Basics
Description
Toxoplasmosis is caused by Toxoplasma gondii, an obligate intracellular protozoan parasite with a complex life cycle, which can cause a wide range of clinical symptoms depending on individual strain virulence and the host immune system. ‚
- Primary infection is often asymptomatic and may result in fever, lymphadenopathy, and eye disease.
- Congenital infection classically presents with triad of chorioretinitis, hydrocephalus, and brain calcifications.
- Reactivation of disease may develop after either primary or congenital infection and most commonly presents as chorioretinitis.
- Patients with immune deficiency can develop brain abscesses, encephalitis, fever of unknown origin, or pneumonia.
Epidemiology
- Toxoplasmosis is the leading cause of death due to foodborne illness in the United States.
- T. gondii is found worldwide and can infect most warm-blooded animals.
- Cats are the definitive hosts, and the parasite replicates sexually in the feline small intestine.
- Vertical transmission is more common with primary infection during pregnancy or within 3 months prior to conception. Treatment of primary maternal infection can decrease fetal transmission rate by half from 50 " “60% to 25 " “30%.
Incidence
Congenital infection in the United States occurs in an estimated 1 per 10,000 live births or 400 new cases annually. ‚
Prevalence
- Worldwide, the rate of infection varies greatly and ranges from 7% to 80%.
- In the United States, overall seroprevalence is 11% but may be as high as 40% in areas with lower socioeconomic status.
General Prevention
- Main risk factors for T. gondii infection are eating raw or rare meat, consuming local cured or smoked meat, working with meat, drinking unpasteurized goat milk, or having more than 3 kittens.
- Untreated or contaminated water is also a risk factor and has been responsible for outbreaks of toxoplasmosis.
- Pregnant women should be counseled to avoid cat feces exposure including gardening, landscaping, and changing litter boxes and to avoid consuming undercooked meat.
Pathophysiology
- Cats shed oocysts in feces, which then sporulate and become infectious.
- Humans are infected by eating raw or undercooked meat infested with oocytes; accidental ingestion of contaminated soil, food, or water; contaminated blood transfusion or organ donation; or via transplacental transmission from mother to fetus.
- In the human host, tissue cysts are formed in skeletal muscle, myocardium, brain, and eyes.
- Tissue cysts persist for the life of the host.
- Reactivation can occur when the immune system is compromised particularly due to T-cell deficiency.
Diagnosis
History
- Exposure to raw meat, unfiltered water, cats or kittens
- Immune deficiency disease
- Maternal illness during pregnancy
Physical Exam
- Primary infection may be asymptomatic.
- Symptoms are nonspecific and include lymphadenopathy, fever, headache, sore throat, malaise, myalgia, or arthralgia. A mononucleosis-like syndrome with rash and hepatosplenomegaly is seen occasionally.
- Congenital infection is asymptomatic at birth in 70 " “90% of patients. Visual impairment, learning disabilities, or mental retardation commonly develop over time.
- Signs of symptomatic congenital infection include rash, generalized lymphadenopathy, hepatosplenomegaly, jaundice, pericarditis, thrombocytopenia, meningoencephalitis, hydrocephalus, microcephaly, and brain calcifications.
- The classic triad of toxoplasmosis in neonates is chorioretinitis, hydrocephalus, and brain calcifications.
- Ocular toxoplasmosis commonly is due to reactivation of chronic infection.
- In persons with secondary immunodeficiency, reactivation disease can result encephalitis, pneumonia, or systemic toxoplasmosis.
Diagnostic Tests & Interpretation
Lab
- Serology testing for T. gondii " “specific antibodies is the primary means of diagnosis.
- The presence of immunoglobulin G (IgG) determines if a person has ever been infected, whereas immunoglobulin M (IgM) or IgG avidity test detect primary infection.
- Pregnant women in high-prevalence area should be screened with both IgM to detect acute infection and IgG for latency. If IgG is present, an avidity test will determine if infection occurred within the last 3 " “4 months.
- Infants suspected of congenital toxoplasmosis should be tested for the presence of T. gondii immunoglobulin A (IgA) in addition to IgG and IgM due to higher sensitivity in this age group.
- As serology testing can vary, any positive tests should be confirmed by a reference laboratory.
- Amniotic fluid may tested for T. gondii DNA.
- Diagnosis can be made by direct observation of the parasite in tissue specimens, cerebral spinal fluid, or biopsy material.
- Immunocompromised patients including those with HIV should be tested for T. gondii " “specific IgG, prior to starting therapy.
Imaging
- Prenatal ultrasound is useful to detect signs of congenital infection including hydrocephalus, brain calcifications, or pericarditis.
- Head CT or MRI will detect calcifications and hydrocephalus.
Diagnostic Procedures/Other
- Ophthalmologic examinations for characteristic retinal lesions
- Hearing exams, as hearing loss may be absent in infancy and develop over time
Differential Diagnosis
- Primary infection
- Epstein-Barr virus (EBV)
- Cytomegalovirus (CMV)
- HIV
- Lymphoma
- Congenital infection
- CMV (calcifications are periventricular)
- Herpes simplex virus (HSV)
- Rubella
- Syphilis
Treatment
Medication
- Most cases of acute infection do not require treatment.
