BackgroundAcute diarrhea is a global health problem, resulting in high morbidity and mortality in children. It has been suggested that enteric pathogen co-infections play an important role in gastroenteritis, but most research efforts have only focused on a small range of species belonging to a few pathogen groups. This study aimed to assess the impact of co-infections with a broad range of enteric pathogens on children aged below five years who suffer from acute diarrhea in southwest China.MethodA total of 1020 subjects (850 diarrhea cases and 170 healthy controls) were selected from four sentinel hospitals in Kunming, Yunnan province, southwest China, from June 2014 to July 2015. Stool specimens were collected to detect five virus (rotavirus group A, RVA; norovirus, NoV; Sapovirus, SaV; astrovirus, As; and adenovirus, Ad), seven bacterial (diarrheagenic Escherichia coli, DEC; non-typhoidal Salmonella, NTS; Shigella spp.; Vibrio cholera; Vibrio parahaemolyticus; Aeromonas spp.; and Plesiomonas spp.), and three protozoan (Cryptosporidium spp., Giardia lamblia, and Blastocystis hominis, B. hominis) species using standard microbiologic and molecular methods. Data were analyzed using the partial least square regression technique and chi-square test.ResultsAt least one enteric pathogen was detected in 46.7 % (n = 397) of acute gastroenteritis cases and 13.5 % (n = 23) of healthy controls (χ2 = 64.4, P < 0.05). Single infection with RVA was associated with acute diarrhea (26.5 % vs. 5.8 %, P < 0.05). The prevalence of a single infection with B. hominis in diarrhea cases was higher than in healthy controls (3.1 % vs. 0.5 %, OR = 4.7, 95 % CI: 1.01–112.0). Single infection with NoV GII was not associated with diarrhea (4.4 % vs. 3.5 %, OR = 1.2, 95 % CI: 0.5–3.3). Single infections with bacterial species were not observed. The prevalence of co-infections with two enteric pathogens in diarrhea cases was higher than in asymptomatic children (20.1 % vs. 5.3 %, P < 0.05). RVA-NoV GII was the most common co-infection in symptomatic children (4.4 %), with it aggravating the severity of diarrhea.ConclusionsAlthough it is clear that RVA has an overwhelming impact on diarrhea illnesses in children, co-infection with other enteric pathogens appears to also aggravate diarrhea severity. These findings should serve as evidence for public health services when planning and developing intervention programs.Electronic supplementary materialThe online version of this article (doi:10.1186/s40249-016-0157-2) contains supplementary material, which is available to authorized users.

Neonatal cholestasis disease (NCD) is a complex and easily mis-diagnosed condition. We analyzed microbiota community structure in feces and measured short-chain fatty acids, bile acids (BAs) and liver function of 12 healthy, 13 NCD, and 13 treated infants after diagnosis. Based on 16S rRNA gene amplicon sequencing and gas-chromatographic-mass-spectrometric analysis of secondary BAs, we identified microbial genera and metabolites that associate with abnormal bile secretion. Streptococcus gallolyticus and Parabacteroides distasonis, and Lactobacillus gasseri had higher relative abundance in healthy and NCD infants respectively. Compared to NCD patients, healthy infants had higher LCA, CDCA and GCDCA fecal concentrations. The three microbial species and three secondary bile acids were selected as potential non-invasive combined biomarkers to diagnose NCD. We propose that microbiotametabolite combined biomarkers could be used for diagnosis of NCD, and this may contribute to improved early clinical diagnosis of NCD in the future. Neonatal cholestasis disease (NCD) affects approximately 1 in every 2500 term infants and is infrequently recognized by primary providers in the setting of physiologic jaundice. Cholestasis jaundice is mostly due to biliary atresia and frequently results from non-biliary atresia 1. The etiology of biliary atresia is unclear but is thought to involve bile duct dysmorphogenesis, viral infection, toxins, chronic inflammation, or autoimmune-mediated bile duct injury 2-5. Non-biliary atresia etiology of neonatal cholestasis may involve bacterial sepsis, galactosemia, tyrosinemia, panhypopituitarism, defective BA synthesis, or obstructive gallstones 1. The complex causes for NCD necessitate improved clinical practice guidelines for the care of infants with cholestasis. Hence, joint general recommendations of the North American Society for Pediatric Gastroenterology, Hepatology, and Nutrition and the European Society for Pediatric Gastroenterology, Hepatology, and Nutrition are available for evaluation of NCD in infants, which identify: 1) the measurement of total and conjugated (direct) serum bilirubin for babies at 2 weeks of age; 2) physical examination for hepatomegaly, splenomegaly and appearance of illness; 3) direct visualization of stool pigment; 4) intra-operative cholangiogram and histological examination of the duct remnant 1. However, infants with biliary atresia usually appear healthy and grow normally, which may deceive the parent or physician into believing that the jaundice is physiologic or caused by breastfeeding 6. Thus, development of new or additional biomarkers is considered important in order to improve the care of NCD. Among the most studied causes of NCD in recent years are metabolic diseases and disorders of bile transport and BA synthesis. Cumulative evidence suggests that the composition and function of the gut microbiota plays a prominent role in the occurrence of human metabolic diseases, including type II diabetes 7 , obesity 8 , liver disease 9,10 , atherosclerosis 11...

