Where is mycobacterium leprae commonly found

Thus far, no alleles with contradictory findings have been noted, although studies have been unable to replicate the implicated alleles because of variations in disease prevalence and history, population allelic frequencies, and scales and method of studies. Being more fatal than leprosy, tuberculosis has also been found to have some selective effects on human evolution reviewed by Gagneux [49].

The results of these and many earlier genetic studies suggest that variations in humans' susceptibility to leprosy involve complex traits of numerous polymorphic alleles.

Yet, the observed odds ratios in Table 2 are relatively small i. Hence, considering leprosy a genetic disease [50] is an exaggeration, as another author has noted [51].

The disease has one cause two species of leprosy bacilli ; without the cause, there is no disease. Knowing the bacillary evolution may lend insights into leprosy pathogenesis. Clinically, leprosy begins insidiously and manifests a spectrum of disease from severe lepromatous leprosy to mild tuberculoid form.

In lepromatous leprosy, particularly late stage, and in DLL caused by M. Bacillemia also occurs, but more than half of the patients have little constitutional response, such as fever.

In tuberculoid leprosy, the host immunity contains the bacilli [40]. These characteristics accord with low acute virulence of the lean indolent bacilli. The heavy bacillary burden in lepromatous leprosy and DLL has been puzzling and interpreted since the s, with revisions, as an antigen-specific weakness of the host immune system in tackling M.

The human immunodeficiency virus HIV pandemic since the s has witnessed, in patients with late-stage HIV infections, similar disseminated M. In this setting, the weak pathogen M. In leprosy, however, the host has almost intact immune function [29] , [55] , so how do the bacilli amass under immune radar?

This paradox points to a bacillary immune evasion [55] , [56] , a notion cherished by immunologists and further supported by recent human genome studies of all polymorphic alleles over a million that showed no severe human defects, as discussed above.

In experimental animal models, M. Here we ascribe origination of this immune tolerance or evasion to the multi-Myr parasitic evolution of the leprosy bacilli in the human lineage. Early in the course, the parasitic lifestyle was harsh because the ancestor of leprosy bacilli had to escape host immune attack. This adaptation, intracellular dwelling, and relaxation initiated the Myr reductive evolution to inactivate genes that were no longer needed.

Eventually, a lean genome with least number of antigens and immunogenicity was molded specifically from this long chase—hide game. The organism also became an obligate human parasite.

Thus, the host immunity drives a parasitic bacterial evolution; this differs from a symbiotic evolution in which the host tames and eventually assimilates the bacterium for mutual benefits. In fact, the M. A study of the PPE38 gene region of clinical M. Therefore, as shown in Table 3 , the parasitic evolution of M.

PGL-1 elicits humoral response in patients, but hardly cellular immunity that actually controls leprosy [55] , [62]. The antibody level to PGL-1 parallels bacillary burden as a diagnostic marker of lepromatous leprosy [62]. Functionally, PGL-1 aids bacillary invasion into Schwann cells [55] , which in turn activates the cells to further spread the bacilli [63].

Studies have also shown convincingly that PGL-1 suppresses or subverts immune defense [64] — [68]. Thus, PGL-1 shields and perpetuates the parasitism. Six genes, likely involved in PGL-1 synthesis, have been identified, without finding of related pseudogenes [65] , suggesting conservation despite genome reduction. In a fatal DLL case caused by M. Finally and above all, the lipid-rich cell wall of the leprosy bacilli, apparent from acid-fast stains and microscopy, the defining feature of mycobacteria, and the strongest defense wall among all bacteria nearly 10, species , remains intact after reductive evolution.

Therefore, it is likely that the lipid-rich cell wall has protected the leprosy bacilli from host clearance and enabled the unique Myr-long parasitic evolution.

