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Dual congenital transmission of Toxoplasma gondii and Sarcocystis neurona in a late-term aborted pup from a chronically infected southern sea otter (Enhydra lutris nereis)

Author:
SHAPIRO, KAREN, MILLER, MELISSA A., PACKHAM, ANDREA E., AGUILAR, BEATRIZ, CONRAD, PATRICIA A., VANWORMER, ELIZABETH, MURRAY, MICHAEL J.
Source:
Parasitology 2016 v.143 no.3 pp. 276-288
ISSN:
1469-8161
Subject:
DNA, Enhydra lutris nereis, Protozoa, Sarcocystis neurona, Toxoplasma gondii, animal tissues, brain, fecundity, females, genotype, hosts, immunohistochemistry, liver, lungs, marine mammals, monitoring, parasites, pathogens, placenta, pups, spleen, thymus gland, tissue culture, toxoplasmosis, transplacental transmission, California
Abstract:
Toxoplasma gondii and Sarcocystis neurona are protozoan parasites with terrestrial definitive hosts, and both pathogens can cause fatal disease in a wide range of marine animals. Close monitoring of threatened southern sea otters (Enhydra lutris nereis) in California allowed for the diagnosis of dual transplacental transmission of T. gondii and S. neurona in a wild female otter that was chronically infected with both parasites. Congenital infection resulted in late-term abortion due to disseminated toxoplasmosis. Toxoplasma gondii and S. neurona DNA was amplified from placental tissue culture, as well as from fetal lung tissue. Molecular characterization of T. gondii revealed a Type X genotype in isolates derived from placenta and fetal brain, as well as in all tested fetal organs (brain, lung, spleen, liver and thymus). This report provides the first evidence for transplacental transmission of T. gondii in a chronically infected wild sea otter, and the first molecular and immunohistochemical confirmation of concurrent transplacental transmission of T. gondii and S. neurona in any species. Repeated fetal and/or neonatal losses in the sea otter dam also suggested that T. gondii has the potential to reduce fecundity in chronically infected marine mammals through parasite recrudescence and repeated fetal infection.
Agid:
5172901