From Big Medical Encyclopedia

TOXOPLASMOSIS (toxoplasmosis) — the parasitic disease caused by protozoa and which is characterized by defeat of nervous and lymphatic systems, eyes, skeletal muscles, a myocardium, etc.

Distinguish the acquired and inborn T.

Vozbuditel of a toxoplasmosis of Toxoplasma gondii it is opened in 1908 by fr. researchers Sh. Nikoll and L. Manceaux who found it in Tunisia in rodents of Ctenodactyluo gundi and the ital. researcher A. Splendore who revealed it in Brazil at rabbits. In the territory of the USSR of toxoplasma were for the first time allocated from gophers by N. A. Gaysky and D. N. Zasukhin in 1930. In 1923 the Czech researcher found J. Janku toxoplasma in an eye of the died child, having proved thereby a susceptibility of people to infection with this parasite. First case inborn T. the person was described by A. Wolf, D. Cowen and P. Paige in 1939. An important milestone in studying of T. there was a development of methods of its immunodiagnosis. Original serological test with dye offered in 1948 Mr. Seybin (A. V. Sabin) and Feldman (N. to A. Feldman) — the Seybin's reaction — Feldman (SRF). Skin test with toksoplazminy was offered the same year by Frenkel (J. To. Frenkel). In 1953 D. Eyles and N. Coleman entered into practice of treatment of T. Daraprimum (Chloridinum) in a combination with streptocides. Systematic situation Toxoplasma gondii remained uncertain before opening by Hutchison (W. M of Hutchison) in 1969 a sexual phase of development of a parasite, edge proceeds in intestines of representatives of the cat family.


Fig. 1. Scheme of a life cycle of the causative agent of toxoplasmosis: I. An abenteric fabric phase — asexual reproduction toksoplazm (an endodiogeniya and an endopolygeny) in an organism of intermediate owners (the person, mammals, birds); II. An intestinal phase — asexual reproduction (schizogony) and a syngenesis (gametogonium) toksoplazm in epithelial cells of intestines of final owners (a cat and other representatives of the cat family); III. A phase of a sporogony which begins in a gleam of intestines of final owners and comes to an end in the environment (the soil, plants, water); and — penetration of the activator (1) into a cell of the owner (the sporozoite, tsistozoit or endozoit), 2 — a cell membrane of the owner, 3 — a kernel of a cell of the owner; — endozoit (4) in a cell of the owner (5 — a parazitoforny vacuole); in — bystry division of an endozoit (6 — an endodiogeniya, 7 — an endopolygeny); — formation of a pseudo-cyst (8) — accumulation of the endozoit surrounded with a cover of a parazitoforny vacuole; d — a rupture of a cell of the owner and an exit of endozoit; e — slow division of endozoit by an endodiogeniya; — an intracellular cyst (9 — tsistozoita); z — the extracellular cyst containing tsistozoita with a trailer arrangement of kernels (10 — own cover of a cyst); and — a schizogony (1 — the sporozoite, endozoit or tsistozoit, 5 — a parazitoforny vacuole, 11 — kernels of cells of an epithelium of a mucous membrane of intestines, 12 — a binuclear schizont in a parazitoforny vacuole of a cell, 13 — a multinuclear schizont in a parazitoforny vacuole, 14 — the mature schizont containing merozoites, 15 — a merozoite — the predecessor of female gametocytes, 16 — a merozoite — the predecessor of men's gametocytes); to — formation of macrogametes (17 — propagation steps of a ma-krogametotsit, 18 — a mature macrogamete); l — formation of microgametes (19 — a one-nuclear microgametocyte, 20 — the growing microgametocyte with the kernel preparing for division, 21 — a multinuclear microgametocyte, 22 — mature microgametes); m — an oocyst in a gleam of intestines after merge of a microgamete and a macrogamete; N — a nesporuliro-bathing oocyst in the environment; about — education two a sporocyst; p — the sporuli-rovanny oocyst containing two sporocysts from a sporozoitama (23 — sporozoita).

Activator T. — the obligate intracellular parasite of Toxoplasma gondii, Eucoccidiida group, the Apicomplexa type, treats fabric tsistoobrazuyushchy koktsidiya. The name of the sort Toxoplasma (Greek toxon onions, an arch, an arch + plasma molded, issued) is defined by a form of a parasite (in the form of a half moon). Development toksoplazm happens to change of owners. Final owners toksoplazm — a cat and nek-ry other representatives cat's, intermediate — mammals (except cat's), wildings (pigs, sheep, etc.), the person and birds, In development toksoplazm are established the following phases: an abenteric fabric phase — asexual reproduction toksoplazm (an endodiogeniya and an endopolygeny) in various tissues of intermediate owners; an intestinal phase — asexual reproduction (schizogony) and a syngenesis (gametogonium) toksoplazm in cells of an epithelium of a mucous membrane of intestines of final owners; the phase of a sporogony, edge begins in a gleam of intestines of final owners and comes to an end in the environment (fig. 1).

Fig. 2. The diffraction pattern received by means of the scanning microscope: endozoita toksoplazm (1), getting into a cell of the owner (2); x 6000
Fig. 3. The diffraction pattern of intracellular eidozoit toksoplazm, breeding by an endodiogeniya: 1 — maternal individuals; 2 — affiliated individuals; 3 — a cell of the owner; 4 — a parazitoforny vacuole of a cell of the owner; 5 — mitochondrions of a cell of the owner: x 50 000.

