What Is Toxoplasma Gondii?

Toxoplasma Gondii is an intracellular parasite, also called a trisomy. Parasitic in cells, flow with the blood, reach all parts of the body, damage the brain, heart, and fundus, causing human immunity to decline and suffering from various diseases. It is obligate intracellular parasites, coccidia, the order Coccidia, isosporidiaceae, Toxoplasma. The life cycle requires two hosts. The intermediate hosts include animals and humans such as reptiles, fish, insects, birds, mammals, and cats and felines.

Toxoplasma gondii belongs to the order Coccidia, Toxoplasmidae, Toxoplasma. The life cycle requires two hosts. The intermediate hosts include animals and humans such as reptiles, fish, insects, birds, mammals, and cats and felines. The life history of Toxoplasma gondii is divided into 5 stages: tachyzoite (trophozoite): rapidly dividing in nucleated cells occupying the host's cytoplasm, called pseudocysts: bradyzoite: secreted The cyst wall slowly proliferates, known as cysts, which contain hundreds of brachiozoites. The schizont stage is the proliferation of merozoites in cat intestinal epithelium by brachizoites or sporozoites, forming merozoites. Gamete phase: Large gamete (female) and small gamete (male), fertilize to form zygotes, and finally develop into oocysts; sporozoite stage: refers to the development and reproduction of sporophytes in the oocysts, forming 2 sporangia, Then each sporangia developed into 4 sporozoites. The first three stages are asexual reproduction and the second two stages are sexual reproduction.

Toxoplasma develops in two stages, the extra-intestinal and intra-intestinal stages. The former develops in a variety of intermediate hosts and cells in the host tissue of terminal infectious disease. The latter develops only in the intestinal mucosal epithelial cells of the final host.

(A) extramucosal stage

Toxoplasma gondii's oocysts, cysts or pseudocysts are swallowed by the intermediate or final host, and sporozoites, bradyzoites or tachyzoites are released in the intestinal cavity. Various nucleated cells in external tissues and organs can also enter cells through phagocytosis and phagocytosis. The body is mainly in the cytoplasm, and can also divide and reproduce in the nucleus. In the acute phase, tachyzoites proliferate rapidly, causing invaded cells to rupture, and tachyzoites invade new cell proliferation. With the formation of body-specific immunity, the proliferation of Toxoplasma tachyzoites in cells slows down and eventually develops into cysts. The worms enter the bradyzoite stage. Encapsulation can persist in the host. When the host's immune function is low, the cysts rupture, releasing a large number of bradyzoites, forming worms, and invading new host cells to proliferate rapidly.

(II) Intestinal mucosal stage

The oocysts, cysts, or pseudocysts are swallowed by the end host and enter the small intestine. Sporozoites, bradyzoites, or tachyzoites can directly invade the small intestinal mucosal epithelial cells to undergo asexual reproduction and form merozoites. After the cell is destroyed, merozoites are released and then invade new epithelial cells. After several generations of proliferation, some merozoites develop into female and male gametophytes in the epithelial cells, which combine to fertilize to become zygotes, and finally develop into oocysts. After the oocysts mature, they escape from the epithelial cells into the large intestine cavity, and are excreted in the stool in vitro. The discharged oocysts mature and become infectious after 2-3 days of development.

There are significant differences in the resistance of Toxoplasma gondii at different developmental stages. The trophozoite is sensitive to temperature and general disinfectants, and can survive for 10 minutes when heated to 54 ° C; it will die in 1 minute in cresol sulfonic acid solution or 1% hydrochloric acid solution. The cysts have a strong resistance. They can survive for 68 days at 4 ° C, and can tolerate 3 hours in gastric juice, but they are not resistant to dryness and high temperature. They die at 56 ° C for 10-15 minutes. The oocysts are highly resistant to commonly used disinfectants such as acids and alkalis, but weak to heat. They die at 80 ° C for 1 minute.

