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