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''[[Mycobacterium tuberculosis]]'' can remain latent in human hosts for decades after an initial infection, allowing it to continue infecting others. It has been estimated that a third of the world population has latent tuberculosis (TB).<ref>{{cite journal | vauthors = Getahun H, Matteelli A, Chaisson RE, Raviglione M | title = Latent Mycobacterium tuberculosis infection | journal = The New England Journal of Medicine | volume = 372 | issue = 22 | pages = 2127–2135 | date = May 2015 | pmid = 26017823 | doi = 10.1056/NEJMra1405427 }}</ref> ''M. tuberculosis'' has many [[virulence factor]]s, which can be divided across lipid and fatty acid metabolism, cell envelope proteins, [[macrophage]] inhibitors, [[kinase]] proteins, [[protease]]s, metal-transporter proteins, and gene expression regulators.<ref>{{cite journal | vauthors = Forrellad MA, Klepp LI, Gioffré A, Sabio y García J, Morbidoni HR, de la Paz Santangelo M, Cataldi AA, Bigi F | display-authors = 6 | title = Virulence factors of the Mycobacterium tuberculosis complex | journal = Virulence | volume = 4 | issue = 1 | pages = 3–66 | date = January 2013 | pmid = 23076359 | pmc = 3544749 | doi = 10.4161/viru.22329 }}</ref>
''[[Mycobacterium tuberculosis]]'' can remain latent in human hosts for decades after an initial infection, allowing it to continue infecting others. It has been estimated that a third of the world population has latent tuberculosis (TB).<ref>{{cite journal | vauthors = Getahun H, Matteelli A, Chaisson RE, Raviglione M | title = Latent Mycobacterium tuberculosis infection | journal = The New England Journal of Medicine | volume = 372 | issue = 22 | pages = 2127–2135 | date = May 2015 | pmid = 26017823 | doi = 10.1056/NEJMra1405427 }}</ref> ''M. tuberculosis'' has many [[virulence factor]]s, which can be divided across lipid and fatty acid metabolism, cell envelope proteins, [[macrophage]] inhibitors, [[kinase]] proteins, [[protease]]s, metal-transporter proteins, and gene expression regulators.<ref>{{cite journal | vauthors = Forrellad MA, Klepp LI, Gioffré A, Sabio y García J, Morbidoni HR, de la Paz Santangelo M, Cataldi AA, Bigi F | display-authors = 6 | title = Virulence factors of the Mycobacterium tuberculosis complex | journal = Virulence | volume = 4 | issue = 1 | pages = 3–66 | date = January 2013 | pmid = 23076359 | pmc = 3544749 | doi = 10.4161/viru.22329 }}</ref>


The development of [[Leprosy|Hansen’s disease]] is caused by infection with either ''[[Mycobacterium leprae]]'' or [[Mycobacterium lepromatosis|''Mycobacterium lepromatosi''s]] with the latter acting as a secondary causal agent. Roughly 200,000 new cases of infection are reported each year, and 80% of new <ref>{{cite journal | vauthors = Ferrell KC, Johansen MD, Triccas JA, Counoupas C | title = Virulence Mechanisms of <i>Mycobacterium abscessus</i>: Current Knowledge and Implications for Vaccine Design | journal = Frontiers in Microbiology | volume = 13 | pages = 842017 | date = 2022-03-03 | pmid = 35308378 | pmc = 8928063 | doi = 10.3389/fmicb.2022.842017 | doi-access = free }}</ref>cases are reported in Brazil, India, and Indonesia.<ref>{{cite journal | vauthors = Sugawara-Mikami M, Tanigawa K, Kawashima A, Kiriya M, Nakamura Y, Fujiwara Y, Suzuki K | title = Pathogenicity and virulence of <i>Mycobacterium leprae</i> | journal = Virulence | volume = 13 | issue = 1 | pages = 1985–2011 | date = December 2022 | pmid = 36326715 | pmc = 9635560 | doi = 10.1080/21505594.2022.2141987 }}</ref> ''M. leprae'' infection localizes within the skin macrophages and Schwann cells found in peripheral nerve tissue.
The development of [[Leprosy|Hansen’s disease]] is caused by infection with either ''[[Mycobacterium leprae]]'' or [[Mycobacterium lepromatosis|''Mycobacterium lepromatosi''s]] with the latter acting as a secondary causal agent. Roughly 200,000 new cases of infection are reported each year, and 80% of new<ref>{{cite journal | vauthors = Ferrell KC, Johansen MD, Triccas JA, Counoupas C | title = Virulence Mechanisms of <i>Mycobacterium abscessus</i>: Current Knowledge and Implications for Vaccine Design | journal = Frontiers in Microbiology | volume = 13 | pages = 842017 | date = 2022-03-03 | pmid = 35308378 | pmc = 8928063 | doi = 10.3389/fmicb.2022.842017 | doi-access = free }}</ref> cases are reported in Brazil, India, and Indonesia.<ref>{{cite journal | vauthors = Sugawara-Mikami M, Tanigawa K, Kawashima A, Kiriya M, Nakamura Y, Fujiwara Y, Suzuki K | title = Pathogenicity and virulence of <i>Mycobacterium leprae</i> | journal = Virulence | volume = 13 | issue = 1 | pages = 1985–2011 | date = December 2022 | pmid = 36326715 | pmc = 9635560 | doi = 10.1080/21505594.2022.2141987 }}</ref> ''M. leprae'' infection localizes within the skin macrophages and Schwann cells found in peripheral nerve tissue.

