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PubMed1992

White blood cells in infants with congenital toxoplasmosis: transient appearance of cALL antigen on reactive marrow lymphocytes.

Existing serological methods for diagnosing congenital toxoplasmosis are inadequate. We have therefore characterized the features of peripheral blood cell counts and smears in a prospective study of 8 affected infants during their first year of life. Enlarged, vacuolated lymphocytes were observed in all patients. Six patients had periods of neutropenia; in 1 patient the neutropenia was severe and prolonged. A bone marrow aspirate from this patient showed enhanced myelopoiesis, and after stimulation with hydrocortisone, but not with adrenaline, his neutrophil count normalized. Phenotyping of his bone marrow cells revealed that approximately 55% of both the immature and mature B lymphocytes were positive for the cALL antigen. Of the 8 patients, 6 had mild eosinophilia, 4 had mild monocytosis and 3 had increased numbers of plasma cells in the peripheral blood. These findings may reflect the activity of the congenital toxoplasma infection and may thus contribute to the diagnosis, particularly in patients with silent serology.

Antigens, Differentiation↗
PubMed1996

High incidence of toxoplasmosis during pregnancy in Nigeria.

Sera from 606 women of child-bearing age from the Benue River Basin area of Nigeria were screened by serological tests to determine the incidence of toxoplasmosis in Nigeria; 43.7% had serologic evidence of infection, increasing from 25% in the group of 15 to 18-year-old women to 71.4% in the 39-42 year age group. Using a previously published epidemiological model, the incidence rate for each age group varied from 0.5% for 15 years old women to 5.3% in the age group 37 years, with an overall rate of 1.8%. Extending this model as it applies to the estimation of incidence of infection during pregnancy, a 5.4% expected rate of seroconversion was found.

Adolescent↗
PubMed1997

Toxoplasmosis in Danish AIDS patients.

Infection with Toxoplasma gondii was studied in 600 patients with AIDS, diagnosed in the eastern part of Denmark from 1980 up to and including 1990. The median age was 38 years, and 223 (44%) had anti-T. gondii IgG antibodies. Of the patients seropositive to T. gondii 61 (27%) developed toxoplasma encephalitis (TE). Few patients received prophylactic treatment with sulfamethoxazole-trimetoprim. In total, 66 patients were diagnosed with TE. One had no serological test performed, and of the remaining 65, 4 (6%) had no anti-T. gondii IgG antibodies. The predictive value of a negative Sabin-Feldman dye test was 99%. The geometric mean dye test titer was higher in patients with TE than in patients without TE. Of the patients with TE 34% had serological reactivation of their T. gondii infection at the time of TE diagnosis, and 34% had detectable T. gondii-specific antibodies in the cerebrospinal fluid. Specific IgM antibodies were found to have little value in the diagnosis of TE, as only 3% had detectable IgM antibodies. Acute toxoplasmosis was the AIDS-defining diagnosis for 23 (35%) of the patients with TE. The median CD4 count at the time of TE was 30 x 10(6)/l, and the median survival time from diagnosis of TE was 9 months.

Acquired Immunodeficiency Syndrome↗
PubMedDate not supplied

Disseminated toxoplasmosis and acquired immunodeficiency syndrome: diagnosis by transmission electron microscopy.

A 43-year-old, bisexual, black man with acquired immunodeficiency syndrome (AIDS), detected by CD4 lymphocyte criteria alone, presented with low-grade fever, chills, malaise, and watery diarrhea of 2 days' duration. Over the next 5 days, he developed a fulminant septicemia-like illness with progressive hypotension, disseminated intravascular coagulation, and very high serum lactic acid dehydrogenase (2,150 U/L) and serum creatine phosphokinase (5,395 U/L) levels, and died. The cause of this illness was not clinically apparent. A bone marrow biopsy performed on the day of his death revealed intracytoplasmic clusters of 3 microns long, oval, basophilic organisms, the exact nature of which was not evident by light microscopy. The diagnosis of disseminated toxoplasmosis (DT) was made only after electron microscopic study of the bone marrow revealed organisms with features typical of Toxoplasma gondii tachyzoites. These features included a multilayered pellicle, a pointed anterior end containing a conoid, up to nine rhoptries, sparse micronemes, and a posterior end containing a nucleus. Some of the organisms had divided by internal budding or endodyogeny. This case illustrates the value of transmission electron microscopy in making the diagnosis of DT.

