Toxoplasmosis is a zoonoticdisease caused by infectionwith the protozoan Toxoplasmagondii
Toxoplasmosis may cause flu-like symptoms in somepeople, but most peopleaffected never develop signsand symptoms.
For infants born to infectedmothers and for people withweakened immune systems,toxoplasmosis can causeextremely seriouscomplications.
•An obligateintracellular parasitic protozoan.
•T. gondii is capable o f infecting virtuallyall warm-blooded animals(lack of hostspecificity).
• Cats are the definitive hosts in which theparasite can undergo sexual reproduction.
•During infection two forms of parasite mayform:
–Tackyzoit: Rapidly growing form (acuteinfection).
–Bradyzoit: Slowly growing form in cysts (chronic infection).
•Tissue cysts formed in any organespecially brain, eyes and strainedmuscles.
•Eating undercooked,contaminated meat .
•Eating food that wascontaminated by knives,utensils, cutting boards andother foods that have hadcontact with raw, contaminatedmeat (cross contamination).
•Drinking water contaminatedwith Toxoplasma gondii.
•Mother-to-child (congenital)transmission.
•Accidentally swallowing theparasite through contactwith cat feces that containToxoplasma.
•Receiving an infected organtransplant or infected bloodvia transfusion, though thisis rare.
•Toxoplasmosis is usually nothing toworry about because the immunesystem is normally strong enough tofight the infection and stop it fromcausing serious illness. After getting theinfection, most people are immune to itfor the rest of their life.
•However, it can lead to seriousproblems in:
–women who become infectedwhile they're pregnant .
–people with weak immune systems.
•Approximately 10-20% of pregnantwomen infected with Tgondii become symptomatic, Themost common signs of infection arelymphadenopathy and fever.
•When a mother is infected with Tgondii during gestation, theparasite may be disseminatedhematogenously to the placenta.When this occurs, infection may betransmitted to the fetustransplacentally.
If infection was shortly beforeconception (within afew weeks before) :
–carries a one percent risk or below oftransmission to the baby, butthere is a risk of miscarriage if the babydoes become infected.
If infection was in the firsttrimester (week one to 12)
–carries about 10-15 percent risk oftransmission to the baby. A babyinfected at this stage has a risk of beingmiscarried or stillbirth.
If infection was inthe second trimester (week13 to 28):
–about 25 percent risk oftransmission. A baby infectedat this stage is less likely to bemiscarried, but is still at risk ofdeveloping severe symptomsas:
• Hydrocephaly (water on thebrain)
•Calcifications of the brain
•Retinochoroiditis(inflammation of theretina)blindness
•Microcephaly.
•Neurological disorders.
If infection was in the thirdtrimester (week 29 to 40)
–Risk of transmitting the infectionrises again if toxoplasmosis iscaught at this stage ofpregnancy, and may be as highas 70–80 percent.
–Most babies infected will beapparently healthy at birth, but alarge proportion will developsymptoms later in life, usuallyeye damage and Neurologicalproblems .
•Retinochoroiditis usuallyresults from reactivation ofcongenital infection, or apart of acute infection.
•When the organismreaches the eye throughthe bloodstream, dependingon the host's immunestatus, a clinical orsubclinical focus of infectionbegins in the retina.
• As the host's immune systemresponds, the cyst forms which isresistant to the host's immunesystem, and a chronic, latent infectionensues.
•The cyst remains in the normal-appearing retina. Whenever thehost's immune function declines forany reason, the cyst wall rupture,releasing organisms into the retina,and the inflammatory process starts.If an active clinical lesion is present,healing occurs as a retinochoroidalscar.
serologic tests.
Amplification of specific nucleic acidsequences (i.e., polymerase chainreaction [PCR]).
Histologic demonstration of theparasite and/or its antigens (i.e.,immunoperoxidase stain).
Isolation of the organism.
Other rarely used methods include:
–demonstration of antigen in serum andbody fluids.
–A toxoplasmin skin test.
–antigen-specific lymphocytetransformation.
•Serologic testing:
•Different serological testsoften measure differentantibodies that possessunique patterns of riseand fall with time afterinfection.
•A combination ofserological tests isfrequently required toestablish whether anindividual has been morelikely infected in thedistant past or has beenrecently infected.
•IgG antibodies:
–IgG antibodies usually appearwithin 1–2 weeks of acquisitionof the infection, peak within 1–2months, decline at variousrates, and usually persist forlife.
–The most commonly used testsfor the measurement of IgGantibody are the Sabin-FeldmanDye Test (DT), ELISA, IFA, andthe modified direct agglutinationtest.
•IgM antibodies:
–IgM antibody titres rise from 5days to weeks following acuteinfection, reaching a maximumwithin 21 days and declinemore rapidly than IgG.
–The most commonly used testsfor the measurement of IgMantibody are ELISA kits, the IFAtest, and the immunosorbentagglutination assay (ISAGA).
•IgA Antibodies:
–IgA antibodies may be detected insera of acutely infected adultsand congenitally infected infantsusing ELISA or ISAGA methods.
–It appears in sera when theparasite attacks the eye(toxoplasmic chorioretinitis).
–In a number of newborns withcongenital toxoplasmosis andnegative IgM antibodies, theserological diagnosis has beenestablished by the presence ofIgA and IgG antibodies.
Note: Ecteric phase is the period whenswitching b/w IgG and IgM production ,results in low levels of both.
•IgE Antibodies:
–IgE antibodies are detectable byELISA in sera of acutely infectedadults, congenitally infected infants.
–The duration of IgE seropositivity isless than with IgM or IgA antibodiesand hence appears useful as anadjunctive method for identifyingrecently acquired infections.
•Histologic diagnosis:
–Diagnosis also can be made by directobservation of the parasite in stainedtissue sections from biopsy.
–Immunoflorscence stain and sabin fieldman stain can be used.
– These techniques are used lessfrequently because of the difficulty ofobtaining these specimens.
•Isolation:
–Parasites can also be isolated fromblood or other body fluids by animalinoculation or cell cultures, but thisprocess can be difficult and requiresconsiderable time.
•PCR:
–Molecular techniques that can detect the parasite'sDNA in the amniotic fluid can be useful in cases ofpossible mother-to-child (congenital) transmission.
–Amniocentesis:
•to identify T. gondii in the amniotic fluid by PCR (the mostsensitive and specific), done if serologic testing cannotconfirm or exclude acute infection, and if there are abnormalultrasound findings suggestive of toxoplasmosis infection.
–Fetal blood sampling (cordocentesis):
•was previously the gold standard for diagnosing fetalinfection but no longer, because of the associated higherfetal risk
•Ocular disease isdiagnosed based onthe appearance ofthe lesions in theeye, symptoms,course of disease,and often serologictesting andmeasuring the levelof IgA.
•There are 2 goals of drug therapy fortoxoplasmosis, depending onwhether or not fetal infection hasoccurred.
–If maternal infection has occurred butthe fetus is not infected, spiramycin isused for fetal prophylaxis (to preventspread of organisms across theplacenta from mother to fetus).
–If fetal infection has been confirmed oris highly suspected, pyrimethamineand sulfadiazine are used for treatmentand decrease in disease severity.
•Do not eat undercooked meat.
•Wash hands after handling rawmeat.
•Keep children's play areas freefrom cat and dog feces.
•Wash your hands thoroughly aftertouching soil that may becontaminated with animal feces.
