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PubMed1999

Reconsidering the pathogenesis of ocular toxoplasmosis.

PURPOSE: To review recent observations regarding the sources of Toxoplasma gondii infection and rates of ocular involvement in cases of infection acquired after birth, and to reconcile them with older observations and widely held beliefs about the pathogenesis of ocular toxoplasmosis. METHOD: A review of pertinent reports from the medical literature. RESULTS: There are several potential sources and routes of infection, including inhalation of spores and ingestion of contaminated drinking water, that were previously unrecognized. Ocular involvement in cases of acquired infection appears to be more common than heretofore believed. A variety of host and parasitic factors may influence rates of ocular infection and the characteristics of ocular disease. CONCLUSIONS: The scars from which recurrent toxoplasmic retinochoroiditis arise may be the result of remote, acquired infections in many cases, rather than the residua of congenital infections, as commonly assumed. A better understanding of the epidemiology of T. gondii infection, as well as the host and parasitic factors that influence disease presentation, is important for developing strategies for prevention and management of ocular toxoplasmosis.

Animals↗
PubMedDate not supplied

Pathology of toxoplasmosis in captive new world primates.

Clinical information was available for 32 of 33 New World primates with fatal toxoplasmosis, all of which were subjected to a variable number of pathological observations. Death without apparent clinical signs occurred in 43.7% of cases. The most common clinical findings were malaise (40.6%), dyspnoea (18.7%), hypothermia (15.6%) and a sero-sanguinous or foamy nasal discharge (12.5%). Nutritional status was good in 71.8%, average in 18.7% and poor in 9.4%. The most common post-mortem findings were pulmonary congestion (78.8%), pulmonary oedema (75.8%), splenomegaly (57.6%) and mesenteric lymphadenitis (54.6%). The most common histopathological findings were multifocal necrotic hepatitis (97%), lymphadenitis (95.4%), interstitial pneumonia (90.3%) and necrotic splenitis (71.4%). The gross post-mortem changes in cebids were more variable than those observed in callitrichids, a fact that may complicate the diagnosis of toxoplasmosis in cebids.

Animals↗
PubMed1994

Toxoplasmosis of the bladder: case report and review of the literature.

Toxoplasma gondii is an intracellular parasite that is responsible for an asymptomatic or minimally symptomatic lymphadenopathy syndrome, which in the immunocompromised host can be life threatening. Toxoplasmosis commonly affects the central nervous system. Genitourinary involvement is uncommon with reported cases limited to Toxoplasma orchitis and the nephrotic syndrome. To our knowledge we report the first case of toxoplasmosis of the bladder as an intravesical mass without central nervous system or other organ involvement in a young man with the acquired immunodeficiency syndrome.

AIDS-Related Opportunistic Infections↗
PubMed2000

[Seroprevalence of toxoplasmosis in women of childbearing age, 1992-1999].

UNLABELLED: To determine the need of prenatal screening for toxoplasmosis in our hospital from a seroepidemiological point of view. PATIENTS AND METHODS: The prevalence of IgG anti-T. gondii was retrospectively analyzed in 7.090 women of childbearing age attended in the Hospital Clínic of Barcelona from February 1992 to April 1999. The association among the seroprevalence and the variables year, age, birthplace (province of Barcelona/other provinces) and place of residence (urban/rural) was analyzed. A decreasing trend was observed in the prevalence (p < 0.001), currently being < 40% in the average women between 15 and 45 years. Infection was also directly related to age of women (p < 0.001) and birthplace out of the province of Barcelona (p = 0.001). Habitat (rural or urban) was not associated with seroprevalence. Prenatal screening for toxoplasmosis is necessary due to the high rate of seronegative women exposed to infection and the evidence of a high number of primoinfections in the childbearing period.

Adolescent↗
PubMed2001

Prenatal diagnosis using polymerase chain reaction on amniotic fluid for congenital toxoplasmosis.

