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Year : 2018  |  Volume : 2  |  Issue : 4  |  Page : 242-246

A review on the shape changes in pathogenic bacteria with emphasis on Mycobacterium tuberculosis

1 Mycobacteriology Research Center, National Research Institute of Tuberculosis and Lung Disease, Tehran, Iran
2 Department of Biotechnology, School of Advanced Technologies in Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran
3 Department of Chemistry, Institute for Chemistry of New Materials, Belarus National Academy of Sciences, Minsk, Belarus
4 The Republican Research and Practical Centre for Epidemiology and Microbiology, Minsk, Belarus

Date of Submission25-Jun-2018
Date of Decision02-Aug-2018
Date of Acceptance05-Aug-2018
Date of Web Publication11-Dec-2018

Correspondence Address:
Dr. Parissa Farnia
Mycobacteriology Research Centre (MRC), National Research Institute of Tuberculosis and Lung Disease (NRITLD), Shahid Beheshti University of Medical Sciences, Tehran
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/bbrj.bbrj_86_18

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Bacteria show a plenty of cellular shapes and can alter their forms. The bacterial cell shape is functionally important. Bacteria have a number of options to select their shapes in order to uptake more nutrient, motility, attachment to surface, symmetrical division of chromosomal elements, and localization of complex secretion apparatuses. Some factors including peptidoglycan and cytoskeleton-like proteins can regulate and keep the bacterial shape. In the case of Mycobacterium tuberculosis, the reported morphological variation in the pathogen are classified into two categories; those which frequently seen at exponential phase of growth that is rod, V, Y-shape, branched, or buds, and those that are seen occasionally under stress or environmental conditions which are round, oval, ultra-virus, spore-like, and cell wall defiant or L-forms. Growth conditions and age of the cells can influence on the shape and size of the pathogen in a range from coccobacilli to long rods. Under unsuitable conditions including starvation or oxygen deprivation, tubercle bacillus assumed a swollen shape without making the vacuolar or globoid bodies. The physical circumstances and nutritional feature will control the temporary lifestyle of the pathogen.

Keywords: Mycobacterium tuberculosis, ovoid, round, shape of pathogens, Y and V form bacilli

How to cite this article:
Farnia P, Farnia P, Ghanavi J, Zhavnerko GK, Poleschuyk NN, Velayati AA. A review on the shape changes in pathogenic bacteria with emphasis on Mycobacterium tuberculosis. Biomed Biotechnol Res J 2018;2:242-6

How to cite this URL:
Farnia P, Farnia P, Ghanavi J, Zhavnerko GK, Poleschuyk NN, Velayati AA. A review on the shape changes in pathogenic bacteria with emphasis on Mycobacterium tuberculosis. Biomed Biotechnol Res J [serial online] 2018 [cited 2022 Oct 7];2:242-6. Available from: https://www.bmbtrj.org/text.asp?2018/2/4/242/247247

  Introduction Top

The shape of bacteria and its impact on bacterial existence in different situations

Bacteria are very different in terms of cell forms and can show a different shape throughout their life cycle. Different cellular forms of bacteria can be very important in their function. One of the new opportunities for examining the importance of cellular functions in different bacterial species is the understanding of more genetic programs based on morphological changes of different species.[1],[2]

The cell wall plays an essential role in determination of bacterial cell shape. However, difference in chemical characteristics of the cell walls is a main challenge in this aspect since such differences can lead to the cell shape perturbations. It has been revealed that the selective pressures motivate various forms of pathogenic bacteria. The shape variations cause suitable adherence to organic and inorganic surfaces, existence under stressful environments or starvation, escape of human complement system, efficient distribution over mucous barriers and tissues, and increase the nutrient intake.[1],[2]

Considering the morphology and arrangement of bacterial cells, they can be classified into some basic forms including cocci and bacilli, spiral bacteria, and other forms.

Cocci: The overall shape of cocci (plural of coccus) is round or approximately round.[3] Diplococci (plural of diplococcus) are spherical bacteria (cocci) that usually appear in pairs of two fused cells. Coccobacilli (plural of coccobacillus) belong to rod-shaped bacteria. A coccobacillus reflects a middle shape between bacillus (elongated) and coccus (round)[4] and is so wide and short that it be similar to a coccus.


