1. LEPROSY
De Leoz, Maria Sabrina C.
De Taza, Kaizette Mieje L

2. What is Leprosy?
A disease caused by the bacteria
Mycobacterium Leprae,
which causes damage to the
skin and the peripheral
nervous system. Chronic
granulomatous disease, similar
to tuberculosis,because it
produces inflammatory
nodules (granulomas) in the
skin and nerves over time.

3. Leprosy develops slowly from 6months up to 40 yrs and results in
skin lesions and deformities, most often affecting the cooler
places on the body (for example, eyes, nose, earlobes, hands, feet,
and testicles) that can be very disfiguring. . Although human-to-
human transmission is the primary source of infection, three other
species can carry and (rarely) transfer M. leprae to humans:
chimpanzees, mangabey monkeys, and nine-banded
armadillos.

4. Etiology
In 1873, Dr. Hansen discovered bacteria in leprosy lesions, suggesting
leprosy was an infectious disease, not a hereditary disease or a
punishment from the gods .
First of all, and quite unexpectedly, the disease was more likely
introduced to West Africa by infected explorers, merchants or colonists
from North Africa or Europe, rather than by migrants from East Africa.
Early humans probably left East Africa to settle in Western and
Southern Africa 50,000 years ago, before humans arrived in the
Eurasian regions, and it seems improbable, according to the analysis
conducted, that these first humans brought leprosy to West Africa.
From West Africa, leprosy was then introduced to the Caribbean
islands, Brazil and probably to other regions of South America through
the slave trade in the 18th century, as isolates with the same profile as
those from West Africa were discovered in these regions.

5. The strain of M. leprae is closer to the type present in Europe and
North Africa, which indicates that colonialism and emigration
from the Old Continent very clearly contributed to introducing
leprosy to the New World. In fact, in the 18th and 19th centuries,
when Scandinavian immigrants settled in the western United
States, many cases of leprosy were reported, while a vast
epidemic was simultaneously ravaging Norway. This hypothesis
is supported by the presence today of a strain with the same
genetic profile as the strain from Europe and North Africa in
armadillos naturally infected in Louisiana (United States), which
undoubtedly originated from human infection.

6. Signs and Symptoms
Early signs and symptoms of leprosy are very subtle and occur
slowly (usually over years).

First symptoms : Numbness and loss of temperature sensation
(cannot sense very hot or cold temperatures)

As the disease progresses : the sensations of touch, then pain,
and eventually deep pressure are decreased or lost.

Long-term developing sequence of events : Relatively painless
ulcers, skin lesions of hypopigmented macules (flat, pale areas of
skin), and eye damage (dryness, reduced blinking) are
experienced before the large ulcerations, loss of digits, and facial
disfigurement develop that begins and continues on the cooler
areas of the body (for example, hands, feet, face, and knees).

8. Mode of Transmission
Leprosy occurs more commonly in males than in females in most
regions of the world. Leprosy is not particularly a disease of children
as was once believed.

transmitted from person to person by aerosol with a high subclinical
rate of infection. Casual contact does not cause leprosy. This contact
may be direct (e.g. skin to skin) or indirect (e.g. contact with soil,
and fomites such as contaminated clothes and linen).

may be transmitted by inoculation, such as by contaminated tattoo
needles.

9. 
The nose is a major portal of exit of organisms of a person affected by
leprosy. Some cases of leprosy harbor millions of Mycobacterium
leprae in their nasal mucosa which are discharged when they sneeze or
blow the nose.

The bacilli can also exit through ulcerated or broken skin of
bacteriologically positive cases of leprosy.

10. Period of Communicability

Leprosy is not usually infectious after three months of continuous
treatment with dapsone or clofazimine, or after two to three weeks of
treatment with rifampicin.
At Carville in 1941, promin, a sulfone drug, showed efficacy but
required many painful injections.
Dapsone pills were found to be effective in the 1950s, but soon
(1960s-1970s), M. leprae developed resistance to dapsone.
Fortunately, drug trials on the island of Malta in the 1970s showed
that a three-drug combination (dapsone, rifampicin [Rifadin], and
clofazimine [Lamprene]) was very effective in killing M. leprae. This
multi-drug treatment (MDT) was recommended by the WHO in 1981
and remains, with minor changes, the therapy of choice. MDT,
however, does not alter the damage done to an individual by M. leprae
before MDT is started.

11. Susceptibility & resistance
Everyone is susceptible to infection, however study results have
suggested a strong age-related susceptibility to being infected or
developing disease following close contact with a multi-bacillary case.
Children aged between five and nine years are at greatest risk. The risk
of progression to leprosy disease following infection is considered to
be approximately the same as tuberculosis which is approximately a
10% lifetime risk.

12. Susceptibility of Leprosy
•
Symptoms and disease progression can differ from
person to person depending on interactions
between the affected person's immune system and
the bacterium. The disease has been difficult to
study in a laboratory setting, but evidence suggests
that variation in disease susceptibility and
symptoms are influenced mainly by human genetic
variation.

13. Methods of Control
•
Steps to control Leprosy:
1. Detection of cases of leprosy and tracing the
contacts especially children of the patient's house.
2. Prevention of contact between the patient and other
normal persons, especially children.
3. Preventive treatment (chemoprophylaxis) with
daps one.

14. 4. Selective isolation or hospitalization of the patient
showing acute reactions or complications.
5. Treatment of infected patients with daps one.
6. Rehabilitation of the patient with suitable
work. Social and psychological rehabilitation is also
necessary.

15. Programs for Prevention
•
Leprosy Control Program: envisions to eliminate
Leprosy as a human disease by 2020 and is
committed to eliminate leprosy as a public health
problem by attaining a national prevalence rate
(PR) of less than 1 per 10,000 population by year

16. WHO gives an overview of leprosy and leprosy
control activities around the world. ILEP Member
Association support leprosy activities on a country-
by-country basis throughout the world. In the USA,
the Center for Disease Control(CDC) , gives general
information about leprosy. The Report of the ILA
technical forum, held in Paris in 2002, reviews much
of the scientific evidence underpinning current efforts
to control leprosy.

17. •
Multi Drug-Therapy(MDT): a therapy introduced
by WHO which consist of two regimens: rifampicin
and dapsone for PB leprosy and
rimfacin ,clozimine and dapsone for MB leprosy.

18. Prevention and Control
•
Prevention of Leprosy for Household Contacts:
For prevention of leprosy, people who live in the
same household as a person with leprosy
(household contacts) will need to be examined by a
physician. These examinations should be repeated
annually for five years. It is important to note that
the degree of natural immunity is high, and there is
often no need for preventative medicine.

19. However, if you are a household contact and you
develop a questionable skin rash, you should have a
skin biopsy to determine whether or not leprosy is
present.

20. •
Tests and Vaccines for the Prevention of Leprosy
Although there is currently no vaccine available for
the prevention of leprosy, researchers are actively
working on developing one.

21. END :)