Value of new rapid tests for the diagnosis of group A streptococcal pharyngitis.
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Biomedical subjects
Publications and source records attributed to S T Shulman.
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To assess the frequency of hospital encoded diagnoses of acute rheumatic fever (ARF) and Kawasaki disease (KD), the two leading causes of acquired heart disease in children in the United States, we performed a survey of the medical record departments of United States children's hospitals and of general hospitals that have at least 400 beds and a pediatric ward. With a simple questionnaire, data were gathered for the years 1984 through 1990 by ICD.9CM codes, with a 58% response rate. About 8000 diagnoses of KD and 6000 diagnoses of ARF were encoded during the study period. Encoded diagnoses of both KD and ARF showed yearly fluctuations in the earlier years (1984 through 1987). For KD there was a general trend toward increasing numbers after 1986. These data are consistent with increased physician awareness and diagnosis of KD. For ARF a gradual decline was observed between 1986 and 1990. About 80% of ARF diagnoses were reported from general hospitals. The much smaller pool of encoded diagnoses of ARF at the children's hospitals showed a 56% increase from 1985 to 1986. These data suggest that the highly publicized increase in cases of acute rheumatic fever in the United States during the mid-1980s may reflect focal rather than nationwide increased activity and that nationally the number of diagnoses of ARF actually may have continued to decline gradually from 1984 through 1990.
Long-term management of patients with Kawasaki disease should be tailored to the degree of coronary arterial involvement. This committee has made recommendations for each risk level about antiplatelet and anticoagulant therapy, physical activity, follow-up assessment by a pediatric cardiologist or primary care physician, and the appropriate diagnostic procedures that may be performed to evaluate cardiac disease. The risk level for a given patient with coronary arterial involvement may change over time because of changes in coronary artery morphology. The recommendations for management presented here are intended as practical interim guidelines until additional prospective or retrospective data are compiled to define more clearly the natural history of Kawasaki disease.
The use of conventional methods to detect a possible infectious cause of Kawasaki disease (KD) has been unsuccessful. Using the polymerase chain reaction and DNA hybridization techniques, we have sought evidence that a known or new herpesvirus, parvovirus, or bacterial pathogen is related etiologically to KD. Peripheral blood DNA from acute KD patients was subjected to amplification and dot-blot hybridization to detect the presence of herpesvirus DNA, and acute KD peripheral blood and serum DNA were subjected to dot-blot hybridization for the presence of parvoviral DNA. All samples were negative for both herpesvirus and parvovirus DNA. In addition, we analyzed buffy-coat white blood cell DNA, synovial fluid DNA, and frozen autopsy and formalin-fixed, paraffin-embedded myocardial tissue DNA from KD patients for the presence of highly conserved bacterial 16S ribosomal RNA gene sequences with the polymerase chain reaction, and all were negative. These results argue against a direct pathogenic role for herpesviruses, parvoviruses, and bacteria in KD. This approach to the detection of highly conserved genomic sequences among broad groups of microorganisms can be adapted for the detection of other groups of microorganisms and may yet prove useful in the search for an etiologic agent of KD.
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We describe two patients with acute myocarditis temporally associated with an acute Shigella sonnei gastroenteritis. This association has not been described in children and should be considered in children with shigellosis who do not respond to rehydration therapies.
We investigated the possible relationship of the distribution of immunoglobulin allotypic markers for susceptibility to Kawasaki disease in Japanese, Japanese-American, and white American populations. The kappa-chain allotype Km1 was present in 25.6% of sera from white patients with Kawasaki disease and in 14.4% of control sera (p < 0.01), and the combination of Km1 with Gm heterozygosity was present in 17.9% of white patients with Kawasaki disease and in 6.4% of control sera (p < 0.0001). In all populations studied, differences were observed between the patients with Kawasaki disease and the race-matched control subjects. The findings support the hypothesis that one or more unknown infectious agents may trigger genetically influenced immune responses that result in clinically recognizable Kawasaki disease.