The immune evasion is likely a gradual and dynamic process with a delicate balance between the bacilli and immunity. If the evasion gains, the disease worsens. If the evasion falls, the immunity prevails. For instance, in patients with borderline lepromatous leprosy, the disease is unstable and may progress towards the severe lepromatous form with increasing bacillary load.

When antimicrobial therapy kills the bacilli, the immunity recovers, leading to inflammatory response known as leprosy reactions, which usually occur after months of treatment [29] , [55]. Notably, the complexity of immune evasion in leprosy requires more studies to refine the details. Linking it with the parasitic adaptive evolution of the bacilli in this proposal unifies its role in pathogenesis, its origin, and its specificity to the human immune system.

In summary, the leprosy bacilli M. They gradually settled in humans or early hominids millions of years ago as obligate intracellular parasites. The unique parasitic evolution may be a key piece in solving the puzzle of leprosy pathogenesis. The long burden of leprosy may have exerted minor selection on human genetic polymorphisms.

Abstract Leprosy is a chronic infection of the skin and nerves caused by Mycobacterium leprae and the newly discovered Mycobacterium lepromatosis. Funding: The authors received no specific funding for this work. Leprosy As a Strictly Human Disease Human beings have contracted leprosy for millennia, as documented in ancient cultures. A chronic infection of the skin and nerves, leprosy is caused by Mycobacterium leprae and the newly discovered Mycobacterium lepromatosis [1] Rare infections in animals have been seen incidentally, such as in chimpanzees and monkeys [2] , [3] , and naturally, such as in armadillos in the southern United States [4] , [5].

Out of Africa with Leprosy The age of human leprosy was further traced by analyzing the parasitic M. Download: PPT. Table 1. Genomes, living styles, and pathogenicity of five Mycobacterium species. New Leprosy Agent M.

Figure 1. Phylogenetic tree of several Mycobacterium species based on the amino acid sequences of rpoB protein. Leprosy and Human Evolution Many studies in the past decades have shown human genetic susceptibility to leprosy, and the clinical manifestations or severity have also been classified by immunity [40]. Table 2. Recent studies of polymorphic single nucleotides in the human genome that are significantly associated with risk for or protection against leprosy.

Insights into Leprosy Pathogenesis Knowing the bacillary evolution may lend insights into leprosy pathogenesis. Table 3. Conclusion In summary, the leprosy bacilli M. Key Learning Points Evolutionary origin and approximate timing of the leprosy bacilli M. Evidence of the parasitic evolution of the bacilli and adaptation to host milieu in explanation of leprosy pathogenesis. Nature — Nat Genet — Am J Clin Pathol — Genome Res — J Bacteriol — References 1.

View Article Google Scholar 2. Lab Anim Sci — View Article Google Scholar 3. View Article Google Scholar 4. N Engl J Med — View Article Google Scholar 5. J Wildl Dis — View Article Google Scholar 6. Science — Clinical infectious diseases: an official publication of the Infectious Diseases Society of America 63 , — Bonnar, P.

Emerg Infect Dis 24 , — Lavania, M. The Journal of communicable diseases 38 , — Turankar, R. Single nucleotide polymorphism-based molecular typing of M. Clinical microbiology and infection: the official publication of the European Society of Clinical Microbiology and Infectious Diseases 20 , O— Dynamics of Mycobacterium leprae transmission in environmental context: deciphering the role of environment as a potential reservoir.

Infection, genetics and evolution: journal of molecular epidemiology and evolutionary genetics in infectious diseases 12 , — Presence of viable Mycobacterium leprae in environmental specimens around houses of leprosy patients. Indian journal of medical microbiology 34 , — International journal of mycobacteriology 4 , 54—59 Detection of viable Mycobacterium leprae in soil samples: insights into possible sources of transmission of leprosy.

Infection, genetics and evolution: journal of molecular epidemiology and evolutionary genetics in infectious diseases 8 , — Holanda, M. Presence of Mycobacterium leprae genotype 4 in environmental waters in Northeast Brazil.

