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PubMed1979

[Occurrence of congenital ocular toxoplasmosis in siblings].

The author points out in connection with the description of two families in which evidently several children suffered damage through toxoplasmosis with which the mother had been infected a long time ago (pseudocoloboma of the macula, changes of the macula similar to juvenile degreneration, abortion and malformations such as anophthalmia, rhinoschisis, cheiloschisis, gnathoschisis and palatoschisis), that low titer levels in the Sabin-Feldmann test and in the complement fixation test are by no means totally insignificant for subsequent pregnancies, as is commonly assumed. In any case, women who have already given birth to children with congenital toxoplasmosis should be subjected to toxoplasmosis treatment, as far as possible, before any new pregnancy.

Adult↗
PubMed1970

Toxoplasmosis of the central nervous system in children.

The clinical symptoms and signs of 17 children with congenital toxoplasmosis of the brain are reported. Moreover the neuropathological lesions of 8 cases were given. The clinical findings of 10 children with acquired toxoplasmosis were tabulated. Problems concerning the diagnosis and differential diagnosis of toxoplasmosis of the central nervous system were discussed.

Brain↗
PubMed1983

[Meningoencephalic and chorioretinal manifestations of toxoplasmosis in an immunodeficient patient].

With reference to a case of malignant toxoplasmosis in a patient with angioimmunoblastic lymphadenopathy, the following features are recalled: in compromised hosts, clinical manifestations of malignant toxoplasmosis are highly variable, with neurologic signs and fever being predominant; the occurrence of lesions of the fundus, such as chorioretinitis, is an essential clue to the diagnosis; serologic tests for toxoplasmosis should be performed routinely at each stage of the disease in order to ascertain seroconversion through comparison with baseline results.

Adult↗
PubMed1978

Congenital toxoplasmosis: chances of occurrence in subsequent siblings.

Occurrence of congenital toxoplasmosis in subsequent siblings after the birth of an affected child is discussed. Toxoplasmic retinochoroiditis was found in 3 surviving siblings. The diagnosis was made by the typical fundus lesions in children, intracranial calcification in one child, and significant positive titer for toxoplasmic antibodies in all the children and the mother, who was asymptomatic. Serology for syphilis, skin tests for histoplasmosis and tuberculosis, blood studies with sedimentation rate, and chest roentgenograms were all negative in mother and all 3 children. The view that transmission of infection from mother to the fetus may result from a chronically infested uterine wall is supported and is thought to be the probable cause in the cases reported here. After the birth of one child with congenital toxoplasmosis, the parents may be reassured about the favorable prognosis of subsequent pregnancies with some reservation. However, it appears unwise to categorically refute the repetition of congenital toxoplasmosis in siblings. It is also suggested that because of possible danger of reactivation, the healed toxoplasmic chorioretinal lesions should be properly monitored if the patient is to be given corticosteroids for any other reason.

Adolescent↗
PubMed1982

Congenital toxoplasmosis: long-term follow-up.

The incidence in Europe is high, about 6 in 1000 births. Five percent of these babies either die or are severely damaged by the disease. In the others most infections are clinically asymptomatic in the neonatal period. In +/- 70% of all infants with congential infections relapses of chorioretinitis give rise to scars in their eyes after a follow-up of 16 years. The relapses were occurring later on both in treated and untreated infants. Most scars were in the periphery of the retina, but scars in the neighbourhood of the macula can threaten the vision. In 1--2% of these children later on uveitis impairing vision due to congenital toxoplasmosis will occur. As a control 117 children in the age 12--14 years without congenital toxoplasmosis were studied. No chorioretinitis-scars were found in the eyes although +/- 50--60% had antibodies against toxoplasmosis, resulting from an acquired infection. The problem of prevention is unsolved. There is no vaccine. Deliberately infecting girls before pregnancy is too dangerous. Screening of pregnant women is possible but no clear-cut safe therapy is available. Screening of the baby after birth is too late.

Adolescent↗
PubMed1995

[A preliminary study on the antenatal diagnosis and prevention of the fetus toxoplasmosis infection].

For those pregnant women with an abnormal pregnancy history, the polymerase chain reaction (PCR) technique was adopted to screening the serum toxoplasmosis DNA (TOX-DNA). Then tests were made for further evidence of TOX-DNA in the amnionic fluids TOX-DNA was examined in cases with blood TOX-DNA positive. Gamma glutamyl transpeptidase (GGT) and alpha-fetoprotein (AFP) in the amnionic fluids were measured for reference, a antenatal diagnosis of the fetal congenital toxoplasmosis infection could thus be made. In the present paper, 9 out of 92 blood specimen were TOX-DNA positive, of the 9 cases, 5 had TOX-DNA and 4 had no TOX-DNA in the amnionic fluid tests. The results of follow-up examination in the 9 cases were in conformity with the ante natal diagnosis. This is an important procedure for diagnosis and prevention of maternal-fetal vertical infection of Toxoplasmosis.

