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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.
PURPOSE: To describe the course of ocular toxoplasmosis during pregnancy. METHODS: This study was a retrospective, non-comparative case series of four pregnant women who were treated for ocular toxoplasmosis during pregnancy. RESULTS: All of the participants had severe and treatment-resistant toxoplasmic retinochoroiditis during pregnancy, leaving three of them with decreased visual acuity in spite of aggressive therapy. Delivery of the infant appeared to help the recovery in two patients. CONCLUSIONS: Pregnant state may provoke the recurrence of ocular toxoplasmosis.
PURPOSE: To describe a case of recurrent frosted branch angiitis after treatment of ocular toxoplasmosis. METHODS: In a 6-year-old boy, we found perivascular, creamy, patchy, retinal sheathing in both eyes without any focal necrotizing retinochoroiditis or scarring. IgM antibodies for toxoplasma gondii were also found. The patient was treated with antitoxoplasmosis medication and a systemic steroid. RESULTS: Several years after treatment of the toxoplasmosis, frosted branch angiitis occurred twice without any retinal scarring or serological evidence of toxoplasmosis. After systemic steroid therapy, the angiitis improved without further complications. CONCLUSIONS: Toxoplasmic retinal vasculitis should be considered as a cause of frosted branch angiitis.
Clinical toxoplasmosis was diagnosed antemortem in two cats being treated with therapeutic doses of cyclosporin. The diagnosis was made by detecting tachyzoites on cytological examination of bronchoalveolar lavage fluid from one case and pleural effusion from the other. Despite early diagnosis and aggressive treatment in both cases, only one cat survived. Reactivation of latent Toxoplasma gondii infection secondary to cyclosporin-induced immunosuppression was considered likely in both cases. The presence of respiratory signs in cats treated with cyclosporin should alert clinicians to the possibility of clinical toxoplasmosis. Consideration should be given to determining the serostatus of cats to T gondii prior to use of drugs which are potent inhibitors of cell mediated immunity, such as cyclosporin. Two cases of feline toxoplasmosis are presented.
Serum samples from 89 cats with serologic evidence of toxoplasmosis were identified by using an enzyme-linked immunosorbent assay (ELISA) that detected Toxoplasma gondii-specific immunoglobulin M (IgM) or T. gondii-specific immunoglobulin G (IgG). Concurrent feline immunodeficiency virus (FIV) infection was detected in 36 cats using an ELISA for detection of FIV-specific IgG. The majority of the cats in both the FIV-seropositive and FIV-seronegative groups were male and > 5 years of age. FIV-seropositive cats were more likely to have T. gondii IgM titers without IgG (P < 0.05) or any T. gondii IgM titer (P < 0.05) than were FIV-seronegative cats. FIV-seronegative cats (1328) had a higher T. gondii IgG geometric mean titer than did FIV-seropositive cats (724) and were more likely to have T. gondii IgG titers > 1:2048 than were FIV-seropositive cats (P < 0.05). Cats with serologic evidence of both T. gondii and FIV infections had persistent T. gondii IgM titers for > 12 weeks. Lymphoblast transformation in response to concanavalin A, T. gondii-specific intracellular antigens, and T. gondii-specific secretory antigens was compared in T. gondii seropositive and FIV-seronegative cats, cats with serologic evidence of T. gondii infection alone, and cats with serologic evidence of concurrent FIV and T. gondii infections. Lymphocytes from all but one cat in the FIV-seropositive group responded to concanavalin A. Whereas lymphocytes from FIV-seronegative cats with serologic evidence of toxoplasmosis responded to T. gondii-specific antigens, four of five of the FIV-seropositive cats with concurrent serologic evidence of toxoplasmosis did not.
Current therapy for toxoplasmosis with a synergistic combination of pyrimethamine plus sulfadiazine or pyrimethamine plus clindamycin is not always efficacious and is frequently discontinued due to intolerable toxic effects in immunocompromised individuals, particularly those with AIDS. Trovafloxacin, a new fluoroquinolone with potent activity against Toxoplasma gondii, was examined for potential synergistic activity when combined with other drugs used for treatment of human toxoplasmosis. Combinations of trovafloxacin with clarithromycin, pyrimethamine, or sulfadiazine demonstrated significantly enhanced activities compared to those observed with each drug alone. Our results suggest that combinations of trovafloxacin and other anti-toxoplasma drugs should be further explored for treatment of toxoplasmosis in humans.
