Rapid detection of Clostridium difficile toxin A in stool specimens

Objective: To evaluate a rapid (15-min) enzyme immunoassay in the format of an individual cassette (ImmunoCard toxin A, Meridian, BMD, Marne-la-Vallée, France) for the detection of Clostridium difficile toxin A in stool specimens.
Methods: We compared this new test with the cytotoxicity assay using MRC-5 cells, the ToxA test (TechLab, BioWhittaker, Fontenay-sous-bois, France) and toxigenic culture for the diagnosis of C. difficile -associated diseases (CDAD). A total of 236 stool specimens collected from 220 patients was simultaneously tested with the four methods. Discordant results were resolved by reviewing patients' clinical records.
Results: The prevalence of CDAD was 13.9%. Test sensitivities and specificities were 100% and 99% respectively for the cytotoxicity assay, 87.5% and 100% for ImmunoCard toxin A, 77.4% and 100% for the ToxA test and 100% and 98% for toxigenic culture.
Conclusions: The ImmunoCard Toxin A is a very rapid, individual and easy-to-perform test for the diagnosis of CDAD. It provides same-day results and may be useful for both guiding appropriate treatment and controlling nosocomial spread of C. difficile.     

Sequence Analysis Demonstrates that VP6, NSP1 and NSP4 Genes of Indian Neonatal Rotavirus Strain 116E are of Human Origin

We have sequenced the genes encoding the inner capsid protein VP6 and the nonstructural proteins NSP1 and NSP4 of the Indian neonatal serotype P8[11]G9 human/bovine reassortant candidate vaccine rotavirus strain 116E. These three genes share a high degree of sequence and deduced amino acid homology with human prototype strain Wa. Our results confirm and extend those of previous RNA-RNA hybridization studies which suggested that these genes are of human origin, and will facilitate examination of the host immune response to 116E induced by natural infection and vaccination. This revised version was published online in July 2006 with corrections to the Cover Date.     

Colonic histopathology in untreated celiac sprue or refractory sprue: Is it lymphocytic colitis or colonic lymphocytosis?

Colonic histopathology in some patients with untreated celiac sprue and refractory sprue has been said to be indistinguishable from lymphocytic colitis, but there have been no objective comparisons on which this is based. The purpose of this study was to determine the prevalence and to characterize the nature of colonic histopathology at the time of diagnosis in patients with celiac or refractory sprue. Colonoscopic biopsy specimens obtained at the time of diagnosis from 16 patients with celiac sprue, six patients with refractory sprue, nine patients with lymphocytic colitis, and five normal controls were analyzed blindly by histological and morphometric methods, quantitating the number and specific subtypes of inflammatory cells within the lamina propria and epithelium. Immunoperoxidase staining of intraepithelial lymphocytes with a monoclonal antibody to CD8 also was performed. Three of 16 patients with untreated celiac sprue (19%) were thought to have colonic histological abnormalities, which by morphometry consisted of slightly increased numbers of lymphocytes in the surface epithelium and lamina propria, many of which were CD8-positive. These abnormalities were distinguishable from lymphocytic colitis by the lack of increased overall lamina propria cellularity and surface epithelial abnormalities, and by fewer intraepithelial lymphocytes. In refractory sprue, colonic histological abnormalities were more frequent than in celiac sprue, occurring in four of six patients (67%), more pronounced, and identical to those in the lymphocytic colitis syndrome. However, colonic intraepithelial lymphocytes in lymphocytic colitis were mostly CD8-positive, whereas those in the colitis of refractory sprue rarely were. Mild colonic lymphocytosis in patients with untreated celiac sprue should be distinguished from lymphocytic colitis by the lack of surface epithelial abnormalities, the lack of increased cellularity of the lamina propria, and the lack of ongoing watery diarrhea after treatment with a gluten-free diet. In contrast, colonic histopathology in refractory sprue is indistinguishable from lymphocytic colitis, although immunohistochemical differences do exist.     

Identification of the membrane protein of porcine epidemic diarrhea virus

Sequence information on the genome of porcine epidemic diarrhea virus (PEDV) has only recently been determined. In contrast, very little is known about the viral proteins. In the present report we have identified the membrane glycoprotein (M) of PEDV by use of rabbit anti-peptide sera and transient expression of the cloned M gene in Vero cells and by expression in the baculovirus system. The native M protein of PEDV is incorporated into virions, is N-glycosylated, and migrates with a relative mobility (Mr) of 27 k in polyacrylamide gels. In contrast, the M protein synthesized by recombinant baculoviruses migrates with a Mr of 23 k, that is, with identical mobility as the deglycosylated product of PEDV. Thus, it appears that M protein specified by the recombinant baculovirus is poorly, if at all, glycosylated. Using monoclonal antibodies and rabbit antipeptide sera specific for the N and C termini of the M protein, we were able to show that a 19 k band detected in PEDV-infected cells but not in virions represented a fragment of M from which the C terminus had been cleaved off. Finally, by electron microscopy and immunogold labelling, the relative orientation of M within the virion envelope was determined as NexoCcyt. In conclusion, all of these data strongly support the hypothesis that PEDV should be classified with the group I coronaviruses.     

