|Year : 2015 | Volume
| Issue : 2 | Page : 346-349
Leprosy: Chronicles of a disabling disease
Spandana Prakash Hegde, Manjunath Mala Shenoy, Malcolm Pinto, Vishal B Amin
Department of Dermatology, Yenepoya Medical College, Yenepoya University, Mangalore, Karnataka, India
|Date of Web Publication||16-Dec-2015|
Manjunath Mala Shenoy
Department of Dermatology, Yenepoya Medical College Hospital, Deralakatte, Mangalore - 575 018, Karnataka
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Hegde SP, Shenoy MM, Pinto M, Amin VB. Leprosy: Chronicles of a disabling disease. Arch Med Health Sci 2015;3:346-9
| Introduction|| |
The history of leprosy dates back to antiquity.  It is a complex disease with multifaceted history ranging from medical-scientific to legal, social, and political.  The word leprosy is derived from the Greek word "lepros," meaning scaly. The disease was named after Gerhard Armauer Hansen as Hansen's disease following his identification of a bacterium, Mycobacterium leprae as the causative agent of leprosy. Despite the various advances in the field of leprosy management, it is still referred to as "living death." 
Historical background of leprosy
The earliest evidence of a leprosy-like disease came from Egypt dating as far back as 1400 BC.  Migration was responsible for the worldwide spread of leprosy.  Studies and analysis of ancient skeletal remains have revealed the existence of leprosy in India since 2000 BC. Leprosy is believed to have been existent in India since 2000 BC based on studies and analysis of ancient skeletal remains.  Leprosy was referred to as kusth in Vedic writings, which is how the disease is known as even to this day in India. 
For several centuries, leprosy was equivalent to adversity, social rejection, and fear. Leprosy was believed to be a disease acquired as a result of evil acts and a penalty for sin. Lepers were treated as outcasts and were prohibited from living in the society amid other people. This led to the establishment of numerous leprosaria, usually outside cities. 
Etiology of leprosy - heritable versus infectious theory
The definitive etiology of leprosy was obscure for a long period.  Dr. Daniel Cornelius Danielssen and Dr. Carl Wilhelm Boeck were the renowned Norwegian leprosy research workers of the 19th century. They were the publishers of a very popular work, "Om Spedalskhed" (On Leprosy). , Danielssen firmly believed in the hereditary theory of leprosy transmission, which was supported by other medical personnel in his era. The infectious nature of the disease remained cryptic for a protracted period of time due to its long period of incubation. 
Gerhard Armauer Hansen was appointed as an Assistant Physician under Danielssen in 1868. He concluded that leprosy was a disease with a definitive etiology and not an inheritable scourge of society. He believed that a bacterium was involved in the transmission of leprosy, thus running into a professional conflict with his superior. This was an innovative hypothesis at a time when the contagion theory of disease transmission was known inadequately, and nobody had demonstrated that bacteria could produce disease in humans. In 1873, he discovered Mycobacterium leprae, which were rod-shaped structures from the nodules of leprosy ([Figure 1] showing ear lobe nodules in lepromatous leprosy). By 1879, he was able to demonstrate a large number of these rod-shaped structures characteristically clustered in parallel cells, through the use of improved staining methods. He postulated that the rod-shaped bacillus was the etiological agent of leprosy. Thus, he was the foremost investigator to propose that microorganisms might be responsible for the causation of a human disease. ,
Albert Neisser, a young bacteriologist from Germany, went on a leprosy research trip to Norway in 1879. During his visit, he had the opportunity to meet Hansen and he also collected tissue materials prepared from nodules of leprosy by Hansen. Being a bacteriologist, Neisser used advanced staining methods and succeeded in getting more convincing results after returning back to Germany. He published his findings in 1880 in the paper "Über die Aetiologie des Aussatzes" without contacting Hansen. , In the meantime, Hansen was also successful in staining his tissue materials using newer staining techniques. 
In 1881, Neisser published an article "Weitere Beitrδge zur Aetiologie der Lepra" in Virchows Archiv in which he claimed to be the discoverer of a microorganism causing human disease without mentioning the contribution of Hansen. This long-lasting conflict came to an end in the Lepra Congress, Berlin, Germany where Hansen was officially declared as the original discoverer of Mycobacterium leprae. 
Gerhard Armauer Hansen devoted his entire lifetime to make landmark achievements in the field of leprosy. He played a major role in revolutionizing the plague of humanity to a specific, treatable disease. 
Genetics of leprosy
Though encounter with M. leprae is essential for the infection to develop, not all persons exposed to the bacilli develop manifestations.  A recessive or codominant mode of inheritance for leprosy was detected in the late 1980s, which has been further supported by various segregation studies. ,,, Host genetic factors may thus play an important role in determining which exposed individuals will develop the disease.  Hence, Danielssen's theory of hereditary affliction of leprosy may again gain importance in the near future, along with Hansen's theory of infectious origin.
