Day 4 M Leprae 30mn.pdfgbbvcgbhhhgdghjjjjj

Day 4 M Leprae 30mn.pdf

1. Professor PonndaraITH,
MD, GS, MPH, PhD
Chair, Academic Board
Faculty of Medicine, UHS
Honorary Professor, Faculty of Health,
University of Technology Sydney (UTS), Australia
Mycobacterium Leprae
Medical Students, Year 4, Semester 1, 2022-2023

2. Learning outcomes
i.Epidemiology
ii.Bacteriology
iii.Mode of contamination and Pathogenesis
iv.Clinical aspects
v.Diagnostic
vi.Management
vii.Treatment and Prevention

3. I-Epidemiology
-The highest prevalence of leprosy are in tropical countries,
especially in Asia and Africa.
-Over 250, 000 new cases of leprosy have been reported
annually in recent years worldwide (WHO, 2009)
-The highest number of cases in the world is still found in
India, with Brazil ranking second.
-India alone accounts for 64 % of all new cases in the world.
-Children comprise 15,000 diagnosed cases within this
significant number
-Globally, 2 to 3 million individuals are living with Leprosy-
related disabilities.

4. II-Bacteriology
▪M.lepraeis an obligate, oxidative resistance,
intracellular acid fast bacillus aerobic and rod-
shaped, that can infect humans and other species
such as armadillos and primates.
▪Morphology and culture:
-Similarity to MT: Gram-Positive, an acid-fast
bacillus, structure and cell wall components
-Differences: Not grown in artificial media or
tissue but multiply when injected into the feet of mice

5. •Disease: Leprosy
•A chronic infectious disease or a chronic
granulomatous disease of the peripheral nerves
and superficial tissues, particularly the nasal
mucosa
•Disease ranges from slowly resolving anesthetic
skin lesion to the disfiguring facial lesions
responsible for the social stigma and ostracism of
the individuals with leprosy (lepers)

6. III-Mode of transmission and pathogenesis
A-Mode of transmission
-Unknown/uncertain.
-50% of patients have a history of intimate contact with
an infected person, commonly a household member
-Untreated lepromatous but not tuberculoid patients,
patients harbor a large numbers of M.lepraein the nasal
mucosa and its secretion.
-Organism is thought to be transmitted by nasal droplets

7. •The milder, tuberculoid form of leprosy is generally
considered noncontagious.
•However, infected soil and insect vectors (bedbugs,
mosquitos) play a role in disease propagation
•Incubation period: very long ranging rom 1 to 2 years to >40
years (average, 5-7 years),

8. B-Pathogenesis
▪Destruction of the nasal bones may lead to collapse of the nose
▪The eye is frequently damaged by direct bacillary invasion,
blindness is a common and tragic complication of untreated
leprosy

9. IV-Types and clinical spectrum
•Tuberculoid leprosy (TL)is at one pole of the spectrum.
✓These patients have one or a few hypopigmented,
hypoestheticmacule with well-defined borders.
✓Rashes in all forms of leprosy are nonpruritic
✓Peripheral nerves may be damaged and enlarged, are
generally asymmetric., and frequently are contiguous to
skin lesions.
•The first sign of leprosy is a non-specific or indeterminate
skin lesion, which is often healed spontaneously anaesthesia
and muscle paralysis

10. •Lepromatous leprosy (LL):is at the other pole of the
spectrum
✓Symmetric skin nodules or plaques loaded with acid-fast
bacilli (AFB) and often have distal peripheral neuropathy
✓Lack of immunity
✓Loss of eyelashes and eyebrows or even loss of body hairs
✓May develop erythema nodosum leprosum (ENL) and
those with diffuse lepromatosismay develop the Lucio’s
phenomenon, a serious reaction associated with
ulcerations (particularly of the legs) that often become
secondarily infected, resulting in bacteremia and death

11. •Borderline leprosy (BL)is in the middle of the spectrum
✓Patients have features of both polar forms
✓This type of leprosy is unstable and may downgrade
nearer the LL pole or may undergo a reversal reaction,
becoming more nearly TT

12. V-Diagnostic and laboratory findings
•History taking
•Based on clinical symptom
•Skin biopsy or nasal smear
•The clinical diagnosis may be confirmed by
•Histological examination of skin biopsies
•Microscopy

23. Lepromatous Leprosy (Early/Late Stages)

24. LepromatousLeprosy Pre-and Post-Treatment

25. Clinical Progression of Leprosy

26. VI-Management
▪Multidrug therapy (MDT): Dapsone, Rifampicin and,
Clofazimine is highly effective
▪National leprosy guideline management
▪Psychological and spiritual welfare

27. How can you prevent leprosy?

28. VII-Prevention
▪The most effective prevention in leprosy, as in tuberculosis,
is the early detection and treatment of infectious cases
▪No vaccines have been prepared for M.leprae.

29. VII-Prevention cont.’

30. Preventing leprosy at a household level
•Some diseases are highly infectious and require people to
quarantine even within their own homes, as we saw with
Covid-19. Leprosy is not one of those diseases.
•If you know that someone in your home has been diagnosed
with leprosy, this means they should have started treatment.
Leprosy is treated with three antibiotics known asMulti Drug
Therapyand once a person has started treatment, they are
no longer infectious and cannot spread the disease.

31. Preventing leprosy at a public health level
•Governments and leprosy NGOs such as the Leprosy Mission
are working in partnership in communities across the world
to distribute an antibiotic that can prevent leprosy.
•This antibiotic (Rifampicin) is being shared with people who
are at most risk of developing the disease. This approach is
known as apost exposure prophylaxis(or PEP for short). If
you are offered PEP, it is important that you take it as the
healthcare professional has explained.

32. References
David Greenwood, Richard Slack, John Peutherer, Mike
Barer. 2007. Medical Microbiology.7
th
ed.
Mark Gladwin, Bill Trattler, 1995 by Medmaster,Inc.
Clinical microbiology