Prematurity and Severity Are Associated With Toxoplasma gondii Alleles (NCCCTS, 1981–2009)

McLeod, Rima; Boyer, Kenneth M.; Lee, Daniel; Mui, Ernest; Wroblewski, Kristen; Karrison, Theodore; Noble, A. Gwendolyn; Withers, Shawn; Swisher, Charles N.; Heydemann, Peter; Sautter, Mari; Babiarz, Jane; Rabiah, Peter; Meier, Paul; Grigg, Michael E.

doi:10.1093/cid/cis258

Cited by 148 publications

(135 citation statements)

References 33 publications

Supporting

Mentioning

131

Contrasting

Unclassified

Order By: Relevance

“…According to recent research in North America, 39% of CT cases (in a sample of 166) were exclusively of type 2 genotype, but the remaining 61% were not. 19 Thus, for North American CT cases we assigned a 39% frequency of chorioretinitis, as in Europe, and to the remaining 61% of patients we assigned the same frequency of sequelae as observed in South American patients. We used the same disease model as reported in a previous paper.…”

Section: Disease Model and Disability Weightsmentioning

confidence: 99%

The global burden of congenital toxoplasmosis: a systematic review

Torgerson

Mastroiacovo

2013

Bull. World Health Organ.

593

486

View full text Add to dashboard Cite

Section: Disease Model and Disability Weightsmentioning

confidence: 99%

The global burden of congenital toxoplasmosis: a systematic review

Torgerson

Mastroiacovo

2013

Bull. World Health Organ.

593

486

View full text Add to dashboard Cite

“…Precautions to prevent infection are important for this group, especially when traveling to areas of the world with higher rates of infection such as much of Latin America. The potential to cause more severe illness is now being associated with specific serotypes of T. gondii 27 and as test development progresses there may be an opportunity in the future to evaluate the prevalence of various T. gondii serotypes in the United States in a representative sample of the population.…”

mentioning

confidence: 99%

Toxoplasma gondii Seroprevalence in the United States 2009–2010 and Comparison with the Past Two Decades

Jones¹,

Kruszon-Moran²,

Rivera³

et al. 2014

The American Society of Tropical Medicine and Hygiene

134

104

View full text Add to dashboard Cite

Abstract. Toxoplasma gondii is a ubiquitous parasite that can cause neurologic and ocular disease. We tested sera from 7,072 people 6 years of age in the 2009-2010 National Health and Nutrition Examination Survey (NHANES) for immunoglobulin G antibodies and compared these results with two previous NHANES studies. The overall T. gondii antibody seroprevalence among persons 6 years of age in 2009-2010 was 13.2% (95% confidence limit [CL] 11.8%, 14.5%) and age-adjusted seroprevalence was 12.4% (95% CL 11.1%, 13.7%); age-adjusted seroprevalence among women 15-44 years of age was 9.1% (95% CL 7.2%, 11.1%). In U.S. born persons 12-49 years of age, the age-adjusted T. gondii seroprevalence decreased from 14.1% (95% CL 12.7%, 15.5%) in NHANES III (1988-1994 to 9.0% (95% CL 7.6%, 10.5%) in NHANES 1999-2004 in NHANES 2009-2010 (P 0.001 linear trend). Although T. gondii antibody presence is still relatively common, the prevalence in the United States has continued to decline.

show abstract

“…The disease caused by T. gondii is usually asymptomatic but can be severe in immunosuppressed individuals, and cyst reactivation causes toxoplasmic encephalitis in AIDS patients (1). In addition, infection of nonimmune women during pregnancy can lead to congenital infection, with hydrocephaly, microcephaly, or intracerebral calcifications occurring in the fetus (2).…”

mentioning

confidence: 99%

Transcriptome Analysis of Mouse Brain Infected with Toxoplasma gondii

et al. 2013

View full text Add to dashboard Cite

c Toxoplasma gondii is an obligate intracellular parasite that invades a wide range of vertebrate host cells. Chronic infections with T. gondii become established in the tissues of the central nervous system, where the parasites may directly or indirectly modulate neuronal function. However, the mechanisms underlying parasite-induced neuronal disorder in the brain remain unclear. This study evaluated host gene expression in mouse brain following infection with T. gondii. BALB/c mice were infected with the PLK strain, and after 32 days of infection, histopathological lesions in the frontal lobe were found to be more severe than in other areas of the brain. Total RNA extracted from infected and uninfected mouse brain samples was subjected to transcriptome analysis using RNA sequencing (RNA-seq). In the T. gondii-infected mice, 935 mouse brain genes were upregulated, whereas 12 genes were downregulated. GOstat analysis predicted that the upregulated genes were primarily involved in host immune responses and cell activation. Positive correlations were found between the numbers of parasites in the infected mouse brains and the expression levels of genes involved in host immune responses. In contrast, genes that had a negative correlation with parasite numbers were predicted to be involved in neurological functions, such as small-GTPase-mediated signal transduction and vesicle-mediated transport. Furthermore, differential gene expression was observed between mice exhibiting the clinical signs of toxoplasmosis and those that did not. Our findings may provide insights into the mechanisms underlying neurological changes during T. gondii infection.T oxoplasma gondii, an obligate intracellular parasite, invades a wide variety of cells in its vertebrate hosts. The disease caused by T. gondii is usually asymptomatic but can be severe in immunosuppressed individuals, and cyst reactivation causes toxoplasmic encephalitis in AIDS patients (1). In addition, infection of nonimmune women during pregnancy can lead to congenital infection, with hydrocephaly, microcephaly, or intracerebral calcifications occurring in the fetus (2).Systemic infection by the proliferating stage of the parasite, the tachyzoite, is efficiently controlled by the cellular immune response. However, the pathogen persists in its slowly replicating stage, the bradyzoite, in tissue cysts mainly within the muscle and brain. In chronic infections, parasites within neurons can directly cause neuronal death and atrophy of neuronal processes, while inflammation via production of nitric oxide (NO) and inflammatory cytokines from microglia or immune cells may contribute to the death of neighboring neurons (3). However, the mechanisms underlying parasite-induced neuronal disorder in the brain remain unclear.In mice and rats, the specificity of behavioral modifications induced by T. gondii has been examined across a broad range of behaviors that primarily concern anxiety and learned fear in these animals (4). Recently, it has been suggested that chronic infection with T...

show abstract

Prematurity and Severity Are Associated With Toxoplasma gondii Alleles (NCCCTS, 1981–2009)

Abstract: NCT00004317.

Cited by 148 publications

References 33 publications

The global burden of congenital toxoplasmosis: a systematic review

The global burden of congenital toxoplasmosis: a systematic review

Toxoplasma gondii Seroprevalence in the United States 2009–2010 and Comparison with the Past Two Decades

Transcriptome Analysis of Mouse Brain Infected with Toxoplasma gondii

Contact Info

Product

Resources

About