AIDS-Related Opportunistic Infections↗
PubMed1996

The evolution of ocular toxoplasmosis in anti-interferon gamma treated mice.

PURPOSE: A clinico-histopathological cross correlation was made to study the mechanism of tissue damage in toxoplasmic retino-choroiditis during an experimental reactivation of chronic toxoplasmosis and to compare the influence of treatment by sulfadiazine on the retinal lesions. METHODS: Chronically infected Swiss-Webster mice were treated, six weeks after infection, with an avirulent strain of Toxoplasma gondii (Beverley strain) with polyclonal rabbit antibody directed against murine interferon gamma. RESULTS: Mice treated by anti-interferon gamma developed clinical lesions between day 5 and day 30 (lesions including single foci of retinochoroiditis, multifocal lesions or diffuse areas of retinal necrosis). These lesions did not arise from borders of pre-existing scars. The retina was photographed with an operating microscope fitted with a 90 diopter lens. Biological study showed a significant rise of parasitic loads in the eye and brain. Histological examination is in favour of free organism dissemination via retinal vessels; the lesions are restricted to the inner retina and ciliary body, the parasites migrated from extra-ocular cysts via the vasculature. No cysts were seen at the beginning of the study; they were found at the scar phase and appeared in mice treated with sulfadiazine. The clinical lesions were not caused by cysts but by coagulated necrosis in the retinal tissue. Parasite migration may have played a trigger role. CONCLUSIONS: The retinal damage was constituted either as a result of a toxic effect of the organisms or as a hypertensive reaction to the toxoplasma organism. The results of this study showed that the treatment with anti interferon gamma was sufficient to reactivate chronic infection.

Adrenal Cortex Hormones↗
PubMed1983

Determination of IgG, IgM and IgA antibody responses in human toxoplasmosis by enzyme-linked immunosorbent assay (ELISA).

A 4-layer modification of ELISA for the determination of toxoplasma antibodies is described. In 103 Finnish blood donors 27 had antibodies against Toxoplasma gondii. One donor had IgM antibodies and IgA antibodies were found in 9. In patients with acute toxoplasmosis a vigorous IgG antibody response resulted in high antibody levels soon after infection, declining gradually to mean adult levels in approximately 2 yr. IgM antibodies appeared during the earliest phases of infection and disappeared as early as in 1 or 2 months in some cases and in most cases by the 6th month after infection. An IgA antibody response was also always seen. It was slower than the IgM response and could therefore be used to improve the laboratory diagnosis especially in cases where IgM antibodies had already disappeared and no further increase in IgG antibodies could be detected.

Antibodies↗
PubMed1990

Toxoplasmosis of the conus medullaris in a patient with hemophilia A-associated AIDS. Case report.

Toxoplasma gondii has been reported to be the most common cause of focal brain lesions in patients with acquired immunodeficiency syndrome (AIDS). A case of intramedullary toxoplasmosis of the conus medullaris is reported in a patient with hemophilia A-associated AIDS. The diagnosis is discussed, with particular emphasis on the magnetic resonance imaging appearance.

Acquired Immunodeficiency Syndrome↗
PubMed2003

Highly endemic, waterborne toxoplasmosis in north Rio de Janeiro state, Brazil.

