Toxoplasma Gondii

Toxoplasma Gondii

Toxoplasma gondii is a microscopic protozoa that causes a disease called toxoplasmosis. The disease is found all over the world. Some estimates suggest that over 30 % of human population is infected. For example, in Germany and France most people carry the parasite, whereas in South Korea it is quite rare. More than 60 million people in the United States are said to be infected. Toxoplasmosis is usually asymptomatic, because our immune system keeps the parasite from causing illness. The disease is more problematic for pregnant women and people who have weakened immune systems. Cats are the primary host and humans and other warm blooded animals are just intermediate hosts. In this sense Toxoplasma gondii is not a pure human parasite.

Toxoplasma gondii is known to change the host's behaviour. Studies show the capability for the parasite to make rats fearless near cats. This indicates the evolutionary need for Toxoplasma gondii to get inside felines. When a rat is eaten by a cat the parasite gets inside the primary host. There have been a few studies with humans, too. Some results indicate a strong correlation between schizophrenia and toxoplasmosis. According to some studies women with toxoplasmosis are more likely to cheat their husbands. Men with the parasite have shown to be more aggressive. Infected humans also have slower reaction times.

Humans get infected by:
blood transfusion or organ transplantation (very rare)
consuming undercooked, infected meat (especially lamb, pork and venison)
ingesting water, soil (for example, putting dirty fingers in your mouth) or anything else that has been contaminated with cat feces
mother-to-child transmission. A pregnant woman, who has just been infected with Toxoplasma gondii can pass the infection to her unborn baby (congenital infection). She might not have any symptoms, but the unborn child might suffer and develop disease.

The life cycle of Toxoplasma gondii starts, when oocysts (resting form of the parasite) exit the primary host (cat) in the feces. Millions of oocysts are shed for as long as three weeks after infection. Oocysts sporulate and become infective within a few days in the environment. The oocysts are found only in the feces of domestic and wild cats. Birds, humans and other intermediate hosts get infected after ingesting water or food contaminated with the cat feces. (Healthy cats can get infected this way, too.) In the gut oocysts transform into tachyzoites which are about 4–8 µm long and 2–3 µm wide. They travel to other parts of the body via bloodstream and further develop into tissue cyst bradyzoites in muscle and neural tissue. Cysts are about 5–50 µm in diameter. They are commonly found in skeletal muscles, brain, myocardium and eyes where they can remain many decades. If a cat (or a human) eats the intermediate host, the tissue cysts get ingested and the parasite activates in the small intestine.



Healthy people who become infected often do not have symptoms because their immune system keeps the parasite from causing sickness. 10–20 % of patients develop sore lymph nodes, muscle pains and other minor symptoms that last for several weeks and then go away (acute toxoplasmosis). The parasites remain in the body as tissue cysts (bradyzoites) and reactivate, if the person becomes immunosuppressed by other diseases or by immunosuppressive drugs.

Usually if a woman has been infected before becoming pregnant, the unborn baby is safe because the mother has developed immunity. If a woman is pregnant and becomes infected with toxoplasmosis during or right before pregnancy, she can transmit the disease to her unborn child (congenital transmission). The earlier the transmission occurs the bigger the effects. Then again, the longer the pregnancy goes on, the more likely is the infection going to occur. This has something got to do with the penetrability of the placenta. Symptoms might include:
miscarriage or stillborn baby
baby born with signs of toxoplasmosis (for example, abnormal enlargement or smallness of the head)
baby with brain or eye damage.

Usually the babies have no symptoms initially, but can develop mental disability, vision loss (ocular toxoplasmosis) and seizures later in life.

Eye disease can be caused by congenital toxoplasmosis or infection after birth or rarely from acute toxoplasmosis as an adult. Eye lesions from congenital infection are often not present at birth but occur in 20–80 % of infected individuals, when they reach adulthood. However, in the U.S. less than 2 % of persons infected after birth develop eye lesions. Eye infection leads to an acute inflammatory lesion of the retina, which leaves retinochoroidal scarring. Symptoms of acute ocular toxoplasmosis include:
blurred or reduced vision
eye pain
redness of the eye
sensitivity to light (photophobia)
tearing of the eyes.

The eye disease can reactivate later in life causing more damage to the retina. If the central structures of the retina are damaged, a progressive vision loss may follow.

People with weakened immune systems may develop central nervous system disease, brain lesions, pneumonitis or retinochoroiditis among other risks. For example, people with AIDS and renewed toxoplasmosis can have symptoms that include:
confusion
fever
headache
nausea
poor coordination
seizures.

If latent (chronic) toxoplasmosis reactivates in immunocompromised pregnant women who were infected before their pregnancy, it might cause congenital infection to the baby.

Toxoplasmosis diagnosis is typically made by serologic tests by detecting immunoglobulin antibodies within several weeks of infection. Your health care provider examines your blood sample to find Toxoplasma-specific IgA, IgG or IgM antibodies. Living parasites can be also found in the sample (blood, cerebrospinal or other body fluids) but the process is more difficult and thus not usually used. Direct observation of the parasite is possible in cerebrospinal fluid (CSF), stained tissue sections or other biopsy samples but these techniques are used less frequently due to their difficulty. A test that measures IgG determines if a person has been infected. Sometimes it is necessary to determine the time of the infection especially if the person is pregnant. For this IgM is detected along with IgG avidity test. Molecular techniques are used for detecting Toxoplasma gondii DNA in the amniotic fluid in cases of congenital transmission (mother-to-child transmission). Ocular toxoplasmosis diagnosis is usually based on symptoms, appearance of lesions in the eye, serologic testing and course of the infection. Serologic tests can be unreliable in immunosuppressed patients.

Toxoplasmosis can be treated with combinations of pyrimethamine with either trisulfapyrimidines or sulfadiazine, plus folinic acid in the form of leucovorin calcium to protect the bone marrow from the toxic effects of pyrimethamine. If this treatment causes hypersensitivity reaction, then pyrimethamine and clindamycin can be used instead. If these drugs are not available, then a combination of sulfamethoxazole and trimethoprim can be used. Pregnant women and babies can be treated but Toxoplasma gondii cannot be eliminated completely. The parasites can remain within tissue cells in a less active stage (cyst) in locations difficult for the medication to get to. A drug called spiramycin is recommended during the first four months whereas sulfadizaine/pyrimethamine and folinic acid for women that have been pregnant for more than four months. PCR (a method to discover parasite DNA) is often performed on the amniotic fluid to find out if the infant is infected. If the infant is likely to be infected, then treatment is done with drugs such as sulfadizaine, pyrimethamine and folinic acid. Congenitally infected babies are treated with sulfonamide and pyrimethamine. Treatment for persons with ocular disease depends on the size of the eye lesion, the characteristics (acute or chronic) and the location of the lesion. Persons with compromised immune systems (such as AIDS patients) need to be treated until their health improves significantly.