Acute Gastrointestinal Infection Research Articles

Genetic diversity of enteric viruses responsible of gastroenteritis in urban and rural Burkina Faso.

Viral gastrointestinal infections remain a major public health concern in developing countries. In Burkina Faso, there are very limited updated data on the circulating viruses and their genetic diversity. This study investigates the detection rates and characteristics of rotavirus A (RVA), norovirus (NoV), sapovirus (SaV) and human astrovirus (HAstV) in patients of all ages with acute gastrointestinal infection in urban and rural areas. From 2018 to 2021, stool samples from 1,295 patients with acute gastroenteritis were collected and screened for RVA, NoV, SaV and HAstV. Genotyping and phylogenetic analyses were performed on a subset of samples. At least one virus was detected in 34.1% of samples. NoV and SaV were predominant with detection rates of respectively 10.5 and 8.8%. We identified rare genotypes of NoV GII, RVA and HAstV, recombinant HAstV strains and a potential zoonotic RVA transmission event. We give an up-to-date epidemiological picture of enteric viruses in Burkina Faso, showing a decrease in prevalence but a high diversity of circulating strains. However, viral gastroenteritis remains a public health burden, particularly in pediatric settings. Our data advocate for the implementation of routine viral surveillance and updated management algorithms for diarrheal disease.

Reported antibiotic use among patients in the multicenter ANDEMIA infectious diseases surveillance study in sub-saharan Africa

BackgroundExposure to antibiotics has been shown to be one of the drivers of antimicrobial resistance (AMR) and is critical to address when planning and implementing strategies for combatting AMR. However, data on antibiotic use in sub-Saharan Africa are still limited. Using hospital-based surveillance data from the African Network for Improved Diagnostics, Epidemiology and Management of Common Infectious Agents (ANDEMIA), we assessed self-reported antibiotic use in multiple sub-Saharan African countries.MethodsANDEMIA included 12 urban and rural health facilities in Côte d’Ivoire, Burkina Faso, Democratic Republic of the Congo, and Republic of South Africa. Patients with acute respiratory infection (RTI), acute gastrointestinal infection (GI) and acute febrile disease of unknown cause (AFDUC) were routinely enrolled, and clinical, demographic, socio-economic and behavioral data were collected using standardized questionnaires. An analysis of ANDEMIA data from February 2018 to May 2022 was conducted. Reported antibiotic use in the ten days prior to study enrolment were described by substance and by the WHO AWaRe classification (“Access”, “Watch”, “Reserve”, and “Not recommended” antibiotics). Frequency of antibiotic use was stratified by location, disease syndrome and individual patient factors.ResultsAmong 19,700 ANDEMIA patients, 7,258 (36.8%) reported antibiotic use. A total of 9,695 antibiotics were reported, including 54.7% (n = 5,299) from the WHO Access antibiotic group and 44.7% (n = 4,330) from the WHO Watch antibiotic group. The Watch antibiotic ceftriaxone was the most commonly reported antibiotic (n = 3,071, 31.7%). Watch antibiotic use ranged from 17.4% (56/322) among RTI patients in Côte d’Ivoire urban facilities to 73.7% (630/855) among AFDUC patients in Burkina Faso urban facilities. Reported antibiotic use included WHO Not recommended antibiotics but no Reserve antibiotics.ConclusionsReported antibiotic use data from this multicenter study in sub-Saharan Africa revealed a high proportion of WHO Watch antibiotics. Differences in Watch antibiotic use were found by disease syndrome, country and health facility location, which calls for a more differentiated approach to antibiotic use interventions including further evaluation of accessibility and affordability of patient treatment.

Salmonella manipulates the host to drive pathogenicity via induction of interleukin 1β.

Acute gastrointestinal infection with intracellular pathogens like Salmonella Typhimurium triggers the release of the proinflammatory cytokine interleukin 1β (IL-1β). However, the role of IL-1β in intestinal defense against Salmonella remains unclear. Here, we show that IL-1β production is detrimental during Salmonella infection. Mice lacking IL-1β (IL-1β -/-) failed to recruit neutrophils to the gut during infection, which reduced tissue damage and prevented depletion of short-chain fatty acid (SCFA)-producing commensals. Changes in epithelial cell metabolism that typically support pathogen expansion, such as switching energy production from fatty acid oxidation to fermentation, were absent in infected IL-1β -/- mice which inhibited Salmonella expansion. Additionally, we found that IL-1β induces expression of complement anaphylatoxins and suppresses the complement-inactivator carboxypeptidase N (CPN1). Disrupting this process via IL-1β loss prevented mortality in Salmonella-infected IL-1β -/- mice. Finally, we found that IL-1β expression correlates with expression of the complement receptor in patients suffering from sepsis, but not uninfected patients and healthy individuals. Thus, Salmonella exploits IL-1β signaling to outcompete commensal microbes and establish gut colonization. Moreover, our findings identify the intersection of IL-1β signaling and the complement system as key host factors involved in controlling mortality during invasive Salmonellosis.

