Toxoplasma gondii

         Toxoplasma gondii infection

                     P.K.Ghatak, MD 

Toxoplasma gondii

Toxoplasma gondii is a protozoa. It lives in cat's intestine as a parasite and is eliminated from cats' body in the feces in a cystic from which can infect mammals and birds. Rodents and small mammals are intermediate and humans are also intermediate host and victims.

Toxoplasma needs a higher concentration of arachidonic acid, a long chain fatty acid, for sexual maturity and reproduction. All species of cat family provide that environment because the enzyme, delta-6-desaturase (D6D), which breaks down arachidonic acid during metabolism, is lacking in he cats' small intestine.

Toxoplasmosis is a medical term describing clinical features of Toxoplasma gondii (T. gondii) infection T. gondii is an obligate intracellular parasite in human and other mammals.

Eating under cooked meat, raw fruits, vegetables and drinking unfiltered water contaminated with cats feces are the main source of human infection. In rare cases blood transfusion, organ transplantation and transplacental infection to the developing fetus can occur. Most infected people show no symptoms, however, the fetuses of women infected for first time during pregnancy and Immunosuppressed people become sick.

There are three infectious forms of T. gondii, - 1.sporozoites - present in the feces of cat as oocysts ( thick wall cysts containing multiple larvae), 2.tachyzoites ( rapidly multiplying by asexual cell division) and 3. bradyzoites (slow growing or dormant) - present in the muscles and organs of infected mammals.

Life cycle of Toxoplasma.

T. gondii has a complex life cycle.

In cats:

All species of cat family are carnivorous , when they devour infected preys , the cysts are released in the small intestine. The wall of the cysts opens and releases sporozoites. Subsequent development of T. gondii takes two different pathways.

1. As a intestinal parasite.

In 3 to 10 days the sporozoites mature as male and female gametes and after mating and begins to reproduce. Million of cysts are excreted daily in the feces for 14 days. In the soil these cysts matures further and becomes infectious in a day or two. The cysts can survive about a year in the soil and water

2. As cysts in muscles and organs,

Some of the released sporozoites penetrate intestinal wall and are carries by the blood to different organs and muscles. The sporozoites asexually divide rapidly and are called tachyzoites. Later, tachyzoites stop dividing and form cysts and are known as bradyzoites. Cysts in the muscles, heart,eyes and other organs can complete their life journey if other carnivores eat the cat.

In rodents, mammals and human:

Infection is via oral route. In the intestine the T. gondii follows the 2nd path described for cat.

                                         Taken from CDC publication.

Primary infection is healthy adults.

About 50% of infected people have no symptoms , the rest have symptoms resembling a flu with slight fever, body aches, cough and sneezing. Cervical lymph node enlargement is a distinct feature, at times, lymph nodes draining the thorax may enlarge. Viral pneumonia like symptoms may develop in some. Rarely skin lesions of various definitions are also described. Cysts, containing a live T. gondii remain in the muscles, brain, heart, eyes and other organ for the rest of the life of an individual.

Pregnancy:

In the first trimester of pregnancy if a woman is infected, there is a good chance that infection from the placenta will pass to the fetus. This may result in a miscarriage and spontaneous abortion. A growing fetus examined by ultrasonography shows growth retardation and a characteristic triad of hydrocephalus, chorioretinitis and areas of calcification of the brain. Eye infection leads to congenital blindness. And sensory deafness in 30% cases.

In last trimester of infection produces mainly blindness.

Latency:

In all healthy people, T. gondii after the initial infection, remains in an inactive state. The organism however is still alive within the cysts and last for the rest of life of the individual.

Reactivation:

When inter-current infections and HIV infection in particular, lowers the cellular resistance or immunosuppressed drugs are used, the cellular resistance breaks down and T. gondii spread through out the body. The CNS and eye symptoms predominate.

The Brain:

Mass lesions, like cerebral lymphoma , are present in many cases; in most of the cases necrotizing lymphocytic vasculitis and microglial nodules around the cysts are present. These produce seizures and symptoms of encephalitis. The common areas of brain are the symmetrical lesions in the white matter of cerebral cortex, thalamus, brain stem, and cerebellum. Symptoms are headaches, confusion, seizure, inability to concentrate, clumsiness of movements, fever and nausea and vomiting.

Eyes:

Necrotizing lesions of choroid and retina of the eyes produce poor vision and blindness.

Diagnosis:

The initial test is IgM and IgG antibodies against T. gondii. If a biopsy is performed the T. gondii is visible within the cells. In most cases, PCR test to detect DNA of T. gondii has become a standard test. In encephalitis the PCR test of CSF is 100% positive .

In suspected mother to fetal transmission, an amniocentesis and PCR test is performed on the amniotic fluid.

Treatment:

Normal adult people with T. gondii infection requires no medication. In a developing fetus, even infection is confirmed, no anti- protozoal drugs are prescribed because of adverse effects. After the birth of the baby the choice of therapy is a combination of Pyrimethamine and Sulfadiazine. Infections of pregnant women if the child is not infected - Spiramycin is preferred therapy. If the child is infected then no treatment is given to mothers in the first trimester because drugs can cause deformed brain development and low platelet count of the child. After 16 weeks of pregnancy, Pyrimethamine and Sulfadiazine plus folinic acid are prescribed.

In all other infections the drug of choice is a combination of Pyrimethamine and Sulfadiazine; Folinic acid is added to prevent anemia.

Children with congenital deafness 16 months of therapy is advocated.

Prophylaxis in HIV infection and immunosuppressed individual.

Pyrimethamine plus Sulfadiazine should be continued.

Vaccine:

No vaccine is available.

Prevention:

Good hygienic measures and avoiding under cooked meat and unwashed fruits and vegetable.