The basic shape of a bacillus (rod-shaped bacterium; plural bacilli) is round-ended cylinder. Bacilli typically are solitary but may associate to make some other forms including diplobacilli, streptobacilli, and palisades.[5] Diplobacilli consist of two bacilli organized side by side with each other. Streptobacilli are bacilli organized in chains. Coccobacilli are oval and resemble to cocci (round bacteria).[5]

Spiral bacteria

The third major bacterial cell morphology is spiral form.[6],[7] Spiral bacteria may be categorized as vibrios, spirilla, or spirochetes (helically twisted cylinders) considering the number of coils per a cell as well as motility, density, and elasticity of the cells.

Other forms

There are some other forms of bacteria such as selenomonads (cylinders curved in one plane) and uncommon square shapes. Bacteria may also appear as tetrads, staphylos, diplos, palizadas, streptos, and so on.

  Variation in the Shape of Mycobacterium Tuberculosis Top

Analysis of the shape of Mycobacterium tuberculosis through atomic and electron microscopes has shown that the bacillus does not constantly appear in the typical rod shape, it can be appear in other forms including granular rod, round, Y, V, ovoid, and club shapes.[8] The most classical form of M. tuberculosis is a slender rod shape that seen in stained smears. However, the bacilli can also be in round form. The number and size of round bacilli are variable in different growth condition [Figure 1].
Figure 1: The most classical form of Mycobacterium tuberculosis is a slender rod shape that seen in stained smears. But the bacilli can be in round form also. The number and size of round bacilli is variable in different growth condition

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Formally, the V-forms of M. tuberculosis arise by any of three methods; (i) germinating of adjacent coccoid elements, (ii) subpolar germination (budding) of rods, and (iii) snapping postfission movements. [Figure 2] shows the V-shape M. tuberculosis recorded by height mode of atomic force microscopy (AFM). In tubercle bacilli, during septum formation, the plasma membrane and inner cell wall grow inward, but the outer cell wall layer remains intact. On completion of septum formation with a cross wall, the inner layer may continue to grow and thus exert pressure upon the outer cell wall layer. The outer layer eventually ruptures first on one side of the cell, and the two daughter cells bend in on the side where the outer layer is still intact forming a “V-form” [Figure 2] and [Figure 3].
Figure 2: The V-shape Mycobacterium tuberculosis recorded by height mode of atomic force microscopy

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Figure 3: The V-shape Mycobacterium tuberculosis

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  Morphological Plasticity Top

Morphological plasticity of bacteria is a mysterious phenomenon, by which microorganisms gain adaptive advantages for growing and dividing in different circumstances.[9]

In the case of M. tuberculosis, there are some forms that are seen occasionally under stress or environmental conditions which are round, oval, ultra-virus, spore-like, and cell wall defiant or L-forms.[8],[10] Dividing M. tuberculosis cells display a greater morphological diversity than is generally regarded. They may appear as an elongated L-form shape also.[8],[10] [Figure 4] shows elongated L-shape M. tuberculosis in exponential phase. [Figure 5] represents variable shapes of tubercle bacilli in exponential phase recorded by AFM. The shape can be L-form, round, and rod shapes.
Figure 4: Elongated L-shape Mycobacterium tuberculosis in exponential phase

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Figure 5: Variable shapes of tubercle bacilli in exponential phase recorded by atomic force microscopy. The shape can be L-form, round, and rod shapes

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L-form bacteria

As it was mentioned above, bacteria can transform into a diversity of shapes during their natural life cycle. In this aspect, bacteria may transform to L-form as a phase of bacteria that have not cell wall (or have a deficient cell wall) and are very small. L-forms are involved in a diversity of infections. L-forms belong to a metagenomic microbiota associated with chronic disease. Hence, they have been the topic of a great deal of investigation by the medical research community.[11]

Up to now, over 50 various species of bacteria able to change into the L-form have known. It is believed that a large number of bacteria could be transformed into L-forms if they treated with the antibiotics that prevent cell wall synthesis. Bacillus anthracis, Helicobacter pylori, Borrelia burgdorferi, M. tuberculosis, Rickettsia prowazekii, and Treponema pallidum have been identified to transform into L-form pathogens involved in chronic infections.[11]

Overall, bacterial species with deficient cell wall are not destroyed by routinely utilized antibiotics. By applying a beta-lactam antibiotic (e.g., penicillin) to a culture of wild-type bacteria on a plate, little colonies of L-form bacteria form on the edges of the  Petri dish More Details.[11] It is illustrated that L-form bacteria duplicate in different approaches such as binary fission, budding, and filamentous growth.[11]

In the host bloodstream, classical shapes of pathogenic bacteria may be found. However, L-form bacteria could effectively enter and contaminate many cells of host immune system. The role of immunity cells is destroying of bacteria. Therefore, once inside white blood cells (specifically macrophages), bacteria can no longer be identified by the host immune system and are capable to persist in the body over long periods of time.[12],[13]

In the case of M. tuberculosis, we studied its elongated L-shape using AFM.[14] [Figure 4] represents elongated L-shape M. tuberculosis in the exponential phase. Dividing M. tuberculosis cells display a greater morphological diversity than is generally regarded. They may appear as an elongated L-form shape also.

