2. It is a non fatal slowly progressive chronic
granulomatous infection
Causetive organism : Mycobacterium
leprae
Incubation period : 2- 20 years
Organs that infected : Nerves (nerve
schawann cells)
Bacteria also invades either dermal nerve
or main peripheral nerve
Cooler parts of the body is mainly affected
such as skin,mouth,eyes,peripheral
nerves,superficial lymph nodes and testes
3. MODE OF TRANSMISSION
Direct contact with untreated leprosy patient
who shed numerous bacilli from damaged
skin,nasal secretion and from mouth
Nasal droplet infection
Infected soil
Mother to infants by milk
Materno –fetal transmission across the
placenta
4. ETIOLOGY
Mycobacterium leprae – intracellular
parasite
The organism is acid fast and
indistiguishable from other mycobacterium
Detected in tissue sections by a modified
stain
6. TUBERCULOID LEPROSY
ORGAN INFECTED –Skin,PNS
T.Leprosy patient have asymmetric enlargement
of one or few peripheral nerves
Mainly affected – Posterior auricular,peroneal
and posterior tibial nerves,with associated
hypoesthesia and myopathy
7. PATHOPHYSIOLOGY
T – cell reach the perineurium
Destruction of Schwann cells
Fibrosis of epineuria
Epithelial granuloma
Necrosis
8. LEPROMATUS LEPROSY
ORGANS INFECTED:Skin nodules, raised
plaques,or diffuse dermal infiltration on
face results in leonine facies
SYMPTOMS : Loss of eyebrows and
eyelashes,dry skin
9. L leprosy bacilli attack
skin, PNS
invade schwann cells
axonal degeneration
bacilli
circulation all organ
10. BORDERLINE LEPROSY
Shows all characteristics of tuberculoid and
lepromatous
INTERMEDIATE LEPROSY
No specific dermatitis may be made
12. 2nd Stage ( secondary stage)
bacteria invade
multiply in nerve fibre
skin becomes thick and wrinkled and ear
become swollen
nodules formed at skin and nose
nodules discharge fluid
14. DIAGNOSIS
Leprosy in most commonly presents with both
characteristic skin lesion and skin
histopathology
Lipromen skin test: Skin smears by splitting
the skin. Scrapping from the cut edges of
dermis and nasal smears
1. Acid fast staining (Ziehl-Neelsen) staining
2. Fite- Faraco staining
3. Gamori methenamine silver staining
15. TREATMENT
Antimicrobial therapy
Dapsone (50-100 mg/dl)
MOA:Inhibits the synthesis of dihydrofolic acid
through competition with para-amino-
benzoate for the active site of
dihydropteroate synthetase
Clofazimine (50-100 mg/dl)- 3 times weekly
MOA: Inhibits mycobacterial growth and binds
preferentially to mycobacterial DNA
16. Rifampine (600mg daily or monthly)
MOA: Inhibits bacterial RNA polymerase, the
enzyme responsible for DNA transcription
Bacillus Calmette–Guérin (BCG) vaccine