SN4 SHORT NOTE 5M ★ High-yield

Describe the pathology of leprosy. Differentiate tuberculoid from lepromatous leprosy.

Pathology · 2nd Professional — Para-Clinical

Definition

Leprosy (Hansen disease) is a chronic granulomatous infection caused by Mycobacterium leprae, an acid-fast bacillus with a special affinity for schwann cells of peripheral nerves and for the skin.

Cannot be cultured in vitro; grown in the armadillo and the mouse footpad
Prefers cooler parts of the body — skin, superficial nerves, nose, testis, eye — which determines the whole clinical picture
Generation time about 12–14 days, the slowest of all bacteria; incubation is 2–5 years or more
India accounts for more than half the world's new cases, so this remains an important subject despite elimination as a public health problem

The Spectrum of Disease

Feature	Tuberculoid (TT)	Lepromatous (LL)
Cell-mediated immunity	Good	Poor or absent
Lepromin test	Positive	Negative
Bacillary load	Paucibacillary — few or no bacilli	Multibacillary — abundant bacilli in globi
Skin lesions	Few, large, well-defined, dry, anaesthetic, hypopigmented	Many, symmetrical, poorly defined, shiny; sensation preserved until late
Nerve involvement	Early, severe, asymmetrical; nerves thickened	Late, symmetrical, "glove and stocking"
Histology	Epithelioid granulomas with Langhans giant cells; nerve destroyed	Sheets of foamy macrophages (lepra or virchow cells) laden with bacilli; a clear GRENZ zone beneath the epidermis
T cell response	TH1, IFN-gamma	TH2, IL-4 and IL-10
Infectivity	Low	High
Course	May heal spontaneously	Progressive; facies leonina, saddle nose, loss of eyebrows

Borderline forms (BT, BB, BL) lie between the two poles and are immunologically unstable, which is why they are the ones that develop reactions

CLINICAL PEARL

Leprosy is the classic demonstration that the host, not the organism, determines the disease. The same bacillus produces a paucibacillary, granulomatous, nerve-destroying illness in a person with good cell-mediated immunity, and a multibacillary, diffusely infiltrative one in a person without it. The tissue damage in tuberculoid leprosy is caused by the immune response itself.

Lepra Reactions

Feature	Type 1 (reversal)	Type 2 (erythema nodosum leprosum)
Mechanism	Type IV (cell-mediated) hypersensitivity	Type III — immune complex deposition
Occurs in	Borderline forms	Lepromatous and borderline lepromatous
Features	Existing lesions become red, swollen and tender; acute neuritis with rapid nerve damage	Crops of tender subcutaneous nodules, fever, arthritis, iritis, orchitis
Treatment	Corticosteroids	Thalidomide or corticosteroids

Reactions are medical emergencies, because irreversible nerve damage and deformity occur within days if untreated

Diagnosis

The cardinal signs — a hypopigmented or reddish patch with definite loss of sensation, a thickened peripheral nerve, or acid-fast bacilli in a slit-skin smear. Any one is sufficient
Slit-skin smear stained by a modified Ziehl–Neelsen (Fite) method; graded by the bacteriological index
Nerves commonly thickened — ulnar at the elbow, common peroneal at the fibular neck, great auricular, posterior tibial
Skin biopsy for histology where the diagnosis is uncertain

Applied Aspects

Multidrug therapy — rifampicin, dapsone and clofazimine; 6 months for paucibacillary and 12 months for multibacillary disease. It is provided free in India
Deformity is caused by nerve damage, not by the bacillus — claw hand, foot drop, lagophthalmos and trophic ulcers all follow anaesthesia and paralysis
Trophic ulceration of the anaesthetic foot is the commonest cause of disability; prevented entirely by protective footwear and daily self-examination
Patients are non-infectious within days of starting rifampicin, which is the single most useful fact for countering stigma
Stigma remains the greatest obstacle to early presentation in India, and late presentation is why deformity persists

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