| pubmed-article:18523590 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:18523590 | lifeskim:mentions | umls-concept:C1655731 | lld:lifeskim |
| pubmed-article:18523590 | lifeskim:mentions | umls-concept:C1413580 | lld:lifeskim |
| pubmed-article:18523590 | lifeskim:mentions | umls-concept:C0040560 | lld:lifeskim |
| pubmed-article:18523590 | lifeskim:mentions | umls-concept:C1274040 | lld:lifeskim |
| pubmed-article:18523590 | lifeskim:mentions | umls-concept:C1412063 | lld:lifeskim |
| pubmed-article:18523590 | lifeskim:mentions | umls-concept:C0314603 | lld:lifeskim |
| pubmed-article:18523590 | lifeskim:mentions | umls-concept:C1521761 | lld:lifeskim |
| pubmed-article:18523590 | lifeskim:mentions | umls-concept:C0205210 | lld:lifeskim |
| pubmed-article:18523590 | pubmed:issue | 6 | lld:pubmed |
| pubmed-article:18523590 | pubmed:dateCreated | 2008-6-4 | lld:pubmed |
| pubmed-article:18523590 | pubmed:abstractText | Primary Toxoplasma gondii infection during pregnancy can be transmitted to the fetus. At birth, infected infants may have intracranial calcification, hydrocephalus, and retinochoroiditis, and new ocular lesions can occur at any age after birth. Not all children who acquire infection in utero develop these clinical signs of disease. Whilst severity of disease is influenced by trimester in which infection is acquired by the mother, other factors including genetic predisposition may contribute. | lld:pubmed |
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| pubmed-article:18523590 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:18523590 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:18523590 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:18523590 | pubmed:issn | 1932-6203 | lld:pubmed |
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