Plasticity of the central nervous system—a neurosurgeon's experience of cerebral compensation and decompensation

Summary Cerebral plasticity constitutes one of the most decisive factors in recovery and readaptation after cerebral lesions. In contrast to the considerable progress in current studies on normal neuronal plasticity including the idea of l'homme neuronal, the concept of plasticity postulated by Albrecht Bethe in 1929 received little attention. The author, as a neurosurgeon, has tried to describe cranial morphological plasticity, morphological and functional plasticity in infantile encephalopathies and especially in hemiatrophic lesions. It is supposed that a true morphological substrate exists due to compensatory hyperplasia of the uninvolved hemisphere.Modern neurosurgical techniques have demonstrated that the functional plastic capacity is much larger than has been supposed, even in the elderly. Some aspects of the mechanisms of compensation and decompensation of cortical and subcortical structures as well as of the central regulation systems are discussed. The full extent of the amazing recovery and functional reorganization is reached by plastic capacity, personal motivation, adequate training and sufficient time.The contribution ends with an exposition of a personal philosophy concerning psycho-somatic dualism, the body-mind problem, the future of the human brain and the ethical outlook, based on the progressive biological evolution of the basal neocortex and the immanent functional development (H. Spatz).In grateful memory of my paternal friends, the great German brain researchers Julius Hallervorden (1882–1965) and Hugo Spatz (1888–1969).     

2019年广东省部分地区感染性腹泻病原学及人轮状病毒分子流行病学特征

目的 对感染性腹泻样本进行检测鉴定,并对轮状病毒A组进行病毒分离,研究2019年广东省部分地区感染性腹泻病原学及轮状病毒分子流行病学特征。方法 2019年1月1日至2020年1月12日,采集广东省广州市、东莞市和江门市临床感染性腹泻患者粪便样本,进行多重RT-PCR扩增和微球杂交技术检测鉴定,并对轮状病毒A组阳性样本进行分离后,采用半巢式PCR试验对阳性细胞培养物进行G/P基因分型。结果 共纳入706例合格病例,病原体总检出率43.06%,病毒检出率18.13%高于细菌检出率8.36%高于寄生虫检出率1.27%。病毒病原谱以轮状病毒A组G9P[8]和诺如病毒GII型感染为主,细菌病原谱以沙门菌和艰难梭菌为主,寄生虫以蓝氏贾第鞭毛虫为首。不同季度、不同年龄组病原谱构成各不相同。轮状病毒A组主要受累群体为≤5岁儿童,主要时间分布于1—4月,基因型呈现多样性,包括G2P[4]、G3P[8]和G9P[8]。结论 2019年广东省部分地区感染性腹泻病毒类病原体高于细菌类高于寄生虫类,轮状病毒A组G9P[8]、诺如GII型、沙门菌和蓝氏贾第鞭毛虫是最主要的病原体,且G9P[8]型A组轮状病毒毒株在轮状病毒感染中占主导趋势。在防控病毒性和细菌性腹泻的同时,应警惕寄生虫所致腹泻并重视混合感染的病原学监测。     

沙棘干乳剂联合布拉氏酵母菌治疗儿童轮状病毒性肠炎的效果及对免疫功能的影响

目的 探讨沙棘干乳剂联合布拉氏酵母菌治疗儿童轮状病毒性肠炎的临床效果。方法 以随机数字表法,将2019年10月—2021年2月收治的106例轮状病毒性肠炎患儿予以分组,对照组53例,给予布拉氏酵母菌治疗,观察组53例,在对照组基础上,加用沙棘干乳剂治疗,对2组临床疗效,症状消失时间,治疗前、后免疫功能变化及用药安全性予以观察。结果 治疗总有效率观察组为96.23%,与照组治疗总有效率84.91%比较,明显较高,差异有统计学意义(χ2=3.975,P<0.05);观察组患儿发热、腹泻、呕吐消失时间为(2.14±0.36)d、(2.75±0.48)d、(1.86±0.31)d, 与对照组(2.59±0.42)d、(3.19±0.51)d、(2.24±0.39)d比较,明显较短,差异有统计学意义(t=5.922、4.574、5.553,P均<0.05);治疗3 d后,观察组血清免疫球蛋白A(IgA)、免疫球蛋白M(IgM)、免疫球蛋白G(IgG)水平为(1.58±0.39)g/L、(1.45±0.33)g/L、(9.82±1.06)g/L,与同期对照组(1.31±0.32)g/L、(1.24±0.31)g/L、(8.96±1.02)g/L比较,明显较高,差异有统计学意义(t=3.896、3.393、4.256,P均<0.05);不良反应发生率观察组、对照组分别为3.77%、7.55%,差异无统计学意义(χ2=0.177,P>0.05)。结论 沙棘干乳剂联合布拉氏酵母菌治疗儿童轮状病毒性肠炎,可促进患儿症状恢复,提高患儿免疫功能,疗效确切,安全性高,值得推广。     

