[Chorioiditis, chorioretinitis].
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Uveitis is the term used to describe most intraocular inflammations. The classification of uveitis into anterior, posterior and diffuse is based on the physical appearance of an inflamed eye. Diagnosis is usually on the basis of a thorough history, a review of systems to uncover any systemic diseases known to be associated with uveitis and a complete eye examination. We review the most common types of uveitis, the pertinent laboratory investigations and different therapeutic aspects.
Toxoplasmosis is a worldwide health problem. Infection of a pregnant woman can result in severe fetal morbidity or in subclinical neonatal infection; most subclinical cases will develop ocular and neurological sequelae. Fetal infection and clinical outcome is related to when in pregnancy toxoplasmosis was acquired. The risk of transmission increases from 14% in the first trimester to 29% in the second and 59% in the third. Conversely, clinical damage decreases from about 80% in the first to 10% in the third trimester, but up to 50% of patients with subclinical congenital toxoplasmosis will develop neurologic and ocular sequelae. Congenital toxoplasmosis can be prevented by identification of non immune women at the beginning of pregnancy, by giving information on how to avoid the infection and by a serological follow-up until the delivery. Serological follow-up is based on repeated testing for specific IgG and IgM, but other serologic methods are necessary to differentiate between acute and chronic infections and possibly on a single serum sample. Procedures to detect fetal infection are ultrasound examination, cordocentesis and amniocentesis; prenatal diagnosis relies on demonstration of toxoplasma in fetal blood or amniotic fluid by mouse inoculation. Very promising results have recently obtained by the PCR-method applied to amniotic fluid samples. All strongly suspected cases of acquired toxoplasmosis in pregnancy have to be treated.
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Focal encephalitis occurred in a girl with activation of chorioretinitis which on clinical and serological grounds was taken to be caused by toxoplasma. The encephalitis and acute ocular inflammation resolved with treatment with pyrimethamine and sulphadiazine. This is presumably an example of reactivation of congenital cerebral toxoplasmosis.
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The eye manifestations of congenital toxoplasmosis were investigated in 38 infants and children. Diagnosis of the congenital ocular lesions was established clinically, using also X-ray, computed tomography and ultrasonography, and confirmed by two immunodiagnostic techniques. Infants and children were examined when one or more characteristic manifestations of ophthalmic disorders were present. Typical symptoms and signs can present at birth or appear later in life. The multiplicity of clinical manifestations is characteristic of the disease. The most common symptom was chorioretinitis (92%), associated in 71% of the cases with other ocular lesions, and the second most common symptom was microphthalmia and strabismus. The inflammatory process also involved the anterior segment of the eye: iridocyclitis, cataract, glaucoma. Other rare findings were hydrocephalus, calcification in the brain, paresis, epilepsy and diminished visual acuity. The study showed that transplacental transmission of Toxoplasma to the fetus can have severe clinical consequences and terminate in fatal ocular impairment.
PURPOSE: To report the association of Fuchs heterochromic cyclitis (FHC) and ocular toxocariasis in a young adult. DESIGN: Observational case report. METHODS: A 26-year-old patient was referred for the management of a unilateral intermediate uveitis associated with a lower peripheral subretinal fibrotic lesion near the pars plana. Diagnosis of FHC was clinically confirmed. Laboratory examination was performed to exclude an infectious condition. RESULTS: LISA assay detected significant levels of IgG directed against Toxocara canis. Toxoplasmic serology was negative, excluding this differential diagnosis. Other examinations, including complete blood cell count, urinalysis, serum angiotensin-converting enzyme, lysosyme, chest CT scan, and syphilis serology were noncontributive. CONCLUSIONS: Previous studies have reported on the association of FHC and other parasitic conditions, such as toxoplasmosis but also on herpetic ocular infections. Serologic analysis for toxocariasis may be proposed in patients with FHC and retinal scars in the absence of toxoplasmosis.
