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The biological mothers of 23 patients presenting with acute chorioretinal toxoplasmosis had sera screened for the presence of antibodies to Toxoplasma gondii. Twenty-two of the mothers (96%) had positive serology and one (4%) had negative serology. This is consistent with the hypothesis that most cases of ocular toxoplasmosis are congenital in origin, but indicates that some cases are due to acquired toxoplasmosis.
We report a follow-up after 25 years of a patient with a congenital bilateral ocular toxoplasmosis who developed Fuchs's heterochromic cyclitis in her left eye. Whether Toxoplasma gondii can cause the development of Fuchs's heterochromic cyclitis, as our case suggests, or whether the iridocyclitis is a secondary ocular response to other agents, is not yet clear.
Congenital toxoplasmosis is essentially characterized on the ophthalmological point view by a pathognomonic focus of necrotic chorioretinitis in the cicatricial stage and taking the aspect of a rose-window, which is seen in more than 50% of the cases. The late recurrences of this ocular toxoplasmosis are not rare and may be seen in nearly one third of the cases. They may be due to a congenital toxoplasmic cyst, which may exist in a healthy retina in the absence of any old cicatricial focus.
Infection by Toxoplasma gondii is very common in cats although most remain disease free. The factors that trigger development of uveitis in some cats infected with T gondii have not been elucidated, but infection by more than one organism may be contributory. In this study, cats chronically infected with T gondii were inoculated with Bartonella henselae followed by FHV-1 to test the hypothesis that immune stimulation by multiple infections will reactivate ocular toxoplasmosis. Anterior uveitis and chorioretinitis were not detected in the cats with chronic T gondii infection thus allowing rejection of the hypothesis using this experimental design.
Using a modified enzyme-linked immunosorbent assay that included dissociation of antigen antibody complexes with 6M urea solution, we analyzed the avidity of Toxoplasma-specific IgG in aqueous humor and serum samples from 24 patients with toxoplasmic chorioretinitis. As a control, we studied aqueous humor and serum samples from 14 cataract patients without history of uveitis and serum samples from 10 patients with recent primary systemic toxoplasmic infection without ocular lesions. IgG avidity was markedly lower in aqueous humor samples from patients with toxoplasmic chorioretinitis than in serum samples, despite those samples presenting higher levels of Toxoplasma-specific IgG than in serum samples. The detection of the low-avidity Toxoplasma-specific antibodies can offer a valuable aid to make a specific etiologic diagnosis and perhaps contribute to understand the pathogenic mechanisms of ocular toxoplasmosis.
High seroprevalence of Toxoplasma and Toxocara spp. in populations of children and adults in Poland constitutes a significant risk of supradiagnosed parasitic eye infections. We described the clinical characteristics in relation to the analysis of comparative immunological profiles of T. gondii-specific antibodies in aqueous humour and serum samples in patients with reactivated retinochoroiditis, and of Toxocara spp. ones in cases with posterior granuloma, fibrotic and calcified tumor-like masses simulating retinoblastoma, detected by ophthalmoscopy and echography. Intraocular synthesis of specific IgG antibodies was detected in anterior eye chamber fluid in 1/2 and 2/3 of patients respectively, strongly suspected of ocular toxoplasmosis or toxocarosis. The evidence of a local production of specific antibodies in intraocular fluid shown by the Western blot seems to be a valuable immunodiagnostic method for a final confirmation of eye lesions of parasitic origin and crucial in the choice of an appropriate treatment regimen.
BACKGROUND: Toxoplasmosis is a leading cause of retinochoroiditis. Conventional multidrug therapy using sulfadiazine, pyrimethamine, and folinic acid is increasingly difficult to procure and administer safely. METHODS: To evaluate the efficacy of trimethoprim-sulfamethoxazole, a fixed-combination antibiotic, patients with active toxoplasmosis were treated with trimethoprim-sulfamethoxazole (Bactrim DS) with or without adjunctive clindamycin and prednisone for 4 to 6 weeks. RESULTS: All patients in this study (n = 16) had resolution of active retinochoroiditis and had improved vision, with an average gain of 5.2 lines of vision. Two patients developed a drug allergy. CONCLUSION: Trimethoprim-sulfamethoxazole appears to be a safe and effective substitute for sulfadiazine, pyrimethamine, and folinic acid (Leucovorin) in treating ocular toxoplasmosis.