Epidemiology

1. Cats and other mammals and birds can be used as storage hosts for Toxoplasma gondii, with cats being the most important. Other encapsulated animals are also a source of infection. Toxoplasma infection in pregnant women is the source of infection for the fetus.

2. way for spreading

(1) Congenital infection: pregnant women infect the fetus through placental transmission. When a pregnant woman is infected with Toxoplasma gondii during pregnancy, the amniotic fluid can also be contaminated through the placenta during the helminthemia period, enter the gastrointestinal tract of the fetus, and cause internal infection.

(2) Acquired infection: The main transmission routes are diet (raw or unripe meat, milk, eggs, etc.), water pollution and close contact with animals (cats, pigs, dogs, rabbits, etc.). Blood transfusion or organ transplantation with toxoplasmosis has also been reported, and transmission through damaged skin mucous membranes or saliva droplets has also been reported.

3 Population susceptibility Populations are generally susceptible. However, infection rates are higher among animal breeders, slaughterhouse staff, and medical staff. Patients with severe diseases, such as malignant tumors, lymphogranuloma, long-term immunosuppressants, and immunodeficiency patients such as AIDS, are more likely to develop toxoplasmosis.

4 The epidemiological characteristics of Toxoplasma gondii infection are distributed globally, but most of them are latent infections. The infection rate in China is O.lo ~ 47.3%, which is higher in rural areas than in urban areas and higher in adults than in children. Animal-related occupations, such as animal breeders, slaughter T-persons, meat and animal fur processors, veterinarians, have higher infection rates.

Pathogenesis and pathology

After toxoplasma invades the human body, it enters the blood circulation through local lymph nodes or directly causes parasitemia. In the early stage of infection, the body has no specific immunity. Toxoplasma gondii in the bloodstream quickly spread and invaded various organs, and rapidly divided and proliferated in the form of tachyzoites in the cells. After the host cell ruptured, the escaped tachyzoites invaded adjacent cells. Repeatedly, it develops into local tissue necrosis

At the same time, it is accompanied by an acute inflammatory reaction mainly with monocyte infiltration. In the chronic infection phase, the spread of helminthemia occurs only when the cysts are ruptured and the body's immunity is low.

Toxoplasma can invade any organ of the human body, and its predominant sites are the brain, eyes, lymph nodes, heart, lungs, liver and muscles. With the formation of body-specific immunity, Toxoplasma gondii in the blood is cleared, and T. gondii forms cysts in the tissue, which can exist in the host for a long time without obvious symptoms. Encapsulation is most common in the brain and eyes, followed by myocardium and skeletal muscle. Once the host's immunity is reduced, in addition to the cyst rupture and escape, the bradyzoites can spread and cause the above-mentioned tissue necrosis, and can also cause the body's rapid-type hypersensitivity reaction, leading to necrosis and a strong granulomatous inflammation reaction.

Lymph nodes are the most frequently affected sites of acquired toxoplasmosis. Its inflammatory response is characteristic, manifested as a high degree of follicular hyperplasia, marginal cells in the germinal center exhibit eosinophilic cytoplasm, and tissue macrophages irregularly aggregate. No typical granulomas were formed in the lymph nodes.

The eye can produce single or multiple necrotic foci. There is infiltration of monocytes, lymphocytes and plasma cells. Lesions or cysts can be seen in the lesion. Necrotizing retinitis is the first lesion, and granulomatous choroiditis, iridocyclitis, cataracts, and glaucoma can follow.

Brain damage can manifest as focal or diffuse meningoencephalitis with necrosis and microglia nodules. Monocytes, lymphocytes, and plasma cells were infiltrated around the necrotic lesions and necrotic lesions. Toxoplasma gondii could be found in the periphery. Congenital toxoplasmosis encephalopathy can still be seen in the periventricular calcification, perivascular inflammation, necrosis and hydrocephalus.

