Despina Contopoulos-Ioannidis1, Kelsey M Wheeler2, Raymund Ramirez3, Cindy Press3, Ernest Mui2, Ying Zhou2, Christine Van Tubbergen2, Sheela Prasad2, Yvonne Maldonado4, Shawn Withers2, Kenneth M Boyer5, A Gwendolyn Noble6, Peter Rabiah7, Charles N Swisher6, Peter Heydemann5, Kristen Wroblewski2, Theodore Karrison2, Michael E Grigg8, Jose G Montoya9, Rima McLeod2. 1. Department of Pediatrics, Division of Infectious Diseases Palo Alto Medical Foundation Toxoplasma Serology Laboratory, California. 2. Departments of Ophthalmology and Visual Sciences and Pediatric Infectious Diseases, Toxoplasmosis Center, Department of Public Health Sciences, University of Chicago. 3. Palo Alto Medical Foundation Toxoplasma Serology Laboratory, California. 4. Department of Pediatrics, Division of Infectious Diseases. 5. Departments of Ophthalmology and Visual Sciences and Pediatric Infectious Diseases, Toxoplasmosis Center, Department of Public Health Sciences, University of Chicago Department of Pediatrics, Rush University Medical Center. 6. Departments of Ophthalmology and Visual Sciences and Pediatric Infectious Diseases, Toxoplasmosis Center, Department of Public Health Sciences, University of Chicago Lurie Children's Hospital, Northwestern Memorial Hospital, Northwestern University, Chicago. 7. Departments of Ophthalmology and Visual Sciences and Pediatric Infectious Diseases, Toxoplasmosis Center, Department of Public Health Sciences, University of Chicago North Shore University Hospital, Evanston, Illinois. 8. Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland. 9. Department of Medicine, Division of Infectious Diseases and Geographic Medicine, Stanford University School of Medicine Palo Alto Medical Foundation Toxoplasma Serology Laboratory, California.
Abstract
BACKGROUND: Family clusters and epidemics of toxoplasmosis in North, Central, and South America led us to determine whether fathers of congenitally infected infants in the National Collaborative Chicago-Based Congenital Toxoplasmosis Study (NCCCTS) have a high incidence of Toxoplasma gondii infection. METHODS: We analyzed serum samples collected from NCCCTS families between 1981 and 2013. Paternal serum samples were tested for T. gondii antibodies with immunoglobulin (Ig) G dye test and IgM enzyme-linked immunosorbent assay. Additional testing of paternal serum samples was performed with differential-agglutination and IgG avidity tests when T. gondii IgG and IgM results were positive and serum samples were collected by the 1-year visit of the congenitally infected child. Prevalence of paternal seropositivity and incidence of recent infection were calculated. We analyzed whether certain demographics, maternal parasite serotype, risk factors, or maternal/infant clinical manifestations were associated with paternal T. gondii infection status. RESULTS: Serologic testing revealed a high prevalence (29 of 81; 36%) of T. gondii infection in fathers, relative to the average seropositivity rate of 9.8% for boys and men aged 12-49 years in the United States between 1994 and 2004 (P < .001). Moreover, there was a higher-than-expected incidence of recent infections among fathers with serum samples collected by the 1-year visit of their child (6 of 45; 13%; P < .001). No demographic patterns or clinical manifestations in mothers or infants were associated with paternal infections, except for sandbox exposure. CONCLUSIONS: The high prevalence of chronic and incidence of recent T. gondii infections in fathers of congenitally infected children indicates that T. gondii infections cluster within families in North America. When a recently infected person is identified, family clustering and community risk factors should be investigated for appropriate clinical management.
BACKGROUND: Family clusters and epidemics of toxoplasmosis in North, Central, and South America led us to determine whether fathers of congenitally infectedinfants in the National Collaborative Chicago-Based Congenital Toxoplasmosis Study (NCCCTS) have a high incidence of Toxoplasma gondii infection. METHODS: We analyzed serum samples collected from NCCCTS families between 1981 and 2013. Paternal serum samples were tested for T. gondii antibodies with immunoglobulin (Ig) G dye test and IgM enzyme-linked immunosorbent assay. Additional testing of paternal serum samples was performed with differential-agglutination and IgG avidity tests when T. gondii IgG and IgM results were positive and serum samples were collected by the 1-year visit of the congenitally infectedchild. Prevalence of paternal seropositivity and incidence of recent infection were calculated. We analyzed whether certain demographics, maternal parasite serotype, risk factors, or maternal/infant clinical manifestations were associated with paternal T. gondii infection status. RESULTS: Serologic testing revealed a high prevalence (29 of 81; 36%) of T. gondii infection in fathers, relative to the average seropositivity rate of 9.8% for boys and men aged 12-49 years in the United States between 1994 and 2004 (P < .001). Moreover, there was a higher-than-expected incidence of recent infections among fathers with serum samples collected by the 1-year visit of their child (6 of 45; 13%; P < .001). No demographic patterns or clinical manifestations in mothers or infants were associated with paternal infections, except for sandbox exposure. CONCLUSIONS: The high prevalence of chronic and incidence of recent T. gondii infections in fathers of congenitally infectedchildren indicates that T. gondii infections cluster within families in North America. When a recently infected person is identified, family clustering and community risk factors should be investigated for appropriate clinical management.
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