Toxoplasmosis

Original article by Lily Stanley | Last updated on 7/6/2014
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Organism

  • Toxoplasma gondii (protozoa)
  • Incubation: 7-14 days

 

Transmission

  • 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.
 

Epidemiology

  • Peak incidence 25-35 years
  • In 10% causes self-limiting non-specific illness
  • 60% risk of transmission to fetus in pregnancy=congenital toxoplasmosis.

 

Pathogenesis

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

Cycle

  • 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. 

Clinical features

Infection is asymptomatic in most immunocompetant people (kids and pregnant women)

Complications

  • 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
  • Microcephaly
  • Hydrocephalus.
  • Developmental delay
  • Epilepsy
  • 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

 

Diagnosis

Serology

  • 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
 

Treatment

  • Only required in healthy individuals if symptoms are severe:
  • Combination of pyrimethaminesulfadiazine 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)

Prevention

  • 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)