⚫
[[File:Three Pathogenic Mycobacteria.png|thumb|A Venn diagram constructed using InteractiVenn<ref>{{cite journal | vauthors = Heberle H, Meirelles GV, da Silva FR, Telles GP, Minghim R | title = InteractiVenn: a web-based tool for the analysis of sets through Venn diagrams | journal = BMC Bioinformatics | volume = 16 | issue = 1 | pages = 169 | date = May 2015 | pmid = 25994840 | pmc = 4455604 | doi = 10.1186/s12859-015-0611-3 }}</ref> using proteomic information. The regions in the diagram represent [[Sequence homology|orthologous]] proteins found in each species (based on OMA identifiers). Unidentified proteins for each species are localized in the unique section for each species.]]
Since 2018, several members of this [[species complex]] are considered synonyms of ''M. tuberculosis'' as far as bacterial nomenclature is concerned. The [[International Journal of Systematic and Evolutionary Microbiology|IJSEM]] article reports that ''M. africanum'', ''M. bovis'', ''M. caprae'', ''M. pinnipedii'' are 99.21–99.92% identical to ''M. tuberculosis'' on the whole-genome level, failing the criteria to be considered independent species. The same applies to "M. canetti", "M. mungi", and "M. orygis", species not validly published. The variation is even below the accepted level for subspecies. The authors note that these names do refer to stable lineages with meaningful clinical distinctions, recommending that them become variants: ''M. bovis'' would become ''M. tuberculosis'' var. ''bovis'', for example.<ref>{{cite journal |last1=Riojas |first1=Marco A. |last2=McGough |first2=Katya J. |last3=Rider-Riojas |first3=Cristin J. |last4=Rastogi |first4=Nalin |last5=Hazbón |first5=Manzour Hernando |title=Phylogenomic analysis of the species of the Mycobacterium tuberculosis complex demonstrates that Mycobacterium africanum, Mycobacterium bovis, Mycobacterium caprae, Mycobacterium microti and Mycobacterium pinnipedii are later heterotypic synonyms of Mycobacterium tuberculosis |journal=International Journal of Systematic and Evolutionary Microbiology |date=1 January 2018 |volume=68 |issue=1 |pages=324–332 |doi=10.1099/ijsem.0.002507}}</ref>


