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BY
ASLAM MATANIA
GROUP-3
FACULTY OF MEDICINE
TSMU
MYCOBACERIUM LEPRAE
INTRODUCTION
 IT IS A GRAM POSITIVE ORGANISM
CAUSING LEPROSY OR HANSEN’S
DISEASE.
 IT IS NON-MOTILE, NON-SPORING,
ACID FAST BACILLI WHICH IS MAINLY
RESPONSIBLE FOR CAUSING DAMAGE
TO NERVES.
– this organism was
described by Hansen
in 1873
–it has not been
cultivated on
nonliving
bacteriologic media
– There are more than
10 million cases of
leprosy, mainly in
Asia
Armauer Hansen in 1873
Cultivation
• No artificial media / tissue
culture available.
• Mouse :
• intradermaly inoculated into
FOOT PADS and develop
local granulomatous lesions
with limited multiplication of
bacilli
• . Inoculated armadillos
develop extensive
lepromatous leprosy
Epidemiology
• Without prophylaxis, about 10% of exposed children
may acquire the disease
• The incubation period is probably 2–10 years.
• The naturally infected armadillos found in Texas and
Mexico probably play no role in transmission of
leprosy to humans.
Pathogenesis
• Source : Nasal or Skin
• discharges from lesion.
Portal of entry: Damaged
• skin -Inoculation.
Nasal mucosa- Inhalation
• MOST OF THE DAMAGE DONE
IS BY ENTERING THE NERVES,
MAINLY SPINAL NERVES AND
CAUSE DAMAGE TO THEM.
• IT LEADS TO LOSS OF
SENSATION OF TOUCH, PAIN,
TEMPERATURE.
• IT LEADS TO WHITE PATCHES ON THE SKIN WHICH
ARISE DUE TO LOSS OF PIGMENTATION FROM SKIN.
• IF THIS DISEASE STARTS DETERIORATING , NODES
APPEAR ON THE SKIN WHICH CONTAINS BUNDLES OF
BACTERIA, SLOWLY IT DISSESEMINATES INTO THE
COMPLETE BODY AND CAUSES FORMATION OF “
GRANULOMA”
• THIS GRANULOMA IS DIFFERENT FROM TUBERCLE
GRANULOMA DUE TO ABSENCE OF CENTRAL
CASEIATING NECROSIS.
STAGES OF LEPROSY
• The disease is divided into two
major types, lepromatous and
tuberculoid, with several
intermediate stages
Tuberculoid leprosy
•Lesions are
large maculae on skin,
superficial nerve
endings.
•CMI is intact.
•Low infectivity
Lepromatous leprosy
• Extensive
maculae,
papules or
nodules;
Extensive
destruction of skin.
•CMI severely depressed
•High infectivity
Regression
Progression
Generalized form with decreased CMI.
“Lepromata” : Granulation tissue
with plenty of vacuolated
cells
Ulceration
Secondary infection &
Mutilation of limbs.
Skin lesions are extensive and bilaterally
symmetrical.
Lepromatous leprosy
Face,ear lobules,hands and feet.
Symmetrical thickening of peripheral nerves &
anesthesia.
Bacilli invade mucosa of Nose , Mouth and
Respiratory tract → shed in secretions.
Bacteremia present.
Auto antibodies are produced.
Lateral part of eyebrows are lost.
Lepromatous leprosy Lepromatous leprosy
Localized form in individuals with
intact CMI.
Skin lesions :
Few hypo or hyper pigmented
macular patches.
Seen on Face, trunk and limbs.
Bacilli are scanty or absent.
Infectivity is low.
Tuberculoid leprosy
Lab. Diagnosis
• Specimens :
1. Scrapings from
Lesion ,Nasal mucosa.
Z-N staining.
Acid fast bacilli within
the undifferentiated
• Live bacilli : Solid, uniformly
stained.
• Dead bacilli :Fragmented
and granular.
• 2. Skin & Nerve biopsy.
• 3.Ear lobules ( Slit skin smear ).
• 5. Lepromin test : To know prognosis.
• Not for diagnosis.
• 6.Molecular diagnosis: Identifying DNA codes
for
• 65 & 18-kDa M.leprae proteins.
Treatment :
• Sulfones such as dapsone are first-line therapy for
both tuberculoid and lepromatous leprosy
• RMP or clofazimine generally is included in the initial
treatment regimens
• Other drugs active against M leprae include
minocycline, clarithromycin, and some
fluoroquinolones.

