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PubMed2005

[Diagnostic difficulties of Toxoplasma gondii infection in pregnant women. Is it possible to explain doubts by polymerase chain reaction?].

OBJECTIVES: Toxoplasma gondii infection during pregnancy is still a difficult problem in the contemporary perinatology. Difficulties met during interpretation of serological tests carried out in pregnant patients to detect Toxoplasmosis implies more and more frequent use of the Polymerase Chain Reaction (PCR). DESIGN: To evaluate the dependence between serological tests and quantity of the Toxoplasma gondii genomes in mothers' blood and amniotic fluid or neonatal blood, the quantitative PCR (q-PCR) method was applied. MATERIALS AND METHODS: The analysis was performed in 81 pregnant women. Maternal blood, amniotic fluid and newborns' umbilical blood samples were evaluated for the presence of Toxoplasma gondii DNA. IgG and IgM Toxoplasma gondii antibodies were evaluated by the ELISA method. RESULTS: High seroprevalence (51.9%) of the Toxoplasma gondii was confirmed. Toxoplasma gondii genetic material in blood and/or amniotic fluid was found in 33 patients. It was stated that quantity of the protozoa and anti-IgM presence in mothers' blood are the factors influencing significantly the Toxoplasma gondii manifestation in amniotic fluid. CONCLUSION: High suitability of PCR in diagnosis of Toxoplasmosis during pregnancy and vertical transmission was confirmed.

Adult↗

PubMed1979

Serological cross-reactions between toxoplasma and hammondia.

Toxoplasma and Hammondia infected mice, dogs, rabbits, and pigs were tested for Toxoplasma antibodies by means of 5 serological methods. All Toxoplasma infected animals showed Toxoplasma-specific antibodies. Only sera of Hammondia infected mice and dogs showed positive serological reactions with Toxoplasma antigen in the SFT, CFT, and ELISA. IFAT and IHA, however, proved to be Toxoplasma-specific. The influence of Hammondia infections on the Toxoplasma serology is discussed.

Animals↗

PubMed1984

Toxoplasmacidal activity of Obioactin derived from hydrolyzed Toxoplasma immune bovine serum in heterologous cell cultures.

Serum samples were collected from Toxoplasma-infected cattle after challenge and 24 h after Toxoplasma lysate injection. They were hydrolyzed with proteinase, HCl and NaOH. Then substances 3,000 to 5,000 in molecular weight were obtained from fractionation by chromatography. Native serum was collected from cattle immune only to Toxoplasma was affected in homologous bovine monocytes. Of the hydrolyzed fractions, one termed Obioactin inhibited the growth of Toxoplasma in heterologous cells, such as mouse macrophages and kidney cells, canine monocytes, and human heart and brain cells. Its toxoplasmacidal activity was presumed to be derived from its non-specific cell potentiating effects. In mice immunized to Toxoplasma peritoneal macrophages released about 10 times as much superoxide (O-2) and hydrogen peroxide (H2O2) as glycogen-elicited macrophages in normal mice. The release of O-2 and H2O2 from glycogen-elicited and resident macrophages in normal mice showed a tendency to increase up to 72 h of incubation with 0.5% Obioactin . No changes in the O-2 and H2O2 release were found in kidney cells during the period of incubation with Obioactin . In those immunized mice activated macrophages and kidney cells inhibited the intracellular multiplication of Toxoplasma parasites remarkably. It was suggested that the increase in O-2 and H2O2 generating activity in the macrophages might be associated with the enhancement of antitoxoplasmatic activity. The mechanism of inhibition of Obioactin , however, might be different from that of mouse macrophages on the multiplication of Toxoplasma in mouse kidney cells.

Animals↗

PubMed1984

Experimental concomitant toxoplasma and malaria infection in rats.