Factors that induce morphological plasticity

As it was mentioned above, bacteria have a number of options to select their shapes. Some circumstantial signals were known to motivate shape plasticity, but the principal molecular reactions are mainly unidentified. However, bacteria assume one shape over another that is guided by a number of elements. For example, to uptake more nutrient in poor-nutrient conditions, bacteria may increase surface area-to-volume ratio resulting in increasing in diffusion of nutrients. Another factor that may influence the bacterial shape is motility. For this reason, flagella are localized at one end of the rod and host proteins are recruited to form actin tail. Attachment to surface by localized adhesion proteins and structures, symmetrical division of chromosomal elements to increases the probability of accurate division of cells, and localization of complex secretion apparatuses are other factors that affect the shape of bacteria.[7]

  Factors That Regulate and Keep the Bacterial Shape Top

The role of peptidoglycan in regulation of cell shape

The main factor that keeps bacterial shape is the cross-linked glycan plexus of peptidoglycan that encloses most bacteria. The peptidoglycan isolated from  Escherichia More Details coli in shape maintenance has been confirmed to maintain the rod-like shape of the bacterium even in the lack of all other substances.[15] Moreover, researchers showed that treatment of bacteria with lysozyme, the agent that degrades peptidoglycan, leads to conversion of the rod-shaped bacteria to round cells.[16]

Other reports demonstrated that hereditary (genetically) shape and size can also control shape and size of bacteria. Therefore, existing peptidoglycan may not simply govern the shape and size.

The role of cytoskeleton in determination of cell shape

Cytoskeletal proteins have a key role in determination of cell shape in eukaryotic cells. Recently, some cytoskeleton-like proteins involved in cell polarization, DNA separation, sporulation, and shape regulation have been discovered in bacteria.

Tubulin-like protein FtsZ was the first cytoskeleton protein discovered in bacteria, deficiency of which in bacteria caused long thread-like cells.[17] FtsZ hydrolyzes GTP to form filaments and construct a ring assembly at the mid-belt of bacterial cells.[18] Moreover, to produce particular cell morphology, FtsZ might control the production and localization of peptidoglycan in a stable manner.[19] In a mechanism that is found uniquely in M. tuberculosis, proteins FtsZ and FtsW interact directly to make an association mediated through cytoplasmic tails.[20] Therefore, FtsW might have a significant role in M. tuberculosis.

An intermediate filament-like protein, called CreS, is recently found in bacterium Caulobacter crescentus. The protein involved in regulating the specific shape.[21] There is no report for the existence of intermediate filaments in tubercle bacillus.

In recent years, actin-like cytoskeletal proteins including MreB, ParM, and MamK have received high attention to study.[18] MreB involves in regulating cell shape and forms microfilament-like spiral filaments near the inner side of cell membrane. Both Mbl and MreBH proteins are significant to make rod shape for Bacillus subtilis by recruiting peptidoglycan-synthesizing enzymes. A large number of coccoid-shaped bacteria (e.g., Staphylococcus, Streptococcus, and Lactococcus) do not have MreB, signifying that the protein is mainly essential for bacteria owing more complicated forms. ParM is shown to include in DNA partitioning and MamK may contribute to organelle positioning.[18]

