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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although not a major public health problem, food-borne parasitic zoonoses in the United States are the cause of numerous diseases that occur widely in the population. The most common food-borne parasitic diseases in the United States are trichinosis, toxoplasmosis, taeniasis/cysticercosis, diphyllobothriasis, and anisakiasis. Since 1947, when the US Public Health Service began to record statistics on trichinosis cases in humans, the numbers of reported cases in the United States have declined markedly, from an average of about 400 with 10-15 deaths reported each year in the late 1940s, to an average of 57 per year with three deaths overall in the 5 years 1982-1986. Each year throughout the world, Toxoplasma gondii infects millions of persons, who contract it either by eating raw or poorly cooked meat from infected animals such as hogs or sheep or by ingesting soil contaminated with cat feces. In the United States between 400 and 10,000 infants are born each year with congenital toxoplasmosis. Toxoplasmic encephalitis, marked by dementia and seizures, has become the most commonly recognized cause of central nervous system opportunistic infection in AIDS patients. Intestinal taeniid tapeworm infection acquired in the United States is almost entirely caused by Taenia saginata, the beef tapeworm. Neurocysticercosis, caused by larvae of the pork tapeworm Taenia solium, is diagnosed in hundreds of persons in the United States every year. Nearly all patients are immigrants or travelers from Mexico and other disease-endemic areas. Diphyllobothriasis and anisakiasis both have increased in recent years in association with increasing popularity of raw fish dishes. Adequate prevention and control of food-borne parasitic zoonoses require continued and improved programs to educate consumers, producers and medical practitioners.
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PMID:Current status of food-borne parasitic zoonoses in the United States. 182 40

A newborn, delivered at term, developed a rapidly increasing hydrocephalus with intracranial calcifications and seizures during the first week of life. Clinical suspicion of congenital toxoplasmosis was at first not confirmed serologically (serum titer in the immunofluorescence test [IFT] of 1:1024 and complement-fixation reaction [CFR] of 1:40 equalling those of the mother; IgM-IFT being negative and the IFT and CFR titers significantly falling within two weeks). But in the further course of the disease the diagnosis of congenital toxoplasmosis was confirmed: 1. Microscopic tachyzoits in CSF when aged six weeks; 2. positive IgM-IFT in serum and CSF from the seventh weeks onwards; 3. steep IFT titer rise in serum and CSF from the 16th week onwards. This case demonstrates that with delayed immune response in the infected child only serial serological tests will exclude or confirm the diagnosis of congenital toxoplasmosis.
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PMID:[Congenital toxoplasmosis with delayed immune response in children. Diagnostic problems]. 355 31

A case of congenital toxoplasmosis is reported in which the patient died at 32 days following seizures, coma and respiratory disturbances. Neuropathological examination showed numerous foci of softening throughout the brain. Histological examination disclosed widespread areas of inflammatory necrosis. Circumscribed areas of granulomatous inflammation were also found. Cysts containing a variable number of microorganisms and toxoplasmas free in the damaged areas were frequently observed. Small calcifications were scattered in the cerebral cortex and basal ganglia. Electron microscopy of postmortem brain specimens demonstrated toxoplasmas at various stages of development. The microorganism is enveloped by a two-layered membrane, the pellicle. Replication occurs in a vacuole inside the host cell. Following replication the newly formed parasites, the trophozoites, are released. Several replications without release may also occur with consequent cyst formation. The motile form of the toxoplasma, the tachyzoite, is fusiform with truncated cone shape of the anterior ending which is the presenting surface modified for host cell penetration. The modality of transplacental transmission and the clinical syndromes associated with toxoplasma infection are discussed. EM even of post mortem material contributes to knowledge of the structure of the parasite and of its life cycles.
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PMID:Congenital toxoplasmosis: histological and ultrastructural study. 708 42