=== Nontuberculosis Mycobacteria ===
=== Nontuberculosis Mycobacteria ===
⚫
[[File:Three Pathogenic Mycobacteria.png|thumb|A Venn diagram constructed using InteractiVenn<ref>{{cite journal | vauthors = Heberle H, Meirelles GV, da Silva FR, Telles GP, Minghim R | title = InteractiVenn: a web-based tool for the analysis of sets through Venn diagrams | journal = BMC Bioinformatics | volume = 16 | issue = 1 | pages = 169 | date = May 2015 | pmid = 25994840 | pmc = 4455604 | doi = 10.1186/s12859-015-0611-3 }}</ref> using proteomic information. The regions in the diagram represent [[Sequence homology|orthologous]] proteins found in each species (based on OMA identifiers). Unidentified proteins for each species are localized in the unique section for each species.]]
A collection of Nontuberculosis Mycobacteria (NTM) that exclude ''M. tuberculosis, M. leprae,'' and ''M. lepromatosis'' are readily available to infect mammalian hosts. Such species are referred to as "atypical mycobacteria." Although person-to-person transmission is rare, transmission of ''M. abscessus'' has been observed between patients with [[cystic fibrosis]].<ref>{{Cite web |date=2019-08-12 |title=Nontuberculous Mycobacteria (NTM) Infections {{!}} HAI {{!}} CDC |url=https://www.cdc.gov/hai/organisms/nontuberculous-mycobacteria.html |access-date=2023-04-28 |website=www.cdc.gov |language=en-us}}</ref> The four primary diseases observed in humans are chronic pulmonary disease, disseminated disease in immunocompromised patients, skin and soft tissue infections, and superficial lymphadenitis. 80-90% of recorded NTM infections manifest as pulmonary diseases.<ref name="To_2020">{{cite journal | vauthors = To K, Cao R, Yegiazaryan A, Owens J, Venketaraman V | title = General Overview of Nontuberculous Mycobacteria Opportunistic Pathogens: <i>Mycobacterium avium</i> and <i>Mycobacterium abscessus</i> | journal = Journal of Clinical Medicine | volume = 9 | issue = 8 | pages = 2541 | date = August 2020 | pmid = 32781595 | pmc = 7463534 | doi = 10.3390/jcm9082541 | doi-access = free }}</ref>
A collection of Nontuberculosis Mycobacteria (NTM) that exclude ''M. tuberculosis, M. leprae,'' and ''M. lepromatosis'' are readily available to infect mammalian hosts. Such species are referred to as "atypical mycobacteria." Although person-to-person transmission is rare, transmission of ''M. abscessus'' has been observed between patients with [[cystic fibrosis]].<ref>{{Cite web |date=2019-08-12 |title=Nontuberculous Mycobacteria (NTM) Infections {{!}} HAI {{!}} CDC |url=https://www.cdc.gov/hai/organisms/nontuberculous-mycobacteria.html |access-date=2023-04-28 |website=www.cdc.gov |language=en-us}}</ref> The four primary diseases observed in humans are chronic pulmonary disease, disseminated disease in immunocompromised patients, skin and soft tissue infections, and superficial lymphadenitis. 80-90% of recorded NTM infections manifest as pulmonary diseases.<ref name="To_2020">{{cite journal | vauthors = To K, Cao R, Yegiazaryan A, Owens J, Venketaraman V | title = General Overview of Nontuberculous Mycobacteria Opportunistic Pathogens: <i>Mycobacterium avium</i> and <i>Mycobacterium abscessus</i> | journal = Journal of Clinical Medicine | volume = 9 | issue = 8 | pages = 2541 | date = August 2020 | pmid = 32781595 | pmc = 7463534 | doi = 10.3390/jcm9082541 | doi-access = free }}</ref>
''[[Mycobacteroides abscessus|M. abscessus]]'' is the most virulent rapidly-growing mycobacteria (RGM), as well as the leading cause of RGM based pulmonary infections. Although it has been traditionally viewed as an opportunistic pathogen like other NTM's, analysis of various virulence factors (VF's) have shifted this view to that of a true pathogen. This is due to the presence of known mycobacterial VFs and other non-mycobacterial VF's found in other prokaryotic pathogens.<ref name="To_2020" />
''[[Mycobacteroides abscessus|M. abscessus]]'' is the most virulent rapidly-growing mycobacteria (RGM), as well as the leading cause of RGM based pulmonary infections. Although it has been traditionally viewed as an opportunistic pathogen like other NTM's, analysis of various virulence factors (VF's) have shifted this view to that of a true pathogen. This is due to the presence of known mycobacterial VFs and other non-mycobacterial VF's found in other prokaryotic pathogens.<ref name="To_2020" />

