- Toxoplasma gondii (protozoa)
- Incubation: 7-14 days
- Via ingestion, inhalation or blood-blood contact.
- 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)
- 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:
- 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
- Measuring IgG (positive within 1-2 weeks and remain so for life)
- Specific IgM and IgA (more useful in neonates)
Can also detect 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)