Hard white nodules and necrotic spots can be seen in the lungs. Spleen enlargement, necrosis, and infiltration around blood vessels ^[1]

Congenital toxoplasmosis

It occurs mainly in the fetus of a pregnant woman who is first infected during pregnancy. Infection in the first and second trimester of pregnancy can cause miscarriage, stillbirth or deformity (such as intracranial calcification, microcephaly, hydrocephalus), intrauterine growth retardation; late pregnancy infection, fetal development can be normal, but premature birth, or Symptoms such as retinal choroiditis, visual impairment, epilepsy, and mental developmental disorders do not develop until months or years after birth.

Acquired toxoplasmosis

The performance is complicated, and the condition is related to the state of human immune function.

1. Most of the patients with normal immune function are recessive infections, and about 10% to 20c / o patients have clinical manifestations with mild cold-like symptoms. 90qo patients have lymphadenopathy but do not have suppuration. Neck and axillary lymph nodes are most commonly affected. Occasionally pneumonia, pleurisy, myocarditis, pericarditis, hepatitis, retinal choroiditis. The course of the disease lasts several weeks or months, even up to 1 year. If the worm cannot be completely removed, it can form a cyst and turn into a latent infection.

2. In patients with immunocompromised function, when acute infection or latent infection is activated, lymph node lesions are not obvious, and they are prone to systemic disseminated infections such as central nervous system involvement.

(1) Diseases of the central nervous system can manifest as encephalitis, meningitis or meningoencephalitis, myelitis, seizures, and mental disorders. Subacute or acute onset, may have fever, headache, jet-like vomiting, varying degrees of consciousness, movement disorders, paresthesia, epilepsy, visual impairment, aphasia, etc. Meningeal irritation signs can be positive and localized signs can be found.

(2) Pulmonary toxoplasmosis is more common in patients with advanced AIDS and is an interstitial pneumonia.

(3) Ocular toxoplasmosis is mainly manifested as retinal choroiditis, which can occur repeatedly. Acute inflammation mainly manifests as eye pain, blurred vision, photophobia and tearing. After the inflammation is relieved, scars are left locally, often involving the macula, blind spots and decreased vision. Can be complicated by retinal detachment, choroidal neovascularization, glaucoma.

(4) Other manifestations such as involvement of the digestive tract,

Complications and sequelae

Survivors of congenital toxoplasmosis often have sequelae, such as mental retardation, visual impairment, epilepsy, and mental retardation. Acquired toxoplasmosis also has sequelae in patients with central nervous system and eyes ^[3]

Strengthen the monitoring and isolation of domestic animals, poultry and suspicious animals; strengthen dietary hygiene management, strengthen the meat quarantine system; educate the public not to eat raw or semi-raw meat, eggs, dairy products; pregnant women do not raise cats, do not touch cats, Cat feces and raw meat. Do not let cats lick their hands, face, and food utensils. Regular routine inspections of Toxoplasma gondii can be used to reduce the incidence of congenital Toxoplasmosis.

Patients in the acute phase should be treated with drugs in time, but there is no ideal drug yet. Ethylpyrimidine and sulfa drugs such as compound sinomine have inhibitory effects on Toxoplasma gondii in the proliferative phase. The combined use of these two drugs can improve the efficacy.

Once the first infection of the pregnant woman is diagnosed, spiramycin should be taken immediately; if the diagnosis of fetal toxoplasmosis is confirmed, it should be changed to pyrimethamine, sulfadiazine and spiramycin. Spiramycin is safe, has little toxic and side effects, good oral absorption, high concentration in tissues, and slow excretion. It is expected to be widely used in the treatment of various toxoplasmosis.

The prevention and control of toxoplasmosis is extremely important, but the ideal method has not yet been found. Therefore, the development of a cheap, safe and effective toxoplasma vaccine is undoubtedly the best control measure. However, there have been no reports of such vaccines being applied to humans ^[4]

Results of antibody tests after pregnancy determine pets' stay:

• Already infected :

If the IgM antibody is positive, it means that there is an infection in the near future, and you cannot temporarily become pregnant. You need to be treated. You can consider pregnancy only after being cured.