OBJECTIVE: To evaluate sensitivity, specificity, and predictive values of a prenatal amniotic fluid (AF) polymerase chain reaction (PCR) test for diagnosis of congenital toxoplasmosis. METHODS: A multicenter prospective study was done on 271 women with proved primary Toxoplasma infection during pregnancy and who had amniocentesis for prenatal diagnosis by PCR. Live-born infants were eligible for analysis only if a serologic follow-up could assess a definitive infection status. RESULTS: Of the 270 evaluable cases, 75 were congenitally infected, 48 of whom had a positive PCR at prenatal diagnosis. Overall sensitivity of PCR on AF was estimated at 64% (95% confidence interval [CI] 53.1%, 74.9%), negative predictive value of 87.8% (95% CI 83.5%, 92.1%), whereas specificity and positive predictive value were 100% (95% CIs 98%, 100% and 92.3%, 100%, respectively). Among cases with congenital toxoplasmosis, there were no significant differences between those with positive or negative PCR with regard to median gestational age at maternal infection, interval between maternal infection and amniocentesis, or duration of treatment before amniocentesis. However, sensitivity of PCR was found to be significantly higher for maternal infections that occurred between 17 and 21 weeks' gestation (P <.02). CONCLUSION: A negative PCR of AF cannot rule out congenital infection. In this case, continuation of treatment with spiramycin combined with ultrasonographic follow-up and postnatal follow-up are warranted. Our results also suggest presumptive treatment combining pyrimethamine and sulfonamides in case of maternal infection occurring late in pregnancy.

Adult↗
PubMed1988

Occlusive hypertrophic arteritis as the cause of discrete necrosis in CNS toxoplasmosis in the acquired immunodeficiency syndrome.

Brain specimens from five immunocompromised patients with CNS toxoplasmosis were studied with immunostaining for toxoplasma antigens and electron microscopy. The tachyzoites or toxoplasma antigens were predominantly localized in walls of hypertrophic, often thrombosed, arteries and adjacent brain tissue at the hyperemic rims of centrally necrotic lesions. This study suggests that in CNS toxoplasmosis of immunocompromised hosts, the organisms primarily invade and spread along segments of small artery walls, causing hypertrophy of arterial walls, thrombotic occlusion of lumens, circumscribed but expansive ischemic necrosis, and extravasation of organisms. Rapid response to chemotherapy can be explained by this preferential parasitism to the arterial walls. Early definitive diagnosis on brain biopsy specimens can be attained by immunostaining.

Acquired Immunodeficiency Syndrome↗
PubMed1993

Toxoplasmosis neuroretinitis.

BACKGROUND: Neuroretinitis is a distinct clinical entity consisting of moderate to severe visual loss, optic nerve head edema, macular exudate in a stellate pattern, and variable vitreous inflammation. Although the etiology is usually postviral or idiopathic, an acute infectious cause occasionally is demonstrated. METHODS: Five juvenile or young adult patients with neuroretinitis are presented with serologic evidence of Toxoplasma gondii infection. Four of the five patients were treated with systemic antibiotics and corticosteroids; one patient was not treated. RESULTS: With a mean follow-up period of 50 months, visual acuity returned to 20/25 or better in four patients, with one patient regaining visual acuity of 20/60. Two patients had one or more recurrent episodes of neuroretinitis, distinguishing toxoplasmosis from idiopathic neuroretinitis, which is usually a monophasic illness. CONCLUSION: Toxoplasmosis infection is a rare, but potentially treatable, form of neuroretinitis and should be included in the differential diagnosis of "Leber's idiopathic stellate retinopathy."

Adult↗
PubMed1988

Outer retinal toxoplasmosis.

Toxoplasma gondii is a neurotrophic organism that affects the neurosensory retina in humans. Typical ocular toxoplasmosis involves the inner retina and is associated with marked vitreous reaction. A subset of this clinical spectrum is characterized by gray-white macular lesions at the level of the outer retina. This outer retinal lesion is associated with little or no vitreous reaction. The authors report five additional cases of outer retinal toxoplasmosis. Recognition of this variation is important; prompt treatment, before serologic confirmation, resulted in marked visual improvement in all cases.

Adolescent↗
PubMed1998

Multiple cases of acquired toxoplasmosis retinitis presenting in an outbreak.

