Advertising Survey

We would like your input on how advertising is currently used in the site.

Please take this short survey to help us out.

Hide this message

Home > Professional Reference > Toxoplasmosis

Print this page

Toxoplasmosis

This PatientPlus article is written for healthcare professionals so the language may be more technical than the condition leaflets. You may find the abbreviations list helpful.

Introduction1,2

Toxoplasmosis is caused by Toxoplasma gondii, an intracellular protozoan parasite. Its main host is the cat. It is one of the most common human parasites. Primary infection is usually subclinical, but sometimes leads to chorioretinitis, or may damage the fetus if acquired in pregnancy. Reactivation of latent infection can occur in immunocompromised patients and may cause life-threatening encephalitis.

Life cycle

T. gondii oocysts are excreted in cat faeces, mature in the environment, and may be ingested by secondary hosts (humans, cattle, sheep, pigs, rodents and birds). In these hosts, there is disseminated infection, which is controlled by the immune response. The active proliferating forms of the organism are called tachyzoites. They can be found in any organ, but occur most commonly in the brain, skeletal muscle and heart muscle.

Following a successful immune response, dormant parasites remain encysted in the host tissues for years. They can reactivate if there is immune suppression - notably, AIDS.

The life cycle is completed by cats eating infected animal tissue.

Transmission

Domestic cats are the main source of infection. Infectious oocysts are excreted by the cat for up to two weeks after the initial infection and can survive in warm, moist soil for more than 1 year.

Humans become infected via the following routes:

  • Ingestion/handling of oocytes from cat faeces - via contaminated soil, water or food.
  • Eating or handling undercooked or raw meat which is infected - mainly pork and lamb.
  • Maternal-to-fetal transmission - occurs almost solely when the primary infection is acquired during pregnancy.
  • Organ transplantation - usually in the context of a donor seropositive for T. gondii and a seronegative recipient.

Epidemiology

T. gondii is worldwide in distribution but the disease occurs less frequently in areas where the environment is unfavorable for the oocysts, such as colder or drier regions and high altitudes. The seroprevalence of populations varies widely, for example:

  • One UK survey found the seroprevalence in pregnant women in the London region was 5.5-12.7%, with variation across geographical areas, and further variation according to country of birth.3
  • By the fourth decade of life, seropositivity for toxoplasmosis is 90% in France, 12.5% in Japan and 60% in the Netherlands.4

Presentation

Toxoplasma infections may present in four main ways:

  1. Acquired infection in immunocompetent adults and children:
    • Asymptomatic in most cases.
    • Approximately 10% have symptoms, e.g. nonspecific illness or isolated lymphadenopathy (of occipital or cervical nodes, usually resolving within 6 weeks).
    • More chronic lymphadenopathy can occur.
    • Rarely, there may be polymyositis, myocarditis, pericarditis,5 pneumonitis,6 hepatitis or encephalitis.
    • Cases of severe, acute disseminated toxoplasmosis in immunocompetent patients, requiring treatment, have been reported from rural French Guiana.These were thought to be due to new, virulent strains of T. gondii.7,8
  2. Ocular toxoplasmosis:4,9
    • Toxoplasmic chorioretinitis can occur in both immunocompetent and immunocompromised patients, through acute infection, reactivation or congenital infection.
    • Presentation varies:
      • Possible symptoms are reduced visual acuity and floaters.
      • The typical ocular findings are focal retinochoroiditis, a nearby retinochoroidal scar, and moderate-to-severe vitreous inflammation.
      • Atypical presentations can occur, such as anterior uveitis, scleritis and optic disc or optic nerve pathologies.
      • Pain is not a common feature (since pain is unusual in chorioretinitis). However, pain may occur in some of the atypical presentations, e.g. with scleritis or endophthalmitis.
    • See also the separate Chorioretinal Inflammation article.
  3. Congenital infection in immunocompetent patients:2,10
    • The mother is usually asymptomatic, although some have malaise and lymphadenopathy or, rarely, chorioretinitis.
    • The fetal consequences are more severe if infection takes place close to conception. The risk of maternal-fetal transmission increases as the pregnancy proceeds, but the consequences become less severe.
    • May cause miscarriage or fetal abnormalities which are detectable on ultrasound.
    • May have no apparent symptoms at birth, with complications developing only later in life.
    • Neonatal features of infection vary and include hydrocephalus, microcephaly, intracranial calcifications, chorioretinitis, strabismus, blindness, epilepsy, developmental delay, thrombocytopenia and anaemia.
    • The classical triad of congenital infection comprises chorioretinitis, intracranial calcifications and hydrocephalus; however, this is rare.
  4. Immunocompromised patients:4
    • Toxoplasmosis can be life-threatening for immunocompromised patients, usually due to reactivation of chronic infection.
    • Toxoplasmic encephalitis is the most common feature, with varying presentations:
    • Other presentations in the immunocompromised are:

