AUTHOR AND EDITOR INFORMATION

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INTRODUCTION

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Background

Toxoplasma gondii is a widely distributed protozoan that usually causes an asymptomatic infection in the healthy host. Toxoplasmosis refers to a symptomatic infection by T gondii and can be acute or chronic. Apart from disease in immunocompromised individuals, congenital toxoplasmosis is the most serious manifestation of infection, resulting from vertical transmission of T gondii from a parasitemic mother to her offspring. The severity of disease depends on the gestational age at transmission. Ophthalmologic and neurologic disabilities are the most important consequences of infection and can be present even when the congenital infection is asymptomatic. Congenital toxoplasmosis is a preventable disease. Prepregnancy screening accompanied by serial titers and appropriate counseling in women with initial negative titers would minimize cases.

Pathophysiology

T gondii is an obligate intracellular protozoan. It has an intestinal and an extraintestinal cycle in cats but only an extraintestinal cycle in other hosts, including herbivores, omnivores, and carnivores.

T gondii exists in 3 forms, as follows:

• Bradyzoites are slowly multiplying organisms contained in tissue cysts, usually localized to muscle (skeletal and cardiac) and brain. They live in their host cells for months to years. Once ingested, gastric enzymes degrade the cyst wall, liberating viable bradyzoites.
• Tachyzoites are rapidly dividing organisms found in tissues during the acute phase of infection. The tachyzoites are the forms responsible for tissue destruction. Multiplication continues until either cyst formation or host cell destruction occurs. After cell death, the free tachyzoites invade other cells and resume rapid multiplication.
• Sporozoites (oocysts) result from the parasite's sexual cycle, which takes place in the epithelial cells of the cat intestine. When eliminated by the cat, these cysts must first undergo sporulation to become infectious, a process that takes 2-3 days in temperate climates and longer in cold climates. Therefore, the risk of infection is minimized if cat litter boxes are cleaned daily. Cats shed 1-100 million oocysts after the first infection, but, because of immunity, reinfection is rarely followed by reshedding of oocysts. Passive antibody transference to newborn kittens does not prevent shedding of oocysts.

Human horizontal infection occurs from ingesting food contaminated with oocysts or poorly cooked food containing tissue cysts (bradyzoites). Although experimental attempts to transmit tachyzoites by arthropods were negative, cockroaches and flies are believed to be able to transport oocysts to water and food. Because parasitemia can persist up to a year in healthy persons, blood transfusion is a potential source of infection. Once the individual is infected, the organism persists as tissue cysts for life. The degree of organ involvement varies considerably among patients but mostly depends on the immune status of the host. Fetuses and immunocompromised patients are most severely affected.

Vertical transmission is the cause of congenital toxoplasmosis. The infection can occur in utero or during a vaginal delivery. Transmission by breastfeeding has not been demonstrated. In general, only primary infection during pregnancy results in congenital toxoplasmosis. Thus, it is exceedingly rare for a woman to deliver a second child with congenital toxoplasmosis unless she is immunocompromised, usually from acquired immunodeficiency syndrome (AIDS). Infections that occur before but within 6 months of conception may result in transplacental transmission. Intrauterine exposure can result in an uninfected infant or infection that ranges from being asymptomatic to causing stillbirth. Approximately 30% of exposed fetuses acquire the infection, but most of the infants are asymptomatic. The severity of infection in the fetus depends on the gestational age at the time of transmission.

In general, earlier infection is more severe but less frequent. As a consequence, 85% of live infants with congenital infection appear normal at birth. Very early infections (ie, occurring in the first trimester) may result in fetal death in utero or in a newborn with severe central nervous system (CNS) involvement, such as cerebral calcifications and hydrocephalus.

Frequency

United States

The frequency of congenital toxoplasmosis depends on the incidence of primary infection in women of childbearing age. The earlier a woman acquires a primary infection, the less likely she is to transmit the parasite to her offspring. Prevalence increases with age. In New York, antibody prevalence was 16% in women aged 15-19 years, 27% in women aged 20-24 years, 33% in women aged 25-29 years, 40% in women aged 30-34 years, and 50% in women older than 35 years. Rates in women of childbearing age in Palo Alto, California, dropped from 27% in 1964 to 10% in 1987. Other areas in the United States report positive antibody titers in women of childbearing age of 30% in Birmingham (1983), 12% in Chicago (1987), 14% in Massachusetts (1998), 3.3% in Denver (1986), 30% in Los Angeles (1993), 12% in Texas (1993), and 13% in New Hampshire (1998).