OBJECTIVE: The purpose of the study was to examine the variability in presentation and outcome of individuals presenting with acquired toxoplasmosis retinitis in the setting of an outbreak of the disease. DESIGN: The study design was a case series. PARTICIPANTS: Twenty-one eyes of 20 patients with equal gender distribution and a mean age of 54 years followed for 38 to 170 weeks (mean 113.7 weeks) were studied. INTERVENTION: Systemic antimicrobials and corticosteroids when indicated were given. MAIN OUTCOME MEASURES: Visual acuity, media inflammation and clarity, resolution of active retinitis, and appearance of recurrence were observed. RESULTS: Fifteen of 21 lesions were active, and 7 of the total number of lesions fell within the macula-peripapillary region. Overall, vision improved with treatment except in cases of macular involvement (3 cases) and persistent vitritis (3 cases). Four recurrences have occurred to date. CONCLUSIONS: This is the largest reported outbreak of acquired toxoplasmosis retinitis occurring within a single outbreak. Twenty-one eyes of 20 patients presented with retinal lesions, and on average, those treated for active retinitis had improvement in vision.

Adolescent↗
PubMed1991

New methods in the diagnosis and management of cerebral toxoplasmosis associated with the acquired immune deficiency syndrome.

Cerebral toxoplasmosis is a life-threatening condition associated with the acquired immune deficiency syndrome (AIDS). Current diagnostic and therapeutic methods have serious limitations. The diagnosis of cerebral toxoplasma infection in a patient with AIDS was assisted by the detection of specific IgM in a highly sensitive immunosorbent agglutination assay and by the demonstration of Toxoplasma gondii nucleic acid in a brain biopsy specimen by means of the polymerase chain reaction. Following initial failure of the patient to respond to treatment with sulphadiazine and pyrimethamine, clinical improvement was observed during treatment with clindamycin followed by dapsone. Further assessment of novel methods in the management of cerebral toxoplasmosis is required.

Acquired Immunodeficiency Syndrome↗
PubMed1984

A family outbreak of toxoplasmosis: a serendipitous finding.

A family outbreak of toxoplasmosis involving five members of a Lebanese family is described. We believe it to be the first reported outbreak of toxoplasmosis in Australia. Kibbi , a traditional Lebanese dish which can occasionally incorporate raw meat, may have been the source of infection. The chance occurrence of an outbreak of hepatitis A in the same family subsequently led us to discover this outbreak.

Adult↗
PubMed1989

Diagnosis of congenital toxoplasmosis in Scotland.

During a period of 10 years (1976-1986) 853 cases of toxoplasmosis were identified serologically in the Toxoplasma Reference Laboratory in Scotland. Suspected cases of infection in pregnancy (29 cases) and of congenital infection (27 cases) were rare but ophthalmic disease was common (224 cases). In two of the congenital cases, maternal infection was identified during pregnancy. The other 25 babies were investigated because of suspected congenital infection. Toxoplasmosis was confirmed retrospectively in 11/25 babies and excluded in two of them. The other 12 cases remain unclassified. Diagnosis of infection in babies was difficult although the introduction of an IgM capture ELISA was of some help. IgM was detected by ELISA in 3/13 congenitally infected babies but by immunofluorescence tests in only one of these. In two antenatal studies, involving 16,000 women, an additional 32 women were identified whose babies might have benefited from treatment or the availability of fetoscopy for early detection of congenital infection.

Animals↗
PubMed1989

Failure to diagnose fatal disseminated toxoplasmosis in a bone marrow transplant recipient: the possible significance of declining antibody titres.

A 46-year-old patient with acute myelogenous leukaemia developed lethal disseminated toxoplasmosis 8 weeks after allogeneic bone marrow transplantation. Clinical features included pulmonary infiltrates, respiratory insufficiency and neurological signs. Post-transplantation toxoplasma serological tests were characterised by declining IgG titres and failure to detect IgM, whereas titres of IgG against the various herpes viruses remained constant and even increased over the same period. Circulating toxoplasma antigen could not be detected. Post mortem, specific immune complexes were identified in serum. Autopsy revealed widely disseminated toxoplasmosis with several foci in the brain, lungs and various other organs as well as concomitant infection with cytomegalovirus.

Animals↗
PubMed1998

[Epidemiologic characteristics of cerebral toxoplasmosis in 399 HIV-infected patients followed between 1983 and 1994].