Outbreak of Gastrointestinal Infections Caused by Yersinia enterocolitica in Children, Medellín, Colombia

Abstract Objective In this study, we describe the clinical and epidemiological characteristics of a cluster of children with acute gastrointestinal (GI) infection caused by Yersinia enterocolitica in Medellín, Colombia. Methods A retrospective descriptive observational study was performed with the information recorded in clinical charts of GI infection cases caused by Y. enterocolitica in pediatric population of two hospital institutions in Medellín, Colombia. The microorganism identification was performed directly from stool samples using molecular biology techniques and from stool cultures using mass spectrometry. Space-time simulations and antibiotic susceptibility profiles were performed using Whonet 5.6 and Clinical and Laboratory Standards Institute 2020 guide. Results A total of 37 cases were identified in children younger than 15 years; between November 2020 and January 2021, 45.9% of cases were in children aged 1 to 5 years. Most children had diarrhea (97.3%) and fever (67.6%), 21.6% had abdominal pain and vomiting, and 13.5% had hyporexia. Sixteen of the patients (43.2%) received azithromycin, 24.3% (n = 9) received ceftriaxone, and 13.5% (n = 5) received a combined treatment of ceftriaxone and azithromycin or azithromycin and metronidazole. Based on space-time simulations, the clonality analysis and the characteristics of the cases suggest a community outbreak of unknown origin. Conclusion Our findings confirm the occurrence of an outbreak related to Y. enterocolitica from the community whose source could not be identified. Although it is presumed that the frequency of this microorganism is low in these regions, the use of new diagnostic tools in clinical microbiology allowed the early identification of the epidemiological event.

Whole-genome-based characterization of Campylobacter jejuni from human patients with gastroenteritis collected over an 18 year period reveals increasing prevalence of antimicrobial resistance.

Campylobacteriosis is the most common cause of acute gastrointestinal bacterial infection in Europe, with most infections linked to the consumption of contaminated food. While previous studies found an increasing rate of antimicrobial resistance (AMR) in Campylobacter spp. over the past decades, the investigation of additional clinical isolates is likely to provide novel insights into the population structure and mechanisms of virulence and drug resistance of this important human pathogen. Therefore, we combined whole-genome sequencing and antimicrobial-susceptibility testing of 340 randomly selected Campylobacter jejuni isolates from humans with gastroenteritis, collected in Switzerland over an 18 year period. In our collection, the most common multilocus sequence types (STs) were ST-257 (n=44), ST-21 (n=36) and ST-50 (n=35); the most common clonal complexes (CCs) were CC-21 (n=102), CC-257 (n=49) and CC-48 (n=33). High heterogeneity was observed among STs, with the most abundant STs recurring over the entire study period, while others were observed only sporadically. Source attribution based on ST assigned more than half of the strains to the 'generalist' category (n=188), 25 % as 'poultry specialist' (n=83), and only a few to 'ruminant specialist' (n=11) or 'wild bird' origin (n=9). The isolates displayed an increased frequency of AMR from 2003 to 2020, with the highest rates of resistance observed for ciprofloxacin and nalidixic acid (49.8 %), followed by tetracycline (36.9 %). Quinolone-resistant isolates carried chromosomal gyrA mutations T86I (99.4 %) and T86A (0.6 %), whereas tetracycline-resistant isolates carried tet(O) (79.8 %) or mosaic tetO/32/O (20.2 %) genes. A novel chromosomal cassette carrying several resistance genes, including aph(3')-III, satA and aad(6), and flanked by insertion sequence elements was detected in one isolate. Collectively, our data revealed an increasing prevalence of resistance to quinolones and tetracycline in C. jejuni isolates from Swiss patients over time, linked to clonal expansion of gyrA mutants and acquisition of the tet(O) gene. Investigation of source attribution suggests that infections are most likely related to isolates from poultry or generalist backgrounds. These findings are relevant to guide future infection prevention and control strategies.