The prevalence of congenital infection can be indirectly estimated from the incidence rate of primary infection during pregnancy by multiplying the number of mothers who acquire infection during pregnancy by the transmission rate of the parasite to the fetus. On the basis of data from the National Health and Nutrition Examination Survey during 1989-1994, the incidence of primary infection for seronegative pregnant women was 0.27%. With 4 million births per year and an overall transmission rate of 33%, approximately 3500 infected children should be born in the United States every year. The rate likely varies by region.

Direct estimates of congenital infection may be derived by measuring anti-Toxoplasma IgM in newborn sera. However, this may underestimate the true incidence because infants with toxoplasmosis may not have demonstrable IgM in up to 20% of cases. In Alabama, the incidence was 0.1 per 1000 births. Health care workers in Massachusetts began screening sera of newborns in 1986. From 1986-1998, a total of 99 cases were detected (incidence of 1 in 10,000 births) in Massachusetts, but at least 6 cases were missed by the screening.

International

Worldwide, the reported incidence of congenital toxoplasmosis is decreasing. The prevalence of positive antibody titers among pregnant women is often higher outside the United States. The rate of positive antibody titers is 81% in the Central African Republic, 48% in Tanzania, 23% in Zambia, 53-58% in Argentina, 36% in Austria, 46% in Belgium, 59% in Chile, 60% in Colombia, more than 75% in Ethiopia, 52% in France, and 46% in Guatemala. The estimated incidence of congenital toxoplasmosis is 6 per 1000 births in France, 2 per 1000 births in Poland, 7-10 per 1000 births in Colombia, and 3 per 1000 births in Slovenia.

Mortality/Morbidity

Fetuses and immunocompromised individuals are at particularly high risk for severe sequelae and even death. Infection acquired postnatally is usually much less severe.

• Newborns with acute congenital toxoplasmosis often die in the first month of life.
• Subacute congenital disease may not be observed until some time after birth, when symptoms start to appear.

Race

The incidence of disease depends on sanitary conditions and culinary habits. The ingestion of raw or poorly cooked meat increases the risk of toxoplasmosis. Individuals with poor sanitary conditions and those who eat raw or poorly cooked meat are at an increased risk of acquiring Toxoplasma infection, unrelated to race.

Sex

Incidence does not significantly vary between the sexes.

Age

Incidence of T gondii antibodies increases with increasing age. The seroconversion rate in women of childbearing age is 0.8% per year. The risk of transplacental transmission is greatest during the third trimester of pregnancy.

CLINICAL

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History

Pediatric toxoplasmosis can be acute or chronic, asymptomatic or symptomatic, and congenital or postnatally acquired.

• Congenital toxoplasmosis is the consequence of transplacental hematogenous fetal infection by T gondii during primary infection in pregnant women. Primary infection in an otherwise healthy pregnant woman is asymptomatic in 60% of cases. Symptoms during pregnancy are frequently mild. The most common manifestations are fatigue, malaise, a low-grade fever, lymphadenopathy, and myalgias. Latent Toxoplasma infection with reactivation during pregnancy may lead to congenital infection only in immunocompromised women (most commonly, those with AIDS).
• The classic triad of chorioretinitis, hydrocephalus, and intracranial calcifications cannot be used as a strict diagnostic criterion for congenital toxoplasmosis because a large number of cases would be missed. Congenital toxoplasmosis may occur in the following forms:
• • Neonatal disease
  • Disease occurring in the first months of life
  • Sequelae or relapse of previously undiagnosed infection
  • Subclinical infection
• When clinically recognized in the neonate, congenital toxoplasmosis is very severe. Signs of generalized infection are usually present, such as intrauterine growth retardation, jaundice, hepatomegaly, splenomegaly, lymphadenopathy, and a rash. Neurologic signs are severe and always present. They include microcephaly or macrocephaly, bulging fontanelle, nystagmus, abnormal muscle tone, seizures, and delay of developmental milestone acquisition.
• • Most cases of chorioretinitis result from congenital infection, although patients are often asymptomatic until later in life. Symptoms include blurred vision, scotoma, pain, photophobia, and epiphora. Impairment of central vision occurs when the macula is involved, but vision may improve as inflammation resolves. Relapses of chorioretinitis are frequent but rarely accompanied by systemic signs or symptoms.
  • Latent toxoplasmosis may reactivate in women with human immunodeficiency virus (HIV) and result in congenital transmission. Congenital toxoplasmosis in the infant with HIV appears to run a more rapid course than in infants without HIV.

