Toxoplasma Lymphadenitis



Toxoplasma Lymphadenitis


Carlos E. Bueso-Ramos, MD, PhD









H&E stain shows Toxoplasma lymphadenitis. Note enlarged follicles with reactive germinal centers, clusters of epithelioid cells encroaching on lymphoid follicles, and monocytoid cells.






H&E-stained section reveals a reactive germinal center with many centroblasts, tingible body macrophages, and epithelioid cells encroaching into the germinal center from the right image.


TERMINOLOGY


Synonyms



  • Glandular toxoplasmosis


  • Piringer-Kuchinka lymphadenopathy



ETIOLOGY/PATHOGENESIS


Toxoplasma gondii Infection



  • T. gondii is a protozoan parasite of the phylum Apicomplexa that can invade many cell types


  • Cat is definitive host for sexual stage of reproduction



    • Trophozoites reproduce in intestinal epithelium, producing oocysts


    • Oocysts are eliminated in feces


    • Oocysts mature to infective stage in soil in 2-21 days


  • Humans and animals are intermediate hosts



    • Ingest oocysts from contaminated soil


    • Humans can ingest oocysts from undercooked meat


  • In humans and animals, oocysts are digested by digestive enzymes



    • Trophozoites are released into intestine



      • Organisms are carried by macrophages within the lymphatic system and blood vessels to internal organs


    • Within macrophages, trophozoites can multiply and become crescent-shaped tachyzoites


  • In immunocompetent patients, tachyzoites usually become segregated into cysts synthesized by host



    • Within cysts, organisms are slow-growing bradyzoites


    • Infection typically resolves


  • In immunodeficient patients, tachyzoites widely disseminate, causing acute infection


CLINICAL ISSUES


Epidemiology



  • Incidence



    • Toxoplasmosis is common parasitic disease worldwide



      • More prevalent in warm and humid climates


    • In USA, toxoplasmosis is most common parasitic infection



      • 50% of USA population have serum antibodies to T. gondii: Evidence of chronic infection


    • T. gondii can be spread transplacentally from mother to fetus



      • 1 in every 1,000 live births in USA


      • ˜ 3,000 births are affected annually


      • Contamination of food &/or water by oocysts commonly causes human infection


      • Potential damage to fetus is greatest with infection in 1st trimester


      • Intrauterine death, microcephaly or hydrocephaly with intracranial calcifications may develop


      • Infections in the 2nd 1/2 of pregnancy are asymptomatic at birth


      • Fever, hepatosplenomegaly, and jaundice may appear


      • Chorioretinitis, psychomotor retardation, seizures appear months or years later


    • Rarely, T. gondii infection can be transmitted via transplanted organ


    • Active infection may result from reactivation of earlier infection



    • Common in patients with cancers and diabetes mellitus


  • Age



    • Children and young adults most often affected


  • Gender



    • Sexes equally affected


Site



  • Lymph nodes are commonly affected (95%)




    • Posterior cervical lymph nodes are characteristic site



      • Often unilateral, firm, 0.5-3.0 cm, tender or nontender


    • Any group of lymph nodes can be involved



      • Other cervical, supraclavicular, occipital, parotid, intramammary regions


    • Generalized lymphadenopathy or hepatosplenomegaly can occur but is unusual


Presentation



  • Asymptomatic infection is common in immunocompetent individuals


  • In immunosuppressed patients, CNS involvement is common


  • Mild malaise, fever, myalgia


  • Pneumonitis, myocarditis, retinitis, pancreatitis, polymyositis, orchitis


Laboratory Tests



  • Sabin-Feldman dye test



    • Highly sensitive and specific


    • T. gondii organisms do not stain with alkaline methylene blue if they have been exposed to serum anti-T. gondii antibodies


    • Positive result: Change from negative to positive or rapidly increasing IgG titers


  • Antibodies to T. gondii can be detected by enzyme immunoassays or indirect immunofluorescence



    • IgM or IgG antibodies against cell wall antigens


    • IgM antibodies present within few days after infection



      • Titers of 1:80 or higher indicate recent infection


      • IgM and IgA antibodies are 93% sensitive detecting congenital toxoplasmosis


    • IgG antibody titers of 1:1,000 occur 6-8 weeks after infection



    • Antibody to 11-kDa sporozoite protein detects infection with oocysts formed in cats


  • Latex agglutination test is available



Prognosis



  • In immunocompetent patients, infection is self-limiting


  • In immunodeficient patients, great risk of acute dissemination



    • Encephalitis, chorioretinitis, pneumonia, and cardiac involvement


    • Death as result of above conditions

Jul 8, 2016 | Posted by in PATHOLOGY & LABORATORY MEDICINE | Comments Off on Toxoplasma Lymphadenitis
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