Caught by ingesting oocysts from cat faeces (in soil or water) or infected meat (but cats are vector). Mother to child transmission occurs only in primary infection, which is usually asymptomatic. About a third of newly infected mothers will transmit infection, but very dependent on gestational age at time of seroconversion; risk rises by 12% per week of gestational age.

Only 4% of those congenitally infected will be symptomatic.

Introduction in the UK of prenatal or neonatal screening for congenital toxoplasmosis would not be justified by the currently available evidence. 1 in 10 000 children is congenitally infected but only five in a million have severe neurological disease in infancy and some 20 or 30 per million develop brain or eye lesions by the age of 3 years… Acquired toxoplasmosis is a bigger problem than congenital (meat and meat products, in some countries water supply). (Journal of Medical Screening 2002;9:135)

Untreated congenital toxoplasmosis with generalized or neurologic abnormalities at presentation almost always develop mental retardation, seizures, and spasticity. For untreated, initially asymptomatic infants studies have found that although the mean IQ was in the average range it was significantly lower (93 versus 110); furthermore, sequelae were common – at a mean age of 8.5 years, uni/bilateral blindness (65%), sensorineural hearing loss (26%), seizures (17%), severe mental retardation (13%), and hydrocephalus or microcephaly (13%).

Early treatment is very effective. A prospective study (n=36) using pyrimethamine and sulfadiazine for 1 year beginning in the first months of life in symptomatic patients had excellent outcomes with nearly 80% having a normal IQ. Seizures, deafness and motor problems resolved in most cases. Poor prognostic factors were hydrocephalus at birth, or high CSF protein (>1g/dl), or hydrocephalus unresponsive to shunting. Other risk factors for poor outcome include diabetes insipidus, apnoea and bradycardia. Microcephaly does not always mean a poor outcome, esp if hydrocephalus does not complicate it.

In pregnancy, IgM is not necessarily diagnostic of recent infection (can persist in adults). If IgG only, probably old infection unless third trimester, so use reference lab if in doubt – do battery of tests incl dye test, IgA, agglutination. Serology not reliable if HIV co-infection. Amnio PCR only 80% sensitive and varies with gestation. Monthly antenatal USS can assess ventricular dilatation, calcification, hepatosplenomegaly. Chorioretinitis in pregnancy thought to be reactivation so not a risk to fetus.

In newborn, IgM, IgA or Sabin Feldman Dye test > 300 IU suggests infection. Avoid using cord blood in case of contamination from maternal blood. If unsure, do PCR and culture from blood, urine, CSF. Characteristic findings (in symptomatic?) are:

Chorioretinitis usually present if clinical disease, seen in 40% if subclinical. Rare in acquired disease (ie lymphadenopathy), only 1.5%.

  • chorioretinitis (always),
  • cerebral calcifications (72%),
  • hydrocephalus (44%),
  • persistent IgG antibodies beyond first year,
  • and Toxoplasma antibodies in Western blot but not present in the mother.

Other initial manifestations include jaundice (64%); hepatomegaly (50%); splenomegaly (56%); abnormal tone (58%); microphthalmia (22%); CSF pleiocytosis (56%); and abnormal CSF protein (59%).

Trial ongoing in Chicago. Regimen (Feigin & Cherry) – First 6 months: pyrimethamine – 15mg/m2 or 1 mg/kg daily else alternate days if difficult to divide tablet). Sulfadiazine – 85mg/kg in 2 divided doses, with folinic acid 5mg every 3 days, IM in young infants, 10mg if bone marrow toxicity, more frequent in young infants. Next 6 months alternate pyri/sulfa with spiramycin 100mg/kg in 2 divided doses monthly. If active chorioretinitis, high CSF protein, jaundice add steroids (pred 1.5mg/kg in 2 divided doses!) until inflammation subsiding, then taper. FBC 2x/week.

Remington + Klein regimen – pyri 2mg/ml, 2mg/kg for 2 days loading then 1mg/kg/d, 3x/wk in second 6/12, sulfa 100mg/ml, 100mg/kg in 2 divided doses, crush 10mg folinic, add to formula M/W/F, pred 1mg/kg in 2 divided doses. Fansidar 1.25mg/kg used in Europe – prob less effective levels, risk of serious adverse reactions, but convenient 2wkly dosing…

Spiramycin is good for infected mums as long as baby is not thought to be infected, where pyrimethamine/sulphadiazine are required. Prenatal treatment using spiramycin or pyrimethamine with sulfadoxine or sulfadiazine from time of diagnosis until 1 year of age has been tried. No RCTs. Metanalysis (n-1745 mothers) showed that early (within 3 weeks of seroconversion) was slightly more effective than later treatment, but that the risk was very dependent on gestation at time of seroconversion. Clinical manifestations in infected children were just as frequent whether prenatally treated or not. But difficult data and very dependent on gestational age at seroconversion. [Lancet Volume 369, Issue 9556 , 13 January 2007-19 January 2007, Pages 115-122]

Differential diagnosis: CMV, Human LCMV (lymphocytic choriomeningitis virus, found in rodents esp hamsters).

[Clin Perinatol 2005;32:705-26. Pediatrics, January 1, 1995, 95:11-20]