Revision as of 17:46, 10 May 2023

Mycobacterium
TEM micrograph of M. tuberculosis
Scientific classification Edit this classification
Domain: Bacteria
Phylum: Actinomycetota
Class: Actinomycetia
Order: Mycobacteriales
Family: Mycobacteriaceae
Genus: Mycobacterium
Lehmann & Neumann 1896[1]
Species

Over 190 species, see LPSN

Synonyms[2]
  • Mycolicibacterium Gupta et al. 2018
  • Mycolicibacillus Gupta et al. 2018
  • Mycolicibacter Gupta et al. 2018
  • Mycobacteroides Gupta et al. 2018

Mycobacterium is a genus of over 190 species in the phylum Actinomycetota, assigned its own family, Mycobacteriaceae. This genus includes pathogens known to cause serious diseases in mammals, including tuberculosis (M. tuberculosis) and leprosy (M. leprae) in humans. The Greek prefix myco- means 'fungus', alluding to this genus' mold-like colony surfaces.[3] Since this genus has cell walls with Gram-positive and Gram-negative features, acid-fast staining is used to emphasize their resistance to acids, compared to other cell types.[4]

Mycobacterial species are generally aerobic, non-motile, and capable of growing with minimal nutrients. The genus is divided based on each species' pigment production and growth rate.[5] While most Mycobacterium species are non-pathogenic, the genus' characteristic complex cell wall contributes to evasion from host defenses.[6]

Microbiology

Morphology

Model of the Mycobacterium spp. cell envelope with 3-D protein structures

Mycobacteria are aerobic with 0.2-0.6 µm wide and 1.0-10 µm long rod shapes. They are generally non-motile, except for the species Mycobacterium marinum, which has been shown to be motile within macrophages.[7] Mycobacteria possess capsules and most do not form endospores. M. marinum and perhaps M. bovis have been shown to sporulate;[8] however, this has been contested by further research.[9] The distinguishing characteristic of all Mycobacterium species is a thick, hydrophobic, and mycolic acid-rich cell wall made of peptidoglycan and arabinogalactan, with these unique components offering targets for new tuberculosis drugs.[10]

Physiology

Many Mycobacterium species readily grow with minimal nutrients, using ammonia and/or amino acids as nitrogen sources and glycerol as a carbon source in the presence of mineral salts. Temperatures for optimal growth vary between species and media conditions, ranging from 25-45 °C.[5]

Most Mycobacterium species, including most clinically relevant species, can be cultured in blood agar.[11] However, some species grow very slowly due to extremely long reproductive cycles, such as M. leprae requiring 12 days per division cycle compared to 20 minutes for some E. coli strains.[12]

Ecology

Whereas Mycobacterium tuberculosis and M. leprae are pathogenic, most mycobacteria do not cause disease unless they enter skin lesions of those with pulmonary and/or immune dysfunction, despite being widespread across aquatic and terrestrial environments. Through biofilm formation, cell wall resistance to chlorine, and association with amoebas, mycobacteria can survive a variety of environmental stressors. The agar media used for most water testing does not support the growth of mycobacteria, allowing it to go undetected in municipal and hospital systems.[13]

Genomics

Comparative analyses of mycobacterial genomes have identified several conserved indels and signature proteins that are uniquely found in all sequenced species from the genus Mycobacterium.[14][15] Additionally, 14 proteins are found only in the species from the genera Mycobacterium and Nocardia, suggesting that these two genera are closely related.[15]

The genomes of some mycobacteria are quite large, such as M. vulneris encoding 6,653 proteins, larger than the ~6000 proteins of eukaryotic yeast.[16]

Protein-Coding Genomic Information
Organism Number of Protein Coding Genes
M. intracellulare 5,289[17]
M. colombiense 5,084[18]
M. leprae 1,603[19]
M. tuberculosis 3,995[19]
M. smegmatis 6,602[20]
M. chelonae 4,948[21]

Pathogenicity

Mycobacterium tuberculosis Complex

Mycobacterium tuberculosis can remain latent in human hosts for decades after an initial infection, allowing it to continue infecting others. It has been estimated that a third of the world population has latent tuberculosis (TB).[22] M. tuberculosis has many virulence factors, which can be divided across lipid and fatty acid metabolism, cell envelope proteins, macrophage inhibitors, kinase proteins, proteases, metal-transporter proteins, and gene expression regulators.[23]

The development of Hansen’s disease is caused by infection with either Mycobacterium leprae or Mycobacterium lepromatosis with the latter acting as a secondary causal agent. Roughly 200,000 new cases of infection are reported each year, and 80% of new[24] cases are reported in Brazil, India, and Indonesia.[25] M. leprae infection localizes within the skin macrophages and Schwann cells found in peripheral nerve tissue.

