What Is Ocular Toxoplasmosis?

Toxoplasmosis is a zoonotic parasitic protozoan that is distributed worldwide, and its pathogen is toxoplasma gondii. Protozoa are intracellular parasites, felines are their terminal hosts, and humans and other mammals are intermediate hosts. Congenital toxoplasmosis caused by fetal infection through the human placenta can also cause acquired acquired toxoplasmosis through the digestive tract, damaged skin and mucous membranes, and blood transfusions or organ transplant infections. Congenital toxoplasmosis is one of the most serious diseases in human congenital infections, with a high mortality rate, mainly manifested as deformed children, low growth and development, and ocular encephalopathy. Acquired toxoplasmosis is mild and has a lower mortality rate, but its clinical manifestations are complex and often atypical, mainly involving lymph nodes, central nerves, and heart organs.

Ocular toxoplasmosis

Epidemiology of Toxoplasma gondii

Pathology of Toxoplasma gondii Figure 1. Epidemic profile Toxoplasma gondii infection is one of the most common animal infectious diseases in the world. Among people in many regions, there is a high proportion of Toxoplasma infection Infected. More than 50% of adults in the United States have been infected; the seroprevalence rate in the South American population is 42% to 83%; in France it is as high as 90%. With the increase of age, the infection rate also increases. For example, the infection rate is 5% to 30% in the population of 10 to 19 years old; while the infection rate is 70% in the population of 50 years and older, but most of the asymptomatic infections are arched. Intraocular inflammation (uveitis) caused by worms has become one of the most common post uveitis in some countries in Europe and the United States (Table 1). It is reported that it accounts for 80% of post uveitis and a high proportion of anti-toxoplasma antibodies are positive in the normal population. Such antibody positives do not indicate that the infection of toxoplasma is the cause of uveitis. The detection of serum and aqueous humor antibodies should be performed at the same time. The diagnosis can only be confirmed when the antibody titer in the intraocular fluid is significantly higher than the serum antibody titer.

Toxoplasma infections are congenital and acquired. The incidence of congenital infections was 0.004% (UK), 0.01% (US), and 0.2% (Norway). About 40% of infected pregnant women pass the disease on to their fetuses, but only on rare occasions after birth, and the vast majority develop neurological and eye diseases later

Although ocular toxoplasmosis can occur at any age, it is more common in 20 to 30 years old, and the incidence rate is similar between men and women.

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(1) Source of infection: A variety of animals, especially felines, are the source of toxoplasmosis. Placenta can cause vertical transmission as a source of infection

(2) Transmission routes: transmission through food, through damaged skin and mucous membranes, through blood transfusion or organ transplantation, and through vertical placental transmission. Among them, ingestion of meat products, eggs, milk, various foods and water contaminated by Toxoplasma gondii at various developmental stages is the main route of transmission.

(3) Susceptible populations: Humans are generally susceptible to Toxoplasma gondii, and fetuses and infants whose immune function is suppressed (such as those receiving immunosuppressive drugs, patients with acquired immunodeficiency syndrome) are more susceptible to infection.

Causes of Toxoplasma gondii

Toxoplasma gondii-Pathogens of infection Toxoplasma gondii can exist in host tissues and body fluids, such as saliva, milk, semen and urine. It exists in 5 forms, namely trophozoites, cysts, schizonts, ligands, and oocysts. Related to pathogenicity and transmission are trophozoites, cysts and oocysts.

The trophozoite exists in the acute phase of the disease. It can enter the cytoplasmic vacuole of any nucleated cell and multiply rapidly by internal budding. The trophozoite released by the rupture of the cell will infect other cells. When the body's immune response is strong or the presence of antibiotics, trophozoites form cysts, and the trophozoites in the cysts are called bradyzoites. Its cyst is composed of two parts of the parasite and the host, so it can be protected from the host's immune system. Encapsulation has a strong resistance, can be latent in the host for several years, without any tissue damage, and can even accompany the host throughout life. This type of cyst is particularly preferred for the retina, central nervous system, skeletal muscle, and heart. Encapsulation rupture can cause a large number of delayed zygote release, causing recurrence of the disease and severe inflammation.

