Mouse model of congenital infection with a non-virulent Toxoplasma gondii strain: Vertical transmission, “sterile” fetal damage, or both?
Congenital transmission of Toxoplasma gondii may occur if the mother gets infected for the first time while pregnant. The risk of mother-to-child transmission depends on the gestation trimester at infection, being lowest in the first and highest in the last. Conversely, fetal damage is frequent and...
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Veröffentlicht in: | Experimental parasitology 2016-07, Vol.166, p.116-123 |
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creator | Vargas-Villavicencio, J.A. Cedillo-Peláez, C. Rico-Torres, C.P. Besné-Mérida, A. García-Vázquez, F. Saldaña, J.I. Correa, D. |
description | Congenital transmission of Toxoplasma gondii may occur if the mother gets infected for the first time while pregnant. The risk of mother-to-child transmission depends on the gestation trimester at infection, being lowest in the first and highest in the last. Conversely, fetal damage is frequent and more severe at the beginning of pregnancy. The objective of this study was to evaluate congenital transmission and pathological aspects in the placenta and the fetus using a mouse model of congenital infection of the second gestation third. Forty-five female BALB/c mice were infected intravenously with 2.5–10.0 × 106 tachyzoites of the ME49 strain at middle gestation. Samples of maternal spleen and fetal/placental units were taken 72 h later. We determined parasite load and vertical transmission by qPCR, as well as damage macroscopically and by histopathology. With the lowest dose, 18% of the fetuses were infected. Also, 40% of fetuses/litter were altered, while this value was 10% in the control group (P |
doi_str_mv | 10.1016/j.exppara.2016.04.002 |
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•Mouse model with Toxoplasma gondii avirulent strain causes infection/damage rates similar to humans.•Up to 105 times tachyzoites in mother infected with ME49 strain as compared to fetus.•Avirulent T. gondii strain causes resorption or abortion without fetal infection.</description><identifier>ISSN: 0014-4894</identifier><identifier>EISSN: 1090-2449</identifier><identifier>DOI: 10.1016/j.exppara.2016.04.002</identifier><identifier>PMID: 27068784</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Animals ; Congenital toxoplasmosis ; Disease Models, Animal ; DNA-Binding Proteins - genetics ; Embryo Loss - parasitology ; Female ; Fetus - parasitology ; Fetus - pathology ; Hemorrhage ; Infectious Disease Transmission, Vertical ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Knockout ; Mouse model ; Necrosis ; Parasite Load ; Parasitic load ; Pathology ; Placenta - parasitology ; Placenta - pathology ; Pregnancy ; Pregnancy Complications, Parasitic - parasitology ; Pregnancy Complications, Parasitic - pathology ; Specific Pathogen-Free Organisms ; Spleen - parasitology ; Thrombosis ; Toxoplasma gondii ; Toxoplasmosis, Animal - congenital ; Toxoplasmosis, Animal - pathology ; Toxoplasmosis, Animal - transmission</subject><ispartof>Experimental parasitology, 2016-07, Vol.166, p.116-123</ispartof><rights>2016 Elsevier Inc.</rights><rights>Copyright © 2016 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c398t-87e339a67a204b4651fc004fbc897cb67137dc0e3f4e212533d5039a7246260e3</citedby><cites>FETCH-LOGICAL-c398t-87e339a67a204b4651fc004fbc897cb67137dc0e3f4e212533d5039a7246260e3</cites><orcidid>0000-0001-6619-2058 ; 0000-0002-3354-4421</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0014489416300649$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27068784$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Vargas-Villavicencio, J.A.</creatorcontrib><creatorcontrib>Cedillo-Peláez, C.</creatorcontrib><creatorcontrib>Rico-Torres, C.P.</creatorcontrib><creatorcontrib>Besné-Mérida, A.</creatorcontrib><creatorcontrib>García-Vázquez, F.</creatorcontrib><creatorcontrib>Saldaña, J.I.</creatorcontrib><creatorcontrib>Correa, D.</creatorcontrib><title>Mouse model of congenital infection with a non-virulent Toxoplasma gondii strain: Vertical transmission, “sterile” fetal damage, or both?</title><title>Experimental parasitology</title><addtitle>Exp Parasitol</addtitle><description>Congenital transmission of Toxoplasma gondii may occur if the mother gets infected for the first time while pregnant. The risk of mother-to-child transmission depends on the gestation trimester at infection, being lowest in the first and highest in the last. Conversely, fetal damage is frequent and more severe at the beginning of pregnancy. The objective of this study was to evaluate congenital transmission and pathological aspects in the placenta and the fetus using a mouse model of congenital infection of the second gestation third. Forty-five female BALB/c mice were infected intravenously with 2.5–10.0 × 106 tachyzoites of the ME49 strain at middle gestation. Samples of maternal spleen and fetal/placental units were taken 72 h later. We determined parasite load and vertical transmission by qPCR, as well as damage macroscopically and by histopathology. With the lowest dose, 18% of the fetuses were infected. Also, 40% of fetuses/litter were altered, while this value was 10% in the control group (P < 0.05). These results are similar to those described in humans in terms of vertical transmission and fetal damage during the second third of gestation. The maternal spleen had 10–1000 times more tachyzoites than the placenta, and the later retained 90–99% of the parasites that could reach the fetus. Nevertheless, we found resorptions, abortions or fetal tissue damage in the presence but also in the absence of parasites. Our data indicate a strong protective effect of maternal organs and the placenta against fetal infection, but extensive damage of the later may led to resorption or abortion without vertical transmission.
