Ocular leprosy is a systemic disease caused by Mycobacterium leprae that commonly involves the eyes through hematogenous spread, resulting in uveitis. It has a prevalence of 1 in 1000 people and can cause blindness in 5-10% of ocular leprosy patients. The disease is classified into 6 types based on bacterial load and immune response. It primarily spreads through droplets from the nose but can also spread through soil, insects, or armadillos. Ocular manifestations include eyelid abnormalities, dacryocystitis, conjunctivitis, keratitis, uveitis, retinal lesions, and cranial nerve palsies. Risk factors for vision loss include multibacillary le

1. OCULAR LEPROSY
P R E S E N T E R : D R . I D D I N D YA B AW E
M O D U L ATO R : D R . A M PA I R E A N N E
M AY 2 0 2 1

2. LECTURE OUTLINE
• Introduction
• Etiology
• Classification of leprosy
• Transmission
• Ocular features
• Complications
• Diagnosis
• Lab investigations
• Management

3. INTRODUCTION
• a.k.a Hansen disease.
• Leprosy is a systemic disease with ocular involvement (most commonly uveitis)
resulting from hematogenous dissemination to the eye
• Prevalence: 1 case per 1000 population
• 5-10% of patients with ocular leprosy are blind
• Ocular involvement in leprosy: 70-75%

4. ETIOLOGY
• Mycobacterium leprae: obligate intracellular aerobic bacilli
• Spread from human-to-human contact
• Acid-fast due to mycolic acid
• M.leprae favour cooler parts of the body e.g skin.

5. 6 CLASSES OF LEPROSY
• Indeterminate
• Tuberculoid
• Borderline tuberculoid
• Borderline
• Borderline lepromatous
• Lepromatous

6. SPREAD
• Mode of transmission: unclear
• Risk factors: over crowding, poverty, poor hygiene
• Route of spread:
-Person to person spread by nasal droplet infection (commonest)
-Soil contamination
-Insect vectors
-Contact with infected armadillos

7. MODES OF INFECTION
• Direct invasion of M.leprae in eyes and surrounding tissues
• Inflammatory lesions: sensitization of ocular tissues to M.leprae antigens, formation of
intravascular immune complexes
• Granulomatous infiltration of CN5 and 7
• Granulomatous infiltration of contiguous structures: eyebrows, eyelids, lid glands,
lacrimal drainage system.
• Secondary infections can also play a role

8. ANALOGY!
Paucibacillary (tuberculoid spectrum)
• 5 lesions and less
• Only ONE nerve trunk is enlarged
• Negative slit skin smear (SSS)
• Asymmetrical
Multibacillary (lepromatous spectrum)
• >5 lesions
• Many nerve trunks are enlarged
• Positive slit skin smear (SSS)
• Symmetrical

9. OCULAR FEATURES OF LEPROSY
• Eyelid and lacrimal glands:
• Eyelid: madarosis, trichiasis, distichiasis, entropion, ectropion, leromatous nodules,
lagophthalmos
• Lacrimal system: dacryocystitis and NLDO, chronic dacroadenitis, DES
• Conjuctiva: chronic conjunctivitis; episcleral nodules (cardinal sign)
• Cornea and sclera: interstitial keratitis, exposure keratopathy (CN 7 palsy), neurotrophic
keratopathy, band keratopathy, corneal opacities, corneal anaesthesia, thickened
nerves, pannus and scarring (corneal pearls), episcleritis and scleritis

10. .
• Dacryocystitis • Erythema nodosum leprae

11. .
• Pannus and scarring

12. SEQUELA OF THE SCLERITIS…

13. INTRAOCULAR
• Granulomatous uveitis: iris atrophy, iris pearls, nodular iris leproma (erythema
nodosum leprosum)
• Pupils:
-Occlusio/seclusion pupillae
-Correctopia, polycoria
-Miosis (sympathetic nerves are preferentially involved)
-Anisocoria, decreased response to light
• Ciliary body: hypotonia, phthisis bulbi
• Cataract, glaucoma

14. NEURO-OPHTHALMIC
• Optic neuritis
• CN palsies
CHOROID AND RETINA:
• Choroidal lepromas
• Retinal scarring and retinal vessels sheathing and fibrosis
• Retinal detachment
• Papillitis