OBJECTIVE: To describe the epidemiological characteristics of toxoplasmic encephalitis in HIV-infected patients with a more than 12-year follow-up. METHODS: From a data base of 1,628 AIDS subjects hospitalized from 1983 to 1994, we studied the epidemiological characteristics of 399 patients with toxoplasmic encephalitis. Diagnosis of toxoplasmic encephalitis was based on the association of central neurological disorders, typical lesions on CT scan or MRI, and favorable outcome under appropriate toxoplasmosis therapy. RESULTS: Four hundred sixty-four cases of toxoplasmic encephalitis were reported in 399 patients (24.5% of the patients with AIDS). The overall incidence was 20.5 per 100 patients-year. Toxoplasmic encephalitis was the first AIDS defining event in 51% of the cases and revealed HIV infection in 13% of the cases. In the remaining 49%, the mean delay from AIDS diagnosis to toxoplasmic encephalitis was 13 months (range: 1-71 months). At the time of diagnosis, mean CD4 count was 44/mm3 (range: 0-408/mm3). Antibodies to Toxoplasma gondii were found in 97% of the cases. Before the first episode of toxoplasmic encephalitis, 58% of the patients were given antiretroviral therapy (mean: 17.8 months; range: 1-64 months). Of the 399 patients with toxoplasmic encephalitis, 366 (92%) did not receive any primary toxoplasmosis prophylaxis. Among them, 205 (56%) did not receive any drug prophylaxis, and 161 (44%) had Pneumocystis carinii pneumonia prophylaxis alone (aerosolized pentamidine). Thirty-three failures were observed (8%) with cotrimoxazole: 14 cases (3%) were considered to have irregular compliance. Sixty-five relapses were observed in 52 patients. At the end of the study 334 patients had died (84%). The median survival was 11.4 months (95% confidence interval, range: 10.4-12.4 months). CONCLUSIONS: Toxoplasmic encephalitis incidence has decreased since the introduction of appropriate drug prophylaxis.

AIDS-Related Opportunistic Infections↗
PubMed2001

Neonatal screening for congenital toxoplasmosis in a cohort of 165 women infected during pregnancy and influence of in utero treatment on the results of neonatal tests.

The aim of this study was to determine the performances of methods used for the neonatal diagnosis of congenital toxoplasmosis. We included 165 pregnant women infected during pregnancy over a 10-year period. Fifty-seven cases of congenital toxoplasmosis were demonstrated (34.5%). Neonatal diagnosis gave positive results in 50 cases (88%). Parasites were isolated from placenta or cord blood in 61% of the infected newborns, more frequently from placenta (60%) than from cord blood (43%). This method was the only criterion of infection in 18% of these infected infants. The detection of specific IgM and IgA antibodies performed on 42 sera of infected infants allowed the diagnosis of congenital infection in 34 cases (81%). IgA antibodies were more frequently detected (60%) than specific IgM (50%). Neonatal and prenatal screening were carried out for 143 pregnant women. This combination diagnosed 39 of 40 infected infants (98%). Prenatal diagnosis identified 30 of 40 cases (75%). Nine cases were diagnosed through neonatal screening and one case with the postnatal follow-up. When prenatal diagnosis was positive, pyrimethamine and sulfadoxine were administered to the mothers (25 cases) in addition to spiramycin. Toxoplasma gondii was less frequently isolated in the placenta and the cord blood of these women (32% and 19%, respectively) than in women treated by spiramycin alone (83% and 63%) proving the antiparasitic action of these drugs. In conclusion, neonatal screening combining parasite detection in placenta and immunological methods on cord blood is essential particularly when prenatal diagnosis is negative. Therefore, when this diagnosis is positive, a treatment with pyrimethamine and sulfamide can be started in the first month of life.

Animals↗
PubMed2000

Fatal toxoplasmosis in brown hares (Lepus europaeus): possible reasons of their high susceptibility to the infection.

