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At least 289 records · Page 16Linked to original sources

PubMed1988

Long-term persistence of Toxoplasma gondii in tissues of pigs inoculated with T gondii oocysts and effect of freezing on viability of tissue cysts in pork.

To study the distribution of tissue cysts in porcine tissues, 16 pigs were fed oocysts of 4 strains of Toxoplasma gondii (4 pigs/strain). Pigs were euthanatized between postinoculation days 103 and 875 and portions of 5 to 14 organs were bioassayed in mice and/or cats for T gondii. For bioassays, 50- to 100-g portions of tissue were incubated in acidic pepsin solution to free bradyzoites from cysts in parenchyma, and washed sediment from the digests of each specimen was inoculated SC into mice (6 mice/organ). For bioassays in cats, a 500-g portion or whole organ was fed to Toxoplasma-free cats (1 cat/organ). Toxoplasma gondii was recovered from tissues of 14 of the 16 pigs (from the brains of 12, hearts of 11, tongues of 10, and diaphragms of 6). Toxoplasma gondii was isolated from commercial cuts of meat from 5 infected pigs; from the arm picnic and ham of 3, Boston butt, spareribs, and tenderloin of 2, and bacon and tailbone of 1. Regarding the 4 pigs euthanatized between postinoculation days 759 and 865, cats shed T gondii oocysts after the ingestion of hearts of all 4; tongues of 3; bacons, hams, arm picnics, Boston butts, spareribs, and diaphragms of 2; and livers, kidneys, and tenderloins of 1. Toxoplasma gondii was found to be inconsistently distributed among the organs and muscles, but overall, tongue and heart were more heavily infected than were other tissues. Tissue cysts in pork were rendered nonviable at -12 C for 3 days.

Animals↗

PubMed1979

Direct development of enteroepithelial stages of Toxoplasma in the intestines of cats fed cysts.

Four newborn (1- to 2-day-old) and two weaned (55- to 67-day-old) Toxoplasma-free cats were killed between 23 and 120 hours after ingestion of Toxoplasma gondii cysts from the brains of infected mice, and the cats' tissues were examined for the development of Toxoplasma. Intraepithelial Toxoplasma types (B, C, and D) were found in sections of small intestine. Homogenates of mesenteric lymph nodes, spleen, and liver of each cat were injected intraperitoneally into each of six weaned Toxoplasma-free cats to test the hypothesis of extraintestinal pregametogonic stages, as proposed by Overdulve (1978). Of the six cats injected with infected feline tissues, none shed oocysts within 17 days. Thus, the hypothesis of extraintestinal pregametogonic stages was not confirmed.

Animals↗

PubMed1981

Protective reaction against malaria infection in mice sensitized with Frozen-thawed toxoplasma tachyzoites.

Mice sensitized with frozen-thawed Toxoplasma antigen emulsified in Freund's Incomplete Adjuvant (FIA) showed high resistance against Plasmodium berghei infection, but not in mice sensitized with paraformaldehyde-fixed. Toxoplasma or saline plus FIA. However, mice which survived from malaria infection did not show any protective reaction against the RH strain inoculation. Furthermore, an immune interferon activity was detected in the supernatant of the spleen cells collected from the mice sensitized with frozen-thawed Toxoplasma and cultured with the specific antigen, however, no Toxoplasma growth inhibitory factor (Toxo-GIF) was found in the same supernatant of lymphokines. From these results, it is suggested strongly that frozen-thawed Toxoplasma antigen could confer nonspecific resistance in mice against Plasmodium infection.

Animals↗

PubMed1984

[Demonstration of antigen-specific suppressor cells in Toxoplasma infection of man].

Detection of antigenspecific suppressor cells in Toxoplasma infection of man. Investigations adapted to demonstrate the action of antigen-specific suppressor cells were carried out in subjects with acute toxoplasmosis (n = 5) and latent infections (n = 16) and compared to non-infected controls (n = 11). The investigations were carried out in vitro in the form of autologous one-way lymphocyte mixed culture. Suppressor cells were activated by toxoplasma lysate antigen (325 micrograms/ml) and, for comparison, by concanavalin A (10 micrograms/ml). Responder cells were stimulated by toxoplasma lysate antigen (200 micrograms/ml). In the acute cases, antigen-specific suppressor cells were identified which caused the lymphocyte transformation to be suppressed (tritium thymidine incorporation) to the same extent as did the mitogen-activated cells. The subjects with latent infections revealed a statistically significant difference (p less than 0.01) between the means of the percentage suppression of suppressor cells activated by toxoplasma lysate antigen or concanavalin A, suggesting a diminishing suppressive action of antigen-specific cells at this stage of infection. In addition to the effect on phagosome formation in macrophages, the activation of suppressor cells too should be considered as a factor of virulence for Toxoplasma gondii.

