Toxoplasmosis

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 

Q. What is the most common clinical manifestation of toxoplasmosis acquired after birth? Asymptomatic localized lymphadenopathy 

Q. What are the most frequently involved lymph nodes in toxoplasmosis? cervical nodes 

Q. What is the most common cause of intracerebral lesions in AIDS patients? Toxoplasmic encephalitis 

Q. What is the most common late presentation of congenital toxoplasmosis? Retinochoroiditis 

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