Toxoplasmosis - disease, protozoal infection caused by obligate intracellular protozoan Toxoplasma gondii, have a complex life cycle.This infection is characterized by a tendency to chronic course with the development of lymphadenopathy, hepatosplenomegaly, CNS, myocardium and eyes.How to cure this disease folk remedies, see here.
final master Toxoplasma can be a house cat, as well as representatives of wild felines.While infecting cats alimentary by parasites penetrate the epithelial cells of the intestine, where, after several generations of asexual form of macro- and microgamete.The sexual process culminates in the formation of oocysts, which are output to the external environment.Man - an intermediate host of the parasite, but does not release the pathogen into the environment and does not pose a danger to others epidemic.In humans, Toxoplasma reproduce only asexually and are two stages of development:
main route of infection of toxoplasmosis - oral (eating raw meat, vegetables and berries, cont
etiology. causative agent of toxoplasmosis - Toxoplasma gondii - is a type of protozoa (Protozoa), class Sporozoa (Srotozoa), detachment of coccidia (Coccidia), the genus Toxoplasma.An obligate intracellular parasite that infects all nucleated cells, mainly gistofagotsitarnoy system.Toxoplasma have a complex life cycle with a change of owner.The ultimate owner of a cat and other felines in the intestine that occurs sexual cycle of development, culminating in the formation of immature cysts, released into the environment with faeces.In soil 3-7 days form oocysts, which are stored within 1.5-2 years.Man is the intermediate host, the body which passes T. gondii asexual development, which includes 2 stages - tachyzoites (breeding of parasites) and bradyzoites (in persistent cysts).Trophozoites characteristic of the acute phase, tissue oocysts - the chronic stage of the disease.
Dimensions parasite trophozoite stage 4-7 x 2-4 micrometers.Cysts are rounded, up to 100 microns in diameter, containing up to 3000-5000 parasites.
cysts and oocysts are resistant to chemotherapeutic drugs, physical and chemical factors, high and low temperatures, well preserved in the soil.
trophozoites sensitive to pyrimethamine, spiramycin, sulfonamides, tetracycline.Quickly killed by drying, warming, under the influence of disinfectants.
Toxoplasma have a tropism for the three groups of bodies, which determines the peculiarity of the clinical picture of the disease:
• to lymphoid tissue - the lymph nodes, liver and spleen;
• to muscle tissue - skeletal muscle, the myocardium;
• to the authorities, "forbidden" for the immune system - to the central nervous system, eyes.
Epidemiology.Toxoplasmosis is a zoonotic infection.
source is domestic and farm animals:
• cats and other members of the cat family, in the gut which passes sexual reproduction of the pathogen with the release of oocysts in the faeces into the environment;
• pigs, cows, sheep, etc., In which the muscle tissue is in the form of Toxoplasma cysts.
1. Alimentary path is carried out by ingestion of oocysts in the gut with the soil contaminated with the feces of cats, and by eating insufficiently cooked meat from infected animals.
2. The parenteral route of infection is described at meat-packing workers, blood transfusion, organ transplant, INTRA-infection.
3. The vertical path is implemented mostly during primary infection during pregnancy (risk of fetal infection is 30-40%).Cases of vertical transmission of pathogens in HIV-infected women with chronic toxoplasmosis reactivation described in recent years.
Current concepts of the pathogenesis of toksoplazmza provide for the existence of two forms of the disease: congenital and acquired.
acquired toxoplasmosis occurs in the transmission of infection or nutritional parenteral routes.Once in the human body, pathogens penetrate the lymphatic pathways in the regional lymph nodes.When sufficient barrier mechanisms of the disease does not develop, the pathogens are killed.Immune deficiency promotes the growth of parasites, their falling into the blood and hematogenous spread to various organs.Parasitemia is usually brief.Toxoplasma accumulate in the liver, spleen, bone marrow, lymph nodes, nervous system, myocardium, skeletal muscles and eyes reproduce in them.Infectious formed granulomas composed of epithelioid cells, macrophages, plasma cells, lymphocytes, eosinophils, and other elements.In the nervous system, eye, skeletal muscle necrosis may develop, followed by the deposition of calcium salts.With the development of the immune response (7 days, 12 minutes) there is a destruction-free and active intracellular parasites.There are only Toxoplasma found in the cysts.As a result of repeated revenue Toxoplasma waste products of the body's sensitization occurs and develops a specific allergy, detectable by intradermal tests with toksoplazminom.