The effect of concomitant toxoplasma and malaria infection on the reticuloendothelial system was investigated in rats. This was evaluated by the level of plasmodial parasitaemia; humoral antibody response; effect on splenic weight; histopathological changes in thymus and spleen; histopathological and histochemical changes in liver. The parasitaemia appeared after 2 days in single malaria and concomitant infections. The peak was reached after 6 days with single and precedent malaria, and after 10 days with precedent toxoplasma. The clearance of parasitaemia was delayed to 30 days with concomitant infections instead of 14 days with single malaria. Higher than normal malarial antibody levels were reached with precedent toxoplasma, while the toxoplasma antibodies were lower than normal in both concomitant infections. There was a significant increase in splenic weight in both precedent malaria and toxoplasma, followed by a decrease which did not return to normal in case of precedent malaria. The thymus was packed with thymocytes in precedent malaria, while depletion in the cortex occurred in precedent toxoplasma. In the liver, there was glycogen depletion and decrease in succinic dehydrogenase activity in both concomitant infections. Choline esterase activity in precedent malaria was decreased and returned to normal on day 40 while in precedent toxoplasma the activity was normal all through the period. The alkaline phosphatase activity was decreased and returned to normal on day 40 in both concomitant infections.

Animals↗

PubMed1980

Vital fluorescence microscopy of lysosomes in cultured mouse peritoneal macrophages during their interactions with microorganisms and active substances. III. Interactions of macrophages with endozoits of Toxoplasma gondii RH strain and their soluble substance.

Macrophages with lysosomes pinpointed by quinacrine-induced fluorescence were infected with the endozoits of Toxoplasma gondii RH strain (peritoneal exudate of infected mouse), or treated with liquid (acellular) fraction of the same exudate. Dead toxoplasmas ingested by macrophages come into contact with the stained lysosomes of the cell and acquire a diffuse fluorescence. Viable toxoplasmas do not give fluorescence, which means that they do not come into contact with lysosomes, either primary or secondary. This supports the hypothesis that toxoplasmas can prevent lysosomes from fusing with the phagosomes of the host cell. Moderate doses of soluble products of toxoplasmas contained in peritoneal exudate cause an excessive output of macrophage lysosomes which points to the activation of macrophages; high doses of challenge inhibit the phagocytosis of toxoplasmas and damage macrophages. The pathogenicity of toxoplasmas due to their ability to inhibit the fusion of lysosomes and phagosomes and the cellular action of their soluble products is discussed.

Acid Phosphatase↗

PubMed1994

Characterization of Toxoplasma and Trichinella isolates from muscles of black bears in Pennsylvania.

During the hunting season of 1992, 322 black bears from Pennsylvania were examined for Toxoplasma gondii- and Trichinella spp-induced infections. Toxoplasma gondii antibodies were found in 79.8% of 322 bears--titer < 1:25 in 65 (20.2%), 1:25 in 18 (5.6%), 1:50 in 11 (34.5%) and 1:500 in 128 (38.7%) bears--by use of the modified agglutination test. Muscle tissues from 89 of these bears were bioassayed for T gondii parasites. Muscles from 64 bears, including heart from 1 bear, and heart alone from another bear, were digested in pepsin, and the digested samples were bioassayed in mice. Toxoplasma gondii was isolated from 5 bears; from the heart of 1, heart and skeletal muscles of 1, and skeletal muscles of 3. The T gondii antibody titers for the 5 bears with detectable T gondii were: > or = 1:25 in all 5 bears by use of the modified agglutination test; < 1:10 (3 bears, considered Toxoplasma-negative), 1:20 and 1:320 by use of the Sabin-Feldman dye test; < 1:64 (3 bears, considered Toxoplasma-negative), 1:128, 1:512 by use of the indirect hemagglutination test, and < 1:16 (2 bears, considered Toxoplasma-negative), 1:32, 1:64, and 1:512 by use of the latex agglutination test. Toxoplasma gondii was not isolated from feces of 5 cats fed muscles from the remaining 25 bears with T gondii antibody titer < 1:25. Tissue cysts of the 4 T gondii isolates from bears were rendered noninfective by freezing at -13 C.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1975

Immunity to Toxoplasma gondii induced in vitro in non-immune mouse macrophages with specifically immune lymphocytes.