Acute Disease↗

PubMed1980

Augmentation of resistance to toxoplasma in mice by pretreatment with attenuated vaccine.

It is well known that certain chronic infectious diseases can be cured by preimmunization of the host against the live vaccine of an attenuated strain of an infectious agent from an attack of a virulent strain of same group of infectious agents. To test for the existence of a similar protective mechanism for Toxoplasma infection in mice, seven groups of mice were first infected with two kinds of low virulence strains (Beverley or S-273). They were challenged with a strong virulence strain (RH) from 2 to 59 weeks after the first immunization. All mice in one group challenged 2 to 3 weeks after the first Beverley immunization survived at rates of 33, 22 and 18 percent respectively, and mice examined at almost the same times after immunization with S-273 showed survival rates of 35, 19 and 52 percent respectively, which indicates a major difference in the number of surviving mice examined after 46-59 weeks. However, the majority of mice killed by a challenge with a virulent strain of Toxoplasma showed prolonged survival times of up to 10 days more than the non-immunized mice. Histological studies of dead mice showed acute bronchitis and/or bronchopneumonia, and a small number of tachyzoites was found in their lungs and other organs. All surviving mice harbored RH parasites in their brains. The present study suggested that mice treated with live vaccine of attenuated Toxoplasma acquired resistance against a challenge of a virulent strain of Toxoplasma. Since the infected mice showed small numbers of parasites and high antibody titers, the cause of death of premunitive mice from highly virulent Toxoplasma might differ from that of non-immune mice.

Animals↗

PubMed1995

Establishment of T-helper type 1- and T-helper type 2-like human Toxoplasma antigen-specific T-cell clones.

As an in vitro model for human cerebral toxoplasmosis, we analysed the interaction between glioblastoma cells, Toxoplasma and Toxoplasma antigen-specific T-helper cells. We established 46 different human CD4+ T-cell clones from four different donors. All T-cell clones responded to Toxoplasma antigen derived from three different Toxoplasma strains. We found that the supernatants of 44 clones induced toxoplasmostasis in glioblastoma cells. The anti-parasitic effector mechanism activated in glioblastoma cells by T-cell supernatants was the induction of the tryptophan-degrading enzyme indolamine 2,3-dioxygenase. Enzyme induction, as well as the anti-parasitic effect, was blocked by a monoclonal antibody directed against interferon-gamma (IFN-gamma), and the addition of L-tryptophan to the cultures completely blocked the anti-parasitic effect induced by T-cell supernatants. The supernatants from two of the 46 established T-cell clones (3A22 and 1A15) were unable to induce indolamine 2,3-dioxygenase activity or, as expected, toxoplasmostasis in glioblastoma cells. We further analysed the supernatants from these two clones, and found that they contained large amounts of IL-4 and no, or only limited amounts of, IFN-gamma. We therefore conclude that Toxoplasma-antigen is able to activate T-helper type 1 (Th1)- and Th2-like human T cells, and only IFN-gamma-producing cells are capable of inducing anti-parasitic effector mechanisms.

Animals↗

PubMed1994

Use of a clinical laboratory database to estimate Toxoplasma seroprevalence among human immunodeficiency virus-infected patients. Overcoming bias in secondary analysis of clinical records.

Knowledge of Toxoplasma seroprevalence among human immunodeficiency virus-infected patients identifies candidates for potential prophylaxis and may influence management among patients who present with mass lesions of the central nervous system. Toxoplasma antibody seroprevalence among persons with human immunodeficiency virus infection varies widely. We utilized an administrative and laboratory database (including 1599 patients with human immunodeficiency virus infection who were receiving medical care at the University of California-San Diego Medical Center, between July 1, 1986, and March 31, 1990) to estimate Toxoplasma seroprevalence. Of the 1599 patients, 344 underwent serum assays for Toxoplasma antibodies. The tested group was similar to other members of the cohort in distributions of sex, race, citizenship, and age. The overall mean (+/- SE) Toxoplasma seroprevalence was 16% +/- 2%. Potential bias in this estimate because of testing indication, misclassification, or testing frequency was small.

Acquired Immunodeficiency Syndrome↗

PubMed1997

Intracellular fate of vacuoles containing Toxoplasma gondii is determined at the time of formation and depends on the mechanism of entry.

