World Leprosy Eradication Day 2025: Bursting Myths & Revealing Facts

World Leprosy Eradication Day 2025: Bursting Myths & Revealing Facts

World Leprosy Eradication Day is observed annually on the last Sunday of January, and in 2025, it will be observed on January 30. This day aims to raise awareness about leprosy, also known as Hansen’s disease, and to promote efforts towards its eradication.

Leprosy is also known as Hansen’s disease, named after the Norwegian physician who discovered the microorganism that caused it in 1874. The microorganism was discovered by Dr. Gerhard Armauer Hansen in 1874, a Norwegian physician who was searching for the unknown bacteria in the skin nodules of lepers, so the illness was called “Hansen’s disease. Leprosy is a chronic infectious disease caused by the bacteria Mycobacterium leprae, which primarily affects the skin, nerves, and mucous membranes. While it is treatable, the disease has historically carried a significant stigma, which has led to discrimination and isolation of affected individuals.

Myths and Misconceptions

Myth: Hansen’s disease is very contagious.

Fact: Hansen’s disease does not spread easily from person to person. You cannot get it through casual contact such as shaking hands, sitting next to, or talking to someone who has the disease.

Myth: There is no cure for Hansen’s disease.

Fact: Leprosy is curable with multi-drug therapy (MDT), a combination of antibiotics. Early diagnosis and treatment can prevent severe disabilities. 

Myth: Hansen’s disease makes your fingers and toes fall off.

Fact: Fingers and toes do not just “fall off” due to Hansen’s disease. The bacteria that cause the disease attacks the nerves of the fingers and toes, causing them to become numb. Injuries like burns, ulcers, and cuts on numb parts can go unnoticed, which may lead to permanent damage or infection, causing loss of the digit. Sometimes, the nerve damage makes muscles in the fingers and toes so weak that the muscles and bones begin to disintegrate and be reabsorbed by the body.

Myth: People with leprosy should be isolated or shunned.

Fact: There’s no need to isolate or segregate people affected by leprosy. With early diagnosis and proper treatment, patients become non-infectious and can continue with their normal lives. Social inclusion and support are crucial in combating the stigma associated with the disease.

Introduction
Leprosy (Hansen’s disease) is a chronic granulomatous disease affecting skin and nerve; it is caused by Mycobacterium leprae. The clinical form of the disease is determined by the degree of cell-mediated immunity (CMI) expressed by that individual towards M. leprae . High levels of CMI with elimination of leprosy bacilli produce tuberculoid leprosy, whereas absent CMI.

Leprosy: Mechanism of Damage and Tissue affected

Mycobacterium leprae reprogram adult Schwann cells by altering host-gene expression. Bacterially reprogrammed cells resemble progenitor/stem-like cells of mesenchymal trait that promote bacterial spread to mesenchymal tissues by redifferentiation. Progenitor/stem-like cells then secrete immune factors, recruit macrophages, transfer bacteria, form granulomas, and disseminate infection

  • Leprosy manifestations are classified along a clinical spectrum of:
    1. Tuberculoid (TT)
    2. Borderline tuberculoid (BT)
    3. Borderline borderline (BB)
    4. Borderline Lepromatous (BL), and
    5. Lepromatous (LL) leprosy.

    Each pole is associated with a characteristic cell-mediated or humoral immune profile. The cell-mediated (Th1) response of the TT pole features the elimination or containment of the organism in granulomas, while the ineffective humoral response at the LL (Th2) pole allows the proliferation of mycobacteria within and around foamy macrophages. Reversal reactions reflect a sudden shift toward the Th1 pole from the BT, BB, or BL state and can lead to irreversible nerve damage (neuritis). Erythema nodosum leprosum (ENL) reactions occur in patients with BL or LL leprosy and reflect an increase in both cell-mediated and humoral responses to M. leprae . ENL is associated with the systemic release of TNF and IL-4, a brisk polymorphonuclear leukocyte (PMN) influx, and antigen-antibody (Ag/Ab) complex deposition. The mechanism of nerve damage is unclear but may involve immune injury due to the release of inflammatory cytokines or activity of cytotoxic T cells, ischemia due to edema within the perineural sheath, apoptosis, or demyelination

Complication of Nerve Damage

  • Dryness
  • Anaesthesia 
  • Paralysis 
  • Contracture
  • Weakness of muscle
  • Tissue destruction on Face, hands and  feet

Epidemiology

Some 4 million people have or are disabled by leprosy.

World-wide active transmission continues, with around 750 000 new cases detected annually, many of them children. About 70% of the world’s leprosy patients live in India, with Brazil, Indonesia, Mozambique, Madagascar, Tanzania and Nepal being the next most endemic countries.