We characterized antigenic markers recognized by human serum samples from patients presenting with acute and chronic toxoplasmosis by the determination of immunoglobulin G (IgG) antibody avidity by a Western blot modified technique (avidity immunoblotting) that includes the dissociation of the antigen-antibody interaction with 6 or 8 M urea solutions. Human serum samples from 20 patients presenting with recent infection and from 20 patients with chronic infection were analyzed. It was observed that bands p16, p32, p38, p40, p43, p54, p60, p66, and p97 were more frequently recognized by low-avidity IgG in recent infection and by high-avidity IgG in chronic toxoplasmosis. From these antigenic bands, p38 can be characterized as an optimal antigenic marker of low avidity for recent forms of toxoplasmosis due to a significant decrease of their frequencies (from 80 to 0%) after treatment with 6 M urea solutions. The p30 antigen was not considered a good marker to distinguish acute from chronic infection since corresponding IgG antibodies were determined to have high avidity in both phases of the infection. Thus, the avidity immunoblotting assay proved to be a useful tool for determining antigenic markers of recent and chronic phases of Toxoplasma gondii infection.
The avidities of Toxoplasma-specific immunoglobulin G serum antibodies were measured in immunocompromised patients presenting with cerebral or extracerebral toxoplasmosis and/or serological reactivation. Since avidity remained high and stable in 39 of 40 patients with toxoplasmosis and 27 of 28 patients with serological reactivation, we conclude that this test cannot help diagnose toxoplasmosis in these patients.
Enzyme-linked immunosorbent assay (ELISA) for toxoplasmosis was evaluated in serum samples presenting defined toxoplasmosis serological patterns, as determined by results in immunoglobulin (Ig)G and IgM immunofluorescence (IgG-IF, IgM-IF), hemagglutination, and complement fixation tests. ELISA was carried out with alkaline phosphatase-labeled anti-IgG and anti-IgM antibodies. Serum titer was expressed as the serum dilution end point determined by mere observation of color development in the test. A straight agreement was found between IgG-ELISA and IgG-IF titers, both in group A sera of ancient infections (patterns II and III) and group B sera of recent infections (pattern I). A similar agreement was found between IgG-ELISA and hemagglutination titers in group A sera, for which coincident IgG-IF and hemagglutination titers are also frequent. However, in group B sera, in spite of the same toxoplasma extract being used to sensitize both plastic surfaces and erythrocytes, IgG-ELISA titers were much higher than hemagglutination titers, in a way similar to that observed for IgG-IF titers. IgM-ELISA was positive in every group B serum, with higher titers than corresponding IgM-IF titers. Occasional low-titered positive IgM-ELISA results were seen for group A sera, sometimes due to IgM-antiglobulin antibodies. An easy test to perform, ELISA seems to be an adequate substitute for toxoplasmosis IF tests for routine purposes.
A polysaccharide fraction from Toxoplasma gondii was adsorbed to polystyrene plates, and the enzyme-linked immunosorbent assay was performed (poly-ELISA) with peroxidase-labeled anti-immunoglobulin G and anti-immunoglobulin M antibodies. A comparison was made with a T. gondii total protein extract ELISA (protein ELISA) in serum samples presenting different toxoplasmosis serological patterns, as indicated by a battery of tests for toxoplasmosis. Very low titers and negative results were seen for immunoglobulin G poly-ELISA both for serum samples corresponding to ancient or transitional-period infections (serological patterns II and III) and for samples of recent or acute toxoplasmosis (pattern I). On the contrary, immunoglobulin M poly-ELISA furnished high titer results for pattern I sera, and a very close agreement of titers was seen between immunoglobulin M protein ELISA and immunoglobulin M poly-ELISA. When the polysaccharide fraction was added to pattern I sera, a complete blocking of immunoglobulin M antibody reactivity resulted only for poly-ELISA. In the same way, the total protein extract could completely block only reactivity for protein ELISA. In both cases, a limited decrease in titers was observed for respective heterologous assays.