In humans, Toxoplasma in the form of cysts can persist indefinitely, mainly in the tissues of the brain, eyes and internal organs.In the future, they die, calcify, resolve.With the development of IDS shell cysts are destroyed and the released parasites multiply, located next to hit the cells can enter the blood stream, which explains the chronic relapsing course of toxoplasmosis.
Pathogenesis of congenital toxoplasmosis are determined by a number of factors.The frequency of vertical transmission of Toxoplasma depends on gestational age.In connection with the "aging" of the placenta is an increase in its permeability, so that the frequency of fetal infection increases with 10% in the first trimester and 60% in the third trimester of pregnancy.On the other hand, play an important role intensity organogenesis, maturation of the immune system and the inflammatory response of the fetus.When the infection in the first trimester half of children the disease is the clinical manifestation, and if infected in the third trimester of congenital toxoplasmosis almost always takes place in the erased or subkli-cal form.
known that fetal inflammatory response matures during ontogeny.In the first trimester of pregnancy is dominated alterative inflammation component and organogenesis intensity is high enough.In connection with this infection during the first two weeks of pregnancy leads to the death of the embryo or blastopatii - systemic pathology similar to a genetic disease.Infection during pregnancy 15-75 days, accompanied by her interruption, or the formation of embryopathy - true malformations at the organ and cellular level.Further organogenesis intensity decreases maturation occurs proliferative component of the inflammatory response.When Toxoplasma infection in pregnancy 76- 180 days, it is possible to interrupt the development or early fetopathy - generalized inflammatory response to the outcome of a fibro-sclerotic deformation bodies (false defects).In the third semester of pregnancy the fetus is formed exudative inflammation component.Infection after 180 days of gestation accompanied by the development of late fetopathy - generalized lesions of various systems and organs (hepatitis, encephalitis, chorioretinitis, carditis, pneumonia, etc.).The defeat of the central nervous system and the eyes with congenital toxoplasmosis occurs at a later date than the pathology of other organs.When infected shortly before delivery the baby is born with the clinic of acute congenital toxoplasmosis.Upon infection in the middle of the third trimester of pregnancy, the acute phase of the disease takes place in utero, and in the clinical symptomatology is dominated by symptoms of CNS and eyes (subacute congenital toxoplasmosis).When infected in the second trimester of acute and subacute stage ends before birth, and congenital toxoplasmosis occurs in the chronic form of clinical manifestation in the form of hydrocephalus, calcification in the brain and chorioretinitis with optic atrophy.Upon infection in even earlier stages of pregnancy the baby is born with the clinic residual forms of congenital toxoplasmosis, which is represented by the gross residual effects.
no generally accepted classification of toxoplasmosis, so in practice we recommend to use a working version of the classification of the disease (Table.).
Classification of toxoplasmosis in children
incubation period acquired toxoplasmosis - from a few days to 3 weeks.
acquired acute and chronic toxoplasmosis can occur with a primary lesion of the lymph nodes (limfonodulyarnaya form), nervous system (meningoencephalitic form), eyes (eye shape), heart (myocarditic form), the lungs (pulmonary form), liver (icteric form)gastrointestinal (intestinal form), skin rash (exanthematous form).Perhaps the formation of a generalized form with a lesion of visceral organs and the nervous system.Often there are erased, subclinical, latent asymptomatic form.
The disease often begins with a prodromal phenomena: malaise, general weakness, headache, loss of appetite, fever, muscle and joint pains.Later on in the first place are the symptoms associated with the predominant localization of infection.
Limfonodulyarnaya form is characterized by an increase in the occipital, cervical, sometimes - axillary and inguinal lymph nodes.Described mezenterealnye lymphadenitis with abdominal pain, loss bronchopulmonary nodes.Lymph nodes reach sizes of 1.5 to 3.5 cm in diameter, painless, elastic consistency, mobile, not soldered to surrounding tissues and among themselves.Often at the same time enlarged liver and spleen size.Possible manifestations of acute tonsillitis.A number of patients glandular form occurs with relapses, which are characterized by an increase in the lymph nodes and tenderness, symptoms of intoxication.
meningoencephalitic form. toxoplasmosis may be the cause of acute, subacute and chronic diseases of the nervous system.It leads to severe lesions both organic and functional.
are the following forms of acquired neyrotoksoplazmoza: cerebral (encephalitis, meningoencephalitis, meningitis, vasculitis, pseudotumor meningoencephalitis), common (meningoen-tsefalopoliradikulonevropatiya, dientsefalit), spinal (myelopathy), peripheral nerve (mono- and polyneuropathy).
