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Mycobacterium leprae

mycobacterium leprae, mycobacterium leprae bacteria
Mycobacterium leprae, also known as Hansen’s bacillus spirilly, mostly found in warm tropical countries, is a bacterium that causes leprosy Hansen's disease It is an intracellular, pleomorphic, acid-fast, pathogenic bacterium M leprae is an aerobic bacillus rod-shaped surrounded by the characteristic waxy coating unique to mycobacteria In size and shape, it closely resembles Mycobacterium tuberculosis Due to its thick waxy coating, M leprae stains with a carbol fuchsin rather than with the traditional Gram stain The culture takes several weeks to mature

Optical microscopy shows M leprae in clumps, rounded masses, or in groups of bacilli side by side, and ranging from 1–8 μm in length and 02–05 μm in diameter

It was discovered in 1873 by the Norwegian physician Gerhard Armauer Hansen, who was searching for the bacteria in the skin nodules of patients with leprosy It was the first bacterium to be identified as causing disease in humans The organism has never been successfully grown on an artificial cell culture medium Instead, it has been grown in mouse foot pads and more recently in nine-banded armadillos because they, like humans, are susceptible to leprosy This can be used as a diagnostic test for the presence of bacilli in body lesions of suspected leprosy patients The difficulty in culturing the organism appears to be because it is an obligate intracellular parasite that lacks many necessary genes for independent survival The complex and unique cell wall that makes members of the Mycobacterium genus difficult to destroy is apparently also the reason for the extremely slow replication rate

Virulence factors include a waxy exterior coating, formed by the production of mycolic acids unique to Mycobacterium

Mycobacterium leprae was sensitive to dapsone diaminodiphenylsulfone, the first effective treatment which was discovered for leprosy in the 1940s, but resistance against this antibiotic has developed over time Therapy with dapsone alone is now strongly contraindicated Currently, a multidrug treatment MDT is recommended by the World Health Organization, including dapsone, rifampicin and clofazimine In patients receiving the MDT, a high proportion of the bacilli die within a short amount of time without immediate relief of symptoms This suggests many symptoms of leprosy must be due in part to the presence of dead cells


  • 1 Pathogenesis
  • 2 Genome
    • 21 Evolution and pseudogenes
    • 22 Applications
  • 3 Ancient Mycobacterium leprae
  • 4 Evolution
  • 5 Diagnostic criteria for leprosy
  • 6 Treatment
  • 7 References
  • 8 External links


The incubation period of M leprae can range between nine months and twenty years It replicates intracellularly inside histiocytes and nerve cells and has two forms One form is tuberculoid, which induces a cell-mediated response that limits its growth Through this form M leprae multiplies at the site of entry, usually the skin, invading and colonizing Schwann cells The microbe then induces T-helper lymphocytes, epitheloid cells, and giant cell infiltration of the skin, causing infected individuals to exhibit large flattened patches with raised and elevated red edges on their skin These patches have dry, pale, hairless centers, accompanied by a loss of sensation on the skin The loss of sensation may develop as a result of invasion of the peripheral sensory nerves The macule at the cutaneous site of entry and the loss of pain sensation are key clinical indications that an individual has a tuberculoid form of leprosy

The second form of leprosy is the lepromatous form This form of the microbe proliferates within the macrophages at the site of entry It also grows within the epithelial tissues of the face and ear lobes The suppressor T-cells that are induced are numerous, however the epithelioid and giant cells are rare or absent With cell-mediated immunity impaired, large numbers of M leprae appear in the macrophages and the infected patients develop papules at the entry site, marked by a folding of the skin Gradual destruction of cutaneous nerves lead to what is referred to as "classic lion face" Extensive penetration of this microbe may lead to severe body damage; for example the loss of bones, fingers, and toes


Mycobacterium leprae has the longest doubling time of all known bacteria and has thwarted every effort at culture in the laboratory Comparing the genome sequence of M leprae with that of M tuberculosis provides clear explanations for these properties, and reveals an extreme case of reductive evolution Less than half of the genome contains functional genes Gene deletion and decay appear to have eliminated many important metabolic activities, including siderophore production, part of the oxidative and most of the microaerophilic and anaerobic respiratory chains, and numerous catabolic systems and their regulatory circuits

