Mycobacterium leprae*

A Microbial Biorealm page on the genus Mycobacterium leprae*

Classification

Higher order taxa

Bacteria; Actinobacteria; Actinobacteria; Actinobacteridae; Actinomycetale; Corynebacterineae; Mycobacteriaceae

Species

NCBI: Taxonomy

Mycobacterium leprae

Description and Significance

Child with leprosy (1)

Mycobacterium leprae is named after Doctor Gerhard Armauer Hansen in 1873. Dr. Hansen discovered the bacteria in the nodules of leprosy patients and determined that it was the cause of the leprosy. Leprosy has been recorded as early as 600-400 B.C. Leprosy is found in countries world wide, but it is common in many countries with a tropical or sub-tropical climate such as Angola, Brazil, and India. In the United States, there are approximately 1000 cases reported and diagnosed each year. In 2004, according to the World Health Organization (WHO) there were an average of 150 cases of leprosy, with 69 new cases and 131 wide-spread cases. In 2005 the WHO reported that there were 286,063 new cases of leprosy worldwide. Mycobacterium leprae has two different forms in which it can express itself, Tuberculoid and Lepromatous. The difference between the two is that Tuberculoid is caused by a faster cellular response to the bacterium, causing disfigurement of the skin, sores, peripheral nerve damage, and progressive debilitation. Lepromatous is a slower cellular response large nodules and bumps on the skin. There are medicines today that can treat leprosy and kill the M. leprae. Victims can choose to either take certain medicines as prescribe by the WHO or can get surgery to help prevent further deterioration.

Genome structure

The M. leprae genome project was sequenced in 2001 by the Sanger Institute. The sequence was found by employing automated DNA sequence analysis of selected cosmids* and whole-genome clones. After the completion of this, the genome sequence was found to contain 3,268,203 base pairs (bp), and to have an average of G+C (Guanine and Cytosine) content of 57.8% However, compared to M. tuberculosis, which are 4,441,529bp and 65.6% G+C, the numbers are much lower. More on numbers, M. leprae contains about 1600 genes and more than 1100 pseudogenes, but again, this is relatively small compared to M. tuberculosis, which contains around 4000 genes. All of these smaller numbers in M. leprae suggest that there is massive decay in it; making it the most striking example of genome reduction in a microbial pathogen.

Cell structure, metabolism & life cycle

M. leprae is a strong acid rod-shaped organism with parallel sides and rounded ends. It is also a gram-positive aerobic and is surrounded by a waxy coating which is unique to Mycobacterium. Because of this waxy coating it is known to have the largest doubling time of all known bacteria (27 hours). And because of this factor, every effort to culture this in the laboratory has proved non-successful. M. leprae is also known to have unique lipids that are linked together with covalent bonding. The waxy coating, that was mentioned earlier, is created because of this bonding at room temperature. Adding this factor to the slow doubling time makes M. leprae very hard to fight against. The metabolism of M. leprae, that was thought to be self-reliant, has been greatly reduced due to the down-sizing of the genome. Many regulatory elements of metabolism, such as producing siderophores, which is a key part of the oxidative, microaerophilic and anaerobic chains, have been lost altogether. Due to all of this lost, M. leprae has become dependent on its host to receive nutrients and metabolites. It has evolved itself to a parasitic role.

Ecology (including pathogenesis)

M. leprae can be typically found in water, soil, or in the air. In fact the DNA from M. leprae has been discovered in several soil samples that are prone to the disease leprosy. But even though it can be found in soil and such, M. leprae is very choosey when picking its hosts. Its ideal conditions are around 33 degree C. This temperature is lower for most mammals, however; so only a few species are known to be carriers of M. leprae. When the disease does affect humans, though; it is usually in the hands and feet because they are the coolest parts of the body. This environment is more suitable for M. leprae to live and thrive.

Describe its habitat, symbiosis, and contributions to environment. If it is a pathogen, how does this organism cause disease? Human, animal, plant hosts? Describe virulence factors and patient symptoms.

Interesting feature

Describe in detail one particularly interesting aspect of your organism or it's affect on humans or the environment.

References

1) "Leprosy Today." World Health Organization. World Health Organization. 10 Oct 2007

Brennan, J. T. Mycobacteria . In Encyclopedia of Microbiology (pp. 312-327). a.

Drugs.com Drug Information Online. (2007, August 17). October 2, 2007

Kazda, J. (2000). The Ecology of Mycobacteria. Kluwer Academic Publishers.

Medline Plus. (2007, September 19). October 1, 2007

Microbiology, T. D. (2007, August 17). Microbiology and Immunology Online. September 29, 2007, from University of South Carolina School of Medicine

Mycobacterium Leprae. (2007, July 21). September 25, 2007

WHO. (2007). September 30, 2007

Infectious Disease (2007) Mycobacterium leprae November 6, 2007

Institute of Tropical Medicine Antwerp (2007) 4 MYCOBACTERIUM LEPRAE November 6, 2007

The Welcome Trust Sanger Institute. (2007) Mycobacterium leprae Genome Project. November 6, 2007

World Health Organization. (2007). November 6, 2007

Edited by the NC State University MB 103 class of 2007.