Male and female CBA mice were used to study in vitro the mechanisms involved in the development and expression of cellular immunity to toxoplasma infection. The lag phase preceding toxoplasma division was delayed in nonimmune macrophages obtained from peritoneal cavities stimulated with thioglycollate. Specific anti-toxoplasma activity was conferred on nonimmune macrophages incubated with toxoplasma-immune spleen lymphocytes and soluble toxoplasma antigen. Treatment of immune spleen cell populations with anti-theta serum plus complement abolished completely their activity of conferring anti-toxoplasma activity on nonimmune macrophages, demonstrating that the essential cells were T lymphocytes. The mediator(s) responsible for the acquisition of immunity to toxoplasma in the nonimmune macrophages were soluble. Heat-inactivated, toxoplasm-immune macrophages of fibroblasts. The findings are related to previous investigations of induced immunity in animals and man.

Animals↗

PubMed1977

Attempted transmission of Toxoplasma gondii infection from pregnant cats to their kittens.

Sixteen 1- to 7-week-old pregnant specific-pathogen free cats were inoculated orally with Toxoplasma gondii cysts. Fetuses and neonatal kittens were examined for toxoplasma infection by inoculating suspensions of their tissues into mice. Toxoplasma gondii was not isolated from 23 fetuses and 16 newborn kittens from 13 queens. Six (3 litters) of the 15 kittens from the 3 remaining queens were killed on the day of or a day after birth, and the remaining 9 kittens were housed with their mothers for 7 to 33 days. None of the 9 kittens from the 2 litters examined between 0 and 33 days of age was infected with T gondii. In the other litter, T gondii was isolated from 3 kittens killed at 9, 16, and 22 days of age but not from 3 littermates killed on days 1, 1, and 22. Internal organs from the 3 kittens with proved toxoplasma infectivity in mice were examined histologically. Multifocal granulomatous encephalitis, hepatitis, nephritis, myocarditis, myositis, and interstitial pneumonia were found in all 3 kittens. Toxoplasma forms were demonstrated histologically in the tissues of 2 of these kittens. The mode of toxoplasma infection in newborn kittens was not determined but did not appear to be either transplacental or via fecal contamination from oocysts excreted by the mother cat. Evidence obtained in these experiments suggests that transplacental toxoplasma infection in the cat is not an important epidemiologic factor in perpetuation of the disease in the feline population.

Animals↗

PubMed1994

Toxoplasma gondii infection & its association with iodine deficiency in a residential school in a tribal area of Maharashtra.

To determine the seroprevalence and incidence of toxoplasmosis, 194 random serum samples of school students aged 10 to 18 yr (n = 178), their teachers (n = 10) and food handlers (n = 6) from a residential tribal school situated in district Dhule, Maharashtra state of western India, were tested. The samples were tested for anti-toxoplasma IgG and IgM antibodies using enzyme linked immuno sorbent assay (ELISA). Active infection was confirmed by a stage-specific direct agglutination test (DAT) using acetone fixed tachyzoites of T. gondii. A serosurveillance for rubella immunity was also simultaneously carried out. The results showed that at the age of 10 yr, all the children were immune to rubella infection and toxoplasma seroprevalence was detected in 20 per cent of the children. Toxoplasma infection was prevalent in 42.8 per cent adolescents, at the age of 18 yr. The average seroprevalence rate of toxoplasma infection was not significantly different in male and female children. The incidence rate of toxoplasma infection was inversely related to increase in age. The school staff comprising teachers and food handlers (aged 27 to 45 yr) showed a toxoplasma seroprevalence rate of 75 per cent (P < 0.001). There was also a significant difference (P < 0.05) in the prevalence of toxoplasmosis in children with grade II goitre (46.1%) and grade I or no goitre (31.8 and 26.5% respectively). The possible association between iodine deficiency and toxoplasma infection is being reported for the first time in this preliminary study.

Adolescent↗

PubMed2025

Serologic and molecular survey of Toxoplasma gondii in Baghdad Province, Iraq.

