Toxoplasmosis is a parasitic disease caused by Toxoplasma Gondii parasitizing in nucleated cells of the human body. These include congenital toxoplasmosis and acquired toxoplasmosis. The main clinical manifestations were mostly recessive infection, and the severe cases were multiple organ damage.
The main clinical manifestations of diseased dairy cattle were elevated body temperature, dyspnea, diarrhea symptom, and central nervous system diseases. The size of the herd, the age of the cattle, the pasture and the location of the water source may all lead to the infection of dairy cows. Let's learn about the following: clinical symptoms of toxoplasmosis in dairy cows, diagnosis and prevention of toxoplasmosis in dairy female cows.
The immune status of the host and the virulence of Toxoplasma Gondii are closely related to the pathogenicity of Toxoplasma Gondii. Toxoplasma Gondii can be divided into attenuated strains and virulent strains according to its reproductive speed, invasiveness, cyst formation, and host mortality. Among them, attenuated strains proliferate slowly after they invade the body, and parasitic in the brain or other tissues can form cysts, but, do not lead to death.
Generally, they can be isolated from carriers without symptoms or recessive infections; virulent strains will multiply rapidly after they invade the body, leading to acute infection and rapid development of the body. Death is usually isolated from animals or humans with acute infections. The less virulent strains isolated from animals or humans will only cause some deaths after inoculating the experimental mice.
However, after many generations in animals, it will lead to increased virulence. At present, the type strain of virulent strain is RH strain, and the type strain of attenuated strain is Bev - Riley strain. Most mammals, poultry, and humans are intermediate hosts because they are susceptible to Toxoplasma Gondii infection, but there are some differences in susceptibility of different kinds of animals to Toxoplasma Gondii.
Whatever way Toxoplasma Gondii invades the body, it will invade the blood circulation directly or through lymph, causing parasitemia, and then gradually spread to other organs and tissues throughout the body. In the early stage of infection, the body has not yet formed a specific immune system function. When Toxoplasma Gondii invades the body, it divides and proliferates rapidly until it causes cell rupture. When the cells rupture, tachyzoites will escape, and then invade the host cells again. Repeated repetitions will lead to local tissue necrosis and acute inflammation. The main feature is monocyte infiltration, which is also the most basic pathological change caused by Toxoplasma Gondii. The size of pathological changes in the body is determined by the rate of proliferation, the time of necrosis and the immune status of the host.
Clinical Symptoms and Anatomical Lesions
The cow babies showed mental depression, increased body temperature, cough, dyspnea, diarrhea, viscous feces discharged from mixed blood, weak constitution, and often died within 2 to 6 days. The cows showed different symptoms after illness, some of them only suffered from abortion; some showed dyspnea, fever, diarrhea, mastitis and neurological symptoms; some had no symptoms.
The dead cattle were dissected and found to have thinner blood, harder to coagulate, and subcutaneous edema of neck; enlargement of lymph nodes in the whole body, especially in mesenteric lymph nodes and hilar lymph nodes, valgus on the section, and bleeding points; effusion in the abdominal cavity, myocarditis in the heart; punctate appearance in nasal cavity and tracheal mucosa Bleeding, lungs were purplish purple, widening of the local interstitium, congestion, and necrosis.
There was a large number of mixed foam fluid flowing out of the section, and there were small nodules and necrotic foci on the surface and sections. The liver was slightly swollen, and there were pale yellow nodules on the surface and sections, which resemble the concentric circles. There was congestion on the surface of the kidneys. The true gastric mucosa is bleeding and necrosis, grey-black and easy to peel off, and the small intestinal mucosa is bleeding.
The body fluids or tissues of suspected or dead diseased cattle were smeared and stained by Giemsa for microscopic examination. Toxoplasma Gondii can be seen in cows infected with the disease. This method is simple to operate, but has a low positive rate and is prone to missed detection.
At present, the common methods of pathogen detection are animal inoculation and isolation or cell culture to detect trophozoites. The susceptible experimental mice were inoculated with samples of disease in the abdominal cavity. After one week, the mice were killed, and the peritoneal fluid was taken for microscopic examination. If the samples were negative, at least three times of blind transmission were required. The samples of disease could also be inoculated with monolayer nucleated cells cultured in vitro.
Because of the deficiency of the Toxoplasma Gondii pathogenic examination and the continuous development of serological technology, the serological diagnosis has been mainly adopted nowadays. Commonly used methods include dye test, enzyme-linked immunosorbent assay, indirect immunofluorescent antibody test, and indirect hemagglutination test.
Molecular biology examination.
In recent years, with the rapid development of molecular biology techniques, the DNA probe, and PCR technology have been able to detect Toxoplasma Gondii infection. Especially, PCR technology has the advantages of early diagnosis, strong specificity, and high sensitivity. It has been used in laboratories with good conditions, but it can not be popularized at the grass-roots level.
