"Hansen's Disease" — Practice

Question 1

Which of the following alone establishes a diagnosis of leprosy?

Accepted Answer

B

Question 2

The commonest peripheral nerve involved in leprosy is the

Accepted Answer

C

Question 3

A 26-year-old has a single well-defined hypopigmented patch with a raised margin, complete sensory loss within it, and a thickened ipsilateral ulnar nerve. Slit-skin smear is negative. Classify and treat.

Accepted Answer

On the Ridley-Jopling spectrum this is tuberculoid or borderline tuberculoid disease, indicated by a single asymmetric well-defined lesion with a negative smear, which reflects strong cell-mediated immunity.

For treatment purposes it is paucibacillary disease, being one to five lesions with a negative smear, so he receives the uniform three-drug regimen of rifampicin, clofazimine and dapsone for six months.

The thickened ulnar nerve requires the closest follow-up. Tuberculoid disease damages nerves early and severely despite having almost no bacilli, because the vigorous granulomatous response destroys the nerve it is defending.

Question 4

A patient two months into multibacillary treatment develops fever, crops of tender red nodules over the limbs, painful eyes and testicular pain. What is this, and should treatment be stopped?

Accepted Answer

Type 2 reaction, erythema nodosum leprosum, an immune complex mediated systemic event occurring in patients with a high bacterial load. The systemic features of fever, iritis and orchitis distinguish it from a type 1 reaction, which is largely confined to existing skin lesions and nerves.

Antileprosy treatment must not be stopped. A reaction is an immunological event rather than treatment failure, and stopping the drugs allows bacterial multiplication to resume while doing nothing for the inflammation.

Severe ENL is treated with corticosteroids, with thalidomide the most effective agent since tumour necrosis factor alpha is central to the pathogenesis, subject to absolute precautions against pregnancy.

Question 5

India declared elimination of leprosy as a public health problem in 2005 yet still reports over 100,000 new cases a year. Explain the apparent contradiction.

Accepted Answer

Elimination was defined as reducing registered prevalence below one case per 10,000 population, and prevalence is a stock measure that falls whenever treatment duration shortens, since patients leave the register sooner. It does not directly measure transmission.

The annual new case detection rate measures incidence and has plateaued rather than fallen since 2005, which means new infections are still occurring at a steady rate. India accounts for roughly 60 per cent of global new cases, and the burden is very unevenly distributed, with around 80 districts exceeding 20 new cases per 100,000. This is why programme indicators have shifted toward grade 2 disability rate, which reflects delay in diagnosis, and toward contact tracing with single-dose rifampicin prophylaxis, which targets transmission directly.

Question 6

Explain why a tuberculoid patient with almost no demonstrable bacilli suffers worse nerve damage than a lepromatous patient teeming with them.

Accepted Answer

Because in leprosy the immune response, not the bacillus, causes the tissue injury.

In tuberculoid disease cell-mediated immunity is vigorous, and the granulomatous inflammation mounted against a handful of organisms sheltering within Schwann cells destroys the nerve in the process of containing them. The result is early, severe damage confined to a small number of nerves, with correspondingly few bacilli on smear.

In lepromatous disease cell-mediated immunity is absent, so bacilli multiply almost unopposed but provoke little inflammatory response. Nerve damage there is caused by sheer bacterial load, appears later, and is widespread but more gradual.

The same logic explains why the borderline groups, whose immunity is unstable, are the ones that react, and why reactions rather than infection account for most disability.

Question 7

A patient who completed treatment two years ago presents with new weakness of foot dorsiflexion over ten days and is reassured that he is cured. Comment.

Accepted Answer

The reassurance is wrong and the delay is harmful. Reactions occur before, during and after completion of treatment, and bacteriological cure does not prevent immunological events.

A new motor deficit indicates acute neuritis, most likely a type 1 reversal reaction affecting the common peroneal nerve, which is superficial at the fibular neck and a characteristic site.

This is urgent because nerve function impairment treated within about six months of onset has a substantially better prospect of recovery than impairment treated later, and every week of delay reduces the chance of regaining dorsiflexion. He needs systemic corticosteroids with a slow taper, splinting to prevent contracture and footwear modification, and documented serial assessment of nerve function to judge response.

Question 8

A patient with a healed plantar ulcer returns with a new deep ulcer under the same metatarsal head, having taken his medication faithfully. What has gone wrong?

Accepted Answer

Nothing has gone wrong with the antibacterial treatment, which is precisely the point.

He has posterior tibial nerve damage giving an anaesthetic sole, so he continues to walk normally on a foot that cannot report injury, and repetitive pressure at the metatarsal head breaks the skin without pain to warn him. Autonomic loss compounds it, since absent sweating leaves the skin dry and fissured.

Antileprosy drugs do not restore sensation and therefore cannot interrupt this cycle. What prevents it is self-care: daily inspection of the feet for injuries he cannot feel, soaking and oiling of dry skin, protective footwear with a moulded insole to redistribute pressure away from the metatarsal head, and immediate rest of any ulcer until healed. Without that, the sequence runs to secondary infection, osteomyelitis and a shortened deformed foot.

Question 9

A patient presents with progressive weakness and sensory loss in an ulnar distribution with a palpably thickened nerve, but has no skin lesion at all. Repeated skin examination is normal. What should be considered?

Accepted Answer

Pure neuritic leprosy, in which nerve involvement occurs without any skin lesion. It is reported far more frequently from India than from most other settings, and it is missed precisely because clinicians search for a patch and conclude that its absence excludes the diagnosis.

The diagnosis rests on the second cardinal sign, a thickened peripheral nerve with sensory loss or weakness in its distribution, which is sufficient on its own. Careful palpation of all accessible nerve trunks and systematic sensory mapping establish it, and nerve biopsy or fine needle aspiration cytology of the nerve may be used where doubt persists.

The practical importance is that these patients present with established nerve damage rather than with a visible lesion, so they are diagnosed late and carry a high burden of disability, and they require the same multidrug therapy plus close monitoring for reactions.

Practice — "Hansen's Disease"

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