BACKGROUND: A prevalent contagious pathogenic parasite that can lead to major health issues is Toxoplasma gondii. AIM: The present study aimed to detect the parasitic immune response and the existence of genomic DNA in the blood of a T. gondii-positive equine. METHODS: Thirty serum samples from horses suspected of having toxoplasmosis were collected from the Al-Rusafa neighborhood in Baghdad. To quantitatively investigate toxoplasma antibody levels in horse serum, an ELISA was used to evaluate immunoglobulin G (IgG) levels. Conventional (PCR) was used to identify T. gondii DNA. RESULTS: The blood levels of IgG immunoglobulin in toxoplasma-infected horses differed significantly (p < 0.01) according to sex and age. Toxoplasma gondii-specific forward and reverse primers were generated using NCBI GenBank software. Toxoplasma genes were amplified using standard PCR. The proposed method can be used as a molecular diagnostic tool for detecting and comparing molecules using a ladder. CONCLUSION: The findings of this investigation were to ascertain whether the T. gondii genotype (UPRTF2 gene) is present. The size band of 443 bp DNA in the blood of toxoplasma-infected horses was confirmed using serological and molecular assessments. There were no statistically significant differences found by the Chi-square (χ2) test between the age groups or sexes of the seropositive and seronegative horses.

Animals↗

PubMed1975

Observations on a feline coccidium with some characteristics of Toxoplasma and Sarcocystis.

Two morphologically different cysts were found in skeletal muscles of mice inoculated with fecal material from a stray cat containing Isopora-type oocysts. The most common cyst contained bradyzoites resembling those of Toxoplasma and resulted from an oocyst measuring 11 times 13 mum which appeared to be identical to that of Toxoplasma. The other cyst, observed in only a few mice, contained bradyzoites resembling those of Sarcocystis, but the oocyst or sporocyst that gave rise to it was overlooked and apparently lost. Two more strains of the parasite resembling Toxoplasma were found in feces of stray cats. When inoculated into mice, the oocyst of this parasite routinely produced chronic infection and formed cysts similar to Toxoplasma in skeletal muscles and occasionally in the central nervous system. The majority of infected mice developed Toxoplasma antibody, but only to low titers. Cats fed carcasses of infected mice remained healthy and shed nonsporulated oocysts following a prepatent period of about 5 days. Cats did not develop Toxoplasma antibody. There was little or no cross immunity between the parasite and T. gondii in cats or mice. Transmission of the parasite between mice by the cyst stage normally was not possible; however, mice inoculated with cortisone acetate did become infected when inoculated with cysts. In other laboratory animals inoculated orally with the oocyst asymptomatic infection was detected in 3 species of rats, in guinea pigs and in dogs, but not in monkeys, pigeons or Japanese qualis. Fluorescent antibody tests on human sera failed to provide evidence of natural human infection with the parasite.

Animals↗

PubMed1995

Toxoplasma gondii surface antigen-1 in sera of HIV-infected patients as an indicator of reactivated toxoplasmosis.

The major surface antigen from the proliferative form of Toxoplasma gondii (P-30 of SAG-1) was chosen as a target for exploration of Toxoplasma gondii reactivation in sera from immunocompromised patients. Samples were obtained from 37 HIV-infected subjects with lymphocyte levels of CD4+ < 200/mm3. The prevalence of IgG antibodies to Toxoplasma gondii was 64.9%. Ten patients had clinical symptoms of reactivated toxoplasmosis; eight of these had Toxoplasma encephalitis. The SAG-1 epitopes were found as circulating antigen in five cases with an immunocapture enzyme immunoassay (EIA). The EIA was improved with an IgG1 monoclonal antibody to SAG-1 and a streptavidinbiotin amplification. The sensitivity, specificity and positive predictive value were 30, 92 and 60%, respectively. The SAG-1 levels were compared with different biological parameters such as HIV p24 antigen, beta 2 microglobulin, CD4+ cell count and IgG antibodies to Toxoplasma gondii. The levels of SAG-1 in these patients were significantly higher than those in the 75 healthy control persons with or without a chronic Toxoplasma gondii infection. Therefore, SAG-1 may be involved as a marker of reactivated toxoplasmosis in HIV-infected patients.

AIDS-Related Opportunistic Infections↗

PubMed2002

Cyst burden in the brains of Wistar rats fed Toxoplasma oocysts.

