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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.