The clinic Toxoplasma meningoencephalitis dominated by signs of CSF hypertension, lesion of the meninges, the brain stem and cerebellum.The character of serous inflammation.Rapidly growing hypertension-hydrocephalic syndrome, which serves as the basis for the erroneous suspicion of a brain tumor.
Chronic acquired toxoplasmosis is often accompanied by lesions of the arachnoid membrane of the brain.Toxoplasma leptomeningity usually diffuse, but it is possible and predominant involvement of the posterior fossa shell, cerebellopontine angle.
The clinic observed bouts of intracranial hypertension, possible involvement in the ependyma of the ventricles of the brain process the development of adhesions at the base of the brain and subsequent hypertensive crises.
organic lesion of the vascular wall and the violation of the innervation of the cerebral vessels leads to the development of cerebral vasculitis, manifested by vascular crises, dynamic disorders of cerebral circulation.
Toxoplasma dientsefalit characterized irritable weakness, mental hyperesthesia, sleep disorders, severe adynamia, endocrine and cardiovascular disorders.
spinal form (myelitis) is rare for subacute disease.Perhaps the prevailing defeat posterior columns.
Defeat of peripheral nerves is observed in most patients with neyrotoksoplazmozom.Patients concerned about pain and paresthesias in extremities, objectively reveals tenderness along the roots and peripheral nerves, tension positive symptoms, peripheral disorders of pain sensitivity, vegetative-trophic disorders (coldness, cyanosis, hypertrichosis, hyperkeratosis, nail violation trophism).
defeat autonomic system is observed in chronic acquired toxoplasmosis and appears Crocq's disease, "marbled pattern" of the skin, skin hyperhidrosis.There are bouts of tachycardia, dizziness, sweating.
Eye shape flows by type of chorioretinitis and granulomatous uveitis.The disease has a chronic relapsing course and is often accompanied by other clinical signs of infection - lymphadenopathy, changes of the heart and nervous system.The ability of the parasites persist for a long time in the retina leads to the possibility of multiple relapses.Initially, changes may occur on retinitis type, and only after repeated relapses in the process involves the choroid.Typically, one eye is affected first, then the second.Changes in both eyes usually proceed the same way.Chronic recurrent course can lead to atrophy of the optic nerve and retina with partial or complete loss of vision.
Cardiac involvement is one of the leading places in frequency among the diseases of internal organs.Develop a focal or diffuse myocarditis, pericarditis.Patients concerned about weakness, fatigue, shortness of breath, palpitations, chest pain.Objectively reveal enlargement of the heart borders, deafness tones, systolic murmur.Possible atrial fibrillation.The ECG show conduction disorders, expanding the PQ complex, negative or biphasic T wave
defeat of the respiratory system, gastrointestinal tract, liver, kidney often develops in patients with generalized form of the disease.
Generalized form accompanied by fever, chills, muscle and joint pains.In the first 3-4 days, the process involved the myocardium, liver, kidney, intestines, nervous system.symptoms of intoxication expressed sharply.Often there maculopapular rash.The disease is characterized by severe, an unfavorable outcome is possible.
acquired toxoplasmosis in some patients has acute course, but often the process becomes chronic.In patients with chronic toxoplasmosis in addition to intoxication and low grade fever reveal lymphadenopathy, hepatosplenomegaly, nerve damage (chronic meningitis), eye (chorioretinitis), liver (chronic hepatitis), the heart (myocarditis).
clinical picture of congenital toxoplasmosis depends on the duration of pregnancy, during which there was infection of the fetus.
Toxoplasma Infection of the fetus after the completion of organogenesis in the last months of pregnancy results in the birth of a child with symptoms of acute generalized form.The disease is characterized by severe general condition, severe intoxication, high body temperature, abundant polymorphic rash (roseolous, pyatnistopapuleznaya, hemorrhagic), hepatosplenomegaly, jaundice of the skin and sclera coloration, generalized lymphadenopathy.Perhaps the development of hemorrhagic syndrome, pneumonia, myocarditis, dyspeptic disorders.The course of acute congenital toksaplazmoza severe, possibly fatal.
Subacute form is observed in the case of infection of the fetus in the last months of pregnancy and the development of acute generalized form in utero.