Physical

• Lymphadenopathy is the most common form of symptomatic acute toxoplasmosis in immunocompetent individuals.
• Patients typically present with painless firm lymphadenopathy that is confined to one chain of nodes, which are most commonly cervical. The suboccipital, supraclavicular, axillary, and inguinal groups may also be involved.
• Other physical manifestations include a low-grade fever, occasional hepatosplenomegaly, and a rash.
• Ophthalmologic examination reveals multiple yellow-white cottonlike patches with indistinct margins located in small clusters in the posterior pole.
• Characteristically, a focal necrotizing retinitis develops that may atrophy and generate black pigment, or it may be associated with panuveitis. Papillitis is usually indicative of CNS disease. Flare-up of congenitally acquired chorioretinitis is often associated with scarred lesions in proximity to the fresh lesions.
• Because of multifocal involvement of the CNS, clinical findings vary widely. They include alterations in mental status, seizures, motor weakness, cranial nerve disorders, sensory abnormalities, cerebellar signs, meningismus, movement disorders, and neuropsychiatric manifestations in patients with immunocompromise.

Causes

• The etiologic agent is T gondii.
• • Congenital disease is passed transplacentally from the newly infected mother to the fetus during pregnancy.
  • Other syndromes may result from newly acquired infection or reactivation of latent infection.
  • Ingestion of meat or foods containing cysts or oocysts present in cat feces can cause infection.
  • Infection can be transmitted by blood transfusion or organ transplantation.
• Hosts who are immunocompromised, especially those with defects in cellular immunity such as AIDS, are also at increased risk for severe disease.

DIFFERENTIALS

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Other Problems to be Considered

Congenital toxoplasmosis - Encephalopathies, erythroblastosis fetalis, lymphocytic choriomeningitis virus infection
Toxoplasma encephalitis (TE) - Vasculitis, progressive multifocal leukoencephalopathy, malignancy, lymphocytic choriomeningitis virus infection

WORKUP

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Lab Studies

• Demonstration of T gondii in blood, body fluids, or tissues is evidence of infection.
• Isolation by mouse inoculation of Toxoplasma from amniotic fluid or placental or fetal tissue is diagnostic of congenital infection.
• Lymphocyte transformation in response to Toxoplasma antigens indicates previous infection in adults.
• Detection of Toxoplasma antigens in blood or body fluids by means of enzyme-linked immunoassay (ELISA) indicates acute infection.
• The Sabin-Feldman dye test is a sensitive and specific neutralization test. It measures IgG antibody and is the standard reference test for toxoplasmosis; however, it requires live T gondii and thus is not available in most laboratories. High titers suggest acute disease.
• The indirect fluorescent antibody (IFA) test measures the same antibodies as the dye test. Titers parallel dye test titers. The IgM fluorescent antibody test can be used to detect IgM antibodies within the first week of infection, but titers fall within a few months.
• The indirect hemagglutination test measures a different antibody than does the dye test. Titers tend to be higher and remain elevated longer.
• The double-sandwich IgM ELISA is more sensitive and specific than other IgM detection tests.
• The IgG avidity test may be able to discriminate acute from chronic infection better than alternative assays, such as assays that measure IgM antibodies. As is true for IgM antibody tests, the avidity test is most useful when performed early in gestation because a chronic pattern occurring late in pregnancy does not rule out the possibility that the acute infection may have occurred during the first months of gestation. A 2-fold rise in serum IgG obtained at 3-week intervals is diagnostic.
• Performing polymerase chain reaction (PCR) on body fluids, including cerebrospinal fluid (CSF), amniotic fluid, bronchoalveolar lavage fluid, and blood, may be useful in establishing the diagnosis.