AIM: To compare the clinical findings in children with symptomatic toxoplasmic ocular lesions attributable to infection acquired before or after birth. METHODS: Cases were prospectively ascertained for 24 months through national surveillance units and reference laboratories in the British Isles. Age and presenting symptoms, site of lesion and visual impairment in children who were classified as acquiring infection either before or after birth on the basis of clinical and serological findings were compared. RESULTS: 31 children had toxoplasmic retinochoroiditis, 15 had congenital infection and all but three of these presented before the age of 4 years. The remaining 16 children acquired toxoplasmosis postnatally, and 14 of 16 presented after the age of 10 years. A further four children had retinochoroiditis due to other causes. The presence of bilateral, multiple or posterior pole lesions did not distinguish between the two groups, but most children (16/19; 84%) presenting with acute ocular symptoms had postnatally acquired infection. Unilateral visual impairment (Snellen < or =6/18) was equally prevalent in the two groups (4/9 before birth v 7/16 after birth; p>0.5). Only two children had bilateral visual impairment, both of whom had congenital infection. No child was blind. CONCLUSIONS: About 50% of children with ocular lesions due to toxoplasmosis had postnatal infection. Retinochoroidal lesions due to infection before and after birth were indistinguishable. The prognosis for bilateral visual function was good, regardless of when infection was acquired.
Toxoplasma infection is associated with acquired immune deficiency syndrome (AIDS), pregnancy, chorioretinitis, etc. Since the number of AIDS patients is increasing rapidly in Thailand and there are few reports about T. gondii immune status in this country. Toxoplasma-specific IgG and IgM antibodies (Ab) were determined in healthy persons and patients with different symptoms who were suspected of toxoplasmosis. Specific IgG Ab were detected in 3.2% of healthy persons, 12.5% of patients with ocular disease and in 42.5% in HIV positive patients. Only 3.1% of patients with ocular disease were positive for specific IgM Ab. No specific IgM Ab were found in the other samples studied.
The authors conducted a retrospective analysis of 201 patients with intermediate, posterior or panuveitis to determine the most frequent etiologies and collect some epidemiological data. A specific diagnosis was made in 70% of the cases: 35% were of infectious origin, 23% were associated with a systemic disease and 24% had a specific ocular condition. The most common entities included toxoplasmosis (24%), sarcoidosis (7.5%) and Behçet disease (5.5%). Birdshot retinochoroidopathy was the most frequent specific ocular disease (3.5%). The findings of this study are compared with those previously published in the literature.
PURPOSE: To report a case of toxoplasmosis with optic nerve and orbital involvement as the initial presentation of HIV infection. METHOD: Case report. RESULTS: A 46-year-old zookeeper, who had had right central retinal vein occlusion (CRVO) 2 weeks previously, presented with painless lid and conjunctival swelling and profound visual loss in his right eye (RE). Examination revealed no light perception (NLP) RE with axial proptosis and ocular motility restriction; fundal examination revealed a clinical picture of an ischaemic CRVO. MRI of the brain and orbit showed ring-enhancing targetoid lesions in the brain and inflammatory changes in the right optic nerve, extraocular muscles and orbital fat. He was subsequently found to be HIV positive and had positive toxoplasma IgG serology. CONCLUSIONS: Immunocompromised individuals have an increased likelihood for more severe and atypical presentations; this highlights the need for increased index of suspicion for HIV infection as ocular or orbital disease may be the first manifestation of life-threatening systemic toxoplasmosis.
An outbreak of systemic toxoplasmosis occurred in October 1977 in Atlanta, Georgia. Thirty-seven people became ill and/or had serologic evidence of acute infection. Epidemiologic study by the Center for Disease Control (CDC) suggested that toxoplasma oocysts from infected cats in a riding stable were the source of infection. Aerolization of oocysts or hand-to-mouth contact were the presumptive means of transmission. All patients were examined and followed for over a year, without evidence of toxoplasma retinochoroiditis. In a four-year follow-up study, only one patient had shown evidence of ocular disease. This suggests that at least some sporadic cases are due to acquired toxoplasmosis.
