Tetanus

Leishmaniasis is a parasitic infection caused by protozoa of the genus Leishmania, transmitted by the bite of infected female sandflies.

Clinical presentation depends substantially on both the specific infecting species and host immune factors, ranging from a self limiting cutaneous lesion to fatal systemic disease if untreated.

• Cutaneous leishmaniasis is the most common clinical form globally, causing localized skin lesions at the site of the sandfly bite.

• Mucocutaneous leishmaniasis, seen predominantly with certain New World species, involves subsequent spread to and destruction of the nasal and oral mucosa, and can occur even after apparent healing of the original cutaneous lesion, sometimes years later.

• Visceral leishmaniasis (kala azar), caused predominantly by Leishmania donovani and Leishmania infantum, involves dissemination to the reticuloendothelial system, and carries high mortality if untreated, making it the most clinically significant form.

• Cutaneous leishmaniasis presents as a papule at the bite site that gradually enlarges into a painless (or minimally painful) ulcer with a raised, indurated border, typically over weeks to months, often eventually healing spontaneously over months to a couple of years, though leaving a disfiguring scar.
• Mucocutaneous leishmaniasis presents with progressive, destructive ulceration of the nasal septum, oral mucosa, and pharynx, causing significant disfigurement and functional impairment if untreated.
• Visceral leishmaniasis presents with prolonged fever (often with a characteristic double daily temperature spike pattern in some descriptions, though this is not universally reliable), marked hepatosplenomegaly (the spleen often massively enlarged), weight loss, and progressive pancytopenia from bone marrow infiltration and hypersplenism, with skin hyperpigmentation in some regions accounting for the name kala azar, meaning "black fever" or "black sickness."
• Immunocompromised patients, particularly those with HIV, are at substantially higher risk of visceral leishmaniasis, and can present atypically, with a higher parasite burden and poorer response to treatment.
• Untreated visceral leishmaniasis carries a very high mortality, typically from secondary bacterial infection, bleeding complications from pancytopenia, or progressive cachexia.

• Microscopic identification of amastigotes in tissue samples remains a mainstay of diagnosis: skin biopsy or scraping from the edge of a cutaneous lesion for cutaneous disease, and bone marrow or splenic aspirate for visceral disease, the latter carrying a small but recognized risk of hemorrhage given the often significantly enlarged, congested spleen.
• Serology (rK39 rapid diagnostic test being widely used and useful in endemic settings) supports the diagnosis of visceral leishmaniasis, though sensitivity can be reduced in HIV co-infected patients, and serology cannot reliably distinguish active from past infection.
• PCR based testing offers high sensitivity and specificity where available, and is increasingly used for both diagnosis and species identification, the latter relevant given that treatment and prognosis can differ by species, particularly for cutaneous and mucocutaneous disease.
• FBC in visceral disease characteristically shows pancytopenia, reflecting bone marrow infiltration and hypersplenism.
• HIV testing should be offered to all patients diagnosed with visceral leishmaniasis, given the strong bidirectional interaction between the two infections.

Differentials for cutaneous disease include other causes of chronic skin ulceration, including mycobacterial infection and fungal infection. Differentials for visceral disease include the broad differential for fever with hepatosplenomegaly and pancytopenia, including malaria, brucellosis, tuberculosis, and hematological malignancy.

• Liposomal amphotericin B is increasingly preferred as first line treatment for visceral leishmaniasis in many settings, given its favorable efficacy and improved safety profile compared to older agents, though access and cost remain limiting factors in some endemic regions.
• Pentavalent antimonials (sodium stibogluconate, meglumine antimoniate) remain widely used, particularly where amphotericin is not accessible, though they carry a more significant side effect profile, including cardiotoxicity, pancreatitis, and nephrotoxicity, requiring careful monitoring during treatment.
• Miltefosine, an oral agent, offers a treatment option that avoids the need for parenteral administration, though with some regional variation in efficacy depending on the infecting species.
• Cutaneous leishmaniasis management is guided by lesion severity, number, location (facial or cosmetically sensitive lesions generally warrant more active treatment), and infecting species: options range from watchful waiting for small, self limiting lesions in low risk locations, through local treatment (intralesional antimonials, cryotherapy, topical paromomycin), to systemic therapy for larger, multiple, or high risk lesions, or those caused by species with a recognized risk of subsequent mucosal spread.
• Mucocutaneous disease requires systemic treatment, typically with amphotericin B or pentavalent antimonials, given the destructive and progressive nature of untreated disease.
• HIV co-infected patients with visceral leishmaniasis require careful specialist management, given higher relapse rates, the need for secondary prophylaxis in some cases, and close coordination between infectious disease and HIV care.
• Prevention centers on sandfly bite avoidance (insecticide treated bed nets, protective clothing, repellents) in endemic areas, alongside broader vector and reservoir control programs.

Referral: infectious disease or tropical medicine for diagnosis and treatment of all forms; hematology if bone marrow aspirate is required for diagnosis or if severe pancytopenia requires additional supportive management.