Introduction
Background
Toxoplasma gondii is an intracellular parasite that affects one third of the world’s population.11 It can affect all mammals who serve as the intermediate host. Cats are the definitive hosts. Toxoplasma may transmitted via hand-to-mouth contact from improper handling of, or ingestion, of raw or undercooked meat containing cysts from cat feces; by congenital transmission from mother to fetus; and rarely by transplantation of infected organs. The life cycle of Toxoplasma species includes tissue cysts in neural (mostly brain) and muscular (mostly skeletal and cardiac) tissue and fecal oocysts within the GI tract. Either may transform after ingestion and become infective over a period of several days.
Acute infection in an immune-competent host usually causes a self-limited, flulike illness. The situation is very different for the fetus or for an individual who is immune compromised due to human immunodeficiency virus (HIV), immune-suppressant drugs, or other illness. Fulminant infection with significant morbidity and mortality or ongoing low-grade symptoms is possible in these populations.
Pathophysiology
T gondii exists in 3 forms: oocysts, tachyzoites, and cysts.
Oocysts
Oocytes exist in cats—the definitive hosts. During acute infection in the cat, millions of oocytes are produced and shed in the cat’s feces for 7-21 days. These sporozoite-containing oocytes transform and become infectious after ingestion.
Tachyzoites
Tachyzoites are the rapidly replicating form of the parasite that occur inside the body of the intermediate host. They can actively penetrate all nucleated cells and form vacuoles. Eventually, the infected cells die and tachyzoites disseminate throughout the body to infect and destroy other tissues including the eye, CNS, skeletal and heart muscle, and placenta. They also cause an inflammatory response. In an immunocompetent host, the tachyzoites transform into bradyzoites, which form cysts.
Cysts
Bradyzoites remain in cysts for the life of the host in the host brain, heart, and skeletal muscle. They can be released from the cyst to transform back into tachyzoites to infect other tissues in immunocompromised hosts. Bradyzoites are morphologically similar to tachyzoites but are much slower replicating.
Human infestation
Humans can become infected with T gondii by ingesting either material contaminated with infectious oocysts or tissue cysts contained in raw or undercooked meat from another intermediate host. T gondii also may be transmitted by transplantation of infected organs, through blood transfusion, and through laboratory accidents. Transplacental transmission of T gondii is the only form of human-to-human transmission of toxoplasmosis. The rate of transplacental transmission has been reported to be 55% for untreated mothers and 25% for treated mothers.
Most cases of toxoplasmosis in the immunocompetent host are subclinical or benign. The most severe symptoms occur in the congenitally acquired form and in immunocompromised hosts. In the immunocompetent host, toxoplasmosis is classified as congenital, acquired, or ocular.
Approximately 10-20% of pregnant women infected with T gondii show clinical signs. The most common finding is lymphadenopathy. If the mother was infected prior to the current pregnancy, virtually no risk of fetal transmission exists. If the mother becomes infected during pregnancy, the fetus is at risk regardless of whether the mother is symptomatic. Fetal infection with T gondii may result in stillbirth or abortion. Congenital infection is most severe if acquired in the first or, in some cases, second trimester. Infection during the second or third trimesters tends to be asymptomatic. Seventy-five percent of infants born with congenital toxoplasmosis infection are asymptomatic. Eight percent show severe CNS impairment, which might not manifest for several years.
Patients with acquired toxoplasmosis can present with a range of clinical manifestations, from subclinical lymphadenopathy (the most common presentation) to fatal, fulminant disease. In the immunocompetent host, infection with T gondii may be indistinguishable from infectious mononucleosis.
Ocular toxoplasmosis occurs from activation of cysts deposited in or near the retina (see Media file 1). Focal necrotizing retinitis is the characteristic lesion. Approximately 35% of all cases of retinochoroiditis can be attributed to toxoplasmosis. Since most cases of ocular toxoplasmosis are the result of congenital infection, clinical manifestation later in life usually represents reactivation of latent infection.
The most severe forms of toxoplasmosis occur in patients who are immunocompromised. Immunocompromised hosts at risk include patients with malignancies, leukemias, collagen-vascular diseases, or acquired immunodeficiency syndrome (AIDS) and organ-transplant recipients. Clinical toxoplasmosis occurs in as many as 40% of patients with AIDS. Clinical toxoplasmosis usually is due to reactivation of latent T gondii infection; therefore, all patients with AIDS with T gondii antibodies are at risk of developing active infection.
Clinical manifestations may mimic those of other opportunistic infections. Necrotizing encephalitis, pneumonitis, and myocarditis are the most common autopsy findings. The most frequent clinical findings reflect involvement of these 3 organ systems, although disseminated toxoplasmosis is being described with increasing frequency. Incidence of toxoplasmic encephalitis in patients with AIDS is correlated directly with the presence of antitoxoplasmal antibodies. In patients with AIDS, CNS involvement is the most common manifestation, ranging from nonspecific, generalized symptoms to focal findings such as headache, altered levels of consciousness, motor impairment, and seizures.
Pulmonary involvement is the second most common manifestation. Clinically, patients may appear to have tuberculosis or infection with Pneumocystis carinii.
Frequency
United States
Toxoplasmosis is the third most fatal food-borne disease in the United States. The overall all seroprevalence in the United States is estimated to be 22.5%. Fifteen percent of women aged 15-44 years are seropositive. Congenital toxoplasmosis is uncommon in the United States and is estimated to occur in 4004000 births per year or 1-10 births per 10,000 live births. Seroprevalence of T gondii varies among populations and correlates with eating and hygiene habits of each population.