Imaging Studies

• Ultrasonography of the fetus to evaluate for evidence of congenital toxoplasmosis can be performed at 20-24 weeks' gestation.
• Computed tomography (CT) of the brain is useful in cerebral toxoplasmosis.
• • In 70-80% of immunodeficient patients with TE, the CT scan depicts multiple bilateral ring-enhancing cerebral lesions.
  • Although multiple lesions are more common, finding a solitary lesion should not exclude TE.
  • The likelihood of TE is approximately 80% in AIDS patients with detectable Toxoplasma IgG and multiple ring-enhancing lesions.
  • Lesions are characteristically hypodense and tend to occur at the corticomedullary junction, frequently involving the basal ganglia.
  • CT frequently underestimates the number of lesions, although delayed imaging after a double dose of intravenous (IV) contrast material may improve the sensitivity of this imaging modality.
  • An enlarging hypodense lesion that does not enhance is a poor prognostic finding.
  • Improvement is seen in up to 90% of patients with AIDS and TE after 2-3 weeks of treatment. Complete resolution lasts from 6 weeks to 6 months; peripheral lesions resolve more rapidly than deeper ones. Radiographic response tends to lag behind clinical response.
• Magnetic resonance imaging (MRI) is the preferred imaging modality to evaluate for lesions.
• • MRI has superior sensitivity, particularly if gadolinium is used for contrast. It can often depict lesions or more extensive disease not apparent on CT scan. Hence, MRI should be used as the initial imaging procedure when feasible and always follow CT demonstration of a single lesion.
  • MRI depicts TE lesions as high signal abnormalities on T2-weighted studies and reveals a rim of enhancement surrounding the edema on T1-weighted contrast-enhanced images.
  • Smaller lesions usually resolve completely on MRI studies within 3-5 weeks, but lesions with a mass effect tend to resolve more slowly and leave a small residual lesion.
• Even characteristic lesions on CT or MRI are not pathognomonic of TE. The major differential diagnosis in patients with AIDS is CNS lymphoma, which appears with multiple enhancing lesions in 40% of cases.
• To evaluate patients with AIDS and focal CNS lesions, a variety of positron emission tomography and radionuclide scans have been used, generally with minimal benefit over the above modalities.

Other Tests

• A skin test showing delayed hypersensitivity to Toxoplasma antigens may be a useful screening test.
• Antibody levels in aqueous humor or CSF may reflect local antibody production and infection at these sites.
• Perform an amniocentesis at 20-24 weeks' gestation in suspected cases of congenital disease.

Procedures

• When single lesions are depicted on MRI, the probability of TE falls and that of lymphoma rises. Brain biopsy is generally required to obtain a definitive diagnosis.

Histologic Findings

The histopathology of toxoplasmosis varies with the immune status of the host. In the healthy host with acquired toxoplasmosis, the characteristic histopathology of the lymph node is diagnostic, despite the relative paucity of organisms present. Typical findings include reactive follicular hyperplasia, irregular clusters of histiocytes encroaching on the margins of germinal centers, and focal distention of sinuses with monocytoid cells. Necrosis, granuloma formation, microabscesses, and vasculitis do not occur. At autopsy of normal hosts, tissue cysts are noted as incidental findings in skeletal muscle and myocardium, invoking little inflammatory response.

By contrast, in patients who are immunodeficient and in children with severe congenital toxoplasmosis, tachyzoite proliferation is accompanied by tissue necrosis and an intense, usually monocytic, inflammatory response. In patients with AIDS, toxoplasmosis typically produces brain abscesses that have a characteristic appearance. A central avascular area is surrounded by a region of necrosis and inflammatory cells that may also contain free and intracellular tachyzoites. Outside of the region of inflammation are cysts.

Demonstration of tachyzoites in a tissue specimen is required for definitive diagnosis of active infection. The presence of multiple cysts near an inflammatory lesion makes the diagnosis highly likely. Stains used to detect tachyzoites or cysts include hematoxylin and eosin, periodic acid-Schiff, and Gomori-methenamine silver. Immunoperoxidase and fluorescein-conjugated antibody stains can also be used. Wright-Giemsa staining of body fluid sediments of biopsy tissue touch preparations is a rapid and simple method for visualizing the organisms.

TREATMENT

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Medical Care

• Outpatient care is sufficient for acquired disease in patients with ocular toxoplasmosis and hosts who are immunocompetent.
• Initial inpatient care is appropriate for patients with CNS toxoplasmosis and immunocompromised hosts with acute disease.
• Usually, no treatment is necessary for asymptomatic hosts, except in those younger than 5 years.
• Symptomatic patients should be treated until immunity is assured.
• Immunocompetent patients who are not pregnant and have no vital organ damage can be observed without therapy. Suppressive therapy must continue for HIV-positive patients with active infection and a CD4+ count less than 200.

Consultations

• Infectious disease specialist
• Ophthalmologist
• Neurologist
• Radiologist

Diet

No special diet is required.

Activity

Limitation of activity depends on the severity of disease and the organ systems involved.