Ocular toxoplasmosis is a potentially blinding intraocular inflammation. The intent of this study was to investigate the role of Fas-FasL interaction in a murine model of acquired ocular toxoplasmosis induced by intracameral inoculation of Toxoplasma gondii. Intraocular inflammation, Fas and FasL expression on lymphocytes and on ocular tissues, the occurrence of apoptosis, and the frequency of CD8(+) and CD4(+) T cells in the infected eyes were analyzed in C57BL/6 (B6) mice. Susceptibility to parasite-induced intraocular inflammation was observed in Fas-deficient (B6-lpr) and FasL-deficient (B6-gld) mice. Inoculation of 5,000 T. gondii tachyzoites induced significant intraocular inflammation associated with increase of Fas and FasL expression in the inoculated eyes of wild-type B6 mice. Flow cytometry demonstrated a significant increase of Fas and FasL expression on the splenocytes from naive mice incubated in vitro with the parasite and on the splenocytes harvested from the infected mice at day 8 after parasite inoculation. Apoptosis of inflammatory cells and cells in ocular tissues was seen, and a greater frequency of CD8(+) than CD4(+) T cells was observed in the infected eyes. The intensity of intraocular inflammation was greater in B6-lpr and B6-gld mice than in wild-type B6 mice (P < 0.05). The results suggest that Fas-FasL interaction associated with apoptosis is involved in the pathogenesis of acquired ocular toxoplasmosis in mice.
Toxoplasmosis is a ubiquitous parasitic infection causing a wide spectrum of diseases. It is usually asymptomatic but can lead to severe ocular and neurological disorders. Among the small-animal models available to study factors that determine susceptibility to toxoplasmosis, the rat appears to be rather similar to humans, particularly in terms of resistance to acute infection. Here, we demonstrate that the Lewis (LEW) rat strain displays an unexpected refractoriness to Toxoplasma infection. Complete resistance was assessed by both negative anti-Toxoplasma serology and lack of detection of the parasite during the course of infection. In this model, sex, age, major histocompatibility complex, and inoculum size had no effect on resistance. Interestingly, progeny from F(1) hybrid crosses between Fischer (F344) or Brown Norway susceptible rats and LEW resistant rats were also fully resistant, showing a dominant effect of the gene or set of genes. Furthermore, resistance of the LEW rat was shown to be dependent on hematopoietic cells and partially abrogated by neutralization of endogenous gamma interferon. To our knowledge, this is the first observation of a rodent strain that is refractory to Toxoplasma infection. This model is therefore an attractive and powerful tool to dissect host genetic factors involved in susceptibility to toxoplasmosis.
Toxoplasma gondii strains were genotyped directly from blood samples of patients with ocular toxoplasmosis. Analysis of nontranscribed spacer 2 revealed that all detected strains belonged to type I, suggesting an association of ocular toxoplasmosis with this type. The method shows the usefulness of blood samples for genotyping in ocular toxoplasmosis.
Toxoplasma immunoglobulin E (IgE) antibodies were evaluated in an immunosorbent agglutination assay (ISAGA) and an enzyme-linked immunosorbent assay (ELISA) to determine their usefulness in the diagnosis of acute infection with Toxoplasma gondii. IgE antibodies were not detected in serum specimens from otherwise seronegative individuals, individuals with chronic toxoplasma infection, or infants without congenital toxoplasmosis. In contrast, they were detected in pregnant women who seroconverted during gestation (100% by ELISA, 63% by ISAGA), patients with toxoplasmic lymphadenopathy (96% by ELISA, 88% by ISAGA), infants with signs of congenital toxoplasmosis which prompted serologic testing in the postnatal period (92% by ELISA, 67% by ISAGA), children and adults with toxoplasmic chorioretinitis (36% by ELISA, 18% by ISAGA), and adult patients with AIDS and toxoplasmic encephalitis (33% by ELISA, 25% by ISAGA). In many of the serum specimens, the titer of IgE antibodies detected by the ISAGA were close to or at the positive cutoff value. The duration of detectable IgE antibodies in patients with acute infections varied considerably among individuals but showed a trend toward a briefer duration by the ISAGA than by the ELISA. These results reveal that recrudescence of IgE antibodies in patients with reactivated chronic infection (toxoplasmic chorioretinitis and toxoplasmic encephalitis) may be useful diagnostically and that demonstration of toxoplasma IgE antibodies is a useful adjunct to currently available serologic tests for the diagnosis of acute toxoplasma infection and toxoplasmosis.