Differential diagnosis2

Investigations2

  • Serology:
    • IgG antibodies arise within 1-2 weeks of infection and persist for life.
    • Absent IgG in pregnant women or the immunocompromised indicates a risk of acquired toxoplasmosis.
    • Presence of IgG in the immunocompromised (e.g. transplant recipients and those with AIDS) indicates a risk of reactivation of latent infection.
    • Tests of the avidity of IgG can help to distinguish recent infection from previous infection.
    • IgM appears in the first week of infection, increases rapidly, and then declines at variable rates. False positives can be a problem.
    • IgM and IgA levels are more useful in neonates.
  • Direct detection:
    • Polymerase chain reaction (PCR) amplification techniques allow detection of T. gondii in blood, body tissues and fluids (including fetal blood or amniotic fluid11). This indicates acute infection and can be used for typing strains of the organism.
    • Tachyzoites (the active form of the parasite) may be found in tissue sections or body fluid smears.
    • The organism can be cultured from blood samples.12
  • Imaging:12
    • MRI or CT scanning for brain lesions (MRI is more sensitive). Typical CNS findings are multiple ring-enhancing lesions.
    • Fetal or neonatal ultrasonography can be used if there is known/suspected transplacental infection. However, the findings are not diagnostic. There may be ventriculomegaly, CNS calcifications, placental changes, hepatomegaly, splenomegaly, ascites, and pericardial or pleural effusion.10,11
  • Trial of therapy:
    • Empirical anti-toxoplasmosis treatment is accepted practice for immunocompromised patients with multiple ring-enhancing brain lesions; patients usually improve within 7-10 days.

Management2

There may be life-threatening illness (usually in immunocompromised patients), with encephalitis, pneumonitis, or myocarditis. Patients may require stabilisation and treatment of acute symptoms such as seizures, respiratory failure and cardiovascular compromise.12

Specific treatment against T. gondii is given, depending on the clinical situation:

  • Immunocompetent adults and children (non-pregnant):
    • Treatment is not usually required unless symptoms are severe, persistent, or incurred through blood products or laboratory transmission.
    • The usual drug combination is pyrimethamine, sulfadiazine and folinic acid for 4-6 weeks.
  • Immunocompromised patients:2
    • For transplant recipients (seropositive donor and seronegative recipient) - trimethoprim/sulfamethoxazole prophylaxis is effective.
    • CNS toxoplasmosis - combinations of drugs are used; for example:
    • Treatment is continued until 4-6 weeks after clinical resolution (may require months of treatment). This is followed by maintenance therapy at lower doses, lifelong or until immunocompetent.
  • Maternal and fetal infection:11
    • It is important to distinguish recent versus past infection.
    • For recently acquired maternal infection, start treatment as soon as possible.
    • There are various treatment regimens, and protocols vary between countries. Spiramycin may reduce vertical transmission, but does not cross the placenta well. Pyrimethamine and sulfadiazine can treat the fetus, but have significant side-effects; pyrimethamine is potentially teratogenic and should not be used in the first trimester.
    • One suggested treatment protocol is:10
      • Spiramycin - started as soon as possible if there is acute maternal infection. This is continued until term, or until fetal infection is documented.
      • For documented fetal infection after 14-18 weeks' gestation - pyrimethamine/sulfadiazine plus folinic acid (not folic acid), with monitoring for haemotoxicity.
    • Other treatment regimens include 3 weeks of pyrimethamine and sulfadiazine, alternating with 3 weeks of spiramycin; or spiramycin plus co-trimoxazole.14
    • Alternative drugs such as azithromycin have been used, although their efficacy is uncertain.
    • Many protocols also treat the child postnatally; recommendations vary as to the duration of treatment.
    • Termination of pregnancy may be considered.
  • Immunocompromised, pregnant women with previous infection:10
    • Pregnant women who have HIV/AIDS with a pre-existing T. gondii infection risk developing severe toxoplasmosis and/or transmitting the infection to the fetus.
    • Fetal transmission in this scenario is rare, and there is little evidence regarding prophylactic treatment. Some authors suggest prophylaxis during pregnancy, using trimethoprim-sulfamethoxazole for those with low CD4 cell counts, or spiramycin for those with higher CD4 counts.
    • Amniotic fluid PCR may be contra-indicated for HIV-infected women because it risks transmission of HIV to the fetus.
    • Clinical infection in the mother is treated similarly to non-pregnant patients.11
  • Ocular toxoplasmosis:

Complications12,15

  • Nervous system involvement can lead to seizures, developmental delay, deafness or other CNS lesions.
  • Ocular disease can lead to visual impairment or, rarely, blindness.
  • Acute infection in the immunocompromised may cause haemodynamic abnormalities similar to septic shock.
  • Life-threatening involvement of internal organs (CNS, heart and lungs) - usually in immunocompromised patients.
  • Other possible, although uncommon, complications in AIDS patients are panhypopituitarism, diabetes insipidus, syndrome of inappropriate antidiuretic hormone secretion, orchitis and myositis.

Prognosis

  • Most cases in immunocompetent healthy individuals remain subclinical or resolve spontaneously.
  • The prognosis in AIDS patients was poor, but has improved considerably since the advent of highly active antiretroviral therapy (HAART).16
  • The overall prognosis with maternal infection is fairly good:17
    • The overall risk of vertical transmission with maternal seroconversion is 26%.
    • Among infected children, 33% have retinal lesion(s), but bilateral visual impairment seems to be unusual; in one survey, no child was blind.18
    • One expert suggested that "the biggest danger to the fetus is not the parasite, but the mothers' anxiety".17
  • The effectiveness of antenatal and postnatal treatment is still debated.19,20

Prevention

Hygiene measures, particularly for pregnant women21 and seronegative immunocompromised patients:

  • Wash hands before handling food.
  • Thoroughly wash all fruit and vegetables, including ready-prepared salads, before eating.
  • Thoroughly cook raw meats and ready-prepared chilled meals.
  • Wear gloves and thoroughly wash hands after handling soil and gardening.
  • Avoid cat faeces in cat litter or in soil.

Some countries, e.g. France, routinely screen pregnant women for toxoplasmosis.19 This is not done in the UK or USA, where prevalences are lower. National Institute for Health and Clinical Excellence (NICE) antenatal care guidelines and the UK National Screening Committee (NSC) concluded that there was insufficient evidence to recommend screening.21,22