Oocysts are produced in feline intestinal cells and are excreted in feces. It can survive 2 years in warm and humid soil. 1 to 21 days after discharge, the oocysts begin to form spores and become mature infectious oocysts. Ingestion of these mature oocysts can cause infection in intermediate or final hosts.

Pathogenesis of Toxoplasma gondii

Gamete mother cell Toxoplasma gondii has two different life histories, namely the asexual phase and the sexual phase. The former occurs in all hosts and the latter occurs only in the intestinal epithelium of the final host. Felines are the only final host. Toxoplasma gossipes sexually in the small intestinal epithelial cells of the final host and asexually in other tissues outside the intestine. Only asexual reproduction occurs in other animals such as cattle, pigs, poultry and humans. These animals and humans are intermediate hosts.

When the mature oocysts or cysts in animal meat are taken up by the intermediate host, the spores, bradyzoites or tachyzoites released from the intestine invade the intestinal wall and enter the monocyte-macrophage system via blood or lymph. The intracellular parasites spread to the brain, retinal lymph nodes, liver, heart, lungs, muscles and other tissues and organs, causing the manifestation of acute infection and inducing the body to produce specific antibodies. Antibodies bind to extracellular trophozoites and eliminate trophozoites through an immune response, but humoral immunity has no effect on pathogens inside the cell, while cellular immunity works on infected cells, inhibits intracellular proliferation, and forms trophozoites. After the immune system clears away free tachyzoites, the patient's symptoms disappear and the disease enters a chronic phase.

When felines ingest oocysts and cysts, spores, bradyzoites, or tachyzoites escape in the small intestine, invade intestinal epithelial cells, and begin merozoite reproduction. After 3 to 7 days, the worms in the epithelial cells formed merozoites and released merozoites after maturation, and developed into male and female gametes. The male and female gametes fertilized into zygotes and formed oocysts. The latter escapes from the epithelial cells and enters the intestinal lumen, where it is excreted with the feces. At this time, the gametoblasts can excrete 12 million oocysts in one day. The oocysts can develop into infectious mature oocysts in 2 to 4 days under the conditions of 25 ° C and suitable humidity.

Clinical manifestations of toxoplasmosis

The clinical manifestations of toxoplasmosis in the eyes vary greatly depending on the mode of infection (congenital or acquired), and the number and age of the protozoa.

1. Congenital toxoplasmosis causes placental infection due to maternal infection with toxoplasmosis and transfers to the fetus. Generally, infection in early pregnancy can cause fetal miscarriage and premature delivery; stillbirth and delivery of infants with congenital toxoplasmosis in late pregnancy. Its main lesions are retinal choroiditis, cerebral edema, cerebral calcification plaques and mental and dyskinesias, that is, the symptoms of central nervous system invasion.

The ocular manifestations of congenital toxoplasmosis are mostly congenital malformations caused by embryonic damage with retinal choroiditis as the main symptoms. There are mainly small eyeballs without eyeballs, congenital absence of iris, choroidal defects, residual vitreous arteries, optic atrophy, and congenital cataracts. And inflammatory damage such as strabismus and retinal choroiditis. Fundus changes can be divided into two types: old lesions and recurrent lesions.

2. Acquired toxoplasmosis in adults acquired chronic toxoplasmosis, more chronic manifestations, especially the lack of other symptoms of congenital toxoplasmosis. Cases with elevated serum antibody titers can be considered new infections or acquired toxoplasmosis. Acquired toxoplasmosis also has systemic changes when there are eye diseases, while those with congenital diseases can have eye diseases alone

Acquired systemic toxoplasmosis infection with ocular symptoms is rare. If ocular damage occurs, its clinical manifestations are limited exudative retinal choroiditis, which can occur in one or both eyes, as seen in recurrent cases of congenital infection. The vision of the affected eye is reduced, and the fundus lesions are mostly located around the macula or optic disc. The retinal gray-white edema at the lesion was unclear, and the retinal edema exudation gradually subsided after 2 to 3 months, and finally it became a scar lesion. This is because the protozoa invades the retinal tissue through the blood stream, causing inflammatory lesions to reproduce in it, causing tissue reactions and necrosis, and causing secondary reactions to the choroid. The path of infection from Toxoplasma gondii to the fundus is most likely to be a bloodstream infection in the macula because the capillary network in the macula is denser than other parts of the retina, which can easily cause protozoan embolism in the capillaries.

