Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “TOXOPLASMA”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,423 records · Page 79Linked to original sources

Nonspecific suppression of primary antibody responses and presence of plastic-adherent suppressor cells in Toxoplasma gondii-infected mice.

The effect of Toxoplasma infection on primary antibody responses to both T-dependent and T-independent antigens was examined in mice. Drastic suppression of primary responses to sheep erythrocytes (SRBC) occurred when mice were immunized 7 days after infection. The suppression was observed in both 2-mercaptoethanol-sensitive and -resistant hemagglutinin responses. Anti-dinitrophenol (DNP) immunoglobulin E and G1 responses to DNP-conjugated keyhole limpet hemocyanin were also suppressed by infection. It was suggested that the suppressive effect is nonspecific for the antigens and immunoglobulin classes produced. Anti-DNP responses to DNP-Ficoll, a T-independent antigen, were suppressed by infection, but the suppressive effect was weaker than that on the responses to SRBC. This suggests that both T and B cells are suppressed by infection. In vitro responses of infected mouse spleen cells to SRBC and DNP-Ficoll confirmed the results of in vivo experiments. In addition, the presence of plastic-adherent suppressor cells was demonstrated in the spleen cells of infected mice, which suppressed the ability of normal mouse spleen cells to mount an SRBC-specific plaque-forming cell response. These plastic-adherent suppressor cells appeared to be a major cause of nonspecific suppression of primary antibody responses in Toxoplasma-infected mice.

Animals↗

A protective role for endogenous tumor necrosis factor in Toxoplasma gondii infection.

The involvement of tumor necrosis factor (TNF) in resistance to Toxoplasma gondii infection was examined by means of experiments in which mice were treated with anti-TNF antibodies prior to infection with ME49, a low-virulence Toxoplasma strain. In (BALB/cBy x C57BL/6J)F1 (CB6F1) mice, which are highly resistant to intraperitoneal (i.p.) infection with T. gondii ME49, 10(4) neutralizing units of anti-TNF caused a significant increase in trophozoite numbers in the peritoneal cavities of infected mice and transient signs of illness but no deaths. i.p. infection of anti-TNF-treated C57BL/6J (B6) mice, which are more susceptible to T. gondii and develop a chronic progressive toxoplasmosis, resulted in death for some of the mice. If the mice were infected perorally, however, and treated with anti-TNF, mortality was extensive in B6 mice but not in CB6F1 mice. Although it was not detected in their sera, TNF was found in the peritoneal fluids of i.p.-infected CB6F1 and B6 mice. Endogenously produced TNF thus appears to be an important mediator of resistance to T. gondii.

Animals↗

Roles of gamma interferon and other cytokines in suppression of the spleen cell proliferative response to concanavalin A and toxoplasma antigen during acute toxoplasmosis.

Suppressed splenocyte proliferation in response to mitogen and toxoplasma lysate antigen (TLA) is observed in mice acutely infected with Toxoplasma gondii. Recently, we reported that NG-monomethyl-L-arginine (NMMA), an inhibitor of reactive nitrogen intermediate (RNI) production, partially restored proliferative responses of splenocytes from infected mice. In the present study we have examined the effect of NMMA on production of cytokines by splenocytes from mice acutely infected with T. gondii and assessed the role of gamma interferon (IFN-gamma) and interleukin-10 (IL-10) in the RNI-mediated suppression. Stimulation with concanavalin A (ConA) or TLA of splenocytes from CBA/Ca mice infected for 7 days resulted in increased production of IFN-gamma, IL-4, and IL-10 but reduced levels of IL-2 when compared with cultures of splenocytes from uninfected mice. Whereas addition of NMMA did not alter levels of cytokines produced by splenocytes from uninfected mice, splenocytes from infected mice stimulated with ConA produced significantly higher levels of IL-10 and reduced levels of IL-2 and IL-4. Addition of anti-IFN-gamma monoclonal antibodies to cultures of spleen cells from mice infected for 7 or 14 days remarkably decreased the levels of nitrite and resulted in a 47- and 4-fold increase in proliferation induced by stimulation with ConA or TLA, respectively. Anti-IL-10 did not reduce levels of nitrite produced in culture but did result in a fourfold increase in the proliferative response of splenocytes from mice infected for 14 days. In vivo administration of anti-IFN-gamma or anti-IL-10 monoclonal antibodies to infected mice partially restored ex vivo spleen cell proliferative responses by approximately 40 and 15%, respectively. Our data indicate that IFN-gamma is important in inducing the RNI-mediated immunosuppression, which, in turn, affects production of cytokines by splenocytes. Our data also demonstrate that IL-10 is involved in the suppression observed but that this activity is independent of RNI.