We have characterized the intracellular fate of Toxoplasma in bone marrow-derived macrophages following two disparate modes of uptake: phagocytosis vs active invasion. The fate of parasite-containing vacuoles was followed by immunofluorescence localization of endogenous endocytic markers to track phagocytic processing in pulse-infected cells. During uptake of both opsonized and dead parasites, host cell plasma membrane MHC class II molecules and FcR were internalized into the phagosome and then gradually lost. Maturation of phagosomes containing Toxoplasma was a rapid, dynamic process of sequential fusion with early endosomes, late endosomes, and lysosomes that was complete within 15 min. Toxoplasma-containing phagosomes were transiently positive for transferrin receptor between 0 and 2.5 min, then contained the cation-independent mannose 6-phosphate receptor between 2.5 and 7.5 min, and finally matured to lysosome-like compartments containing lysosomal membrane glycoprotein 1 and the proton pump, but lacking cation-independent mannose 6-phosphate receptor. Toxoplasma-containing phagosomes also sequentially acquired host proteins that regulate endocytic fusion including rab5, N-ethylmaleimide-sensitive factor, and rab7. In marked contrast, MHC class II molecules and FcR were excluded from the parasitophorous vacuole formed by active parasite invasion. The parasitophorous vacuole also failed to acquire any host compartmental markers or fusion proteins analyzed. Our results indicate that Toxoplasma evades endocytic processing due to an absence of host regulatory proteins necessary to drive endocytic fusion, and that this divergence from normal maturation occurs during the formation of the primary vacuole.

Animals↗

PubMed1976

Effects of Corynebacterium parvum treatment and Toxoplasma gondii infection on macrophage-mediated cytostasis of tumour target cells.

Injection of mice with Corynebacterium parvum or living or killed Toxoplasma gondii was studied to determine the efficacy of these treatments in activating peritoneal macrophages to inhibit the uptake of [3H]TdR (cytostasis) by tumour target cells in vitro. In the presence of activated macrophages from mice treated i.p. with a wide dose range of either C. parvum or living Toxoplasma, cytostasis was usually greater than 99%. This population of activated macrophages was transient in C. parvum-treated mice, but persists, probably for life, in Toxoplasma-infected mice. Whereas the i.p. route of administration of C. parvum was more efficient in activating macrophages than the i.v. route, the s.c. route appeared to be relatively ineffective. Treatment with killed Toxoplasma by any route was also relatively ineffective in activating macrophages. In contrast Toxoplasma infection resulted in highly activated peritoneal macrophages, regardless of the route of administration. Depending upon the route of initial treatment, the route of readministration of C. parvum had either no appreciable effect or resulted in a marked alteration in the cytostatic capacity of peritoneal macrophages.

Animals↗

PubMed2000

Neosynthesized IgG detected by Western blotting in Toxoplasma-seropositive heart or lung transplant recipients.

Toxoplasmosis is a life-threatening disease in heart- or lung transplant recipients that can result either from the reactivation of a latent infection or from an organ-transmitted infection. The diagnosis of acute toxoplasmosis is easy in cases of seroconversion following a mismatch. However, when the recipient is Toxoplasma-seropositive before transplantation, usual serological techniques do not allow the differentiation between endogenous and organ-related reinfection. The aim of this study was to determine whether western blotting could contribute to this differentiation. Sequential sera from two heart- and one liver- and lung transplant patients whose anti-Toxoplasma antibody titers strongly increased after transplantation, were analyzed by western blotting. Neosynthesized IgG were observed on blots incubated with the sera from two patients who had received transplants from Toxoplasma-seropositive donors, whereas no neosynthesized IgG was detected on blots from the patient who had received a transplant from a Toxoplasma-seronegative donor. Our results suggest that the detection of neosynthesized IgG in the recipient may be related to the recognition of a new parasite strain possibly brought by the transplant from a Toxoplasma-seropositive donor.

Adolescent↗

PubMed1987

Assessment of therapy for toxoplasma encephalitis. The TE Study Group.

Toxoplasma encephalitis has been reported as a life-threatening opportunistic infection among patients with the acquired immune deficiency syndrome. The TE Study Group was established to address clinical questions about Toxoplasma encephalitis by retrospectively reviewing available data. The medical centers selected were those reporting Toxoplasma encephalitis to the Centers for Disease Control or to one of the principal investigators. Sixty-eight histologically confirmed cases of Toxoplasma encephalitis were reported by investigators at 31 medical centers; 61 of the patients received some therapy. Overall prognosis was poor. The median survival following initiation of therapy was four months. Patients described as "alert" at initiation of therapy survived significantly longer than those described as "lethargic" or "stuporous." No beneficial or harmful effects could be attributed to the use of corticosteroids. Toxicity attributed to pyrimethamine and sulfonamide therapy was reported in 60 percent of patients. Leukopenia, rash, and thrombocytopenia were common during therapy. A clinical relapse of Toxoplasma encephalitis was reported in 50 percent of patients discharged from the hospital.