Prevention and control measures
In dairy farms, the diseased cattle can be treated by intramuscular injection of 20 mg/kg compound sulfonamide into Methoxypyrimidine sodium injection according to their body weight. The first dosage should be doubled, 1-2 times a day for 2 weeks. It is also possible to inject 0.05 mL/kg "Set" (the main ingredients are anti-pathogen, Silver Ring snake venom and artemisinin) into the muscle according to the body weight, once a day for three days, and add appropriate B vitamins and vitamin C to the feed to improve the body's resistance and accelerate recovery.
It should be noted that Toxoplasma encephalitis occurs at the end of the disease because the parasite invades the brain of the diseased cattle, causing it to fall into a coma and difficult to breathe. Especially when accompanied by subcutaneous emphysema, the effect of drug treatment will deteriorate and death will occur. Therefore, prevention and treatment should be carried out as soon as possible after dairy farmers discover the disease. Also, the use of prednisone, cortisone, dexamethasone and other drugs can effectively alleviate symptoms, but can quickly cause Toxoplasma encephalitis and Toxoplasma sepsis, so the use of these drugs is not allowed.
Morphology of Toxoplasma Gondii
Tachyzoite is banana-shaped or half-moon-shaped, with a sharp front end and a blunt back end. The length is 3 to 7 microns and the width is 2 to 4 microns. After Giemsa staining, the cytoplasm was blue and the nucleus was purple-red, which was slightly behind the center of the worm.
Intracellular parasitic tachyzoites proliferate continuously, usually consisting of several to more than ten. Their aggregates enclosed by host cell membranes have no real cyst wall, which is called pseudocyst.
The cyst is round and has a flexible and tough cyst wall secreted by the parasite. It contains dozens to thousands of bradyzoites. Bradyzoites are found in the brain, skeletal muscle, retina and other tissues with a diameter ranging from 5 to 100 microns, and can survive in tissues for a long time.
Life history of Toxoplasma Gondii
The development process in the final host: after felines swallowed oocysts, cysts or pseudocysts, sporozoites, bradyzoites or tachyzoites escaped from the small intestine and invaded the epithelial cells of the small intestine to develop and proliferate, forming merozoites. Merozoites are released after maturation and then invade other intestinal epithelial cells to form the next generation of merozoites.
After several generations, some of the merozoites developed into female and male gametophytes and then continued to develop into female and male gametophytes. Female and male gametes fertilize into zygotes, continue to develop into oocysts, escape from epithelial cells into the intestinal cavity, and excrete in vitro with feces. Infectious mature oocysts developed after 2 to 4 days at 25 C and suitable humidity. Toxoplasma Gondii can also proliferate asexually in the parenteral tissues of cats.
The development process in the intermediate host: when the cysts or false cysts in cat feces or animal meat are swallowed by intermediate hosts such as humans, sheep, pigs, and cows, sporozoites, retards or Tachycolones can escape from the intestine, invading the intestinal wall, parasite through blood or lymph into mononuclear macrophages, and spread to all organs of the body. Officials, such as the brain, eye, liver, heart, lung, muscle, etc., enter cells to form pseudocysts by fission or end bud proliferation.
When cells rupture, tachyzoites invade other tissue cells. When the body's immune function is normal, some tachyzoites invade the host cells, especially the brain, eyes, skeletal muscle and other tissues. The growth rate of the worm slows down and secretes cystic substances to form cysts. Envelopes can live in the host for months, years or longer. When the body's immune function is low or defective, it can induce the development and rupture of cysts, release slow-actin, enter the bloodstream and invade other tissue cells to form pseudocysts and continue to grow and proliferate.
Toxoplasma Gondii, unlike most other intracellular parasitic pathogens, can infect almost all types of cells. When Toxoplasma Gondii enters the blood from the invading site, it spreads all over the body and quickly enters the monocyte-macrophage and the organs and tissues of the host cells to reproduce until it is dilated and broken. The escaped protozoa (tachyzoites) can invade the adjacent cells, again and again, thus causing focal necrosis of local tissues and the inflammatory reaction of surrounding tissues. This is the basic pathological change in the acute stage.
If the patient's immune function is normal, it can quickly produce specific immunity to eliminate Toxoplasma Gondii and form recessive infection; protozoa can also form cysts and long-term latency in vivo; once the body's immune function is reduced, the bradyzoites in the cysts will break out and cause recurrence. If the patient's immune function is impaired, the worms multiply in large numbers, causing disseminated damage throughout the body. Toxoplasma Gondii can also act as an antigen, causing allergic reactions and inflammation in the flesh teeth. Also, the focal lesions caused by Toxoplasma Gondii can cause serious secondary lesions, such as small thrombosis, local tissue infarction, surrounding with hemorrhage and inflammatory cells, forming cavities or calcification over time.
Toxoplasma Gondii can invade various organs and tissues. The most common sites of the lesions are the central nervous system, eyes, lymph nodes, heart, lung, liver, and muscle.
