IVD of Leishmania

Leishmania

Leishmania is an intracellular parasitic flagellate whose main host is vertebrates. There are four species of Leishmania parasites in humans, with sandflies as the main vector. Leishmaniasis is a parasitic infection caused by the protozoa Leishmania. After infection, due to the destruction of macrophages, patients develop clinical symptoms such as fever, anemia, and swollen lymph nodes. In addition, Leishmania donovani (L. donovani) can parasitize the internal organs and cause kala-azar. Currently, in vitro diagnosis (IVD) of Leishmania is carried out through immunological examination and molecular biology methods.

IVD of LeishmaniaFig1. The life cycle of Leishmania parasites. (Kaye P, et al., 2011)

Main Steps of IVD for Leishmania

  • Antibody testing. Enzyme-linked immunosorbent assay (ELISA), indirect hemagglutination test (IHA), convective immunoelectrophoresis (CIE), indirect fluorescence test (IF), direct agglutination test and Dip-stick method were used to detect specific antibodies in the patient's serum.
  • Serum circulating antigen detection. Monoclonal antibody-antigen spot test (MeAb-AST) has high sensitivity and specificity for diagnosing kala-azar.
  • Pathogen testing. Smear staining and culture methods. The puncture smear is stained with Gibbs or Wright, and then the puncture is inoculated into the culture medium for observation.
  • Molecular biology technology. Higher specificity and sensitivity of PCR technology can distinguish various Leishmania genera.

Transmission and Infection Process

Sandfly Bite: The transmission occurs when an infected female sandfly bites a human. During the blood meal, the sandfly injects the infective stage of the parasite, known as promastigotes, into the human skin.

Promastigote Transformation: Once inside the human body, the promastigotes are phagocytized by macrophages or other types of mononuclear phagocytic cells.

Amastigote Formation: Inside the phagocytic cell, the promastigotes transform into amastigotes, which are the intracellular form of the parasite. The amastigotes multiply within the phagolysosomes of these cells.

Cell Burst and Spread: The infected cells eventually burst, releasing the amastigotes which then infect new macrophages. This leads to the clinical manifestations of leishmaniasis.

Creative BioMart provides high-quality recombinant Leishmania proteins used for IVD, including ELISA, lateral flow assay, western blot, and other immunoassays.

Clinical Manifestations

The disease can present in various forms, primarily based on the species of Leishmania involved and the immune response of the host:

  • Cutaneous Leishmaniasis: Characterized by skin sores or ulcers at the site of the sandfly bite.
  • Mucocutaneous Leishmaniasis: Involves the mucous membranes of the nose, mouth, and throat. It can lead to severe disfigurement.
  • Visceral Leishmaniasis (Kala-Azar): Affects internal organs like the spleen, liver, and bone marrow, and can be fatal if untreated.

Classifications of Leishmania

Leishmania species are primarily classified based on the clinical syndromes they cause and their geographical distribution. The major species and complexes involved in human disease include:

Leishmania donovani Complex:

Includes Leishmania donovani and Leishmania infantum (syn. Leishmania chagasi).

Primarily responsible for visceral leishmaniasis (Kala-Azar).

Found in parts of East Africa, India, and the Mediterranean region.

Leishmania mexicana Complex:

Includes Leishmania mexicana, Leishmania amazonensis, and Leishmania venezuelensis.

Primarily responsible for cutaneous leishmaniasis.

Found in Central and South America.

Leishmania braziliensis Complex:

Includes Leishmania braziliensis, Leishmania guyanensis, and Leishmania panamensis.

Primarily responsible for mucocutaneous leishmaniasis.

Found in South America.

Leishmania major and Leishmania tropica:

Responsible for old world cutaneous leishmaniasis.

Found in the Middle East, Central Asia, and Africa.

Leishmania aethiopica:

Causes both cutaneous and diffuse cutaneous leishmaniasis.

Found in Ethiopia and Kenya.

Highlights of Our Products

  • It is widely used and suitable for downstream immunological experiments.
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Our Outstanding Advantages

  • Provide high-quality service, high-level experiments, and reliable analysis.
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Case Study

Case 1: Sharifi M, Shiravi T, Bolouki A, Motamed Shariati M. Palpebral leishmaniasis. Clin Case Rep. 2024 Jul 16;12(7):e9197. doi: 10.1002/ccr3.9197. PMID: 39015213; PMCID: PMC11250501.

Leishmaniasis can mimic many conditions, including hordeolum, basal cell carcinoma, and squamous cell carcinoma. The presence of kinetoplast in free-form or intramacrophage amastigotes, ensuring us to establish the microscopic diagnosis of leishmaniasis.

Fig2. Ocular leishmanial lesion involving the left upper eyelid before the treatment (left upper) and 6 months after treatment (right upper). Direct smear from the skin ulcer shows amastigotes in the cytoplasm of macrophages (lower image, black arrow).

Case 2: Shmueli M, Ben-Shimol S. Review of Leishmaniasis Treatment: Can We See the Forest through the Trees? Pharmacy (Basel). 2024 Feb 8;12(1):30. doi: 10.3390/pharmacy12010030. PMID: 38392937; PMCID: PMC10892631.

Leishmaniasis treatment is difficult, with several factors to be considered. In this review, the authors aim to describe the diverse treatment options for different clinical manifestations of leishmaniasis. For each currently available treatment, they will discuss the various considerations mentioned above (efficacy, ease of use, safety, and cost).

Fig3. Visceral leishmaniasis in a 4-year-old patient. Amastigotes in bone marrow biopsy (right) are notable.

Case 3: Veras PST, de Santana MBR, Brodskyn CI, et al. Elucidating the role played by bone marrow in visceral leishmaniasis. Front Cell Infect Microbiol. 2023 Oct 4;13:1261074. doi: 10.3389/fcimb.2023.1261074. PMID: 37860064; PMCID: PMC10582953.

Visceral leishmaniasis (VL), the most severe form, can be life-threatening if left untreated. Parasites can spread systemically within the body, infecting a range of organs, such as the liver, spleen, bone marrow and lymph nodes. Dogs exhibit clinical and pathological similarities to human VL and are valuable models for studying disease progression. The review emphasizes the need for future research to enhance our understanding of VL and identify potential targets for novel diagnostic and therapeutic approaches.

Fig4. Hematological alterations in bone marrow and peripheral blood during CVL. This image depicts the common hematological changes observed in the peripheral blood of dogs infected with L. infantum. Although the underlying causes appear to differ from those in humans, dogs with CVL commonly exhibit anemia along with thrombocytopenia, eosinopenia, and lymphopenia. By contrast, leukocytosis associated with neutrophilia and monocytosis in CVL was also described in CVL.