Leprosy ( communicable disease)

1. LEPROSY AND ITS
TRETMENT THERAPY
Presenter: Prabesh Budhathoki
Program: Bachlore in pharmacy
Semester: 5th
Roll No: 25

2. —Mother Teresa
“The biggest diseases today is not
lyprosy or tuberclosis, but rather the
feeling of being unwanted ”

3. Prevention
Introduction
Types Diagnosis and
treatment
01
History Sings and
symptoms
04
03
05 06 07
Table of contents
Mode of tranmission
08 09
Complication Refrenc
es

4. Introductio
n
01
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5. INTRODUCTI
ON
Leprosy is a chronic infectious disease caused by a
bacillus, Mycobacterium leprae.
Incubation period of this disease is 5 years , on average.
M leprae multiplies slowly and Symptoms may occur
within 1 year but can also take as long as 20 years or
even more.
It primarily affects the nerves of the extremities, the skin,
the lining of the nose, and the upper respiratory tract.
Leprosy is also known as Hansen’s disease.
Hansen’s disease produces skin ulcers, nerve damage,
and muscle weakness. If it isn’t treated, it can cause
severe disfigurement and significant disability.
Hansen’s disease is common in many countries,
especially those with tropical or subtropical climates.

6. It is an intracellular, aerobic, acid-fast, rod-shaped bacillus, surrounded by the
characteristic waxy coating, which is one of the most important virulence factors .

7. Histor
y 02

8. History
Hansen’s disease is one of the oldest diseases in
recorded history. The first known written reference to
Hansen’s disease is from around 600 B.C.
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
For the first time, leprosy has been described in osteo-
archaeological remains founded in India and dated to
2000 BC .

9. Geographical distribution of leprosy

10. Signs and
Symptoms
03

11. Signs and symptoms
Skin
symptoms
● Discolored patches of skin, that may be numb and look
faded
● Growths (nodules) on the skin
● Thick, stiff or dry skin
● Loss of eyebrows or eyelashes
Damage to
the nerves
● Numbness of affected areas of the skin
● Muscle weakness or paralysis
● Enlarged nerves
● Eye problems that may lead to blindness
Mucous
membrane
s
● A stuffy nose
● Nosebleeds

12. A
picture
is worth
a
thousan
d words

14. Mode of
transmission
04

15. How do people get Hansen’s
disease?
Air-borne
transmission
Through inhalation of bacilli
Maaterno-
foeataltransmission
across placenta
Transmission from milk of
leprosy patient to infant
Direct contact
With leprosy patient who shed numerous
bacilli from damaged skin nasal secretion,
mucous membrene of mouth and hair
follicles

16. Types of
Leprosy
05

17. •indeterminate (I)
•tuberculoid (TT)
•borderline tuberculoid (BT)
•mid - borderline (BB)
•borderline lepromatous (BL)
•lepromatous (LL)
Classification of Hansen's Disease (leprosy)
based on clinical evaluation, skin smears from
several sites and ideally at least an initial
biopsy

18. Classification according to WHO
While this classification gives one considerable information about the disease
in an immunologic sense, the use of the World Health Organization's limited
duration multidrug therapy has led to the widespread adoption of the WHO
classification. This includes only the following:
•single lesion paucibacillary (SLPB)
•paucibacillary (PB) i.e., those with two to five lesions
•multibacillary (MB) with six or more lesions

19. Diagnosis
06
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it

20. Recommendation
It is recommended to base the diagnosis of leprosy on
the following:
• clinical examination, with or without slit-skin smears or
pathological examination of biopsies (conditional recommendation,
very low quality evidence).