Document references

  1. Kumar P; Clarke M; Clinical Medicine, 6th Ed, (2005). WB Saunders: London
  2. Montoya JG, Liesenfeld O; Toxoplasmosis. Lancet. 2004 Jun 12;363(9425):1965-76. [abstract]
  3. Ades AE, Parker S, Gilbert R, et al; Maternal prevalence of Toxoplasma antibody based on anonymous neonatal Epidemiol Infect. 1993 Feb;110(1):127-33. [abstract]
  4. Wu L et al; Ophthalmologic Manifestations of Toxoplasmosis, Medscape, Jan 2011
  5. Sagrista-Sauleda J, Permanyer-Miralda G, Juste-Sanchez C, et al; Huge chronic pericardial effusion caused by Toxoplasma gondii. Circulation. 1982 Oct;66(4):895-7. [abstract]
  6. De Salvador-Guillouet F, Ajzenberg D, Chaillou-Opitz S, et al; Severe pneumonia during primary infection with an atypical strain of Toxoplasma gondii in an immunocompetent young man. J Infect. 2005 Dec 9. [abstract]
  7. Bossi P, Bricaire F; Severe acute disseminated toxoplasmosis. Lancet. 2004 Aug 14-20;364(9434):579.
  8. Carme B, Demar M, Ajzenberg D, et al; Severe acquired toxoplasmosis caused by wild cycle of Toxoplasma gondii, French Emerg Infect Dis. 2009 Apr;15(4):656-8. [abstract]
  9. Smith JR, Cunningham ET Jr; Atypical presentations of ocular toxoplasmosis. Curr Opin Ophthalmol. 2002 Dec;13(6):387-92. [abstract]
  10. Montoya JG, Remington JS; Management of Toxoplasma gondii infection during pregnancy. Clin Infect Dis. 2008 Aug 15;47(4):554-66. [abstract]
  11. Giannoulis C, Zournatzi B, Giomisi A, et al; Toxoplasmosis during pregnancy: a case report and review of the literature. Hippokratia. 2008 Jul;12(3):139-43. [abstract]
  12. Becker JU et al; Toxoplasmosis in Emergency Medicine, Medscape, Mar 2010
  13. Dedicoat M, Livesley N; Management of toxoplasmic encephalitis in HIV-infected adults (with an emphasis on resource-poor settings).; Cochrane Database Syst Rev. 2006 Jul 19;3:CD005420. [abstract]
  14. Valentini P, Annunziata ML, Angelone DF, et al; Role of spiramycin/cotrimoxazole association in the mother-to-child transmission of toxoplasmosis infection in pregnancy. Eur J Clin Microbiol Infect Dis. 2008 Aug 21. [abstract]
  15. Weiss LM, Dubey JP; Toxoplasmosis: A history of clinical observations. Int J Parasitol. 2009 Jul 1;39(8):895-901. Epub 2009 Feb 13. [abstract]
  16. Contini C; Clinical and diagnostic management of toxoplasmosis in the immunocompromised patient. Parassitologia. 2008 Jun;50(1-2):45-50. [abstract]
  17. Peyron F; When are we going to celebrate the centenary of the discovery of efficient Mem Inst Oswaldo Cruz. 2009 Mar;104(2):316-9. [abstract]
  18. Stanford MR, Tan HK, Gilbert RE; Toxoplasmic retinochoroiditis presenting in childhood: clinical findings in a UK Br J Ophthalmol. 2006 Dec;90(12):1464-7. Epub 2006 Aug 9. [abstract]
  19. Garcia-Meric P, Franck J, Dumon H, et al; (Management of congenital toxoplasmosis in France: current data). Presse Med. 2010 May;39(5):530-8. Epub 2009 Nov 18. [abstract]
  20. Stanford MR, Gilbert RE; Treating ocular toxoplasmosis: current evidence. Mem Inst Oswaldo Cruz. 2009 Mar;104(2):312-5. [abstract]
  21. Antenatal care: routine care for the healthy pregnant woman, NICE Clinical Guideline (March 2008)
  22. Gilbert RE, Peckham CS; Congenital toxoplasmosis in the United Kingdom: to screen or not to screen? J Med Screen. 2002;9(3):135-41. [abstract]

Internet and further reading

  • Elsheikha HM; Congenital toxoplasmosis: priorities for further health promotion action. Public Health. 2008 Apr;122(4):335-53. Epub 2007 Oct 26. [abstract]
  • Safadi MA, Berezin EN, Farhat CK, et al; Clinical presentation and follow up of children with congenital toxoplasmosis in Brazil. Braz J Infect Dis. 2003 Oct;7(5):325-31. [abstract]

Acknowledgements

EMIS is grateful to Dr N Hartree for writing this article and to Dr Laurence Knott for earlier versions. The final copy has passed scrutiny by the independent Mentor GP reviewing team. ©EMIS 2011.
Document ID: 736
Document Version: 22
Document Reference: bgp376
Last Updated: 11 Apr 2011
Provide feedback