acid fast bacilli
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ACID FAST BACILLI
Mycobacterium leprae
First discovered by Norwegian Microbiologist Gerhard Hansen 1873
The leprosy bacillus
Hansen’s bacillus
strict parasite(doesn’t grow in artificial media )
The slowest growing specie of Mycobacteria
morphology & staining characteristics similar with M.tuberculosis
Causes a disease which is known from ancient times because of its sever disfigurement
It was known as a divine curse
Mycobacterium leprae
Mycobacterium leprae
Non spore and capsule forming
Non motile
Staining ( acid alcohol fast )
Ziehl Nielsen Stain
Resistant many years in human dead body
Mycobacterium leprae
Mycobacterium leprae
Epidemiology and transmission- word wide disease - Not restricted to warm climate - 500,000 to 1000,000 cases (mostly
in Asia, Africa. Central and southAmerica and pacific Islands)
- In USA 300 to 500 people per year
Mycobacterium leprae
Transmission
Directly inoculation into skin and mucus membrane through contact with leprotics
Mechanical vectors
Inhalation of droplets
Mycobacterium leprae
Humans are the most important reservoir host of leprosy
Armadillos are the only animal which can harbor a spice of mycobacteria genetically identical to M.leprae
A new zoonotic disease
Mycobacterium leprae
Mycobacterium leprae
Factors influence susceptibility to leprosy- living and health condition - weakness of immunity system( defects in
the regulation of T- cells )- genetic factors - long term household contact with
leprotics- poor hygiene - poor nutrition & crowded conditions
Mycobacterium leprae
Pathogenicity Not highly virulent
Chronic disease
Macrophages destroy bacilli mostly
4 – 12% It develops intracellular in macrophages (weakned and slow response of T- cells ) ١٢
Mycobacterium leprae
Acid fast bacilli
Strict human pathogens
Cannot be cultivated in-vitro
Armadillo’s used for obtaining M leprae
Transmission - ? Air borne
Low infectivity - prolonged contact required
Spectrum of clinical presentations dependent on host –parasite interactions
Tuberculoid BorderlineTuberculoid
Borderline lepromatous
Lepromatous
Mycobacterium leprae
Usual incubation period 2-5 years Varies from 3 months to 40 years Small spotty colored lesions on the skin of
trunks and extremities Infects skin macrophages and schwann cells
of peripheral nerves
Mycobacterium leprae
Progress of M.leprae causes three types of leprosy :
Tuberculoid leprosy
Lepromatous leprosy
Borderline leprosy
Mycobacterium leprae
Tuberculoid leprosy Superficial form of leprosy Asymmetrical shallow skin lesions Destroying of PNS filaments Anesthesia and local paralysis Lesions appear as thin granulomas with
enlarge dermal nerves Loss of pain reception and feeling Easily treated
Tuberculoid leprosy
Mycobacterium leprae
lepromatous leprosy Disfiguration of skin (face,ears …)
It is marked by chronicity and severcomplications
Widespread disseminations
Primarily grow in macrophages ofcooler regions including nose ,ears,eyebrows, chin & testes
Mycobacterium leprae
Face of afflicted person folds and granulomous thickenings called lepromas
Lepromas are caused by massive intracellular overgrowth of M.leprae
Loss of sensitivity
Advanced LL predisposes patient to trauma and mutilation ,secondary infections, blindness and kidney and respiratory failure
Mycobacterium leprae
Mycobacterium leprae
Mycobacterium leprae
borderline leprosy intermediate form of leprosy Depends to treatment and immunologic competence Can be changed to TL and LL Damage to nerves that control muscles of hand and
feet Subsequent wasting of muscles and loss of control
produces drop foot and claw hand Trauma ,loss of fingers and toes
Mycobacterium leprae
Diagnosis Symptomology,Microscopic examination of
lesions ,and patient history Feather test Numbness in the hands and feet, loss of heat
and cold sensitivity ,muscle weakness, thickened earlobes and chronic stuffy nose
Mycobacterium leprae
Lab diagnosis
Detection of acid fast bacilli (ZiehlNielsen) in smears of skin lesion Lepromin test
Mycobacterium leprae
Treatment and prevention
Therapy is effective in the early stage
Multiple drug therapy is necessary because of increase of resistant strains
Tuberculoid leprosy
Rifampin +Dopsone for 6 months
Mycobacterium leprae
Lepromatous leprosy
Rifampine,dapsone and clofazimine 2years
Dopsone for an indeterminate period oftime (more than 10 years )
Mycobacterium leprae
Prophylaxis and control
1 Constant surveillance of population
2 Chemoprophylaxis of healthy persons in
close contact with leprotics
3 Isolation of leprosy patients
Mycobacterium leprae
Non tuberculous mycobacteria
M avium complex(MAC)M avium complex(MAC)
M avium intracellulareM avium intracellulare
severe RTIsevere GI infectionsepticaemia
Infection of cervical lymph nodesPresents as cervical lymphadenopathyTreatment – surgery
Immuno competent hostImmuno competent host
Immuno deficient hostImmuno deficient host
AIDS
Non tuberculous mycobacteria
M ulceransM ulcerans
M fortuitum / M cheloneiM fortuitum / M chelonei
Injection related abscessesAssociated with sternal wound infections
following cardio-thoracic surgery
‘Burundi’ ulcer Prolonged incubation required for growth
Non tuberculous mycobacteria
M KANSASIIM KANSASII
Infection of respiratory compromised hostsPresent like pulmonary tuberculosisTreatment – resistant to anti TB drugs
M SCROFULACEUMM SCROFULACEUM
Infection of cervical lymph nodesPresents as cervical lymphadenopathy
Treatment – surgery