Introduction.

Hansen's disease also known as leprosy is caused by the bacteria named

Mycobacterium leprae sp. which is also a type of obligate acid-fast bacillus. Unlike other
bacteria under the same genus, mycobacteria, this species does not grow in any artificial
media or tissue culture.
Leprosy principally only attacks skin and peripheral nerves in the hands and feet,
upper respiratory tract and mucous membrane which then lead to impairment in sensual and
motor function.
Up till now, the exact mode of transmission of leprosy is still uncertain but according to
Centre of Disease Control (CDC), the bacteria can spread from person to person by air and
direct touch. It might also occur if you are exposed to other nasal fluids (also known as
secretions) that being said, that these secretions contain the bacteria that caused leprosy.
Now, however, the disease is very rare and easily treated with multi-drug therapy
(MDT). Early diagnosis and treatment usually prevent disability related to the disease (WHO,
2014).
The objectives of this assignment are to report and measure leprosy morbidity and
mortality trends: the status of M. leprae detection and treatment outcomes for leprosy.
The objectives that will also cover the aetiology, pathophysiology and
epidemiology of leprosy.

History.
In the face of being broadly believed as an historical moment in health, leprosy rests a
surprisingly widespread disease in the 21st century. In 1985, leprosy was still reflected as a
major public health problem in 122 countries.
Hitherto, 2 to 3 million people worldwide are permanently disabled because of leprosy.
Leprosy is a painful condition that can leave its victims deformed and crippled.
Contrary to popular perception, leprosy does not directly cause body parts to fall off of
their own. Instead, they become disfigured as an indirect result of other symptoms. Leprosy is
caused by the bacteria Mycobacterium leprae first identified by Gerhard Hansen in 1873.
Malaysia is not excluded from the pandemic of leprosy. Although the incidence of
leprosy in Malaysia is declining, it is still a public health problem. The disease was probably
introduced into the country in the nineteenth century by Chinese and Indian immigrants
among whom the disease was prevalent.
In 1926, the Leper Enactment Act 1926 was established which required compulsory
notification and isolation of leprosy patients.
As a result, the National Leprosy Control Centre (NLCC) was built in Sungai Buloh,
Selangor. In 1969, the National Leprosy Control programme was launched with the objective
of early case finding and decentralisation of treatment of leprosy. The centre covers an
area of 562 acres of low hilly land and is among the largest in the British Commonwealth. It
has a hospital with 855 beds, an old leprosy settlement of 2000 bed chalets, an administration
block and a research unit.
The National Leprosy Control Programme was launched in 1969 in West Malaysia
and extended into the East Malaysian states of Sarawak and Sabah in 1974 and 1985
respectively. The diagnosis of leprosy is confirmed by skin or nerve biopsy. The treatment of
leprosy patients is fully integrated with basic medical and health services in Malaysia. This has
resulted in 63% decline in the number of patients in the NLCC over a span of 20 years (19701990).
The treatment of leprosy patients is integrated with basic Medical and Health services
in Malaysia. With the implementation of Multiple Drug Therapy in 1985, the National
prevalence rate of leprosy has reduced from 5.7 per 10,000 in 1983 to 1.7 per 10,000 in 1992.
The Research Unit in NLCC was established in 1950, where cultivation of
Mycobacterium leprae using mouse foot-pad technique is done.
2

The mouse foot-pad technique for cultivation of Mycobacterium leprae was started in
the Research Unit of NLCC, Sungai Buloh in the year 1969. Presently this technique is used
for drug susceptibility/ resistancy testing and the drugs tested include Dapsone, Clofazimine
and Rifampicin. .

Aetiology
Leprosy is caused by the bacteria Mycobateria leprae sp. It is the first bacterial
pathogen acknowledged affecting human, it rests one of the few that is non-cultivable in vitro.
It is an intracellular, gram-positive, acid-fast bacterium. M. leprae is a rod-shaped aerobic
bacillus.
M. leprae prefer to grow in cooler regions of the body. The bacillus is dependent on
the metabolic products of the host, which explain its long incubation period and incapability to
grow in vitro. Since the bacteria does not grow in vitro, understanding its biology is a challenge
that takes time and money.
The bacteria was first discovered by Norwegian physician, Gerhard Armauer Hansen
thus named in honour of him (Hansens disease) who first identified the causative organism
in 1873.
There are three (3) types of leprosy characterised by its severity:
1. Tuberculoid (paucibacillary).
2. Lepromatous (multibacillary).
3. Borderline or dimorphous (intermediate-certain)
The category is based on the number of bacteria present: paucibacillary (small) and
multibacillary (many) and by the number of poorly pigmented numb skin patches present, with
paucibacillary (<5) and multibacillary (>5).

