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MaijaLappalainen
KlausHedman
VedranStefanovic

Toxoplasmosis

Essentials

  • The most common latent protozoan infection in humans
  • The infection is usually dangerous only in pregnancy or in an immunocompromised patient.
  • The transmission is usually from cat faeces, soil, or inadequately cooked meat.
  • Symptomatic disease is the consequence of a primary infection or the reactivation of a latent infection.

Causative agent

  • Toxoplasma gondii is a parasitic protozoon belonging to sporozoa (Coccidia).
  • Toxoplasma exists in three forms, all of which may infect humans: oocyst, tissue cyst and tachyzoite.

Epidemiology

Transmission

  • The primary host of Toxoplasma gondii is the cat. Seroprevalence is higher in older cats than in younger ones. Feeding cats with raw food is also for them a risk factor for acquiring toxoplasma infection.
    1. Oocysts are excreted in feline faeces as the organism replicates in the cat's small intestine during an acute toxoplasm infection.
      • The oocysts remain infective in the nature even for months and may contaminate drinking water, soil or human food.
    2. Tachyzoites are rapidly replicated in the cells of the host during an acute toxoplasm infection (either primary infection or activation of a latent infection) and are spread to different organs via blood circulation.
      • A mother's primary toxoplasm infection during pregnancy may be vertically transmitted through the placenta to the foetus by tachyzoites. The risk of transmission is 30% on the average.
      • Primary infection in the mother poses a danger to the foetus, but a reactivation does not.
      • In rare cases, a tachyzoite infection may also be spread through blood transfusion or by a puncture injury.
    3. Tissue cysts are formed by the immune response of the host after a toxoplasm infection. They are found in the skeletal muscles, in the heart muscle and in the brain. They represent the latent form of a toxoplasm infection.

Global importance

  • The most common protozoan infection in humans. Prevalence correlates e.g. with the level of environmental and food hygiene and with climatic conditions.
  • Symptomatic disease is a consequence of either a primary infection or the activation of a latent infection.
  • The infection is usually dangerous only during pregnancy or in immunocompromised patients.
  • Infection is usually spread through food - inadequately cooked meat or unwashed/unpeeled vegetables or fruits - originally contaminated by soil (feline faeces).

Symptoms

  • Acquired infection is usually asymptomatic in a basically healthy patient.
  • The incubation period of a symptomatic infection is 10-14 (-21) days.
  • When symptoms exist, lymphadenopathy is the most common manifestation. Toxoplasma infection is the cause in 3-7% of cases of clinically significant lymphadenopathy.
  • Fever, fatigue, night sweats, sore throat and muscle pain are the most common symptoms.
  • Hepatosplenomegaly and maculopapular rash may also occur.
  • Atypical lymphocytes may be found in the peripheral blood.
  • In immunocompromised patients, the clinical manifestations are often severe. Patients may develop encephalitis, pneumonia or myocarditis, and the infection may be fatal. The clinical picture may sometimes be severe even in immunocompetent patients.
  • Congenital toxoplasmosis is a generalized infection with symptoms of CNS inflammation.
    • The disease results from primary infection of the mother during pregnancy. The risk of transmission from mother to foetus is 10% in the first trimester and 70% in the third trimester of pregnancy.
    • Infection early in pregnancy usually results in severe disease.
    • The disease is chronic and causes visual and/or CNS defects with the years in 85-90% of the patients.
  • In chronic active toxoplasmosis, symptoms and signs persist for months or even years. In these patients the parasite or its DNA can be detected in blood.
  • Retinochoroiditis is the most common lesion in ocular toxoplasmosis (pictures and ). Toxoplasmic eye disease has also been reported in association with acute infection.

Diagnosis

  • The diagnosis of primary infection is usually serological.
    • Toxoplasma-specific IgG and IgM antibodies are first determined from one serum sample (1-2 ml).
    • According to the result of the IgM test the avidity of IgG may be determined, and in infants, if needed, also IgA (special test, not available in all laboratories).
  • Toxoplasma nucleic acid detection tests from the blood, cerebrospinal fluid, amniotic fluid or tissues can be performed if there are special indications. Serological testing is always the first-line examination.
  • Diagnosis of congenital toxoplasmosis after birth usually requires several serum samples.