INTRODUCTION: Toxoplasma gondii is a ubiquitous parasite of all species of mammals and birds (1). Most often the infection in the immunocompetent persons is asymptomatic. Symptoms (if present) are usually mild and self-limited. Infection in the fetus and immunodeficient patients may lead up to clinically severe and often fatal toxoplasmosis (2). ETIOLOGY: Toxoplasma exists in three forms: oocysts, tissue cysts and tachyzoites. The definitive hosts of Toxoplasma are members of the cat family. They shed unsporulated oocysts in the feces. After sporulation oocysts become infectious. Tachyzoites are crescent-shaped forms responsible for manifestations of acute Toxoplasma infection in the intermediate hosts (6,7). Cysts are formed, particularly in brain, heart muscle and skeletal muscles. The cyst forms of the parasite are seen in the latent stage of the infection. Postnatally acquired toxoplasmosis is a consequence of infection from cysts (by ingestion of undercooked meat of infected animals), oocysts (by ingestion of soil, fruits, vegetables contaminated by cat feces) and tachyzoites (by blood transfusion). Congenital Toxoplasma infection causes congenital toxoplasmosis. PATHOGENESIS: Some authors represented the concept that latent (chronic) infection with Toxoplasma during pregnancy can result in congenital infection in the offspring (8-11). Now it is generally agreed that congenital transmission of Toxoplasma occurs only when the infection is acquired during gestation (6,7, 12-16). More than half of the fetuses escape infection, one-third are definitely infected, and the infection is more often subclinical than clinically obvious (15). The fetus is infected hematogenously from inflammatory foci in the placenta formed during parasitemia in the mother. CLINICAL MANIFESTATIONS: Approximately 75% of congenitally infected newborns are asymptomatic. Wilson's study indicates that nearly all such children will develop adverse sequelae (neurologic, intellectual, audiologic and ophthalmologic) 21). Severe forms of congenital toxoplasmosis occur only in 10% of infected offsprings. Clinical manifestations of congenital toxoplasmosis are different. Clinical findings in patients with congenital toxoplasmosis may include: chorioretinitis and other ocular findings, central nervous system abnormalities (such as microcephaly, hydrocephalus, encephalomyelitis, seizures and mental retardation), icterus, hepatosplenomegaly, rash, anemia, erythroblastosis, thrombopenia. INCIDENCE: Incidence of human congenital toxoplasmosis is different in different countries. The incidence in Britain is 0.6 subclinical infection and 0.09 severe illnesses per 1000 births (22). The incidence in USA is between 1/1000 and 1/8000 live births (23). In France the incidence is 1/2000. In Slovenia the incidence is 2.3 cases per 1000 births (25). DIAGNOSIS: Diagnostic methods are: 1. Isolation of the parasite from the placenta, blood, body fluids (by inoculation of specimens into mice or tissue cultures). 2. Histologically by demonstration of tachyzoites in tissue sections or smears of body fluids. 3. Serologic diagnosis. The most important diagnostic methods are serologic tests. For diagnosis of congenital toxoplasmosis determination of IgM antibody (in the serum of newborn infant) has the greatest importance. The fetus is able to produce IgM specific antibody. The presence of IgM antibodies in serum obtained from the neonate is an evidence of fetus infection in utero. Maternal IgM antibodies do not pass the placenta. IgM antibodies may be demonstrable by indirect fluorescent antibody test (IgM-IFA), enzyme linked immunosorbent assay (IgM-ELISA), double sendwich IgM enzyme-linked immunosorbent assay (DS-IgM-ELISA), IgM immunosorbent agglutination assay (IgM-ISAGA) and reversed enzyme immunoassay (REI). For diagnosis of congenital toxoplasmosis the next tests are also applied: Sabin-Feldman Dye test, indirect fluorescent antibody test for IgG antibodies (IgG-IFA) and enzyme
A gross, light, and electron microscopic study of the eyes from 35 consecutive autopsy cases of the acquired immune deficiency syndrome revealed cotton-wool spots (71% of cases), retinal hemorrhage in areas without cytomegalovirus infection (40%), cytomegalovirus retinitis (34%) with associated retinal detachment, Roth's spots (23%), retinal microaneurysms (20%), papilledema (14%), conjunctival Kaposi's sarcoma (9%), cryptococcal chorioretinitis (6%), Mycobacterium avium-intracellulare in retina and in choroidal granulomas (6%), ischemic maculopathy (6%), bilateral keratitis (3%), and herpes simplex retinitis (3%). Ocular infection with candida or toxoplasmosis were not found in this autopsy series. Immunocytologic studies demonstrated deposition of immunoglobulins in arteriolar walls, consistent with immune complex mediated disease. Ultrastructural studies showed a vasculopathy in the areas near cotton-wool spots. A mechanism is proposed linking the deposition of immune complexes with subsequent small vessel lesions, ischemia, cotton-wool spots and later spread of cytomegalovirus to retina via damaged vascular endothelium.