Intestinal toxicity to CTLA-4 blockade driven by IL-6 and myeloid infiltration.

Immune checkpoint blockade (ICB) has revolutionized cancer treatment, yet quality of life and continuation of therapy can be constrained by immune-related adverse events (irAEs). Limited understanding of irAE mechanisms hampers development of approaches to mitigate their damage. To address this, we examined whether mice gained sensitivity to anti-CTLA-4 (αCTLA-4)-mediated toxicity upon disruption of gut homeostatic immunity. We found αCTLA-4 drove increased inflammation and colonic tissue damage in mice with genetic predisposition to intestinal inflammation, acute gastrointestinal infection, transplantation with a dysbiotic fecal microbiome, or dextran sodium sulfate administration. We identified an immune signature of αCTLA-4-mediated irAEs, including colonic neutrophil accumulation and systemic interleukin-6 (IL-6) release. IL-6 blockade combined with antibiotic treatment reduced intestinal damage and improved αCTLA-4 therapeutic efficacy in inflammation-prone mice. Intestinal immune signatures were validated in biopsies from patients with ICB colitis. Our work provides new preclinical models of αCTLA-4 intestinal irAEs, mechanistic insights into irAE development, and potential approaches to enhance ICB efficacy while mitigating irAEs.

Dual RNA-seq reveals a type 6 secretion system-dependent blockage of TNF-α signaling and BicA as a Burkholderia pseudomallei virulence factor important during gastrointestinal infection

ABSTRACT Melioidosis is a disease caused by the Gram-negative bacillus Burkholderia pseudomallei (Bpm), commonly found in soil and water of endemic areas. Naturally acquired human melioidosis infections can result from either exposure through percutaneous inoculation, inhalation, or ingestion of soil-contaminated food or water. Our prior studies recognized Bpm as an effective enteric pathogen, capable of establishing acute or chronic gastrointestinal infections following oral inoculation. However, the specific mechanisms and virulence factors involved in the pathogenesis of Bpm during intestinal infection are unknown. In our current study, we standardized an in vitro intestinal infection model using primary intestinal epithelial cells (IECs) and demonstrated that Bpm requires a functional T6SS for full virulence. Further, we performed dual RNA-seq analysis on Bpm-infected IECs to evaluate differentially expressed host and bacterial genes in the presence or absence of a T6SS. Our results showed a dysregulation in the TNF-α signaling via NF-κB pathway in the absence of the T6SS, with some of the genes involved in inflammatory processes and cell death also affected. Analysis of the bacterial transcriptome identified virulence factors and regulatory proteins playing a role during infection, with association to the T6SS. By using a Bpm transposon mutant library and isogenic mutants, we showed that deletion of the bicA gene, encoding a putative T3SS/T6SS regulator, ablated intracellular survival and plaque formation by Bpm and impacted survival and virulence when using murine models of acute and chronic gastrointestinal infection. Overall, these results highlight the importance of the type 6 secretion system in the gastrointestinal pathogenesis of Bpm.

Abstract 5545: Intestinal toxicity to CTLA-4 blockade driven by IL-6 and myeloid infiltration

Abstract Immunotherapies such as anti-CTLA-4 immune checkpoint blockade (ICB) have revolutionized cancer treatment, yet quality of life and continuation of therapy can be constrained by off-target tissue damage or immune-related adverse events (irAEs). At present, there is limited understanding of irAE mechanisms, hampering development of approaches to mitigate their damage. We addressed this problem by generating animal models of intestinal irAE. Our results show that disruption of homeostatic immunity by genetic predisposition to intestinal inflammation or acute gastrointestinal infection sensitizes mice to anti-CTLA-4-mediated intestinal toxicity. Inflammation-prone mice treated with anti-CTLA-4 showed neutrophil accumulation, systemic interleukin-6 (IL-6) release, and dysbiosis. Significantly, IL-6 blockade combined with antibiotic treatment improved anti-CTLA-4 therapeutic efficacy and reduced intestinal irAEs. Immune signatures were validated in biopsies from patients who developed colitis during ICB, supporting the utility of our models. This study provides new pre-clinical models, mechanistic insight into irAEs, and potential approaches to enhance ICB efficacy while mitigating irAEs. Citation Format: Yifan Zhou, Yusra B. Medik, Bhakti Patel, Daniel B. Zamler, Sijie Chen, Thomas Chapman, Sarah Schneider, Rachel L. Babcock, Taylor T. Chrisikos, Laura M. Kahn, Allison M. Dyevoich, Elizabeth M. Park, Alexandria P. Cogdill, Daniel H. Johnson, Sarah B. Johnson, Khalida M. Wani, Debora A. Ledesma, Courtney W. Hudgens, Jingjing Wang, Md Abdul Wadud Khan, Aron Y. Joon, Weiyi Peng, Haiyan S. Li, Reetakshi Arora, Ximing Tang, Maria Gabriela Raso, Xuegong Zhang, Wai Chin Foo, Michael T. Tetzlaff, Gretchen E. Diehl, Karen Clise-Dwyer, Elizabeth M. Whitley, Matthew M. Gubin, James P. Allison, Patrick Hwu, Nadim J. Ajami, Adi Diab, Jennifer A. Wargo, Stephanie S. Watowich. Intestinal toxicity to CTLA-4 blockade driven by IL-6 and myeloid infiltration [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 5545.