Group A rotavirus (RVA) is one of the leading cause of acute diarrhea worldwide, the RVA-related disease burden and the genotypes of RVA is important reference to introduce RVA variance to national immunisation programmes, 1,121 diarrhea cases and 319 healthy controls were recruited from four sentinel hospital outpatient from July 2014 to June 2015. The prevalence of RVA was 244 (21.8%) in gastroenteritis cases and in 12 (3.8%) in healthy controls across all age group (OR = 7.12, 95%CI = 3.93-12.89); the detection rate of RVA in diarrhea patients under 5 years was more higher than in diarrhea cases over 5 years (26.1%, 222/850; 8.1%, 22/271, respectively, P = 0.000). Of 244 RVA strains isolated from acute diarrhea cases, G9 (66.4%) was predominant G genotype, followed by G3 (18.7%), G1 (8.9%), and G1G3 (3.8%); P[8] was the overwhelming prevalence P genotype, followed by P[4] (4.7%); G9P[8] (54.9%) was most common G and P Combination, followed by G3P[8] (17.6%) and G1[8] (8.6%). The conclusion of the study was important to provide reference for introducing the RVA vaccine to prevent and control RVA-associated disease burden. J. Med. Virol. 89:71-78, 2017. © 2016 Wiley Periodicals, Inc.

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Background: Although existing studies have suggested the involvement of the infrapatellar fat pad (IPFP) during the development of knee osteoarthritis (OA), the role of IPFP is still controversial. This study aimed to investigate the biochemical effects of osteoarthritic IPFP on cartilage and the underlying mechanisms.Methods: Human IPFP and articular cartilage were collected from end-stage OA patients during total knee arthroplasty. IPFP derived fat-conditioned medium (FCM) was used to stimulate human primary chondrocytes and cartilage explants. CCK8 was used to detect the viability of human chondrocyte. qRT-PCR and western blotting was performed to evaluate the balance of extracellular matrix (ECM) catabolism and anabolism in human chondrocytes with FCM stimulation. Functional effect of osteoarthritic IPFP was also demonstrated in human articular cartilage by ex vivo assay. Activation of relative pathways and its effects on chondrocytes were assessed through immunoblotting and inhibition experiments, respectively. Neutralization test was performed to identify the main factors and their associated pathways responsible for the effects of IPFP.Results: Osteoarthritic IPFP-derived FCM signi cantly induced extracellular matrix (ECM) degradation in both human primary chondrocytes and cartilage explants. Several pathways, such as NF-κB, mTORC1, p38MAPK, JNK, and ERK1/2 signaling were signi cantly activated in human chondrocytes with osteoarthritic IPFP-derived FCM stimulation. Interestingly, inhibition of p38MAPK and ERK1/2 signaling pathway could alleviate the detrimental effects of FCM on chondrocytes while inhibition of other signaling pathways had no similar results. In addition, IL-1β and TNF-α instead of IL-6 in osteoarthritic IPFP-derived FCM played a key role in cartilage degradation via activating p38MAPK rather than ERK1/2 signaling pathway.Conclusions: Osteoarthritic IPFP induces the degradation and in ammation of cartilage via activation of p38MAPK and ERK1/2 pathways, in which IL-1β and TNF-α act as the key factors. Our study suggests that modulating the effects of IPFP on cartilage may be a promising strategy for knee OA intervention.