A nine-week-old Caucasian male presented with right ptosis and right exotropia due to a third cranial nerve palsy. Symmetrical macular lesions and a paramacular hyperpigmented lesion with overlying vitreous cells in the left eye were compatible with congenital toxoplasmosis. Computer tomography demonstrated calcifications in the periventricular and midbrain regions where the oculomotor nerve exits the brainstem. The diagnosis was confirmed by the toxoplasma indirect fluorescent antibody titer greater than 1:2048 for the infant and greater than 1:512 for the mother. Treatment was instituted with pyrimethamine, sulfadiazine and folinic acid. Neurologic sequelae included a right hemiparesis, infantile seizures, and generalized developmental delay. A Mueller's muscle resection (RUL) combined with 9-mm recession of the right lateral rectus and 7-mm resection of the right medial rectus muscles produced minimal ptosis and right exotropia one year later. the child now prefers to fix with the right eye and a vertical nystagmus is evident in the left eye. To our knowledge this is the first reported case of an infant with noncomitant strabismus due to congenital toxoplasma cranial nerve involvement. The finding of an acquired third cranial nerve palsy accompanied by progressive neurologic sequelae warrants consideration of congenital toxoplasmosis.
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PMID:Congenital toxoplasmosis associated with acquired oculomotor nerve (CN III) palsy. 717 24

Between December 1981 and May 1991, 44 infants and children with congenital toxoplasmosis were referred to our study group. A uniform approach to evaluation and therapy was developed and is described herein along with the clinical characteristics of these infants and children. In addition, case histories that illustrate especially important clinical features or previously undescribed findings are presented. Factors that contributed to the more severe disabilities included delayed diagnosis and initiation of therapy; prolonged, concomitant neonatal hypoxia and hypoglycemia; profound visual impairment; and prolonged, uncorrected increased intracranial pressure with hydrocephalus and compression of the brain. Years after therapy was discontinued, three children developed new retinal lesions (without loss of visual acuity when therapy for Toxoplasma gondii was initiated promptly), and three children experienced a new onset of afebrile seizures. Most remarkable were the normal developmental, neurological, and ophthalmologic findings at the early follow-up evaluations of many--but not all--of the treated children despite severe manifestations, such as substantial systemic disease, hydrocephalus, microcephalus, multiple intracranial calcifications, and extensive macular destruction detected at birth. These favorable outcomes contrast markedly with outcomes reported previously for children with congenital toxoplasmosis who were untreated or treated for only 1 month.
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PMID:Early and longitudinal evaluations of treated infants and children and untreated historical patients with congenital toxoplasmosis: the Chicago Collaborative Treatment Trial. 805 36

Toxoplasmosis is caused by infection with the protozoan parasite Toxoplasma gondii. In the United States, approximately 85% of women of childbearing age are susceptible to acute infection with T. gondii. Acute infections in pregnant women may cause serious health problems when the organism is transmitted to the fetus (congenital toxoplasmosis), including mental retardation, seizures, blindness, and death. An estimated 400 to 4000 cases of congenital toxoplasmosis occur in the U.S. each year. Manifestations of congenital toxoplasmosis may not become apparent until the second or third decade of life. Serologic tests are used to diagnose acute infection in pregnant women, but false-positive tests occur frequently, therefore, serologic diagnosis must be confirmed at a reference laboratory before treatment with potentially toxic drugs should be considered. Much of congenital toxoplasmosis can be prevented by educating women of childbearing age and pregnant women to avoid eating raw or undercooked meat, to avoid cross-contamination of other foods with raw or undercooked meat, and to use proper cat-litter and soil-related hygiene.
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PMID:Congenital toxoplasmosis: a review. 1133 76

Approximately 85 percent of women of childbearing age in the United States are susceptible to acute infection with the protozoan parasite Toxoplasma gondii. Transmission of T. gondii to the fetus can result in serious health problems, including mental retardation, seizures, blindness, and death. Some health problems may not become apparent until the second or third decade of life. An estimated 400 to 4,000 cases of congenital toxoplasmosis occur in the United States each year. Serologic tests are used to diagnose acute T. gondii infection in pregnant women. Because false-positive tests occur frequently, serologic diagnosis must be confirmed at a Toxoplasma reference laboratory before treatment with potentially toxic drugs is considered. In many instances, congenital toxoplasmosis can be prevented by educating pregnant women and other women of childbearing age about not ingesting raw or undercooked meat, using measures to avoid cross-contamination of other foods with raw or undercooked meat, and protecting themselves against exposure to cat litter or contaminated soil.
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PMID:Congenital toxoplasmosis. 1277 62

