Toxoplasmosis

Toxoplasmosis is a disease caused by the obligate intracellular parasite Toxoplasma gondii. Transmission occurs either through ingestion of cysts found, for example, in raw meat or cat feces, or from mother to fetus through the placenta. The clinical presentation depends on the patient's immune status: In immunocompetent individuals, 90% of cases are harmless and asymptomatic, with the remaining 10% displaying mild mononucleosis-like symptoms. In immunosuppressed patients (e.g., those who are HIV-positive), infection may result in cerebral toxoplasmosis (headache, confusion, focal neurologic deficits) or toxoplasmic chorioretinitis (eye pain, reduced vision). Treatment is indicated for immunosuppressed patients, infected mothers, congenital toxoplasmosis, and immunocompetent patients with more severe symptoms. The treatment of choice is usually a combination of pyrimethamine, sulfadiazine, and leucovorin (folinic acid), with the exception of new infections during pregnancy, which are treated with spiramycin.

For the congenital variant and how to manage infection in pregnant women, see toxoplasmosis during pregnancy.

• Prevalence
  • In the US: ∼ 10% of adults
  • In some tropical climates: up to 95%

References:^[1]

Epidemiological data refers to the US, unless otherwise specified.

• Pathogen: Toxoplasma gondii, an obligate intracellular, single-celled protozoan
• Route of transmission
  • Oral ingestion: The oocysts are excreted in the feces of cats (final host) and are orally ingested by other mammals such as humans, hoofed animals, and birds (intermediate hosts). Primary modes of transmission include the following:
    • Cat feces
    • Raw or insufficiently cooked meat (most common)
    • Unpasteurized milk (especially goat milk)
  • Transplacental transmission: see toxoplasmosis during pregnancy
  • Via organ transplantation or blood transfusion

References:^[2]

• Incubation time: 3 days to 3 weeks
• Immunocompetent patients
  • Mainly asymptomatic (90% of cases)
  • Symptomatic (< 10% of cases): mononucleosis-like symptoms with bilateral cervical adenopathy (but negative heterophile antibody test)
  • Lifelong immunity following infection
• Immunosuppressed patients (e.g., AIDS): primary infection or reactivation in previously infected individuals
  • Cerebral toxoplasmosis (the most common neurological AIDS-defining illness)
  • Ocular toxoplasmosis

References:^[3]

Cerebral toxoplasmosis

• Description
  • Caused by reactivation of T. gondii in immunocompromised individuals
  • Most common neurological disorder associated with AIDS (considered an AIDS-defining condition)
• Clinical features (symptomatic usually if CD4 count < 100 cells/μL)
  • Fever
  • Headache
  • Mental status changes
  • Seizures
  • Focal neurological deficits
• Diagnostics
  • CT or MRI with contrast: multiple ring-enhancing lesions (brain abscesses); predominantly in the basal ganglia and/or the subcortical white matter
  • Serology: detection of anti-toxoplasma IgG antibodies
  • Biopsy: rarely performed due to the risk associated with obtaining a brain specimen
    • Toxoplasma tachyzoites and bradyzoites
    • Chronic inflammation and necrosis of brain tissue
• Treatment: : see “Treatment” section
• Prophylaxis
  • Adequate HIV treatment (cART)
  • TMP/SMX

Ocular toxoplasmosis

• Chorioretinitis
  • Acute toxoplasmosis; (current focal infection): yellow-white retinal lesion; , marked vitreous reaction; , concomitant vasculitis; , defects in the visual field at the site of inflammation
  • Previous toxoplasmosis (previous focal infection): formation of scars with white atrophic areas and surrounding dark, sharply-defined pigmentation
  • Recurrent focal infection usually develops at chorioretinal scars.
  • Congenital toxoplasmosis is almost always accompanied by the formation of scars of the macula and corresponding visual impairment.
• Special form: retinochoroiditis juxtapapillaris (Jensen disease)
  • Peripapillary zonal inflammation with nerve fiber layer defects
  • Visual field defects
  • Treatment: sulfonamide, pyrimethamine, folinic acid, clindamycin

References:^[4][5]

• Serology
  • IgM antibody test: positive within first week of acute infection
  • IgG antibody test; : positive 2 weeks following infection and remains positive for life
• PCR: sample is taken from amniotic fluid in case of suspected intrauterine disease
• CT/MRI: of the brain for suspected cerebral toxoplasmosis (see cerebral toxoplasmosis)

• Immunocompetent patients usually do not require treatment.
• Medical therapy
  • Indications
    • Immunosuppression (e.g., HIV)
    • Infected pregnant women (for both pre-existing and new infections)
    • Severe symptoms in immunocompetent patients
  • First choice
    • Spiramycin if maternal infection before the 18^th week of pregnancy is suspected/confirmed and infection of the fetus is not suspected/documented (see toxoplasmosis during pregnancy) ^[6]
    • Combination treatment with pyrimethamine, sulfadiazine, and leucovorin (folinic acid) in all other cases
  • Duration: minimum of 4–6 week

References:^[7]