MEDICATION

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The currently recommended drugs for T gondii infection act primarily against the tachyzoite form; thus, they do not eradicate the encysted form (bradyzoite). Pyrimethamine is the most effective agent and is included in most drug regimens. Leucovorin (folinic acid) should be administered concomitantly to avoid bone marrow suppression. Unless circumstances arise that preclude using more than one drug, a second drug, such as sulfadiazine or clindamycin, should be added. The efficacy of azithromycin, clarithromycin, atovaquone, dapsone, and cotrimoxazole (ie, trimethoprim-sulfamethoxazole) is unclear; therefore, they should only be used as alternatives in combination with pyrimethamine. The most effective available therapeutic combination is pyrimethamine plus sulfadiazine or trisulfapyrimidine (ie, combination of sulfamerazine, sulfamethazine, and sulfapyrazine). These agents are active against tachyzoites and are synergistic when used in combination.

Additional therapy with corticosteroids (prednisone, 1 mg/kg/d) should be considered with markedly elevated CSF protein (>1g/dL) and vision-threatening chorioretinitis.

Drug Category: Sulfonamide antimicrobials

These agents exert bacteriostatic action through competitive antagonism with para-aminobenzoic acid (PABA). Microorganisms that require exogenous folic acid and do not synthesize folic acid (pteroylglutamic acid) are not susceptible to the action of sulfonamides. Resistant strains are capable of using folic acid precursors or preformed folic acid. These agents exist as 3 forms in serum—free, conjugated (ie, acetylated and possibly others), and protein bound. The free form is considered to be therapeutically active.

Drug Category: Antiprotozoal and antimycobacterial agents

Dapsone, a sulfone that has been widely used in the treatment of leprosy, has been administered in combination with pyrimethamine for prophylaxis against malaria. It is marketed as Maloprim, a combination of pyrimethamine 25 mg and dapsone 100 mg, for malaria prophylaxis. Dapsone with trimethoprim is used as an alternative to trimethoprim-sulfamethoxazole for the treatment of mild-to-moderate Pneumocystis carinii pneumonia, and dapsone alone can be used for prophylaxis. Dapsone and pyrimethamine have also been used in patients with HIV and low CD4+ T-cell counts to prevent T gondii encephalitis.

Drug Category: Lincosamide antimicrobials

These agents inhibit bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest.

Drug Category: Antiprotozoal agents

Protozoal infections occur throughout the world and are a major cause of morbidity and mortality in some regions. Patients who are immunocompromised are especially at risk. Primary immune deficiency is rare; whereas, secondary deficiency is more common. Immunosuppressive therapy, cancer and its treatment, HIV infection, and splenectomy may increase vulnerability to infection. Infectious risk is proportional to neutropenia duration and severity. Protozoal infections are typically more severe in immunocompromised patients than in immunocompetent patients.

Drug Category: Macrolide antimicrobials

Azithromycin is an azalide, a subclass of macrolide antibiotics, for oral administration. Azithromycin is derived from erythromycin; however, it differs chemically from erythromycin in that a methyl-substituted nitrogen atom is incorporated into the lactone ring.

Spiramycin is a macrolide antibiotic with an antibacterial spectrum similar to that of erythromycin and clindamycin. It is bacteriostatic at serum concentrations but may be bactericidal at achievable tissue concentrations. Its mechanism of action is unclear, but it acts on the 50S subunit of bacterial ribosomes and interferes with translocation. Absorption from the gastrointestinal (GI) tract is irregular (20-50% of PO dose absorbed). Following PO administration, peak plasma levels are achieved within 2-4 h. Spiramycin has a longer half-life than erythromycin and sustains higher tissue levels.

Drug Category: Antidote

Supplemental folinic acid is coadministered to prevent hematologic adverse effects caused by bone marrow suppression.

FOLLOW-UP

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Further Inpatient Care

• Standard precautions are recommended.

Further Outpatient Care

• Follow-up visits should occur every 2 weeks until the patient is stable, then monthly during therapy.
• Obtain complete blood count weekly for the first month, then every 2 weeks.
• Perform renal and liver function tests monthly.

Deterrence/Prevention

• Preventing the infection is particularly important for women who are pregnant and for patients who are seronegative and immunocompromised.
• • Avoid consuming raw or undercooked meat, unpasteurized milk, and uncooked eggs.
  • Wash hands after touching raw meat and after gardening or having other contact with soil.
  • Wash fruits and vegetables.
  • Avoid contact with cat feces.
  • To attempt to prevent congenital toxoplasmosis, routine serologic screening of pregnant women has been performed in order to identify fetuses at risk of becoming infected.
• When feasible, avoid transfusions of blood products from a donor who is seropositive to a patient who is seronegative and immunocompromised.
• If possible, recipients who are seronegative should receive transplanted organs from donors who are seronegative.