OBJECTIVE: The study was to evaluate the diagnostic efficacy of nested polymerase chain reaction (nPCR) using primers targeting B1 gene of Toxoplasma gondii (T. gondii) with Witmer Desmonts coefficient (WDC) technique in intraocular fluids of clinically suspected toxoplasma retino choroiditis (TRC) patients. MATERIALS AND METHODS: Two hundred and seventy eight specimens from 189 patients (25 TRC patients and 164 controls) consisting of 189 serum samples and 89 intraocular fluids were included in the study. The clinical specimens were categorized into TRC patients (typical TRC lesion-group I & atypical TRC lesion-group II) and controls (voluntary blood donors-group III, patients undergoing uncomplicated cataract surgery-group IV, ocular inflammation of non-toxoplasma origin-group V). Detection of anti T. gondii IgG and IgM antibodies in serum samples and intraocular fluids were performed and WDC was calculated by the standard method. The standardized nPCR was applied on the 89 intraocular fluids. RESULTS: Clinical diagnosis of TRC based on fundus examination was considered to be the "gold standard." Anti T. gondii IgG/IgM antibodies were detected in serum by ELISA in 95.6% of 25 clinically suspected TRC patients (gp I and II), 28% of gp III, 40.4% of gp IV, and in 58.3% of gpV. Witmer Desmont's coefficient was positive in 72.7% (16/22) and nPCR in 59.1% (13/22) of TRC patients (gp I and II). Both WDC and nPCR were negative in all the controls. The difference in sensitivity of WDC and nPCR was not statistically significant (p=0.5247). CONCLUSIONS: Though both WDC and nPCR were reliable diagnostic techniques for ocular toxoplasmosis, nPCR is more acceptable because of the amount of specimen(s) required, rapidity, cost effectiveness, and direct evidence of T. gondii DNA in the intraocular fluids.
Seventeen patients with active toxoplasmic retinochoroiditis were treated for four weeks, seven with clindamycin alone and ten with a combination of clindamycin and sulfadiazine. The follow-up period ranged from six months to four years. Results of the Sabin-Feldman dye test were positive in all patients. Five of the seven patients treated with clindamycin alone showed improvement two weeks after treatment was begun, while eight of the ten patients treated with combined clindamycin and sulfadiazine showed both subjective and objective improvement within ten days and signs of healing within three weeks. Since clindamycin and sulfadiazine operate on unrelated metabolic pathways of Toxoplasma, they may act synergistically. A regimen consisting of this combination may be appropriate for the treatment of ocular toxoplasmosis.
The clinical aspect of congenital toxoplasmosis is sometimes typical, sometimes atypical. The advantage of the serological study of the aqueous is an early diagnosis and an early treatment for less expense. The classical treatment relies on the therapeutic association Pyrimethamine + Adiazine + corticosteroids which will be used during acute phases, at ordinary doses, but may be prolonged further over many months in difficult cases. Severe forms are those that are spontaneously severe or increased with the exclusive use of corticosteroids in previous attacks, noticeably when injected by local route, and in bilateral forms. Prevention of ocular toxoplasmosis is represented by the detection of sero-conversion in mother and treatment in the newborn. Due to the legal aspect of this procedure in France, the incidence of congenital toxoplasmosis has already decreased during the past years and will continue to diminish in the next future. However the possibility of acquired forms cannot be excluded, even in non immuno-depressed patients.
Six monkeys had prior systemic immunization followed by intraretinal challenge to each eye with Toxoplasma antigens. All eyes developed iridocyclitis, vitritis, and retinal edema, but no necrotizing retinochoroiditis. One-half of the eyes were then challenged with living organisms and the other one-half with Toxoplasma antigens. All eyes developed iridocyclitis, vitritis, and retinal edema, but no necrotizing retinochoroiditis. Four months later, the right eye of each monkey was challenged with living Toxoplasma organisms injected intraretinally. Each injected eye developed iridocyclitis, vitritis, and retinal edema 24 hours after injection, and all developed a retinal vasculitis 6 days after injection. One injected eye developed a papillitis. A subcutaneous booster of living Toxoplasma organisms in four of the monkeys failed to produce a reactivation of the iridocyclitis, vitritis, and vasculitis. These findings suggest that hyperimmunization provides protection against the development of a necrotizing toxoplasmic retinochoroiditis in nonhuman primates and that it may lead to retinal vasculitis and iridocyclitis. This study also serves as an animal model of retinal vasculitis in ocular toxoplasmosis.
