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Congenital Toxoplamsosis

Congenital Toxoplamsosis. Casey Muir MS III UNSOM. Toxoplasma gondii Ubiquitous obligate intracellular protozoan parasite Exists in 3 forms: Oocyst (shed only in cat feces) Tachyzoite (rapidly divides, acute phase of infection) Bradyzoite (slow growing w/in tissue cysts)

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Congenital Toxoplamsosis

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  1. Congenital Toxoplamsosis Casey Muir MS III UNSOM

  2. Toxoplasmagondii • Ubiquitous obligate intracellular protozoan parasite • Exists in 3 forms: • Oocyst (shed only in cat feces) • Tachyzoite (rapidly divides, acute phase of infection) • Bradyzoite (slow growing w/in tissue cysts) • Leading cause of blindness in South America (not in N. America/Europe) • Once infected parasite lies dormant in neural & muscle tissue, never eliminated— large majority of immunocompetent humans maintains in dormant form. Micro Review

  3. Oocytes in Cats Feces • Oocytes are shed only in cat feces (millions of oocysts over 1-3 wks during primary infection) • Oocysts become infective 1-5 days later & can remain infectious for over 1 yr (esp in warm/humid environments. • Bradyzoites in Undercooked or Cured Meats • Main source of Maternal infection in developed temperate climate countries Sources of Infection

  4. Usually Asymptomatic • Symptomatic infection typically a heterophile-negative mononucleosis syndrome (LAD, fever, HSM) Maternal Infection

  5. Incidence of congenital toxoplasmosis 1-2 / 1000 live births • Acutely infected mother transmits to child 30-40% of cases • Rarely transmission can occur after reactivation of disease in immunocompromised pregnant mother • Placental Blood Flow correlates directly w/ • Transmission Rates • Timing of Fetal Infection • As Gestational Age of Maternal Infection Increases: • Risk of infection infant INCREASES (90% or greater near term) • Time between maternal and fetal infection DECREASES • Severity of fetal disease DECREASES Transmission

  6. Many Infants are Asymptomatic at Birth • Classic Triad (CHIC) • Chorioretinitis • Hydrocephalus • Intracerebral Calcifications • Characterisitcs/common other findings: • Fever • SGA • Early-onset Jaundice • HSM • Thrombocytopenia • Generalized Maculopapular Rash • Generalized LAD • Seizures (further brain imaging shows diffuse cortical calcifications; contrast to CMV which shows periventricular pattern) Symptoms

  7. Subclinical Congenital Toxoplasmosis cases who did not receive tx are at highest risk • Chorioretinitis/Vision Loss (most common late finding) • Mental Retardation • Deafness • Seizures • Spasticity/Palsies • Hydrocephalus/Microcephalous Long-Term

  8. Serologic Tests for Diagnosis • Seroconversion • Fourfold increase in Ab titer • Positive IgMAb titer • Positive PCR for T. gondii in peripheral WBCs, CSF, serum, or amniotic fluid • Additional Info • IgG-specific Ab’s (peak concentration 1-2 months, remains positive indefinitely) • Measurement of IgA & IgEAb’s can be useful to confirm the disease Diagnosis

  9. Ophthalmologic evaluation • Auditory evaluation • Neurologic evaluation (head computed tomography & CSF examination) Follow-up Testing

  10. Symptomatic and Asymptomatic Congenital Infections treat with: • Pyrimethamine (supplemented with folic acid) & Sulfadiazine • Duration of tx often prolonged (up to 1 year) Treatment

  11. Marcdante KJ, Kliegman RM, Jenson HB, Behrman RE. Nelson Essentials of Pediatrics 6th Edition. Philadelphia, PA: Saunders Elsevier;2011. • Gavinet MF, Robert F, Firtion G, Delouvrier E, Hennequin C, Maurin JR, Tourte-Schaefer C, Dupouy-Camet J. Congenital toxoplasmosis due to maternal reinfection during preganancy. Journal of Clincal Microbiology. 1997 May;35(5):1276-7. • Thiébaut R, Leproust S, Chêne G, Gilbert R. Effectiveness of prenatal treatment for congenital toxoplasmosis: a meta-analysis of individual patients' data. Lancet. 2007;369(9556):115. • Eichenwald HF. A study of congenital toxoplasmosis with particular emphasis on clinical manifestations, sequelae and therapy. In: Human Toxoplasmosis, Siim JC (Ed), Munksgaard, Copenhagen 1959. References

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