B-cell-intrinsic MHCII signaling limits bacteremia and systemic invasion by Citrobacter rodentium

Abstract B-cell-intrinsic major histocompatibility complex class II (MHCII) antigen presentation is central to the development of T-cell-dependent antibody responses. However, the physiological significance of B-cell-intrinsic MHCII signaling during homeostatic conditions and infection are unknown. Here, using a B-cell-intrinsic MHCII knockout mouse model, we demonstrate that B-cell-intrinsic MHCII signaling is important for the development of systemic IgG1 and mucosal, high-affinity IgA responses. We also show that the conditional ablation of MHCII signaling on B cells results in a change in the microbiota composition, exhibiting a significant increase in the mucin-degrading bacteria Akkermansia muciniphila. This change in the microbiome is also associated with elevated bacterial dissemination from the gut into the systemic compartment under homeostatic conditions. Additionally, using a Citrobacter rodentium model of acute gastrointestinal infection, we also demonstrate the relevance of B-cell-intrinsic MHCII signaling in limiting invasion of the systemic compartment by an opportunistic enteric pathogen. Results from these experiments demonstrate that B-cell-intrinsic MHCII signaling is an important factor minimizing the physiological cost of microbial colonization of the gut. Supported by NIH R21AI142409, R01AI155887

Intestinal inflammation alters the antigen-specific immune response to a skin commensal.

SUMMARYResident microbes in skin and gut predominantly impact local immune cell function during homeostasis. However, colitis-associated neutrophilic skin disorders suggest possible breakdown of this compartmentalization with disease. Using a model wherein neonatal skin colonization by Staphylococcus epidermidis facilitates generation of commensal-specific tolerance and CD4+ regulatory T cells (Tregs), we ask whether this response is perturbed by gut inflammation. Chemically induced colitis is accompanied by intestinal expansion of S. epidermidis and reduces gut-draining lymph node (dLN) commensal-specific Tregs. It also results in reduced commensal-specific Tregs in skin and skin-dLNs and increased skin neutrophils. Increased CD4+ circulation between gut and skin dLN suggests that the altered cutaneous response is initiated in the colon, and resistance to colitis-induced effects in Cd4creIl1r1fl/fl mice implicate interleukin (IL)-1 in mediating the altered commensal-specific response. These findings provide mechanistic insight into observed connections between inflammatory skin and intestinal diseases.

Antiviral Activities of Carbazole Derivatives against Porcine Epidemic Diarrhea Virus In Vitro.

Porcine epidemic diarrhea virus (PEDV), an enteric coronavirus, causes neonatal pig acute gastrointestinal infection with a characterization of severe diarrhea, vomiting, high morbidity, and high mortality, resulting in tremendous damages to the swine industry. Neither specific antiviral drugs nor effective vaccines are available, posing a high priority to screen antiviral drugs. The aim of this study is to investigate anti-PEDV effects of carbazole alkaloid derivatives. Eighteen carbazole derivatives (No.1 to No.18) were synthesized, and No.5, No.7, and No.18 were identified to markedly reduce the replication of enhanced green fluorescent protein (EGFP) inserted-PEDV, and the mRNA level of PEDV N. Flow cytometry assay, coupled with CCK8 assay, confirmed No.7 and No.18 carbazole derivatives displayed high inhibition effects with low cell toxicity. Furthermore, time course analysis indicated No.7 and No.18 carbazole derivatives exerted inhibition at the early stage of the viral life cycle. Collectively, the analysis underlines the benefit of carbazole derivatives as potential inhibitors of PEDV, and provides candidates for the development of novel therapeutic agents.