BACKGROUND: Cytomegalovirus (CMV) and Toxoplasma gondii both cause necrotizing retinopathy in immunosuppressed hosts. Because of the high prevalence of serum antibodies to these agents in the general population and the risks associated with retinal biopsies, diagnosis of these infections is usually based on clinical findings alone, but the two infections can be confused with one another because of similar clinical features. Accurate diagnosis is critical, however, because both diseases are treatable but require different medical therapies. METHODS: Case histories were reviewed for five immunosuppressed patients with necrotizing retinopathy, which was initially diagnosed incorrectly as CMV retinopathy but was subsequently found to be toxoplasmic retinochoroiditis. Correct diagnosis was based on retinal biopsy (2 cases) or rapid response to antiparasitic drug therapy (3 cases). Factors were sought that might help differentiate toxoplasmic retinochoroiditis from CMV retinopathy at presentation. RESULTS: In all cases, the character of retinal opacification (densely opaque, thick) and the appearance of lesion borders (smooth, nongranular) was different from that typically seen with CMV retinopathy. These cases also were characterized by prominent anterior chamber and vitreous inflammatory reactions (four of five cases) and relative lack of retinal hemorrhage. One patient subsequently developed CMV retinopathy; characteristics of the two lesions in the same eye highlighted the differences between these two infections. CONCLUSION: Clinicians should consider ocular toxoplasmosis as a cause of necrotizing retinopathy in immunosuppressed patients and consider an empiric course of antiparasitic therapy for lesions with features described in this report.
PURPOSE: To ascertain the clinical features, visual outcome, and recurrence rates of ocular toxoplasmosis (OT) in a large series of patients. To determine the efficacy of various treatment strategies and identify the patients at risk of visual loss. DESIGN: Retrospective noncomparative observational case series. PARTICIPANTS: One hundred fifty-four consecutive patients with active lesions of OT (first attack and/or recurrence) were identified in a cohort of 1300 consecutive patients with uveitis. Mean follow-up was 5.8 years. INTERVENTION: A review of the medical records of 154 patients with active OT. MAIN OUTCOME MEASURES: Patients were subdivided according to clinical and laboratory criteria. Numerous variables were compared per patient and group, including age and gender distribution, onset and course of infection, clinical ocular features, laboratory data, therapeutic strategies and their outcomes, number of recurrences, complications, final visual acuity, and features associated with poor visual outcome. RESULTS: Primary retinal lesions were observed in 28% and a combination of active lesions and old retinochoroidal scars in 72% of the patients at first presentation to the ophthalmologist. Mean age at first presentation with an active OT lesion was 29.5 years. Patients with primary OT were older than those with a combination of active lesions and old scars (P < 0.001). Serologic characteristics of the acute phase of systemic infection were found in 11% of the patients. Ocular involvement in these patients was associated with advanced age at onset (P < 0.001) and was characterized by severe intraocular inflammation. Most (82%) of the patients with serologic characteristics of the acute phase of systemic infection had primary lesions (compared with 23% of OT in the chronic phase of systemic infection; P < 0.001). Extensive retinal lesions were more frequently observed during the acute phase of systemic infection (P = 0.02) and in patients with primary OT (P < 0.04). Recurrences, which developed in 79% of all patients followed for more than 5 years, were located predominantly in previously affected eyes (with old scars) in contrast to the sporadic cases of recurrence in the healthy contralateral eye (P < 0.0001). Standard short-term therapeutic modalities had no effect on visual outcome or future recurrence rates. Legal blindness in one or both eyes was confirmed for 24% of the patients. Blindness of both eyes was more frequent in patients with congenital OT (P < 0.001). Risk factors for visual loss included congenital infection, OT manifesting during the acute phase of systemic infection, central location and/or extensive retinal lesions, and the administration of corticosteroids without a shield of antiparasitic drugs. CONCLUSIONS: Legal blindness in at least one eye developed in 24% of the patients with OT. Recurrences, which developed in 79% of the patients with long-term follow-up, were located predominantly in eyes with toxoplasmic scars. Various short-term therapeutic modalities had no effect on visual outcomes or future recurrence rates, with the exception of a poor visual outcome for patients who received corticosteroids without a shield of antiparasitic drugs.
