 Toxoplasmosis is a zoonotic disease caused by infection with the protozoan Toxoplasma gondii  Toxoplasmosis may cause flu- like symptoms in some people, but most people affected never develop signs and symptoms.  For infants born to infected mothers and for people with weakened immune systems, toxoplasmosis can cause extremely serious complications.

An obligate intracellular parasitic protozoan. T. gondii is capable o f infecting virtually all warm-blooded animals(lack of host specificity). Cats are the definitive hosts in which the parasite can undergo sexual reproduction. During infection two forms of parasite may form: –Tackyzoit: Rapidly growing form (acute infection). –Bradyzoit: Slowly growing form in cysts ( chronic infection). Tissue cysts formed in any organ especially brain, eyes and strained muscles.

Eating undercooked, contaminated meat. Eating food that was contaminated by knives, utensils, cutting boards and other foods that have had contact with raw, contaminated meat (cross contamination). Drinking water contaminated with Toxoplasma gondii.

Mother-to-child (congenital) transmission. Accidentally swallowing the parasite through contact with cat feces that contain Toxoplasma. Receiving an infected organ transplant or infected blood via transfusion, though this is rare.

Toxoplasmosis is usually nothing to worry about because the immune system is normally strong enough to fight the infection and stop it from causing serious illness. After getting the infection, most people are immune to it for the rest of their life. However, it can lead to serious problems in: –women who become infected while they're pregnant. –people with weak immune systems.

Approximately 10-20% of pregnant women infected with T gondii become symptomatic, The most common signs of infection are lymphadenopathy and fever. When a mother is infected with T gondii during gestation, the parasite may be disseminated hematogenously to the placenta. When this occurs, infection may be transmitted to the fetus transplacentally.

 If infection was shortly before conception (within a few weeks before) : –carries a one percent risk or below of transmission to the baby, but there is a risk of miscarriage if the baby does become infected.  If infection was in the first trimester (week one to 12) –carries about percent risk of transmission to the baby. A baby infected at this stage has a risk of being miscarried or stillbirth.

 If infection was in the second trimester (week 13 to 28): –about 25 percent risk of transmission. A baby infected at this stage is less likely to be miscarried, but is still at risk of developing severe symptoms as: Hydrocephaly (water on the brain) Calcifications of the brain Retinochoroiditis (inflammation of the retina)  blindness Microcephaly. Neurological disorders.

 If infection was in the third trimester (week 29 to 40) –Risk of transmitting the infection rises again if toxoplasmosis is caught at this stage of pregnancy, and may be as high as 70–80 percent. –Most babies infected will be apparently healthy at birth, but a large proportion will develop symptoms later in life, usually eye damage and Neurological problems.

Retinochoroiditis usually results from reactivation of congenital infection, or a part of acute infection. When the organism reaches the eye through the bloodstream, depending on the host's immune status, a clinical or subclinical focus of infection begins in the retina.

As the host's immune system responds, the cyst forms which is resistant to the host's immune system, and a chronic, latent infection ensues. The cyst remains in the normal- appearing retina. Whenever the host's immune function declines for any 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 retinochoroidal scar.

 serologic tests.  Amplification of specific nucleic acid sequences (i.e., polymerase chain reaction [PCR]).  Histologic demonstration of the parasite and/or its antigens (i.e., immunoperoxidase stain).  Isolation of the organism.  Other rarely used methods include: –demonstration of antigen in serum and body fluids. –A toxoplasmin skin test. –antigen-specific lymphocyte transformation.

Serologic testing: Different serological tests often measure different antibodies that possess unique patterns of rise and fall with time after infection. A combination of serological tests is frequently required to establish whether an individual has been more likely infected in the distant past or has been recently infected.

IgG antibodies: –IgG antibodies usually appear within 1–2 weeks of acquisition of the infection, peak within 1–2 months, decline at various rates, and usually persist for life. –The most commonly used tests for the measurement of IgG antibody are the Sabin-Feldman Dye Test (DT), ELISA, IFA, and the modified direct agglutination test. IgM antibodies: –IgM antibody titres rise from 5 days to weeks following acute infection, reaching a maximum within 21 days and decline more rapidly than IgG. –The most commonly used tests for the measurement of IgM antibody are ELISA kits, the IFA test, and the immunosorbent agglutination assay (ISAGA).

IgA Antibodies: –IgA antibodies may be detected in sera of acutely infected adults and congenitally infected infants using ELISA or ISAGA methods. –It appears in sera when the parasite attacks the eye (toxoplasmic chorioretinitis). –In a number of newborns with congenital toxoplasmosis and negative IgM antibodies, the serological diagnosis has been established by the presence of IgA and IgG antibodies. Note: Ecteric phase is the period when switching b/w IgG and IgM production, results in low levels of both.

IgE Antibodies: –IgE antibodies are detectable by ELISA in sera of acutely infected adults, congenitally infected infants. –The duration of IgE seropositivity is less than with IgM or IgA antibodies and hence appears useful as an adjunctive method for identifying recently acquired infections.

Histologic diagnosis: –Diagnosis also can be made by direct observation of the parasite in stained tissue sections from biopsy. –Immunoflorscence stain and sabin field man stain can be used. – These techniques are used less frequently because of the difficulty of obtaining these specimens. Isolation: –Parasites can also be isolated from blood or other body fluids by animal inoculation or cell cultures, but this process can be difficult and requires considerable time.

PCR: – Molecular techniques that can detect the parasite's DNA in the amniotic fluid can be useful in cases of possible mother-to-child (congenital) transmission. – Amniocentesis: to identify T. gondii in the amniotic fluid by PCR (the most sensitive and specific), done if serologic testing cannot confirm or exclude acute infection, and if there are abnormal ultrasound findings suggestive of toxoplasmosis infection. – Fetal blood sampling (cordocentesis): was previously the gold standard for diagnosing fetal infection but no longer, because of the associated higher fetal risk

Ocular disease is diagnosed based on the appearance of the lesions in the eye, symptoms, course of disease, and often serologic testing and measuring the level of IgA.

There are 2 goals of drug therapy for toxoplasmosis, depending on whether or not fetal infection has occurred. –If maternal infection has occurred but the fetus is not infected, spiramycin is used for fetal prophylaxis (to prevent spread of organisms across the placenta from mother to fetus). –If fetal infection has been confirmed or is highly suspected, pyrimethamine and sulfadiazine are used for treatment and decrease in disease severity.

Do not eat undercooked meat. Wash hands after handling raw meat. Keep children's play areas free from cat and dog feces. Wash your hands thoroughly after touching soil that may be contaminated with animal feces.