Pathophysiology.
The pathophysiology of leprosy can be easily guessed with the known aetiology. Once
M. leprae entered a host, it needed more time to replicate and grow including people with
immunodeficiency.
The route of entry is thru respiratory tract by direct contact or air droplets that
contained the bacteria. Prone to replicate around wet/ damp areas; skin and nerves, Schwann
cell.
Can withhold its life outside human body up to a week. Incubation is long and
asymptomatic ranging from 4 to 8 years.
Leprosy is harmful to the body by disabling the function of sensory and motor
(peripheral neuritis). Furthermore, the injury of the 7th and 5th cranial nerves exposed patients
to trauma, sepsis and possible blindness.

Clinical Manifestations.
Leprosy attacks skin, nerves and eyes thus causing systemic failure. Patients
generally present with skin lesions, weakness or numbness caused by a peripheral-nerve
lesion or a burn.
Patients with dimorphous leprosy may develop nerve pain, sudden palsy, eye pain or
a systemic febrile illness.
The signs and symptoms of leprosy are:
1. Skin lesions.
2. Thickened peripheral nerves.
3. Acid-fast bacilli on skin smears or biopsy.
The nerves most often involved are the
1. Ulnar (elbow),
2. Median (wrist),
3. Radial (wrist),
4. Peroneal (knee),
5. Posterior tibial and sural (ankle),
6. Facial and great auricular (posterior triangle of the neck).
7. Affected nerves may be enlarged and tender.
Blindness is a devastating complication of leprosy in patients with anaesthetic hands and
feet. Eyelid closure is impaired when the facial nerve is affected. Damage to the trigeminal
(5th) nerve causes anaesthesia of the conjunctiva and the cornea, which is then susceptible
to trauma and ulceration.
Tuberculoid leprosy has a good prognosis. It may self-heal, and peripheral nerve
damage is limited.
Borderline tuberculoid is when the skin lesions are similar to those in tuberculoid leprosy,
but more numerous. Peripheral nerve damage may be widespread and severe. Borderline
leprosy is unstable; patients have numerous skin lesions varying in size, shape and
distribution. Annular lesions with a broad, irregular edge and a sharply defined, punched-out
centre are characteristic. Nerve damage is variable.
Borderline lepromatous leprosy is characterized by widespread of small macules.
Patients may experience type 1 and type 2 reactions. Peripheral nerve involvement is
widespread.
6

Lepromatous leprosy patients with untreated polar lepromatous leprosy may be

carrying 1011 M. leprae. The earliest lesions are ill-defined.

Clinical Characteristics

Lepromatous

Tuberculoid

Skin and nerves

Widely disseminated

One or few sites,

asymmetrical.

-Number and distribution

Skin lesions
Definition:
i. Clarity of margin
ii. Elevation of margin

I. Poor
II. Never

I. Good
II. Common

Color
i. Dark skin
ii. Light skin

III. Slight hypopigmentation III. Hypopigmentation

IV. Slight erythema
IV. Coppery or red

Surface

Smooth, shin.

Dry, scaly.

Central healing
Sweat and hair growth

None.
Impaired late

Common
Impaired early

Loss of sensation

Late

Early and marked

Nerve enlargement and

Late

Early and marked

Bacilli (Bacterial Index)

Many (5 or 6+)

Absent (0)

Natural outcome

Progression

Healing

Other tissues

Upper respiratory mucosa,

None

damage

eye, testes, bones, muscle

Reactions

Immune complexes

Cell-mediated

Gradually, the skin becomes infiltrated and thickened. Dermal nerves are destroyed,
sweating is lost and glove-and-stocking neuropathy is common. Nerve damage to large
peripheral nerves occurs late in the disease.
The collapse of the bridge of the nose results from bacillary destruction of the bony
nasal spine. Testicular atrophy is caused by diffuse infiltration and the acute orchitis that
occurs with type 2 reactions. This results in azoospermia and gynaecomastia.

Type 1 reaction. This man developed erythematous, oedematous lesions on his face and trunk 6 weeks after starting
treatment.

Type 1 reaction. This woman developed acute ulnar nerve neuritis as part of the reversal reaction, leading to overnight loss
of function. Early clawing and swelling of the hand is visible.