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The induction of coronary arteritis in mice by Lactobacillus casei cell wall (CW) is thought to represent an animal model of Kawasaki disease. Treatment of vascular endothelial cells (EC) in vitro with supernatants from CW stimulated human mononuclear cells (MNC) enhanced adherence of human polymorphonuclear leukocyte (PMN) to human EC, and EC expression of intercellular adhesion molecule-1 (ICAM-1) but not HLA-DR. Supernatants contained high concentrations of tumor necrosis factor-alpha (TNF-alpha) and PMN adherence correlated directly with the concentration of TNF-alpha. Intravenous human gamma globulin (IVGG) preparations did not block the effect of cytokine containing MNC supernates upon EC, ICAM-1 expression by EC, or PMN adherence to prestimulated EC. However, both EC ICAM-1 expression and enhanced PMN adherence to EC by CW induced MNC supernatants were blocked by anti-TNF-alpha treatment. The initial coronary inflammatory reaction in the mouse model appears to involve PMN adherence to vascular EC that have been activated by TNF-alpha released by MNC after stimulation with CW.
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Three American infants with Kawasaki disease (KD) complicated by peripheral extremity gangrene are reported. Eight such patients (only 1 from Japan) have been reported previously. These 11 patients, infants less than 7 months old at onset of KD, are predominantly non-Asian. At least nine had associated giant coronary aneurysms, and eight had associated peripheral arterial aneurysms. In eight infants the diagnosis of KD was not established and therapy was not instituted until greater than or equal to 14 days after onset. Peripheral ischemia initially was noted 15-31 days after onset. Although the pathogenesis of this complication is not well understood, it likely includes some combination of local peripheral arteritis, arteriospasm, thrombosis peripherally and/or more proximally (e.g., in an axillary artery aneurysm), and cardiogenic shock. Treatment may include use of antiinflammatory agents such as salicylates and intravenous gamma globulin, vasodilative agents and/or methods, and thrombolytic and/or anticoagulant agents in an attempt to prevent the potentially devastating consequences of progressive gangrene.
OBJECTIVES: To evaluate both the frequency and route of endotracheal colonization of intubated children by pathogens and to assess the usefulness of Pediatric Risk of Mortality scoring and measurement of gastric pH in predicting this colonization. DESIGN: Prospective data collection. SETTING: A multidisciplinary pediatric ICU. PATIENTS: Nineteen children with medical/surgical problems who were intubated for at least 4 days. INTERVENTIONS: Buccal mucosa, and endotracheal and gastric aspirates were cultured for pathogens immediately after endotracheal intubation and daily for 4 to 5 days. Pediatric Risk of Mortality scores were calculated at the time of endotracheal intubation; gastric pH was measured each time that the cultures were obtained. MEASUREMENTS AND MAIN RESULTS: The buccal mucosae of ten (53%) of 19 children were colonized with Candida species at the time of endotracheal intubation. This colonization correlated with the degree of physiologic instability as measured by Pediatric Risk of Mortality scores (12.9 +/- 2.8 SEM for those patients colonized vs. 4.9 +/- 1.0 for those patients not colonized; p = .01), but not with preintubation antibiotic therapy. Eleven (58%) children acquired 27 endotracheal pathogens after the day of intubation. The buccal mucosa was the initial site of colonization of 19 (70%) of 27 of the acquired pathogens. A gastric pH of > 3.0 at the time of intubation correctly predicted colonization in nine of 11 children (p < .025, Fisher's exact test); a Pediatric Risk of Mortality score of > 8 at the time of endotracheal intubation correctly predicted colonization in eight of 11 patients (p < .05, Fisher's exact test). CONCLUSIONS: Colonization of the buccal mucosa appears to be the crucial antecedent to endotracheal colonization in children. In children, gastric pH and Pediatric Risk of Mortality scores at the time of endotracheal intubation can predict pathogenic endotracheal colonization within 4 days of intubation. Selective decontamination regimes may be appropriate for these patients, especially those regimes that are directed to the buccal mucosa.