Toxoplasmosis uveitis is a specific parasitic lesion of the posterior parts of the uveal tract with a tendency to generalize the process. Common symptoms for all forms are a decrease in visual acuity, the appearance of “fog” in front of the eyes. In the generalized variant, photophobia and pain develop in the projection area of the orbit. Diagnostics includes external examination, ophthalmoscopy, biomicroscopy, visometry, biopsy, gonioscopy, cytological examination, ELISA. Treatment tactics are reduced to taking synthetic antibacterial agents in combination with sulfonamides and folic acid. In order to limit the inflammation zone, laser coagulation is performed.
H20.9 Unspecified Iridocyclitis
Toxoplasmosis uveitis is an acute or chronic disease of the vascular membrane of the eye of inflammatory origin caused by toxoplasma. For the first time, parasites having a similar structure to the pathogens of toxoplasmosis in animals were isolated from the membranes of the eyeball in 1923. In 1952 , experts were able to identify T. gondii in the tissues of the eyeball. In 90% of cases with congenital toxoplasmosis, the organ of vision is involved in the pathological process. Approximately 75% of patients have binocular eye damage. The prevalence among the total number of congenital pathologies of the eyeball is 18-45%. The acquired form of toxoplasmous uveitis can develop at any age, in 30-50% of cases it is manifested by the clinic of posterior uveitis.
The causative agent of toxoplasmosis uveitis is Toxoplasma gondii, which belongs to the type of protozoa, the class of spores. The life cycle consists of two phases of development – sexual and asexual. The process of reproduction of toxoplasmas occurs only in the intestinal epithelial cells of cats. The phase of asexual development is realized in the cells of most human organs and tissues, including the eyeball. This stage of the life cycle is characterized by a tendency to invasion, which causes not only functional, but also organic changes in the organ of vision in toxoplasmosis uveitis.
The congenital form of the disease is observed with a vertical (transplacental) pathway of transmission of the pathogen from mother to child. The cause of acquired toxoplasmosis uveitis is infection from carnivores, farm animals or birds. Cats and pigeons are more often carriers. Pathogens enter the systemic bloodstream through small skin lesions or intact mucous membrane. A less common way of infection is alimentary, which is realized when eating meat of sick animals, as well as vegetables and fruits that have not been fully processed. The development of toxoplasmosis uveitis may be associated with blood transfusion or transplantation of infected organs.
The penetration of pathogens into the lymph nodes leads to regional lymphadenitis. Foci of infection are formed during the dissemination of toxoplasma in the bloodstream. The occurrence of toxoplasmosis uveitis is possible only when an infectious agent penetrates through the hematophthalmic barrier. Less often, visual dysfunction is observed in violation of the permeability of the blood-brain barrier and damage to the visual cortex of the brain.
From a clinical point of view, specialists in the field of ophthalmology distinguish between congenital and acquired forms of the disease. In most cases, the vascular membrane is involved in the pathological process, so toxoplasmosis uveitis is manifested by symptoms of chorioretinitis. Generalized uveitis develops less often. At the same time, the anterior parts of the eyeball remain intact. The organ of vision is more often affected in the chronic period of the disease. The acquired form of the disease in the absence of violations by the immune system proceeds latently. With a chronic course, the pathogen can be in the persistence stage for a long time and provoke the periodic development of relapses.
Clinical manifestations of the congenital form of toxoplasmosis uveitis depend on which trimester of pregnancy the infection occurred. Infection in the first trimester is incompatible with life, with infection in the second and third trimesters, a subacute or chronic course of toxoplasmosis infection is noted. Very rarely, toxoplasmous uveitis occurs latently and is only the cause of the development of secondary strabismus. This variant of pathology is often combined with oligophrenia, hydrocephalus, microphthalmos, malignant course of myopia.
Clinical manifestations of the acute stage of toxoplasmosis uveitis occur with a decrease in resistance and reactivity of the body. The first symptoms are a decrease in visual acuity, image distortion, the appearance of “fog” or “flies” in front of the eyes. The function of central and twilight vision is mainly impaired. Hyperemia of the orbital conjunctiva, photophobia and pain syndrome are characteristic only for the generalized form of toxoplasmosis uveitis involving the anterior parts of the eyeball. The acute course of the disease may be accompanied by hyperthermia.
