Ocular toxoplasmosis

Introduction to Ocular Toxoplasmosis Toxoplasmosis is also a common cause of potentially blinding eye disease, and ocular eye lesions caused by toxoplasma infection are most common with retinal choroiditis. basic knowledge The proportion of illness: 0.002% Susceptible people: no special people Mode of infection: digestive tract spread Complications: glaucoma, cystoid edema, choroidal neovascularization

Cause of ophthalmic toxoplasmosis

Causes:

The toxoplasma can be present in host tissues and body fluids, such as saliva, milk, semen and urine. It exists in five forms, namely trophozoites, cysts, schizonts, ligands and oocysts. Diseases and transmission are related to trophozoites, cysts and oocysts.

The trophozoite exists in the acute phase of the disease. It can enter the cytoplasmic vacuoles of any nucleated cells and rapidly multiply in the way of internal sprouting, causing the cells to rupture. The released trophozoites will infect other cells, when the body's immune response is strong or there is antibiotics. When the trophozoite forms a cyst, the trophozoite in the capsule is called a eutrophozoite. Its cyst is composed of the components of the parasite and the components of the host, so it is protected from the host immune system, and the capsule has Strong resistance, can be lurking in the host for several years, without any tissue damage, or even with the host's life. This kind of cyst especially favors the retina, central nervous system, skeletal muscle and heart, etc. The release of euphratica causes recurrence of the disease and severe inflammation.

The oocysts are produced in the intestinal cells of the cat family and are excreted in the feces. In warm and humid soil, it can survive for 2 years. After 1 to 21 days after discharge, the oocysts begin to form spores, thus becoming mature. Infectious oocysts that ingest these mature oocysts can cause infection in the intermediate or terminal host.

Pathogenesis:

The toxoplasma has two different life histories, the asexual phase and the sexual phase. The former occurs in all hosts, the latter occurs only in the intestinal epithelium of the terminal host, and the feline is the only terminal host, toxoplasma. Sexual reproduction occurs in the terminal host intestinal epithelial cells, while asexual reproduction occurs in other tissues outside the intestine, and only asexual reproduction occurs in other animals such as cattle, pigs, poultry and humans. These animals and humans are intermediate hosts.

When the cysts in mature oocysts or animal meat are ingested by the intermediate host, spores, tachyzoites or tachyzoites released from the intestine enter the intestinal wall and enter the mononuclear-macrophage system via blood or lymph. Intracellular parasitism and spread to the brain, retina, lymph nodes, liver, heart, lungs, muscles and other tissues and organs, causing acute phase infection, inducing the body to produce specific antibodies, antibodies and extracellular trophozoites, through The immune response clears the trophozoites, but humoral immunity has no effect on the pathogens in the cells. Cellular immunity acts on the infected cells, inhibits intracellular proliferation, and forms trophozoites. When the immune system clears free tachyzoites After that, the patient's symptoms disappear and the disease enters the chronic phase.

When the feline ingests the oocysts, the cysts, tachyzoites or tachyzoites escape in the small intestine, invade the intestinal epithelial cells and begin schizogulation, and after 3 to 7 days, the worms in the epithelial cells Formation of schizont, mature to release merozoites, and develop into male and female gametes, male and female gametes fertilized into zygotes and form oocysts, the latter escape from the epithelial cells into the intestinal lumen, with the feces discharged to the body, at this time gametes The formation of mother cells can excrete 12 million oocysts in one day. The oocysts can develop into infectious mature oocysts in 2 to 4 days at 25 ° C and suitable humidity conditions.

Toxoplasma infection is mainly caused by ingestion of unripe foods containing tissue capsules (especially meat). Secondly, accidental inhalation or ingestion of fecal fecal contaminants can also cause infection and can also be obtained by ingesting unsterilized Goat milk, raw or unwashed vegetables, blood transfusions, organ transplants, etc., if the infection occurs before pregnancy or during pregnancy, infection can occur through the placenta.

