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PubMed1992

Pulmonary toxoplasmosis in AIDS.

The chest radiographs obtained in nine patients with acquired immunodeficiency syndrome (AIDS) and pulmonary toxoplasmosis were reviewed. In three patients, a bilateral, diffuse, fine to medium reticulonodular pattern indistinguishable from that seen in Pneumocystis carinii pneumonia (PCP) was observed. In six patients, however, a bilateral, predominantly coarse, nodular pattern was observed. This type of abnormality is unusual with PCP, and its presence may help in distinguishing between pulmonary infections caused by Toxoplasma gondii and P carinii. Other opportunistic pneumonias occurring in patients with AIDS, including tuberculosis, histoplasmosis, and coccidioidomycosis, might show similar coarse, nodular opacities on chest radiographs and thus may not be differentiated from pulmonary toxoplasmosis. No hilar or mediastinal adenopathy was observed. Two patients had pleural fluid. Radiologists familiar with the chest radiographic appearance of T gondii pneumonia could be first to suggest this unusual complication of AIDS.

Acquired Immunodeficiency Syndrome↗
PubMed2006

[Acute toxoplasmosis: clinical and laboratory data in eleven patients].

INTRODUCTION: The clinical and laboratory data of immunocompetent patients with acute toxoplasmosis (AT) are described. PATIENTS AND METHODS: We performed a retrospective study of patients with AT attended between 1996 and 2004. Diagnostic criteria consisted of compatible clinical findings (generalized and cervical lymphadenopathies) and specific serology against Toxoplasma gondii (high IgG and IgM and/or reactive IgA). IgG and IgM determinations were performed by ELFA and IgA determinations by ELISA. IgM-CMV, heterophil antibodies, hemogram, hepatic chemistry were also determined and funduscopic examination was performed. RESULTS: Eleven immunocompetent patients with AT were evaluated. The mean age was 8.8 years (95 % CI: 3.6-12.9). The patients were evaluated between the first and the third month after symptom onset. Of the 11 patients, hard elastic lymphadenopathies were found in 10, single cervical lymphadenectomy in three and generalized lymphadenectomy in seven. One patient showed no symptoms. In one patient, nodal histology showed the Piringer-Kuchinka triad. None of the patients showed alterations in the hemogram, hepatic chemistry or funduscopic examination. The mean IgG value was 4.143 UI/ml (95 % CI: 2.570 and 5.717). IgM was reactive in nine of the 11 patients (81.8 %) and IgA in seven out of 10 patients (70 %). In all patients, at least one of these two immunoglobulins was reactive. In all patients, clinical outcome was favorable without parasiticide treatment. CONCLUSION: Except for one asymptomatic patient, all the patients had generalized lymphadenopathies and only 27.2 % showed cervical lymphadenopathies. A negative IgM or IgA result does not rule out a diagnosis of AT. Parasiticide treatment is unnecessary in this entity. Acute toxoplasmosis should be considered early in children with lymphadenopathies to avoid invasive procedures.

Acute Disease↗
PubMed1999

Presumed congenital ocular toxoplasmosis in two successive siblings.

We present the cases of 2 consecutive siblings with bilateral macular lesions, for which there is strong clinical and laboratory evidence supporting the diagnosis of congenital ocular toxoplasmosis. These cases raise the possibility of maternal parasitemia during Toxoplasma gondii reinfection, leading to transmission to the fetus and congenital ocular toxoplasmosis despite prior immunity and lack of an immune disturbance in the mother.

Adolescent↗
PubMed1987

Pityriasis lichenoides et varioliformis acuta and acquired toxoplasmosis.

A patient presented with a typical pityriasis lichenoides et varioliformis acuta (PLEVA) and disclosed serological evidence of an active and recent toxoplasmosis. Specific treatment of toxoplasmosis promptly and definitively resolved PLEVA lesions. Serological tests for Toxoplasma gondii should be performed in all PLEVA patients.

Female↗
PubMed1992

Absence of sensorineural hearing loss in treated infants and children with congenital toxoplasmosis.

