Zheng Qi  2021-03-15

Visceral Leishmaniasis (VL, Kala-azar) Core Symptoms

VL is the most life-threatening form of leishmaniasis, caused by Leishmania donovani or related species that invade the body’s reticuloendothelial system. Its hallmark clinical features include prolonged, irregular bouts of fever that can last for weeks, progressive massive enlargement of the spleen, and significant unintended weight loss. Other common associated signs are moderate enlargement of the liver, severe normocytic normochromic anemia, reduced white blood cell and platelet counts, persistent cough, recurrent diarrhea, and generalized swollen lymph nodes.

These symptoms are highly non-specific, and easily mimic the presentation of malaria, typhoid fever, tuberculosis, chronic schistosomiasis and severe childhood malnutrition, leading to frequent misdiagnosis in low-resource endemic settings. In regions where malaria and VL co-circulate, local clinical guidelines recommend suspecting VL immediately in any patient with fever lasting 2 weeks or longer that shows no response to standard antimalarial treatment, after confirmed drug-resistant malaria has been ruled out. As the disease progresses, patients rapidly develop severe malnutrition and become highly vulnerable to life-threatening intercurrent secondary bacterial infections. Without timely intervention, the untreated mortality rate of VL can reach up to 95%.

Post-Kala-Azar Dermal Leishmaniasis (PKDL) Key Features

PKDL is a unique dermatological complication that occurs almost exclusively in L. donovani endemic zones across East Africa and South Asia, with over 90% of cases developing 6 months to 1 or more years after patients have completed standard VL treatment and their systemic visceral symptoms have fully resolved. A small subset of cases may appear concurrently with active untreated VL, and extremely rare primary PKDL cases with no prior recorded VL history have also been documented in endemic communities.

The earliest visible presentation of PKDL is scattered, patchy hypopigmented macules that are easily misidentified as vitiligo in initial clinical assessments. As the condition advances, these lesions evolve into raised erythematous papules, infiltrative plaques, and firm granulomatous nodules that are most densely distributed across the face, neck, and upper limbs. Unlike cutaneous leishmaniasis, PKDL lesions never ulcerate, and they lack the skin sensory loss, eyebrow shedding and peripheral nerve enlargement that are characteristic of leprosy, the other common differential diagnosis. Most PKDL patients have no systemic symptoms and appear otherwise healthy, but their skin lesions are packed with infectious parasites, making them persistent, hidden reservoirs that sustain ongoing local sandfly-borne transmission for years if left untreated.

Edited by: Secretariat of the Asia-Pacific Network for Drug and Diagnostics Innovation
Produced by: Zheng Qi
Reviewed by: Zhang Haobing
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