Revista da Sociedade Brasileira de Medicina Tropical 50 , — Arraes, M. Natural environmental water sources in endemic regions of northeastern Brazil are potential reservoirs of viable Mycobacterium leprae. Memorias do Instituto Oswaldo Cruz , — Desikan, K.

Extended studies on the viability of Mycobacterium leprae outside the human body. Leprosy review 66 , — Mohanty, P. Viability of Mycobacterium leprae in the environment and its role in leprosy dissemination. Indian journal of dermatology, venereology and leprology 82 , 23—27 Wheat, W.

Long-term survival and virulence of Mycobacterium leprae in amoebal cysts. Avanzi, C. Red squirrels in the British Isles are infected with leprosy bacilli. Science New York, N. Simpson, V. Leprosy in red squirrels on the Isle of Wight and Brownsea Island.

The Veterinary record , — Truman, R. Probable zoonotic leprosy in the Southern United States. The New England journal of medicine , — Honap, T.

Mycobacterium leprae genomes from naturally infected nonhuman primates. Donoghue, H. Journal of medical microbiology 50 , — Vera-Cabrera, L. Journal of clinical microbiology 53 , — Monot, M.

On the origin of leprosy. Tsai, Y. Rapid method for separation of bacterial DNA from humic substances in sediments for polymerase chain reaction. Applied and Environmental Microbiology 58 , — Watson, R. Purification and characterization of a common soil component which inhibits the polymerase chain reaction.

Canadian journal of microbiology 46 , — Singh, P. Insight into the evolution and origin of leprosy bacilli from the genome sequence of Mycobacterium lepromatosis. Cole, S. Repetitive sequences in Mycobacterium leprae and their impact on genome plasticity. Leprosy review 72 , — Braet, S. Journal of clinical microbiology 56 Comparative genomic and phylogeographic analysis of Mycobacterium leprae.

Nature genetics 41 , — Benjak, A. Phylogenomics and antimicrobial resistance of the leprosy bacillus Mycobacterium leprae. Nature communications 9 , Download references.

The authors gratefully acknowledge all patients and control participants. We thank Dr. You can also search for this author in PubMed Google Scholar. Correspondence to Annemieke Geluk.

Reprints and Permissions. Detection of Mycobacterium leprae DNA in soil: multiple needles in the haystack. Before the introduction of multi-drug therapy in the early s, leprosy could only be slowed but not cured, as the bacteria could not be killed.

Now, with the use of antibiotics and with other medicines, the disease is curable. Once a person with leprosy begins appropriate treatment, they quickly become non-infectious. There is no vaccine generally available to specifically prevent leprosy. However, the vaccine against tuberculosis TB , called the BCG vaccine, may provide some protection against leprosy.

This is because the organism that causes leprosy is closely related to the one that causes TB. This page has been produced in consultation with and approved by:. Acne is common and can make people of all ages feel embarrassed, but treatments can help if acne is causing distress. Anthrax is a rare but potentially fatal bacterial disease that occasionally infects humans.

The Western obsession with cleanliness may be partly responsible for the increase in allergic asthma and conditions such as rhinitis. Careful prescribing of antibiotics will minimise the emergence of antibiotic resistant strains of bacteria. Aspergillus is a fungus that commonly grows on rotting vegetation. It can cause asthma symptoms. Content on this website is provided for information purposes only. Information about a therapy, service, product or treatment does not in any way endorse or support such therapy, service, product or treatment and is not intended to replace advice from your doctor or other registered health professional.

The information and materials contained on this website are not intended to constitute a comprehensive guide concerning all aspects of the therapy, product or treatment described on the website.

All users are urged to always seek advice from a registered health care professional for diagnosis and answers to their medical questions and to ascertain whether the particular therapy, service, product or treatment described on the website is suitable in their circumstances.

The State of Victoria and the Department of Health shall not bear any liability for reliance by any user on the materials contained on this website.