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A vival toxoplasmosis infection was diagnosed in 188 cases (3,8%) out, of 49,582 pregnant women routinely screened. 4 children live with congenital toxoplasmosis. Follow-up studies showed that 33 children have specific antibodies, 5 are with suspect clinical findings. Therefore is the conclusion that more late signs of connatal toxoplasmosis are to be detected by follow-up investigations.
Toxoplasmosis is caused by the parasite Toxoplasma gondii. It is acquired from undercooked meat or from food or fomites contaminated by cat feces. The disease can be transmitted to the fetus only during maternal parasitemia, which is associated with primary infection. Extrapolation from current data suggests that there are 140 to 1400 cases of congenital toxoplasmosis per year in Canada and that 70 to 280 of the infants are severely affected at birth; many of the others suffer sequelae later in life. Serologic diagnosis of primary infection in the mother is quite sensitive and specific. Diagnosis in the infant is more difficult and may take several months. Prenatal treatment of the woman and postnatal treatment of the infant are hampered by the lack of proven efficacy as well as ethical and compliance problems. Preventive serologic screening and prophylaxis have the same drawbacks. Educating young women to avoid infection is an inexpensive, low-risk intervention that would be the preferred preventive strategy if it could be shown to be effective. Immunization may prove to be the most cost-effective method of preventing congenital toxoplasmosis if a safe and effective vaccine is developed.
In Toulouse, various epidemiological works and biological results regarding toxoplasma infection permitted us to study immunity in pregnant women. 66 to 70% are immunized. Incidence of acquired toxoplasmosis is 1 to 2 for 1,000 pregnancies. Carefully planned, regionalized programs with obstetricians and pediatricians are realized to prevent congenital toxoplasmosis. Epidemiological studies may be realized to estimate the prevalence and the incidence of congenital toxoplasmosis before such programs can be recommended on a national scale in tropical area.
The occurrence of toxoplasmosis is described in the cat-mother and three kittens. Clinical symptoms were not significant: bristled hair, conjunctivitis, sneezing and hypertrophy of mandibular and popliteal lymph nodes. The titres of antibodies to Toxoplasma gondii were demonstrated in all kittens and also in the cat: Sabin-Feldman reaction titre 4-32, complement-fixing reaction titre 5-40. Microprecipitation in agar gel was positive in all animals. Oocytes of Toxoplasma gondii were eliminated through faeces by the cat and two 16-day-old kittens. An isolation trial on white mice with a negative finding of toxoplasmosis (inoculation of brain, liver and spleen samples) has demonstrated toxoplasmosis in all animals under study. Most probably the kittens were infected transplacentally.
The indices of seasonal changes in the proportion of population allergopositive to toxoplasmosis were determined by analyzing the results of intracutaneous tests made in 61,324 pregnant women in Novokuznetsk between 1964 and 1974. Indices exceeding the average monthly level were registered in March-July and in September-October. Taking into account the modal term during which allergization develops in a patient from the moment of toxoplasmic invasion, a high risk of toxoplasmosis infection is likely to be present mainly during winter and spring (December-May), as well as summer (July-August) periods. Researchers should pay attention to the nature of the seasonal prevalence of the epidemic process of toxoplasmosis.
The pyrimethamine-sulfadoxine combination, active against acute toxoplasmosis in the mouse, was administered to 24 children with congenital toxoplasmosis in doses of 500 mg sulfadoxine and 25 mg pyrimethamine per 20 kg bodyweight once every fortnight. The drug appeared to be as effective as other sulfonamide-pyrimethamine combinations. It was generally well tolerated and was withdrawn in only 3 patients on account of minor side-effects. Giving pyrimethamine-sulfadoxine together with folinic acid is a much simpler treatment of congenital toxoplasmosis than the usual ones.
The risk of acquired toxoplasmosis during pregnancy (1.2% of susceptible women) and of transmission of Toxoplasma gondii to the fetus (1% of neonates) was estimated from results of serial serological tests done in 15 132 pregnant women from 1977 to 1982. Congenital toxoplasmosis was studied in the product of 47 induced abortions and in 34 neonates. In aborted fetuses, congenital toxoplasmosis was established by serological tests in 3 cases and based on histological findings in 4. Among the neonates, 11 cases are reported; the 5 severe cases are due to early contamination.
A 40-year-old man had disseminated toxoplasmosis preceded by miliary tuberculosis and associated with skin anergy. In previously reported cases of disseminated toxoplasmosis, the three organs most commonly involved were brain, heart, and lungs. The histopathologic picture of toxoplasmal lymphadenopathy was not present in our case or in previously reported cases. Therefore, we believe that the diagnosis of disseminated toxoplasmosis should not be rejected simply because of the likely absence of toxoplasmal lymphadenopathy in biopsy material. The thymus in our case was morphologically abnormal and showed features suggestive of an autoimmune process.