Curative treatment of congenital toxoplasmosis is based on the association of pyrimethamine and sulfonamide. There is currently no pediatric galenic formulation. We report the case of a newborn child affected by asymptomatic congenital toxoplasmosis who received an overdose of pyrimethamine. The patient received a dose of pyrimethamine 4 times, equal to 100 times the recommended dose, due to an error in the prescription. He had partial seizures 48 h after the last medicinal absorption. We noted a lack of appetite and vomiting, with a favorable progression in 5 days. Blood analysis showed isolated, spontaneously regressive moderate cholestasis. We propose a pharmacological clarification on the treatment of congenital toxoplasmosis.
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PMID:[Neonatal intoxication with pyrimethamine: risk due to the absence of pediatric formulation?]. 2188 64

Toxoplasmosis is a rare disease caused by intracellular protozoan parasite, Toxoplasma gondii. Though most patients with toxoplasmosis are asymptomatic, congenital toxoplasmosis in the fetus can cause ocular involvement such as chorioretinitis and central nervous system disease including intracerebral calcification, nystagmus, hydrocephalus and microcephaly. Also, these brain lesions can cause seizure secondarily. Our patient was diagnosed with congenital toxoplasmosis, based on toxoplasma-specific serologic test with typical clinical symptoms, including chorioretinitis, nystagmus, hydrocephalus and cerebral palsy. Her brain imaging findings revealed not only the multifocal encephalomalacia, but also multifocal cerebral calcification including intracerebral calcification in left perihippocampal region. Her epileptogenic zone was defined as mesial temporal lobe including hippocampus on left side by seizure semiology, electroencephalogram and neuroimaging including single photon emission computed tomography and 18F-Fluorodeoxyglucose positron-emission tomography. Her seizures were refractory to multiple anti-epileptic drugs. We report a patient with congenital toxoplasmosis who showed intractable mesial temporal lobe epilepsy.
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PMID:Mesial Temporal Lobe Epilepsy in Congenital Toxoplasmosis: A Case Report. 2615 72

Congenital toxoplasmosis (CT) results from transplacental passage of Toxoplasma gondii to the fetus during acute maternal infection. Our study aims to report clinical and biological patterns of 35 cases of CT diagnosed at the department of the Parasitology of the Pasteur Institute of Tunis and to access the performance of prenatal and early postnatal diagnosis techniques. Serological screening of maternal infection was performed by Immunoglobulin (Ig) M and IgG detection and IgG avidity determination. Prenatal diagnosis was based on both Toxoplasma DNA detection in the amniotic fluid and monthly ultrasound examinations. polymerase chain reaction analysis on amniotic fluid, performed only in 15 cases, detected Toxoplasma's DNA in five cases (33.3%). Ultrasound examination did not reveal any morphological abnormalities. Thirty newborns had serological criteria of Toxoplasma infection. Congenital toxoplasmosis diagnosis was confirmed in 23 cases (76.6%) by immunoblot. Among the 35 born-infants, five (14.3%) were symptomatic: three had chorioretinitis at the first clinical ocular examination, one had neurological symptoms (seizures) with positive parasite DNA in cerebral spinal fluid, and one had both ophthalmological and neurological damages- chorioretinitis and intracranial calcifications in the computed tomography scan. Thirty-four of 35 infected children were treated with pyrimethamine-sulfadiazine combination. Four (11.7%) of the treated infants showed abnormal hematological values because of the treatment side effect. Serological rebound was observed in seven infants. A screening program and a diagnostic algorithm in pregnant women should be implemented in Tunisia to improve the follow-up of seronegative ones and to prevent CT cases.
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PMID:Congenital Toxoplasmosis in Tunisia: Prenatal and Neonatal Diagnosis and Postnatal Follow-up of 35 Cases. 2966


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