TO FIND OUT ETIOLOGY AND CLINICAL PROFILE OF PATIENTS OF ACUTE KIDNEY INJURY AT TERTIARY CARE CENTRE OF INDORE

Background & Method: Present Study was done with an aim to find out Etiology and clinical profile of patients of Acute Kidney Injury at Tertiary Care Centre of Indore. After taking institutional ethical clearance and written consent from the patients a cross sectional observational study was conducted on 100 Patients admitted in Intensive Care Unit of INDEX MEDICAL COLLEGE AND RESEARCH CENTRE who have clinical and / or biochemical evidence of acute kidney injury, detailed thorough history taking, general physical examination, systemic examination and routine and specific lab investigations, were done to find out the underlying etiology, clinical features and outcome of Acute Kidney Injury.
 Result: This study includes various etiology of acute kidney injury in the current study. Most common cause being AGE (30%) followed by septicemia (16%) and poisoning (14%). In present study 75 % of cases were of Pre Renal AKI. Post Renal and Renal AKI was present in 13% and 12% respectively.
 Conclusion: The variety of clinical features were recorded and studied, the most commonly observed clinical feature was oliguria closely followed by malaise and vomiting in acute kidney injury. Acute gastrointestinal infection was the most common cause of acute kidney injury. Other frequent causes were septicemia, poisoning, multi organ dysfunction syndrome.
 Keywords: Etiology, clinical & Acute Kidney.

TREATMENT OF ACUTE INTESTINAL INFECTION IN MINKS

The article presents the results of studies on the effectiveness of the multicomponent drug Nifulin (powder for oral administration) in the treatment of acute gastrointestinal infection in minks. The active pharmaceutical ingredients (API) of the drug are metronidazole, furazolidone and oxytetracycline hydrochloride. The researches were conducted on 135 minks of standard dark brown breed at the age of 4–5 months with acute gastrointestinal infection. To isolate and identify pathogens from sick minks with intestinal infection, samples of feces were taken, and from animal’s corpses – samples of parenchymal organs. On the basis of clinical signs of the disease and results of bacteriological researches of biomaterial, a diagnosis – salmonellosis has been put. The test for the sensitivity of bacteria-isolates to oxytetracycline showed a high degree of sensitivity of isolated strains of Salmonella to this antibiotic.
 Nifulin was administered orally at a dose of 0,3g/kg body weight with food three times a day for 3 days. For laboratory tests blood sampling was performed from 10 animals before treatment and on the 10th day from the latest application of the drug.
 Morphological studies of blood samples of sick minks before treatment established a significant increase in the number of leukocytes, and in leukoformula – an increased relative number of rod-nucleated neutrophils and lymphocytes, a decreased number of segmentonuclear neutrophils. Biochemical studies of blood serum revealed a decrease in total protein content, increased transaminase enzyme activity and increased urea and creatinine content, compared with physiological norms.
 On the 10th day after antibiotic therapy hematological studies established a reliable decrease in the relative number of leukocytes by 65,4%, in the number of rod-nucleated neutrophils by 1,3 times and in the number of lymphocytes by 1,9 times, an increase in the number of segmentonuclear neutrophils by 1,4 times. The results of biochemical tests of mink’s serum blood indicated a reliable increase in the total protein content by 18% and increased ALT and AST enzyme activity, compared with the physiological values. The increase in serum AST activity in 1.8 times was noted, that can be explained, as a consequence of the disease, and the influence of antibiotics on the mink’s liver functional state. In this case, a decrease in urea content in 1.3 times and creatinine content – in 1.5 times was determined, the values of these indicators were normalized, indicating the restoration of the physiological state of the mink’s kidneys.
 As a result of the treatment of minks the clinical signs of the disease were gradually disappeared: diarrhea stopped, body temperature and respiratory frequency normalized, general condition has improved. In most animals (130 goals) clinical recovery came. During the application of Nifulin manifestations of adverse reactions or negative effects in the experimental minks were not observed.

Suppression of PTRF Alleviates Post-Infectious Irritable Bowel Syndrome via Downregulation of the TLR4 Pathway in Rats.