The first genome sequence of a strain of M leprae, was completed in 1998 The genome sequence of a strain originally isolated in Tamil Nadu, India and designated TN, was completed in 2013 The sequence was obtained by a combined approach, employing automated DNA sequence analysis of selected cosmids and whole-genome 'shotgun' clones After the finishing process, the genome sequence was found to contain 3,268,203 base pairs bp, and to have an average G+C content of 578%, values much lower than the corresponding values for M tuberculosis, which are 4, 441,529 bp and 656% G+C

Evolution and pseudogenes

Mycobacterium leprae has undergone a dramatic reduction in genome size with the loss of many genes This genome reduction is not complete and numerous genes are still present as non-functional pseudogenes Downsizing from a genome of 442 Mbp, such as that of M tuberculosis, to one of 327 Mbp would account for the loss of some 1200 protein-coding sequences There is evidence that many of the genes that were present in the genome of the common ancestor of M leprae and M tuberculosis have been lost in the M leprae genome 1500 genes are still common to both M leprae and M tuberculosis


Information from the completed genome can be useful to develop diagnostic skin tests, to understand the mechanisms of nerve damage and drug resistance and to identify novel drug targets for rational design of new therapeutic regimens and drugs to treat leprosy and its complications

Ancient Mycobacterium leprae

Almost complete sequences of M leprae from medieval skeletons with osteological lesions suggestive of leprosy from different Europe geographic origins were obtained using DNA capture techniques and high-throughput sequencing HTS Ancient sequences were compared with those of modern strains from biopsies of leprosy patients representing diverse genotypes and geographic origins, giving new insights in the understanding of evolution, course through history, phylogeography of the leprosy bacillus and the disappearance of leprosy from Europe

Verena J Schuenemann et al demonstrated a remarkable genomic conservation during the past 1000 years and a close similarity between modern and ancient strains, suggesting that the sudden decline of leprosy in Europe was not due to a losing of virulence but due to extraneous factors, such as other infectious diseases, changes in host immunity or improved social conditions

The geographic occurrence of M leprae include:Angola, Brazil, Central African Republic, Democratic Republic of Congo, Federated States of Micronesia, India, Kiribati, Madagascar, Nepal, Republic of Marshall Islands, and United Republic of Tanzania


The closest relative to Mycobacterium leprae is Mycobacterium lepromatosis These species diverged 139 million years ago 95% highest posterior density 82 million years ago – 214 million years agoThe most recent common ancestor of the extant M leprae strains was calculated to have lived 3,607 years agoThe estimated substitution rate was 767 x 10−9 substitutions per site per year - similar to other bacteria

A study of genomes isolated from medieval cases estimated the mutation rate to be 613 × 10−9 The authors also showed that the leprosy bacillus in the Americas was brought there from Europe

It has been estimated that the ancestors of M leprae and M tuberculosis separated 36 million years ago

Another study suggested that M leprae originated in East Africa and spread from there to Europe and the Middle East initially before spreading to West Africa and the Americas in the last 500 years

Diagnostic criteria for leprosy

Diagnostic criteria for leprosy:The diagnosis of leprosy is primarily a clinical one In one Ethiopian study, the following criteria had a sensitivity of 94% with a positive predictive value of 98% in diagnosing leprosy Diagnosis was based on one or more of three signs:

  1. Hypopigmented or reddish skin patches with definite loss of sensation
  2. Thickened peripheral nerves
  3. Acid-fast bacilli on skin smears or biopsy material


Multidrug therapy MDT Antibiotics that destroy M leprae bacilli include:dapsone, rifampin, clofazamine, fluoroquinolones, macrolides, and minocycline

A preventative measure of M leprae is to avoid close contact with infectious people who are untreated The Bacillus Calmette–Guérin BCG vaccine offers a variable amount of protection against leprosy in addition to its main target of tuberculosis Armadillos are also known hosts for Mycobacterium leprae and have infected humans in the southeastern United States, although the geographic range of the disease and its complexity has been spreading


