Toxoplasmosis Disease Facts

Toxoplasmosis

• Caused by infection with the protozoan Toxoplasma gondii, an obligate intracellular parasite.
• Only 10-20% of toxoplasmosis cases in adults and children are symptomatic.
• Toxoplasmosis is a serious and often life-threatening disease in immunodeficient patients.
• Congenital toxoplasmosis may manifest as a mild or severe neonatal disease, with onset during the first month of life or with relapse of a previously undiagnosed infection at any time during infancy or later in life.

Life Cycle of Toxoplasma gondii

• T. gondii has two distinct life cycles: the sexual cycle occurs only in cats, the definitive host, and the asexual cycle occurs in other mammals (including humans) and various strains of birds.
• The asexual cycle consists of two forms: tachyzoites (the rapidly dividing form observed in the acute phase of infection) and bradyzoites (the slowly growing form observed in tissue cysts).

Transmission

• T. gondii oocysts, tachyzoites, and bradyzoites can cause infection in humans.
• The tissue cysts are up to 60μm in diameter, each containing up to 60,000 organisms.
• Extracellular tachyzoites are cleared from host tissues, and intracellular parasites differentiate into occult bradyzoite forms.

Changes in T-Lymphocyte Levels

• Alterations in subpopulations of T lymphocytes are profound and prolonged during acute acquired T. gondii infection.
• These have been correlated with disease syndromes but not with disease outcome.

Retinochoroiditis

• Retinochoroiditis usually results from reactivation of congenital infection, although cases have been recorded that were part of acute infection.
• There are five hypotheses related to the inflammatory process of ocular toxoplasmosis.

Signs and Symptoms

• In immunocompetent personnel:
  • Cervical lymphadenopathy
  • Fever, malaise, night sweats, and myalgias
  • Sore throat
  • Retroperitoneal and mesenteric lymphadenopathy with abdominal pain
  • Retinochoroiditis
• In immunodeficient patients:
  • CNS toxoplasmosis occurs in 50% of patients
  • Seizure, dysequilibrium, cranial nerve deficits, altered mental status, focal neurologic deficits, headache
  • Encephalitis, meningoencephalitis, or mass lesions
  • Hemiparesis and seizures have been reported
  • Visual changes

Congenital Toxoplasmosis

• This is most severe when maternal infection occurs early in pregnancy.
• 15-55% of congenitally infected children do not have detectable T. gondii –specific IgM antibodies at birth or early infancy.
• Approximately 67% of patients have no signs or symptoms of infection.
• Retinochoroiditis occurs in about 15% of patients, and intracranial calcifications develop in 10%.

Ocular Toxoplasmosis

• Patients develop retinochoroiditis (focal necrotizing retinitis).
• Symptoms include:
  • Impaired vision - Either sudden or gradual, depending on the site of infection
  • Blurred vision
  • Scotoma
  • Pain
  • Photophobia
  • Floaters
  • Red eye
  • Metamorphopsia

Diagnosis

• Direct detection of T. gondii organisms in blood, body fluids, or tissue using PCR.
• Indirect detection of immunoglobulin G (IgG) is possible within 2 weeks of infection using ELISA test.
• Diagnostic procedures:
  • Lumbar puncture
  • Brain biopsy
  • Lymph node biopsy
  • Amniocentesis

Treatment

• Act primarily against the tachyzoite form of T. gondii; thus, they do not eradicate the encysted form (bradyzoite).
• Pyrimethamine is the most effective agent.
• Leucovorin (ie, folinic acid) should be administered concomitantly to prevent bone marrow suppression.

Prevention

• Avoid eating raw meat, unpasteurized milk, and uncooked eggs, oysters, clams, and mussels.
• Wash hands after touching raw meat.
• Wear gloves when gardening or handling soil and wash hands afterwards.
• Wash fruits and vegetables.
• Avoid contact with cat feces.