Since 2018, several members of this species complex are considered synonyms of M. tuberculosis as far as bacterial nomenclature is concerned. The IJSEM article reports that M. africanum, M. bovis, M. caprae, M. pinnipedii are 99.21–99.92% identical to M. tuberculosis on the whole-genome level, failing the criteria to be considered independent species. The same applies to "M. canetti", "M. mungi", and "M. orygis", species not validly published. The variation is even below the accepted level for subspecies. The authors note that these names do refer to stable lineages with meaningful clinical distinctions, recommending that them become variants: M. bovis would become M. tuberculosis var. bovis, for example.[26]

Nontuberculosis Mycobacteria

A Venn diagram constructed using InteractiVenn[27] using proteomic information. The regions in the diagram represent orthologous proteins found in each species (based on OMA identifiers). Unidentified proteins for each species are localized in the unique section for each species.

A collection of Nontuberculosis Mycobacteria (NTM) that exclude M. tuberculosis, M. leprae, and M. lepromatosis are readily available to infect mammalian hosts. Such species are referred to as "atypical mycobacteria." Although person-to-person transmission is rare, transmission of M. abscessus has been observed between patients with cystic fibrosis.[28] The four primary diseases observed in humans are chronic pulmonary disease, disseminated disease in immunocompromised patients, skin and soft tissue infections, and superficial lymphadenitis. 80-90% of recorded NTM infections manifest as pulmonary diseases.[29] M. abscessus is the most virulent rapidly-growing mycobacteria (RGM), as well as the leading cause of RGM based pulmonary infections. Although it has been traditionally viewed as an opportunistic pathogen like other NTM's, analysis of various virulence factors (VF's) have shifted this view to that of a true pathogen. This is due to the presence of known mycobacterial VFs and other non-mycobacterial VF's found in other prokaryotic pathogens.[29]

Virulence Factors

Mycobacteria have cell walls with peptidoglycan, arabinogalactan, and mycolic acid; a waxy outer mycomembrane of mycolic acid; and an outermost capsule of glucans and secreted proteins for virulence. It constantly remodels these layers to survive in stressful environments and avoid host immune defenses. This cell wall structure results in colony surfaces resembling fungi, leading to the genus' use of the Greek prefix myco-.[30] This unique structure makes penicillins ineffective, instead requiring a multi-drug antibiotic treatment of isoniazid to inhibit mycolic acid synthesis, rifampicin to interfere with transcription, ethambutol to hinder arabinogalactan synthesis, and pyrazinamide to impede Coenzyme A synthesis.[6]

Mycobacterial Infection Information
Organism Common Symptoms of Infection Known Treatments Reported Cases (Region, Year)
M. tuberculosis Fatigue, weight loss, fever, hemoptysis, chest pain.[31] isoniazid INH, rifampin, pyrazinamide, ethambutol.[32] 1.6 Million (Global, 2021)[33]
M. leprae Skin discoloration, nodule development, dry skin, loss of eyebrows and/or eyelashes, numbness, nosebleeds, paralysis, blindness, nerve pain.[34] dapson, rifampicin, clofazimine.[34] 133, 802 (Global, 2021)[35]
M. lepromatosis Skin discoloration, nodule development, dry skin, loss of eyebrows and/or eyelashes, numbness, nosebleeds, paralysis, blindness, nerve pain.[34] dapson, rifampicin, clofazimine.[34] Estimated in conjunction with M. leprae
M. avium complex Tender skin, development of boils or pus-filled vesicles, fevers, chills, muscle aches.[36] clarithromycin, azithromycin, amikacin, cefoxitin, imipenem.[37] 3000 (US, Annual estimated)[38]
M. abscessus complex Coughing, hemoptysis, fever, cavitary lesions.[39] clarithromycin, amikacin, cefoxitin, imipenem.[39] Unknown