Complications: Complications of toxoplasmosis include secondary glaucoma, macular edema, retinal vascular obstruction, retinal neovascularization, and choroidal neovascularization, which can cause vision loss.

Eye Toxoplasmosis Diagnosis

The diagnosis of rubella virus toxoplasmosis in the eye should have the following conditions: the clinical process and manifestations of the fundus lesions meet the characteristics of the typical ocular toxoplasmosis; serological tests are positive for anti-toxoplasma antibodies; except for other possible causes that cause similar fundus lesions. Because the clinical manifestations of fundus toxoplasmosis are complicated and often difficult to distinguish from other chorioretinitis, laboratory tests and serological antibody determinations are the main basis for the diagnosis of toxoplasmosis. Because there is no significant correlation between the level of antibody and the severity of eye disease, any patient with a positive serum anti-toxoplasma antibody, regardless of the potency, can be diagnosed as long as there are typical clinical manifestations and fundus changes. The comparison test of aqueous humor antibody and serum antibody is valuable for diagnosing ocular toxoplasmosis. In addition, try to rule out other common causes of uveitis, such as chorioretinitis caused by tuberculosis, syphilis, and viruses.

Fundus fluorescein angiography shows strong fluorescence in active lesions of toxoplasmosis. Early leakage and late staining can be observed in areas of vasculitis. Other manifestations include window-like defects, late scleral staining, and choroidal neovascularization. Optical coherence tomography (OCT) tests revealed retinal inflammation and edema. None of these tests are specific for toxoplasmosis.

Differential diagnosis:

Congenital toxoplasma infection in newborns should be distinguished from some viral infections (such as rubella virus, cytomegalovirus, herpes simplex virus) and other infections (such as tuberculosis, syphilis, acquired immunodeficiency syndrome), and should be distinguished from Retinoblastoma choroidal defect, permanent primitive vitreous hyperplasia, etc.

According to clinical manifestations, retinitis caused by herpes simplex virus and those caused by toxoplasma are easy to distinguish. However, congenital active retinitis caused by cytomegalovirus or retinitis caused by immunodeficiency patients is sometimes difficult to distinguish. Serological examination and urine examination can help differentiate diagnosis.

Eye Toxoplasmosis-Examination

1. The fluorescein fundus angiography (FFA) and indocyanine green angiography check the active lesions of toxoplasmosis in the eye. The fluorescein fundus angiography shows weak fluorescence in the center of the lesion early, and fluorescein leaks later. Scar lesions may show early weak fluorescence due to retinal pigment epithelium proliferation, or see through fluorescence due to retinal pigment epithelial atrophy. Irregular retinal pigment epithelium atrophy and proliferation lead to a mottled appearance, with late stage staining of the lesions. Patients with neuroretinitis or neuritis often show intense fluorescence at the optic disc margin. Patients with retinal vasculitis can see vascular leakage and late vascular wall staining, and can also find lesions such as intraretinal arteriovenous short circuit, retinal choroid short circuit, macular cystic edema, and choroidal neovascular membrane. Indocyanine green angiography can show weak or strong fluorescence in the early stage of active lesions, and strong fluorescence in the later stages. Early recurrent lesions not found with ophthalmoscope and fluorescein fundus angiography can also be found.

2. CT and magnetic resonance examination can find calcification and brain lesions in the brain, which is of great help in the diagnosis of intracranial toxoplasma infection.

Treatment: The treatment measures for toxoplasmosis in the eye depend on the nature of the lesion, the severity and the period. Old lesions generally do not require treatment; localized exudative lesions can be treated with anti-toxoplasma; recurrent lesions are allergic reactions caused by ruptured cysts or the protozoa are released for infection, and anti-toxoplasmic drugs combined with corticosteroids should be used to treat the lesion Can be used for preventive photocoagulation after remission.