Animals↗
PubMed1995

[A clinicopathological study of eighteen autopsy cases with acquired toxoplasmosis].

Eighteen autopsy cases of acquired toxoplasmosis in New York City were studied. Seventeen cases were with acquired immunodeficiency syndrome (AIDS) and one patient with Hodgkin's disease. All 18 cases involved the brain and nine of them disseminated to the heart (8 cases), lung (4 cases), pancreas (3 cases), alimentary tract (2 cases) and urogenital organs (3 cases). The authors divided the acquired toxoplasmosis into (1) immunocompetent, (2) immunocompromised and (3) immunodeficient types. The autopsy findings showed that the brain, heart and lung were the most susceptible organs. Pseudocysts were also found in lungs and alimentary tract, suggesting an autoinfection by swallowing sputum containing Toxoplasma. Toxoplasma in the urogenital organs might become a source for sexual transmitted toxoplasmosis.

Acquired Immunodeficiency Syndrome↗
PubMed1993

[Treatment of ocular toxoplasmosis. Part 1: Basic principles and diagnosis].

Ocular toxoplasmosis is a frequent cause of ocular inflammation which threatens central visual acuity. New concepts of treatment are important alternatives for the well known therapy with pyrimethamine and sulphadiazine. They cause less side effects and result in better compliance. Up to know prospective randomized trials are still missing although they might prove the value of medical treatment in ocular toxoplasmosis. Nevertheless it is generally accepted that ocular toxoplasmosis should be treated when central visual function is threatened. Treatment strategy is influenced by general symptoms, especially in children and immunocompromised patients. In this paper opportunities for treatment are discussed. Relevant microbiological, immunological and epidemiological fundamentals are mentioned as well as serological tests.

Clindamycin↗
PubMed1993

[Toxoplasmosis and pregnancy: is it possible to simplify the diagnostic procedures?].

About 1% of all pregnancies in France are complicated by a primary infection with toxoplasmosis. The risk for the fetus being affected increases during the pregnancy but the seriousness of the effect on the fetus becomes less with more advanced pregnancies. Treatment of the mother using Spiramycin have been proven to be efficient, lessening the risk for the fetus being affected. The diagnosis of the fetus being affected rests on a whole bundle of presumptive evidence culled from non-invasive methods and invasive methods which are not without risk. (Direct or over-enthusiastic diagnostic techniques or none at all). We have studied a series of 101 primary infections with toxoplasmosis for which we have not carried out any invasive diagnostic techniques. The long term results in 77 infants show no difference in fetal morbidity and better results as far as mortality are concerned. We therefore propose simplifying the diagnostic approach in cases of primary infection with toxoplasmosis during pregnancy.

Decision Trees↗
PubMed1997

Immune response in a murine model of congenital toxoplasmosis: increased susceptibility of pregnant mice and transplacental passage of Toxoplasma gondii are type 2-dependent.

We used a model of acquired toxoplasmosis to study the immune response in pregnant BALB/c mice (IL-4+/+) and in pregnant transgenic IL-4-deficient BALB/c mice (IL-4-/-) during acute toxoplasmosis. Female BALB/c mice were infected orally by 20 tissue cysts of the avirulent PRU strain of Toxoplasma gondii on day 11 of pregnancy. Splenocyte cultures were used to explore proliferative responses and cytokine production in vitro. Parasite loads were determined in the lungs on day 7 post-infection and in the brain on day 30 post-infection. After infection, cultured spleen cells from pregnant mice produced more IFN-gamma (a Type I cytokine) and more NO than non pregnant mice, and the Type 2 response (IL-4 and IL-10) was weak. Although this kind of immune response may be required for mice to recover from toxoplasmosis, pregnant mice were more susceptible to infection than non pregnant mice, as illustrated by a larger parasite load in lungs and brain. Pregnant IL-4-/- mice showed lower susceptibility to T. gondii infection and a lower materno-fetal transmission rate (24% vs. 53% infected fetuses) without increased production of Type I cytokines (IFN-gamma and NO). These data indicate that Type 2 response plays an important role in increasing mouse susceptibility to T. gondii infection during pregnancy and that IL-4 and pregnancy-associated substances increase the transplacental passage of T. gondii.

Animals↗
PubMed1992

Skeletal muscle toxoplasmosis in patients with acquired immunodeficiency syndrome: a clinical and pathological study.