US Food and Drug Administration Analysis of Patient-Reported Diarrhea and Its Impact on Function and Quality of Life in Patients Receiving Treatment for Breast Cancer

ObjectivesMany trials conclude “no clinically meaningful detriment” to health-related quality of life (HRQL) or function between arms, even when notable differential toxicity is observed. Mean change from baseline analyses of function or HRQL can possibly obscure important change in subgroups experiencing symptomatic toxicity. We evaluate the impact of diarrhea, a key treatment arm toxicity, on patient-reported HRQL and functioning in clinical trials submitted to US Food and Drug Administration.MethodsThis study used 4 randomized, breast cancer trials (adjuvant to late-line metastatic) as case examples. Diarrhea, physical functioning (PF), and global health status and quality of life (GHS/QoL) from the European Organisation for Research and Treatment of Cancer Quality of Life Questionnaire-C30 were analyzed at baseline and approximately 3 and 6 months.ResultsGenerally, patients reporting very much diarrhea at months 3 and 6 had worse PF (9-19 points lower) and GHS/QoL (16-19 points lower) than patients reporting no diarrhea regardless of treatment arm. In the change from baseline analysis, patients reporting very much diarrhea also experienced a greater decrease in PF (6-13 points) and GHS/QoL (6-16 points) versus patients reporting no diarrhea in both arms.ConclusionsIn trials with moderate to large differences in symptomatic toxicity by arm, reporting “no meaningful difference in functioning and HRQL between arms” based on mean change from baseline analysis is insufficient and may obscure important impacts on subgroups experiencing symptomatic adverse events. Additional exploratory analyses with simple data visualizations evaluating functioning or HRQL in patient subgroups experiencing expected symptomatic toxicities can further inform the safety and tolerability of an investigational agent.     

Diarrhea Predominant-Irritable Bowel Syndrome (IBS-D): Effects of Different Nutritional Patterns on Intestinal Dysbiosis and Symptoms

Irritable Bowel Syndrome (IBS) is a chronic functional gastrointestinal disorder characterized by abdominal pain associated with defecation or a change in bowel habits. Gut microbiota, which acts as a real organ with well-defined functions, is in a mutualistic relationship with the host, harvesting additional energy and nutrients from the diet and protecting the host from pathogens; specific alterations in its composition seem to play a crucial role in IBS pathophysiology. It is well known that diet can significantly modulate the intestinal microbiota profile but it is less known how different nutritional approach effective in IBS patients, such as the low-FODMAP diet, could be responsible of intestinal microbiota changes, thus influencing the presence of gastrointestinal (GI) symptoms. The aim of this review was to explore the effects of different nutritional protocols (e.g., traditional nutritional advice, low-FODMAP diet, gluten-free diet, etc.) on IBS-D symptoms and on intestinal microbiota variations in both IBS-D patients and healthy subjects. To date, an ideal nutritional protocol does not exist for IBS-D patients but it seems crucial to consider the effect of the different nutritional approaches on the intestinal microbiota composition to better define an efficient strategy to manage this functional disorder.     

Gut Microbiota Prevents Sugar Alcohol-Induced Diarrhea

While poorly-absorbed sugar alcohols such as sorbitol are widely used as sweeteners, they may induce diarrhea in some individuals. However, the factors which determine an individual’s susceptibility to sugar alcohol-induced diarrhea remain unknown. Here, we show that specific gut bacteria are involved in the suppression of sorbitol-induced diarrhea. Based on 16S rDNA analysis, the abundance of Enterobacteriaceae bacteria increased in response to sorbitol consumption. We found that Escherichia coli of the family Enterobacteriaceae degraded sorbitol and suppressed sorbitol-induced diarrhea. Finally, we showed that the metabolism of sorbitol by the E. coli sugar phosphotransferase system helped suppress sorbitol-induced diarrhea. Therefore, gut microbiota prevented sugar alcohol-induced diarrhea by degrading sorbitol in the gut. The identification of the gut bacteria which respond to and degrade sugar alcohols in the intestine has implications for microbiome science, processed food science, and public health.