Because of the high degree of infestation in women capable of bearing children in Europe (70 to 80%) with Toxoplasma gondii the authors have studied all babies admitted for clinical treatment at the institute of Paediatrics in Lublin for clinical and serological indications of a connatal toxoplasmosis. In the period between January 1977 and December 1978, 133 babies showed positive findings. The most frequently occurring findings were lesions of the central nervous system (hydrocephalus 21 X, microcephaly 8 X, porencephaly 18 X, convulsions and psychomotor retardation 11 X, subdural hygroma and haematoma 34 X, encephalomeningitis 7 X). Intracranial calcifications within the classical triad were only found in two cases. Other internal lesions without cerebral deficiency symptoms were found in 18 children. The authors point out the possible connection between vascular lesions caused by toxoplasmosis and subdural effusions. One might think of both permeability disturbances and direct vascular lacerations. The treatment consisted in repeated punctures, trepanations and antibiotics (Spiramycin, Daraprim, Orisul). The serological proof of the presence of toxoplasmosis may well lag behind the clinical symptoms.
The clinical symptoms of toxoplasmosis in man are very various and often uncharacteristical. Until now there are no statistical evaluations on the frequency of different clinical appearances of the disease. A comparison of the clinical symptoms and the results of serology was made on 14 618 patients with suspected toxoplasmosis, who were divided into groups in regard to their age and clinical symptoms. Suggestions for the diagnosis of toxoplasmosis are given by this evaluation.
Toxoplasmosis is an anthropo-zoonosis caused by the protozoa Toxoplasma gondii. The frequency of infection in the population of adults is estimated at 30-50%. Acquired toxoplasmosis takes a differentiated clinical course. It is usually symptomless or the symptoms are indistinct. In case of immunosuppressive treatment of the host severe Toxoplasma gondii infections can occur. There also is a possibility of transmission of the protozoa via transplant from the donor to the recipient as well as the possibility of reinfection of the acquired infection. In perinatal medicine toxoplasmosis plays a particularly important part due to the possibility of the transmission from mother to foetus. It seems therefore that women who are chronically treated with immunosuppressive eg after a renal transplant deserve special medical attention.
BACKGROUND: We describe a child and an adult infected with the human immunodeficiency virus (HIV) who developed cerebral lesions consistent with toxoplasmosis. A biopsy in the child and IgG ELISA in both patients confirmed the diagnosis of Toxoplasma gondii. The patients were initially treated with pyrimethamine, however, computerized tomography studies (CT scan) revealed progression of a left frontal and temporoparietal lesion. Therapy in the child was changed to pyrimethamine, clindamycin, and azithromycin. Repeat CT scan showed further disease progression and therapy was changed to high-dose pyrimethamine (3 mg/kg/d) and azithromycin. A subsequent CT scan disclosed further radiologic progression with increasing edema. The adult patient developed a maculopapular rash during attempted treatment with pyrimethamine. METHODS: Introduction of 2 (trans-4[4 chlorophenol] cyclohexy[3-hydroxy-1, 4 naphthoquinone] (HNPQ) an experimental antiparasitic compound previously used only in adult HIV clinical trials, was instituted in the child and rapid oral desensitization to pyrimethamine was initiated in the adult patient. RESULTS: HNPQ resulted in resolution of the cerebral lesion in the child and rapid oral desensitization to pyrimethamine produced an excellent clinical response in the adult. To our knowledge, these are the first cases of childhood and adult cerebral toxoplasmosis treated successfully with HNPQ and rapid oral desensitization to pyrimethamine. CONCLUSION: HNPQ and pyrimethamine desensitization should be considered as alternate modes of therapy in patients who become intolerant or fail to respond to traditional therapy for toxoplasmosis.
Toxoplasmosis is a parasitic infection divided into congenital and acquired forms. In the latter form, malaise, fatigue, and lymphadenopathy are commonly found, and submandibular lymphadenopathy is sometimes a manifestation. In children, cervical lymph nodes usually are affected. This is a case of a 13-year-old boy suffering from acquired toxoplasmosis, in which submandibular lymphadenopathy was the only clinical sign of the disease. Meticulous history taking, clinical examination, and specific serological tests should be performed in these cases. Positive serological results will confirm toxoplasmosis infections. Conservative treatment must be attempted initially.
BACKGROUND: IgM serologic response in the diagnosis of acute toxoplasmosis presents interpretation problems. A comparative study with IgA detection of antibodies was performed. METHODS: A parallel serologic study was carried out with IgM and IgA enzymoimmunoassay enhancement techniques in the sera of patients suspected of having toxoplasmosis. RESULTS: Positive results for IgM and/or IgA were presented in 74 sera (47 patients): 86.3% for the former and 58.9% for the latter (p < 0.001). The group of IgA-/IgA+ sera presented a low mean of proportionality index (PI): 1.6 versus the IgM+ sera group in the context of IgG seroconversion with a PI of 3.4 (p < 0.001). Out of the 9 patients with demonstrated IgG, all were IgA+ and seven IgM+. CONCLUSIONS: The present data seem to support greater specificity of the determination of IgA antibodies than that of IgM in the diagnosis of acute toxoplasmosis.
