecular techniques applied to M. tuberculosis, have resulted in sequencing and annotation of entire genome, comprising about 4000 genes.4 Currently, whole genome sequencing (WGS) has evolved into a powerful automated tool within the contemporary clinical microbiology laboratory, which provides a comprehensive method for M. tuberculosis identification and importantly concurrent detection of mutations that predict resistance to first- and second-line antimycobacterial drugs.5

Mycobacteria divide every 18–24 hours compared to every 1–2 hours for most other bacterial pathogens. Mycobacteria have traditionally been cultured on egg-potato–based solid media, Lowenstein-Jensen (L-J) slants, or Middlebrook 7H10 or 7H11 agar-based solid media. Following a 3- to 4-week incubation, an array of biochemical tests and additional growth on artificial media have been necessary traditionally to distinguish M. tuberculosis from the other multiple species of mycobacteria.6 Final identification by these nearly ...

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