Intermediate owners, including and the person, can catch or sporozoitam from the sporulirovanny oocysts which got to the soil with excrements of cats (or from hands, a floor, furniture, the objects of use contaminated by excrements of cats), or the tsistozoita from cysts which are contained in tissues of other intermediate owners (in particular, at the use by people in food of insufficiently thermally processed meat); or the endozoita which are also contained in tissues of intermediate owners (penetration through the injured skin during the processing of carcasses of the infested animals). In a human body (the intermediate owner), sporozoita, endozoita and tsistozoita actively get into cells (fig. 1, I, and, fig. 2) various fabrics and bodies where there takes place sexless development. It consists in reproduction in their way of an endodiogeniya — internal budding (fig. 1, I, c) therefore two daughter cells (fig. 1, I, in, are formed; fig. 3), and endopolygenies, at a cut is formed four and more affiliated individuals (fig. 1, I, in, 7). The rhythm of reproduction of endozoit is defined by duration of development of one generation toksoplazm and can be bystry (3 — 5 hours) at an acute current of T. or slowed down (10 — 15 hours and more) at chronic T. At an acute current of an invasion as a result of repeated divisions of endozoit pseudo-cysts (fig. 1, I, 8) — the accumulations of endozoit of one generation surrounded with a cover of the parazitoforny vacuole created by a cell of the owner are formed. The struck cell overflowed with endozoita collapses (fig. 1, I, e), endozoita actively are implemented into the next cells where again sexless development begins (fig. 1, I, a — d). At chronic T. slow temn reproduction of endozoit (fig. 1, I, e) leads to formation of the tsistozoit (fig. 1, I, g) which are in cysts and continuing to breed slowly (fig. 1, I, h).

Endozoita (tachyzoites) also the sizes 2 — 4 X 4 — 7 microns have the form of a half moon with the rounded-off back end. During the coloring across Romanovsky cytoplasm of endozoit of bluish-gray color, and a kernel — red-violet.

Tsistozoita (bradyzoites), especially in large cysts, have the extended form, their kernels are considerably displaced by the back end of a body. In large cysts cytoplasm of tsistozoit is painted less intensively or at all is not painted. The size (diameter) of cysts is more often than 50 — 70 microns, sometimes — 100 — 200 microns, and quantity of tsivtozoit in them — several thousands. In smears from a brain and prints of the internals painted across Romanovsky (see. Romanovsky — Gimza a method ), large cysts have an appearance of roundish coarse-grained educations due to preferential coloring of kernels.

Final owners (cats) can also catch the toksoplazma which are at different stages of development — sporozoitam, tsistozoitam, endozoitam (fig. 1, II) that determines duration of the period from the moment of infection prior to allocation of oocysts to the environment: at infection of a sporozoitama — 20 days and more, tsistozoitam — 3 — 10 days, endozoitam — 19 days. Development toksoplazm in cells of an epithelium of a mucous membrane of intestines of a cat begins with process of a schizogony (fig. 1, 11, i). At the same time it is formed several morphologically various types of merozoites, one of to-rykh are so-called predecessors of the sexual stages of female (fig. 1, II, 15) and men's (fig. 1, II, 16) gametotspt following them. Sexual development toksoplazm in an organism of a cat begins with formation of macrogametocytes (fig. 1, II, to, 17) and microgametocytes (fig. 1, II, l, 19 — 21). Their development leads to formation of macrogametes (fig. 1, II, to, 18) and microgametes (fig. 1, II, 22). Microgametes get into a mature macrogamete and as a result of fertilization the oocyst forms (fig. 1, II, l). The oocyst destroys an epithelial cell of intestines of the final owner (cat) and comes in his gleam, and then with excrements — to the environment (fig. 1, III, m) (to the soil, in water, to plants), gets on objects of use, a hand. Under favorable conditions for aeration and a temperature schedule within 2 — 5 days there is a maturing of an oocyst of N education in it two sporotsnst (fig. 1, III, o), and then in everyone a sporocyst — four sporozoit (fig. 1, III, o).

Sporozoita of 1,5x7 microns in size develop in the oocysts having the rounded oval form and diameter from 9 to 14 microns. Oocysts, as well as sporocysts concluded in them, are surrounded with a dense colourless two-layer cover.

The acquired toxoplasmosis — the disease which is most extended from all zoonoz. Its activator or specific toksoplazmenny antibodies in blood serum are found in representatives of all groups of wild vertebrata and all types of domestic animals. The Toksoplazmenny invasion occurs at people everywhere, on all continents and in all klimatogeografichesky zones. Prevalence of T. as a rule, higher in territories with roast and a humid climate, and also among country people.

In the countries of the Central Africa and South America infectiousness of the population of T. reaches 60 — 90%, in countries of Western Europe and North America — 25 — 50%, in Southern and Southeast Asia — 5 — 25%. In view of the fact that acquired by T. in most cases proceeds as an asymptomatic carriage or subclinically, its diagnosis is difficult also the systematic accounting of incidence of T. does not exist. It is considered that is infested by toksoplazma apprx. 1/4 — 1/3 world's populations. In the USSR the disease is also revealed, including in districts of Far North. Its distribution among people very unevenly that is defined by a combination natural and economic living conditions of life. The greatest influence on distribution of T. among people render number in settlements of cats, custom of consumption in food of insufficiently thermally processed meat, level a dignity. cultures of the population.


there are natural and sinantroiny centers of the acquired T. V the natural centers (see. Natural ochagovost ) circulation of the activator happens generally on a chain the victim — a predator where a final owner are representatives of the cat family, and intermediate — the person, numerous mammals and birds. In dispersion toksoplazm the greatest role belongs to migratory birds. In the natural centers people catch T. rather seldom. In the synanthropic centers the activator T. circulates with the participation of cats as final owners. Among intermediate owners the most struck with T. there are pigs, sheep, rabbits, hens, mice, and from wild birds — sparrows.

Intensity of the natural and synanthropic centers is defined by the number and an invazirovannost of representatives of the cat family, and also small rodents and birds. Domestic mammals and synanthropic birds are infested by toksoplazma considerably more often than wild, and in general the flow of parasites from the synanthropic centers in natural is more constant and intensive, than the return. Are the main source of an invasion for people; the animals (mammals and birds) infected with toksoplazma, meat to-rykh it is eaten crude or insufficiently processed thermally; the cats disseminating oocysts with excrements in the environment (soil), and indoors contaminating them furniture, floors, etc., and also hands of the people contacting to cats, especially children. The person infested by toksoplazma epidemiologically significant source of an invasion is not; only at inborn T. a source of an invasion for the child is mother who gave birth to him (see below the Inborn toxoplasmosis).