Despite the limitations, the available data lead to the conclusion that treatment of the mother may be of benefit to the fetus. To date, harmful effects of maternal therapy on the fetus have not been substantiated. Current recommendations for fetal therapy of toxoplasmosis include the initiation of spiramycin in the pregnant woman when acquired toxoplasmosis is strongly suspected in pregnancy. Prompt detection of infection in the mother is important in order to start therapy as early as possible. An attempt to determine the status of the fetus is undertaken by prenatal diagnostic procedures such as amniocentesis, cordocentesis, and ultrasonography. After confirmation of fetal infection, repeated courses of a combination of pyrimethamine, sulfadiazine, and folinic acid should be alternated with courses of spiramycin. If the fetus is not infected, spiramycin should be continued in repeated courses or throughout pregnancy. Pregnancy termination tends to be reserved for cases in whom ultrasonographic examination demonstrates the fetus to be severely affected. The importance of postnatal follow-up and treatment, although not addressed in this article, must be emphasized. The advent of fetal therapy offers hope that the problem of congenital toxoplasmosis will become less common. In addition to currently available options, the future may offer new avenues of therapy, such as the possibility of treating infected fetuses by the intra-amniotic infusion of drugs.
The diagnosis of cerebral toxoplasmosis in an immunosuppressed patient is based on computer tomography (CT) findings and response to specific empiric treatment. Although infrequent, cerebral toxoplasmosis has been described in patients undergoing bone marrow transplantation (BMT) with lesions compatible with this diagnosis always being found on cranial CT. The case of a patient with Burkitt's lymphoma who received BMT and developed convulsive crisis with repeatedly normal cranial CT scans during the course of severe immunosuppression (graft versus host disease and treatment with 3 immunosuppressive drugs) is presented. Post mortem study demonstrated cerebral cysts of Toxoplasma gondii with slight perilesional inflammatory infiltrate. Normal CT in patients with neurologic foci and severe immunosuppression following BMT does not exclude the diagnosis of cerebral toxoplasmosis, therefore more sensitive diagnostic techniques should be performed, particularly in areas in which infection by toxoplasma is endemic.
Prophylaxis against toxoplasmosis with weekly administration of pyrimethamine/sulfadoxine (Fansidar) was assessed for efficacy and toxicity in bone marrow transplant (BMT) recipients over a 21 month period. Sixty-nine of 90 consecutive seropositive patients were evaluable. Fansidar was administered from the time of established engraftment (median day 40, range days 13-100). Medication was scheduled to be continued until 6 months or longer in cases of continued immunosuppression (median 10 months, range day 72 to 22 months). No proven case of toxoplasmosis occurred in patients receiving prophylaxis. In addition, there were no cases of Pneumocystis carinii. Side-effects included BM suppression requiring cessation (n = 4) or interruption (n = 8) of therapy and rash (n = 1). To evaluate toxicity associated with prolonged therapy, 42 evaluable patients were assessed at 6 months following transplant (or at least 4 months of continuous treatment). Haematological toxicity was minimal and compounded in three patients showing moderate derangement by cytomegalovirus infection and graft-versus-host disease. Fansidar is an effective prophylactic agent against toxoplasmosis in BMT patients.
An indirect hemagglutination test (IHAT) for toxoplasmosis and electrocardiogram (EKG) were performed to 11,161 apparently healthy inhabitants with negative IHAT for Chagas' disease, from 259 rural and periurban localities sited in the first seven regions of Chile (geographic area of distribution of Chagas' disease in the country). The age of the 11,161 examined people ranged between 5 and 94 years, being 4,518 males and 6,643 females. The IHAT for toxoplasmosis was considered positive with titers > or = 1:16. This test resulted positive in 3,519 (31.1%) persons (30.8% in males and 32.0% in females). Positivity of the IHAT increased from 21.2%, in the youngest group (< 10 years) up to 46.9% in the oldest group (> or = 60 years). Different types of EKG alterations were observed in 10.9% of the IHAT positive individuals and in 7.9% of the IHAT negative ones. In both groups the percentages of altered EKG increased parallel with age. The overall difference of percentages of altered EKG in IHAT positive and IHAT negative persons has a statistical significance with p < 0.001. This study suggest the convenience to consider toxoplasmosis as a cause of chronic myocardiopathy in epidemiological studies on Chagas' disease, because a possible Toxoplasma gondii infection may contribute to overincrease the magnitude of the impact of Trypanosoma cruzi in the generation of the quoted myocardiopathy.