21. How is the disease diagnosed?
Biopsy
presence of acid-
fast bacilli in a
slit-skin smear
Muscles
weakness
thickened or
enlarged peripheral
nerve, with loss of
sensation and/or
weakness of the
muscles supplied by
that nerve;
Phyical
examination
Definite loss of
sensation in a pale
(hypopigmented)
or reddish skin
patch
The diagnosis of leprosy in current practice is based on the presence of at least one of the
three cardinal signs

22. Treatment of
leprosy
07

23. Anti-leprotic Drugs
Antitubrcular
drugs
RIFAMPIN
ETHIONAMID
E
Other antibiotic
OFLOXACIN
MOXIFLOXCIN
MINOCYCLINE
CHARITHROMYCINE
sulfone
DAPSONE
Phenazin
e
CLOFAZIMIN
E
1 2 3 4

24. ● Dapsone is a diamino diphenyl sulfone drug
● It is simplest , oldest , chepest and most active and most common drugs.
● Dapsone is structurally related to the sulphonamides and is bacteriostatic in nature
Dapsone
Mechanism of action :
Dapsone is chemically related to sulfonamides and has the same mechanism of action, i.e.
inhibition of PABA incorporation into folic acid by folate synthase. The antibacterial action of
dapsone is antagonized by PABA. It is leprostatic at very low concentrations, while growth of
many other bacteria sensitive to sulfonamides is arrested at relatively higher concentration .

25. Contraindication
• Hypersensitivity to Dapsone
• A low G6PD level
• Cardiopulmonary disease
• Allergy to sulfonamide antibiotics

26. ● Dapsone is completely absorbed after oral administration and is widely
distributed in the body, though penetration in CSF is poor
● It is 70% plasma protein bound, but more importantly it is concentrated in
skin (especially lepromatous skin), muscle, liver and kidney.
● Dapsone is acetylated as well as glucuronide and sulfate conjugated in
liver
● Metabolites are excreted in bile and reabsorbed from intestine, so that
ultimate excretion occurs mostly in urine.
● The plasma t½ of dapsone is variable, though often > 24 hr
● The drug is cumulative due to retention in tissues and enterohepatic
circulation.
● Elimination takes 1–2 weeks or longer.
pharmacokinetics

27. USES: DDS
• Leprosy
• Pneumolytic pneumonia in HIV patients
• Chloroquine resistant malaria
• Nodular type Acne vulgaris
ADVERSE EFFECTS
• Hemolytic anemia
• Mthemoglobinemia
• Anorexia
• Headache
• Cutaneous reaction like photoxicity , hypermelanosis , allergic rashes
• Hepatitis
• Agranulocytes
• DOSE: 100mg

28. Clofazimine (Clo)
• It is a dye with leprostatic and antiinflammator properties. Often used in the
combination with rifampicin and multidrug therapy for the treatment of leprosy.
• When used alone, the clinical response to clofazimine is slower than that to dapsone,
and
resistance develops in 1–3 years. Dapsoneresistant M. leprae respond to clofazimine
but
apparently after a lag period of about 2 months.
Mechanism of action :
Clofazimine works by interfering with DNA template function and inhabiting bacterial
proliferation.

29. • Clofazimine is orally active (40–70% absorbed).
• It accumulates in macrophages and gets deposited in
many tissues including subcutaneous fat, as needle-
shaped crystals.
• However, entry in CSF is poor.
• The t½ is 70 days so that intermittent therapy is possible
PHARMACOKIETICS
ADVERSE EFFECTS
• GI symptoms-nausea, vomiting, cramps , diarrhoea
• Imparts a harmless red color to feces, urine , sweat, tears and
saliva
• Deposition of clofazimine in the small intestine
• produces the most serious side effects-intestinal obstruction,
pain and bleeding
• Clofazimine causes reversible reddish-black discoloration of
the skin in most patients.

30. CONTRAINDICATION
Clofazimine is to be avoided during early
pregnancy and in patients with liver or kidney
damage.
DOSE:
50-100 mg/day orally

31. Rifampicin
This important tuberculocidal drug is also the most potentcidal drug for
M.leprae; rapidly renders leprosy patients noncontagious.
Upto 99.99% M.leprae are killed in 3–7 days by 600 mg/day dose.
Clinical effects of rifampin are very rapid; nasal symptoms in lepromatous
leprosy subside within 2–3 weeks and skin lesions start regressing by 2
months. However, nerve damage already incurred is little benefited.