[Display omitted]
•Mouse model with Toxoplasma gondii avirulent strain causes infection/damage rates similar to humans.•Up to 105 times tachyzoites in mother infected with ME49 strain as compared to fetus.•Avirulent T. gondii strain causes resorption or abortion without fetal infection.</description><subject>Animals</subject><subject>Congenital toxoplasmosis</subject><subject>Disease Models, Animal</subject><subject>DNA-Binding Proteins - genetics</subject><subject>Embryo Loss - parasitology</subject><subject>Female</subject><subject>Fetus - parasitology</subject><subject>Fetus - pathology</subject><subject>Hemorrhage</subject><subject>Infectious Disease Transmission, Vertical</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Mouse model</subject><subject>Necrosis</subject><subject>Parasite Load</subject><subject>Parasitic load</subject><subject>Pathology</subject><subject>Placenta - parasitology</subject><subject>Placenta - pathology</subject><subject>Pregnancy</subject><subject>Pregnancy Complications, Parasitic - parasitology</subject><subject>Pregnancy Complications, Parasitic - pathology</subject><subject>Specific Pathogen-Free Organisms</subject><subject>Spleen - parasitology</subject><subject>Thrombosis</subject><subject>Toxoplasma gondii</subject><subject>Toxoplasmosis, Animal - congenital</subject><subject>Toxoplasmosis, Animal - pathology</subject><subject>Toxoplasmosis, Animal - transmission</subject><issn>0014-4894</issn><issn>1090-2449</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkc1u1DAQxy0EotvCI4B85NCEsePECZeqqiggFXEpXC3HmWy9Suxge0u59QV4A3i5Pgle7cK1J2us_8dofoS8YlAyYM3bTYl3y6KDLnkeSxAlAH9CVgw6KLgQ3VOyAmCiEG0njshxjBsAaBkXz8kRl9C0shUr8uuz30aksx9won6kxrs1Opv0RK0b0STrHf1h0w3V1HlX3NqwndAleu3v_DLpOGu69m6wlsYUtHXv6DcMyZockGcXZxtjzjilD_e_Y8JgJ3y4_0NH3FUMetZrPKU-0N6nm7MX5Nmop4gvD-8J-Xr5_vriY3H15cOni_OrwlRdm4pWYlV1upGag-hFU7PRAIixN20nTd9IVsnBAFajQM54XVVDDdkguWh4k_9PyJt97hL89y3GpPKaBqdJO8z3UKyFVjLgdfO4VHayFoI3O2m9l5rgYww4qiXYWYefioHaQVMbdYCmdtAUCJWhZd_rQ8W2n3H47_pHKQvO9gLMN7m1GFQ0Fp3BwYaMSA3ePlLxF56zre4</recordid><startdate>201607</startdate><enddate>201607</enddate><creator>Vargas-Villavicencio, J.A.</creator><creator>Cedillo-Peláez, C.</creator><creator>Rico-Torres, C.P.</creator><creator>Besné-Mérida, A.</creator><creator>García-Vázquez, F.</creator><creator>Saldaña, J.I.</creator><creator>Correa, D.</creator><general>Elsevier Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>M7N</scope><orcidid>https://orcid.org/0000-0001-6619-2058</orcidid><orcidid>https://orcid.org/0000-0002-3354-4421</orcidid></search><sort><creationdate>201607</creationdate><title>Mouse model of congenital infection with a non-virulent Toxoplasma gondii strain: Vertical transmission, “sterile” fetal damage, or both?</title><author>Vargas-Villavicencio, J.A. ; Cedillo-Peláez, C. ; Rico-Torres, C.P. ; Besné-Mérida, A. ; García-Vázquez, F. ; Saldaña, J.I. ; Correa, D.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c398t-87e339a67a204b4651fc004fbc897cb67137dc0e3f4e212533d5039a7246260e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Animals</topic><topic>Congenital toxoplasmosis</topic><topic>Disease Models, Animal</topic><topic>DNA-Binding Proteins - genetics</topic><topic>Embryo Loss - parasitology</topic><topic>Female</topic><topic>Fetus - parasitology</topic><topic>Fetus - pathology</topic><topic>Hemorrhage</topic><topic>Infectious Disease Transmission, Vertical</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>Mouse model</topic><topic>Necrosis</topic><topic>Parasite Load</topic><topic>Parasitic load</topic><topic>Pathology</topic><topic>Placenta - parasitology</topic><topic>Placenta - pathology</topic><topic>Pregnancy</topic><topic>Pregnancy Complications, Parasitic - parasitology</topic><topic>Pregnancy Complications, Parasitic - pathology</topic><topic>Specific Pathogen-Free Organisms</topic><topic>Spleen - parasitology</topic><topic>Thrombosis</topic><topic>Toxoplasma gondii</topic><topic>Toxoplasmosis, Animal - congenital</topic><topic>Toxoplasmosis, Animal - pathology</topic><topic>Toxoplasmosis, Animal - transmission</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Vargas-Villavicencio, J.A.