Educationally significant hearing loss has been reported in 10% to 15% of children with congenital toxoplasmosis. As part of a pilot study to assess feasibility and safety of prolonged therapy for congenital toxoplasmosis, 30 congenitally infected infants and children were evaluated for auditory function. Serial testing, beginning within 2 months of birth, was performed. Availability of auditory brainstem response (ABR) testing made evaluation at an earlier age than previously possible. Six (20%) of the 30 infants had mild to moderate conductive type hearing loss associated with otitis media. No infant or child had sensorineural hearing loss. The better outcome we observed compared to previous reports of a 15% to 26% incidence of sensorineural hearing loss and 10% to 15% incidence of educationally significant, bilateral hearing impairment may be related to early initiation and/or prolonged institution of antimicrobial therapy. Continued followup to exclude progressive hearing impairment and study of larger numbers of children are needed to verify these preliminary findings.

Audiometry, Evoked Response↗
PubMed1981

Pathogenesis of acute toxoplasmosis in specific-pathogen-free cats.

Systemic toxoplasmosis was produced in specific-pathogen-free cats by intravenous inoculation with Toxoplasma gondii tachyzoites. Infectious organisms were recovered from all tissues studied, but the number of organisms recovered from liver, lungs and spleen was 10-fold to 10,000-fold higher than from heart and brain. The occurrence and severity of Toxoplasma-induced lesions correlated with the number of infectious organisms recovered from the various tissues. In nonlymphoid tissues, the Toxoplasma-associated lesions consisted of multifocal necrosis, usually with demonstrable organisms. Lesions in the spleen and mesenteric lymph nodes consisted of reticuloendothelial and lymphoid hyperplasia, with few demonstrable organisms. Pneumonitis was severe and sometimes fatal in the early stages of systemic toxoplasmosis. Light- and electron-microscopic studies showed that the earliest lung lesions were randomly distributed infiltrates of neutrophils, eosinophils, and mononuclear cells into alveolar walls. Later lesions were diffuse alveolar necrosis, pneumocytic hyperplasia, and extensive fibrinocellular exudates in alveoli. Tachyzoites were present in cytoplasmic vacuoles of fibroblasts, macrophages, type I and II pneumocytes, bronchiolar epithelial cells, bronchiolar smooth muscle cells, endothelial cells, neutrophils, and eosinophils, and circulating monocytes. Replication of organisms was found in all parasitized cell types except neutrophils and eosinophils.

Acute Disease↗
PubMed1997

Epizootic disseminated toxoplasmosis in captive slender-tailed meerkats (Suricata suricatta).

Fatal disseminated toxoplasmosis was diagnosed in seven captive slender-tailed meerkats (Suricata suricatta) according to clinicopathologic findings and immunohistochemistry. Five of nine meerkats died during an outbreak in late 1994. These included four kits (2.5 to 4.5 months old) and a 4-year-old meerkat. Two other meerkats, both adults, died in 1992 and 1995. Respiratory insufficiency (4/7) and incoordination (3/7) were the most consistent clinical signs. although two of seven meerkats died unexpectedly. At necropsy, the lungs were reddened and noncollapsed (6/7), and had multiple pale round foci (4/7). Yellow foci of necrosis in mesenteric lymph nodes (4/7), splenomegaly (3/7), and hydropericardium (3/7) were other common gross findings. Microscopically, interstitial pneumonia was present in all seven meerkats, being acute to subacute in six of them. Type 2 pneumocyte hyperplasia, aggregates of foamy macrophages, and giant cells were consistently seen. Multifocal to locally extensive necrosis of mesenteric lymph nodes (4/7), mild to severe multifocal necrotizing hepatitis (5/6), and mild nonsuppurative encephalitis (4/6) were also seen. Toxoplasma-like organisms were consistently associated with these lesions and were stained by the avidin biotin peroxidase procedure with an antiserum that does not cross-react with Neospora caninum. Meerkats were most likely infected after an oral, primary exposure to Toxoplasma. Several observations indicate that meerkats may be highly susceptible to toxoplasmosis.

