Toxoplasmosis is an infectious disease caused by pathogenic protozoan Toxoplasma gondii, which proceeds with a polymorphic clinical picture. There are congenital and acquired toxoplasmosis.
Etiology . Toxoplasma - unicellular parasites of the semilunar form, 2-4 microns wide and 4-7 microns long, mobile, multiply intracellularly. Withstand freezing for several days. Heating to t ° 56-60 ° kills parasites within 5-15 minutes, and boiling - instantly. Do not tolerate drying out and direct sunlight. In raw milk, 24 hours are saved. Poorly tolerate acidic media. In normal gastric juice, survive for 30 minutes. 1% phenol solution, 2% chloramine solution, 50% alcohol kill toxoplasma within 5-10 minutes.
Epidemiology . Detection of the pathogen in wild animals (rodents, predators), as well as in birds, substantiates the existence of primary natural foci. The source of infection are domestic animals (horse, large and small cattle, rabbits, etc.), as well as birds (chickens, ducks, pigeons, etc.). Infected dogs and cats are of great epidemiological importance. In the acute course of toxoplasmosis, the pathogen is excreted with saliva, urine, feces, milk, conjunctival secret; with prolonged flow - with saliva, feces, urine. Infection occurs with the use of infected foods (meat, milk, raw eggs); at workers of meat-packing plants, slaughterhouses, cattle-breeding farms - through damaged skin, mucous membranes. Transmissible transmission of infection through ticks is possible.The
Fig. 1. Toxoplasma in the smear from the organs of the mouse (fixation with methyl alcohol, coloring according to Romanovsky - Giemsa): a and b - resting forms; c-the stage of division; g and g are divided forms. Fig. 2. Pseudocyst of toxoplasma in the macrophage (from the exudate of the infected mouse). Fig. 3. Toxoplasma, located in the vacuoles in the rat brain; 15th day after infection. Fig. 4. Three cysts in the rat brain, the 25th day after infection (Figures 3 and 4 - fixation in the Carnoy fluid, color according to Romanovsky - Giemsa). (According to SG Vasin.)
Pathogenesis and pathological anatomy . When infected, toxoplasma penetrates into the lymphatic pathways and then into the bloodstream. The generalization of infection leads to the formation of local lesions in various organs.
Inflammatory proliferative-granulomatous changes of reticulo-lymphocytic elements appear in the tissues. In necrotic areas lime is secondarily deposited, characteristic calcifications are formed (in the soft meninges, the cortex, the cerebellum , the ventricles of the brain). Perhaps asymptomatic carriage of toxoplasm; causative agents in the form of cysts persist in the skeletal musculature, myocardium, and brain. Disintegration of cysts leads to activation of infection, secondary generalization with a specific allergy .The
Clinical picture of acquired toxoplasmosis . In the acute course of acquired toxoplasmosis, several clinical forms are distinguished.
1. Lymphoglandular (glandular) form is characterized by an increase in lymph nodes (cervical, axillary, inguinal), fever, angina, enlargement of the liver and spleen. In the blood - moderate leukocytosis, lymphocytosis, monocytosis. The glandular form is more often noted in children and young people.
2. The eye shape is accompanied by the phenomena of central chorioretinitis , acute conjunctivitis, uveitis , iritis. There is a decrease and loss of vision. Eye damage can be the only manifestation of the disease.
3. The exanthema form begins with a chill and an increase in temperature, marked by a general intoxication right up to the development of the status typhosus. On the 4th-7th day there is a profuse maculopapular rash that lasts up to 2 weeks. There may be an increase in lymph nodes, liver, spleen. Often there are pneumonia , myocarditis, lesions of the central nervous system.
4. The cerebral (meningoencephalitic) form is characterized by a high temperature, symptoms of severe brain damage and its membranes.
5. Visceral forms are manifested in the form of myocarditis, pneumonia, interstitial hepatitis.
In the chronic course of acquired toxoplasmosis, subfebrile temperature, head and muscle pain remain for a long time, angina , minor enlargement of the lymph nodes are noted. Characteristic neuro-psychic and neuroendocrine manifestations - paresis, paralysis, epileptiform cramps , vegetative-vascular disorders, dysfunction of the sexual glands, pituitary gland, thyroid gland , eyes. Often observed hepatitis, splenomegaly , myocarditis, pneumonia. Sometimes only a laboratory test determines the toxoplasmic etiology of the disease.
Fig. 1. Paroxysus toxoplasmosis chorioretinitis in a man of 43 years. Fig. 2. Late relapse of toxoplasmosis chorioretinitis in a woman of 57 years. Fig. 3 and 4. Congenital focal chorioretinitis of the right (Figure 3) and left eye (Figure 4) in the girl is 15 years old.