Many persons infected with Toxoplasma gondii develop ocular lesions. Immunologic parameters in the response to T. gondii were evaluated in infected persons with and without ocular lesions and in noninfected controls. Subjects were divided into groups on the basis of presence of serum antibodies to T. gondii, presence of ocular lesions, and clinical history. Production of interleukin-2 and interferon-gamma by peripheral blood mononuclear cells from patients with probable congenital toxoplasmosis was decreased, compared with that in persons with presumed acquired infection. Cell proliferation and delayed-type skin reaction induced by soluble toxoplasma tachyzoite antigen followed the same pattern. Asymptomatic persons showed high levels of interleukin-12 and interferon-gamma, whereas persons with ocular lesions had high interleukin-1 and tumor necrosis factor-alpha responses toward soluble toxoplasma tachyzoite antigen. These data suggest that patients with ocular disease due to congenital infection show tolerance toward the parasite. Furthermore, susceptibility to ocular lesions after acquired toxoplasmosis is associated with high levels of interleukin-1 and tumor necrosis factor-alpha, whereas resistance is associated with high levels of interleukin-12 and interferon-gamma.
HISTORY AND GENERAL INVESTIGATIONS: In February 1993 a 53-year-old immunocompetent man presented at our department with blurred vision on the right eye for 6 weeks. Following a journey to Guatemala in November 1992 he had developed undulating fever up to 40 degrees C (later subfebrile temperature) with loss of weight (15 kg), dysesthesia mainly in the feet and general weakness. He was hospitalized at a general hospital and treated with different antibiotics. Various examinations showed normal results, like cranial computer tomography, and serological tests for virus, bacteria or malaria. Only the transaminases and the borrelia serology (IgG: 1:80, IgM:neg.) were slightly elevated, and the abdominal sonography revealed a moderate hepatomegaly. OPHTHALMOLOGICAL FINDINGS: Visual acuity was 1.0 in both eyes. The right eye showed fatty retrocorneal precipitates, cellular infiltration of the anterior chamber and vitreous and a focal retinochoroiditis next to the superior temporal vessels (Fig. 1a), with corresponding defect in visual field and nerve fiber layer (Fig. 1b, c). Serology established the diagnosis of an acute generalized toxoplasmosis (IgM ISAGA i.S.: 1:1,600; IgM-AK IFT i.S.: 1:128, KBR i.S.: 1:320). THERAPY AND CLINICAL COURSE: After adequate chemotherapy ocular symptoms and dysesthesia improved rapidly. The temperature stayed low and the liver parameters returned to normal. CONCLUSION: The ophthalmoscopic finding of an acute focal retinochoroiditis played an important role for the diagnosis of an acute generalized toxoplasmosis in a patient with fever of unknown origin. Ocular manifestation is rare in acute generalized toxoplasmosis.
Toxoplasmosis is a common opportunistic pathogen in patients with acquired immunodeficiency syndrome (AIDS). It usually presents with ocular, central nervous system, or pulmonary disease. Gastric toxoplasmosis is uncommon in AIDS patients, especially in the absence of central nervous system manifestations. In the few reported cases, patients have presented with abdominal pain and other digestive complaints that usually are attributed to the more common gastrointestinal manifestations of human immunodeficiency virus infection. We describe a 49-year-old man with AIDS who presented with abdominal pain, diarrhea, dry cough, and systemic symptoms and was diagnosed with toxoplasmosis by a gastric biopsy.