Animals↗
PubMed2003

Frosted branch angiitis and late peripheral retinochoroidal scar in a patient with acquired toxoplasmosis.

PURPOSE: To report a case of acute frosted branch angiitis associated with acquired toxoplasmosis in which a late peripheral chorioretinal scar developed. RESULTS: A 32-year-old man without systemic symptoms presented with sudden visual loss in his left eye. Examination demonstrated frosted branch angiitis without necrotizing chorioretinitis. Serologic tests showed elevated Toxoplasma gondii-specific immunoglobulin M antibody titers. Antitoxoplasmic therapy and oral steroids healed the ocular inflammation. In a follow-up visit one year later, a peripheral chorioretinal scar was noted. CONCLUSIONS: Acute frosted branch angiitis without focal necrotizing chorioretinitis can be a manifestation of acquired toxoplasmosis. This could be an important, and sometimes forgotten, sign of the disease.

Adult↗
PubMedDate not supplied

Reactivation of ocular toxoplasmosis in fellow unaffected eye.

PURPOSE: To report a case of reactivation of ocular toxoplasmosis in fellow unaffected eye. METHODS: Case report. RESULTS: A 15 year old girl, known to have right ocular toxoplasmosis previously, has presented with one week history of sudden left visual deterioration and pan uveitis. Her condition was improved on intensive steroid treatment. CONCLUSIONS: Reactivation of such lesion in fellow unaffected eye is quite rare. Various choices of treatment are available and there are also different techniques to treat. A review of treatment based on this pathology is briefly discussed.

Adolescent↗
PubMed2003

Comparison of two DNA targets for the diagnosis of Toxoplasmosis by real-time PCR using fluorescence resonance energy transfer hybridization probes.

BACKGROUND: Toxoplasmosis is an infectious disease caused by the parasitic protozoan Toxoplasma gondii. It is endemic worldwide and, depending on the geographic location, 15 to 85% of the human population are asymptomatically infected. Routine diagnosis is based on serology. The parasite has emerged as a major opportunistic pathogen for immunocompromised patients, in whom it can cause life-threatening disease. Moreover, when a pregnant woman develops a primary Toxoplasma gondii infection, the parasite may be transmitted to the fetus and cause serious damage. For these two subpopulations, a rapid and accurate diagnosis is required to initiate treatment. Serological diagnosis of active infection is unreliable because reactivation is not always accompanied by changes in antibody levels, and the presence of IgM does not necessarily indicate recent infection. Application of quantitative PCR has evolved as a sensitive, specific, and rapid method for the detection of Toxoplasma gondii DNA in amniotic fluid, blood, tissue samples, and cerebrospinal fluid. METHODS: Two separate, real-time fluorescence PCR assays were designed and evaluated with clinical samples. The first, targeting the 35-fold repeated B1 gene, and a second, targeting a newly described multicopy genomic fragment of Toxoplasma gondii. Amplicons of different intragenic copies were analyzed for sequence heterogeneity. RESULTS: Comparative LightCycler experiments were conducted with a dilution series of Toxoplasma gondii genomic DNA, 5 reference strains, and 51 Toxoplasma gondii-positive amniotic fluid samples revealing a 10 to 100-fold higher sensitivity for the PCR assay targeting the newly described 529-bp repeat element of Toxoplasma gondii. CONCLUSION: We have developed a quantitative LightCycler PCR protocol which offer rapid cycling with real-time, sequence-specific detection of amplicons. Results of quantitative PCR demonstrate that the 529-bp repeat element is repeated more than 300-fold in the genome of Toxoplasma gondii. Since individual intragenic copies of the target are conserved on sequence level, the high copy number leads to an ultimate level of analytical sensitivity in routine practice. This newly described 529-bp repeat element should be preferred to less repeated or more divergent target sequences in order to improve the sensitivity of PCR tests for the diagnosis of toxoplasmosis.

Animals↗
PubMed1983

Fatal CNS toxoplasmosis in a homosexual man.