Six strains of Toxoplasma oocysts were used to infect groups of 4-24 Wistar rats, with each rat being fed 10(1)-10(4) oocysts from a single strain. After 2 months, the rats were killed, their brains screened for Toxoplasma cysts and then bioassayed in mice if negative. Toxoplasma was either observed in the form of brain cysts or was recovered using the bioassay, from 113 out of 138 (82%) rat brains. As few as ten oocysts were capable of initiating a brain infection that lasted for at least 2 months in eight of the nine rats inoculated. However, judging from bioassay 10(2)-10(4) oocysts did not give rise to progressively higher rates of infection. Brain cysts were seen in only 68 of 138 rats (49%). The number of Toxoplasma cysts formed in the brains of rats was generally in the order of tens to hundreds. The frequency of infection in the brains with Toxoplasma and the number of brain cysts formed appeared to be influenced by the individual resistance of the rats as well as by the doses of oocysts and the Toxoplasma strains used. The information gathered is considered to be a basis for a rat model of immunity against acquired toxoplasmosis.

Animals↗

PubMedDate not supplied

Performance characteristics of a commercial antibody-capture enzyme immunoassay for detection of Toxoplasma-specific IgM antibodies.

Antibody-capture enzyme immunoassay (EIA) for the detection of Toxoplasma-specific IgM has been shown to provide significantly higher specificity than the indirect IgM EIA. A new commercially available antibody-capture EIA (PLATELIA Toxo IgM EIA) converted 99 out of 100 false-positive Toxo-plasma IgM determinations to true negative. Experiments using Toxoplasma IgM calibrators demonstrated the antibody-capture EIA is approximately eightfold more sensitive than a new automated microparticle EIA for Toxoplasma IgM antibodies (IMX Toxo IgM EIA), and approximately equal in sensitivity to the indirect immunofluorescence assay. Precision studies of the antibody capture EIA using low, medium, and high calibrators gave coefficients of variation ranging from 3.0%-4.5% for within-run and 5.2%-11.4% for run-to-run variation experiments. Interference from high levels of bilirubin, albumin, hemoglobin, and lipid was not detected. Sera from patients with inflammatory or infectious disorders were tested for interference in the antibody-capture EIA. False-positive Toxoplasma IgM results were not observed, but low-level negative interference was detectable when patient sera was mixed with Toxoplasma-positive sera. Preparations of purified human IgM also produced negative interference in the antibody-capture EIA for Toxoplasma IgM.

Animals↗

PubMed2005

Toxoplasma gondii is capable of exogenous folate transport. A likely expansion of the BT1 family of transmembrane proteins.

Folates are key elements in eukaryotic biosynthetic processes. The protozoan parasite Toxoplasma gondii possesses the enzymes necessary for de novo folate synthesis and has been suggested to lack alternative mechanisms for folate acquisition. In this paper, we present a different view by providing evidence that Toxoplasma is capable of salvaging exogenous folates. By monitoring uptake of radiolabeled folates by parasites in axenic conditions, our studies revealed a common folate transporter that has a high affinity for folic acid. Transport of this compound across the parasite plasma membrane is rapid, biphasic, temperature dependent, bi-directional, concentration dependent and specific. In addition, morphological evidence demonstrates that fluorescent methotrexate, a folate analog, is internalized by Toxoplasma and shows localization reminiscent to the mitochondrion. The presence of putative folate transporter genes in the Toxoplasma genome, which are homologous to the BT1 family of proteins, suggests that Toxoplasma may encode proteins involved in folate transport. Interestingly, genome analysis suggests that the BT1 family of proteins exists not only in Toxoplasma, but in other Apicomplexan parasites as well. Altogether, our results not only have implications for current therapeutic regimens against T. gondii, but they also allude that the folate transport mechanism may represent a novel Apicomplexan target for the development of new drugs.

Amino Acid Sequence↗

PubMed2004

Intranasal immunisation with Toxoplasma gondii tachyzoite antigen encapsulated into PLG microspheres induces humoral and cell-mediated immunity in sheep.