The present article describes the clinical and pathological findings in 5 human immunodeficiency virus (HIV)-infected patients with muscle toxoplasmosis. The patients had marked lymphopenia (5/5), with less than five CD4+ cells/mm3 (3/3), when they developed fever (5/5), and multiorgan failure (5/5), including diffuse encephalitis, pneumonia, pancytopenia, and myopathy. Muscle involvement included weakness and wasting (4/5), myalgias (3/5), and high serum creatine kinase levels (3/3). Serology for toxoplasmosis showed high IgG titers in 3 patients (3/4). Anti-Toxoplasma therapy resulted in complete recovery in 2 patients. Muscle toxoplasmosis was detected by biopsy (3/5) or postmortem evaluation (2/5), and was identified using immunocytochemistry and electron microscopy. Toxoplasma cysts were detected in 0.5 to 4% of muscle fibers close to or remote from necrotic fibers and inflammatory infiltrates. Muscle fibers strongly expressed the major histocompatibility complex class I antigen (2/2) as in polymyositis. We suggest that Toxoplasma gondii should be sought by muscle biopsy in patients who have acquired immunodeficiency syndrome with fever, encephalitis, multiorgan dysfunction, and elevated serum creatine kinase levels of obscure origin.

Acquired Immunodeficiency Syndrome↗
PubMed1993

Diagnosis of pulmonary toxoplasmosis by bronchoalveolar lavage in cardiac transplant recipients.

We report two cases of fatal, clinically unsuspected disseminated toxoplasmosis that developed following orthotopic cardiac transplantation. Toxoplasma gondii trophozoites, pseudocysts, and cysts were best visualized on hematoxylin and eosin and Giemsa-stained cytospin preparations of bronchoalveolar lavage fluid. Post-mortem examination in both cases revealed disseminated toxoplasmosis with extensive involvement of the lungs and heart. The patients, who were seronegative for antibody to T. gondii prior to transplantation, received organs from donors whose serology status was unknown. Demonstration of anti-toxoplasma antibodies post-transplantation occurred in both cases. Bronchoalveolar lavage may be useful in diagnosis of pulmonary toxoplasmosis. Clinicians, pathologists, and cytopathologists must consider T. gondii in the differential diagnosis of pneumonia in the immunocompromised patient, especially cardiac transplant patients.

Adult↗
PubMed1991

A novel IgM-indirect hemagglutination test for the serodiagnosis of acute toxoplasmosis.

A new indirect hemagglutination (M-Toxo-IHA) test was standardized for the serodiagnosis of acute toxoplasmosis. The reagent for this test consisted of stabilized human red cells coated with a Toxoplasma gondii heat-stable alkaline-solubilized extract which reacted predominantly with IgM antibodies found in serum samples from patients with a recent infection. Almost no reactivity was verified with serum samples from chronic or ancient toxoplasmosis. The reagent preparation was simple and obviated prior fractionation of parasite components reactive with IgM antibodies. Rheumatoid factor or high levels of IgG antibodies did not interfere in the M-Toxo-IHA test. A total of 358 serum samples was assessed for the evaluation of this test, comprising sera from patients with recent and ancient toxoplasmosis, from non-related diseases, as well as from clinically healthy individuals with no previous T. gondii infections. Serodiagnostic performance of the M-Toxo-IHA test in terms of sensitivity, specificity, efficiency, and positive and negative predictive values was verified, and the values obtained were 1.000, 0.985, 0.989, 0.952, and 1.000, respectively, in relation to IgM-immunofluorescence or IgM-capture ELISA. Six different batches of reagent, successively produced for the current study, provided reproducible results and were stable for at least 22 months at 4 degrees C.

Acute Disease↗
PubMed1989

Hemichorea-hemiballismus associated with acquired immune deficiency syndrome and cerebral toxoplasmosis.

A young woman had hemichorea-hemiballismus subsequently found to be secondary to a cerebral toxoplasmosis infection complicating human immunodeficiency virus infection. This patient had the sixth reported case of acquired immune deficiency syndrome (AIDS) with hemichorea-hemiballismus, and each has been secondary to cerebral toxoplasmosis. The presence of hemichorea-hemiballismus in a young patient should suggest a diagnosis of AIDS and in particular the diagnosis of secondary cerebral toxoplasmosis. Other movement disorders that occur in AIDS are discussed.

Acquired Immunodeficiency Syndrome↗
PubMed1996

Choreoathetosis in acquired immune deficiency syndrome patients with cerebral toxoplasmosis.