After the body infects the toxoplasma, B cells are activated to produce anti-toxoplasma antibodies (IgM, IgA, IgE and IgG). The antibodies bind to the trophozoites and can be thawed by the classical complement pathway, and the trophozoites bound to the antibodies It is not able to pass through the cell membrane and enter the cell, and it is easily destroyed by phagocytic cells.

The cellular immune response plays a more important role in the development of the disease, characterized by activation of macrophages, natural killer cells (NK cells) and T cells, which are activated by phagocytosis of antibody-regulated toxoplasma. Produces IL-2 and -tumor necrosis factor, stimulates CD8 T cells and NK cells to produce -interferon, which greatly enhances the killing effect of macrophages on toxoplasma, activated macrophages through the production of toxic oxygen and Nitrogen intermediates and arachidonic acid metabolites, thereby enhancing the killing ability of intracellular Toxoplasma. In addition, -interferon can inhibit the replication of toxoplasma in retinal pigment epithelial cells; macrophage released cytokines can It stimulates CD4 Th1 cells to produce IL-2, which also activates cytotoxic T cells and NK cells, which attack the cells infected with Toxoplasma gondii, while CD4 Th2 cells activate IL-4, IL-5 and IL-10. It can then regulate the cellular immune response so that the inflammatory response is not too strong.

Ocular toxoplasmosis prevention

Since toxoplasmosis infection is mainly caused by ingestion of contaminated food or meat containing cysts, the prevention is mainly to avoid food contamination and not to eat unripe and possibly contaminated food. The specific measures are as follows:

1 Strengthen the monitoring and isolation of livestock, poultry and suspicious animals;

2 Strengthen food hygiene management and education, establish and improve the health quarantine system for meat products;

3 do not eat raw meat or undercooked meat, meat should be cooked at 60 ° C for at least 15min, or frozen at -20 ° C for 24h to completely destroy the capsule;

4 do not eat food that may be contaminated by cat feces;

5 do not eat raw eggs or unsterilized milk;

6 fruit, cooked vegetables should be fully washed before eating;

7 do not drink water that may be contaminated;

8 pregnant women do not raise cats, avoid contact with cats, cat feces and raw meat, do not let cats pick up hands, face and utensils;

9 blood collection and blood transfusion should be strictly controlled to avoid the use of blood from seropositive people, and also to avoid the blood of the positive person to the negative;

10 Clean the cat litter every day and remove the oocysts to avoid infective trophozoites.

Ocular toxoplasmosis complications Complications glaucoma macular cystic edema choroidal neovascularization

Complications of ocular toxoplasmosis include secondary glaucoma, cystoid macular edema, retinal vascular occlusion, retinal neovascularization, choroidal neovascularization, etc., which can cause vision loss.

Ocular toxoplasmosis symptoms Common symptoms Congenital toxoplasma fundus changes uveitis retinal edema optic atrophy cerebral edema

The clinical manifestations of toxoplasmosis vary widely depending on the type of infection (innate or acquired) and the number and age of infected protozoa.

1. Congenital toxoplasmosis: due to infection of toxoplasmosis during maternal pregnancy, which causes placental infection and metastasis to the fetus, usually in the early pregnancy can cause fetal abortion, premature delivery; in the late pregnancy, birth and birth congenital arch In babies with worm disease, the main lesions are retinal choroiditis, cerebral edema, cerebral calcification plaques, and mental and motor disorders, which are mainly caused by the central nervous system.

Congenital toxoplasmosis is characterized by retinal choroiditis. Congenital malformations caused by embryonic damage, mainly small eyeballs, no eyeballs, congenital aniridia, choroidal defects, residual vitreous arteries, optic atrophy, congenital In cataract and strabismus, inflammatory damage causes retinal choroiditis, and fundus changes can be divided into two types: old lesions and recurrent lesions.