Toxoplasma Gondii (T. Gondii) is an important opportunistic pathogenic parasite with worldwide distribution. Human infections are quite common and mostly recessive. The National Collaborative Group for Investigation and Research of Toxoplasmosis in Human and Livestock (1983-1986) investigated 81 968 residents in 141 counties of 19 provinces (municipalities directly under the Central Government and autonomous regions) by IHA method. The results showed that the positive rate of serum Toxoplasma antibody was 0.33%-11.79%, with an average positive rate of 5.16%.
A national survey of the status of important human parasitic diseases (2001-2004) reported that 47 444 people were detected by ELSA in 15 provinces (municipalities directly under the Central Government and autonomous regions). The results showed that the positive rate of serum antibodies was 0.79%-16.810/, with an average positive rate of 7.88%. The positive rate of antibodies increased with age.
1. Sources of infection
Cats that excrete Toxoplasma Gondii oocysts with their feces are the most important source of infection, followed by other mammals, birds and other warm-blooded animals infected with Toxoplasma Gondii. Toxoplasma Gondii can infect the fetus through the placenta, so infected mothers are also the source of infection.
Ways of transmission
Congenital infection of Toxoplasma Gondii refers to the infection of the fetus through maternal placenta; acquired infection of Toxoplasma Gondii refers to the transmission of human digestive tract mucosa, skin damage, blood transfusion, organ transplantation, and other ways.
Human beings are generally susceptible to Toxoplasma Gondii, especially fetuses, infants, pets, cattle breeders, slaughtermen and people with low or deficient immunity.
Toxoplasma Gondii oocysts have strong resistance in the outside world. They are distributed in cold zone, temperate zone, and tropical zone. There is no strict geographical distribution boundary. People infected with Toxoplasma Gondii are related to pet raising and eating habits. In the process of adding T to food, cross-contamination can increase the chance of Toxoplasma Gondii infection.
Clinical manifestations of toxoplasmosis
Toxoplasma Gondii infection has two ways: congenital and acquired. Most women infected with Toxoplasma Gondii during pregnancy can cause congenital infection of the fetus. Normally, there are no obvious clinical symptoms and signs in infants and young children. When the immune function is low due to various reasons, the central nervous system damage may occur in childhood, and Retinochoroiditis may occur in adulthood. A few women infected with Toxoplasma Gondii at the early stage of pregnancy may suffer from abortion, premature delivery, stillbirth or malformation. Infection with Toxoplasma Gondii at the middle and late stages of pregnancy may cause diseases or malformations in the brain, eyes, liver, heart, lung and other parts of the fetus after birth.
After acquired infection with Toxoplasma Gondii in patients with normal immune function, most of them did not show obvious clinical symptoms and signs and were recessive infections. When the immune function is low or deficient, Toxoplasma Gondii can invade various organs of the human body and cause corresponding serious clinical manifestations, such as Toxoplasma encephalopathy, Toxoplasma ophthalmopathy, Toxoplasma hepatopathy, Toxoplasma myocardial pericarditis, Toxoplasma pneumonia, etc.
Clinical manifestations include encephalitis, meningitis, meningoencephalitis, epilepsy, mental disorders, headache, vertigo, delirium, myalgia, lymphadenopathy, etc. Toxoplasma tachyzoites can be found in cerebrospinal fluid.
Toxoplasma Gondii ophthalmopathy
The main clinical manifestations were recurrent, limited and necrotizing Retinochoroiditis. The clinical manifestations were blurred vision, eye pain, photophobia, blindness, and tears. The fundus of the eye showed posterior retinal edema and macular exudative lesions. Fresh lesions have blurred borders, cyan-grey, slightly raised, and retinal hemorrhage around them. Old lesions are satellite-like scattered white circular plaques and pigmented plaques, or macular pigmented epithelial exfoliation.
Toxoplasma Gondii destroys hepatocytes causing inflammation, infiltration and local necrosis of the liver parenchyma. The clinical manifestations are loss of appetite, pain in the liver area, ascites, mild jaundice, cirrhosis of the liver, splenomegaly and so on. The course of the disease is long and easy to recur.
Toxoplasma myocardial pericarditis
Clinically, fever, abdominal pain, tonsillitis, eyelid edema can occur, often without obvious abnormal symptoms of the heart, palpitation, jugular vein enlargement, chest pain, dyspnea, and occasionally pericardial frictional sounds can be heard. In severe cases, blunt pain and acute pain may occur in front of a chest or behind the sternum. Pain radiates to the neck and shoulder. Heart failure may occur if not treated in time.
Clinical manifestations include cough, expectoration, chest pain, shortness of breath, pulmonary beep, and X-ray examination of inflammatory infiltration. Most of the lung lesions were complicated with cytomegalovirus and bacterial infection, showing interstitial and lobular pneumonia.
Toxoplasma Gondii infection in early pregnancy can cause abortion, premature birth and stillbirth through the placental barrier. It can be seen that anencephalus, hydrocephalus, microcephaly, microphthalmos, and mental retardation are the most serious diseases in human congenital infection.