Complications

• Seizure disorder or focal neurologic deficits may occur in CNS toxoplasmosis.
• Partial or complete blindness may occur with ocular toxoplasmosis.
• Multiple complications may occur with congenital toxoplasmosis, including mental retardation, seizures, deafness, and blindness.

Prognosis

• Relapse often occurs in patients with immunocompromise if treatment is stopped.
• Treatment may prevent the development of untoward sequelae in both symptomatic and asymptomatic infants with congenital toxoplasmosis.

Patient Education

• Mothers who are infected must be completely informed of potential consequences to their fetus.
• Explain prevention methods, such as protecting children's play areas from cat litter.
• For excellent patient education resources, visit eMedicine's Brain and Nervous System Center . Also, see eMedicine's patient education article Brain Infection.

MISCELLANEOUS

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Medical/Legal Pitfalls

• Misdiagnosis is possible.

MULTIMEDIA

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Media file 1:  Toxoplasma gondii trophozoites in tissue culture.
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Media type:  Photo

REFERENCES

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• Beaman MH. Toxoplasmosis. In: Rakel, ed. Conn's Current Therapy. 53rd ed. Philadelphia, Pa: WB Saunders. 2001;156-162. [Full Text].
• Bonfioli AA, Orefice F. Toxoplasmosis. Semin Ophthalmol. Jul-Sep 2005;20(3):129-41. [Medline].
• Boyer KM. Diagnostic testing for congenital toxoplasmosis. Pediatr Infect Dis J. 2001;20:59-60. [Medline].
• Foulon W, Naessens A, Ho-Yen D. Prevention of congenital toxoplasmosis. J Perinat Med. 2000;28:337-45. [Medline].
• Gardner WG. Toxoplasmosis. In: Dambro MR, ed. Griffith's 5-Minute Clinical Consult. Philadelphia, Pa: Lippincott Williams & Wilkins. 1999;1090-1091. [Full Text].
• Hill DE, Chirukandoth S, Dubey JP. Biology and epidemiology of Toxoplasma gondii in man and animals. Anim Health Res Rev. Jun 2005;6(1):41-61. [Medline].
• Jones JL, Lopez A, Wilson M, et al. Congenital toxoplasmosis: a review. Obstet Gynecol Surv. 2001;56:296-305. [Medline].
• McLeod R, Boyer K, Roizen N, et al. The child with congenital toxoplasmosis. Curr Clin Top Infect Dis. 2000;20:189-208. [Medline].
• Montoya JG, Rosso F. Diagnosis and management of toxoplasmosis. Clin Perinatol. Sep 2005;32(3):705-26. [Medline].
• Peyron F, Wallon M. Options for the pharmacotherapy of toxoplasmosis during pregnancy. Expert Opin Pharmacother. 2001;2:1269-74. [Medline].
• Pinon JM, Dumon H, Chemla C, et al. Strategy for diagnosis of congenital toxoplasmosis: evaluation of methods comparing mothers and newborns and standard methods for postnatal detection of immunoglobulin G, M, and A antibodies. J Clin Microbiol. 2001;39:2267-71. [Medline].
• Remington JS, Mc Leod R, Thulliez P. Toxoplasmosis. In: Remington JS and Klein JO,eds. Infectious Diseases of the Fetus and Newborn. 2001;205-346.
• Robert-Gangneux F. Contribution of new techniques for the diagnosis of congenital toxoplasmosis. Clin Lab. 2001;47:135-41. [Medline].
• Schwartzman JD. Toxoplasmosis. Curr Infect Dis Rep. 2001;3:85-89. [Medline].
• Tenter AM, Heckeroth AR, Weiss LM, et al. Toxoplasma gondii: from animals to humans. Int J Parasitol. 2000;30:1217-58. [Medline].
• Tierney LM Jr, McPhee SJ, Papadakis MA. Toxoplasmosis. In: Current Medical Diagnosis & Treatment. 40th ed. McGraw-Hill. 2001;1444-7.
• Trikha I, Wig N. Management of toxoplasmosis in AIDS. Indian J Med Sci. 2001;55:87-98. [Medline].

Article Last Updated: Mar 30, 2006