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Mycobacterium leprae by aslam matania

  • 1. BY ASLAM MATANIA GROUP-3 FACULTY OF MEDICINE TSMU MYCOBACERIUM LEPRAE
  • 2. INTRODUCTION  IT IS A GRAM POSITIVE ORGANISM CAUSING LEPROSY OR HANSEN’S DISEASE.  IT IS NON-MOTILE, NON-SPORING, ACID FAST BACILLI WHICH IS MAINLY RESPONSIBLE FOR CAUSING DAMAGE TO NERVES.
  • 3. – this organism was described by Hansen in 1873 –it has not been cultivated on nonliving bacteriologic media – There are more than 10 million cases of leprosy, mainly in Asia Armauer Hansen in 1873
  • 4. Cultivation • No artificial media / tissue culture available. • Mouse : • intradermaly inoculated into FOOT PADS and develop local granulomatous lesions with limited multiplication of bacilli • . Inoculated armadillos develop extensive lepromatous leprosy
  • 5. Epidemiology • Without prophylaxis, about 10% of exposed children may acquire the disease • The incubation period is probably 2–10 years. • The naturally infected armadillos found in Texas and Mexico probably play no role in transmission of leprosy to humans.
  • 6. Pathogenesis • Source : Nasal or Skin • discharges from lesion. Portal of entry: Damaged • skin -Inoculation. Nasal mucosa- Inhalation • MOST OF THE DAMAGE DONE IS BY ENTERING THE NERVES, MAINLY SPINAL NERVES AND CAUSE DAMAGE TO THEM. • IT LEADS TO LOSS OF SENSATION OF TOUCH, PAIN, TEMPERATURE.
  • 7. • IT LEADS TO WHITE PATCHES ON THE SKIN WHICH ARISE DUE TO LOSS OF PIGMENTATION FROM SKIN. • IF THIS DISEASE STARTS DETERIORATING , NODES APPEAR ON THE SKIN WHICH CONTAINS BUNDLES OF BACTERIA, SLOWLY IT DISSESEMINATES INTO THE COMPLETE BODY AND CAUSES FORMATION OF “ GRANULOMA” • THIS GRANULOMA IS DIFFERENT FROM TUBERCLE GRANULOMA DUE TO ABSENCE OF CENTRAL CASEIATING NECROSIS.
  • 8. STAGES OF LEPROSY • The disease is divided into two major types, lepromatous and tuberculoid, with several intermediate stages
  • 9. Tuberculoid leprosy •Lesions are large maculae on skin, superficial nerve endings. •CMI is intact. •Low infectivity Lepromatous leprosy • Extensive maculae, papules or nodules; Extensive destruction of skin. •CMI severely depressed •High infectivity Regression Progression
  • 10. Generalized form with decreased CMI. “Lepromata” : Granulation tissue with plenty of vacuolated cells Ulceration Secondary infection & Mutilation of limbs. Skin lesions are extensive and bilaterally symmetrical. Lepromatous leprosy
  • 11. Face,ear lobules,hands and feet. Symmetrical thickening of peripheral nerves & anesthesia. Bacilli invade mucosa of Nose , Mouth and Respiratory tract → shed in secretions. Bacteremia present. Auto antibodies are produced. Lateral part of eyebrows are lost.
  • 13. Localized form in individuals with intact CMI. Skin lesions : Few hypo or hyper pigmented macular patches. Seen on Face, trunk and limbs. Bacilli are scanty or absent. Infectivity is low. Tuberculoid leprosy
  • 14. Lab. Diagnosis • Specimens : 1. Scrapings from Lesion ,Nasal mucosa. Z-N staining. Acid fast bacilli within the undifferentiated • Live bacilli : Solid, uniformly stained. • Dead bacilli :Fragmented and granular.
  • 15. • 2. Skin & Nerve biopsy. • 3.Ear lobules ( Slit skin smear ). • 5. Lepromin test : To know prognosis. • Not for diagnosis. • 6.Molecular diagnosis: Identifying DNA codes for • 65 & 18-kDa M.leprae proteins.
  • 16. Treatment : • Sulfones such as dapsone are first-line therapy for both tuberculoid and lepromatous leprosy • RMP or clofazimine generally is included in the initial treatment regimens • Other drugs active against M leprae include minocycline, clarithromycin, and some fluoroquinolones.