With generalized uveitis, the lesion of the anterior parts of the eyeball proceeds in the form of a toxic-allergic reaction provoked by a specific inflammation of the uveal vascular membrane of the eye. The most common concomitant pathologies observed in toxoplasmosis uveitis are myopia, cataract and coloboma of the choroid, ptosis of the eyelids. The complicated course of the disease is indicated by choroidal neovascularization.
The diagnosis of toxoplasmosis uveitis is based on an ophthalmologist conducting an external examination, ophthalmoscopy, biomicroscopy, visometry, biopsy, gonioscopy, cytological examination, enzyme immunoassay (ELISA). External examination of patients with congenital toxoplasmous uveitis reveals hyperemia of the bulbar conjunctiva, ptosis of the eyelid, nystagmus. Ophthalmoscopically visualized lesion of the central parts of the fundus. The focus of inflammation or chorioretinal granuloma with a white-yellow or brown tint most often have a diameter of about ⅓ of the diameter of the optic nerve disc. Less often, large foci are formed, the diameter of which is larger than the diameter of OND.
Prolonged course of toxoplasmosis uveitis leads to degeneration of the affected area with the subsequent development of coagulation necrosis. During ophthalmoscopy, a rounded white focus with clearly defined scalloped edges is determined. On the periphery of the focus of atrophy, there is an accumulation of pigment, intra- and subretinal hemorrhage. The generalized form of toxoplasmous uveitis involving the anterior part of the eyeball is characterized by the appearance of precipitates on the cornea. Gonioscopy reveals a cellular suspension in the anterior chamber.
During biomicroscopy with a slit lamp in acute course of toxoplasmous uveitis, areas of hemorrhage, exudate accumulation, vitreous turbidity are determined. Endozoites can be detected in the exudate or inside the cells of the uveal tract structures during cytological examination of the biopsy. Cysts contain cystozoites. The presence of toxoplasmas can be confirmed by biopsy of intact tissues along the periphery of the zone of specific inflammation or necrosis. Biomicroscopy with acquired toxoplasmosis uveitis allows to identify a large number of precipitates in the posterior parts of the eyeball, multiple posterior synechiae in combination with vitreous opacity. During ELISA in the acute phase of the disease, the titer of antitoxic antibodies of the IgM class increases. Isolated detection of IgG indicates a chronic course of toxoplasmosis uveitis or a reactivation phase.
The tactics of treatment of toxoplasmosis uveitis is determined by the form and features of the course of the disease. Immunomodulators, restorative agents are used. Specific therapy is indicated only for patients at risk of decreased visual acuity. The drugs of choice are drugs from the group of synthetic antibacterial drugs in combination with sulfonamides. The course of treatment lasts from 2 to 4 weeks. Throughout the course, the use of folic acid and general blood analysis in dynamics are shown. This is due to the fact that drugs of these groups can lead to a decrease in the level of leukocytes and platelets. In case of isolated development of toxoplasmosis uveitis, parabulbar administration of glucocorticoids is recommended. In the case of the development of systemic manifestations of toxoplasmosis, pulse therapy with glucocorticoids is indicated.
If surgical intervention is necessary, antitoxoplasmosis therapy should be carried out in the pre- and postoperative period. Laser coagulation is performed to delimit the zone of inflammation, but is not used to remove toxoplasmosis foci, which is associated with their deep location and a high risk of postoperative complications. If a large atrophic focus is detected in a patient with a congenital form of toxoplasmosis uveitis, specific treatment is recommended only if a relapse of the disease occurs.
Prognosis and prevention
Specific preventive measures have not been developed. Nonspecific prevention of toxoplasmosis uveitis is aimed at strengthening immunity. If necessary, immunomodulators are prescribed. Also, patients need to normalize sleep and rest, avoid stressful situations. The risk of infection is reduced by following the rules of personal hygiene, pet care, proper heat treatment of food.
The prognosis depends on the severity of the disease. In mild forms, special therapy is not required, since toxoplasmosis uveitis is characterized by a favorable course. With moderate uveitis, the use of immunomodulators and stimulation of the body’s defenses contribute to achieving long-term remission. Infection of a woman in the first trimester of pregnancy is associated with an unfavorable prognosis for the fetus.