International
In France and Germany, as many as 80% of the general population has serologic evidence of subclinical T gondii infection.
Mortality/Morbidity
In the United States, approximately 225,000 cases of toxoplasmosis occur per year, and 5000 hospitalizations and 750 deaths occur.
Race
No difference between races is reported.
Sex
Although toxoplasmosis is well studied in women of childbearing age because of its detrimental effects on the fetus, no difference in prevalence between the sexes is reported.
Age
No difference in seroprevalence by age is reported.
Clinical
History
- Immunocompetent individuals
- Usually asymptomatic
- Nonspecific, flulike illness
- Ocular toxoplasmosis (chorioretinitis)
- Usually painless
- Impaired vision, either sudden or gradual
- May see floaters
- Immunocompromised individuals
- May have flulike symptoms
- Seizure, dysequilibrium, cranial nerve deficits, altered mental status, focal neurologic deficit
- Congenital toxoplasmosis
- Petechia
- Visual defects
Physical
- Immunocompetent individuals
- Usually asymptomatic
- Isolated cervical or occipital adenopathy, nontender, last 4-6 weeks
- Infrequently, may cause myocarditis, polymyositis, pneumonitis, hepatitis, encephalitis
- Ocular toxoplasmosis (chorioretinitis)
- White focal lesions with inflammation of vitreous (the classic “headlight in the fog” appearance)
- Recurrent lesions at the border of the chorioretinal scars
- Congenital toxoplasmosis
- Usually normal prenatal sonogram
- Prenatal sonogram may show intracranial calcifications, dilated ventricles, enlarged liver, ascites, and thickened placenta
- Neonatal hydrocephalus, microcephaly, intracranial calcifications, chorioretinitis, strabismus, blindness, epilepsy, psychomotor or mental retardation, thrombocytopenia (petechia), anemia
- Rare classic triad - Chorioretinitis, hydrocephalus, cerebral calcifications
- Immunocompromised individuals
- May be gradual onset over a few weeks
- May be present as sudden confusion manifesting over days
- Neurologic signs may be present: Seizure, mental status change, focal motor deficits, cranial nerve disturbances, sensory disturbances, cerebellar abnormalities, movement disorders, neuropsychiatric findings
- Chorioretinitis
- Pneumonitis (more common in patients who have undergone bone marrow transplantation and in patients with AIDS)
- Septic shock-like presentation
Causes
- Immunocompetent individuals - Oral-fecal acquisition of parasite from cat feces or eating contaminated, undercooked meat (especially pork and lamb)
- Ocular toxoplasmosis (chorioretinitis)
- Usually reactivation of congenital infection
- Few cases recorded as part of acute infection
- Immunocompromised individuals - Almost always reactivation of chronic infection
- Congenital toxoplasmosis
- Parasite crosses the placenta from maternal circulation and then enters the fetus.
- Infection is less frequent but more serious if mother becomes infected from up to 3 months before pregnancy until end of the second trimester.
- Infections are more frequent but less severe if maternal infection occurs in the third trimester.
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| Multimedia: Toxoplasmosis |
| References |
| Next Page » |
References
Garcia LS, Bruckner DA. Diagnostic Medical Parasitology. 111-121. 3rd ed. American Society of Microbiology: Washington DC; 1997:423-424; 577-589.
Hardman JG, Limbird LE. Protozoal infections. In: Goodman LS, et al, eds. Goodman & Gilman's The Pharmacological Basis of Therapeutics. 9th ed. New York: McGraw-Hill; 1992:989.
Hoeprich PD, Jordan MC, Ronald AR. Infectious Diseases. In: A Treatise of Infectious Processes. Lippincott-Raven Publishers; 1994:1201-1213.
Reese RE, Betts RF. A Practical Approach to Infectious Diseases. 648-649. Philadelphia, Pa: Little, Brown & Co; 1996:755-759; 1274-1275.
Robert-Gangneux F, Gavinet MF, Ancelle T, Raymond J, Tourte-Schaefer C, Dupouy-Camet J, et al. Value of prenatal diagnosis and early postnatal diagnosis of congenital toxoplasmosis: retrospective study of 110 cases. J Clin Microbiol. Sep 1999;37(9):2893-8. [Medline].
Sanford JP, Gilbert DN, Moellering RC. The Sanford Guide to Antimicrobial Therapy. Hyde Park, Vt: Antimicrobial Therapy, Inc; 1997:86-87.
Wong SY, Remington JS. Biology of Toxoplasma gondii. AIDS. Mar 1993;7(3):299-316. [Medline].
Buzoni-Gatel D, Werts C. Toxoplasma gondii and subversion of the immune system. Trends Parasitol. Oct 2006;22(10):448-52. [Medline].
Davaro RE, Thirumalai A. Life-threatening complications of HIV infection. J Intensive Care Med. Mar-Apr 2007;22(2):73-81. [Medline].
Dodds EM. Toxoplasmosis. Curr Opin Ophthalmol. Dec 2006;17(6):557-61. [Medline].
Montoya JG, Liesenfeld O. Toxoplasmosis. Lancet. Jun 12 2004;363(9425):1965-76. [Medline].
Further Reading
Keywords
Toxoplasma gondii, T gondii, T gondii infection, toxoplasmosis, ocular toxoplasmosis cat feces, undercooked meat , congenital toxoplasmosis, acquired toxoplasmosis, toxoplasmosis in immunocompromised host, exposure to cats, retinochoroiditis, food-borne disease
