Toxoplasmosis is a parasitic disease caused by the protozoa Toxoplasma gondii, whose main reservoir is in cats, although it can infect most mammals. In humans, it can cause an acute, vague flu-like illness, sometimes with myalgia and lymphadenopathy, which can last from several weeks to months, although it can often be asymptomatic.
Toxoplasmosis is endemic worldwide and infects up to 50% of the world population. This is around 20% in most developed nations. It is not entirely clear what proportion of people completely clear the infection, and what proportion enter the “latent phase”.
Prevention is by proper food preparation and thorough cooking. It is also important to practice good hygiene when cleaning cat litter trays if these are present in the home.
In most healthy individuals the acute infection becomes latent or is cleared. In a small number of cases it can cause severe complications, such as eye damage (chorioretinitis), seizures and anaemia. These complications are only usually seen in those with underlying immunosuppression (such as in HIV / ADIS), and can also be seen in neonates born to mothers with toxoplasmosis.
Toxoplasmosis is one of the TORCH infections – which are associated with adverse outcomes pregnancy. Despite this, there is not form screening programme in the UK or Australia as part of antenatal screening – due to the high false positive rate and difficulty interpreting blood results (differentiating between previous, latent and active infection).
- Toxoplasma gondii (protozoa)
- Incubation: 7-14 days
- Via ingestion (usually of uncooked meat), inhalation or blood-blood contact.
- Can be from poor hand washing after handling uncooked meat, or touching soil, or handling cat faeces
- Infects bowel (poorly cooked meat), lung or broken skin.
Found in tissue of most warm blooded mammals but cats are the only hosts for its definitive life cycle.
- Peak incidence 25-35 years
- In 10% causes self-limiting non-specific illness
- 60% risk of transmission to fetus in pregnancy=congenital toxoplasmosis.
T.gondii has 2 distinct life cycles.
- Sexual reproduction (only in the definitive cats= the definitive host)
- Asexual reproduction in other mammals (including humans)
The bacteria has 2 forms:
- Tachyzoites which are rapidly dividing and observed in acute infection phase
- Bradyzoites which are slow growing and seen in tissue cysts
- A cat becomes infected with T gondii by eating contaminated meat containing bradyzoites
- Macro and micro-gametocytes fuze to form zygotes in the GI tract
- They undergo change and are shed a oocysts
- Within these, zygotes divide into sporoziotes which become infectious about 24 hrs after being shed in cat faeces (and can remain so for up to 1 year in humid environments)
- Humans ingest the T.gondii
- Sporozoites are released from oocysts and the organisms enter GI tract cells by a process similar to phagocytosis
- Tachyzoites multiply within the cells
- Cells rupture releasing tachyzoites infect adjoining cells and are spread via the lymphatic and bloodstream to other tissues.
- As the tachyzoites proliferate they produce necrotic foci surrounded by inflammatory reaction.
- Tissue cysts with bradyzoites form in the tissues and remain for the whole lifespan of the host.
- The normal immune response eventually clears tachyzoites from tissues.
- The cysts produce little.no inflammatory response but can reactivated in immune-compromised patients.
Infection is asymptomatic in most immunocompetant people (kids and pregnant women). Presenting features can include:
- Brain abscess resulting in epilepsy/focal neurological deficit
- Permanent visual impairment (rarely, blindness)
- Haemodynamic abnormalities similar to septic shock can develop in immunocompromised patients.
Congential toxoplasmosis can result in:
- Retinochoroidosis (aka chorioretinitis)
- Developmental delay
- Thrombocytopenia and anaemia
- Babies can have no apparent symptoms at birth, but complications may develop later in life.
- Worse outcome if infection acquired in 1st trimester but higher chance of vertical transmission later in pregnancy
The risk of congenital toxoplasmosis is greatest if the infection is caught during pregnancy (rather than before pregnancy). For those with positive Toxoplasma gondii antibodies at the start of pregnancy, they are likely immune, or have latent infection, and thus the risk is lower.
- This risk is generally higher in developed countries, because in these countries, the general population has a low chance of previous infection, and thus a low chance of immunity. For example, it is estimated 60-80% of Australians are NOT immune.
- The mother to child transmission rate if acquired during pregnancy is 10-20%
- The risk of transmission in highest in the third trimester
- The risk of severe congenital toxoplasmosis is greatest if it is acquired in the first trimester
Screening for toxoplasmosis in early pregnancy is not currently recommended due to the high false positive rate and difficulty of interpreting test results to assess if there is truly an acute infection – and therefore difficulty in knowing if any treatment is warranted. Screening can cause a great deal of anxiety for expectant parents.
- Serum IgG – positive within 1-2 weeks and remains so for life
- Specific IgM and IgA (more useful in neonates, and can help to determine if the infection is acute)
- Toxoplasmosis can also be detected via PCR or culture
- Only required in healthy individuals if symptoms are severe:
- Combination of pyrimethamine, sulfadiazine and folinic acid for approx 4-6 weeks.
- Differs in immunocompromised patients (who may also require lifelong maintenance therapy)
- In pregnant women add in Spiramycin to reduce vertical transmission (and need to monitor for haemotoxicity of pyimethamine and sulfadiazine)
- Hygiene measures (especially for pregnant women immunocompromised patients)
- (Wash hands and food before eating, well cook meats, avoid handling cat faeces)
- UK does not routinely screen pregnant women (unlike France where prevalence is much higher)