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Ocular toxoplasmosis in consecutive siblings is rare. We report positive ocular and serologic findings in three consecutive teenaged siblings. Results of immunologic studies that were performed on members of the family failed to reveal deficiencies.
Of 60 attacks of ocular toxoplasmosis, in 37 (62%) no apparent macular problems were demonstrated on inspection, in seven (12%) active retinitis was evident within 5 degrees of the umbo, and in seven (12%) some evidence was shown of mild macular edema; severe edema, such as cystoid macular edema, was uncommon.
A 30-year-old woman was treated with unrelated HLA-compatible bone marrow transplantation for acute myeloid leukemia. Examination of her bone marrow smears because of fever and pancytopenia revealed the presence of Toxoplasma cysts. Although Toxoplasma cysts are rarely found in the bone marrow, bone marrow examination in the immunocompromised patient offers rapid diagnosis of systemic toxoplasmosis.
We reviewed the clinical, neuroradiological, and serological findings in 27 patients with cerebral toxoplasmosis complicating the acquired immune deficiency syndrome, 19 of whom were also analyzed neuropathologically. The clinical manifestations of this disorder varied, ranging from headache and fever to coma. However, the characteristic presentation included focal neurological symptoms and signs, usually of subacute onset. In addition, two-thirds of the patients exhibited more generalized cerebral dysfunction with confusion and lethargy. The computed tomographic (CT) scan most commonly revealed ring contrast enhancement, which appeared to correlate best with the histological presence of vascular proliferation and inflammation surrounding the abscesses. However, in 5 patients the CT scan revealed either homogeneous enhancement or no enhancement, and in 3 patients the scans were negative. In general, CT scans underrepresented the number of lesions eventually documented pathologically. Double-dose contrast administration and preliminary experience with magnetic resonance imaging suggested that these techniques were superior to standard CT scanning in detecting Toxoplasma lesions. All patients were seropositive for IgG antibody against Toxoplasma gondii in blood, both before the onset of illness and at the time of presentation, although titers in some patients were as low as 1:8 and most patients did not exhibit rising titers. Prompt therapy resulted in rapid clinical improvement, documented by CT scan, associated with the development of an organizing tissue response in the host and elimination of free organisms. Response to treatment was sufficiently rapid in most patients to allow a trial of therapy as the favored approach to diagnosis.
A case of retrovesical squamous cell carcinoma associated with acquired toxoplasmosis is presented. To date only six cases with retrovesical carcinoma have been reported in the literature. Although it is difficult to make a preoperative diagnosis of this rare neoplasm, transrectal longitudinal ultrasonography was diagnostically valuable, and serial measurements of serum squamous cell antigen (SCC-Ag) were useful for monitoring the clinical course.
The wall of intact tissue cysts in the brains of mice with congenital toxoplasmosis was investigated using light and electron microscopy. Impregnation of the wall with reduced silver salts and protargol silver suggested that it was composed, at least in part, of components derived from the neuronal cytoskeleton. Electron microscopy extended these observations and revealed that intact cysts were separated from the extracellular compartment by a layer of neurofibrillae enclosed within the host cell membrane. It is suggested that this may be a means whereby intact Toxoplasma tissue cysts are protected from the host's immune response.
Prenatal diagnosis of congenital toxoplasmosis relies on the PCR test on amniotic fluid and ultrasound follow-up of the fetus. We report two cases of toxoplasma infection during the first trimester of gestation with a discrepant diagnosis of fetal infection. PCR performed more than four weeks after the estimated date of contamination was negative. Ultrasound follow-up was normal up to the third trimester when major hydrocephalus was detected, leading to pregnancy termination. In both cases, post-mortem examination revealed a diffuse infection with severe brain lesions. These observations confirm the necessity to continue a monthly ultrasound follow-up, even if amniocentesis is negative, in case of fetal toxoplasma infection in pregnancy.