A compromised cellular immunity associated with an increased frequency of tumors and fatal opportunistic infections has recently been reported in homosexual men. We studied a homosexual man with fatal CNS toxoplasmosis to emphasize the value of CT in CNS toxoplasmosis and to alert neurologists to potentially curable opportunistic infections.

Central Nervous System Diseases↗
PubMed1996

Clinical features, outcome and survival from cerebral toxoplasmosis in Edinburgh AIDS patients.

Nineteen cases of cerebral toxoplasmosis (CTOX) are reported from a group of Edinburgh AIDS patients. All patients were severely immunodeficient at the time of presentation with CD4 count < 50 cells/mm3. Thirteen patients had suffered a previous AIDS-defining illness. In Edinburgh, CTOX has developed in 48% of patients who are seropositive for toxoplasma and have a CD4 count < 50 cells/mm3. It is estimated that at least half of the toxoplasma seropositive patients will develop CTOX if they survive for 21 months after reaching a time in their illness when the CD4 count = 50 cells/mm3. The incidence of CTOX in toxoplasma-seronegative patients with a CD4 count < 50 cells/mm3 is 1.3%. All patients showed improvement on treatment and there was no correlation between clinical or radiological features and patient survival. Those patients unable to tolerate first choice anti-toxoplasma therapy had a significantly shorter survival than the remainder but there was no single therapeutic regimen which conferred a survival advantage. Eighteen patients had died at the time of study and the median survival following diagnosis of cerebral toxoplasmosis was 10 months (range 3-38 months). Postmortem examination of the brain was available in 8, 4 of whom had concomitant cerebral lymphoma. The survival from AIDS or CD4 count = 50 cells/mm3 did not differ significantly between those with treated CTOX and a control group who had no toxoplasma infection, suggesting that treatment is reasonably effective. CTOX is a disease associated with severe HIV-related immunodeficiency and, in those with a CD4 count < 50 cells/mm3, occurs more than 35 times as frequently in toxoplasma-seropositive than toxoplasma-seronegative patients. Treatment is effective but the outcome of treated disease cannot be predicted from presenting clinical or radiological features. Concomitant space-occupying cerebral pathology is evident in 50% of post-mortem examinations.

Acquired Immunodeficiency Syndrome↗
PubMedDate not supplied

Ocular toxoplasmosis in HIV infection.

Toxoplasmosis accounts for 1-3% of ocular infections in patients with AIDS1. There are a variety of clinical manifestations that can be confused with other ocular disease. It may be the first manifestations of intracranial and disseminated Toxoplasma gondii infection. Prompt recognition and early treatment with antiparasitic drug therapy will prevent widespread tissue destruction, preserve vision and reduce dissemination. This current review will provide a broad-based overview of toxoplasmosis and ocular infection.

AIDS-Related Opportunistic Infections↗
PubMed2003

Testing for toxoplasmosis in pregnancy: a study of the routines in primary antenatal care.

OBJECTIVES: The question of benefit of screening for antibodies against Toxoplasma gondii in pregnancy to prevent impairment in the infant has not been settled. Despite this, it is believed that such testing is common. The aim of this study was to describe the test routines and to identify factors associated with testing in primary antenatal care. SETTING: Ulleval University Hospital, Oslo, Norway. METHODS: All women who gave birth at Ulleval University Hospital, Oslo, Norway, in May 2000 were included. The number of antibody tests during pregnancy was obtained from the patient registry at the department of microbiology at the same hospital. RESULTS: 81% (361/446) had been tested for antibodies against Toxoplasma gondii during pregnancy. Women attending primary antenatal care at a specialist in obstetrics and gynaecology were most likely to be tested. Among women with no signs of prior toxoplasmosis, 35% (110/317) were tested only once. DISCUSSION: The majority of pregnant women are being tested for toxoplasmosis even though such testing has no documented preventive effect and has not been recommended.

Adult↗
PubMed1997

Acute toxoplasmosis in squirrel monkeys.