In Campos dos Goytacazes, northern Rio de Janeiro state, Brazil, reports of uveitis consistent with toxoplasmosis led to a survey of the prevalence and risk factors for Toxoplasma gondii infection in 1997-1999. The survey population was selected randomly from schools, randomly chosen communities, and an army battalion. Serum samples from 1,436 persons were tested. With results adjusted for age, 84% of the population in the lower socioeconomic group was seropositive, compared with 62% and 23% of the middle and upper socioeconomic groups, respectively (p<0.001). When multivariate analysis was performed, drinking unfiltered water was found to increase the risk of seropositivity for the lower socioeconomic (odds ratio [OR]: 3.0, 95% confidence interval [CI] 1.3 to 6.9) and middle socioeconomic (OR: 1.7, 95% CI 1.2 to 2.3) populations. We also found a high T. gondii seroprevalence in this Brazilian community. Drinking unfiltered water increased the risk of T. gondii seropositivity, indicating the potential importance of oocyst transmission in water in this region.

Adolescent↗
PubMed2006

Waterborne toxoplasmosis, Brazil, from field to gene.

Water was the suspected vehicle of Toxoplasma gondii dissemination in a toxoplasmosis outbreak in Brazil. A case-control study and geographic mapping of cases were performed. T. gondii was isolated directly from the implicated water and genotyped as SAG 2 type I.

Animals↗
PubMed1995

Lymphadenitis in experimental murine toxoplasmosis induced by intramuscular injection of tachyzoites.

When tachyzoites (RH strain) of Toxoplasma gondii are injected intramuscularly, experimental mice survive up to 7 days, 1-2 days longer than those infected intraperitoneally. We observed sequential histopathological changes in inguinal lymph nodes after intramuscular injection of tachyzoites to thighs of specific pathogen free (SPF) mice. Initial findings on 1 or 3 days after the injection were reactive germinal centers, distended sinuses and epithelioid cell clusters in cortical and paracortical regions. Later on 5 days after the injection, however, effacement of nodal structure with depletion of cells and focal necrosis were observed. Necrotizing lymphadenitis in the experimental murine toxoplasmosis suggests the causal relation between T. gondii infection and the human disease.

Animals↗
PubMed1978

A comparative study of some combined treatment regimens in acute toxoplasmosis in mice.

The effectiveness of five treatment regimens was compared to mice during acute and late infection with Toxoplasma gondii. Parasitic cure rates, as judged by failure of brain tissue from surviving mice to produce infection when inoculated into clean mice, were as follows: pyrimethamine + sulfamethoxypyridazine, 92%; clindamycin + sulfamethoxypyridazine, 75%; spiramycin + sulfamethoxypyridazine, 16.7%; trimethoprim + sulfamethoxypryridazine alone, 0%. Pyrimethamine + sulfamethoxypyridazine was the most effective combination against acute toxoplasmosis in mice.

Acute Disease↗
PubMed1992

Construction of a genomic DNA library of the Toxoplasma gondii ZS2 strain, screening of specific clones, and DNA diagnosis of toxoplasmosis.

We have constructed a genomic DNA library of the Toxoplasma gondii ZS2 strain and isolated a specific cloned DNA sequence from this organism. The restriction map of this cloned 1.1-kb DNA fragment was analyzed. Southern and dot-blot analyses showed that the 32P-labeled DNA fragment hybridized to parasite DNA, to DNAs from peripheral blood leukocytes and the thymus of baby pigs that were artificially infected with T. gondii, and to DNAs of T. gondii-positive anencephalic and hydrocephalic fetuses. It did not hybridize with DNA from controls, (i.e., normal human and baby pig peripheral blood leukocytes, spleen of normal mice, Plasmodium falciparum, Pneumocystis carinii, and pBR322). As few as 100 T. gondii parasites or 500 pg of purified DNA from T. gondii can be detected by dot-blot hybridization. This probe method was specific and sensitive, and has been used successfully in detecting various clinical cases of toxoplasmosis with T. gondii.

Animals↗
PubMed1993

Laboratory-acquired malaria, leishmaniasis, trypanosomiasis, and toxoplasmosis.

Because of renewed interest in parasitic diseases, increasing numbers of persons in clinical and research laboratories have the potential for exposure to parasites and therefore are at risk for acquiring parasitic infections. In this review of laboratory-acquired parasitic infections, we concentrate on protozoan diseases that frequently have been reported to be laboratory acquired: malaria, leishmaniasis, trypanosomiasis (American and African), and toxoplasmosis. These diseases can be severe, even fatal, and may be difficult to diagnose. Many laboratorians who have acquired these diseases did not recall having had an accident. Of those with recognized accidents, needlestick injuries were the most common. Laboratories should have established protocols for handling specimens that may contain viable organisms and for responding to laboratory accidents.