Patients with congenital toxoplasmosis occasionally show rises in serum antibodies to Toxoplasma gondii (serological rebound), but the underlying cause remains unclear. The acute or chronic presence of available antigen often causes the appearance, in the peripheral blood, of cells actively secreting specific antibody. We have evaluated the capacity of circulating blood cells from 91 children born to T. gondii-infected mothers to actively synthesize anti-T. gondii antibodies according to their serological status. Supernatants from 7-day cultures of peripheral blood mononuclear cells were evaluated for antibody by cytofluorimetry. Only 1 of 49 subjects with low and stable serum antibody titers produced specific antibodies on cultures, while 9 of 22 subjects with recent rebound were positive. One of the positive children alone showed clinical signs of parasite activity. These observations suggest that rebound may be associated with production of available parasite antigens, possibly associated with reactivation. Differentiation from other causes, such as polyclonal B cell stimulation, would improve our ability to detect clinically significant reactivation and to prevent complications.
This paper describes a rhesus monkey model to study congenital transmission and the prenatal diagnosis of Toxoplasma gondii infection. Transmission to the fetus was investigated after maternal infection in the second (Day 90) or third trimester (Day 130) of pregnancy. A parasitemia was induced and lasted for about 10 days as proven by mouse inoculation and nested PCR on whole blood samples and peripheral blood mononuclear cells. Transmission of T. gondii was proven in 4 of 9 (44%) fetuses in the second trimester and in 3 of 9 fetuses in the third trimester of gestation. Six of the 7 proven fetal infections could be diagnosed antenatally. Postnatally, 4 additional fetuses that most likely were congenitally infected were found, although this could not formally be proven. The mothers of these 4 fetuses were infected in the third trimester. If we accept this group as being antenatally infected, an overall transmission rate is found of 11 of 18 cases (61%). This rate is similar to that found in humans. This is the first description of a monkey model for congenital toxoplasmosis, that is suitable to study the approach of antenatal diagnosis and the effectivity of treatment, with obvious relevance for Toxoplasma infections in humans.
DNA and mRNA amplification by the polymerase chain reaction (PCR), immunohistochemical, and histopathology were performed in the eyes and brains from C57BL/6 mice infected with an avirulent strain of Toxoplasma gondii (ME49). Focal ocular inflammation and retinal pigment epithelial involvement were commonly observed after 15 days of infection. Four weeks after infection a stable number of cysts was observed in the brain but rarely in the eye, and they did not elicit an inflammatory response. In most of the ocular lesions the presence of the parasite could not be demonstrated even with the PCR technique. B1 DNA fragments of T. gondii were detected in only 4 of 11 eyes tested by PCR and Southern blot hybridization. Treatment of mice with mAbs against T cells (CD4 plus CD8) or cytokines (IFN-gamma or TNF-alpha) resulted in a marked increase of ocular lesions, more often associated with the presence of the parasite and the severity of inflammatory response. This model and the techniques utilized here can improve our understanding of the respective roles of parasite proliferation and immune mechanisms involved in the pathogenesis of acquired ocular toxoplasmosis.
Toxoplasmosis may cause serious problems after organ transplantation. For treatment of active infection, pyrimethamine combined with a sulfonamide is recommended. During oral sulfadiazine therapy, a significant decrease in cyclosporine concentrations was observed in three heart transplant recipients. This interaction has not been reported previously.
Four patients with AIDS presented with a rapidly fatal global neurological illness. CT did not show any focal lesion and gross post mortem examination of the brain was normal in three of the four cases. Microscopic examination revealed numerous widespread microglial nodules in the brain parenchyma, most containing central toxoplama cysts or free tachyzoites. Such diffuse, non-necrotic, "encephalitic" forms of cerebral toxoplasmosis appear unique to AIDS and, to our knowledge, have not been documented previously. They represent a treatable, often misdiagnosed cause of diffuse neurological involvement in AIDS patients.
