Introduction
Toxoplasmosis is caused by the obligate, intracellular protozoan parasite Toxoplasma gondii
-the only Definitive hosts are cats
-In the majority of infected persons, toxoplasmosis is chronic, asymptomatic, and self-limiting
-it is contracted through the consumption of poorly cooked meat or the ingestion of oocytes in food or water contaminated with cat feces; rarely via blood transfusion or organ transplantation
-Toxoplasma form oocysts in cats. After ingestion, oocysts become tachyzoites in humans and form tissue cysts mostly in skeletal muscle, eye, brain, placenta,and myocardium
Symptoms & Signs
Most individuals are asymptomatic, but severe disease is often seen in the immunocompromised individuals
-Toxoplasmosis occurs in four major clinical forms:
Infection in Immunocompetent persons
-infectious mononucleosis like clinical syndrome
-self-limiting febrile lymphadenopathy which can be non-tender cervical lymphadenopathy or generalized lymphadenopathy; fever, headache, malaise, fatigue, sore throat and myalgias
Infection in Immunocompromised persons
-often secondary to reactivation of latent infection
-fever, headaches, seizures, mental status changes, encephalopathy, meningoencephalitis, mass lesions, multiple necrotizing brain lesions
-The most common clinical manifestation of toxoplasmosis acquired after birth is asymptomatic localized lymphadenopathy
Congenital infection
-Transplacental transmission highest in third trimester
-Newborns may show low birthweight, hepatosplenomegaly, jaundice, anemia, chorioretinitis, blindness, microcephaly, hydrocephalus, abortion, stillbirth, tram-track intracerebral calcifications, deafness, mental retardation, blueberry muffin lesions (dermal erythropoiesis), purpura
Ocular toxoplasmosis
Pain, photophobia, visual changes, uveitis, focal necrotizing retinochoroiditis, chorioretinal scar, glaucoma, blindness
Diagnosis
-The primary method of diagnosis is serology
-Identification of tachyzoites in tissue or body fluids: With Wright or Giemsa stains, tachyzoites are crescent-shaped and have a prominent, centrally placed nucleus.
-Pregnancy: PCR of amniotic fluid
-Newborns: IgM or IgA antibody tests
-CT and MRI scans: show multiple ring-enhancing cerebral lesions
Treatment
Immunocompetent patients with only lymphadenopathy: do not require treatment
Immunocompromised patients: Pyrimethamine plus sulfadiazine; given with leucovorin/folinic acid to limit bone marrow toxicity; Pyrimethamine is not used during the first trimester of pregnancy due to its teratogenicity; trimethoprim-sulfamethoxazole is an effective alternative; Clindamycin can be used in sulfonamide-allergic patients
Congenital infection: Oral pyrimethamine, sulfadiazine, and folinic acid for 1 year; Spiramycin is used to prevent congenital infection
Ocular toxoplasmosis: Pyrimethamine and either sulfadiazine or clindamycin for 1 month
- What is the most common clinical manifestation of toxoplasmosis acquired after birth? Asymptomatic localized lymphadenopathy
- What are the most frequently involved lymph nodes in toxoplasmosis? cervical nodes
- What is the most common cause of intracerebral lesions in AIDS patients? Toxoplasmic encephalitis
- What is the most common late presentation of congenital toxoplasmosis? Retinochoroiditis