A major drawback in Hansen's experiments on leprosy was his inability to grow the lepra bacillus in vitro, which has still not been cultivable.  Bilford in 1956 suggested that lepra bacillus probably preferred to multiply in the cooler regions of the susceptible host. Shepard in 1960 successfully inoculated the footpads of mice with M. leprae due to the coolness of this area compared to other body parts of the mouse and other warm-blooded animals. 
Eleanor Storrs revolutionized the concept of experimental leprosy by documenting the presence of leprosy infection in the nine banded armadillos.  Hence, in 1969 a group of armadillos were inoculated with M. leprae. A high percentage of inoculated animals developed a massive, disseminated infection. A single armadillo was able to supply over a trillion bacilli. Hence, armadillo became the sole major source of M. leprae needed to conduct experiments throughout the world. 
Treatment of leprosy
Chaulmoogra oil and gurjon oil were being used for the treatment of leprosy. Sushrutha Samhita has documented the usage of chaulmoogra oil in India for treating leprosy in 600 BC. In the 1870s, Surgeon Dougall started using gurjon oil, a tree extract from the islands of Andaman and Nicobar topically for the treatment of leprosy.  Chaulmoogra oil was extracted from Chaulmoogra tree (Taraktogenos kurzi) from Northeast India and Marotti (Hydnocarpus wightiana), a tree indigenous to Kerala. In the early decades of the 20th century, Sir Leonard Rogers and Ernst Muir administered chaulmoogra oil orally as well as injected subcutaneously and intravenously as sodium chaulmoograte and sodium hydnocarpate.  The utility of gurjon oil showed a marked decline as patients reported milder reactions and softer skin with chaulmoogra oil. Albeit the lack of evidence suggestive of its efficacy, chaulmoogra oil remained the mainstay of treatment in India till 1946, which marked the beginning of the dapsone era. 
In 1941, dapsone was first used by Faget et al. for the treatment of leprosy in Carville, Louisiana, USA. A halt in the progression of the disease was observed following parenteral administration of intravenous injections of sodium salt of dapsone. Dapsone was introduced in India as a treatment of leprosy by Robert Cochrane. There was no specified duration of dapsone monotherapy and patients received treatment for a variable period of time ranging from 1 year to over 20 years. 
The early 1960s witnessed the beginning of dapsone resistance, which by the late 1970s spread like an epidemic causing disruption of leprosy control activities. , Hence, there was a need for efficacious multi drug regimens, which could provide an adequate cure and prevent the development of drug resistance. 
Era of multidrug therapy
The need for extremely long-term treatment when using dapsone, coupled with the worsening problems of dapsone resistance, led to the beginning of multidrug therapy (MDT) in 1982 as recommended by a World Health Organization (WHO) Study Group on Chemotherapy of Leprosy for Control Programmes.  MDT was prescribed in the form of rifampicin, clofazimine, and dapsone for at least 2 years in lepromatous and borderline (multibacillary) leprosy, and rifampicin and dapsone for 6 months in tuberculoid (paucibacillary) leprosy.  Since its introduction, MDT has undergone various modifications. In 1992, MDT was being administered for a period of 24 months, which in 1998 was subsequently reduced to 12 months. Currently, 12 months of MDT is being given for multibacillary cases and 6 months of MDT for paucibacillary cases all over India. 
Thalidomide for erythema nodosum leprosum (ENL)
In an attempt to lessen the need for medication to control painful neuritis and other symptoms associated with ENL, thalidomide was prescribed as a sedative by Sheskin. He observed that each of these pts with severe ENL improved dramatically within 1-2 days. Thus, thalidomide, a drug which had a dreadful reputation has been responsible for a vast reduction in the occurrence of disability among leprosy patients. 
Newer drugs in the treatment of leprosy
In the last two decades, many new drugs have shown excellent antileprosy activity in animal studies and clinical trials.  Moxifloxacin, a broad spectrum fluoroquinolone was found to have more bactericidal action than ofloxacin against M. leprae in the footpads of mice.  Rifapentin and rifabutin, derivatives of rifamycin, have also proven to be more beneficial than rifampicin. Other newer antileprosy drugs include minocycline, clarithromycin, brodimoprim, fusidic acid, deoxy fructo serotonin, linezolid, and diarylquinolones. ,
Leprosy control programs in India
The National Leprosy Control Program (NLCP) was started by the Government of India based on a survey, education, and treatment (SET) strategy. In 1983, following the introduction of MDT, the NLCP was renamed as the National Leprosy Eradication Program (NLEP) with an ongoing SET strategy.  Leprosy was declared eliminated (prevalence rate <1/10,000) as a public health problem in India at a national level on December 31, 2005. 