Five cases of acute toxoplasmosis in caged squirrel monkeys (Saimiri sciureus) were reviewed. The early stages of systemic toxoplasmosis were present in all cases. In the liver, there were multiple foci of hepatocellular necrosis. The lung had diffuse interstitial pneumonia. Tachyzoites were mainly seen associated with lesions in the liver, lung, and spleen. Immunohistochemically, tachyzoites reacted with T. gondii antibody. Electron-microscopically, intracellular tachyzoite was surrounded by a thin wall and was in a membrane-bound parasitophorus vacuole.

Animals↗
PubMed1993

Septic shock due to toxoplasmosis in patients infected with the human immunodeficiency virus.

PURPOSE: To describe the presentation and clinical course of septic shock due to Toxoplasma gondii in patients infected with the human immunodeficiency virus (HIV). PATIENTS AND METHODS: From April 1988 to February 1992, nine HIV-infected patients were admitted because of predominant septic shock (7 patients) or developed septic shock in the ICU (2 patients). The recent CD4+ cell count ranged from 2 to 84 x 10(6)/L. RESULTS: The main clinical features were (1) a history of fever for longer than 15 days, with a recent increase to more than 39.5 degrees C; (2) a recent history of dyspnea (< 15 days, 8 cases; < 7 days, 3 cases); and (3) recent onset of thrombocytopenia (6 of 9 cases). All patients were in shock (hyperkinetic profile in 6 of 7; hypokinetic in 1 of 7), and 8 of 9 were in respiratory distress (ratio of PaO2 over fractional concentration of oxygen in the inspired gas of 117 +/- 23; range, 88 to 155). Chest roentgenograms revealed diffuse alveolar infiltrates in six of nine cases. The serum lactate dehydrogenase (LDH) activity was 6,510 +/- 5,080 IU/L (range, 1,010 to 15,450 IU/L). Serologic tests for T gondii were negative in two cases. Toxoplasma gondii was isolated from lung (9/9), bone marrow (5/7), or blood (2/2). One, 3, and 2 patients had brain, ocular, and myocardial involvement, respectively. No other microbial pathogens were isolated. Seven patients died, 5 less than 3 days after admission. CONCLUSION: Disseminated toxoplasmosis can cause septic shock in HIV-infected patients. In two cases, the disease was probably a primary infection. The association of high fever, acute dyspnea, recent onset of thrombocytopenia, and a very high level of LDH activity is suggestive of disseminated toxoplasmosis.

AIDS-Related Opportunistic Infections↗
PubMedDate not supplied

Precocious puberty: an endocrine manifestation in congenital toxoplasmosis.

We reviewed retrospectively seven children with congenital toxoplasmosis and precocious puberty. All seven showed very high levels of LH (25.2-155.0 IU/ml) and FSH (7.1-38.2) upon stimulation with GnRH. Three of them showed low GH response to an insulin tolerance test. All the children had severe mental retardation. We emphasize that children with congenital toxoplasmosis should have their hypothalamopituitary function evaluated even in subclinical situations that could be responsible for endocrinological disturbances such as precocious puberty.

Child↗
PubMed2000

Prevention of congenital toxoplasmosis.

In utero infection with Toxoplasma gondii may result in congenital defects such as hydrocephalus, chorioretinitis and mental retardation; these defects may be present at birth or may develop later in life. Prevention of this disease can be achieved in different ways. The most effective measure is to prevent the acquisition of the disease during pregnancy by avoiding risk factors for Toxoplasma gondii infection. Health education may decrease the incidence of toxoplasmosis during pregnancy by 60%. A second preventive measure is based on serologic screening during pregnancy to identify infected women. Treatment during pregnancy results in a significant reduction in the incidence of sequelae including severe handicaps. A third possible intervention is treating infected neonates. Antibiotic treatment of infected children has a beneficial effect on the development of sequelae and the sooner therapy is started after birth, the better the outcome. This overview presents the potential benefits and harms of these different options available for the prevention of congenital toxoplasmosis.

Animals↗