  Microscopic Anatomy of Mycobacterium Tuberculosis Top

In 1874, the first Mycobacterium was isolated by Hansen and called Mycobacterium leprae. The discovered bacterium has been resistant against all efforts to cultivate it in vitro. Eight years later, Koch discovered the tubercle bacillus M. tuberculosis.[22] The effective staining models of Ehrlich (1887)[23] and Ziehl (1883)[24] confirmed the Koch discovery. M. tuberculosis seems as straight or slightly curved rods under light microscope. Growth conditions and age of the cells can influence on the shape and size of the pathogen in a range from coccobacilli to long rods. The length of the bacilli have been reported to be 1–10 μm in length (typically 3–5 μm) and their width is 0.2–0.6 μm. In few studies, the probability of morphological variations in the shape of M. tuberculosis has been discussed.[25],[26],[27],[28],[29],[30] The researchers showed that under unsuitable conditions including starvation or oxygen deprivation, tubercle bacillus assumed a swollen shape without making the vacuolar or globoid bodies.[30] These first reports were based on stained preparations and criticized frequently.[31] Nowadays, it is revealed that M. tuberculosis is a metabolically flexible pathogen.[32],[33],[34] The pathogen is both prototrophic (because it can make all its nutrients from basic carbon and nitrogen sources) and heterotrophic bacterium (since it can utilize already synthesized organic nutrients as a source of carbon and energy). Tubercle bacilli has a remarkable capacity to adjust to environmental alterations throughout the course of infection.[35],[36],[37],[38],[39],[40] The physical circumstances and nutritional feature will control the temporary lifestyle of the pathogen. The mentioned environmental variations include lack of nutrient, hypoxia, amount of heat, PH, salinity, and different extracellular stress situations.[30],[41],[42],[43],[44],[45],[46],[47],[48],[49] Certainly, in most of the cases, we do not know if shape changes beneficial, because few experiments have addressed the question. Knowledge of the physiology of M. tuberculosis during this process has been limited by the slow growth of the bacterium in the laboratory and other technical problems such as cell aggregation. Recent advances in microscopy techniques have revealed adaptive changes in size and shape of bacilli under stress conditions.[45],[46],[50],[51],[52],[53],[54] Briefly, the reported morphological variation in M. tuberculosis are classified into two categories; those which frequently seen at exponential phase of growth that is rod, V, Y-shape, branched or buds and those that are seen occasionally under stress or environmental conditions which are round, oval, ultra-virus, spore-like, and cell wall defiant or L-forms.[8],[55]

