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Key messages

  • Eighty-five per cent of infants congenitally infected with toxoplasmosis appear normal at birth.
  • The risk of fetal infection with toxoplasmosis is lowest in early pregnancy, but most fetuses infected early have severe consequences.
  • Congenital infection can occur during pregnancy or the peripartum period.
  • Treatment for toxoplasmosis consists of prolonged therapy for the first year of life.

Toxoplasmosis is a congenital infection that can occur during pregnancy or the peripartum period. The timing of infection is important in regards to the severity of neonatal illness.

Toxoplasma gondii is a protozoan parasitic organism. The domestic cat is the primary host. Infection can be contracted by:

  • ingesting oocytes present in faecal material of infected hosts
  • eating pseudocysts present in undercooked meat.

Although 15 per cent of women report an acute flu-like illness with lymphadenopathy, most have no symptoms.

Risk of fetal infection

The risk of fetal infection is lowest in early pregnancy, but most fetuses infected early have severe consequences.

  Risk of fetal infection  Severe consequences of infection

 1st trimester 

 10% 

 70%

 3rd trimester 

 60% 

 <1%

Clinical features

Infants congenitally infected with toxoplasmosis can be:

  • completely asymptomatic
  • unaffected at birth and manifest problems later
  • severely affected in-utero and at birth.

Infection usually affects the neurological and haemopoietic systems. The classical tetrad described by Sabin in 1942 includes:

  • hydrocephalus/microcephaly
  • chorioretinitis
  • seizures
  • other evidence of CNS involvement (including calcification).

Haemopoietic manifestations

Haemopoietic manifestations include:

  • hydrops due to anaemia
  • rash due to thrombocytopenia purpura
  • blueberry muffin appearance (seen in 25 per cent of generalised infection)
  • lymphadenopathy
  • hepatosplenomegaly.

Neurological manifestations

Neurological manifestations include:

  • seizures
  • hydrocephalus with bulging fontanelle
  • microcephaly
  • chorioretinitis can be present early or develop later.

Generalised features

Generalised features include:

  • lethargy and malaise
  • poor feeding
  • vomiting
  • diarrhoea
  • temperature instability
  • jaundice.

Investigation

Antenatal diagnosis

Antenatal diagnosis can be performed using fetal blood sent for:

  • PCR
  • IgM assay
  • culture.

Postnatal diagnosis

Postnatal investigations include:

  • specific IgM or IgA in cord or baby's blood
  • maternal IgM and IgA
  • FBE (anaemia/thrombocytopenia)
  • liver function tests
  • culture by inoculation of blood/placenta in mice
  • cranial US (hydrocephalus and calcification)
  • CT scan (more sensitive than ultrasound at identifying calcification)
  • ophthalmological review.

Management

Treatment consists of prolonged therapy for the first year of life with:

  • pyrimethamine - 1 mg/kg every 12 hours for 2 days, then 1mg/kg/day for 6 months, then 3 times/week until 12 months.
  • sulphadiazine (50 mg/kg orally, twice daily)
  • folinic acid - 10mg, 3 times a week (M, W, F) for 12 months is added to prevent bone marrow suppression. This should continue for 1 week after ceasing pyrimethamine.

An alternative regime aimed at minimising hepatotoxicity may be used:

  • 4 x 21 day cycles of pyrimethamine, sulphadiazine and folinic acid
  • spiramycin (50 mg/kg, orally twice daily) used for 30 days in between.

The addition of steroids in severe infection has been suggested, but no evidence exists for this practice.

Ongoing opthalmological and developmental follow-up is essential.

Outcome

Infants symptomatic at birth have high incidence of long-term difficulties including:

  • chorioretinitis (over 90 per cent)
  • developmental delay (50 per cent)
  • seizures (40 per cent)
  • microcephaly (20 per cent)
  • deafness
  • hydrocephalus.

Outcome data for infants who are asymptomatic at birth is scant.

In ‘asymptomatic’ neonates, it appears that a significant number develop long-term sequelae if left untreated.

Up to 92 per cent develop long-term problems, usually due to ophthalmological disease. Chorioretinitis may not become evident for many years.

Although prolonged therapy reduces the incidence of sequelae compared with untreated infants sequelae may still occur (over 80 per cent).

Prevention

Prevention of toxoplasmosis is aimed at preventing ingestion of infected material through antenatal education. This includes pet, personal and food hygiene.

Pregnant women should be warned to avoid foods and other products that may be contaminated with the oocytes including care when handling, feeding or cleaning up after the family cat.

There may be a role for advocating against acquiring a new cat in households with pregnant women.

More information

Further reading

  • Palasanthiran, P. (et al). 'Management of Perinatal Infections'. Australian Society for Infectious Diseases. 2014
  • Isaacs D, Moxon ER. ‘Handbook of Neonatal Infections - a practical guide’. WB Saunders, London. 1999.
  • Remington JS, Klein JO. ‘Infectious Diseases of the Fetus and Newborn Infant’ 5Th Ed. WB Saunders, Philadelphia. 2000.
  • Davies EG, Elliman DAC, et al. ‘Manual of Childhood Infections’. WB Saunders, London, 1996.
  • Jeffries DG, Hudson CN. ‘Viral infections in Obstetrics and Gynaecology’. Arnold, London, 1999.
  • Jones JL. Lopez A. Wilson M. Schulkin J. Gibbs R. Congenital toxoplasmosis: a review. Obstetrical & Gynecological Survey. 56(5):296-305, 2001 May
  • Beazley DM. Egerman RS. Toxoplasmosis. Seminars in Perinatology. 22(4):332-8, 1998 Aug.
  • Neonatal Pharmacopoeia RWH

Get in touch

Centre of Clinical Excellence - Women and Children
Safer Care Victoria

Version history

First published: May 2014

Last reviewed: October 2018

Review by: August 2019

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Page last updated: 12 Nov 2020

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