Transfer toksoplazm happens hl. obr. orally (infection of a tsistozoitama and sporozoitama). Also the possibility of penetration of the activator through the injured skin (in the form of endozoit) at employees of meat-processing plants, fur farms, etc. (is not excluded during the processing of the infested animals). Isolated cases of infection of people at organ and tissue transplantation are described.

Intensity of epidemic process at T. is defined by probability for the person to catch the parasite who is at one of two stages of his development: sporozoitam or tsistozoitam. The risk of infection of a sporozoitama is defined by extent of environmental pollution cats and level a dignity. cultures of the population, risk of infection of a tsistozoitama — the frequency of the use of the crude or insufficiently thermally processed meat. In the majority of the synanthropic centers of T. the specified factors of transfer interact that determines not only the general level of a prevalence of the population, but also unequal risk of infection in various age and sexual groups. About an invazirovannost of the population of a toksoplazmama and its dynamics judge by the size of the immune layer defined by a skin allergy test with toksoplazminy or serological tests. At low level dignity. cultures of the population the risk of infection of children of a toksoplazmama can be so considerable that more than a half of the children's population is infested by 7 — 10 years. In the countries of Europe and the USA where the alimentary way of infection (tsistozoitama) prevails, children are surprised rather seldom, the maximum of a prevalence is the share of adults. Women are usually struck a little more often than men, hl. obr. owing to a habit of many of them to taste crude mincemeat. Toksoplazmam also workers of slaughters and meat-processing plants are much more struck, vt. doctors.

Infection of T. can happen because of existence of various mechanisms of transfer of the activator at all seasons of the year. Nevertheless it is noted spring (March — May) and autumn (September — October) increase in frequency of positive skin test and reaction of binding complement. Incidence of toksoplaz-menny lymphadenitis (the most often diagnosed form T.) it is dated for winter and spring seasons and it is the share generally of women at the age of 17 — 26 years.

Level and dynamics of incidence of T. remain insufficiently studied by hl. obr. because of difficulties of its diagnosis and absence in this regard obligatory registration of patients with this invasion.

The pathogeny

From places of implementation the activator is brought by macrophages in limf, system, causing development lymphadenitis (see). At the generalization of process which is followed by receipt of the activator in blood (parasitemia), toxoplasma are carried on all organism and are fixed in various bodies and fabrics (in a nervous system, eyes, a liver, a spleen, limf, nodes, skeletal muscles, a myocardium) with education in them intracellular accumulations of the activator. Quite often in places of accumulation of a parasite there are inflammatory ochazhka from the outcome in a necrosis with the subsequent education on their place petrifikat (see). Toxoplasma in an organism of the owner cause formation of specific antibodies, to-rye limit rough reproduction of a parasite. However these antibodies are not able to interfere with long experience of parasites in fabrics and bodies in a stage of cysts. In a pathogeny of T. influence of waste products and disintegration toksoplazm, allergic reorganization of an organism plays a role.

Pathological anatomy

Pathoanatomical changes at acquired by T. are studied insufficiently. Most constantly is surprised limf, system, first of all zadnesheyny, submaxillary, axillary, inguinal and mesenteric limf. nodes. At the same time limf, nodes are increased in sizes at the expense of a hyperplasia, quite often in them there are focal accumulations of lymphocytes, histiocytes, and also plasmocytes, neutrophilic and eosinophilic granulocytes with impurity of huge multinucleate cells. The spleen is surprised less often, its moderate hyperplasia is possible. Damage of a liver — hepatitis is characteristic with cholestasias (see), small sites of a necrosis and miliary granulomas (see). Inflammatory changes and in bilious ways are noted. Damage of muscles, first of all sural, hips, the lower half of a back less often than others, in particular a myocardium is typical. In the thickness of the affected muscle consolidations, often spindle-shaped form (sites of an interstitial productive miositis), focal necroses of a muscle come to light. Similar character infiltrates are available in interstitial tissue of lungs, kidneys and other bodies. In lungs transformation of cells of an epithelium into huge multinucleate cells is possible. A brain at acquired by T. is surprised to a lesser extent, than at inborn. At the same time the small centers of a necrosis are found, petrifikata seldom meet. In hard cases are noted morfol. the changes characteristic of encephalitis (see) or an encephalomeningitis (see the Brain). Damage of eyes is characterized by focal necroses, a productive inflammation of a retina and a choroid.


Immunity at T. unsterile. Its development is caused by constant antigenic stimulation of an organism of the owner endozoita in the beginning, and later, in a stage of a per-sistention of the activator — tsistozoitam. Persistent in a fabric cyst of a tsistozoita continuously allocate immunogene metabolites (see. Antigens ), the cysts passing through a cover. Thanks to it it is long a certain tension of the immunity, insufficient to prevent development of persistent stages of a parasite, but quite effectively protecting an organism from a recurrence and reinfestations is maintained.

A clinical picture

Acquired by T. it is characterized by polymorphism of manifestations. Depending on duration of disease distinguish acute and chronic forms.

Incubation interval (see) lasts from 3 days to several months. In most cases at an acute form acquired by T. there are no expressed displays of a disease: only the general weakness, muscle pains, dispeptic frustration, an indisposition, decrease in working capacity can take place. The disease is distinguished seldom and the wedge, recovery with preservation in fabrics of cysts toksoplazm and from the outcome in an asymptomatic carriage toksoplazm comes to an end resistant (see. Carriage of contagiums , invasions). About the postponed invasion it is possible to judge by positive serological tests and by skin test, edges quite often remains positive throughout all human life.