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Conflicts of interest

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  References Top

Yang DC, Blair KM, Salama NR. Staying in shape: The impact of cell shape on bacterial survival in diverse environments. Microbiol Mol Biol Rev 2016;80:187-203.  Back to cited text no. 1
Velayati AA, Farnia P. Diversity in cell shape of Mycobacterium tuberculosis. Atlas of Mycobacterium tuberculosis. Ch. 3. London: Academic Press; 2016.  Back to cited text no. 2
Madigan M, Martinko J. Brock Biology of Microorganisms. 11th ed.. Prentice Hall: USA; 2006.  Back to cited text no. 3
Ingelfinger, F. Dorland's Medical Dictionary. Saunders Press, 1999.  Back to cited text no. 4
Tortora GJ, Funke BR, Case CL. Functional anatomy of prokaryotic and eukaryotic cells. Microbiology: An Introduction. Pearson Education. 2004. p. 113-8.  Back to cited text no. 5
Csuros M. Microbiological Examination of Water and Wastewater. Boca Raton, Florida: CRC Press; 1999. p. 16-7.  Back to cited text no. 6
Young KD. The selective value of bacterial shape. Microbiol Mol Biol Rev 2006;70:660-703.  Back to cited text no. 7
Velayati AA, Abeel T, Shea T, Konstantinovich Zhavnerko G, Birren B, Cassell GH, et al. Populations of latent Mycobacterium tuberculosis lack a cell wall: Isolation, visualization, and whole-genome characterization. Int J Mycobacteriol 2016;5:66-73.  Back to cited text no. 8
  [Full text]  
Shen JP, Chou CF. Morphological plasticity of bacteria-open questions. Biomicrofluidics 2016;10:031501.  Back to cited text no. 9
Velayati AA, Farnia P. Shape variation in Mycobacterium tuberculosis. Iran J Clin Infect Dis 2011;6:95-101.  Back to cited text no. 10
Casadesús J. Bacterial L-forms require peptidoglycan synthesis for cell division. Bioessays 2007;29:1189-91.  Back to cited text no. 11
Kanneganti TD, Lamkanfi M, Kim YG, Chen G, Park JH, Franchi L, et al. Pannexin-1-mediated recognition of bacterial molecules activates the cryopyrin inflammasome independent of toll-like receptor signaling. Immunity 2007;26:433-43.  Back to cited text no. 12
Rolhion N, Darfeuille-Michaud A. Adherent-invasive Escherichia coli in inflammatory bowel disease. Inflamm Bowel Dis 2007;13:1277-83.  Back to cited text no. 13
Zhavnerko G, Nikolaevich Poleschuyk N. Mycobacterium under AFM tip: Advantages of polyelectrolyte modified substrate. Int J Mycobacteriol 2012;1:53-6.  Back to cited text no. 14
  [Full text]  
Weidel W, Frank H, Martin HH. The rigid layer of the cell wall of Escherichia coli strain B. J Gen Microbiol 1960;22:158-66.  Back to cited text no. 15
Lederberg J. Bacterial protoplasts induced by penicillin. Proc Natl Acad Sci U S A 1956;42:574-7.  Back to cited text no. 16
Lutkenhaus JF, Wolf-Watz H, Donachie WD. Organization of genes in the ftsA-envA region of the Escherichia coli genetic map and identification of a new fts locus (ftsZ). J Bacteriol 1980;142:615-20.  Back to cited text no. 17
Hett EC, Rubin EJ. Bacterial growth and cell division: A mycobacterial perspective. Microbiol Mol Biol Rev 2008;72:126-56.  Back to cited text no. 18
Young KD. Bacterial shape. Mol Microbiol 2003;49:571-80.  Back to cited text no. 19
Datta P, Dasgupta A, Bhakta S, Basu J. Interaction between ftsZ and ftsW of Mycobacterium tuberculosis. J Biol Chem 2002;277:24983-7.  Back to cited text no. 20
Ausmees N, Jacobs-Wagner C. Spatial and temporal control of differentiation and cell cycle progression in caulobacter crescentus. Annu Rev Microbiol 2003;57:225-47.  Back to cited text no. 21
Koch R. The etiology of tuberculosis. Berl Klin Wochenschr 15. 1882: 221-30.  Back to cited text no. 22
Ehrlich P. About the Methylene Blue Reaction of the Living Nervous Substance. Deutsche Medizinische Wochenschrift 1886;12:49-52.  Back to cited text no. 23
Ziehl F. To color the tubercle bacillus. Dtsch Med Wochenschr. 1882; 8:451.  Back to cited text no. 24
Malassez L, Vignal W. On the microorganism of the Zoological tuberculosis. Arch Physiol Norm Pathol 1884;3:81-105.  Back to cited text no. 25
Nocard ME, Roux E. On the bacilli culture of tuberculosis. Ann Inst Pasteur 1887;1:19-29.  Back to cited text no. 26
Metschnikoff VE. On the phagocytic role of tubercle giant cells. Virchows Arch Path Anat. 1888;113:63-94.  Back to cited text no. 27
Lubarsch O. To the knowledge of ray fungi. Z Hyg InfektionsKrankh. 1899;31:187-220.  Back to cited text no. 28
Fischel F. On the morphology and biology of the tubercle bacillus. Klin Wochschr 1893;30:989-93.  Back to cited text no. 29
Vera HD, Rettger LF. Morphological variation of the tubercle bacillus and certain recently isolated soil acid fasts, with emphasis on filtrability. J Bacteriol 1940;39:659-87.  Back to cited text no. 30
Porter KR, Yegian D. Some artifacts encountered in stained preparations of tubercle bacilli: II. Much granules and beads. J Bacteriol 1945;50:563-75.  Back to cited text no. 31
