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Background: Over the past few decades, candidiasis is a disease of growing incidence that parallels the increasing number of immunocompromised people. The entity of recurrent candidal infections has been defined as at least four symptomatic episodes at the last year. Candida albicans pathogen acts as activating surface for complement deposition i.e., covalent binding of C3b. Opsonization is the process of  deposition of complement fragments on the surface of pathogen that allows their recognition, ingestion, and destruction by macrophages, phagocytic cells, neutrophils, and monocytes. IgG antibodies and C3 fragments are the classical opsonins. Phagocytes express specific receptors for C3 fragments. Complement opsonization resulting from the direct activation of the alternative pathway on pathogen surface allows their elimination by phagocytes before the mounting of an adaptive immune response and the appearance of antibodies. Aim of the work: The aim of the present work is to clarify the relation between serum complement (C2&C4) and recurrent candidal infections. Patients and Methods: A case control study. Sera were obtained from 50 recurrent candidal infection patients and 30 healthy volunteers. C2 levels were measured using ELISA with standard kits from EIAab R&D Systems. C4 levels were measured using   Automated Chemistry ELISA with standard kits from EIAab R&D Systems. Results: Serum complement C2 was significantly lower among the cases with recurrent candidal infection (65.63±48.35pg/ml) than in healthy volunteers 200.29± 358.43) with p-value= 0.01. Conclusion: Recurrent candidal infection can be caused by low (C2) level in patient's serum. There is significant alteration in complement (C2) level (P ≤ 0.01). There is no significant alteration in complement (C4) level (P ≥ 0.05). Serum complement (C2) level can be used as a laboratory investigation for patients with recurrent candidal infections especially those with associated systemic disease.

Assessment of complement (C2&C4) in patients with recurrent candidal infections