Acute Disease↗

Resistance to Cryptococcus neoformans is associated with an inflammatory response to Toxoplasma gondii in the central nervous system of mice.

We have studied the resistance of Toxoplasma gondii-infected mice to subsequent infection with Cryptococcus neoformans. Mice infected with the moderately virulent ME49 strain of T. gondii are resistant to proliferation of yeast cells in their brains after intravenous inoculation of the serotype A C. neoformans strain 184. The resistance serves to limit proliferation of yeast cells that colonize the brain. Maximal levels of resistance correlate not with maximal systemic specific anti-Toxoplasma resistance but rather with high levels of inflammatory response, presumably to parasites released from cysts in the brain. Resistance is localized, as mice infected with ME49 show only limited resistance in their lungs after intratracheal instillation of yeast cells, but there is substantial protection against development of cerebral cryptococcosis.

Animals↗

Counter-protective role for interleukin-5 during acute Toxoplasma gondii infection.

The role of interleukin-5 (IL-5) during Toxoplasma gondii infection was investigated by comparing disease progression in IL-5 gene deficient (IL-5-/-) mice and their wild-type (WT) counterparts on a C57BL/6 background. IL-5-/- mice infected orally with T. gondii were less susceptible to infection than WT mice as demonstrated by reduced mortality rates. Consistent with this data, orally infected IL-5-/- mice had less severe pathological changes in their small intestines than WT mice at 8 days postinfection. At this time, splenocytes and mesenteric lymph node cells derived from IL-5-/- mice produced levels of IL-12, interferon-gamma (IFN-gamma), IL-4, IL-10, and nitric oxide (measured as nitrite) similar to those derived from WT mice when stimulated with Toxoplasma lysate antigen. However, peak serum IL-12 and IFN-gamma levels (at days 6 and 8, respectively) were significantly higher in IL-5-/- mice than in WT mice. In addition, WT mice but not IL-5-/- mice had raised levels of eosinophils in their peripheral blood between days 5 and 8 following infection. Oral administration of N omega-nitro-L-arginine methyl (from day 4 postinfection) increased mortality rates in both IL-5-/- and WT mice, indicating a protective role for nitric oxide during the early stages of oral T. gondii infection. In comparison with oral infection, no difference in mortality was observed between IL-5-/- and WT mice following intraperitoneal infection with T. gondii, with all mice surviving until 35 days postinfection. Similarly, no significant differences were observed in the severity of the meningitis, perivascular cuffing, or number of microglial nodules or parasites in the brains of intraperitoneally infected mice. Together, these results demonstrate a detrimental role for IL-5 during the early stage of oral infection with T. gondii which is associated with increased small-intestine pathology, eosinophilia, and reduced plasma IL-12 and IFN-gamma levels.

Acute Disease↗

Role of NK cells and gamma interferon in transplacental passage of Toxoplasma gondii in a mouse model of primary infection.

Protective immunity in mice infected with Toxoplasma gondii is mainly mediated by NK cells, CD4 and CD8 T cells, and type 1 cytokines, such as gamma interferon (IFN-gamma). To clarify the roles of NK cells and IFN-gamma in protection against primary congenital toxoplasmosis, we used recombination activating gene 2 knockout (RAG-2(-/-)) mice, which lack T and B lymphocytes, in comparison with the wild-type BALB/c model. RAG-2(-/-) mice had a significantly lower risk of fetal toxoplasmosis than BALB/c mice (25 versus 63.9%; P = 0.003). This protection was associated with an increased number of maternal NK cells, IFN-gamma secretion by spleen cells, and decreased parasitemia. In the RAG-2(-/-) mice, NK cell depletion increased both the rate of fetal infection, to 56.5% (P = 0.02), and the blood parasite burden. Conversely, in the BALB/c mice, this treatment did not modify maternofetal transmission or the blood parasite burden. Neutralization of IFN-gamma in both infected RAG-2(-/-) and BALB/c mice decreased congenital Toxoplasma transmission, contrasting with an exacerbation of maternal infection. These data suggest that a partially protective immunity against congenital toxoplasmosis is achieved due to the increased number of NK cells in RAG-2(-/-) mice. However, it seems that IFN-gamma enhances, directly or indirectly, the transplacental transmission.

