SN7 SHORT NOTE 5M

Describe the drugs used in visceral leishmaniasis and the basis of the elimination programme in India.

Pharmacology · 2nd Professional — Para-Clinical

The Disease and the Challenge

Visceral leishmaniasis (kala-azar) is caused by Leishmania donovani, transmitted by the sandfly, and is characterised by fever, massive splenomegaly, pancytopenia and wasting; it is fatal if untreated.

India accounts for a substantial share of the global burden, concentrated in Bihar, Jharkhand, West Bengal and eastern Uttar Pradesh
The parasite lives inside macrophages, which is why drugs must reach the reticuloendothelial system — a property the lipid amphotericin formulations possess naturally
Post-kala-azar dermal leishmaniasis (PKDL) follows treatment in a proportion of patients and acts as a reservoir for transmission, so its detection and treatment are essential to elimination

Drugs

Drug	Route and regimen	Notes
Liposomal amphotericin B	Single intravenous dose of 10 mg/kg	First-line in India; cure rates above 95%; a single dose makes directly observed treatment feasible and is the foundation of the elimination programme. Requires cold chain and intravenous access
Miltefosine	Oral, 28 days	The first effective oral antileishmanial — a major advance for rural care. Causes vomiting and diarrhoea; teratogenic with a long half-life, so contraception is required for 3 months afterwards; resistance is emerging with monotherapy
Paromomycin	Intramuscular, 21 days	An aminoglycoside; cheap; ototoxic and hepatotoxic; used in combination regimens
Pentavalent antimonials (sodium stibogluconate)	Intramuscular or intravenous, 28–30 days	The historical standard, now abandoned in Bihar because of resistance exceeding 60%; cardiotoxic (QT prolongation, sudden death), pancreatitis, hepatotoxicity
Combination regimens	Single-dose liposomal amphotericin with miltefosine or paromomycin	Shorten treatment, reduce cost and protect against resistance

CLINICAL PEARL

Antimonial resistance in Bihar is the clearest case study of how resistance destroys a drug regionally. Decades of unsupervised, incomplete and underdosed treatment in the private sector selected resistance until cure rates fell below 40%, while the same drug still worked elsewhere in the world. The lesson is that resistance is created locally by how a drug is used — and that a national programme with supervised, complete regimens is what protects the replacement.

Elimination Strategy

Early diagnosis and complete treatment — the rK39 rapid diagnostic test allows diagnosis in the field without splenic aspiration
Single-dose liposomal amphotericin B, which removes the adherence problem entirely
Vector control — indoor residual spraying against the sandfly, which breeds in cracks in mud walls and organic matter
Active case detection and treatment of PKDL, since these patients sustain transmission between epidemics
HIV co-infection complicates treatment, causes relapse and requires secondary prophylaxis
India has come close to the elimination target of under 1 case per 10,000 population at block level — a genuine public health achievement in which the change in drug regimen played a decisive part

Applied Aspects

Suspect kala-azar in prolonged fever with splenomegaly and pancytopenia in anyone from or travelling to an endemic district; it is frequently misdiagnosed as malaria, tuberculosis or haematological malignancy
Never use monotherapy where resistance is established; combination and single-dose regimens both treat and protect
Counsel women on miltefosine about contraception for 3 months after treatment, given its teratogenicity and long half-life
Treat PKDL actively rather than as a cosmetic problem, since it is the reservoir that restarts epidemics
Free diagnosis and treatment through the national programme removes cost as a barrier; the remaining barriers are awareness, distance and delayed presentation
The kala-azar story shows what changes outcomes — a shorter, supervised, effective regimen delivered through a programme, rather than a more potent molecule

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