Early diagnosis of congenital toxoplasmosis is rendered difficult when specific immunoglobulin M (IgM) and/or IgA antibodies are absent in the blood of the newborn infant. Since maternal IgG antibodies can cross the placenta, determination of IgG antibodies in newborn infants has hitherto not been used routinely for the diagnosis of congenital infection. The aim of this study was to assess the diagnostic usefulness of an immunoblot assay which compares the early IgG profiles between the mother and her child (comparative IgG profile between mother and child; CGMC test) directed against a total cell lysate of Toxoplasma gondii tachyzoites. Serum samples from 97 newborn infants at risk of toxoplasma infection were obtained from umbilical cord blood at birth or postnatally until 3 months of life and were directly compared with serum samples from the respective mothers. Congenital toxoplasmosis was diagnosed only when IgG-reactive protein bands that were present in any newborn serum samples were absent in the corresponding maternal serum sample. Congenital infection was defined by conventional serological assays when IgM and/or IgA antibodies were present in newborn infant blood or when IgG titers rose within the first 12 months or were persistently stable for more than 8 months. Using these criteria, congenital infection was definitely confirmed in 11 cases. Three additional cases were diagnosed based on indicative data. The CGMC test, which was performed without knowledge of the results of conventional serologal assays, had sensitivity and specificity of 82.4 and 93.0%, respectively, and positive and negative predictive values of 73.7 and 95.7%, respectively. When true positives and true negatives were considered, the comparative IgG profile had a ratio of 90.9% true results. The CGMC test thus is useful as an additional assay for the rapid diagnosis of congenital toxoplasmosis when paired serum samples from mother and child are available.
The most common presentation of symptomatic postnatally acquired toxoplasmosis in immunocompetent patients is painless cervical adenopathy. Acute visceral manifestations are associated in rare cases. We report 16 cases of severe primary toxoplasmosis diagnosed in French Guiana during a 6.5-year period. All of the subjects were immunocompetent adults hospitalized with clinical presentations consisting of a marked, nonspecific infectious syndrome accompanied by an altered general status with at least one visceral localization, mainly pulmonary involvement (14 cases). Acute toxoplasmosis was diagnosed according to the results of serological tests suggestive of recent primary infection and the absence of an alternative etiology. Recovery was rapid following specific antitoxoplasmosis treatment. Thirteen of the 16 patients had consumed game in the 2 weeks before the onset of the symptoms, and in eight cases the game was considered to have been undercooked. Toxoplasma strains, which were virulent in mice, were isolated from three patients. Microsatellite analysis showed that all of these isolates exhibited an atypical multilocus genotype, with one allele found only for isolates of this region.
Disseminated toxoplasmosis is a life-threatening disease in liver transplant recipients that can result from an organ-transmitted infection. We report here a case of fatal disseminated toxoplasmosis after orthotopic liver transplantation from a seropositive donor (immunoglobulin G [IgG](+) and IgM(-)) in a patient who was nonimmune for toxoplasmosis prior to transplantation. Quantitative PCR analyses of various clinical specimens, including serum samples, appeared retrospectively to be a valuable diagnostic tool that might guide therapeutic attitudes.
AIMS: To investigate the efficacy of azithromycin in patients with ocular toxoplasmosis. METHODS: 11 immunocompetent patients with ocular toxoplasmosis were treated with azithromycin (500 mg the first day, followed by 250 mg/day for 5 weeks). Ocular and systemic examinations were performed during active retinitis episodes and all patients were followed for at least 1 year. RESULTS: The intraocular inflammation disappeared within 4 weeks in seven patients, including two cases with progressive retinitis despite previous treatment with pyrimethamine, sulphadiazine, and folinic acid. Recurrence of retinitis occurred in three patients (27%) within the first year of follow up. No systemic side effects of azithromycin were encountered. CONCLUSION: These results indicate that although azithromycin cannot prevent recurrent disease it may be an effective alternative for patients with ocular toxoplasmosis who cannot tolerate standard therapies.