Animals↗

Acquired toxoplasma encephalitis.

Toxoplasma was the cause of encephalitis in a 4 year old boy. He recovered completely after treatment with pyrimethamine and sulphadimidine. Toxoplasma encephalitis has a high mortality, and active treatment is recommended.

Child, Preschool↗

Toxoplasma encephalitis complicating Hodgkin's disease.

A case of Toxoplasma encephalitis is described in a patient who had received much immunosuppressive therapy for Hodgkin's disease. Such cases have been reported in immune suppressed patients outside the United Kingdom, but a search of the literature has not revealed any previous reports from this country. Since Toxoplasma gondii is a frequent pathogen and states of immune suppression are becoming more common, further cases, can be expected. Recognition of the clinical and pathological features is important because the condition can be treated.

Adult↗

Toxoplasma infection and pathological outcome of pregnancy.

To better evaluate the role of infection with Toxoplasma gondii in the outcome of pregnancy, 2,108 women with unsuccessful pregnancies (1,747 with spontaneous abortion, 187 with preterm delivery, 126 who delivered stillborn infants, and 48 whose offspring presented with clinical signs at birth) were tested for toxoplasma IgG and IgM antibodies during late pregnancy and/or up to 6 weeks after its termination. A nonpregnant group consisting of 157 women and a group of 568 women with a normal pregnancy were included as controls. The parameters observed were the prevalence of infection and the rates of acute and chronic infections. A causal relationship was established between acute infection during pregnancy and preterm delivery, stillbirth, and birth of infants with abnormal cranial volume, whereas there was no such association between acute toxoplasmosis and spontaneous abortion, or chronic infection and any of the pathological entities.

Acute Disease↗

Laser photocoagulation around the foci of toxoplasma retinochoroiditis: a descriptive statistical analysis of 35 patients with long-term follow-up.

Thirty-five patients with toxoplasma retinochoroiditis, receiving medical treatment and then treated with laser photocoagulation around the foci, were retrospectively evaluated for the risk of recurrence of the retinochoroiditis with a Kaplan-Meier representation. The recurrence rates with 95% symmetric confidence intervals were: at 1 year, 12.7 + or - 13%, at 2 years, 19.8 + or - 15%; at 3 years, 24.0 + or - 16%; at 4 years, 33.3 + or - 19%; at 5,6 and 7 years, 53.5 + or - 21%; at 8 and 9 years 66. 8 + or - 22%. With the data provided by our series, it is not possible to show the efficacy of laser photocoagulation as a prevention of recurrence in toxoplasma retinochoroiditis. Moreover, because of their heterogeneity, the recurrence rates from the literature cannot provide precise data for a comparison. Concerning the laser-induced thermal damage, the potential therapeutic mechanism of the laser procedure is discussed.

Adolescent↗

Huge chronic pericardial effusion caused by Toxoplasma gondii.

Two patients who had a huge pericardial effusion of at least 9 and 14 years' duration caused by cardiac toxoplasmosis are reported. Toxoplasma gondii were seen in the pericardial fluid, and serologic evidence also demonstrated the activity of the infection. These cases illustrate both the need to exclude toxoplasmosis in chronic pericardial effusion of unknown cause and the possibility of seeing toxoplasma in the pericardial fluid of patients with active toxoplasmic pericarditis. Moreover, in endemic areas, cardiac toxoplasmosis may not be an exceptional cause of chronic pericardial effusion.

Adult↗

Sulfadiazine-induced multiple urolithiasis and acute renal failure in a patient with AIDS and Toxoplasma encephalitis.