Diagnosis of primary toxoplasma infection during pregnancy

  • Positive IgG antibodies and negative IgM antibodies to toxoplasma in the first sample taken before pregnancy or during the first trimester indicate an established immunity, and the foetus is safe.
  • Low avidity of IgG in an IgM-positive woman, on the other hand, suggests recent primary infection. Borderline avidity warrants follow-up.
  • If the results of the antibody assay suggest a primary toxoplasma infection during pregnancy, refer the woman to the prenatal clinic in a hospital for further investigations and treatment.

Treatment and prognosis , Management of Toxoplasmic Encephalitis in HIV-Infected Adults

  • Toxoplasmosis will usually resolve spontaneously after the symptomatic period that may last from a few days to a few weeks. Treatment is indicated in
    • patients with severe infection
    • immunocompromised patients
    • pregnant women with primary infection
    • infants with congenital toxoplasma infection.
  • Toxoplasmosis during pregnancy should always be treated in specialized care setting.
    • If toxoplasma nucleic acid detection test in the amniotic fluid is negative, the treatment consists of azithromycin 500 mg × 1 on 3 consecutive days. This is repeated during the following weeks at least 3 times.
    • If the infection has spread into the uterus (PCR +), a triple treatment is introduced: sulphadiazine (3 g/day), pyrimethamine (25 mg/day) and folinic acid (5 mg twice per week) in 3 weeks. Subsequently, azithromycin 500 mg × 1 is given as 3-day courses during the following 3 weeks. These cycles are alternated until delivery. The treatment prevents approximately 40-50% of infections.
  • Pyrimethamine use is associated with risk of severe adverse effects (bone marrow toxicity).
  • Pregnancy need not be interrupted if repeated foetal ultrasound is normal, toxoplasma-PCR from amniotic fluid is negative and antiparasitic treatment is given.
  • The option of terminating the pregnancy should be restricted only to those primary infections where the foetus is diagnosed to be infected (PCR from amniotic fluid positive for toxoplasma) and ultrasonography reveals abnormal findings.
  • The same drugs are used as alternating therapy in the treatment of congenital toxoplasmosis with doses suitable for a newborn infant.

Prevention

Advice for pregnant women on avoiding toxoplasma infection

  • Prevention is based on good hand and food hygiene.
    • Eat meat only if it is well cooked.
    • Wash kitchen utensils and your hands after handling raw meat.
    • Wash or preferably peel vegetables and fruits.
    • Let others empty the cat litter box or if you do it yourself, wear gloves and wash hands afterwards. The cat litter box should be emptied once a day because the toxoplasma organisms that potentially exist in the cat's feces become infective only after approximately 24 hours.
    • Wash hands after gardening or spending time at a sandpit for children.

Screening for primary toxoplasmosis during pregnancy

  • Arguments for and against the screening of pregnant women have been voiced.

    References

    • Remington JS, McLeod R, Desmonts G. Toxoplasmosis. In book: Remington JS, Klein JO, toim. Infectious diseases of the fetus and newborn infant. 4. edition. Philadelphia: W.B. Saunders 1994, p. 140-267
    • Koppe JG, Loewer-Sieger DH, de Roever-Bonnet H. Results of 20-year follow-up of congenital toxoplasmosis. Lancet 1986;1(8475):254-6. [PubMed]
    • Hedman K, Lappalainen M, Seppäiä I et al. Recent primary toxoplasma infection indicated by a low avidity of specific IgG. J Infect Dis 1989;159(4):736-40. [PubMed]
    • Hohlfeld P, Daffos F, Costa JM et al. Prenatal diagnosis of congenital toxoplasmosis with a polymerase-chain-reaction test on amniotic fluid. N Engl J Med 1994;331(11):695-9. [PubMed]
    • Berrebi A, Kobuch WE, Bessieres MH et al. Termination of pregnancy for maternal toxoplasmosis. Lancet 1994;344(8914):36-9. [PubMed]
    • Lappalainen M, Koskela P, Hedman K et al. Incidence of primary toxoplasma infections during pregnancy in southern Finland: a prospective cohort study. Scand J Infect Dis 1992;24(1):97-104. [PubMed]
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    • Kaye A. Toxoplasmosis: diagnosis, treatment, and prevention in congenitally exposed infants. J Pediatr Health Care 2011;25(6):355-64. [PubMed]
    • Robert-Gangneux F. It is not only the cat that did it: how to prevent and treat congenital toxoplasmosis. J Infect 2014;68 Suppl 1():S125-33. [PubMed]