In nek-ry cases at an acute form acquired by T. it is observed generalization (see) process; the disease develops gradually. Temperature increases usually to 38 °, rather often increase limf, nodes, to-rye are soldered among themselves, painless, dense. The sizes vary them from 0,5 — 1 cm to 3 — 4 cm. Simultaneous increase in different groups peripheral limf, nodes is noted (cervical, axillary, inguinal, etc.). Increase limf, nodes of an abdominal cavity, a mediastinum can be observed. Sometimes there is widespread rozeolezno-papular rash. Quite often the liver and a spleen increase, the clinic sometimes develops myocarditis (see), to-ry has an infectious and allergic origin. Pains in heart, heartbeat, an asthma are noted. The beginning can be oligosymptomatic or hidden, degree of manifestation of symptoms is defined by prevalence and sharpness of process in a myocardium, on an ECG various disturbances of a rhythm and conductivity can be revealed. The stated above wedge, a picture of generalization of process at an acute form acquired by T. it is observed seldom, various combinations of the specified symptoms are registered more often. In more hard cases of T. defeat of c is possible. and. page in the form of encephalitis or mennngo-encephalitis (see the Brain) with a picture of diffusion or focal damage of a brain and covers (a sharp headache, vomiting, the mennngealny phenomena, convulsive attacks with a loss of consciousness, defeat of cranial nerves, a monohemiparesis, a hemiplegia, cerebellar frustration). At the same time there are various mental disturbances depending on localization of inflammatory process in a brain. Syndromes of stupefaction are characteristic (see. Consciousness ). Acute acquired by T. in some cases passes into chronic, it is frequent with local defeats of bodies and systems.

Hron. acquired by T. the erased wedges, manifestations are inherent that complicates diagnosis. Complaints at such patients of the general character — on a headache, fatigue, weakness, emotional instability, subfebrile temperature. Changes from internals usually are not observed, but can develop focal and diffusion myocarditis, hron. intersticial pneumonia (see), bronchitis (see), hron. gastritis (see), a coloenteritis (see), cholecystitis (see), hepatitis (see), various disturbances of a musculoskeletal system — arthralgia (see), a miositis (see), an atrophy of muscles (see the Atrophy muscular), etc. Sometimes specific inflammatory diseases of female generative organs — a salpingo-oophoritis develop (see. Adnexitis ), an endometritis (see. Metroendometritis ), characterized by the long course, disturbances of menstrual function, infertility.

Most hard proceeds hron. acquired by T. with involvement in process of a brain and its covers, eyes. Damage of a brain and covers is characterized by a long long-term current with periodic aggravations and considerable polymorphism a wedge, manifestations: disturbance of intelligence, memory, an adynamy (see. A psychoorganic syndrome), encephalitis, an encephalomeningitis, an arachnoiditis (see), an encephalomyeloradiculitis, etc. Development of epileptiform attacks is possible (see. Epileptiform syndrome). Usually at aggravations there are sudden attacks of alarm or fear, irascibility with a bystry exhaustion, the phenomena of a derealization (see), twilight stupefaction (see), dysphorias (see). Frustration of a body scheme (see), metamorphopsias are frequent (see). Mental disorders are often combined with diencephalic pathology (see. Hypothalamic syndrome). Against the background of an asthenic state it can be observed depressive and senestopathetically - hypochiondrial syndromes (see. Depressive syndromes, Hypochiondrial syndrome ).

Character and the course of damages of eyes are very various. Front and back uveites (see), exudative and proliferative retinites (see), the disseminated chorioretinitis meet (see the Choroiditis). The central chorioretinitis is most often observed, to-ry begins a picture of an acute serous retinitis. On a back pole unsharply limited center of gray-green color is found various size. Near the center, in a retina or under it, hemorrhages are visible. Degree of a vision disorder in many respects depends on localization of the centers. Damage of eyes in the form of a chorioretinitis, a uveitis, an atrophy of an optic nerve (see) the wedge, manifestation hron can sometimes be the only thing. the acquired toxoplasmosis.

The diagnosis

Considerable distribution of infectiousness of a toksoplazmama of the population and the large number of positive serological and allergic tests connected with it as at almost healthy faces, and patients with other diseases which do not have relations to T., demands the careful relation to diagnosis. Diagnosis of T. the wedge, a picture can be put only after an exception of all other diseases with similar. It is based on a wedge, displays of a disease, to-rye often have the erased character, and these laboratory researches. Such wedge, signs as long have relative diagnostic value subfebrile condition (See), a lymphadenopathy, increase in a liver and spleen, damage of eyes, and also the calcificats in a brain found at rentgenol. research.

Among laboratory diagnostic methods there is a T. have the greatest value immunol. methods; parazptol. methods (microscopy of smears and cuts of fabrics and bodies, a biological test on laboratory animals) broad use in practice of intravital diagnosis of T. did not receive because of difficulties of detection small, located intracellularly toksoplazm, short duration of a parasitemia, labor input of researches, etc. However the microscopic method of a research (see) with coloring of drugs across Romanovsky or flyuorestseiny is widely used in pilot studies and at autopsy.

For immunol. diagnoses current-soplazmennoy of an invasion are offered allergic reaction — skin test (see) with toksoplazminy (KP), and also serol. the Seybpn's reaction — Feldman (SRF), fixations of the complement (RSK) in standard option and drop modification (see Reaction of binding complement), an indirect gemagglyutinatsna — RNGA (see. Hemagglutination ), an indirect immunofluorescence — RNIF (see the Immunofluorescence), enzyme-mechennykh of antibodies — REMA (see. An enzyme-immunological method), etc. RSF belongs to type of antigenneytralizuyushchy reactions and is based on the principle of loss by a live parasite, on to-ry specific antibodies influenced, abilities it is intravital to perceive paint; at the same time as antigen use live toxoplasma. Immunol. the methods applied to diagnosis of T., have rather high specificity. Thanks to it negative reactions with big reliability exclude an invazirovannost of the inspected person; positive reactions almost with the same reliability indicate existence toksoplazm in a human body at the time of inspection. However it is not necessary to revaluate values of laboratory researches. Detection of parasites or positive immunol. tests with obviousness confirm an invasion of an organism of a toksoplazmama, but it is not obligatory — about a disease of T. Skin test with toksoplazminy is least informative in this respect, edges becomes positive on 4 —-y to week and later after infection and remains such in most cases for life. RNIF becomes positive since the end of the first week, initial credits 1:20 — 1:40 reach 1:1000 on 6 — the 8th week of an invasion and decrease to 1:80 — 1:20 in hron. stages of a disease. RSK becomes positive (a caption 1:4) on 2 — to the 3rd week after infection, credits it reach a maximum (1:32 and more) on 2 — the 4th month, and to 6 — to the 12th month in most cases RSK becomes negative. Results of a single serological research have no great diagnostic value. In most cases a solid data yield only comparative results immunol. inspections in dynamics (transition of negative reaction in positive, significant growth in credits at repeated inspection), and also a combination of several tests. For a fresh toksoplazmenny invasion, including inborn, dominance in blood serum of macroglobulins therefore important diagnostic value was gained by reactions for identification of immunoglobulins of a class M (see is characteristic. Immunoglobulins ), in particular RNIF. Due to the existence of cross-reactions of toksoplazmenny antigen with the serums containing a rhematoid factor (see), and also antinuclear antibodies, it is necessary to interpret with care positive serological tests on T. in the minimum credits (RSK less than 1:4, the REEF less than 1:20 etc.).

