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Kotton, Camille

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Kotton

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Camille

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Kotton, Camille
Author's Publications: search.filters.isAuthorOfPublication.d5048c4f-15b3-430d-8921-68a578987d83

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    Chagas disease reactivation in a heart transplant patient infected by domestic Trypanosoma cruzi discrete typing unit I (TcIDOM)
    (BioMed Central, 2015) Costales, Jaime A.; Kotton, Camille; Zurita-Leal, Andrea C.; Garcia-Perez, Josselyn; Llewellyn, Martin S.; Messenger, Louisa A.; Bhattacharyya, Tapan; Burleigh, Barbara
    Background: Trypanosoma cruzi, causative agent of Chagas disease, displays high intraspecific genetic diversity: six genetic lineages or discrete typing units (DTUs) are currently recognized, termed TcI through TcVI. Each DTU presents a particular distribution pattern across the Americas, and is loosely associated with different transmission cycles and hosts. Several DTUs are known to circulate in Central America. It has been previously suggested that TcI infection is benign and does not lead to chronic chagasic cardiomyopathy (CCC). Findings: In this study, we genotyped T. cruzi parasites circulating in the blood and from explanted cardiac tissue of an El Salvadorian patient who developed reactivation Chagas disease while on immunosuppressive medications after undergoing heart transplant in the U.S. as treatment for end-stage CCC. Parasite typing was performed through molecular methods (restriction fragment length polymorphism of polymerase reaction chain amplified products, microsatellite typing, maxicircle sequence typing and low-stringency single primer PCR, [LSSP-PCR]) as well as lineage-specific serology. We show that the parasites infecting the patient belong to the TcI DTU exclusively. Our data indicate that the parasites isolated from the patient belong to a genotype frequently associated with human infection throughout the Americas (TcIDOM). Conclusions: Our results constitute compelling evidence in support of TcI DTU’s ability to cause end-stage CCC and help dispel any residual bias that infection with this lineage is benign, pointing to the need for increased surveillance for dissemination of this genotype in endemic regions, the USA and globally.
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    Transmission of Lymphocytic Choriomeningitis Virus by Organ Transplantation
    (New England Journal of Medicine (NEJM/MMS), 2006) Fischer, Staci A.; Graham, Mary Beth; Kuehnert, Matthew J.; Kotton, Camille; Srinivasan, Arjun; Marty, Francisco; Comer, James A.; Guarner, Jeannette; Paddock, Christopher D.; Demeo, Dawn; Shieh, Wun-Ju; Erickson, Bobbie R.; Bandy, Utpala; DeMaria, Alfred; Davis, Jeffrey P.; Delmonico, Francis; Pavlin, Boris; Likos, Anna; Vincent, Martin J.; Sealy, Tara K.; Goldsmith, Cynthia S.; Jernigan, Daniel B.; Rollin, Pierre E.; Packard, Michelle M.; Patel, Mitesh; Rowland, Courtney; Helfand, Rita F.; Nichol, Stuart T.; Fishman, Jay; Ksiazek, Thomas; Zaki, Sherif R.
    Background In December 2003 and April 2005, signs and symptoms suggestive of infection devel- oped in two groups of recipients of solid-organ transplants. Each cluster was inves- tigated because diagnostic evaluations were unrevealing, and in each a common do- nor was recognized. Methods We examined clinical specimens from the two donors and eight recipients, using viral culture, electron microscopy, serologic testing, molecular analysis, and histo- pathological examination with immunohistochemical staining to identify a cause. Epidemiologic investigations, including interviews, environmental assessments, and medical-record reviews, were performed to characterize clinical courses and to determine the cause of the illnesses. Results Laboratory testing revealed lymphocytic choriomeningitis virus (LCMV) in all the recipients, with a single, unique strain of LCMV identified in each cluster. In both investigations, LCMV could not be detected in the organ donor. In the 2005 cluster, the donor had had contact in her home with a pet hamster infected with an LCMV strain identical to that detected in the organ recipients; no source of LCMV infection was found in the 2003 cluster. The transplant recipients had abdominal pain, altered mental status, thrombocytopenia, elevated aminotransferase levels, coagulopathy, graft dysfunction, and either fever or leukocytosis within three weeks after transplan- tation. Diarrhea, peri-incisional rash, renal failure, and seizures were variably present. Seven of the eight recipients died, 9 to 76 days after transplantation. One recipient, who received ribavirin and reduced levels of immunosuppressive therapy, survived. Conclusions We document two clusters of LCMV infection transmitted through organ trans- plantation.