Old lesions: children with fundus examination can be seen with scarring changes, the acute phase occurs mostly in the fetal period or shortly after birth, typical old lesions are often bilateral, mostly located in the macula, sometimes seen around the optic disc and the equator, Recently, it has been reported that peripheral lesions are more common. The lesions have 2 to 3 optic disc diameters. The center of the lesion is gray-white proliferation tissue, no neovascularization, surrounded by melanin, arranged in a zigzag pattern. The lesions are clearly defined with the surrounding normal retina. There may be one to several small melanin hyperplasia around the lesion, which is the result of recurrence of inflammation.

Recurrent lesions: Most of the toxoplasmosis is a recurrence of congenital infections. About 1/3 of congenital cases may recur, and the age of recurrence is 11 to 40 years old. There are many reasons for recurrence. Parasitic rupture and proliferation of protozoan cysts in the retina, or allergic to proteins of encapsulated contents and tissue disruptors, or by pathogen-bearing cells entering the ocular tissue, often occurring at or around the edge of old lesions, acute phase It is characterized by focal yellow-white exudation lesions, where there is retinal edema, mild uplift, and unclear borders. The single lesion is about 1 optic disc diameter, the retinal vessels in the lesion are involved, the diameter is irregular, and the artery is segmented. The shape changes, the white sheath around the vein, the vitreous opacity, can also cause anterior uveitis and post-iris adhesion. After 2 to 3 months, the inflammation gradually subsides, the vasculitis disappears, the boundary of the lesion is clear, and the pigment gradually appears on the edge. It is a typical old lesion after 1 to 2 years.

2. Acquired toxoplasmosis : Adult acquired toxoplasmosis, with more chronic manifestations, especially in the absence of other symptoms of congenital toxoplasmosis, elevated serum antibody titers, can be considered new infection or acquired Toxoplasmosis, the congenital person may have only a single eye disease when there is eye disease in the bow torsion.

Congenital systemic toxoplasmosis infection with ocular symptoms is rare, such as eye damage, the clinical manifestations of localized exudative retinal choroiditis, as seen in the recurrence of congenital infections, can be monocular or binocular, The visual acuity of the affected eye decreased, and the fundus lesions were mostly located in the macula or around the optic disc. The retinal gray edema of the lesion was unclear. The retinal edema exudation gradually subsided after 2 to 3 months, and finally the scar lesion was caused by the protozoan menstrual blood. The flow invades the retinal tissue, causing and inducing inflammatory lesions, causing tissue reactions and necrosis, and causing secondary reactions of the choroid. The infection path from the toxoplasma to the fundus is mostly in the macula, and is likely to be a bloodstream infection. Because the macular network of the macula is denser than other parts of the retina, it is easy to cause embolization of the protozoa in the capillaries.

Examination of ocular toxoplasmosis

The diagnosis of toxoplasmosis infection is based on typical ocular and systemic clinical manifestations, direct observation of pathogens, specific antibody detection and polymerase chain reaction.

Pathogen examination

(1) Smear staining method: In the acute phase of the disease, blood, cerebrospinal fluid, urine and milk may have trophozoites. These specimens are centrifuged, and the precipitate is used as a smear, which can be observed under the microscope by Ji's staining. The chronic phase can be observed by biopsy after hematoxylin-eosin staining or silver staining.

(2) Animal inoculation or cell culture: A sample of the patient is inoculated into the abdominal cavity of a sensitive animal, and the peritoneal fluid is examined under a microscope one week later, or inoculated in a single layer of nucleated cells cultured in vitro.

2. Serological methods : In most cases, the pathogenic examination of toxoplasma is difficult and the positive rate is not high. Therefore, serological examination is often used, but the simple serological method cannot confirm the diagnosis, especially for the suspected eye arch. In patients with physical diseases, serum anti-toxoplasma antibody detection can only be used as a diagnostic reference. More importantly, the detection of intraocular liquid toxoplasma antibodies should be performed.

Commonly used serological tests include Sabin-Feldman dye test, complement binding test, hemagglutination reaction, immunofluorescence-labeled antibody test, enzyme-linked immunosorbent assay, immunoblot assay and immunoadsorption agglutination test.