- Persons with eye disease, severe organ damage, pregnant women, congenital infection (symptomatic or asymptomatic), and immunocompromised hosts should be treated.
- Therapy is a combination of pyrimethamine and sulfadiazine.
- Folinic acid is also given to protect against the hematologic side effects of pyrimethamine.
- Spiramycin treatment of pregnant women may reduce congenital transmission.
- Treatment is prolonged and congenital infection is treated for 1 year.
- Trimethoprim/sulfamethoxazole should be used for prophylaxis to prevent disease in those with HIV infection and CD4 count less than 100/ ˇ ¼L or severe immunosuppression with known IgG antibody to toxoplasma.
Ongoing Care
Follow-up Recommendations
- Children with congenital infection should be monitored for neurologic manifestations, including hearing loss and chorioretinitis that may develop over time.
- Ophthalmologic exams and audiometry should be performed periodically for at least the first 10 years of life after congenital infection.
- Head circumference should be monitored due to development of hydrocephalus in congenital infections.
Prognosis
- Congenital infections are also mostly asymptomatic at birth; however, hearing loss, vision loss, and seizures may present months to years later.
- Bad neurologic outcomes are associated with early maternal infection, lack of prenatal treatment, presence of chorioretinitis, and clinical signs noted at birth.
- Treatment improves clinical outcomes, including cognitive function.
- Immunocompromised patients require chronic suppressive therapy until demonstrated immune recovery.
- Appropriately treated patients typically due well.
Complications
- Congenital infection
- Chorioretinitis
- Hydrocephalus
- Seizures
- Intellectual delay
- Seizures
- Sensorineural hearing loss
- Microcephaly
- Primary infection: Rare complications are myocarditis, pericarditis, pneumonia, meningitis, or encephalitis.
Additional Reading
- Berrebi ‚ A, Assouline ‚ C, Bessieres ‚ MH, et al. Long-term outcome of children with congenital toxoplasmosis. Am J Obstet Gynecol. 2010;203(6):552.e1 " “e6. ‚ [View Abstract]
- Del Pizzo ‚ J. Focus on diagnosis: congenital infections (TORCH). Pediatr Rev. 2011;32(12):537 " “542.
- McLeod ‚ R, Boyer ‚ K, Karrison ‚ T, et al. Outcome of treatment for congenital toxoplasmosis, 1981-2004: the National Collaborative Chicago-Based, Congenital Toxoplasmosis Study. Clin Infect Dis. 2006;42(10):1383 " “1394. ‚ [View Abstract]
- Rober-Gangneux ‚ F, Darde ‚ M. Epidemiology of and diagnostic strategies for toxoplasmosis. Clin Microbiol Rev. 2012;25(2):264 " “296. ‚ [View Abstract]
Codes
ICD09
- 130.9 Toxoplasmosis, unspecified
- 771.2 Other congenital infections specific to the perinatal period
- 130.4 Pneumonitis due to toxoplasmosis
- 130.2 Chorioretinitis due to toxoplasmosis
- 130.7 Toxoplasmosis of other specified sites
- 130.0 Meningoencephalitis due to toxoplasmosis
ICD10
- B58.9 Toxoplasmosis, unspecified
- P37.1 Congenital toxoplasmosis
- B58.3 Pulmonary toxoplasmosis
- B58.01 Toxoplasma chorioretinitis
- B58.2 Toxoplasma meningoencephalitis
- B58.89 Toxoplasmosis with other organ involvement
SNOMED
- 187192000 Toxoplasmosis (disorder)
- 73893000 Congenital toxoplasmosis (disorder)
- 187196002 Toxoplasma pneumonitis (disorder)
- 187194004 Toxoplasmosis chorioretinitis
- 17949000 Meningoencephalitis due to acquired toxoplasmosis (disorder)
- 192701001 Toxoplasma encephalitis (disorder)
FAQ
- Q: What newborns require evaluation for congenital toxoplasmosis?
- A: Newborns with known maternal disease or concerning exposure and those with hydrocephalus, intracranial calcifications, strabismus, intrauterine growth restriction, or other concern for congenital infection should have serologic testing for T. gondii specific IgG, IgM, and IgA.
- Q: How do people get toxoplasmosis?
- A: By ingesting oocytes from undercooked meat, drinking unpasteurized milk, or by exposure to cat feces in litter or soil.
- Q: Who is at risk developing severe toxoplasmosis?
- A: Infants born to mother infected with T. gondii during pregnancy and persons with immune suppression due to acquired immune deficiency syndrome (AIDS), chemotherapy, or organ transplantation.
- Q: How can I prevent toxoplasmosis?
- A: Thoroughly cook meat, wash all fruits and vegetables well, eat only pasteurized dairy products, and wash hands well after contact with sand or soil.