At a blood analysis comes to light leukopenia (see), the relative lymphocytosis (see the Leukocytosis), can be an eosinophilia (see).

by Fig. 4. Roentgenogram of a skull (side projection) of the patient with a toxoplasmosis: shooters specified shadows of multiple petrifikat in a brain

Specific rentgenol. signs at T. does not happen. The most frequent rentgenol. manifestation of T. the centers of calcification — a petrifikata (see) a brain are, to-rye are found on survey roentgenograms of a skull (see. Kraniografiya ). They, as a rule, multiple, are located more often in both hemispheres, the sizes make them from several millimeters to 1 — 1,5 cm. Form of petrifikat roundish or wrong (fig. 4). Intracerebral calcificats at T. it is necessary to differentiate with focal calcifications of other etiology, to-rye are observed as at healthy faces (calcification of a pinus, firm meninx, vascular textures of side cerebral cavities), and at various diseases (tubercular meningitis, calciphied hematomas, cysticercosis, etc.). Therefore rentgenol. the symptomatology shall be considered in a complex with clinical and serological data. At an acute form T. defeats of a respiratory organs are possible, to-rye increases limf, nodes of roots of lungs come to light radiological in the form of strengthening of the pulmonary drawing, focal and infiltrative shadows, an exudate in a pleural cavity. These changes have no specific character.

Most often T. it is necessary to differentiate with various inf. diseases, diseases of blood, a lymphogranulomatosis (see), collagenic diseases (see), tuberculosis (see), an arachnoiditis (see), encephalitis (see), oligophrenias (see) other etiologies, an exogenous pathopsyhosis (see. Mental diseases), epilepsy (see), at damage of eyes — with a chorioretinitis (see the Choroiditis).


Treatment of patients to the acquired T. it is carried out in specialized departments depending on preferential organ pathology. Use etiotropic drugs in combination with pathogenetic therapy or only pathogenetic therapy. Faces with an asymptomatic carriage toksoplazm are regarded as the healthy, not needing specific or other look treatments. Causal treatment acute and chronic T. 7 — 10 days consist in use of Chloridinum in combination with sulfanamide drugs (Sulfadimezinum, Sulfapyridazinum, sulfadimethoxine, Etazolum, Norsulfazolum) cycles for 5 days with breaks between them. Carry usually out 3 cycles that makes one course. The adult appoint Chloridinum in a dose of 0,025 g in the first days 4 times, and in the next days — 2 times a day; Sulfadimezinum — in the first days on 3 — 4 g in 3 — 4 receptions, in the next days — on 2 — 3 g a day. At the same time for the prevention of side effect of Chloridinum it is shown folic to - that.

Contraindications to use of Chloridinum and sulfanamide drugs are diseases of the hemopoietic bodies, kidneys with disturbance of their functions, and also a decompensation of cordial activity. At intolerance of Chloridinum appoint Aminochinolum on 0,15 g 2 — 3 times a day within 7 days. Treatment is carried out by three cycles with breaks in 10 days. At intolerance of sulfanamide drugs lincomycin is appointed sick. However the effect of treatment at the same time is much lower.

Pathogenetic therapy is defined by character of the developing syndromes at defeat of c. N of page, cardiovascular system, sexual sphere etc.

Treatment of mental disorders is carried out by psychotropic drugs (see. Psychopharmacological means); the choice of drugs is defined by the prevailing syndrome.

The forecast

After postponed acquired by T. there can be irreversible changes from a brain, the damages of eyes, internal and generative organs resulting in disability.


the Important place in prevention of T. occupies observance of rules of personal hygiene, in particular washing of hands after contact with crude meat since endozoita lose viability even under the influence of mains water.

Meat products can be eaten only after the corresponding heat treatment (cysts toksoplazm perish at t 66 ° above within several minutes). Tasting of crude mincemeat is not recommended. The crude meat which is subject to long-term storage should be frozen at t ° — 20 ° that leads to death of fabric cysts within a day.

In excrements of a cat of an oocyst and prisoners of a sporozoita in them keep viability up to 2 years, it is difficult to destroy them by means of usual desinfectants. Therefore the most effective preventive measure is prevention of pollution of the soil excrements of cats. For achievement of this purpose of neglected cats it is necessary to destroy. Domestic cats cannot be fed with crude meat, it is recommended to inspect periodically them on T. and to destroy sick animals. Excrements of domestic cats need to be deleted daily.

An inborn toxoplasmosis

the Inborn toxoplasmosis develops as a result of transplacental infection of a fruit from mother, sick T. The frequency of an inborn toksoplazmenny invasion specified by various researchers fluctuates from 0,05 to 7 — 8 on 1000 live-born; the indicator 1 — 6 on 1000 live-born is most often given.