(1) Sabin-Feldman dye test: This is an accurate test method for detecting anti-toxoplasma antibodies. Other test methods often use this method as a calibration standard. The principle is to combine the patient's serum or other body fluids with complement and live toxoplasma. Culture, add dyes to quantify antibodies, this test can detect early infections, have good sensitivity and specificity for acute and chronic infections, but because this method uses live toxic toxoplasma, in view of safety Consider that many laboratories do not use this test method.

(2) Complement binding test: When the circulating antibody has a high level, the complement binding test has higher sensitivity and is helpful for the observation of elevated antibody levels, mainly for the diagnosis of acquired toxoplasmosis infection, but In the early and chronic stages of infection, the diagnostic value of such tests is limited, so this method should be used in conjunction with other methods.

(3) Hemagglutination test: The hemagglutination test has high sensitivity and specificity for both acute and chronic phases, but there are large variations in such tests in different laboratories, for early infections and congenital infections. The diagnosis is of little value and should be used in conjunction with other tests.

(4) Immunofluorescence-labeled antibody test: Immunofluorescein-labeled antibody assay is simple and easy, can determine the increase of early antibody levels, can quantify IgM and IgG, is a commonly used detection method, but in the presence of cross-reactive antibodies , it can not produce definite results, such as rheumatoid factor can cause false positive IgM results, anti-nuclear antibodies can also cause IgM, IgG false positive results, for cytomegalovirus, Epstein-Barr virus, hepatitis A virus, secondary syphilis, etc. Cross-reactions can also cause false positive results for IgM.

(5) Enzyme-linked immunosorbent assay: This test method has high sensitivity and specificity and is the most commonly used detection method. The double sandwich method is superior to the immunofluorescein-labeled antibody test in detecting IgM, and rheumatoid-like Factors, antinuclear antibodies, etc. do not affect the test results, and their sensitivity is high. IgM antibodies can be detected within a few months after infection, and can be used to observe changes in IgM after infection.

(6) Immunoadsorption agglutination test: This test method can simultaneously detect anti-toxoplasma IgA and IgM antibodies with high sensitivity and specificity. IgA disappears usually faster than IgM, and IgA usually does not exist in chronic phase. Simultaneous presence often indicates an acute infection, so it is of great value in the diagnosis of primary infection during pregnancy.

(7) Western blotting test: Western blotting test has high sensitivity and is of great value in the diagnosis of congenital toxoplasmosis infection.

3. Polymerase chain reaction (PCR) : Polymerase chain reaction is a method for mass amplification of specific DNA sequences (or genes) in vitro. The process is basically similar to intracellular DNA replication. This reaction requires a reaction. DNA sequence of interest, a pair of primers and four deoxyribonucleotide triphosphates and a thermostable DNA polymerase.

Amniotic fluid PCR detection is helpful for intrauterine toxoplasmic infection. PCR detection of aqueous humor and vitreous can be used for the diagnosis of ocular toxoplasmosis. Cerebrospinal fluid testing can be used for the diagnosis of toxoplasmic infection of toxoplasma.

4. Other laboratory tests : blood routine tests have certain help for congenital infections. Patients usually have anemia, thrombocytopenia, leukopenia or increase, eosinophilia, and acquired eosinophils. Increased cells, and elevated transaminase, increased intracranial toxoplasmosis, cerebrospinal fluid pressure, yellowing, lymphocytosis and increased protein concentration.

1. Fluorescein fundus angiography (FFA) and indocyanine green angiography: active lesions of ocular toxoplasmosis, fluorescein fundus angiography showed weak fluorescence in the early stage of the lesion, followed by fluorescein leakage, scar lesions Retinal pigment epithelial proliferation may show early weak fluorescence, or manifested as transflective fluorescence due to atrophy of retinal pigment epithelium. Irregular retinal pigment epithelial atrophy and proliferation lead to a mottled appearance, late edge staining, neuroretinitis or nerve Inflammatory patients usually have strong fluorescence at the edge of the optic disc. Patients with retinal vasculitis can see vascular leakage and staining of the posterior vessel wall. It can also be found in intraretinal arteriovenous short circuit, retinal choroidal short circuit, cystoid macular edema, choroidal neovascular membrane and other diseases. Indocyanine green angiography can show weak fluorescence or strong fluorescence in the early stage of active lesions, strong fluorescence in the late stage, and early recurrent lesions that can not be detected by ophthalmoscope and fluorescein fundus angiography.