15. WHAT ARE THE POSSIBLE MECHANISMS
OF PANNUS AND SCARRING?
• Lid lesions
• Interstitial keratitis
• Exposure keratopathy
• Neurotrophic keratopathy
• Secondary infective keratitis

16. COMPLICATIONS
• Glaucoma and cataract
• Madarosis, trichiasis
• Corneal hypoesthesia
• Facial nerve palsy with lagopthalmos
• Beading of corneal nerves, scleritis, epiphora

17. DIAGNOSIS
• Based on morphological characteristics
• Lepra bacilli demonstrated from lacrimal fluid and/or conjunctival scrapping is
supplementary
HISTOPATHOLOGY:
• Skin biopsy: numerous acid-fast bacilli which may form clumps called globi
LAB INVESTIGATIONS:
• Microscopic evaluation of tissues
• Lepromin-intradermal skin test: uses killed M.leprae. Not diagnostic. Distinguishes
tuberculoid from lepromatous patients
• Fernandez reaction (induration detectable at 24-48 hours): indicates delayed-type
hypersensitivity to M. leprae

18. MANAGEMENT
• Frequent washing with clean water (boiled and cooled)
• Local antibiotics
• Rest to the eye
• Refer if it doesn’t improve in 48 hours

19. TREATMENT OF LEPROSY -ADULTS
Drugs used
(adults)
Dosage Freq of admin Criteria
MB leprosy Rifampicin 600mg Once monthly Completion of
Dapsone 100mg Daily 12 monthly pulses
Clofazimine 300mg Once monthly
Clofazimine 50mg Daily
PB leprosy Rifampicin 600mg Once monthly Completion of
Dapsone 100mg Daily 6 monthly pulses

20. TREATMENT OF LEPROSY - CHILDREN
(10-14 YEARS OF AGE)
Drugs used Dosage Frequency of
admin
Criteria
MB leprosy Rifampicin 450mg Once monthly Completion of
Dapsone 50mg Daily once 12 monthly pulses
Clofazimine 150mg Monthly
Clofazimine 50mg Every other day
PB leprosy Rifampicin 450mg Once monthly Completion of
Dapsone 50mg Daily 6 monthly pulses

21. TREATMENT OF CHILDREN <10 YEARS
• Rifampicin: 10mg per kilogram
• Clofazimine: 6mg per kilogram monthly and 1mg per kilogram per body weight daily
• Dapsone: 2mg per kilogram body weight daily

22. RISK FACTORS FOR THE SEVERE VISUAL
IMPAIRMENT IN LEPROSY PATIENTS:
• Multibacillary Leprosy
• Active disease for more than 10 years
• Type 2 immune reactions, with or without iritis
• Facial skin lesion or large facial skin infiltration
• Lagophthalmos
• Corneal hypoesthesia or anesthesia
• Scleritis
• Patients with only one eye or vision severely reduced to begin with
• Coexisting diseases like diabetes or glaucoma

23. REFERENCES
• Yanoff M, Duker Jay S. Ophthalmology. 3rd edition. Mosby Elsevier; 2008
• WHO Leprosy Today, 2014: www.who.int/lep
• WONG
• Leprosy Fact Sheet; WHO, 2017:
http://www.searo.who.int/entity/global_leprosy_programme/topics/factsheet/en/
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• Ffytche TJ, McDougall AC. Leprosy and the eye: a review. J R Soc Med. 1985; 78(5): 397–400
• Kanski J, Bowling B. Clinical Ophthalmology - A Systematic Approach. 7th ed. Mosby
Elsevier; 2011
• M Hogeweg, JE Keunen. Prevention of blindness in leprosy and the role of the Vision 2020
Programme. Eye. 2005: 19, 1099–1105.
• KM Waddell, PR Saunderson. Is leprosy blindness avoidable? The effect of disease type,
duration, and treatment on eye damage from leprosy in Uganda. BJO 1995; 79: 250-256
• International Centre for Eye Health, London School of Hygiene & Tropical Medicine.
Leprosy and the eye. Comm Eye Health - teaching set, 2010
• KJ Thompson et al. Patterns of ocular morbidity and blindness in leprosy – a three centre
study in Eastern India. Lepr Rev. 2006: 77, 130 – 140