OBJECTIVE: To report a patient with sulfadiazine-induced urolithiasis and acute renal failure. CASE SUMMARY: A patient with AIDS who was being treated with pyrimethamine and sulfadiazine for Toxoplasma encephalitis developed lumbar pain, dysuria, urinary frequency, and hematuria. Acute renal failure was found and numerous crystals of sulfadiazine were seen in the urine. Multiple calculi of up to 2 cm in diameter in both kidneys were noted on ultrasound. The patient was treated with intravenous fluids and alkalinization of the urine with rapid improvement. An intravenous urographic study performed 2 days later showed no evidence of calculi and renal function was normal. DISCUSSION: Patients with AIDS and Toxoplasma encephalitis may have several predisposing conditions that can lead to the development of sulfadiazine-induced crystalluria, including poor fluid intake, fever, diarrhea, and hypoalbuminemia, in addition to the high doses of the drug required and the prolonged period of treatment. CONCLUSIONS: This potentially serious complication can be managed easily with conservative treatment. Clinicians should be aware of this complication as it is expected to occur more frequently as more patients are treated with sulfonamides and patients with AIDS experience longer survival rates.

AIDS-Related Opportunistic Infections↗

Toxoplasma and coxiella infection and psychiatric morbidity: a retrospective cohort analysis.

BACKGROUND: It has been suggested that infection with Toxoplasma gondii is associated with slow reaction and poor concentration, whilst infection with Coxiella burnetii may lead to persistent symptoms of fatigue. METHODS: 425 farmers completed the Revised Clinical Interview Schedule (CIS-R) by computer between March and July 1999 to assess psychiatric morbidity. Samples of venous blood had been previously collected and seroprevalence of T. gondii and C. burnetii was assessed. RESULTS: 45% of the cohort were seropositive for T. gondii and 31% were positive for C. burnetii. Infection with either agent was not associated with symptoms reflecting clinically relevant levels of concentration difficulties, fatigue, depression, depressive ideas or overall psychiatric morbidity. CONCLUSIONS: We do not provide any evidence that infection with Toxoplasma gondii or Coxiella burnetii is associated with neuropsychiatric morbidity, in particular with symptoms of poor concentration or fatigue. However, this is a relatively healthy cohort with few individuals reporting neuropsychiatric morbidity and therefore the statistical power to test the study hypotheses is limited.

Adult↗

Serological diagnosis of toxoplasmosis: usefulness of IgA detection and IgG avidity determination in a patient with a persistent IgM antibody response to toxoplasma gondii

We report the detection of specific IgA antibodies and the determination of IgG avidity in sequential serum samples from a patient exhibiting significant levels of Toxoplasma-specific IgM antibodies for seven years after the onset of the clinical symptoms of toxoplasmosis. IgM antibodies were detected by an indirect immunofluorescence test and by three commercial enzyme-linked immunosorbent assays (ELISA). Anti-T. gondii IgA was quantified by the alpha-capture ELISA technique using a commercial kit. As defined by the manufacturer of the IgA ELISA test used, most patients with acute toxoplasmosis have antibody levels > 40 arbitrary units per ml (AU/mL). At this cut-off level, the patient still had a positive ELISA result (45 AU/mL) in a serum sample taken one year after the beginning of clinical manifestations. The IgG avidity-ELISA test was performed with the Falcon assay screening test (F.A.S.T.(R)) - ELISA system. Avidity indices compatible with a recent Toxoplasma infection were found only in serum samples taken during the first 5 months after the onset of the clinical symptoms of toxoplasmosis. These results show that the interpretation of positive IgM results as indicative of recently acquired toxoplasmosis requires additional laboratory confirmation either by other tests or by the demonstration of a significant rise in the antibody titers in sequential serum samples.

Journal Article↗

Parkinsonian symptoms as an initial manifestation in a Japanese patient with acquired immunodeficiency syndrome and Toxoplasma infection.

We studied a Japanese patient who developed parkinsonian symptoms over 3 months before the diagnosis of acquired immunodeficiency syndrome. Brain MRI showed multiple lesions with mass effect and ring enhancement in the basal ganglia and subcortical white matter suggesting Toxoplasma infection. Anti-Toxoplasma therapy and highly active antiretroviral therapy for 6 months allowed improvement of parkinsonism, brain MRI findings, and immune system.