Transfer toksoplazm from mother to a fruit happens in the transplacental way. At the same time there are two points of view on dependence of infection of a fruit on a form of a toxoplasmosis (acute or chronic) at mother. G. Desmonts with sotr. (1969), Rov-Bonnet (H. Roever-Bonnet, 1970), Kuvre (J. Couvreur, 1975), Larsen (J. Larsen, 1977), Talkhammer (O. of Thalhammer, 1979), V. N. Nikiforov (1981), etc. is considered that toxoplasma are transferred to a fruit only in the presence at the pregnant woman acute acquired by T., the Crimea it caught during pregnancy. At the same time 3/4 been born children remain asymptomatic carriers and only at 1/4 clinically expressed symptomatology develops. Infection of the woman T. to or in the first 2 months of pregnancy does not lead to transfer of activators to a fruit. Disease of the woman T. at the end of the first and throughout the second trimester of pregnancy leads to infection of a fruit in 40% of cases, in the third trimester — in 60% of cases. However A. G. Pap with sotr. (1964), N. I. Popova (1973) N other observed the repeated birth of sick children at the women suffering hron. the acquired T.

Zarazheniye of a fruit can occur only at development in women parazitemgsh. Character and degree of manifestation patomorfo l. changes in bodies and fabrics of a fruit, and also outcome inborn T. depend on duration and intensity of the parasitemia arising at a fruit as a result of transition through a placenta of endozoit from mother, virulence toksoplazm, age of a fruit by the time of infection, extent of development in its organism of protective mechanisms.

Circulating in blood of a fruit of toxoplasma are brought in all bodies and fabrics that causes polymorphism a wedge, pictures. Defeat of a fruit leads to abortions, mertvorozhdeniyakhm, and also to heavy damages of bodies, often incompatible with life — anencephalias (see the Brain), anophthalmias (see the Anophthalmus), etc. At infection in late terms of development the expressed changes from c are observed. N of page and eyes.

Langer (H. Langer, 1963), Verner (N. Werner) et al. (1963), A. K. Yygiste, D. N. Zasukhin (1976) consider that he is especially dangerous to a fruit hron. a toksoplazmozny endometritis at mother. In this case infection of a fruit can occur also in the absence of a parasitemia at the pregnant woman.

Pathological anatomy inborn T. it is studied most in detail. At early stages of a course of a disease of manifestation generalized. In all struck bodies, in the locations toksoplazm, there are sites of a necrosis and widespread infiltrates which are located preferential in interstitial fabric and consisting of lymphocytes, histiocytes, and also plasmocytes, neutrophilic and eosinophilic granulocytes. Damage of a liver — intersticial hepatitis (see) with small sites of a necrosis and the expressed periportal infiltration, after replaced by fibrosis is most often observed. Along with it in a liver the centers of an extramedullary hemopoiesis come to light. The spleen of a giperplazirovan, is possible moderate infiltration by its eosinophilic granulocytes. In a myocardium, a respiratory organs, adrenal glands, less often other internals small sites of a necrosis (see) and the expressed infiltration of interstitial fabric are found. Focal changes arise also in a brain and eyes.

Fig. 5. Macrodrug of a brain of the newborn at an inborn toxoplasmosis (a horizontal section through hemicerebrums, a dorsal view): shooters specified the cysts located preferential on border between gray and white matter.

At infection of a fruit shortly before the birth the acute form of a disease proceeds also after the birth of the child. During the progressing of a disease damage of a brain prevails. In it are found toxoplasma, there are dystrophic changes, and then a necrosis. Exudative reaction is expressed poorly. Note I macrophagic reaction, in a cut the cells, generally glial origin englobing activators and decomposition products of nek-rotizirovanny tissue of brain participate. In blood vessels — swelling of an endothelium, growth of cells of an adventitia, staz and quite often thrombosis. The secondary focal aseptic kollikvatsionny necrosis is caused by defeat of vessels (see) tissues of a brain. The centers of a necrosis have various size, are located asymmetrically, preferential in a cerebral cortex and in a subependimarny zone of side ventricles. At hard proceeding process these centers merge in the continuous yellowish strips going along crinkles of a brain. Defects of an ependyma of ventricles can come to light; vascular textures and a meninx are quite often thickened, whitish or yellowish color. Further the mass of a necrosis resolves with formation of cysts (fig. 5), to-rye especially often is located on border between gray and white matter of big parencephalons. Cysts contain cerebrospinal liquid, in their walls the macrophages containing decomposition products of tissue of brain in cytoplasm are found. On the periphery of cysts growths of a glia with sharp consolidation of substance of a brain are found (see. Cyst ). Also vascular textures and soft meninx are exposed to a sclerosis. Due to the disturbance of outflow of cerebrospinal liquid the hydrocephaly (see) reaching sometimes considerable degree develops. To it there is a calcification with powdered or granular, and sometimes massive adjournment of salts of calcium. At inborn T. disturbance of development of a brain is often noted, in particular the underdevelopment of a share or even big cerebral hemispheres is possible.

At this time also changes of eyes can come to light. They consist in focal infiltration of covers of an eye and in development of small sites of a necrosis that leads to a thickening of a retina and a choroid, with development in the subsequent granulyatsionny fabric.

Symptoms inborn T. can be revealed already at the birth of the child. Most of researchers distinguish acute, subacute and chronic phases of a disease. The acute phase (stage of generalization) is characterized by the general serious condition, temperature increase (subfebrile, is more rare high), jaundice, increase in a liver and spleen, emergence of rash — rozeolezny, papular, hemorrhagic. Dispeptic frustration, intersticial pneumonia (see), myocarditis are possible (see). Lymphadenitis is expressed poorly. Defeat of a nervous system is shown by slackness, drowsiness, concern, hypotonia of muscles, nystagmus (see), squint (see). In blood — an eosinophilia, limfomonotsitoz; it is noted hamaturia (see). The disease can accept a subacute current in process of subsiding of inflammatory processes in various bodies of the patient.