</creatorcontrib><creatorcontrib>Cedillo-Peláez, C.</creatorcontrib><creatorcontrib>Rico-Torres, C.P.</creatorcontrib><creatorcontrib>Besné-Mérida, A.</creatorcontrib><creatorcontrib>García-Vázquez, F.</creatorcontrib><creatorcontrib>Saldaña, J.I.</creatorcontrib><creatorcontrib>Correa, D.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><jtitle>Experimental parasitology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Vargas-Villavicencio, J.A.</au><au>Cedillo-Peláez, C.</au><au>Rico-Torres, C.P.</au><au>Besné-Mérida, A.</au><au>García-Vázquez, F.</au><au>Saldaña, J.I.</au><au>Correa, D.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Mouse model of congenital infection with a non-virulent Toxoplasma gondii strain: Vertical transmission, “sterile” fetal damage, or both?</atitle><jtitle>Experimental parasitology</jtitle><addtitle>Exp Parasitol</addtitle><date>2016-07</date><risdate>2016</risdate><volume>166</volume><spage>116</spage><epage>123</epage><pages>116-123</pages><issn>0014-4894</issn><eissn>1090-2449</eissn><abstract>Congenital transmission of Toxoplasma gondii may occur if the mother gets infected for the first time while pregnant. The risk of mother-to-child transmission depends on the gestation trimester at infection, being lowest in the first and highest in the last. Conversely, fetal damage is frequent and more severe at the beginning of pregnancy. The objective of this study was to evaluate congenital transmission and pathological aspects in the placenta and the fetus using a mouse model of congenital infection of the second gestation third. Forty-five female BALB/c mice were infected intravenously with 2.5–10.0 × 106 tachyzoites of the ME49 strain at middle gestation. Samples of maternal spleen and fetal/placental units were taken 72 h later. We determined parasite load and vertical transmission by qPCR, as well as damage macroscopically and by histopathology. With the lowest dose, 18% of the fetuses were infected. Also, 40% of fetuses/litter were altered, while this value was 10% in the control group (P < 0.05). These results are similar to those described in humans in terms of vertical transmission and fetal damage during the second third of gestation. The maternal spleen had 10–1000 times more tachyzoites than the placenta, and the later retained 90–99% of the parasites that could reach the fetus. Nevertheless, we found resorptions, abortions or fetal tissue damage in the presence but also in the absence of parasites. Our data indicate a strong protective effect of maternal organs and the placenta against fetal infection, but extensive damage of the later may led to resorption or abortion without vertical transmission.
[Display omitted]
•Mouse model with Toxoplasma gondii avirulent strain causes infection/damage rates similar to humans.•Up to 105 times tachyzoites in mother infected with ME49 strain as compared to fetus.•Avirulent T. gondii strain causes resorption or abortion without fetal infection.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>27068784</pmid><doi>10.1016/j.exppara.2016.04.002</doi><tpages>8</tpages><orcidid>https://orcid.org/0000-0001-6619-2058</orcidid><orcidid>https://orcid.org/0000-0002-3354-4421</orcidid></addata></record> |
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subjects | Animals Congenital toxoplasmosis Disease Models, Animal DNA-Binding Proteins - genetics Embryo Loss - parasitology Female Fetus - parasitology Fetus - pathology Hemorrhage Infectious Disease Transmission, Vertical Male Mice Mice, Inbred BALB C Mice, Inbred C57BL Mice, Knockout Mouse model Necrosis Parasite Load Parasitic load Pathology Placenta - parasitology Placenta - pathology Pregnancy Pregnancy Complications, Parasitic - parasitology Pregnancy Complications, Parasitic - pathology Specific Pathogen-Free Organisms Spleen - parasitology Thrombosis Toxoplasma gondii Toxoplasmosis, Animal - congenital Toxoplasmosis, Animal - pathology Toxoplasmosis, Animal - transmission |
title | Mouse model of congenital infection with a non-virulent Toxoplasma gondii strain: Vertical transmission, “sterile” fetal damage, or both? |
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