Leishmaniasis

Also known as: Kala azar, Visceral leishmaniasis

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.

Clinical toolsCalculators

BMI GCS EDD Parkland Formula

Corrected Sodium Corrected Calcium Anion Gap Creatinine Clearance Insulin Calculations qSOFA Wells PE Wells DVT CHA₂DS₂-VASc HAS-BLED CURB-65 Centor/McIsaac

Pott Disease

Pott disease is tuberculous spondylitis, spinal involvement by Mycobacterium tuberculosis, most commonly reaching the spine via hematogenous spread from a primary (often pulmonary) focus, though the primary site is frequently no longer clinically active by the time spinal disease presents.

It remains an important cause of spinal infection globally, particularly in TB-endemic regions, and is a leading infectious cause of potentially preventable paraplegia if diagnosis is delayed.

The thoracolumbar spine is most commonly affected, with infection typically starting in the anterior vertebral body (adjacent to the richly vascularized subchondral region) and spreading beneath the anterior longitudinal ligament to involve adjacent vertebrae and the intervening disc, a pattern distinguishing it from pyogenic spondylodiscitis.

Onset is typically insidious, over weeks to months, with back pain (often the earliest and most persistent symptom), low grade fever, night sweats, and weight loss.

As vertebral body destruction progresses, a gibbus deformity (an angular kyphosis) may develop.

Neurological complications ("Pott's paraplegia") result from spinal cord compression by an epidural abscess, granulation tissue, or direct bony collapse and instability, presenting with progressive limb weakness, sensory loss, and bladder/bowel dysfunction, and represent a genuine spinal emergency requiring urgent recognition.

A cold abscess (paravertebral or psoas abscess, so termed given the relative absence of the acute inflammatory signs seen with pyogenic infection) may track along fascial planes and present as a soft tissue mass at a site distant from the spine itself, classically in the groin along the psoas sheath.

MRI with contrast is the imaging investigation of choice, showing vertebral body destruction, disc space narrowing, paraspinal or epidural collection, and the degree of any cord compression, with substantially higher sensitivity than plain radiography, particularly for early disease
Plain radiographs may show vertebral body collapse and disc space narrowing but are typically only positive once substantial bone destruction (often 30 to 50%) has occurred
Microbiological confirmation via CT-guided or open biopsy of the affected vertebra or paraspinal collection, sent for Ziehl-Neelsen or auramine staining, mycobacterial culture (though slow, taking weeks), and, where available, GeneXpert MTB/RIF for rapid molecular confirmation and detection of rifampicin resistance
Assessment for a primary or concurrent TB focus (CXR, sputum studies where relevant), and HIV testing given the strong association and mutual influence on presentation and management
Inflammatory markers (ESR, CRP) are typically elevated but non-specific

Standard antituberculous therapy as detailed in the Tuberculosis entry: intensive phase with isoniazid, rifampicin, pyrazinamide, and ethambutol for 2 months, followed by a continuation phase of isoniazid and rifampicin, with spinal TB total treatment duration generally extended to 9 to 12 months given the poorer drug penetration into avascular, necrotic bone and disc tissue and the higher relapse risk compared with pulmonary disease
Pyridoxine (vitamin B6) 10 to 25 mg PO od co-administered with isoniazid to reduce peripheral neuropathy risk
Bracing or immobilization may be used adjunctively for spinal stability and pain relief in selected cases, per orthopedic or spinal surgery input
Surgical intervention (decompression, debridement, and, where instability results, spinal stabilization/fusion) is indicated for significant or progressive neurological deficit, spinal instability, failure to respond to medical therapy alone, or a large abscess requiring drainage; surgery does not replace the need for the full antituberculous drug course
Close neurological monitoring throughout treatment given the risk of neurological deterioration even after treatment initiation, particularly in the first weeks

Referral: spinal surgery for any neurological deficit, instability, or significant abscess; infectious disease or respiratory medicine for antituberculous therapy coordination and monitoring; HIV testing and, where positive, coordinated HIV and TB management per the principles in the Tuberculosis and HIV entries.

Leishmaniasis

Overview

Clinical Features

Diagnosis

Management

Overview

Clinical Features

Diagnosis

Management