In a subacute phase (a stage of active encephalitis) slackness, drowsiness or excitement, vomiting (see), spasms (see), a tremor (see Trembling), paralyzes, paresis (see Paralyses, paresis), temperature increase, changes are observed from eyes (an opacity of the vitreous body, a chorioretinitis, an iridocyclitis, a nystagmus, squint), increase in intracranial pressure. In cerebrospinal liquid (see) protein content increases, the moderate lymphocytic cytosis (proteinaceous and cellular dissociation) is noted. Gradually hydrocephaly develops.

In hron. to a phase (a stage of postencephalitic defect) there are irreversible changes of c. the N of page who are followed by hydrocephaly or a nanocephalia, attacks of concern, spasms, lag in intellectual development to degree of a deficiency of intellect and an idiocy (see Oligophrenias), relative deafness (see), deafness (see), and also irreversible changes of eyes in the form of a microphthalmia (see an Eye, anomalies of development), a chorioretinitis (see the Choroiditis), atrophies of an optic nerve (see. Optic nerve ).

Inborn T. the long time can proceed latentno, and postencephalitic defect in some cases is found at children at more advanced age. Spasms, a chorioretinitis can develop at the age of 2 — 7 years, and signs of an oligophrenia become obvious at preschool or even school age, at the same age more expressed there are headaches, working capacity decreases. The disease can proceed for many years.

Diagnosis inborn T. the wedge, pictures and results of a laboratory research of the child and his mother is based on data (see above the section «The Acquired Toxoplasmosis, the Diagnosis»). Negative or slabopolozhitelny serological tests at children of early age are caused by immaturity of an immunological defense system therefore at suspicion on T. it is reasonable to conduct examination of mother. Slabopolozhitelny serological tests at newborns and babies can be also result of passive transfer of antibodies from mother. Positive takes of serological inspection of mother at typical a wedge, manifestations at the child and identification at it the increasing dynamics of credits of specific antibodies allow to make the diagnosis inborn to T. By a valuable method in diagnosis inborn T. at newborns detection by means of reaction of an indirect immunofluorescence (Remington's test) of IgM of antibodies, to-rye, unlike easier IgG is, do not pass through a placental barrier. Detection of IgM at the child demonstrates development in his organism of own IgM in response to a pre-natal invazirovaniye of a toksoplazmama.

Fig. 6. Roentgenogram of area of eye-sockets of the patient with an inborn toxoplasmosis (direct projection): the right eye-socket is more left (an anizoorbitalny symptom).

At rentgenol. researches on kraniogramma of patients to inborn T. symptoms of hydrocephaly in the form of change of a form and the sizes of a skull, a premature sinostozirovaniye of seams, consolidation of a coronal seam, thinning of bones of a calvaria can come to light (see Kraniografiya, the Skull). Also inborn defects in scales of frontal and occipital bones, the anizoorbitalny symptom which is characterized by various size of eye orbits (fig. 6) are observed.

The differential diagnosis is carried out with a rubella (see), a cytomegaly (see), listeriosis (see), sepsis (see), syphilis (see), etc. Newborns have an encephalomeningitis (see Meningitis) caused by toksoplazma it is necessary to differentiate with the acquired encephalomeningitis of other etiology and with an intracranial birth trauma (see).

Treatment is carried out by Chloridinum in combination with sulfanamide by preparatakhm. Chloridinum to children till 1 year appoint in a dose 1 mg/kg a day. A daily dose of Chloridinum for children from 1 year to 3 years — 0,01 g, from 4 to 7 years — 0,02 g, from 8 to II years — 0,03 g, from 12 to 15 years — 0,04 g (the daily dose is given in 2 receptions). Etazolum or Sulfadimezinum appoint 0,1 — 0,2 g/kg in a daily dose. To children 1 years instead of Etazolum and Sulfadimezinum are more senior it is possible to appoint sulfanamide drugs of the prolonged action, napr, sulfadimetoksinony Conduct 3 courses of treatment for 5 — 7 days with a break of 7 — 10 days, in the absence of sufficient effect — 5 courses. Are shown Prednisolonum (1 mg/kg a day taking into account a day-night rhythm of function of adrenal glands), and also B1, B6 vitamins, ascorbic and folic to - you. At aggravations inborn T. treatment is repeated. Appoint fortifying and symptomatic therapy.

Treatment is most effective in an acute phase of a disease and can lead to an absolute recovery, in a subacute phase — effect satisfactory. Treatment in hron. to a phase it is inefficient.

Prevention inborn T. consists in the prevention acquired by T. at women, identification and treatment of the pregnant women suffering from T.

A toxoplasmosis at pregnant women

Acquired by T. at pregnant women, in addition to described above a wedge, symptoms, is followed by changes of a mucous membrane of a uterus — a toksoplazmenny endometritis, to-ry can lead to disturbance fiziol. conditions of development of fetal egg after implantation and to a misbirth (see). Besides, at T. there are dystrophic, inflammatory processes in a placenta, uteroplacental blood circulation is broken that promotes development of functional insufficiency of a placenta. At the expressed dysfunction of a placenta there can be a threat of abortion in early terms; lag in fetation with a hypotrophy or his pre-natal death is possible.

At dispensary observation for pregnant women in clinic for women it is necessary to reveal women of risk group concerning a possible toksoplazmozny invasion, and also to hold events for prevention of complications during pregnancy and the birth of the child with inborn T.

For identification of risk group to all pregnant women at primary appeal to clinic for women carry out immunol. researches — skin test with toksoplaz-miny or serological tests (RNIF, RSK, etc.). Pregnant women with positive immunol. tests, i.e. immune, in further observation and furthermore do not need etiotropic treatment. Pregnant women with negative immunol. (not immune) T can catch reactions. at this pregnancy. Therefore it is shown repeated immunol. inspection of these women in the second and third trimesters of pregnancy. Preservation of negative tests testifies to absence of infection.