Two unusual cases of cerebral toxoplasmosis in AIDS patients are presented. Two homosexual males aged 33 and 52 years in CDC stage IV C1 complained of memory loss during the past 6 months, as well as weight loss and mild fever. They showed severe intellectual deterioration and discrete basal ganglia dysfunction. Motor performance and cognitive function as well as the conventional EEG findings were grossly abnormal. MRI was normal in the younger patient but showed signal-intensive zones in the basal ganglia and cortical atrophy in the older one. CSF and serological antibody tests were normal; immunological function was severely impaired. The patients were diagnosed as late "HIV-related dementia". Both deteriorated rapidly and died within a few weeks. Neuropathological examination revealed histologically severe Toxoplasma gondii encephalitis, involving the basal ganglia in particular. It is concluded that in AIDS patients with a severely impaired immune status cerebral opportunistic infection may present as dementia with mild basal ganglia impairment in the absence of other focal neurological signs or the characteristic radiological findings.
Authors report a case of fatal CNS toxoplasmosis in a young homosexual man suffering from Kaposi angio-sarcoma. This paper is principally concerned with CT scan and neuropathological correlations.
A study of 31 observations of congenital toxoplasmosis shows that there is a clear relationship between the cerebral lesions as observed on CT scan, neurological symptoms, and the date of maternal infection. The appearance of the CT scan is characteristic of cases with early maternal seroconversion (before the 20th week of pregnancy), of cases with maternal infection between the 20 and 30th week of pregnancy, and of cases with late maternal seroconversion (after the 30th week of pregnancy). Preventive maternal treatment does not change the pattern of the cerebral lesions observed on CT scan and thus proves ineffective in conferring real protection.
The pathological changes, host-parasite relationship and structure of the tissue cysts in the brains of mice chronically infected with four different strains of Toxoplasma gondii were examined by light and electron microscopy. In mice infected with the mouse-adapted ME49 strain for 4, 8, 12, 16 and 25 weeks, the pathological changes consisted of moderate to severe meningitis and cuffing of blood vessels by inflammatory cells. At 4 weeks post-infection (p.i.), lymphocytes were the major cell type, but at later time points, plasma cells predominated. Large numbers of cysts were observed at between 4 and 12 weeks p.i., with a decrease being seen at 16 weeks p.i. Microglial nodules, many containing tachyzoites or bradyzoites, were present at all time points. In contrast, the three strains isolated from patients with the acquired immune deficiency syndrome (AIDS) resulted in no meningitis in two cases (DEY, DAG) and in mild meningitis in one case (WIL), although all three showed some cuffing of blood vessels. In addition, only very low numbers of cysts and nodules were observed. Ultrastructurally, the cysts of all four strains were seen to be located within host cells. The cysts of the ME49 strain differed from those of the other strains in that a proportion contained immature and dividing bradyzoites at all time points, whereas those of the other strains contained only mature bradyzoites. From the observation of nodules with parasites and cysts with immature zoites, it would appear that the ME49 strain may result in an unstable chronic infection with a continuous turnover of cysts, a feature that should be taken into consideration when this strain is used as an experimental model of chronic toxoplasmosis.
Reactivation of chronic, latent infection of Toxoplasma gondii has been observed previously in transplant patients and malignancies treated with immunosuppressive drugs. Recently it has emerged as the most common recognized central nervous system infection in acquired immunodeficiency syndrome (AIDS) patients, seen in 6-20% of all AIDS cases. It produces diffuse encephalopathy or space-occupying and necrotic lesions. Contrary to classical toxoplasmosis, the serological diagnosis is unreliable and the therapeutical response in most cases is poor.
Bronchoalveolar lavage (BAL) fluid from 47 immunocompromised patients (26 with AIDS and 21 patients on immunosuppressive therapy) was analysed for the presence of Toxoplasma gondii DNA by means of the polymerase chain reaction (PCR). Specific target DNA derived from the B1 and P30 gene of Toxoplasma gondii was detected in BAL fluids from three patients with AIDS (6.4%). Pneumonia as the presenting feature of disseminated toxoplasmosis was confirmed by both clinical findings and by detection of Toxoplasma gondii DNA in blood obtained from two patients. The findings indicate that PCR has potential value in the detection of Toxoplasma gondii as an etiologic agent of atypical pneumonia in immunocompromised patients.