History

Cladogram of Key Species

Mycobacteria have historically been categorized through phenotypic testing, such as the Runyon classification of analyzing growth rate and production of yellow/orange carotenoid pigments. Group I contains photochromogens (pigment production induced by light), Group II comprises scotochromogens (constitutive pigment production), and the non-chromogens of Groups III and IV have a pale yellow/tan pigment, regardless of light exposure. Group IV species are "rapidly-growing" mycobacteria compared to the "slowly-growing" Group III species because samples grow into visible colonies in less than seven days.[5]

Because the International Code of Nomenclature of Prokaryotes (ICNP) currently recognizes 195 Mycobacterium species, classification and identification systems now rely on DNA sequencing and computational phylogenetics. The major disease-causing groups are the Mycobacterium tuberculosis complex (tuberculosis), Mycobacterium avium complex (mycobacterium avium-intracellulare infection), M. leprae and M. lepromatosis (leprosy), and Mycobacterium abscessus (chronic lung infection).[3]

Microbiologist Enrico Tortoli has constructed a phylogentic tree of the genus' key species based on the earlier genetic sequencing of Rogall, et al. (1990), alongside new phylogentic trees based on Tortoli's 2017 sequencing of 148 Mycobacterium species:[40]

Phylogenetic tree of slowly-growing members of the Mycobacterium genus
Phylogenetic tree of rapidly-growing members of the Mycobacterium genus, alongside the M. terrae complex.[41]

Proposed division of the genus

Gupta et al. have proposed dividing Mycobacterium into five genera, based on an analysis of 150 species in this genus. Due to controversy over complicating clinical diagnoses and treatment, all of the renamed species have retained their original identity in the Mycobacterium genus as a valid taxonomic synonym:[42][43]

  • Mycobacterium based on the Slowly-Growing Tuberculosis-Simiae clade
  • Mycobacteroides based on the Rapidly-Growing Abscessus-Chelonae clade
  • Mycolicibacillus based on the Slowly-Growing Triviale clade
  • Mycolicibacter based on the Slowly-Growing Terrae clade
  • Mycolicibacterium based on the Rapidly-Growing Fortuitum-Vaccae clade

Diagnosis

The two most common methods for visualizing these acid-fast bacilli as bright red against a blue background are the Ziehl-Neelsen stain and modified Kinyoun stain. Fite's stain is used to color M. leprae cells as pink against a blue background. Rapid Modified Auramine O Fluorescent staining has specific binding to slowly-growing mycobacteria for yellow staining against a dark background. Newer methods include Gomori-Methenamine Silver staining and Perioidic Acid Schiff staining to color Mycobacterium avium complex (MAC) cells black and pink, respectively.[4]

While some mycobacteria can take up to eight weeks to grow visible colonies from a cultured sample, most clinically relevant species will grow within the first four weeks, allowing physicians to consider alternative causes if negative readings continue past the first month.[44]

Mycobacteriophages

Mycobacteria can be infected by mycobacteriophages, a class of viruses with high specificity for their targets. By hijacking the cellular machinery of mycobacteria to produce additional phages, such viruses can be used in phage therapy for eukaryotic hosts, as they would die alongside the mycobacteria. Since only some mycobacteriophages are capable of penetrating the M. tuberculosis membrane, the viral DNA may be delivered through artificial liposomes because bacteria uptake, transcribe, and translate foreign DNA into proteins.[45]

Mycosides

Mycosides are glycolipids isolated from Mycobacterium species with Mycoside A found in photochromogenic strains, Mycoside B in bovine strains, and Mycoside C in avian strains.[46] Different forms of Mycoside C have varying success as a receptor to inactivate mycobacteriophages.[47] Replacement of the gene encoding mycocerosic acid synthase in M. bovis prevents formation of mycosides.[48]

References

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  2. ^ Euzéby JP, Parte AC. "Mycobacterium". List of Prokaryotic names with Standing in Nomenclature (LPSN). Retrieved June 16, 2021.[permanent dead link‍]
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  22. ^ Getahun H, Matteelli A, Chaisson RE, Raviglione M (May 2015). "Latent Mycobacterium tuberculosis infection". The New England Journal of Medicine. 372 (22): 2127–2135. doi:10.1056/NEJMra1405427. PMID 26017823.
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