Edson NL. The intermediary metabolism of the mycobacteria. Bacteriol Rev 1951;15:147-82.  Back to cited text no. 32
Ramakrishnan T, Murthy PS, Gopinathan KP. Intermediary metabolism of mycobacteria. Bacteriol Rev 1972;36:65-108.  Back to cited text no. 33
Niederweis M. Nutrient acquisition by mycobacteria. Microbiology 2008;154:679-92.  Back to cited text no. 34
Mccune RM Jr., Tompsett R. Fate of Mycobacterium tuberculosis in mouse tissues as determined by the microbial enumeration technique. I. The persistence of drug-susceptible tubercle bacilli in the tissues despite prolonged antimicrobial therapy. J Exp Med 1956;104:737-62.  Back to cited text no. 35
Mattman LH. Cell wall-deficient forms of mycobacteria. Ann N Y Acad Sci 1970;174:852-61.  Back to cited text no. 36
Nyka W. Studies on the effect of starvation on mycobacteria. Infect Immun 1974;9:843-50.  Back to cited text no. 37
Takahashi S. L-phase growth of mycobacteria 2. Consideration on the survival of tubercle bacillus in caseous lesion (author's transl). Kekkaku 1979;54:231-5.  Back to cited text no. 38
Khomenko A, Fadeeva N, Golyshevskaia V. Morphologic and biochemical changes in Mycobacterium tuberculosis during chemotherapy. Probl Tuberk 1983;(7):48-53.  Back to cited text no. 39
Wayne LG. Dormancy of Mycobacterium tuberculosis and latency of disease. Eur J Clin Microbiol Infect Dis 1994;13:908-14.  Back to cited text no. 40
Smeulders MJ, Keer J, Speight RA, Williams HD. Adaptation of Mycobacterium smegmatis to stationary phase. J Bacteriol 1999;181:270-83.  Back to cited text no. 41
Höner zu Bentrup K, Russell DG. Mycobacterial persistence: Adaptation to a changing environment. Trends Microbiol 2001;9:597-605.  Back to cited text no. 42
Young M, Mukamolova GV, Kaprelyants AS. Mycobacterial dormancy and its relation to persistence, Mycobacterium: molecular microbiology. Horizon Bioscience, London, United Kingdom. 2005. p. 265-230.  Back to cited text no. 43
Anuchin AM, Mulyukin AL, Suzina NE, Duda VI, El-Registan GI, Kaprelyants AS, et al. Dormant forms of Mycobacterium smegmatis with distinct morphology. Microbiology 2009;155:1071-9.  Back to cited text no. 44
Velayati AA, Farnia P, Masjedi MR, Ibrahim TA, Tabarsi P, Haroun RZ, et al. Totally drug-resistant tuberculosis strains: Evidence of adaptation at the cellular level. Eur Respir J 2009;34:1202-3.  Back to cited text no. 45
Farnia P, Mohammad RM, Merza MA, Tabarsi P, Zhavnerko GK, Ibrahim TA, et al. Growth and cell-division in extensive (XDR) and extremely drug resistant (XXDR) tuberculosis strains: Transmission and atomic force observation. Int J Clin Exp Med 2010;3:308-14.  Back to cited text no. 46
Singh B, Ghosh J, Islam NM, Dasgupta S, Kirsebom LA. Growth, cell division and sporulation in mycobacteria. Antonie Van Leeuwenhoek 2010;98:165-77.  Back to cited text no. 47
Shleeva MO, Bagramyan K, Telkov MV, Mukamolova GV, Young M, Kell DB, et al. Formation and resuscitation of “non-culturable” cells of rhodococcus rhodochrous and Mycobacterium tuberculosis in prolonged stationary phase. Microbiology 2002;148:1581-91.  Back to cited text no. 48
Shleeva MO, Kudykina YK, Vostroknutova GN, Suzina NE, Mulyukin AL, Kaprelyants AS, et al. Dormant ovoid cells of Mycobacterium tuberculosis are formed in response to gradual external acidification. Tuberculosis (Edinb) 2011;91:146-54.  Back to cited text no. 49
Velayati AA, Farnia P, Ibrahim TA, Haroun RZ, Kuan HO, Ghanavi J, et al. Differences in cell wall thickness between resistant and nonresistant strains of Mycobacterium tuberculosis: Using transmission electron microscopy. Chemotherapy 2009;55:303-7.  Back to cited text no. 50
Velayati AA, Farnia P, Hoffner S. Drug-resistant Mycobacterium tuberculosis: Epidemiology and role of morphological alterations. J Glob Antimicrob Resist 2018;12:192-6.  Back to cited text no. 51
Velayati AA, Farnia P, Merza MA, Zhavnerko GK, Tabarsi P, Titov LP, et al. New insight into extremely drug-resistant tuberculosis: Using atomic force microscopy. Eur Respir J 2010;36:1490-3.  Back to cited text no. 52
Velayati AA, Farnia P. Division-cycle in Mycobacterium tuberculosis. Int J Mycobacteriol 2012;1:111-7.  Back to cited text no. 53
  [Full text]  
Farnia P, Farhadi T, Farnia P, Ghanavi J, Velayati AA. A review on the C-terminal domain of channel protein with necrosis-inducing toxin as a novel necrotizing toxin of Mycobacterium tuberculosis. Biomed Biotechnol Res J 2018;2:100-5.  Back to cited text no. 54
  [Full text]  
Velayati AA, Farnia P. Morphological characterization of Mycobacterium tuberculosis. Understanding Tuberculosis-Deciphering the Secret Life of the Bacilli. London: InTech; 2012.  Back to cited text no. 55


  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]

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