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Toxoplasma infection in kidney donors and transplant recipients from Western Mexico: A one‐year follow‐up
Author(s) -
GalvánRamírez María Luz,
SánchezOrozco Laura V.,
AndradeSierra Jorge,
MendozaCabrera Salvador,
EvangelistaCarrillo Luis Alberto,
Rodríguez Pérez Laura R.,
Chiquete Erwin,
ArmendárizBorunda Juan
Publication year - 2019
Publication title -
transplant infectious disease
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.69
H-Index - 67
eISSN - 1399-3062
pISSN - 1398-2273
DOI - 10.1111/tid.13139
Subject(s) - seroconversion , toxoplasma gondii , medicine , toxoplasmosis , antibody , immunology , kidney transplantation , transplantation , virology
Abstract Purpose Solid organ transplant recipients are highly susceptible to Toxoplasma gondii infection. We aimed to describe the 12‐month follow‐up risk of seroconversion in renal transplant recipients. Methodology Anti‐ T gondii antibodies were investigated in donors and recipients of renal transplants. In donors, anti‐ T gondii were evaluated before transplantation. In recipients, anti‐ T gondii were monitored over a 12‐month period to evaluate potential seroconversion or reactivation. IgG and IgM anti‐ T gondii antibodies were investigated through enzyme immunoassay and Western blot. Molecular diagnosis was performed on peripheral blood leukocytes using PCR to amplify fragments corresponding to the T gondii B1 gene and the repetitive 529‐bp element. Results The basal frequency of seropositive IgG anti‐ T gondii antibodies was higher in donors than in recipients (38.4% vs 25.2%; P = .03). During the 12‐month follow‐up, the accumulated seroconversion to IgG and IgM antibodies was 3/99 (3.0%), and the accumulated reactivation was 11/99 (11.0%). None of the samples exhibited positivity to T gondii DNA. Conclusions This study showed that there is an increased risk of seroconversion or reactivation in renal transplant recipients over a 12‐month follow‐up. Our data suggest that prophylaxis with trimethoprim and sulfamethoxazole effectively prevented toxoplasmosis, since neither T gondii DNA nor clinical toxoplasmosis was detected.