1.What is Toxoplasma gondii?
Toxoplasma gondii is a parasite (protozoan) that lives in the host cells and is called Toxoplasma gondii because its trophozoites are bow-shaped. There are 5 forms in the life history of Toxoplasma gondii, namely trophozoites, encysts, schizonts, gametophytes and oocysts. The first 3 stages are asexual reproduction and the last 2 stages are sexual reproduction. Toxoplasma gondii requires dual hosts to complete its life history: in the final host (cats and other felines), all five forms are present; in the intermediate host (including birds, mammals and humans), only asexual reproduction is present. The oocysts are infectious after maturation, and when swallowed by cats or felines, the zygotes in the oocysts escape in the intestine and invade the mucosal epithelial cells at the end of the ileum for cleavage and proliferation, and the cleavage zygotes escape after cell rupture and invade nearby cells to continue cleavage and proliferation, while some develop into male and female gametophytes, which proliferate to form oocysts that enter the intestinal lumen and are excreted in the feces. If the oocysts are swallowed, they enter the small intestine and then the zoospores pass through the intestinal wall and spread throughout the body with the blood or lymphatic circulation, reproducing in tissue cells by rapid endospore proliferation. The individual inside the pseudocyst is the trophozoite, which is a common form in the acute infection period. After the rupture of tissue cells, the trophozoites are dispersed and then invade other tissue cells, so repeatedly proliferate, and the body gradually develops immunity, so that the protozoan reproduction slows down, and the cyst wall is formed, called the cyst. The cysts can exist in the body for months, years, or even for life.
The disease caused by infection with Toxoplasma gondii is called toxoplasmosis.
2. How is toxoplasmosis transmitted?
Many mammals and avian species can be reservoir hosts for Toxoplasma gondii, but their epidemiological significance varies. Cats are the most important source of infection, followed by pigs, sheep, dogs, and rats. Toxoplasma gondii is present in the urine, feces, saliva and sputum of patients in the acute stage, but it cannot survive in the outside world for a long time, except for pregnant women who can transmit it to their fetus through the placenta, the significance of patients as a source of infection is small.
The transmission route of toxoplasmosis is: congenital transmission: after acute infection of the mother during pregnancy, 30% to 60% can be transmitted to the fetus through the placenta. The rate of infection in the first trimester is low, but infection can lead to severe congenital toxoplasmosis, and later infection is often asymptomatic, but the rate of fetal infection can reach 65%. Acquired transmission: mainly through oral infection, eating food contaminated with oocysts, undercooked meat and eggs containing encysts and pseudocysts, or unsterilized milk, and drinking contaminated water, can be infected. Toxoplasma gondii in the sputum and saliva of cats, dogs and other animals can invade human body through close contact with mucous membranes and broken skin.
3.Who is susceptible to Toxoplasma gondii infection?
Humans are generally susceptible to Toxoplasma gondii. The fetus of a newly infected pregnant woman has a high rate of infection. The susceptibility of young children is also high. People with low immune function, such as those receiving immunosuppressive therapy, tumor and AIDS patients, are susceptible to Toxoplasma gondii infection, and most of them are dominantly infected. Animal breeders, slaughterhouse workers and medical personnel are more likely to be infected.
Toxoplasmosis has a global distribution and is extremely common in both animals and humans, but most are recessive infections or carriers of the protozoa. Seroepidemiological surveys show that Toxoplasma gondii is prevalent in domestic animals, with the highest seropositivity rate in cats (15.16%-73%), followed by pigs, dogs, sheep, cattle and horses. The infection rate of human varies from 0.5% to 47.3%.
4.What are the clinical manifestations of toxoplasmosis?
Most of them are asymptomatic carriers, and only a few of them have the disease. The manifestations are complex and varied.
(1) Congenital toxoplasmosis: After a pregnant woman transmits Toxoplasma gondii to her fetus, the fetus may suffer from varying degrees of developmental damage or even death. The rate of fetal infection is related to the gestational age of the mother at the time of initial infection, with the rate of infection being lower the earlier the infection. The degree of fetal damage is the opposite, the earlier the infection the more severe the fetal damage. If the fetus is infected at 1 to 3 months of gestational age, it often causes miscarriage, stillbirth or birth of non-viable children or children with developmental defects. If the infection occurs between 4 and 6 months of gestational age, stillbirth, premature birth and serious brain and eye disorders will occur. If the infection occurs at 7 to 9 months of gestational age, fetal development is generally normal, but there may be premature births, or symptoms such as heart malformation, deafness, microcephaly or mental retardation may appear gradually after several months or even years of birth.
(2) Acquired toxoplasmosis: more complex than congenital toxoplasmosis, the condition is related to the host’s immune function. In acquired toxoplasmosis in people with normal immune function, most of them are asymptomatic or only have enlarged cervical lymph nodes. Approximately 10% to 20% show fever, general malaise, night sweats, muscle aches, rash, generalized lymph node enlargement, and hepatomegaly and splenomegaly. The most common sites of invasion are the neck, suboccipital, supraclavicular, axillary and inguinal areas, and deep lymph nodes such as mediastinum, mesentery and retroperitoneum may also be enlarged. Symptoms and signs usually last 1 to 3 weeks, with a few lasting up to 1 year. Individual patients may present with more severe manifestations such as persistent high fever, pneumonia, pleural effusion, pericarditis, myocarditis, and meningoencephalitis. The risk of acquired toxoplasmosis in immunocompromised individuals is extremely high, especially with recurrence of latent infection, which can be widely disseminated and fatal in multiple organs. Manifestations include.