Animals↗
PubMed1997

A maternal screening program for congenital toxoplasmosis in Quindio, Colombia and application of mathematical models to estimate incidences using age-stratified data.

We studied 937 pregnant women from Quindio, Colombia for the presence of specific anti-Toxoplasma gondii IgG antibodies using the indirect immunofluorescence antibody technique (IFAT-IgG). Specific anti-T. gondii IgM antibodies detected using the immunosorbent agglutination assay (ISAgA-IgM) were investigated in patients with high titers in the IFAT-IgG (dilutions > or = 1:1,024). We used mathematical models based on the age prevalence results of the IFAT-IgG to estimate the number of seroconversions and these were compared with the results predicted by the IgM based-incidence results. We found 15 positive cases by ISAgA-IgM and we were able to follow the children of six mothers from this group in which we found one case of congenital toxoplasmosis with the development of a retinal scar despite prenatal and postnatal treatment. The estimation of new cases for the annual total of pregnancies (approximately 8,000) in the Quindio region was 30-120 according to the ISAgA-IgM results and 57-85 using mathematical models. Thus, mathematical models based on age prevalence can give useful estimations of the magnitude of the problem.

Adolescent↗
PubMed2003

[Ocular toxoplasmosis].

PURPOSE: To update the current concepts in ocular toxoplasmosis. METHODS: Interpretation of recent publications, meeting information and personal experience. RESULTS: Most important aspects related to transmision of the parasite and clinical presentation of the ocular disease are discussed. Special issues on diagnosis and therapy are also mentioned. CONCLUSION: A correct knowledge of the epidemiology may allow a decrease in the ocular disease and a better diagnosis will be possible by recognizing the clinical presentations. Therapies have not changed significantly over the last years.

Humans↗
PubMedDate not supplied

Cutaneous manifestations of disseminated toxoplasmosis in an immunosuppressed dog.

A 3.5-year-old, castrated male, giant schnauzer was presented with alopecic pustular dermatitis. Immune-mediated hemolytic anemia had been diagnosed 45 days previously. At the time of presentation, the dog was receiving prednisone, azathioprine, and cyclosporine. Cutaneous protozoosis was diagnosed, and postmortem examination revealed protozoa within cutaneous, cardiac, pancreatic, and pulmonary tissues. The protozoa divided by endodyogeny, had the morphology of Toxoplasma gondii (T. gondii) tachyzoites, and stained positively with T. gondii polyclonal antibodies but not with antibodies to Neospora caninum or Sarcocystis neurona. Immunosuppression may have predisposed this dog to disseminated toxoplasmosis.

Animals↗
PubMedDate not supplied

Concurrent toxoplasmosis and feline infectious peritonitis in a cat.

A 13-year-old, 4-kg, neutered male Maine coon presented with ascites. Toxoplasma gondii tachyzoites were seen within neutrophils and macrophages, and free within the abdominal fluid. At necropsy, many abdominal organs were positive for feline infectious peritonitis (FIP) antigens using immunohistochemical staining. This apparently is the first report of concurrent toxoplasmosis and FIP in a domestic cat.

Animals↗
PubMed1978

Congenital toxoplasmosis in Tasmania.

In a prospective study, 9037 cord sera from Tasmanian children were tested using the Toxoplasma indirect fluorescent antibody test (IFAT). There were 494 positive reactors at the screening titre of 1:64. These reacting sera were titrated out and were also tested in the immunoglobulin M (IgM) Toxoplasma IFAT. No specific IgM antibodies were detected, but, even so, 33 of the sera had titres of 1:512 or greater. Repeat samples from 20 of the children with high titres revealed a substantial decline in titre. It is believed that these results indicate that congenital toxoplasmosis is not an important cause of perinatal morbidity in Tasmania.

Antibodies↗