Acquired Immunodeficiency Syndrome↗

PubMed1982

The role of hypersensitivity reactions to toxoplasma antigens in experimental ocular toxoplasmosis in nonhuman primates.

To assess the role of ocular hypersensitivity reactions to Toxoplasma antigens in previously sensitized ocular tissues, we used a nonhuman primate model of ocular toxoplasmosis. Each eye of eight monkeys was inoculated with living Toxoplasma organisms into the inner retinal layers. All eyes developed necrotizing retinochoroiditis. Healing of the lesion occurred with the formation of a retinochoroiditic scar. Four months later, Toxoplasma antigens were injected through the right internal carotid artery. Four weeks after this, Toxoplasma antigens were inoculated into the left retina. Iritis, vitritis, and retinal edema occurred in response to the administration of the antigens, but no recurrent necrotizing retinochoroiditis was produced in this model. These findings suggested that hypersensitivity to Toxoplasma antigens does not play a major role in triggering recurrences of toxoplasmic retinochoroiditis in nonhuman primates.

Animals↗

PubMed1985

Influence of Toxoplasma on manifestations of Moloney virus infections.

Considerable evidence documents the importance of co-factors, including the immune response, in expression of oncogenicity of tumour viruses. To determine whether a common protozoal infection that can depress lymphocyte function alters manifestations of oncogenic virus infection, a mouse model of Toxoplasma infection with depressed T lymphocyte function was developed. In this model, Toxoplasma depressed blastogenic transformation to the T-cell mitogen Concanavalin A and primary antibody response to sheep red blood cells which requires T cell help. Uninfected and Toxoplasma-infected mice were then infected with Moloney leukaemia or Moloney sarcoma viruses and development of lymphoma and sarcoma were evaluated. Toxoplasma infection, which induced depression of T-cell function, decreased the incidence of Moloney sarcoma virus induced rhabdomyosarcomas but did not alter progression or regression of tumour in those mice that developed tumour. Conjoint infection with Toxoplasma and Moloney leukaemia virus did not increase incidence of lymphoma when compared with incidence of lymphoma in mice infected with Moloney leukaemia virus alone.

Animals↗

PubMed1981

IgM enzyme-linked immunosorbent assay test for the diagnosis of congenital Toxoplasma infection.

An IgM enzyme-linked immunosorbent assay, developed for detection of IgM antibodies to Toxoplasma gondii, was evaluated to define its usefulness for diagnosis of congenital Toxoplasma infection. Sera from 51 infants suspected of having congenital Toxoplasma infection but in whom this diagnosis was ruled out were negative in the IgM-ELISA test. Fifty of them were also negative in the IgM-fluorescent antibody test; the one which was positive was from an infant with congenital syphilis who had circulating rheumatoid factor. Of 55 sera from newborn infants with proved congenital Toxoplasma infection, the IgM-ELISA test was positive in 43 (72.7%), whereas the IgM-IFA test was positive in only 14 (25.4%). Of those sera obtained during the first 30 days of life the infected infants, 81.2% were positive in the IgM-ELISA test, whereas only 25% were positive in the IgM-IFA test. The Igm-ELISA test avoids the false-positive results owing to RF and the false-negative results owing to competition from high levels of maternal IgG antibody which occur in the IgM-IFA test. We conclude that the IgM-ELISA test is highly sensitive and specific for diagnosis of congenital Toxoplasma infection.

Child, Preschool↗

PubMed1994

Outcome of Toxoplasma gondii mismatches in heart transplant recipients over a period of 8 years.

Donor-related infection due to Toxoplasma gondii is a well-recorded complication of cardiac transplantation. In order to assess the efficacy of co-trimoxazole in small doses as prophylaxis for primary Toxoplasma gondii infection in seronegative heart and heart-lung transplant recipients receiving organs from seropositive donors, we reviewed the serostatus and clinical outcome of all such mismatched transplants performed at our unit over a period of 8 years. Of 310 transplants performed between May 1985 and May 1993, donor and recipient serum samples were available for 257 heart and 33 heart-lung transplants. Of these, 13 (4.5%) were toxoplasma mismatches. Post-transplant review serum samples were available for 3 months or longer for nine of the 13 mismatches. The first three patients received co-trimoxazole 480 mg bd orally for 3 months (regimen A) while the remainder received only the standard prophylaxis designed for Pneumocystis carinii i.e., 960 mg bd orally three times per week for 3 months (regimen B). Seroconversion was demonstrated in only one patient (regimen A). Furthermore, none of the mismatched patients developed serious infection compatible with primary toxoplasmosis. We therefore conclude that in centres with a low prevalence of toxoplasma seropositivity, testing of donor and recipient serum for Toxoplasma gondii antibody should be performed only when clinically indicated and, in addition, standard prophylaxis for Pneumocystis carinii may be adequate for preventing primary toxoplasmosis.