  1. ^ Ryan KJ, Ray CG, eds 2004 Sherris Medical Microbiology 4th ed McGraw Hill pp 451–3 ISBN 0-8385-8529-9 
  2. ^ a b McMurray DN 1996 "Mycobacteria and Nocardia" In Baron S; et al Baron's Medical Microbiology 4th ed University of Texas Medical Branch ISBN 0-9631172-1-1 
  3. ^ Shinnick, Thomas M 2006 "Mycobacterium leprae" In Dworkin, Martin; Falkow, Stanley; Rosenberg, Eugene; Schleifer, Karl-Heinz; Stackebrandt, Erko The Prokaryotes Springer pp 934–944 doi:101007/0-387-30743-5_35 ISBN 978-0-387-25493-7 
  4. ^ Hansen GHA 1874 "Undersøgelser Angående Spedalskhedens Årsager Investigations concerning the etiology of leprosy" Norsk Mag Laegervidenskaben in Norwegian 4:1–88 
  5. ^ Irgens L 2002 "The discovery of the leprosy bacillus" Tidsskr nor Laegeforen 122 7:708–9 PMID 11998735 
  6. ^ "Leprosy Hansen's disease - Blue Book - Department of Health and Human services, Victoria, Australia" ideashealthvicgovau Retrieved 2015-11-17 
  7. ^ Truman RW, Krahenbuhl JL; Krahenbuhl 2001 "Viable M leprae as a research reagent" Int J Lepr Other Mycobact Dis 69 1:1–12 PMID 11480310 
  8. ^ a b Cole ST, Brosch R, Parkhill J, et al 1998 "Deciphering the biology of Mycobacterium tuberculosis from the complete genome sequence" Nature 393 6685:537–44 doi:101038/31159 PMID 9634230 
  9. ^ Narayanan S, Deshpande U; Deshpande 2013 "Whole-Genome Sequences of Four Clinical Isolates of Mycobacterium tuberculosis from Tamil Nadu, South India" Genome Announc 1 3:e00186–13 doi:101128/genomeA00186-13 PMC 3707582  PMID 23788533 
  10. ^ Cole ST, Eiglmeier K, Parkhill J, et al 2001 "Massive gene decay in the leprosy bacillus" Nature 409 6823:1007–11 doi:101038/35059006 PMID 11234002 
  11. ^ Schuenemann VJ, Singh P, Mendum TA, et al July 2013 "Genome-wide comparison of medieval and modern Mycobacterium leprae" Science 341 6142:179–83 doi:101126/science1238286 PMID 23765279 
  12. ^ "Risk of Exposure | Hansen's Disease Leprosy | CDC" wwwcdcgov Retrieved 2015-11-17 
  13. ^ Singh P, Benjak A, Schuenemann VJ, Herbig A, Avanzi C, Busso P, Nieselt K, Krause J, Vera-Cabrera L, Cole ST 2015 Insight into the evolution and origin of leprosy bacilli from the genome sequence of Mycobacterium lepromatosis Proc Natl Acad Sci U S A 11214:4459-4464
  14. ^ Schuenemann VJ, Singh P, Mendum TA, Krause-Kyora B, Jager G, et al 2013 Genome-wide comparison of medieval and modern Mycobacterium leprae Science 341:179–183
  15. ^ Djelouadji Z, Raoult D, Drancourt M 2011 Palaeogenomics of Mycobacterium tuberculosis:epidemic bursts with a degrading genome Lancet Infect Dis 118:641-650
  16. ^ Monot M, Honoré N, Garnier T, Araoz R, Coppée JY, Lacroix C, Sow S, Spencer JS, Truman RW, Williams DL, Gelber R, Virmond M, Flageul B, Cho SN, Ji B, Paniz-Mondolfi A, Convit J, Young S, Fine PE, Rasolofo V, Brennan PJ, Cole ST 2005 On the origin of leprosy Science 3085724:1040-1042
  17. ^ "Leprosy:MedlinePlus Medical Encyclopedia" wwwnlmnihgov Retrieved 2015-11-17 
  18. ^ Duthie MS, Gillis TP, Reed SG; Gillis; Reed November 2011 "Advances and hurdles on the way toward a leprosy vaccine" Hum Vaccin 7 11:1172–83 doi:104161/hv71116848 PMC 3323495  PMID 22048122 CS1 maint:Multiple names:authors list link
  19. ^ "Zoonotic Leprosy in the Southeastern United States" wwwcdcgov 

External links

  • The genome of Mycobacterium leprae
  • "Mycobacterium leprae" NCBI Taxonomy Browser 1769 

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