Brown hares (Lepus europaeus) trapped in the countryside and domestic rabbits were experimentally infected with Toxoplasma gondii (K7 strain) oocysts. Hares (n=12) were divided into groups of 4 and infected with 10, 10(3) and 10(5) oocysts. Rabbits (n=12) were infected in the same way. The experimentally infected animals were monitored for 33 days after infection (p.i.). Most of the infected hares demonstrated behavioural changes, and all of them died between 8 and 19 days p.i. Three of the rabbits demonstrated only clinical changes related to the concurrent pasteurellosis. The typical pathological finding in the hares were haemorrhagic enteritis, enlargement and hyperaemia of mesenteric lymph nodes, splenomegaly and multiple miliary necrotic lesions in the parenchyma of the liver and other organs. Pathological changes in the rabbits were less pronounced than in the hares. In rabbit brains, tissue cysts of the T. gondii were found. The incidence of T. gondii antibodies both in the hares and the rabbits was first ascertained on day 7 p.i. On day 12 p.i., antibodies were already found in all the animals infected. Antibody titres in indirect fluorescence antibody test (IFAT) using the anti-rabbit conjugate were markedly higher in rabbits than in hares. In all hares, T. gondii was isolated post mortem from the liver, brain, spleen, kidney, lung, heart and skeletal muscles. Although T. gondii was also isolated in all rabbits, it was not always isolated in all their organs. In all hares, parasitemia was demonstrated on days 7 and 12 p.i. The percentage of rabbits with detected parasitemia was lower. In hares, a decrease in the numbers of leukocytes during the infection was observed. No such decrease was observed in the rabbits. The lymphocyte activity after the stimulation with non-specific mitogens showed significant differences between the hares and the rabbits even before the infection. After the infection, the hares infected with 10(3) and 10(5) doses and in rabbits infected with a 10(5) dose showed a decrease of lymphocyte activity. Rabbits infected with a 10(3) dose showed an increase of the lymphocyte activity. While in hares toxoplasmosis was an acute and fatal disease, the infection in rabbits had subclinical manifestations only and easily passed to a latent stage. The different courses of toxoplasmosis in the hare and the rabbit may be due to the differences in the natural sensitivity of the two species to the T. gondii infection or a negative impact of stress to the immune status of hares.

Animals↗
PubMed2002

A review of toxoplasmosis in wild birds.

Toxoplasma gondii affects most species of warm-blooded animals, including birds. There is considerable confusion regarding the identity of T. gondii-like parasites and the diagnosis of toxoplasmosis in wild birds. In this review, T. gondii-like infections in different species of wild birds are reviewed with particular reference to prevalences, clinical signs, pathology, diagnosis, and treatment. Although subclinical T. gondii infections are prevalent in many avian species, toxoplasmosis can be clinically severe in pigeons and canaries. Blindness associated with T. gondii in canaries is reviewed in detail.

Animals↗
PubMed1997

Experimental toxoplasmosis in broiler chicks.

To evaluate chicken toxoplasmosis both as an economic and a public health subject, 84 broiler chicks of a commercial strain, 30 days old, were distributed into seven groups of 12 birds (three replications of four chicks) experimentally infected with three developing T. gondii stages of the P strain as follows: tachyzoites, intravenous (two groups: 5.0 x 10(5) and 5.0 x 10(6)), cysts, per os (two groups: 1.0 x 10(2) and 1.0 x 10(3)) and oocysts, per os (three groups: 5.0 x 10(2), 5.0 x 10(3) and 5.0 x 10(4)). Twelve chicks received only a placebo (control group). During the next 30 days the following parameters were estimated: productivity (weight gain and feed conversion), clinical signs, including rectal temperature and parasitemia (bioassay). No clinical signs suggesting toxoplasmosis were seen and no statistical differences on productivity standards were found in comparison between inoculated and control chicks. However, fowls inoculated with tachyzoites and oocysts occasionally showed hyperthermia. Some haematological changes were detected in fowls inoculated with T. gondii. Anatomo-histopathological changes were not observed. From 14 parasitemias detected, 35.7% appeared on the 5th day after inoculation and 57.1% of them resulted from oocysts inoculation. After 30-35 days all birds were slaughtered: fragments from 12 organs or tissues from each of them were subjected to artificial peptic digestion and after that injected into T. gondii antibody-free mice (IIFR). T. gondii was detected in brain (12), pancreas (five), spleen (five), retina (five), kidney (two), heart (four), proventriculus (three), liver (two), intestine (two), lung (one), and skeletal muscle (one). Similar to observations with parasitemia, from 42 T. gondii isolations, 59.5% came from chicks which had received oocysts. It can thus be inferred that the developing form, expelled by cats, is the most important for T. gondii chicken infection and that brain is the most infected organ in birds. Attention must be paid to the potential importance of chicken meat in public health, since T. gondii was isolated from skeletal and heart muscles.

Animals↗