Proteins from a crude extract of Toxoplasma gondii tachyzoites were encapsulated into poly(D,L-lactide-co-glycolide) (PLG) micro- and nano-particles with a mean encapsulation efficiency of 80%. An intranasal immunisation and infection experiment using 24 sheep was conducted to compare the immune responses elicited by intranasal administration of soluble and particulate T. gondii antigen (with and without cholera toxin). Sheep immunised with particulate toxoplasma antigen produced enhanced levels of both local and systemic antigen-specific IgA antibody, and showed increased cellular immune responses with a corresponding increase in IFNgamma production. After challenge with toxoplasma oocysts larger quantities of both nasal and systemic IgG were measured more rapidly in all animals immunised with toxoplasma antigen than animals infected with oocysts, suggesting a secondary-type IgG response. A slight modification of the febrile response to toxoplasma infection could be observed in animals immunised with particulate toxoplasma antigen and cholera toxin, although none of the immunised animals were protected against the challenge infection. These studies show that intra-nasal delivery has the potential to be an effective route for mucosal immunisation in sheep.

Adjuvants, Immunologic↗

PubMed1984

Analysis of the roles of immune interferon (IFN-gamma) and colony-stimulating factor(s) in the induction of macrophage anti-toxoplasma activity.

Lymphokine-enriched, cell-free supernatants from specific antigen-stimulated spleen cells of toxoplasma-immune mice lacking detectable anti-toxoplasma antibody could generate effective anti-toxoplasma activity within normal (non-immune) murine peritoneal macrophages. Such supernatants also contained high levels of IFN-gamma as well as Ia-antigen(s) inducing activity. Supernatants from ConA stimulated normal (non-immune) spleen cells with high IFN-gamma, as well as CSF-containing supernatants from lung explants, lacked the capacity to induce anti-toxoplasma activity within peritoneal macrophages. ConA-stimulated spleen cell supernatants with high IFN-gamma titers but not CSF-enriched lung explant supernatants could induce the expression of macrophage cell surface Ia-antigen(s). Based on the results of our experiments, we have been able to eliminate the direct (by itself) role of IFN-gamma or CSF in generating macrophage anti-toxoplasma activity. However, the possibility that molecules like IFN-gamma or CSF synergize together with other immune spleen cell-derived factor(s) in the generation of effective macrophage anti-toxoplasma activity has not been ruled out.

Animals↗

PubMed1985

Contribution of immune interferon (IFN-gamma) in lymphokine-induced anti-toxoplasma activity: studies with recombinant murine IFN-gamma.

Recombinant E. coli-derived murine interferon gamma (cDNA IFN-gamma) per se induced resident mouse peritoneal macrophages (MPM) and mouse embryo cells to exert marked antitoxoplasma activity. This capacity of cDNA IFN-gamma was abrogated by a specific antiserum to cDNA IFN-gamma which could only neutralize the antiviral activity mediated by this product, whereas a rabbit antiserum directed against murine IFN-alpha/beta proved ineffective in neutralizing these functions. It has been found that rabbit antiserum to cDNA IFN-gamma could also neutralize IFN-gamma-mediated antiviral activity present in crude lymphokine-enriched supernatants of antigen-stimulated toxoplasma-sensitized spleen cells (Toxo-LK) but proved ineffective in abolishing the capacity of Toxo-LK to trigger macrophage anti-toxoplasma activity. The data obtained suggest that macrophage anti-toxoplasma activity induced by Toxo-LK may be an interplay of multiple factor(s) and that Toxo-LK preparations contain soluble factor(s) other than IFN-gamma, which can induce macrophages to kill intracellular Toxoplasma. Experiments in which crude Toxo-LK preparations were incubated with lectin concanavalin A (Con A) showed that this treatment resulted in a block of anti-toxoplasma arming factor(s) activity, as well as a significant reduction of IFN-gamma-mediated antiviral activity present in Toxo-LK. By contrast, no significant difference was observed in the macrophage anti-toxoplasma activity mediated by Con A or untreated cDNA-IFN-gamma.

Animals↗