At nek-ry not immune pregnant women at repeated inspections positive seroconversion, i.e. immunol can be observed. reactions become positive that testifies to infection of T. at this pregnancy. These pregnant women make risk group and demand careful observation (emergence a wedge, symptoms of a disease and increase in dynamics of an antiserum capacity). At emergence of subfebrile condition, increase limf, nodes or other symptoms, rise of two or more cultivations of blood serum of antiserum capacities in RNIF or RSK at repeated researches surely are attracted consultants (the infectiologist and the parasitologist) for specification of the diagnosis of T. Appointment and performing treatment of pregnant women shall be proved by clinical and laboratory inspection. It is necessary to exclude the numerous diseases having similar a wedge, a picture with T., to specify the general and epidemiol. anamnesis. At assessment immunol. reactions it is necessary to consider a frequent invazirovannost of pregnant women. If at pregnant women low antiserum capacities remain and there is no wedge, displays of a disease, then this state is considered as primary carriage toksoplazm, not demanding treatment. Considerable increase of antiserum capacities in RNIF and RSK, emergence a wedge, symptoms of a disease at the pregnant woman allows to make the diagnosis acute to T.

The absolute indication to performing etiotropic treatment is acute, acquired during this pregnancy, the T. To the pregnant women who caught or had T. before the real pregnancy, specific treatment do not appoint.

Treatment shall be complex and include causal treatment and funds allocated for improvement of uteroplacental blood circulation, prevention of a hypoxia of a fruit. Causal treatment is carried out according to Methodical recommendations M3 of the USSR 1981, proceeding from situation that infection of a fruit of T. perhaps only in case of primary invazi-rovaniye of mother. From etiotropic means apply Chloridinum in combination with Sulfadimezinum (see above the section «The Acquired Toxoplasmosis, Treatment»). At the same time it is necessary to appoint ascorbic and folic to - that, the hyposensibilizing drugs. Because of possible teratogenic impact on a fruit of himiopreparat treatment of pregnant women is carried out since the second trimester of pregnancy. Only at kliniko-immunol. to a picture acute T. in the first trimester of pregnancy when there is a big risk of damage of a fruit, it is necessary to recommend abortion according to medical indications. To women with hron. to the acquired T. abortion is not shown since there is no danger of infection of a fruit.

Childbirth at the women infested by toksoplazma before the real pregnancy should be accepted in fiziol. obstetric department, and caught during this pregnancy — in observation department.

Prevention of T. at pregnant women it is similar to prevention acquired by T.

Bibliography: Akinshina G. T. and D e with m about N. Penetration toksoplazm strains of different virulence in cells of the owner, Veterinary science, No. 12, page 80, 1977; Becker S. M. Pathology of pregnancy, M., 1975; The Life cycle toksoplazm, under the editorship of I. G. Galuzo, Alma-Ata, 1974; Zasukhin D. N. and Shevkunova E. A. Some results of studying of a toxoplasmosis, M., 1969; Yygiste A. K. and Zasukhind. N. Problema of toksoplazmozny embrioiatiya, Owls. medical, No. I, page 107, 1975; Kazantsev A. P. and Popova N. I. Pre-natal infectious diseases of children and their prevention, page 150, JI., 1980; Kopp V. D. and Fadeyeva M. A. To a question of prevention of an inborn toxoplasmosis, Vopr. okhr. mat. also it is put., t. 10, No. 1, page 82, 1965; To about r about in and c - a cue of JI. To., etc. Toxoplasmosis, Kiev, 1966, bibliogr.; Lysenko A. Ya. Toxoplasmosis, M., 1980; The Manna is N about in And. C. A role of X-ray inspection in recognition of a toxoplasmosis, Vopr. okhr. mat. also it is put., t. 10, No. 6, page 36, 1965; Mikhalev P. In, e-naylo S. P. and Mikhalev JI. B. About oneiric and oneiric states at a cerebral toxoplasmosis, Zhurn. neuropath, and psikhiat., t. 78, No. 2, page 251, 1978; Pavlova M. V. To radiodiagnosis of intracranial calcificats at a toxoplasmosis, Vestn. rentgenol. and radio-gramophones., No. 4, page 46, 1964; Fathers A. G. Toksoplazmoz at pregnant women, Kiev, 1972, bibliogr.; A problem of a toxoplasmosis, under the editorship of D. N. Zasukhin, M., 1980, bibliogr.; Talkhammer O. Toxoplasmosis as inborn disease and its prevention, Vopr. okhr. mat. also it is put., t. 20, No. 4, page 29, 1975; II and N-zerling A. V., Medvedev N. Yu. and Karpova O. B. To a problem of a toxoplasmosis, Arkh. patol., t. 40, century 12, page 10, 1978; Shpak N. I. Toxoplasmosis of an eye, M., 1978, bibliogr.; Berger J. and. Piekarski G. Einfluss der Standar-disierung auf den Ausfall der Toxoplasmose-Serologie, Zbl. Bakt., I. Abt. Orig., Bd 236, S. 543, 1976; Desmonts G. Couvreur J. Congenital toxoplasmosis, New Engl. J. Med., v. 290, p. 1110, 1974; Infectious diseases of the fetus and newborn infant, ed. by J. Remington a. J. Klein, p. 191, Philadelphia, 1976; Johnson A. M. a. o. Relationship between spontaneous abortion and presence of antibody to toxoplasma gondii, Med. J., Aust., v. 1, p. 579, 1979; L a r s e n J. W. Congenital toxoplasmosis, Teratology, v. 15, p. 213, 1977; Miller E. C. Die Bedeutung der Toxoplasmose fiir die Schmangerschaft, Z. arztl. Fortbild., Bd 71, S. 1097, 1977; Nizel-Simiftska W. Stan psychiczny dzieci z dodatnimi odczy-nami serologicznymi w kierunku toksoplaz-mozy, Psychiat. pol., t. 14, s. 241, 1980; Toxoplasmose, hrsg. v. G. Wildftihr u. W. Wildftihr, Jena, 1975.

Century of H. Nikiforov; G. T. Akinshina (etiol.), V. V. Kitayev (rents.), M. V. Korkina (psikhiat.), A. Ya. Lysenko (epid., prevention, lab. diagnosis), E. T. Mikhaylenko, A. A. Nesterov (a toxoplasmosis at pregnant women), A. V. Tsinzerling (a stalemate. An.).