Toxoplasmosis

Published on 09/02/2015 by admin

Filed under Allergy and Immunology

Last modified 09/02/2015

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Toxoplasmosis

Learning Objectives

At the conclusion of this chapter, the reader should be able to:

• Describe the etiology and epidemiology of toxoplasmosis.

• Explain the signs and symptoms of acquired and congenital toxoplasmosis infection.

• Discuss the immunologic manifestations and diagnostic evaluation of toxoplasmosis, including the quantitative determination of IgM antibodies to Toxoplasma gondii.

• Analyze a case study related to toxoplasmosis.

• Correctly answer case study related multiple choice questions.

• Be prepared to participate in a discussion of critical thinking questions.

• Describe the principle, interpretation, and limitations of the TORCH procedure.

• Correctly answer end of chapter review questions.

Key Terms

Epidemiology

T. gondii was first discovered in a North African rodent and has been observed in numerous birds and mammals worldwide, including human beings. It is a parasite of cosmopolitan distribution able to develop in a wide variety of vertebrate hosts.

Human infections are common in many parts of the world. The prevalence of infection in adults ranges from less than 10% to more than 90%; higher prevalences tend to occur at lower elevations and in latitudes closer to the equator. The highest recorded rate (93%) was in Parisian women who preferred undercooked or raw meat; a 50% rate of occurrence was documented in the children of these women. Toxoplasma infection rates vary around the world. In the United States, it’s about 10% to 15%, while rates in Europe and Brazil are much higher, around 50% to 80%. These are only estimates. Calculating exact rates is difficult because most infected people don’t have any symptoms.

Toxoplasmosis is not passed from person-to-person, except in cases of mother to child (congenital) transmission and blood transfusion or organ transplantation. People typically become infected by three principal routes of transmission:

The definitive host is the house cat and other members of the Felidae family (Fig. 20-1). Domestic cats are a source of the disease because oocysts are often present in their feces. Accidental ingestion of oocysts by human beings and animals, including the cat, produces a proliferative infection in the body tissues. Fecal contamination of food or water, soiled hands, inadequately cooked or infected meat, and raw milk can be major sources of human infection. The risk for infection is higher in many developing and tropical countries, especially when people eat undercooked meat, drink untreated water, or are extensively exposed to soil.

image
Figure 20-1 Life cycle of Toxoplasma gondii. (Adapted from Katz SL, Gershon AA, Wilfert CM, Krugman S editors: Infectious diseases of children, ed 9, St Louis, 1992, Mosby.)

Organ transplant recipients can become infected by receiving an organ from a Toxoplasma-positive donor. Transfusion-transmitted toxoplasmosis has been associated with the use of leukocyte concentrates. Patients at risk are those receiving immunosuppressive agents or corticosteroids. Laboratory workers who handle infected blood can also acquire infection through accidental inoculation.

Transplacental Transmission

All mammals, including human beings, can transmit the infection transplacentally. Transplacental transmission usually takes place in the course of an acute but inapparent or undiagnosed maternal infection. Evidence has shown that the number of infants born in the United States each year with congenital T. gondii infection is considerably higher than the 3000 previously estimated. It is estimated that 6 of 1000 pregnant women in the United States will acquire primary infection with Toxoplasma during a 9-month gestation. Approximately 45% of women who acquire the infection for the first time and who are not treated will give birth to congenitally infected infants. Consequently, the expected incidence of congenital toxoplasmosis is 2.7/1000 live births.

It is recommended that all pregnant women be tested for toxoplasmosis immunity. If a patient is susceptible, screening should be repeated during pregnancy and at delivery. Prevention of infection in pregnant women should be practiced to avert congenital toxoplasmosis (Box 20-1). To further prevent infection of the fetus, women at risk should be identified by serologic testing and pregnant women with primary infection should receive drug therapy.

Box 20-1   Methods for Prevention of Congenital Toxoplasmosis

Avoid touching mucous membranes of the mouth and eye while handling raw meat.

Wash hands thoroughly after handling raw meat.

Wash kitchen surfaces that come in contact with raw meat.

Cook meat to >18.8° C (65.8° F); smoke it or cure it in brine.

Wash fruits and vegetables before consumption.

Prevent access of flies, cockroaches, and other insects to fruits and vegetables.

Avoid contact with or wear gloves when handling materials that are potentially contaminated with cat feces (e.g., cat litter boxes) and when gardening.

Signs and Symptoms

In adults and children other than newborns, toxoplasmosis is usually asymptomatic. A generalized infection probably occurs. Although spontaneous recovery follows acute febrile disease, the organism can localize and multiply in any organ of the body or the circulatory system.

Toxoplasma can be harmful to individuals with suppressed immune systems. Toxoplasmic encephalitis in AIDS patients may result in death, even when treated (Fig. 20-2). Persons at risk can be identified by screening patients positive for human immunodeficiency virus (HIV) for antibody to T. gondii.

image
Figure 20-2 Toxoplasmic meningoencephalitis.
Shown are magnetic resonance imaging (MRI) brain scans of patients with AIDS. Arrows indicate areas infected with toxoplasmosis.

Acquired Infection

When seen, symptoms are frequently mild. Toxoplasmosis can simulate infectious mononucleosis, with chills, fever, headache, lymphadenopathy, and extreme fatigue. Primary infection may be promoted by immunosuppression. A chronic form of toxoplasmic lymphadenopathy exists. T. gondii presents a special problem in immunosuppressed or otherwise compromised hosts. Some of these patients have experienced reactivation of a latent toxoplasmosis. These patients have included those with Hodgkin’s and non-Hodgkin’s lymphoma, as well as recipients of organ transplants.

Reactivation of cerebral toxoplasmosis is not uncommon in patients with AIDS, in whom toxoplasmic meningoencephalitis is almost always a reactivation of a preexisting latent infection, most often occurring when the total CD4 count falls below 100 × 109/L. T. gondii–seropositive, HIV-infected patients may develop toxoplasmic encephalitis because of the following: (1) genetic susceptibility in the human immune response to T. gondii; (2) subtle differences in patients’ immunocompromised status; (3) differences in the virulence of individual strains of T. gondii; (4) possible recurrent infections with different strains; and (5) variable coinfections with other opportunistic pathogens.

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