• Primary infection :

If the antibodies are negative, it means that the body has not been infected, so be careful before and after pregnancy. If you find it difficult to ensure good hygiene, it is best to avoid pets during pregnancy for insurance purposes. Because there is no relevant antibody in the body. It is best to review the pregnancy early, middle and late. After the child has some immunity, he can pick it up and raise it for himself.

• Non-primary infections:

If the IgM antibody is negative and the IgG antibody is positive, but the antibody titer is not high, it may be chronic infection or previous infection. If you have been infected with Toxoplasma before pregnancy, you are no longer in danger of being infected after pregnancy. Because only pregnant women who have not been infected with Toxoplasma before pregnancy can have a primary (primary) infection during pregnancy that can be transmitted to the fetus. At this time, if pets stay with them, they need to pay attention to hygienic habits to avoid getting infected.

• Clean room with germs and antibodies:

It is impossible for humans to completely avoid Toxoplasma as much as they want to survive in a sterile room. A few germs not only have no great harm, but also can promote and increase children's immune antibodies to Toxoplasma gondii. Otherwise, a child who does not have antibodies to Toxoplasma gondii, one day, the primary infection (that is, the first or first infection) will be more harmful. Just like a child in a sterile room, it is the same reason that a cold germ can be fatal.

• Infant disease immunity, breast milk immunity:

In women with toxoplasmosis, the fetus must be infected if there is blood sowing during pregnancy (ie, toxoplasma, sphincter, and cuspid activity). 80% of all fetuses are patients with latent chronic toxoplasmosis. During lactation, the baby becomes "immunized with the disease", so despite the presence of Toxoplasma gondii in the breast milk, the baby is not a big deal. Every time it is fed, a live vaccine is given. Babies can grow as usual.

• Pet detection antibodies:

Detection of Toxoplasma gondii on pets. If the pet is not infected, you can keep it at home, but avoid the pet from contacting the outside during pregnancy. If the pet is already infected, you need to keep the pet in a treatment institution, and then treat the pet with Toxoplasma gondii.

• "Rational" treatment of "Toxoplasma":

The detection technology of Toxoplasma gondii in China is not developed, and the incidence of Toxoplasma gondii in China is not high. Therefore, the domestic knowledge of Toxoplasma gondii is relatively small, and most of the medical staff just have no contact experience, just talk and talk on paper. And media and hospital hype are always a commercial method. Pregnant women need multiple parties to "synthesize and collect the true information about the truth" to be a mother's "sense and responsibility". Since it is to be a mother, it should be beyond ordinary people. Be rational and calm, and check from multiple sources.

Regional and recessive hazards of Toxoplasma gondii infection: Toxoplasma gondii has a worldwide distribution and can be infected by humans and many animals. 25% -50% of the world is infected, and the positive infection rate in China is 5% -20%. In some areas, it is over 30%. Adults infected with this parasite are like having a mild flu, and children or fetuses are more affected if they become infected. Researchers at the University of Oxford believe that children infected with more of the parasite will develop ADHD and decline in IQ. Research by American scientist Torrey has shown years ago that those who raised cats in childhood were 53% more likely to develop schizophrenia in adulthood than those who did not. This means that if a child is breast-feeding and cats live together at home, he is also 51% more likely to develop schizophrenia in adulthood than other babies.

(3) If you are a very careful person who is afraid of chances, even if you want to give a member of your family-pets, be sure to find a good home for your pets, you are all it once depended on. Or, you can pick it up when your child grows up. While a mother grants life to future generations, it is also a necessary course for humans to teach the beautiful souls of future generations. American biologist Kevin Lafferty said cat lovers don't have to be upset about a theoretical infection. A "modern" cat that eats safe cat food and does not need to catch mice generally does not pass "Toxoplasma gondii" to humans. Although there is such a possibility, the probability is not high. "A pet cat doesn't mean it can become infected," he said.