Toxoplasmosis Symptoms

Signs and Symptoms in Immunocompetent Patients

• Cervical lymphadenopathy
• Fever, malaise, night sweats, and myalgias
• Sore throat
• Retroperitoneal and mesenteric lymphadenopathy with abdominal pain
• Retinochoroiditis

Symptoms 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
• Visual changes
• Flulike symptoms and lymphadenopathy
• Myocarditis and pneumonitis are reported
• Toxoplasmic pneumonitis can occur: nonproductive cough, dyspnea, chest discomfort, and fever

Congenital Toxoplasmosis

• 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
• Intracranial calcifications develop in 10%
• Infected newborns have anemia, thrombocytopenia, and jaundice at birth
• Microcephaly has been reported
• Affected survivors may have intellectual disability, seizures, visual defects, spasticity, hearing loss, or other severe neurologic sequelae

Tissue Cysts

• 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
• Preferentially located in the neural and muscle tissues
• Rupture periodically, releasing bradyzoites that are normally destroyed by the host's immune response

Changes in T-lymphocyte Levels

• Alterations in subpopulations of T lymphocytes are profound and prolonged during acute acquired T gondii infection
• Correlated with disease syndromes but not with disease outcome
• Some patients have lymphocytosis, increased suppressor T-cell counts, and a decreased helper-to-suppressor T-cell ratio

Retinochoroiditis

• Results from reactivation of congenital infection
• 5 hypotheses related to the inflammatory process of ocular toxoplasmosis:
  • Infection and inflammatory response after spontaneous cyst rupture
  • Parasitic toxic mediators released from T gondii
  • Lytic effect of inflammatory mediators
  • Delayed-type hypersensitivity reaction to antigens of T gondii
  • Cell-mediated immunity against retinal antigens

Ocular Toxoplasmosis

• Patients develop retinochoroiditis (focal necrotizing retinitis)
• Yellowish white, elevated cotton patch with indistinct margins
• Lesions may occur in small clusters
• Congenital disease usually is bilateral, and acquired disease usually is unilateral
• Symptoms include:
  • Impaired vision
  • 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 may be performed:
  • Lumbar puncture
  • Brain biopsy
  • Lymph node biopsy
  • Amniocentesis (at 20-24 weeks' gestation if congenital disease is suggested)

Treatment

• Act primarily against the tachyzoite form of T gondii; do not eradicate the encysted form (bradyzoite)
• Pyrimethamine is the most effective agent
• Leucovorin (folinic acid) should be administered concomitantly to prevent bone marrow suppression
• Unless circumstances preclude using more than 1 drug, a second drug (e.g., sulfadiazine, clindamycin) should be added