The aim of our study was to evaluate both the incidence and the pathologic and clinical features of extrapyramidal disorders in a population of acquired immune deficiency syndrome (AIDS) patients with cerebral toxoplasmosis. Of 240 AIDS patients evaluated in the 1985-1994 period, 50 of them were diagnosed to have cerebral toxoplasmosis on the basis of the following criteria: occurrence of specific antibodies, computed tomography and/or magnetic resonance imaging (MRI), and regression of the symptoms after specific therapy. Three of 50 (6%) had hemichoreoathetosis. In the first case, the disorder began as a dyskinesia of the left hand that subsequently spread to the whole ipsilateral arm and assumed the features of choreic athetotic movements. The other two cases were characterized by left hemisomatic distal choreic movements. Therapy with pyrimethamine and sulfadiazine led to a complete recovery of the extrapyramidal signs in two cases and to improvement in the third. According to our observations, the onset of these movement disorders could not be related to the dimension of the lesion or to the edema, but to a specific localization in subthalamic nucleus, in subthalamic/pallidal, and pallidal/thalamic pathways. MRI seems the elective tool to perform a more accurate study of the anatomic areas involved in this pathway and to verify their integrity. Cerebral toxoplasmosis in AIDS can be considered as a new etiopathogenic cause of choreoathetosis.

AIDS Dementia Complex↗
PubMed2002

Prenatal diagnosis of congenital toxoplasmosis.

Ninety-three pregnant women with Toxoplasma gondii seroconversion during pregnancy underwent prenatal diagnosis of fetal toxoplasmosis. The following tests were used: (1). amniocentesis for mouse inoculation (93 subjects), (2). amplification of T. gondii DNA by polymerase chain reaction (PCR) (79 subjects), and (3). cordocentesis for the detection of T. gondii-specific IgM antibodies (13 subjects). All patients had serial ultrasonographic scans to detect those fetuses with abnormalities that could be associated with congenital toxoplasmosis. Eighteen pregnancies (19.4%) had evidence of vertical transmission. A total of 11/18 (61.1%) had positive amniotic mouse inoculation test, while 10/12 (83.3%) had positive PCR results. The combination of both tests allowed the prenatal diagnosis in 17/18 infected fetuses (94.4%). All patients who underwent cordocentesis for the detection of T. gondii-specific IgM antibodies had negative results. However, in two of the above cases fetal toxoplasmosis was detected by amniotic fluid studies. In five of the infected fetuses there were abnormal ultrasonographic findings. All pregnancies with evidence of vertical transmission were terminated, whereas the remaining pregnancies proceeded normally to term. The present data showed that amniotic fluid studies, preferably PCR amplification of T. gondii DNA, are the best diagnostic tools for the detection of vertical transmission in pregnancies with seroconversion during pregnancy.

Adult↗
PubMed1989

Hypothalamo-pituitary dysfunction in congenital toxoplasmosis.

Three patients with congenital toxoplasmosis and hypothalamo-pituitary dysfunction are reported. All three children were growth hormone (GH) deficient, two were gonadotropin deficient and one had precocious puberty in addition to central diabetes insipidus (DI). It is suggested that congenital toxoplasmosis might result in a neuro-endocrine disturbance and thus be an organic cause of hypopituitarism. Pituitary function and growth should be monitored in children with congenital toxoplasmosis.

Female↗
PubMed1995

Value of specific immunoglobulin A detection by two immunocapture assays in the diagnosis of toxoplasmosis.

The diagnosis of Toxoplasma gondii infection is currently based on immunological tests, but tests for IgG and IgM antibodies alone are often insufficient to assess the risk of active disease, especially during pregnancy and in immunodeficient subjects. The supplementary diagnostic value of testing for antitoxoplasmic IgA in cases of acute, chronic, congenital and reactivated toxoplasmosis, relative to classical immunological tests, was evaluated using two immunocapture tests, one based on tachyzoite agglutination and the other on an immunoenzymatic complex recognizing the membrane protein P30 of Toxoplasma gondii. A total of 4,541 sera from 395 uninfected subjects, 468 immunized subjects with chronic infection, 117 subjects with acute infection and 403 children, 103 of whom had congenital toxoplasmosis, was tested. Specific IgA tests were negative in the nonimmune population, but tests for this immunoglobulin subtype became positive very rapidly during primary infection, and IgA disappeared more rapidly than IgM. In the children infected in utero, specific IgA was detected more frequently than IgM. In contrast, in a population of HIV-seropositive subjects with clinical toxoplasmosis, tests for IgA were poorly sensitive. The two tests for specific IgA produced similar results, except in the early stages of primary infection, in which immunoenzymatic testing for anti-P30 IgA was less sensitive than the agglutination method.

Agglutination Tests↗