[2] It is an acid-fast, Gram-positive, rod shaped bacterium and an obligate intracellular parasite, which means, unlike its relative Mycobacterium tuberculosis, it cannot be grown in cell-free laboratory media.

[3] This is likely due to gene deletion and decay that the genome of the species has experienced via reductive evolution, which has caused the bacterium to depend heavily on its host for nutrients and metabolic intermediates.

[3] It is an aerobic bacillus (rod-shaped bacterium) with parallel sides and round ends, surrounded by the characteristic waxy coating of mycolic acid unique to mycobacteria.

[11] The bacteria grow best at 27 to 30 °C, making the skin, nasal mucosa and peripheral nerves primary targets for infection by Mycobacterium leprae.

[14] Mycobacterium leprae has an unusually lengthy doubling time (ranging from 12 to 14 days compared with 20 minutes for Escherichia coli), as well as its inability to be cultured in the laboratory.

The complex and unique cell wall that makes members of the genus Mycobacterium difficult to destroy is also the reason for its extremely slow replication rate.

[18] Since in vitro cultivation is not generally possible, it has instead been grown in mouse foot pads,[14] and in armadillos due to their low core body temperature.

[21] Many of the catabolic pathways present in other Mycobacterium species are compromised, due to the absence of enzymes that play key roles in degradation of nutrients.

[21] Mycobacterium leprae has lost the ability to use common carbon sources, such as acetate and galactose, in its central energy metabolism pathways.

[23] 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.

[23][27] Due to Mycobacterium leprae's reliance on a host organism, many of the species' DNA repair functions have been lost, increasing the occurrence of deletion mutations.

Petidoglycan biosynthesis also require murG, murF, MurE, murY, murC, and murD, the remaining six essential enzymes for mycobacterium leprae.

[31][better source needed] The bacterium has a global distribution in humans but the highest prevalence is in sub-Saharan Africa, Asia and South America.

Mycobacterium leprae DNA was detected in soil from houses of leprosy patients in Bangladesh, armadillos' holes in Suriname and habitats of lepromatous red squirrels in the British Isles.

[34] A zoonotic transmission pathway from exposure to armadillos has been proposed, with human patients from a previous study in southeastern United States shown to be infected with the same armadillo-associated Mycobacterium leprae genotype.

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.

With cell-mediated immunity impaired, large numbers of Mycobacterium leprae appear in the macrophages and the infected patients develop papules at the entry site, marked by a folding of the skin.

[44] The symptoms of a Mycobacterium leprae infection, also known as leprosy, are skin sores that are pale in color, lumps or bumps that do not go away after several weeks or months, nerve damage which can lead to complications with the ability to sense feeling in the arms and legs as well as muscle weakness.

[47] In squirrels, according the to Veterinary Pathology Unit of the University of Edinburgh, " The disease is unmistakeable: there is gross swelling and loss of hair around the snout, lips, eyelids, ears, genitalia and sometimes feet and lower limbs.

[51] Effectiveness of the treatment can be determined with the use of an acid-fast stain of Mycobacterium leprae from a skin smear to estimate the number of bacilli still present in the patient.

[54] Dapsone competitively inhibits the enzyme dihydropteroate synthase (DHPS) resulting in decreases the production of tetrahydrofolate, which is an essential component of nucleic acid biosynthesis in M. leprae.

Rifampin will interrupt binding of the β-subunit of the DNA-dependent RNA polymerase, which will uncouple mRNA production and results in cell death.

The binding of clofazimine to mycobacterial DNA can has been proven as weakly bactericidal against Mycobacterium leprae in mice, which is why it is not suitable for single drug therapy for leprosy.

[57] Drug resistance in Mycobacterium leprae is thought to be from genetic alterations in the antibiotic targets and a reduction in cell wall permeability.

The efflux pumps contributing to drug resistance and virulence in M. tuberculosis have been retained throughout the genome reductive evolution that Mycobacterium leprae underwent.

[58] Mycobacterium leprae was discovered in 1873 by the Norwegian physician Gerhard Armauer Hansen (1841–1912), and was the first bacterium to be identified as a cause of disease in humans.