Hansen’s Disease: Symptoms, Causative Agent, Pathogenesis and Treatment

Hansen’s Disease or Leprosy


  • Hansen’s disease, also known as leprosy, is an ancient disease appearing throughout written history.
  • Disfigurement, loss of limbs, and blindness can result from skin and peripheral nerve involvement.
  • The number of new cases of Hansen’s disease has decreased dramatically since the introduction of multi-drug therapy; today it is most often seen in tropical or developing countries.
  • Still, millions of people continue to suffer from the residual effects of their disease and the stigma associated with it.
  • In the United States, about 100 cases are reported annually.

Signs and Symptoms of Hansen’s disease

  • Hansen’s disease begins gradually, months or sometimes years after exposure.
  • Onset is characterized by pigmentation changes and increased or decreased sensation in certain areas of skin.

Early symptom of leprosy

  • These areas may thicken—losing hair, sweat glands, and all sensation.
  • The nerves of the arms and legs may become visibly enlarged with accompanying pain, later changing to numbness.
  • Loss of nerve activity can lead to muscle wasting, ulceration, and finally loss of fingers or toes due to unnoticed or untreated injury.
  • In more severe cases, changes are most obvious in the face, with thickening of the nose and ears and deep wrinkling of the facial skin.
  • Collapse of the supporting structure of the nose leads to congestion and bleeding.
Effects of Leprosy
Absence of fingers and sunken nose as a result of severe Effects of Leprosy

Causative Agent of Hansen’s disease

  • Mycobacterium leprae is aerobic, rod-shaped, and acid-fast.
  • It grows very slowly with a generation time of about 12 days, and prefers the slightly cooler temperatures of the body’s extremities.
  • Hansen’s disease is usually diagnosed based on clinical findings, but skin biopsy specimens that show acid-fast rods can provide an early indication of nerve invasion.
Mycobacterium leprae in a Biopsy Specimen
Acid-fast stain reveals red dense masses of the bacterial cells, a typical finding in lepromatous leprosy.
  • Despite many attempts, M. leprae has not been grown in the absence of living cells.
  • It can, however, grow in the footpads of mice, in armadillos, and in mangabey monkeys.
  • Moreover, a DNA library of M. leprae has been made and expressed in E. coli, providing large quantities of the organism’s antigens for study.

Pathogenesis of Hansen’s disease

  • Mycobacterium leprae is the only known human pathogen that preferentially infects peripheral nerves.
  • From there, the course of the infection depends on the immune response of the host.
  • In most cases, cell-mediated immunity develops against the invading bacteria, and activated macrophages limit.
  • The disease often spontaneously stops progressing, and the nerve damage, although permanent, does not worsen.
  • This limited type of Hansen’s disease, in which cell-mediated immunity successfully stops the proliferating bacteria, is called tuberculoid leprosy (also called paucibacillary Hansen’s disease).
  • People with tuberculoid leprosy rarely, if ever, transmit the disease to others.
  • When cell-mediated immunity to M. leprae fails to develop or is suppressed, unrestricted growth of M. leprae occurs, leading to a form of Hansen’s disease called lepromatous leprosy (also called multibacillary Hansen’s disease).
  • The bacteria first multiply in the cooler tissues of the body, notably in skin macrophages and peripheral nerves, and later throughout the body.
  • The tissues and mucous membranes contain billions of M. leprae, but there is almost no inflammatory response to them.
  • Mucus of the nose and throat contains high numbers of the pathogen, which can easily be transmitted to others.

Epidemiology of Hansen’s disease

  • Transmission of Mycobacterium leprae is by direct human to human contact.
  • The source of the organisms is mainly nasal secretions of lepromatous cases, which can transport M. leprae to mucous membranes or skin abrasions of other individuals.
  • Even then, the disease develops in only a tiny minority, being controlled by immune defenses in the rest.
  • Natural infections with M. leprae also occur in wild ninebanded armadillos, possibly due to their relatively low body temperature suitable for replication of the bacterium.
  • Gene sequencing studies of animals in the southern United States confirm that the same strain of M. leprae is found in both humans and armadillos.
  • Interaction with armadillos in these regions may explain cases of leprosy seen in individuals who have not traveled to a part of the world where the disease is considered endemic nor had contact with those who have.
  • Eradication of Hansen’s disease, defined as less than 1 case per 10,000 individuals, has been achieved in most countries where the disease was endemic.
  • It is difficult to completely eradicate, however, due to the long generation time of M. leprae.
  • The long generation time results in an incubation period of about 3 years (range, 3 months to 20 years), during which time the disease can remain undetected.

Treatment and Prevention of Hansen’s disease

  • Early treatment can keep Hansen’s disease from progressing.
  • Since 1995, the World Health Organization has provided free multidrug therapy to patients, radically reducing the number of cases.
  • Tuberculoid leprosy can be successfully treated by a combination of dapsone and rifampin administered for 6 months.
  • Lepromatous leprosy is generally treated for a minimum of 2 years, with addition of a third drug, clofazimine, to the treatment process.
  • Multiple drug therapy is required to prevent drug-resistant strains from developing.
  • No proven vaccine to control Hansen’s disease is yet available.

Some features of Hansen’s disease are summarized in table

Signs and symptoms Skin lesions that lack sensation, deformed face, loss of fingers or toes
Incubation period 3 months to 20 years; usually 3 years
Causative agent Mycobacterium leprae, an acid-fast rod that has not been grown in the absence of living cells
  • Invasion of small nerves of skin;
  • Multiplication in the macrophages;
  • Course of disease depends on immune response of the host;
  • In tuberculoid leprosy, activated macrophages limit the growth of the bacterium but the damage to infected nerve cells leads to disabling deformities;
  • In lepromatous leprosy, cell-mediated immunity fails, allowing unrestrained growth of M. leprae.
Epidemiology Direct contact with M. leprae from mucous membrane secretions.
Treatment and prevention Treatment: Antimicrobial medication. Prevention: No vaccine.

Reference and Sources

  • https://healthjade.net/lepromatous-leprosy/
  • https://en.wikipedia.org/wiki/Leprosy
  • https://www.researchgate.net/publication/11019269_Leprosy_A_problem_solved_by_2000
  • https://quizlet.com/279492025/bio105-exam-iii-resume-on-lecture-mon-312-flash-cards/
  • https://quizlet.com/293935816/microbiology-final-exam-flash-cards/
  • https://quizlet.com/31630694/chapter-26-flash-cards/
  • https://quizlet.com/17662722/microbiology-final-flash-cards/
  • https://www.nejm.org/doi/full/10.1056/NEJMoa1010536
  • https://www.pnas.org/content/112/51/E7118

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