32. • Ofloxacin
• Many fluoroquinolones like ofloxacin, pefloxacin, moxifloxacin,
sparfloxacin are highly active against M.leprae, but ciprofloxacin has
poor activity.
• Clinically, ofloxacin has been used to the largest extent. As a
component of MDT, it has been found to hasten the bacteriological
and clinical response. It is cidal to M.leprae, and
• in one study, over 99.9% bacilli were found to be killed by 22 daily
doses of ofloxacin monotherapy.
• However, it is not yet included in the standard treatment protocols, but
can be used
• in alternative regimens in case rifampin cannot be used, or to shorten
the duration of treatment and reduce chances of drug resistance. Its
safety during long-term use is not well documented.
• Dose: 400 mg/day.
• Moxifloxacin is the most potent fluoroquinolone against M. leprae.
Recently, it has been tried in some combination regimens with good
clinical and bacteriological results

33. REGIMENS
Adults: Tuberculoid (TT & BT) (WHO classification Paucibacillary, “PB”)
Agent Dose Duration
Dapsone 100 mg daily 12 months, and then
therapy discontinued
Rifampicin 600 mg daily 12 months, and then
therapy discontinued
Adults: Lepromatous (LL, BL, BB) (WHO classification Multibacillary, “MB”)
Agent Dose Duration
a
Dapsone 100 mg daily 24 months, and then
therapy discontinued
Rifampicin 600 mg daily 24 months, and then
therapy discontinued
Clofazimine
b
50 mg daily 24 months, and then
therapy discontinued

34. Treatment for children: Tuberculoid (TT & BT) (WHO Paucibacillary, “PB”)
Agent Dose Duration
Dapsone 1 mg/ Kg daily 12 months, and then therapy
discontinued
Rifampicin 10-20 mg/ Kg daily (not > 600) 12 months, and then therapy
discontinued
Treatment for children: Lepromatous (LL, BL, BB) (WHO Multibacillary, “MB”)
Agent Dose Duration
Dapsone 1 mg/ Kg daily 24 months, and then therapy
discontinued
Rifampicin 10-20 mg/ Kg daily (not > 600) 24 months, and then therapy
discontinued
Clofazimine 1.0 mg/ Kg daily
c
24 months, and then therapy
discontinued

35. Alternative Anti-Microbial Agents
• Minocycline, 100 mg daily, can be used as a substitute for Dapsone in individuals
who do not tolerate this drug. It can also be used instead of Clofazimine, although
evidence of the efficacy of its anti-inflammatory activity against Type 2 reactions is
not as substantial as the evidence for Clofazimine.
• Clarithromycin, 500 mg daily is also effective against M. leprae, and can be used as
a substitute for any of the other drugs in a multiple drug regimen.
• Ofloxacin, 400 mg daily, may also be used in place of Clofazimine, for adults. This
is not recommended for children.

36. . Recommended regimens for drug-resistant leprosy

37. Complication and
prevention
08

38. complication
The complication of leprosy are not due to the effect of the mycobacteria themselves , but rather due to
the nerve compression that is secondar immune reaction of the host.
Leprosy Reactions
Leprosy reactions occur during, before, or after treatment of leprosy. They exacerbate the neuropathy unless
promptly treated, but are immunological in origin. They are of two types - type 1 or reversal reactions, and type 2
or erythema nodosum leprosum.
Leprosy reactions must be treated in a timely and effective manner to prevent nerve compression and resulting
sensory loss, which inevitably leads to mutilating deformity. The reactions involve increased pain, inflammation,
and infiltration. All of these should be managed to prevent nerve damage.
Ophthalmologic Involvement
Leprosy can cause eye damage both through the involvement of the branches of the facial nerve innervating the
eye or by direct infection of the skin or the eye. Either of these leads to:
•Inability to close the eyelids (lagophthalmos)
•Keratitis due to exposure, absence of tears, and drying, leading to corneal ulcers
•Iridocyclitis
•Cataract secondary to eye disease