Background: Accumulating evidence suggests that the polymerase I and transcript release factor (PTRF), a key component of the caveolae structure on the plasma membrane, plays a pivotal role in suppressing the progression of colorectal cancers. However, the role of PTRF in the development of functional gastrointestinal (GI) disorders remains unclear. Post-infectious irritable bowel syndrome (PI-IBS) is a common functional GI disorder that occurs after an acute GI infection. Here, we focused on the role of PTRF in the occurrence of PI-IBS and investigated the underlying mechanisms. Methods: Lipopolysaccharide (LPS) (5 μg/ml) was used to induce inflammatory injury in human primary colonic epithelial cells (HCoEpiCs). Furthermore, a rat model of PI-IBS was used to study the role of PTRF. Intestinal sensitivity was assessed based on the fecal water content. A two-bottle sucrose intake test was used to evaluate behavioral changes. Furthermore, shRNA-mediated knockdown of PTRF was performed both in vitro and in vivo. We detected the expression of PTRF in colonic mucosal tissues through immunohistochemistry (IHC), western blotting (WB), and immunofluorescence (IF) analysis. Luciferase activity was quantified using a luciferase assay. Co-localization of PTRF and Toll-like receptor 4 (TLR4) was detected using IF analysis. The activation of the signaling pathways downstream of TLR4, including the iNOs, p38, extracellular signal-regulated kinase (ERK), and c-Jun N-terminal kinase (JNK) pathways, was detected via WB. The levels of NO, IL-1β, IL-6, and TNF-α were measured using enzyme-linked immunosorbent assays. Results: LPS significantly induced PTRF expression and signaling downstream of TLR4, including p38, ERK, and JNK pathways, in HCoEpiCs. Moreover, shRNA-mediated knockdown of PTRF in HCoEpiCs significantly decreased the phosphorylation of JNK, ERK, and p38 and iNOS expression. In PI-IBS rats, the lack of PTRF not only reduced fecal water content and suppressed depressive behavior but also increased the body weight. Furthermore, we found a strong co-localization pattern for PTRF and TLR4. Consistently, the lack of PTRF impaired TLR4 signaling, as shown by the decreased levels of p-JNK, p-ERK, and p-p38, which are upstream factors involved in iNOS expression. Conclusion: PTRF promoted PI-IBS and stimulated TLR4 signaling both in vitro and in vivo. The results of this study not only enlighten the pathogenesis of PI-IBS but also help us understand the biological activity of PTRF and provide an important basis for the clinical treatment of PI-IBS by targeting PTRF.

Real-time gastrointestinal infection surveillance through a cloud-based network of clinical laboratories.

Acute gastrointestinal infection (AGI) represents a significant public health concern. To control and treat AGI, it is critical to quickly and accurately identify its causes. The use of novel multiplex molecular assays for pathogen detection and identification provides a unique opportunity to improve pathogen detection, and better understand risk factors and burden associated with AGI in the community. In this study, de-identified results from BioFire® FilmArray® Gastrointestinal (GI) Panel were obtained from January 01, 2016 to October 31, 2018 through BioFire® Syndromic Trends (Trend), a cloud database. Data was analyzed to describe the occurrence of pathogens causing AGI across United States sites and the relative rankings of pathogens monitored by FoodNet, a CDC surveillance system were compared. During the period of the study, the number of tests performed increased 10-fold and overall, 42.6% were positive for one or more pathogens. Seventy percent of the detections were bacteria, 25% viruses, and 4% parasites. Clostridium difficile, enteropathogenic Escherichia coli (EPEC) and norovirus were the most frequently detected pathogens. Seasonality was observed for several pathogens including astrovirus, rotavirus, and norovirus, EPEC, and Campylobacter. The co-detection rate was 10.2%. Enterotoxigenic E. coli (ETEC), Plesiomonas shigelloides, enteroaggregative E. coli (EAEC), and Entamoeba histolytica were detected with another pathogen over 60% of the time, while less than 30% of C. difficile and Cyclospora cayetanensis were detected with another pathogen. Positive correlations among co-detections were found between Shigella/Enteroinvasive E. coli with E. histolytica, and ETEC with EAEC. Overall, the relative ranking of detections for the eight GI pathogens monitored by FoodNet and BioFire Trend were similar for five of them. AGI data from BioFire Trend is available in near real-time and represents a rich data source for the study of disease burden and GI pathogen circulation in the community, especially for those pathogens not often targeted by surveillance.

Determinants of Work-Related Risks among Veterinary Clinical Students in South West Nigeria.