(i) Central nervous system infection: focal encephalopathy with manifestations of intracerebral occupying lesions, such as headache, hemiparesis, seizures, visual impairment, coma, etc. may occur; some develop diffuse encephalopathy with rapid progression and signs of impaired consciousness and meningeal irritation; others develop spinal cord lesions with limb movement disorders and sensory abnormalities.
②Pulmonary infection: It is mostly seen in patients with advanced AIDS. The manifestation is prolonged fever, cough and dyspnea. Enlarged lymph nodes and interstitial pneumonia, bronchopneumonia, etc. are seen on chest x-ray.
③Ocular toxoplasmosis: The main manifestation is retinal chorioretinitis, 80% involving macular area, with blurred vision, blind spot, photophobia, pain, tear overflow, and central vision loss, etc.
④ Systemic infection: Those with primary or secondary immune deficiency (such as Hodgkin’s disease, lymphoma, AIDS, etc.) can develop systemic infection with high fever, maculopapular rash, myalgia, arthralgia, headache, vomiting, delirium and other symptoms, and encephalitis, myocarditis, pneumonia, hepatitis, gastroenteritis, etc.
5.What are the laboratory items to check Toxoplasma gondii?
Light microscopy is commonly used to examine pathogens. Smears of various body fluids such as cerebrospinal fluid, sputum, chest and abdominal fluid, bone marrow, etc., prints or sections of placenta, lymph nodes or other tissues are taken, stained and examined microscopically, and trophozoites and encapsulation can be found. Blood, bone marrow, cerebrospinal fluid, anterior chamber fluid, exudate, sputum, or biopsied tissues such as lymph nodes, muscle, tonsils, liver and spleen can also be taken from patients and inoculated with animal or tissue cultures to isolate and identify Toxoplasma gondii. Immunological tests include intradermal toxoplasmin test, indirect fluorescent antibody technique (IFAT), indirect hemagglutination test (IHA) and micro enzyme-linked immunosorbent assay (ELISA), which are important methods to assist in diagnosis and epidemiological investigation.
6.How to treat Toxoplasma gondii?
The main targets of anti-Toxoplasma treatment are
①Acquired infected persons with normal immune function presenting with important organ involvement, such as ocular and cerebral toxoplasmosis.
(2) Acute and occult Toxoplasma gondii infections in immunocompromised patients.
③Children with congenital toxoplasmosis.
(iv) Pregnant women whose serological test has changed from negative to positive (recent Toxoplasma gondii infection). Anti-Toxoplasma gondii trophozoites are effective, but their envelopes are not effective, so they are prone to recurrence.
(1) Commonly used anti-Toxoplasma drugs and treatment protocols
Commonly used anti-Toxoplasma drugs include etanercept, sulfadiazine (or sulfadiazine, sulfadimethoxine, compound sulfamethoxazole), spiramycin, clindamycin, azithromycin, roxithromycin and artemisinin, pentazocine, etc. Induction maintenance therapy is mostly used, i.e., 4 to 6 weeks of high-dose combination therapy with multiple anti-Toxoplasma drugs (induction intensive therapy), followed by a reduction in the type and dose (1/2 the amount of intensive therapy) for long-term maintenance.
Preferred combination therapy regimen.
①Ethylaminopyrimidine 200 mg for the first dose in adults, followed by 50-75 mg/d orally; 1 mg/(kg.d) in children, divided into 2 oral doses.
②Folic acid 10-20 mg/d, may be increased to 50 mg/d, orally or intravenously or intramuscularly.
Sulfasalazine 4-6g/d orally in 4 doses for adults, 150 mg/(kg.d) orally in 4 doses for children, or instead of sulfasalazine, colistin 600mg/d for adults (dose can be increased to 1200/d) orally or intravenously every 6h, 10-25 mg/d orally or intravenously in 4 doses for children.
Alternative combination therapy regimens.
①Compound sulfamethoxazole 3-5 mg/d (based on TMP content) every 6h, orally or intravenously.
②Ethylaminopyrimidine and folinic acid, dosage and administration are the same as the preferred regimen.
(③Clarithromycin 500-1000 mg/d orally every 12h; or azithromycin 1200-1500 mg/d orally.
(2) Anti-Toxoplasma treatment for pregnant women
Once the diagnosis is confirmed, anti-Toxoplasma treatment should be administered as soon as possible. Spironolactone can be used, 2-4g/d, 4 times, 3 weeks as a course of treatment, and then repeat treatment at 1 week interval. Clindamycin can also be used, 600-900 mg/d. Do not use ethacrynic acid to prevent teratogenicity.
7.How to prevent toxoplasmosis?
(1) Popularize the knowledge of toxoplasmosis and raise the awareness of toxoplasmosis. Improve environmental hygiene, strengthen the management of water, manure and livestock. Do not eat raw meat and undercooked meat. Do not come into close contact with cats, dogs and other animals. Do not keep cats or have close contact with them during pregnancy. Strictly disinfect the placenta or aborted stillbirth of patients and diseased animals. Slaughterhouse and meat processing plant staff should be tested regularly for serum antibodies so that Toxoplasma gondii infection can be detected and treated in a timely manner.
(2) Pregnant women who are seronegative are Toxoplasma susceptible and need to avoid infection the most to prevent congenital toxoplasmosis.