Epidemiology.
Leprosy still remains as main global concern to date. There are about 650,000 new
cases per year, 70% of which are in India. In all new cases seen in the UK, infection was
acquired overseas. HIV infection is not a risk factor for the development of leprosy, but may
worsen leprous neuritis.
Infected individuals discharge bacilli from their nose. Infection occurs through the nose
followed by haematogenous spread to skin and nerve. The incubation period of M. leprae is 2
to 5 years in tuberculoid disease and 812 years in lepromatous disease.
In 2001, registered cases of leprosy in Sabah were 206 and the rate of prevalence
was less than one per 10,000 population (0.7/10,000 population). However, five districts with
prevalence rate of more than one in every 10,000 population are from districts of Kota
Kinabalu, Kudat, Semporna, Tawau and Lahad Datu.
Notification on leprosy in year 2000 was 61 cases whereas in 2001 it was 72 new
cases. Amongst these cases, 44 (61%) are immigrants and 28 (39%) cases were Malaysian.
In this analysis, all patients diagnosed were treated with MDT regime since year 1999. Total
number of defaulters were less than 22%.

Year

Case

Completed

Abandoned

analysed

treatment (%)

treatment (%)

Death (%)

Others (%)

1994

2024

83.6

12.2

4.2

1995

1924

82.1

9.2

5.04

3.7

1996

2028

86.7

6.1

5.03

2.2

1997

1876

82.46

10.02

3.46

4.05

1998

2035

79.4

10.8

3.5

6.3

1999

2048

83.1

8.3

3.4

5.2

Table 1. Cohort analysis Sabah, 1994-1996

Year

Malaysian

Immigrants

Total

Notified

Rate per

Total

Notified

Rate per

population

new cases

100k

population

new cases

100k

population

population

1996

1775500

28

1.58

747100

39

5.22

1997

1879700

32

1.70

748200

37

4.72

1998

1989800

33

1.66

823100

51

6.19

1999

2106400

24

1.14

864000

38

4.39

2000

2229800

21

0.94

906900

40

4.41

2001

1952300

28

1.43

764500

44

5.76

Table 2. Notification rate of new cases of leprosy amongst immigrants and Malaysians, Sabah 1996-2001.

Year

Total cases

Regular with treatment follow-

Treatment defaulters

registered

up (number and percentage).

(number and percentage).

1999

221

173 (78%)

48 (22%)

2000

215

171 (80%)

44 (20%)

2001

206

178 (86%)

28 (14%)

Table 3. Registered leprosy cases on Multiple Drug Therapy (MDT), Sabah 1999-2001.

Prevalence rate of leprosy in Sabah.

10

Investigations.
Tuberculoid leprosy in these patients, lymphocytes respond to M. leprae antigens
in vitro. Skin tests with lepromin (a soluble M. leprae sonicate preparation) elicit strongly
positive responses. This strong cell-mediated response clears antigen, but with concomitant
local tissue destruction.
Lepromatous leprosy these patients have specific cell mediated anergy (a state of
immune unresponsiveness) to M. leprae and their lymphocytes do not respond to M. leprae
antigens in vitro. They are unresponsive to intradermal challenge with lepromin. Lepromatous
patients exhibit specific T cell failure and macrophage dysfunction. Immune-mediated
reactions: acute immune-mediated reactions are a serious complication of leprosy.
Both T cells and macrophages are involved when there is a M. leprae infection.
Type 1 reactions are episodes of delayed hypersensitivity occurring at sites of localization
of M. leprae antigens.
Type 2 reactions acute, nodular, erythematous eruption that usually is limited to the extensor
aspects of the lower legs (erythema nodosum leprosum) results from immune complex
deposition.
Diagnosis is clinical, by the finding of a cardinal sign of leprosy, and is supported by
acid-fast bacilli in slit-skin smears or typical histology on skin biopsy. Skin biopsy reviewed
by an experienced health practitioner is invaluable in classifying the patient and to rule out
other diseases.
Skin lesions should be tested for anaesthesia. The peripheral nerves should be
palpated for thickening and tenderness. There are no serological tests that detect leprosy
across the spectrum. Polymerase chain reaction analysis for M. leprae DNA has not been
developed as a diagnostic tool.
Differential diagnosis of leprosy is the most common cause of peripheral nerve
thickening. Uncommon conditions such as CharcotMarieTooth disease and amyloid are
differentiated from leprosy by the absence of skin lesions and acid-fast bacilli. The anaesthesia
of tuberculoid and borderline tuberculoid lesions differentiates them from other conditions
resembling leprosy like in vitiligo and mycotic skin infections.

