Occult group B streptococcal infection: an important cause of intrauterine asphyxia.
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Biomedical subjects
Publications and source records attributed to E G Chalhub.
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Schizencephaly means clefts in the brain and refers to that condition of dysmorphogenesis in which there are bilateral, usually symmetrical, clefts in the region of the central sulcus. This condition is readily demonstrated by computed tomography and is associated with severe mental retardation. We add three case studies to those previously recorded in the literature.
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Eleven children with bacterial meningitis were treated intravenously with amoxicillin sodium to evaluate the efficacy of the parenteral form of amoxicillin for this serious infection and to measure the penetration of the drug into cerebrospinal fluid (CSF). The infecting organisms were Haemophilus influenzae in nine cases and Streptococcus pneumoniae in two. Nine patients had optimal responses to amoxicillin sodium, 200 mg/kg per day for 14 days. Bacteria were also eradicated from CSF of the other two, but one experienced fever and culture-negative CSF pleocytosis after cessation of amoxicillin, and the other developed H. influenzae empyema 2 weeks after termination of therapy. By comparison, 7 of 10 children with meningitis responded optimally to ampicillin (nonrandomized design) during the period of study. The mean peak CSF concentration of amoxicillin was 3.14 mug/ml (ca. 7% of the concomitant mean peak serum level) early during therapy. However, meningeal penetration of the drug declined to a mean peak of 0.63 mug/ml on the final day of therapy. Mild transient neutropenia, noted in five patients, was the most common side effect of amoxicillin sodium therapy; five patients treated with ampicillin also experienced reversible neutropenia. Thus, intravenous amoxicillin sodium provided therapy for bacterial meningitis comparable to that of ampicillin in this limited case-control study.
True congenital herpes simplex viral (HSV) infections have been reported infrequently and have been associated with various 'congenital' malformations. Microcephaly, microphthalmia, intracranial calcifications, chorioretinitis, congenital heart disease and abnormal digits have been associated with presumed congenital HSV infection. This report describes the clinical and pathological features of an infant with a congenital type-II HSV infection. In addition to the findings previously reported with this form of HSV infection, extensive hepatic calcifications, osseous lesions and cataracts were observed for the first time. The effect of congenital HSV infection on the developing central nervous system is discussed.
The factors underlying acute infantile hemiplegia are seldom identified. Coxsackie A9 focal encephalitis was documented for the first time in a 3-month-old infant with fever, hemiconvulsions, and hemiplegia followed by a static motor deficit and epilepsy. It has been suggested that the acute infantile hemiplegia associated with encephalitis results from an arteritis or venous sinus thrombosis with subsequent cerebral infarction. However, this was not observed in our patient. Rather, a series of brain scans, computerized tomograms, and a cerebral angiogram clearly documented the evolution of a focal necrotizing encephaloclastic process resulting in a porencephalic cyst. Serial cerebrospinal fluid viral cultures were necessary to isolate the etiologic agent (tcoxsackie A9). The infant did not have a neutralizing antibody response to the infecting viral agent despite an apparently intact immune system, which possibly may be explained by the developed of immune tolerance or an insufficient amount of infecting viral antigen. This emphasizes that serologic studies alone may not be adequate to document an acute central nervous system viral infection. This patient also typifies the poor prognosis in infants presenting with acute hemiplegia, fever, and convulsions in the absence of cerebrovascular occlusion.
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Similar movement disorders developed in two 8-year-old retarded children while they were receiving phenytoin. Seizures subsequent to a diphtheria-pertussis-tetanus immunization had developed in each child at 1 to 2 months of age. A static encephalopathy ensued, characterized by mental retardation, ataxia, spasticity, and a mixed seizure disorder. Intermittent dystonia and choreoathetosis developed insidiously while serum phenytoin concentrations were in the therapeutic range. Sustained dystonia and choreoatheosis developed 2 hours after an oral provocation with phenytoin. The baseline abnormalities on the electroencephalogram remained unchanged during the choreoathetosis. Recognizable metabolic abnormalities known to be associated with similar movement disorders were excluded. It was concluded from these studies that the movement disorder is secondary to phenytoin and can occur at therapeutic serum concentrations. Phenytoin is a central anticholinergic agent and a central stimulant of serotonin, and may induce movement disorders as a result of altering these neurotransmitters in the brain. The variable expression of these movement disorders may relate to the nature of the preexisting striatal insult.
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The present investigation was undertaken to determine if a candidate live vaccine virus, influenza A/Hong Kong/68-ts-1 [E] (H3N2), induced heterologous interference against an interferon-sensitive, wild-type, parainfluenza type 1 challenge virus. The parainfluenza virus was administered 7 days after Hong Kong/68-ts-1 [E] virus infection. The clinical response, daily quantitative virus shedding, interferon production, and serum and nasal wash antibody responses were determined in an experimental group (influenza A virus followed by parainfluenza virus) and 10 volunteers in a control group (parainfluenza virus only). The volunteers were selected on the basis of susceptibility to the two viruses, i.e. serum hemagglutination-inhibition antibody titer of is less than or greater to 1:8 for influenza virus and low nasal wash antibody titer (is less than or greater to 1:8) for parainfluenza virus. Despite a 100% infection rate in the Hong Kong/68-ts-1 [E] vaccinees, no heterologous interference was induced against the parainfluenza type 1 virus challenge.
An infant with the linear nevus sebaceous syndrome also had new findings of porencephaly and nonfunctioning major cerebral venous sinuses. This infant is the first described with the syndrome to undergo angiographic study. Similar nonfunctioning major cerebral venous sinuses are seen in the Sturge-Weber syndrome. A leptomeningeal angioma recently was reported in a newborn with the linear nevus sebaceous syndrome. The central nervous system disturbances in this syndrome might be secondary to developmental vascular anomalies. Therefore, the linear nevus sebaceous syndrome exhibits important similarities to the Sturge-Weber variety of neurocutaneous syndrome.
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