Toksoplasmosis

Understanding?
Toxoplasmosis is a disease caused by the parasite Toxoplasma gondii, which has been known to cause birth defects (congenital anomalies) in infants and miscarriage (abortion) in pregnant women. Toxoplasma infection can be either single or in combination with other infection from group-KM TORSH.
Transmission source is feces furry animals, especially cats. Its modes of transmission to humans via:
Food and vegetables / fruits contaminated with animal feces furry (cat). Eating undercooked meat from infected animals. Through blood transfusions or organ transplants from infected donors Toxoplasma. In congenital (inherited) from mothers to their babies when pregnant women were infected during the first months of her pregnancy. Toxoplasmosis in pregnant women can cause miscarriage, premature birth, stillbirth, birth defects or congenital Toxoplasma infection. When pregnant women are infected with toxo-plasma then the risk of congenital toxoplasmosis in infants at birth ranged between 30-40%. Congenital Toxoplasma infection can result in children born damaged eye, perkapuran brain, and mental retardation, but often these symptoms are not seen in newborn babies (neonates). Several factors may account for the appearance of symptoms is a function of the placenta as a barrier (barrier), immune status (immune) pregnant women, and gestational age when the occurrence of infection in the mother. The greater the gestational age when the occurrence of infection, the greater the likelihood of congenital Toxoplasma infection in the fetus. On the other hand, the increasingly early occurrence of infection in the fetus, the more severe damage (disorder) that may occur in the fetus and the greater the likelihood of abortion.
The life cycle of the parasite Toxoplasma
Toxoplasma gondii is widespread in nature in humans and animals and is one of the most frequent cause of infections in humans worldwide. This is a protozoan parasite belonging to Coccidia, and has 3 (three) form:
Oocysts (resistant forms which are in the outside environment). Trofozoit (vegetative form and proliferative). Cysts (resistant form inside the human body and animals). Toxoplasma breed in the intestines of animals, especially furry cat, resulting in the release of oocysts with cat feces. A cat may spend up to 10 million oocysts daily for 2 weeks. Oocyst sporozoites forming within 1 to 3 days and remain infective for months to a year in the soil moist and hot, is not sunshine. Soils contaminated with animal feces (cat) causes infection in mice and birds, which then will cause reinfection back on the cat. In this way the parasite's life cycle is complete. Children can also become infected by playing in soil contaminated cat feces. Land is also a source of infection for herbivores such as goats, sheep, pigs and cattle. Due to persistent infection in most animals is chronic, then the meat is raw or undercooked be a source of infection for humans and carnivores.
Symptoms and clinical manifestation of toxoplasmosis
Symptoms that arise in Toxoplasma infection is not typical, so people often do not realize that he had been exposed to infection. But once exposed to the parasite Toxoplasma infection will persist (persistent) in the form of cysts in the organs of the patient's body during its life cycle. Clinical symptoms are most often met by enlarged lymph nodes (lymph) is known as lymphadenopathy, which can be accompanied by fever. Lymph glands in the neck are most often attacked. Other symptoms of acute toxoplasmosis is a fever, stiff neck, muscle aches (myalgia), joint pain (arthralgia), rash, gidu (urticaria), hepatosplenomegaly or hepatitis.
Clinical form of toxoplasmosis is most often in children is an infection of the retina (chorioretinitis), usually occur in adolescence or adulthood. In children, strabismus is an early symptom of chorioretinitis. When the macula is affected, then the vision sen-tralnya will be disrupted.
In patients with immunodeficiencies such as patients with immune defects, cancer, tissue transplant recipients who received immunosuppressant treatment, symptoms can be mild to severe central nervous system such as encephalopathy, meningoense-falitis, or mass lesions of the brain and mental status changes, headache, focal abnormalities cerebral and seizures, even in people with AIDS often lead to death.
Congenital toxoplasmosis is a clinical manifestation of neurological disorders: hydrocephalus, mikrose-phallic, seizures, psychomotor delay, perkapuran (calcification) rontgenkepala abnormal in photographs. In addition it seems too impaired vision: mikroftalmi, cataracts, re-tinokoroiditis; also hearing loss, and systemic disorders: hepatosplenomegaly, lymphadenopathy, and fever of unknown cause.
