Toxoplasmosis - Toxoplasma gondii
also see
TORCH
Etiology: Intracellular protozoan parasite
Epidemiology: Incidence 1/1000 to 1/10000 live births; Source: Feces of newly
infected cat, undercooked pork
Pathogenesis: Mother infected during pregnacy, worst in 1st trimester
- 40-60% of women infected during pregnancy deliver an infected infant
- 70-90% asymptomatic at birth
- Transmission rates increase with increasing gestation: average
transmission rate is approximately 15% for the first trimester, 30% for the
second trimester, and 60% for the third trimester. (vs rubella which is most
transmissible in 1st trimester)
- Infection early in pregnancy most often results in the most severe sequelae
in the infant; Severity decreases with later fetal transmission (same as in
rubella)
Presentation:
- Classic Triad: Chorioretinitis, hydrocephalus, cerebral calcification
- General: SGA, premature, LAD
- Neuro: Hypotonia, Convulsions
- Skin: Various rashes (MP, bluish), petechia, jaundice
- GI: HSM, vomiting, diarrhea, feeding problems
- CV: Myocarditis
- Eye: Strabismus
- Heme: Thrombocytopenia
- Presentation in adults:
The majority of cases of acquired Toxoplasma infection in immunocompetent
adults and children are subclinical. When symptomatic infection does occur, the
only clinical finding may be focal lymphadenopathy, most often involving a
single site about the head and neck. Less commonly, acute infection is
accompanied by a mononucleosis-like syndrome that is characterized by fever,
malaise, sore throat, headache, myalgia, and an atypical lymphocytosis. Nearly
all cases of symptomatic acquired toxoplasmosis in immunocompetent individuals
are self-limiting, although adenopathy may persist for months.
- Acquired toxoplasmosis in immunocompromised hosts can result in encephalitis,
pneumonitis, or less commonly, systemic toxoplasmosis. Most cases are caused by
reactivation of latent infection, with local and distant spread of organisms
from tissue cysts.
Diagnosis:
- Acute Toxoplasma infection in pregnancy is usually subclinical;
most cases remain undiagnosed unless antenatal antibody screening is
performed.
- Prenatal: PCR, isolation from fetal blood or amniotic fluid
- Postnatal: (+) IgM or IgA within first 6 months of life or (+) IgG titers
beyond first 12 months of life (these are persistently positive); Transplacental IgG antibodies
usually become undetectable by 6 to 12 months of age.
Treatment: Interrupts acute disease
- Adults:
Because most cases of acquired acute toxoplasmosis are self-limiting (although
adenopathy may persist for months), specific
drug therapy usually is not required. Symptomatic infections occurring in immunocompromised patients warrant combined chemotherapy with anti-Toxoplasma
drugs. Combination therapy with pyrimethamine, sulfadiazine, and folinic acid (leucovorin)
should be administered for 4 to 6 weeks after clinical symptoms and signs of
active infection have resolved.
- Congenital toxoplasmosis: 1 yr oral pyrimethamine with sulfadiazine
(+leucovorin=folinic acid). Therapy generally is continued up to 1 year,
although the optimal duration has not been established.
- Prednisone if chorioretinitis or CSF protein is greater than 1000
Toxoplasma infection can occur by ingestion of oocysts following
the handling of contaminated soil or cat litter or the consumption of
contaminated water or food sources (such as unwashed garden vegetables). The
oocysts in stool become infectious 24 hours or more after they are shed by a
cat. During a primary infection, a cat can shed millions of oocysts daily for 1
to 3 weeks. The oocysts are very hardy and may remain infectious for more than 1
year (especially in warm, humid environments). Transmission also can occur by
ingestion of tissue cysts present in undercooked meat (especially pork, mutton,
and beef).
Diagnostic testing is the best means to distinguish CMV infection from
toxoplasmosis because many of their clinical features overlap. Toxoplasmosis
is more apt to present with chorioretinitis and scattered cerebral
calcifications; CMV infection more frequently is associated with periventricular
calcifications. CMV is diagnosed best by culture of the infant’s urine in the
first 3 to 4 weeks of life. Serologic testing of maternal and infant sera is the
best method for diagnosing congenital toxoplasmosis, but it is less useful in
identifying CMV infection.
References:
CHLA Board Review 2005
American Academy of Pediatrics. Toxoplasma gondii infections. In:
Pickering LK, ed. 2000 Red Book: Report of the Committee on Infectious
Diseases. 25th ed. Elk Grove Village, Ill: American Academy of Pediatrics;
2000:583-586
Boyer KM, Remington JS, McLeod RL. Toxoplasmosis. In: Feigin RD, Cherry JD, eds.
Textbook of Pediatric Infectious Diseases. 4th ed. Philadelphia, Pa: WB
Saunders Co; 1998:2473-2490
Lynfield R, Guerina NG. Toxoplasmosis. Pediatr Rev. 1997;18:75-83
Remington JS, McLeod R, Desmonts G. Toxoplasmosis. In: Remington JS, Klein JO,
eds. Infectious Diseases of the Fetus & Newborn Infant. 4th ed.
Philadelphia, Pa: WB Saunders Co; 1995:140-247