In vitro lymphocyte proliferative responses to purified toxoplasma antigens and the retinal S-antigen were evaluated in 40 patients with ocular toxoplasmosis; 16 (40%) had a positive in vitro response to the retinal S-antigen. The proliferative responses to the 2G11 (p22) toxoplasma membrane antigen approached that of a crude antigen preparation of Toxoplasma gondii, whereas the response to the 1E11 immunodominant p30 membrane antigen was considerably less striking. HLA typing was also performed, and none correlated to S-antigen or toxoplasma reactivity. The evidence strongly suggests that patients with a clearly infectious ocular disorder may have part of their disease mediated by a putative autoimmune mechanism. An immune response to the 2G11 toxoplasma antigen may increase the risk of developing ocular disease or a substrain of toxoplasma with 2G11 as its immunodominant membrane antigen may have a greater affinity for the retina.
BACKGROUND: Ocular disease is a frequent manifestation of congenital Toxoplasma gondii infection. There are only limited data available in the literature concerning early stages of this disease in fetuses and infants. The purpose of our study was to characterize histopathological features in the eyes of 10 fetuses and 2 infants with congenital toxoplasmosis. METHODS: Fifteen eyes from 10 fetuses, 3 eyes from 2 premature infants, and both eyes from a 2-year-old child with congenital toxoplasmosis were examined by light microscopy. Immunohistochemical analysis to identify inflammatory cells and T gondii antigens was performed. The findings in infected eyes were compared with those of age-matched control eyes. RESULTS: Retinitis (10/18 eyes), retinal necrosis (4/18 eyes), disruption of the retinal pigment epithelium (12/18 eyes), and choroidal inflammation and congestion (15/18 eyes) were characteristic findings. Optic neuritis was present in 5 of 8 fetal eyes with associated optic nerve available for evaluation. An eye obtained from a 32-week-old fetus showed retinal rosettes at the edge of a scar. T cells predominated in retinal lesions and choroid. Parasites were identified by immunohistochemical analysis in 10 of 18 eyes. CONCLUSIONS: Ocular toxoplasmosis causes irreversible damage to the retina in utero. The fetus and infant mount inflammatory responses that may contribute to ocular damage. These findings have important implications for serological screening programs and in utero therapy.
Toxoplasmosis accounts for 1-3% of ocular infections in patients with AIDS1. There are a variety of clinical manifestations that can be confused with other ocular disease. It may be the first manifestations of intracranial and disseminated Toxoplasma gondii infection. Prompt recognition and early treatment with antiparasitic drug therapy will prevent widespread tissue destruction, preserve vision and reduce dissemination. This current review will provide a broad-based overview of toxoplasmosis and ocular infection.
The limitations of serological assessment in toxoplasma infection of the eye are well recognised, but the predictive value of clinical examination is not defined. We undertook a prospective investigation into the role of clinical examination and of serological findings in cases of suspected toxoplasma infection of the eye by means of the dye test and multiple IgM assays. Seventy-four cases of retinal disease and 202 control patients were studied. Patients with retinal disease had a significantly higher incidence of toxoplasma seropositivity than the control group. This was because some patients with retinal disease had acquired the infection congenitally. Half the patients investigated for toxoplasmosis were seronegative. Possible explanations for these findings included misdiagnosis, clinical uncertainty, or, the use of serology testing in the confirmation of other diseases. An excess of IgM reactivity among the retinal disease group may indicate low level immunoglobulin-M production associated with an acute exacerbation of ocular toxoplasmosis. There is a need to consider invasive procedures in cases of ocular infection and for novel techniques to aid the diagnosis of toxoplasma retinochoroiditis.