AIDS-Related Opportunistic Infections↗

Diffusion-weighted MRI of cerebral toxoplasma abscess.

OBJECTIVE: This retrospective study reports the diffusion-weighted MRI appearance of Toxoplasma abscesses, rim-enhancing cerebral masses resulting from toxoplasmosis infection. In all patients, the signal intensity of the abscess core on diffusion-weighted MRI was equal to or less than that of normal, unaffected cerebral white matter and the measured apparent diffusion coefficient was greater than that of unaffected white matter. Histopathology revealed necrotic tissue in the center of these abscesses but no purulent fluid. CONCLUSION: Unlike pyogenic abscesses, the core tissue of rim-enhancing Toxoplasma abscesses shows no restriction of water diffusion.

Adult↗

Suppression of intestinal and hepatic cytochrome P4503A in murine Toxoplasma infection. Effects of N-acetylcysteine and N(G)-monomethyl-L-arginine on the hepatic suppression.

1. Cytochrome P4503A (CYP3A) expression was studied in a murine model of infection. Mice were infected with a cystogenic strain of Toxoplasma gondii and microsomes were prepared for liver homogenates and jejunum villus tip enterocytes on day 10 postinfection. Total cytochrome P450 (CYP) and CYP3A were quantitated, and CYP3A activity was determined. 2. In the infected mouse, total CYP and CYP3A contents fell in the liver (-39 and - 49% respectively) and intestine (-43 and - 48 % respectively), as did the rate of metabolism of erythromycin (Ery) and cyclosporine A (CyA), two markers of CYP3A activity (-36 and -26% in the liver, -35 and -58% in the intestine). 3. To determine the mechanism(s) involved in the depression of hepatic CYP3A, infected mice were treated on day 7.5 post-infection with a monoclonal antibody raised against interferon-gamma (anti-IFN-gamma, or from days 7.5 to 10 post-infection with either N(G)-monomethyl-L-arginine (NMMA), an inhibitor of reactive nitrogen intermediates (RNI) production, or N-acetylcysteine (NAC), a reactive oxygen intermediates (ROI) scavenger. 4. Total CYP content was restored in the liver of infected mice treated with anti-IFN-gamma, but with marked interindividual variability. NAC treatment led to a recovery in the liver of total CYP content (+35 %), CYP3A content (total recovery), and the rates of Ery (+59%) and CyA (+87%) metabolism, whereas inconsistent results were obtained with NMMA. These results suggest that NAC, but probably not NMMA, partially protects hepatic CYP3A from Toxoplasma-mediated suppression in mouse.

Acetylcysteine↗

Toxoplasma antibodies by indirect latex agglutination tests in zoo animals.

Total of 216 animals conserved in Seoul Grand Park were examined on the antibody titers of Toxoplasma by the indirect latex agglutination test, 20 out of 131 cases (15.3%) in mammals, 2 out of 75 cases (2.7%) in birds, and none in reptiles, according to species, 15 out of 68 species (22.1%) in mammals, 2 out of 36 species (5.6%) in birds showed positive antibody titers when the titers of 1:32 or higher were regarded as positive. In mammals, it appeared as positive in 2 out of 6 cases (1 out of 3 species ) in marsupials, 1 out of 15 cases (1 out of 11 species) in primates, 1 out of 1 case in bats, 6 out of 13 cases (5 out of 10 species) in carnivores, 1 in 12 cases (1 species out of 3) in odd-toed ungulates, 9 out of 80 cases (6 species out of 38) in even-toed ungulates, and none in rodents and in whales. In birds, 1 out of 21 cases (1 out of 7 species) in gallinaceous birds and 1 out of 6 (5 species ) in parrots appeared to have the positive antibody titers of Toxoplasma. And, none of reptiles showed positive. Frequencies of positive antibody titers were high in 1: 64, 9 cases in mammals followed by 1: 32, 6 cases, 1: 128, 3 cases, and 1: 256, 2 cases, respectively. Two positive cases in birds appeared to be 1: 64.

Journal Article↗