This document summarizes key information about leprosy (Hansen's disease):
- Leprosy is caused by Mycobacterium leprosy, an acid-fast bacillus first identified in 1873. It primarily affects the skin, nerves, and mucous membranes.
- Clinical presentation ranges from tuberculoid leprosy with few lesions and intact immunity, to lepromatous leprosy with widespread lesions and impaired immunity. The Ridley-Jopling classification further categorizes types of leprosy.
- Diagnosis involves examination of skin and nerve lesions along with bacterial index testing. The Mitsuda reaction skin test assesses host immunity and prognosis.
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Do you know Mycoacterium leprae cannot e cultured in normal medium? Do you know leprosy is one of the least contagious diseases? To know more interesting facts see the slide
Do you know Mycoacterium leprae cannot e cultured in normal medium? Do you know leprosy is one of the least contagious diseases? To know more interesting facts see the slide
This ppt contains all the information about the Epidemiology of leprosy. It is useful for students of the medical field learning Preventive and social medicine, Swasthavritta (Ayurved), and everyone who is interested in knowing about it
"A Study of Clinical Profile of Leprosy in Post Leprosy Elimination Era"iosrjce
IOSR Journal of Dental and Medical Sciences is one of the speciality Journal in Dental Science and Medical Science published by International Organization of Scientific Research (IOSR). The Journal publishes papers of the highest scientific merit and widest possible scope work in all areas related to medical and dental science. The Journal welcome review articles, leading medical and clinical research articles, technical notes, case reports and others.
Mycobacterium is a genus of Actinobacteria, given its own family, the Mycobacteriaceae. Over 190 species are recognized in this genus. This genus includes pathogens known to cause serious diseases in mammals, including tuberculosis (Mycobacterium tuberculosis) and leprosy (Mycobacterium leprae) in humans.
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Mycobacterium leprae
1. Dr. V. S. Vatkar
Asso Prof,
Microbiology Department
2. * Causative agent of Leprosy
* Vedic times (Kustha Roga) in
Sushruta Samhita and Biblical
times in Middle East and
Hippocrates,460 BC
* G H Armauer Hansen
(1873)in Norway
* Not possible to cultivate the
bacillus in culture media
3.
4. * Straight or slightly curved rod
* 1- 8µm 0.2- 0.5µmˣ
* obligate intracellular pathogen
* Gram positive, less acid fast : 5% H2SO4
* Glia: bacilli bounded together by lipid like
substance : ‘Cigar bundle’ appearance
* Globi : masses of glia are known as globi
*Strict aerobe
5. * Virchow’s cells : cigar bundle of
bacilli inside lipid laden macrophages
*Undifferentiated histiocytes / foamy
cells
* Morphological index: % of uniformly
stained bacilli in tissue : method of
assessing pt’s progress who is on
chemotherapy.
* Bacteriological index : no of bacilli in
a tissue
6. * ICRC (Indian Cancer Research
Centre),Bombay (1962) : AFB isolated
from leprosy pts employing human
foetal spinal ganglion cell culture
* Shephard ( 1960) : Lepra bacilli can
multiply in footpads of mice at 20 C
with development of granuloma in 1-6
mnths
7. * Thymectomy done to inhibit CMI or
administration of antilymphocyte
serum, generalized inf is produced
stimulating Lepromatous Leprosy
* Nine banded armadilo : highly
susceptible, generalised inf with
lepromatous leprosy
* Natural ds seen in Chimpanzees in
west Africa
* Generation time : 12-13 days
9. * Warm climate : 9-16 days
* Moist soil : 46 days
* Direct sunlight : 2 hours
* UVL : 30 mins.
10. *Leprosy is a chronic granulomatous
disease of humans, involving the skin,
peripheral nerves, nasal mucosa and
any organ of the body
11. *Believed to be highly contagious ds
*Due to fear, ignorance, superstitious
beliefs and deformities –
disfigurements causes social stigma
*Pts were considered UNCLEANE &
out casted
*Today early diagnosis & effective
treatment- deformities can be
prevented
12. *Incubation period:
*3-5yrs (vary between 2 & 40
yrs)
*Due to longer generation time
*Lepromatous leprosy has longer
generation time than
tuberculoid type
16. *Low host resistance
*Large no Bacilli seen and globi seen
inside the macrophage
*superficial nodules – (Lepromata) :
contain granulation tissue and vacuolated
cells , Lesions on face : LEONINE face
*Nodules ulcerate, sec.infection,
distortion and mutilation
*Bacilli invade the mucosa of the nose,
mouth & URT : bacilli shed in nasal &
oral secretions
17. *Nerve involvement : Very LATE
*RES, Eyes, Kidneys,testes,bones
*Bacillemia : common
*Humoral immune response broad & CMI
deficient, poor prognosis
*Antibodies in high titre against mycobacteria
and Autoantibodies : common
*Biological false positive reaction +ve
*Lepromin test : negative
20. * scanty bacilli in the lesions
