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Chapter 12 :

Author: Jeffrey D. Kravetz1
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Affiliations: 1: Veterans Affairs Healthcare System, West Haven, CT 06516, and Yale University School of Medicine, New Haven, CT 06520
Content Type: Monograph
Publication Year: 2009

Category: Clinical Microbiology

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Abstract:

is an obligate intracellular protozoan that has the ability to infect all mammals, as well as birds and rodents, who serve as intermediate hosts. In immunocompetent hosts, 90% of primary infections caused by are asymptomatic. Reactivation of can thus lead to long-term consequences of a primary infection that occurred in the remote past. has a complex life cycle, with both asexual and sexual reproduction leading to the formation of three different forms of the protozoan. Congenital toxoplasmosis results from the transplacental transmission of infective tachyzoites from a mother with a primary toxoplasmosis infection. Ocular toxoplasmosis can occur in both immunocompetent and immunocompromised hosts and can lead to wide array of symptoms, from asymptomatic retinal scars to blindness requiring enucleation. Clinically, ocular toxoplasmosis can cause a range of symptoms. In Tanzania, a study of 849 pregnant women revealed evidence of congenital toxoplasma infection in 0.8% of newborns. Thus, though congenital toxoplasmosis in the United States is uncommon, its frequency in other countries makes it a worldwide newborn health problem. Most cases of toxoplasma encephalitis occur in human immunodeficiency virus (HIV)-infected individuals with AIDS. Other risk factors associated with toxoplasma encephalitis include lymphoma (either Hodgkin’s or non-Hodgkin’s lymphoma), treatment with immunosuppressants for other malignancies or following organ transplantation, and use of high-dose steroids.

Citation: Kravetz J. 2009. , p 217-228. In Fratamico P, Smith J, Brogden K (ed), Sequelae and Long-Term Consequences of Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555815486.ch12
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Toxoplasma gondii
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Citation: Kravetz J. 2009. , p 217-228. In Fratamico P, Smith J, Brogden K (ed), Sequelae and Long-Term Consequences of Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555815486.ch12
/content/10.1128/9781555815486.ch12.ch12fig01
Figure 1.
Risk of congenital infection according to duration of gestation at maternal seroconversion. (Reprinted from [ ] with permission from Elsevier.)
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10.1128/9781555815486/ch12fig1.gif
Image of Figure 1.
Figure 1.

Risk of congenital infection according to duration of gestation at maternal seroconversion. (Reprinted from [ ] with permission from Elsevier.)

Citation: Kravetz J. 2009. , p 217-228. In Fratamico P, Smith J, Brogden K (ed), Sequelae and Long-Term Consequences of Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555815486.ch12
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Figure 2.
Risk of developing clinical signs (not necessarily symptomatic) before age 3 years according to gestational age. (Reprinted from [ ] with permission from Elsevier.)
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10.1128/9781555815486/ch12fig2.gif
Image of Figure 2.
Figure 2.

Risk of developing clinical signs (not necessarily symptomatic) before age 3 years according to gestational age. (Reprinted from [ ] with permission from Elsevier.)

Citation: Kravetz J. 2009. , p 217-228. In Fratamico P, Smith J, Brogden K (ed), Sequelae and Long-Term Consequences of Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555815486.ch12
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Figure 3.
Seroprevalence of , by age and sex; Third National Health and Nutrition Examination Survey, 1988–1994. White bars represent males, black bars represent females. In the age group 30 to 39 years (*), seroprevalence was higher in males than in females ( = 0.02). Among children under 12 years (†), seroprevalence estimates are unstable because of low sample representation in these categories. (Reprinted from the [ ] with permission of Oxford University Press.)
10.1128/9781555815486/ch12fig3_thmb.gif
10.1128/9781555815486/ch12fig3.gif
Image of Figure 3.
Figure 3.

Seroprevalence of , by age and sex; Third National Health and Nutrition Examination Survey, 1988–1994. White bars represent males, black bars represent females. In the age group 30 to 39 years (*), seroprevalence was higher in males than in females ( = 0.02). Among children under 12 years (†), seroprevalence estimates are unstable because of low sample representation in these categories. (Reprinted from the [ ] with permission of Oxford University Press.)

Citation: Kravetz J. 2009. , p 217-228. In Fratamico P, Smith J, Brogden K (ed), Sequelae and Long-Term Consequences of Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555815486.ch12
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Figure 4.
T1-weighted axial gadolinium-enhanced magnetic resonance image of toxoplasmosis encephalitis. (Image reprinted with permission from eMedicine.com, 2008; available at http://emedicine.medscape.com/article/344706-overview.)
10.1128/9781555815486/ch12fig4_thmb.gif
10.1128/9781555815486/ch12fig4.gif
Image of Figure 4.
Figure 4.

T1-weighted axial gadolinium-enhanced magnetic resonance image of toxoplasmosis encephalitis. (Image reprinted with permission from eMedicine.com, 2008; available at http://emedicine.medscape.com/article/344706-overview.)

Citation: Kravetz J. 2009. , p 217-228. In Fratamico P, Smith J, Brogden K (ed), Sequelae and Long-Term Consequences of Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555815486.ch12
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Tables

Toxoplasma gondii
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Citation: Kravetz J. 2009. , p 217-228. In Fratamico P, Smith J, Brogden K (ed), Sequelae and Long-Term Consequences of Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555815486.ch12
/content/10.1128/9781555815486.ch12.ch12tab01
Table 1.
Counseling for reduction of primary toxoplasmosis in women of childbearing age
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Table 1.

Counseling for reduction of primary toxoplasmosis in women of childbearing age

Citation: Kravetz J. 2009. , p 217-228. In Fratamico P, Smith J, Brogden K (ed), Sequelae and Long-Term Consequences of Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555815486.ch12

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