Examination
Diagnosis of toxoplasmosis disease generally enforced because of kecenderu with that lead to disease, among others, a history:
infertility, abortion, stillbirth, congenital abnormalities keep furry pets such as cats Examination of the currently used to diagnose toxoplasmosis is serologically, by examining the anti (antibody) IgG and IgM Toxsoplasma gondii. IgM antibodies formed during the acute infection (5 days after infection), titernya increase rapidly (80 to 1000 or more) and will subside within a relatively short time (several weeks or months). IgG antibodies formed much later (1-2 weeks after infection), which will increase titernya in 6-8 weeks, then decreased and can survive in a long time, months or even more than a year. Therefore, the findings of IgG antibodies is considered as an infection that had been a long, while the presence of IgM antibodies means a new infection or re pengakifan old infection (reactivation), and the risk of babies exposed to congenital toxoplasmosis. How high levels of antibodies to declare a person already infected with Toxoplasma are extremely diverse, depending on how worn calibration and quality control of raw and limitations of each laboratory. One example that can be pointed out is the result of research conducted by the Rev. Teguh S et al. (1998), which states a mother classified as positive when titer IgGnya 2949 IU / ml or IgM 0.5 IU / mL, while classified as negative when the IgG titer <> Not all pregnant women infected with Toxoplasma will transmit toxoplasmosis to her baby ba-Waan. When the examination of the mother before pregnancy showed positive IgG antibodies against toxoplasma, means the mother is infected long, but it does not mean that 100% baby will be free of congenital toxoplasmosis. If the new serological examination performed during pregnancy, then:
when the IgG (+) and IgM (-); considered a long infection and risk of fetal infection is low enough so that there are some experts who argue not need to be treated, unless the patient is suffering from immune disorders. when the IgG (+) and IgM (+); test should be repeated again three weeks later. IgG titer was not increased when it is considered that the infection occurred before the pregnancy and the risk to the fetus is quite low, whereas if the titers increased 4-fold IgG and IgM remained positive, then this means that there has been a new infection and the fetus is at risk of miscarriage or congenital toxoplasmosis. if IgG (-) and IgM (-); does not mean free from congenital toxoplasmosis, it is the mother of this examination should be repeated every 2-3 months for menasah seroconversion (negative to positive change). When pregnant women are found IgM (+) then treatment is certain to be given and repeated ultrasound examinations to determine fetal abnormalities.
serial ultrasound every 3 weeks to determine any abnormalities, eg, ascites, enlarged brain cavities (ventriculomegaly) (V / H), pemesaran liver (hepatomegaly), perkapuran (calcification) of the brain. If there are abnormalities in the fetus should be considered for the lawyer-ending (termination) of pregnancy. if possible, fetal blood sampling performed at 20-32 weeks gestation for culturing parasites (inoculation) in mice. When the inoculation gave positive results then need to be considered for termination of pregnancy. after the baby is born to do a complete examination of the infant, including: blood sampling talipusat when newly born babies to fetal antibody serology or isolation of T. gondiii, point-light eye examination (fundoscopy), and ultrasound or x-ray of the skull. The diagnosis of congenital toxoplasmosis in infants is more difficult to set because the clinical symptoms of congenital Toxoplasma infection are very diverse and often subclinical (not shown) in neonates. Therefore, serological testing should be done also in neonates, especially when the mother is infected during pregnancy is known. IgG antibodies can cross the placenta, whereas IgM antibodies can not penetrate the placenta. Thus, if the baby's blood was found on IgG antibodies may simply represent the transfer (transfer) maternal IgG, and gradually be depleted. At age 2-3 months, babies can already form IgG antibody alone, when the baby is infected then the concentration of congenital Toxoplasma IgGnya will begin to increase again after the IgG derived from his mother out. But if IgM antibodies are found, then this shows a real infection in infants (congenital toxoplasmosis).
Treatment
To control this persistent infection, is generally required an adequate immune response (adequate). Toxoplasma Patients with normal immune systems do not require treatment, unless symptoms are severe or ongoing. Toxoplasmosis in immunodeficient patients should be treated because it can lead to death.
Toxoplasmosis in pregnant women need to be treated to prevent congenital toxoplasmosis in infants. Drugs that can be used for pregnant women is spiramycin 3 g / day divided in 3-4 doses regardless of gestational age, or if required it can be given in the form of a combination of pyrimethamine and sulfadiazine after a gestational age above 16 weeks.
In infants suffering from congenital toxoplasmosis whether symptomatic or not, should be given treatment to prevent further disorder. The drugs used were:
Pyrimethamine 2 mg / kg for two days, then 1 mg / kg / day for 2-6 months, dikikuti with 1 mg / kg / day 3 times a week, plus Sulfadiazine or trisulfa 100 mg / kg / day divided in two doses, plus Folinat acid 5 mg / two days, or with the combination treatment: Spiramycin dose of 100 mg / kg / day divided into 3 doses, alternating each month with pyrimethamine, Prednisone 1 mg / kg / day in 3 divided doses until no improvement korioreti-Nitis. Need to be performed serology tests to determine whether continued treatment is still necessary. As a new strategy for tackling problems that Toxoplasma infection is persistent, use a combination of immunotherapy and treatment of antimicrobial substances.Cellular immunologic defects treated with immunomodulators (Isoprinosine or levamisole), while the infection is controlled by administering spiramycin. The combination treatment is intended to provide support for the news Pende by increasing cellular immunologic reaction and simultaneously control the infection toksoplasmanya.