39. • Neurological Complications
• In leprosy, the peripheral nerve trunks are invaded by the bacilli and inflammatory cells.
This will cause neuritis, the features of which include tenderness, thickening, and
irregularity of the nerve, as well as sensorimotor involvement. This usually comes on in a
subacute manner, and the changes may be silent in some cases.
• The nerve changes lie at the root of the typical deformities characteristic of leprosy. In
most patients, a mixed or sensorimotor neuropathy occurs. This involves a single nerve.
As a result of skin denervation, the associated glands and hair follicles die, which results
in skin dryness, fissuring, and ulceration. Neuropathic pain may also occur.
• The breaching of the integument gives rise to secondary infection of underlying bone
and soft tissue. Finally the bone is resorbed at the site of infection, giving rise to
deformity. The bone involvement may also lead to gross deformation of the nose
skeleton and ensuing creation of a saddle-nose deformity.
• The nerves commonly involved include the facial, trigeminal, ulnar, median, and radian
nerves, as well as the common fibular and posterior tibial nerves. Involvement of the
facial nerve leads to failure of eyelid closure and lagophthalmos. The nasal mucosa
becomes dry and hypoesthetic, as does the cornea and conjunctiva.

40. ● Systemic Changes
● Systemic involvement may occur in patients with multibacillary leprosy as a result of leprosy reactions, or les
commonly because of infection by the bacteria in the blood stream. Renal damage may occur due to type 2
reactions or by secondary amyloidosis affecting many organs.
● This is most commonly observed when leprosy takes a chronic course with many reactions occurring and
being treated. Renal affection may manifest as glomerulonephritis, interstitial nephritis, or other renal
conditions. As a result, renal failure may ensue.
● Pulmonary tuberculosis is often seen. The upper airway is affected in many cases. Generalized abnormalitie
of the peripheral vessels and endothelial cell infection are common, with ischemic ulceration and autonomic
dysfunction of the cardiovascular system. Peripheral arteries may show abnormalities.
● Orchitis is common (90 percent), with the potential for infertility and impotence. A third of patients may have
adrenocortical lesions with iatrogenic adrenocortical failure. Hepatic amyloidosis may occur, while
pancytopenia due to infiltration of bone marrow, bacteremia, and lymphadenopathy are often seen.

41. Prevention
• The best way to prevent is early diagnosis and treatment of people who are inflected .
• Prevention of contact with droplets from nasal and other secretions from patients with untreated m .
leprae infection is currently the most effective way to avoid the disease.
• For household contact immediate and annual examinations are recommended for at least five years
after last contact with a person who is infectious .
• Look themselves over daily for ulcers or wounds and care for them properly
• Avoid plastic footwear or gloves which trap moisture and cause ulceration
• Cover wounds with clean bandages and look after them well
• Protect hands and feet from inadvertent injury
• Use the right tools to prevent the use of too much force which could injure the patient
• Be aware of signs of neuropathy
• Moisturize the skin to prevent dryness and fissuring which invite ulceration and infection
• Seek treatment of eye inflammation at the earliest to preserve vision

42. ● AUTHOR (YEAR). Title of the publication.
Publisher
● https://apps.who.int/iris/bitstream/handle/10665/26
2297/PMC2427498.pdf?sequence=1
● https://www.webmd.com/skin-problems-and-
treatments/guide/leprosy-symptoms-treatments-
history
● https://www.healthline.com/health/leprosy#types
● https://www.hrsa.gov/hansens-
disease/diagnosis/recommended-treatment
● https://apps.who.int/iris/bitstream/handle/10665/27
4127/9789290226383-
eng.pdf?sequence=58&isAllowed=y
● https://www.who.int/health-
topics/leprosy#tab=tab_
References

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