*Few skin lesions : Sharply demarcated,
annular macular hypoigmented
anaesthetic pathes, Deformities in
hands and feet
* Early neural involvement: common
nerve : ULNAR nr & Post-auricular nr
(enlarged & thickened)
* Medial popliteal nr: never involved
21. * Scanty bacilli in lesions
* Min. infectivity
* CMI adequate
* Lepromin test: positive
* Antimycobacterial antibodies - rare
* Autoantibodies – rare
* Good prognosis
24. * Possess characteristics of TL and LL
* May shift to any one depending on
chemotherapy or alterations in host
resistance
25. * Unstable : tissue reaction: no
characteristics of either LL or TT type
*One or two Hypopigmented patches &
definite sensory impairment
*Lesions : bacteriologically negative
* Spontaneous healing
* Some may progress to TT / LL
26. * Humans : only source of inf (TL or LL)
* Mode of entry : RT or thr’ skin
* Asymptomatic inf quite common in
endemic areas
* bacilli continue to shed from nose &
skin for 2-3 yrs before S/S of ds seen in
pt
* Not highly communicable ds
* I P : 2-5 yrs, as long as 30 yrs
27. *Direct contact: person to person
*Indirect contact: infected soil,
fomites (cloths & linens)
*Direct dermal inoculation during
tattooing
*Environmental factors: rural areas,
moist soil, humidity, over crowding
*Males affected twice common than
females
28. * High degree of innate
immunity exists in human
beings
* Humoral & CMI
* Humoral Ab do not have
harmful effects on lepra
bacilli
29. * Capable of destroying the
bacilli
* Phagocytose the bacilli
* Sp.humoral antibodies absent
* Ig levels same
* Alb: Glob ratio is same
* Deficiency of CMI : deve LL
30. * No deleterious effect on the bacilli
* Delayed hypersensitivity is absent
* Macrophages phagocytose the bacilli
but do not kill them
* Grow inside the cell
32. *People with low CMI: LL
*Delayed type of hypersensitivity: to lepra Ag
*Virchow’s Lepra Cell: macrophages unable to kill
intracellular bacilli but bacilli proliferate inside the
cells
*Ag Specific: CMI deficient in LL pts, not susceptible
to any opportunistic infections
*CD4 & CD8 ratio: reverse (1:2) in LL, CD8 cells are
prominent in circulation & in granulomas
*Prominent T2H response: in LL pts: T2H specific
cytokines: IL4,IL5, IL6 & IL10 leads to exaggerated Ab
response so auto Ab common, False +ve VDRL test
33. *DTH response: lepromine test positive
*CMI intact , prominent T1H response:
release of T1H specific cytokines like
IL2, INF-γ which activates
macrophages
*CD4 & CD8 ratio: Normal, CD4 cells:
seen in circulation & in granulomas
* Normal humoral response
34. *Deformities: 25% untreated cases develop deformities,
may due to
*Nerve injury: ms weakness, paralysis
*Facial deformities or loss of eyebrows
*Infection or injury (ulcers)
*Common deformities:
*Face Leonine facies, sagging face, saddle nose & corneal
opasity
*Hands: claw hand , wrist drop
*Feet: foot drop, clawing of toes, inversion of foot &
planter ulcers
35. *Type I : Lepra reaction
- In borderline
- Pts.on chemotherapy
- Influx of lymphocytes in lesion
- Shift to tuberloid morphology
- Erythema & swelling
-Pain & tenderness
- CMI deficient : lesion may shift to Lpromatous pattern
36. *Type II ( Erythema
Nodosum Leprosum)
*In LL & BL
*With few mnths. chemotherapy
*Tender, inflammed subcut. nodules
appear with fever, lymphadenopathy
*Arthur type response
*Dead cells
37. *Mitsuda in 1919
*Skin test: delayed type of
hypersensitivity test
*Ag lepromin : boiled,emulsified
lepromatous tissue rich in lepra bacilli
, intradermal injection of lepromin
38. Biphasic reaction :
1. Fernandez reaction: erythema &
induration
In 24-48 hrs and stays for 3-5 days
analogous to TT
2. Mitsuda reaction
Late reaction in 1-2 wks.
Peak in 1-4 wks. And then subsides,
indurated nodule which may ulcerate
39. *Modern Ag – standardized
*Lepra bacillus content is 4 10 7ˣ
Lbac./ml
*Std. lepromins from armadillo
40. *Classify lesions of leprosy pts
*Assess prognosis & treatment
*Assess resistance of individuals
to leprosy
41. *Tuberculoid leprosy.
*Indicates a good prognosis.
*Indicates resistance to
leprosy.
*Conversion of negative
reaction to positive reaction is
the evidence of improvement.
43. *Specimen from nasal mucosa,skin
lesions and ear lobules
*Internal septum
*From 5-6 different areas
*Z-N staining
44. *1-10 bacilli in 100 fields = 1 +
*1-10 bacilli in 10 fields = 2 +
*1-10 bacilli in 1 field = 3 +
*1-100 bacilli per field = 4 +
*1-1000 bacilli in per field = 5 +
*More than 1000 bacilli,clumps and globi
in every field is 6 +
45. *BI = Totaling no.of bacilli (live or
dead) seen /oil immersion field
total No.of smears examined
Min 4 skin lesions, a nasal swab, both the
ear lobes have to be examined
46. *Dapsone 100 mg + rifampicin 600
mg for 6 months ( for TT & BT)
Dapsone 100 mg
Rifampicin 600 mg for 2 years
Clofazime 50 mg
50. *Chorioallantoic membrane of fertile hen’s egg.
*Tissue culture of rat fibroblast origin.
*Growth appears in 8 – 12 days.
*DNA study show no relation to M.leprae.