Adolescent↗

PubMed1989

Elevated Toxoplasma IgG antibody in patients tested for infectious mononucleosis in an urban emergency department.

There are many infectious causes of fatigue, sore throat, and fever, including mononucleosis and toxoplasmosis. Toxoplasma antibody testing is rarely performed in most emergency departments; as a result, toxoplasmosis is diagnosed infrequently. We obtained Toxoplasma IgG IFA titers on ED patients who had mononucleosis testing performed to determine the frequency of toxoplasmosis in this population. Two hundred sixty patients were included in our study. Eleven (4.2%) had a positive mononucleosis test, and 14 (5.4%) had a positive Toxoplasma titer. In the detection of toxoplasmosis, Toxoplasma IgG titers of 1:1,024 or greater have been shown to be a sensitive means of detecting infection in the first six months. Further testing with IgM titers is needed to establish a positive diagnosis when necessary. We found more patients with elevated Toxoplasma IgG titers than with positive heterophil antibody titers in an ED population tested for mononucleosis over a two-year period. We conclude that toxoplasmosis may be as common as mononucleosis in our ED and that clinicians should consider this pathogen when working up patients with appropriate symptoms.

Adolescent↗

PubMed1992

Secretion of Toxoplasma gondii-specific antibody in vitro by peripheral blood mononuclear cells as a new marker of acute toxoplasmosis.

Antigen-specific antibody secretion in vitro by peripheral blood mononuclear cells (PBMC) reflects an in vivo stimulation of the immune system by the antigen. Primary infection of immunocompetent patients with T. gondii causes an acute infection followed by chronic toxoplasmosis. We examined in vitro anti-Toxoplasma antibody production by PBMC during the acute and chronic phases of toxoplasmosis. PBMC from patients with acute or chronic toxoplasmosis and seronegative subjects were cultured for up to 6 days. Anti-Toxoplasma antibodies were assayed in supernatants by ELISA and immunoblotting. Anti-Toxoplasma antibodies were detected in supernatants of PBMC from 29 pregnant women who seroconverted during gestation. PBMC from 17 patients who had chronic toxoplasmosis and PBMC from 10 seronegative healthy controls did not secrete Toxoplasma-specific antibodies. This in vitro antibody secretion was spontaneous, active and transient since it disappeared between 11 and 24 weeks after seroconversion. Anti-Toxoplasma antibody secretion by PBMC from patients with acute toxoplasmosis is consistent with an in vivo stimulation of the immune system by T. gondii antigens. Our results represent a new approach for studying the immunological response during T. gondii infection and could have important implications for the diagnosis of acute and re-activated toxoplasmosis.

Acute Disease↗

PubMed1994

Toxoplasma gondii: detection of antibodies in human saliva and serum.

Saliva samples from 27 patients with a recent toxoplasma infection were tested for specific IgG, IgM and IgA antibodies to Toxoplasma gondii. Thirteen of the 27 saliva samples were positive for IgG anti-T. gondii by direct agglutination and 8 of the 27 were positive for IgM anti-T. gondii by an immunosorbent agglutination assay. Twenty of the 27 saliva samples were positive for IgG antibody on toxoplasma immunoblots with three major immunodominant antigens; 38, 30 and 35 kDa. IgA results on toxoplasma immunoblots were positive for all three groups tested, recently infected patients, chronically infected and seronegative adults without distinguishing between them. The 35 and 43 kDa antigens were the most frequently detected proteins. IgM in saliva gave negative or very weak reactions. None of the eight seronegative or the 17 chronically infected adults gave positive results in any of the tests performed to detect IgG or IgM in saliva. Serial saliva and serum samples from a laboratory-infected patient were collected and tested for toxoplasma-specific IgG, IgM and IgA. IgG in saliva was detected by 27 days post infection (p.i.) and was negative by 81 days p.i.; it detected mainly the 38 and 30 kDa antigens. IgM in saliva was detected by 11 days p.i. and was negative by 81 days p.i., with no reaction on immunoblots.

Acute Disease↗