All new cases seen in the UK have acquired their infection abroad. Age, sex and household contact are important determinants of leprosy risk; leprosy incidence reaches a peak at 10-14 years, and an excess of male cases has regularly been found. HIV infection is not a risk factor for leprosy. HIV/leprosy co-infected patients have typical skin lesions and typical leprosy histology and granuloma formation, even with low circulating CD4 counts.

Transmission

Untreated lepromatous patients discharge bacilli from the nose. Infection occurs through the nose, followed by haematogenous spread to skin and nerve. The incubation period is 2-5 years for tuberculoid cases and 8-12 years for lepromatous cases.

Pathogenesis

  1. leprae has a predilection for Schwann cells and skin macrophages, and the host response is critical in determining the outcome of infection. There are three important aspects of leprosy pathogenesis: the spectrum of immune responses, nerve damage and immune-mediated reactions.

At the tuberculoid pole, well-expressed CMI and delayed hypersensitivity control bacillary multiplication; organised epithelioid granulomas are seen in tissue biopsies. In the lepromatous form, there is cellular energy towards M. leprae, resulting in abundant bacillary multiplication. Between these two poles is a continuum, varying from patients with moderate CMI (borderline tuberculoid) to patients with little cellular response (borderline lepromatous). The polar groups are stable but the central groups are immunologically unstable.

Both T cells and macrophages are important in the response to M. leprae antigens. Tuberculoid patients have a Thl-type response to M. leprae.

Clinical features

Patients commonly present with skin lesions  or the effects of a peripheral nerve lesion, weakness or an ulcer in an anaesthetic hand or foot. Borderline patients may present with a reaction, nerve pain, sudden palsy and multiple new skin lesions.

• Skin: The most common skin lesions are macules or plaques. In lepromatous leprosy, papules, nodules or diffuse infiltration of the skin occur. Tuberculoid patients have few, hypopigmented lesions whilst lepromatous patients have numerous, sometimes confluent lesions.

  • Anaesthesia: Anaesthesia occurs in skin lesions when dermal nerves are involved or in the distribution of a large peripheral nerve. In skin lesions the small dermal sensory and autonomic nerve fibres are damaged, causing local sensory loss and loss of sweating within that area.

• Peripheral Neuropathy: Peripheral nerve trunks are affected at ‘sites of predilection’. These are the ulnar (elbow), median (wrist), radial (humerus) causing wrist drop, radial cutaneous (wrist), common peroneal (knee), posterior tibial and sural nerves at the ankle, facial nerve as it crosses the zygomatic arch, and great auricular in the posterior triangle of the neck. Damage to peripheral nerve trunks produces characteristic signs with regional sensory loss and dysfunction of muscles supplied by that peripheral nerve. All these nerves should be examined for enlargement and tenderness and tested for motor and sensory function. The central nervous system is not affected.

• Eye involvement: Blindness due to leprosy is a devastating complication for a patient with anaesthetic hands and feet. Eyelid closure is impaired when the facial (7th) nerve is affected. Damage to the trigeminal (5th) nerve causes anaesthesia of the cornea and conjunctiva. The cornea is then susceptible to trauma and ulceration.

CARDINAL FEATURES OF LEPROSY

  • Skin lesions, typically anaesthetic at tuberculoid end of spectrum
  • Thickened peripheral nerves
  • Acid-fast bacilli on skin smears or biopsy


Investigation 

The diagnosis is clinical, made by finding a cardinal sign of leprosy and supported by finding acid-fast bacilli in slit skin smears or typical histology in a skin biopsy. Skin lesions should be tested for anaesthesia. The peripheral nerves should be palpated for thickening and tenderness.

Neither serology nor PCR testing for M. leprae DNA is sensitive or specific enough for diagnosis.

Slit skin smears

The bacterial load is assessed by scraping dermal material onto a glass slide. The smears are then stained and acid-fast bacilli are scored on a logarithmic scale: the bacterial index (BI). Smears are useful for confirming the diagnosis and monitoring response to treatment. 


Reference
1.https://continentalhospitals.com/blog/stigma-surrounding-leprosy-breaking-misconceptions/#:~:text=Historically%2C%20this%20myth%20led%20to,cases%20reported%20worldwide%20in%202020.

2.https://www.researchgate.net/figure/The-leprosy-spectrum-and-possible-mechanisms-of-tissue-damage-Leprosy-manifestations-are_fig1_49646466

3. https://www.sci.news/biology/article00829.html

4.https://archive.org/details/davidsons-principles-and-practice-of-medicine-24th-ed-full-version

About the author

Dr Mansi Tyagi

Dr. Mansi Tyagi, BHMS (SHMC), DNHE is a reowned Homoeopathic Consultant and the Marketing Head and Homeopathic Editor at BJain Books. With a strong foundation in homeopathy from the prestigious Dr. B. R. Sur Homoeopathic Government Medical College and a specialization in Diet and Nutrition, she is passionate about promoting holistic health and well-being. Dr. Mansi combines her clinical expertise with her Medical writing to advance knowledge in the field of homeopathy.