11

Management.
WHO recommendations for chemotherapy of leprosy are listed in table below. Firstline antileprotic drugs are Rifampicin, Dapsone and Clofazimine.

Type of leprosy

Paucibacillary

Multibacillary

Regimen

Monthly supervised

Daily self-administered

Rifampicin, 600 mg

Dapsone, 100 mg

Rifamcipin, 600 mg

Rifamcipin, 50 mg

Chlofaziminem, 300 mg

Dapsone, 100 mg

Duration of
treatment

6 months

12 months

Any patient with acid-fast bacilli on skin smear or biopsy should be treated for
multibacillary disease. Patients with high bacterial loads (on skin biopsy or slit-skin smear)
need treatment with multi-drug therapy for at least 24 months. Clinical improvement is rapid
and toxicity is uncommon.
New nerve damage that occurred to any patient with motor or sensory loss of less
than 6 months duration should receive a 6-month course of oral corticosteroids as for the
treatment of type 1 reactions.
Patient education is vital. Patients must be reassured that, within a few days of
chemotherapy, they will no longer be infectious and can lead a normal social life. It should be
emphasized that care and awareness of their limbs is as important as chemotherapy.
Preventing disability nerve damage produces anaesthesia, dryness and muscle
weakness, which lead to misuse of the affected limb and resultant ulceration, infection and,
ultimately, severe deformity. Dryness predisposes to cracking of the skin and secondary
infection; it can be alleviated by soaking the feet and applying oil-based creams.
Physiotherapy can prevent contractures, muscle atrophy and over-stretching of
paralysed muscles.

12

Principles of management of leprosy reactions are:

1. Control the acute inflammation and ease the pain.
2. Treat the neuritis.
3. Halt eye damage.
Type 1 reactions should be treated using Prednisolone, 40 mg/day PO. initially reduced
by 5 mg/day each month.
Vaccines there is no specific vaccine against leprosy, but several trials have shown
BCG to be protective.

13

Conclusion.
In todays world, thousands of people across the globe will stop to remember those
who suffer this horrendous effects of leprosy.
World Leprosy Day helps to focus on the needs of the very poorest of people and
with leprosy. It helps to tell story to people who simply dont know that leprosy still exists and
most importantly, that it can be cured.

Discussion.
With the resurgence of TB as a global concern, immediate attention has to be given
to this disease in all sectors of health systems and community.
Although a Plan of Action in prevention and control of TB at the national level is
available, every district needs to develop its own specific action plan, because, to be
effective, action plans must address local issues such as disease patterns and resource
availability.
Although the prevalence rate of leprosy is less than 1 case per 10,000 population,
new cases continue to be detected. Total commitment of everyone will make a difference in
the prevention and control of tuberculosis and leprosy in Malaysia.

14

Bibliography.
Dony, J.F., Ahmad, J. & Khen Tiong, Y. 2004, "Epidemiology of tuberculosis and leprosy,
Sabah, Malaysia", Tuberculosis (Edinburgh, Scotland), vol. 84, no. 1-2, pp. 8-18.

Bedford, K.J.A. 2008, Gombak and its patients: provision of healthcare to the Orang Asli
(indigenous minority) of peninsular Malaysia, ProQuest, UMI Dissertations Publishing.

Weinstein, D.E. 2000, "Mycobacterium leprae and neuropathies", Trends in microbiology, vol.
8, no. 4, pp. 156-157.

"Communicable Diseases Department, Leprosy FAQ". World Health Organization. 2006-0525. Retrieved 2010-01-31.

Chehl S, Job CK, Hastings RC (1985). "Transmission of leprosy in nude mice". Am J Trop
Med Hyg 34 (6): 11616.

Britton, W.J. & Lockwood, D.N. 2004, "Leprosy", The Lancet, vol. 363, no. 9416, pp. 12091219.

Fadzilah K. Mouse footpad studies in National Leprosy Control Centre. Proceedings of the
National Leprosy Seminar, Malaysia, July 26-29, 1992.

Jayalakshmi P, Looi LM, Lim KJ, Rajagopalan K. Autopsy findings in 35 cases of leprosy in
Malaysia. Int J Leprosy 1987; 55: 510-4.

15