The prevalence rate of leprosy in India as on March 2015 was 0.69/10000.  Thirty three states/union territories (UTs) had attained the level of leprosy elimination till April 2013.  Currently, the World Health Organization's global strategy for leprosy control focuses on reducing the rate of new leprosy cases with grade 2 disabilities per 100,000 in the population by at least 35% of 2010's level by the end of 2015. 
| Conclusion|| |
A brief look into the pages of history gives us an understanding of the way in which leprosy has evolved in the aspects of etiopathogenesis, treatment, and rehabilitation. Mahatma Gandhi had said "Leprosy work is not merely medical relief but it is transforming the frustration of life into joy of dedication and personal ambition into selfless services."  January 30, the martyrdom day of Gandhiji is observed as Anti-Leprosy Day to commemorate his selfless service, compassion, and care toward people suffering from leprosy.
In this era of elimination, though the stigma and prejudice against leprosy has reduced markedly, the deformities and disabilities left behind warranty active participation of non-governmental organizations (NGOs) in rehabilitating the affected people. With all the landmark achievements in the battle against leprosy and the renewed commitment from the dermatologists and NGOs, we hope to make India and the world free of leprosy.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Azizi MH, Bahadori M. A history of leprosy in Iran during the 19 th
and 20 th
centuries. Arch Iran Med 2011;14: 425-30.
Pandya SS. Historical background. In: Kar HK, Kumar B, editors. IAL Text Book of Leprosy. 1 st
ed. New Delhi: Jaypee Brothers Medical Publishers; 2010. p. 3-23.
Joshi PL. National scenario, national leprosy eradication programme (NLEP) and new paradigms. In: Kar HK, Kumar B, editors. IAL text book of leprosy. 1 st
ed. New Delhi: Jaypee Brothers Medical Publishers; 2010. p. 35-43.
Robbins G, Tripathy VM, Misra VN, Mohanty RK, Shinde VS, Gray KM, et al
. Ancient skeletal evidence for leprosy in India (2000 B.C.). PLoS One 2009;4:e5669.
Whonamedit? A dictionary of medical eponyms. Norway. Gerhard Henrik Armauer Hansen. Inc.; 1994-2015. Available from: http://www.whonamedit.com
. [Last accessed on 2015 Oct 05].
Ghosh S, Chaudhuri S. Chronicles of Gerhard Henrik Armauer Hansen′s life and work. Indian J Dermatol 2015; 60:219-21.
Misch EA, Berrington WR, Vary JC Jr, Hawn TR. Leprosy and the human genome. Microbial Mol Biol Rev 2010;74:589-620.
Feitosa MF, Borecki I, Krieger H, Beiguelman B, Rao DC. The genetic epidemiology of leprosy in a Brazilian population. Am J Hum Genet 1995;56:1179-85.
Lazaro FP, Werneck CC, Cobat MA, Prevedello FC, Pimentel RP, Macedo GM, et al
. A major gene controls leprosy susceptibility in a hyperendemic isolated population from North of Brazil. J Infect Dis 2010;201:1598-605.
Abel L, Demenais F. Detection of major genes for susceptibility to leprosy and its subtypes in a Caribbean island: Desirade Island. Am J Hum Genet 1988;42:256-66.
Haile RW, Iselius P, Fine PE, Morton NE. Segregation and linkage analyses of 72 leprosy pedigrees. Hum Hered 1985; 35:43-52.
Trautman JR. The history of Leprosy. In: Hastings RC, editor. Leprosy. 2 nd
ed. USA: Churchill Livingstone; 1994. p. 11-25.
Gautam VP. Treatment of leprosy in India. J Postgrad Med 2009;55:220-4.
World Health Organization. Report of the third meeting of the Scientific Working Group (SWG) on the Chemotherapy of leprosy (THELEP). 1980. Available from: http://www.who.int/lep/resources/MDT02.pdf.
Noordeen SK. Leprosy control through multidrug therapy (MDT). Bull World Health Organ 1991;69:263-9.
Sehgal VN, Sardana K, Dogra S. The imperatives of leprosy treatment in the pre- and post-global leprosy elimination era: Appraisal of changing the scenario to current status. J Dermatol Treat 2008;19:82-91.
Rao PN, Jain S. Newer management options in leprosy. Indian J Dermatol 2013;58:6-11.
Giridhar BK. Chemotherapy: Drugs used in leprosy including newer drugs. In: Kar HK, Kumar B, editors. IAL Text Book of Leprosy. 1 st
ed. New Delhi: Jaypee Brothers Medical Publishers; 2010. p. 335-52.
Shetty VP. Challenges facing the control of leprosy in the Indian context. Ann Acad Med Singapore 2010;39:1-3.
Pannikar V. Enhanced global strategy for further reducing the disease burden due to leprosy: 2011-2015. Lepr Rev 2009;80:353-4.
Kumar B. World Leprosy Day 2015: Renewing commitment for a leprosy free world! Indian J Med Res 2015;141:1-4.