2. CT and magnetic resonance examination: intracerebral calcification and brain lesions can be found, which is important for the diagnosis of intracranial toxoplasmosis infection.

Diagnosis and diagnosis of ocular toxoplasmosis

diagnosis

Diagnosis of ocular toxoplasmosis should have the following conditions: the clinical course and manifestations of fundus lesions are consistent with the characteristics of the above-mentioned typical ocular toxoplasmosis; serological examination is positive for anti-toxoplasma antibodies; except for other possible causes of fundus-like lesions, due to fundus The clinical manifestations of toxoplasmosis are complicated and often difficult to distinguish from other chorioretinitis. Therefore, laboratory tests and serological antibody determination are the main basis for the diagnosis of this disease. Because there is no significant correlation between the level of antibody and the severity of eye disease, serum Anti-toxoplasma antibody positive, regardless of potency, as long as the typical clinical manifestations and fundus changes, can diagnose ovistoidosis, the comparison of serum antibody to serum antibody is valuable for the diagnosis of ocular toxoplasmosis, in addition Try to rule out other common causes of uveitis, such as choroidal retinitis caused by tuberculosis, syphilis, and viruses.

Fundus fluorescein angiography shows strong fluorescence in active lesions of toxoplasmosis, early leakage and late coloration can be observed in vasculitis, other manifestations include window-like defects, late scleral staining and choroidal neovascularization, optical coherence tomography (OCT) tests showed retinal inflammatory edema, and these tests were not specific for ocular toxoplasmosis.

Differential diagnosis

Neonatal congenital toxoplasma infection should be differentiated from some viral infections (such as rubella virus, cytomegalovirus, herpes simplex virus) and other infections (such as tuberculosis, syphilis, acquired immunodeficiency syndrome), and should also be Retinoblastoma, choroidal defect, permanent primordial vitreous hyperplasia.

According to the clinical manifestations, herpes simplex virus-induced retinitis and toxoplasma are easy to identify, but cytomegalovirus-induced congenital active retinitis or retinitis caused by immunodeficiency patients is sometimes difficult to identify, serological examination And urine tests help to differentiate the diagnosis.

Recurrent ocular toxoplasmosis is sometimes similar to purulent chorioretinitis, with fresh retinal choroidal lesions around the old lesions, but claudication chorioretinopathy often presents a spiral choroidal retinal scar around the optic disc, without Inflammation of the anterior segment of the eye and vitreous, in addition, recurrent toxoplasmic retinal choroiditis should also be associated with herpes simplex virus, herpes zoster virus, cytomegalovirus, etc., retinitis, fungal retinitis, septic retinitis, Identification of retinitis caused by sarcoma, syphilis, tuberculosis, etc.

Cat scratches often manifest as neuroretinitis. Serological tests and specific antibodies are useful for differential diagnosis. Cat scratches can sometimes cause anterior chamber empyema, which is generally not caused by ocular toxoplasmosis.

If the patient has a single large uplifted choroidal inflammatory lesion, it should be considered to distinguish from retinopathy caused by Toxoplasma gondii. Specific antibody detection may be helpful for diagnosis. Indirect ophthalmoscopy is used to find the choroid larvae of the surrounding area for diagnosis. Also helpful.

The punctate outer retinopathy caused by ocular toxoplasmosis should be associated with acute posterior multifocal squamous pigment epithelial lesions, punctate choroidal lesions, multifocal choroiditis, diffuse unilateral subacute neuroretinitis, etc. Identification.

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