SERODIAGNOSIS OF LEISHMANIASIS

Leishmaniasis is a spectrum of diseases ranging in severity from cutan eous (CL), post-kala-azar dermal (PKDL), and diffuse cutaneous (DCL) t o mucocutaneous (MCL) and visceral (VL) infections that are endemic in 86 tropical and subtropical countries around the world, accounting fo r 75,000 deaths per year. Different forms of leishmaniases are general ly caused by different distinct species of Leishmania having a digenet ic life cycle alternating between an aflagellated amastigote form repl icative within the macrophages of the host and a flagellated promastig ote form that multiplies within the gut of the sandfly. VL, MCL, PKDL, DCL, and CL forms of the disease can be arranged on a priority basis in accordance with the humoral immune responses of host. Generally, th e cell-mediated immunity, particularly the delayed-type hypersensitivi ty to leishmanial antigens, is associated with CL, MCL, PKDL, and cure d VL cases. The serodiagnosis of leishmaniasis appears to be an altern ative to parasite detection in biopsy samples either by the staining o f amastigotes or by culturing the amastigotes, which transform to a pr omastigote form and replicate. A battery of immunological procedures h ave been developed or adapted to demonstrate either humoral or cell-me diated immune responses against Leishmania for diagnosis and epidemiol ogical survey. The sensitivity and specificity of such diagnostic meth ods depend on the type, source, and purity of antigen employed, as som e of the leishmanial antigens have common cross-reactive epitopes shar ed with other microorganisms, particularly Trypanosoma, Mycobacteria, Plasmodia, and Schistosoma. Serodiagnostic techniques for the detectio n of antileishmanial antibodies have been employed with about 72 to 10 0, 23 to 90, 83, and 33 to 100% success in VL, CL, MCL, and PKDL patie nts, respectively. The Leishmanin skin test (LST) is useful to detect MCL and CL, with about 100 and 84% success, respectively. In PKDL, the gradual fall of antileishmanial antibody titer to some extent and the rise of delayed hypersensitivity to the parasite antigen are the char acteristic features associated with the chronicity of the disease. The use of whole promastigote as the source of antigens in the direct agg lutination test (DAT) and immunofluorescent test (IFAT) gave cross-rea ctions with the sera of leprosy, tuberculosis, and African trypanosomi asis patients. Again, the use of cell-free extracts of promastigotes g enerally gave false positive results with the sera of normal human and Chagas' disease, leprosy, tuberculosis, and malaria patients in enzym e-linked immunosorbent assay (ELISA), dot ELISA, immunodiffusion, immu noelectrophoresis, and counter-current immunoelectrophoresis tests. Le ishmanial proteinase, gp63, is not species specific, but appears to be Leishmania specific, so it can be used to detect a case of leishmania sis. Acid phosphatase and the dp72-kDa protein of L. donovani cross-re acts with the sera of leprosy patients. Active VL cases are confirmed by the positive results obtained for antileishmanial antibody detectio n and negative for LST. The titers of antibodies against excreted fact or (EF) or lipophosphoglycan (LPG) or lipophosphopolysaccharide (LPPS) of Leishmania were found to be insignificant for serodiagnostic purpo ses. Use of ConA-positive glycoproteins released or secreted by promas tigotes of L. donovani showed 100% positive reactions with VL in immun oelectrophoresis. An LPS-like antigen of L. major promastigotes could detect 90% of confirmed CL cases with radioimmunoassay. Detection of l eishmanial antigens circulating in immune complexes is considered an i ndication of active leishmanial infection.