Veterinary practices or activities expose professionals, including students, to hazards associated with animal contact. To describe workplace health and safety status and risk factors associated with hazards among veterinary clinical students in South West Nigeria, a cross-sectional survey was conducted using a semistructured questionnaire. Data on demographics, health and safety (HS) status, work-related hazards, healthcare facilities, and immunisation history were obtained. Of 167 students recruited, 100 (60.2%) were males, and >77.1% fell within the age group of 21–25 years. Many participants (77.0%) reported the lack of active HS committee. Exposures to various physical hazards (PHs) such as needlestick injuries (NSIs, 41.5%), animal scratches (42.0%), animal kicks (33.0%), falls/slips (25.0%), and, less frequently, animal bites (13.8%) were reported. Allergies (35.9%) and acute gastrointestinal infection (25.6%) mainly after contact with dogs presented with parvoviral enteritis were reported. For chemical hazards, 27.8% and 29.0% of participants indicated having had eye burn and choke on exposure to formalin. No adequate immunisation against either tetanus, rabies, or both was provided (<18%). An association between accommodation type and students' level of health and safety training was observed (OR = 0.46, 95% CI: 0.241–0.897, p=0.02), and frequencies of student contact with various animal types were strongly associated with exposures to different physical and biological risks (p < 0.05). This study revealed poor health and safety training, practices, and increased exposure of students to a wide range of hazards. Therefore, the development of mitigation programmes in veterinary schools becomes critical to safeguard students' wellbeing.

Clostridium difficile caused changes in fatty acids profile and resolvin D1 content in plasma of infected patients.

Clostridium difficile infection (CDI) is an acute gastrointestinal infection caused by anaerobic, toxin-producing bacteria. During the course of CDI, there is a general inflammatory state. In order to gain a deeper understanding of the role of fatty acids (FAs) in the pathogenesis of acute infection we analyzed their plasma content in both patients with CDI and controls. The study groups included 40 patients with CDI and 40 healthy volunteers. Plasma FA content was analyzed by gas chromatography, resolvin D1 (RvD1) level using ELISA assay, and we assessed the white blood cell (WBC) count, neutrophil count and C-reactive protein (CRP) level. Patients with CDI were characterized by significantly higher values of WBC, neutrophils, platelets and CRP compared with the control group. The saturated FA index was statistically higher and total n-3 FA was significantly decreased in the plasma of CDI patients as compared with the control group. RvD1 content was significantly higher in the control group as compared with patients with CDI. In patients with good outcomes, we probably observed the effective resolution of inflammation, as reflected in n-3 FA metabolism and their significant decrease in plasma. This may indicate the therapeutic role of n-3 FA in CDI infection.

Seasonal influenza vaccine and Guillain-Barré syndrome: A self-controlled case series study.

To evaluate the risk of Guillain-Barré syndrome (GBS) following seasonal influenza vaccination based on French nationwide data. All cases of GBS occurring in metropolitan France between September 1 and March 31 from 2010 to 2014 were identified from the French national health data system. Data were analyzed according to the self-controlled case series method. The risk period started 1 day after the patient received vaccine (D1) until 42 days after vaccination (D42). The incidence of GBS during this risk period was compared to that of the control period (D43-March 31). The incidence rate ratio (IRR) was estimated after adjusting for seasonality and presence or not of acute infections. Between September and March, of the 2010/2011 to 2013/2014 influenza vaccination seasons, 3,523 cases of GBS occurred in metropolitan France and were included in the study. Among them, 15% (527 patients) had received influenza vaccination. A total of 140 patients developed GBS during the 42 days following influenza vaccination. The crude risk of developing GBS was not significantly increased during the 42 days following influenza vaccination (IRR, 1.02; 95% confidence interval [CI], 0.83-1.25; p = 0.85). This result remained nonsignificant after adjustment for calendar months and the incidence of acute gastrointestinal and respiratory tract infections (IRR, 1.10; 95% CI, 0.89-1.37; p = 0.38). In contrast, the risk of GBS was fourfold higher after acute respiratory tract infection (IRR, 3.89; 95% CI, 3.52-4.30; p < 0.0001) or gastrointestinal infection (IRR, 3.64; 95% CI, 3.01-4.40; p < 0.0001). No association between seasonal influenza vaccination and GBS was shown during the 42 days following vaccination.

Acute Febrile Illness Among Children in Butajira, South-Central Ethiopia During the Typhoid Fever Surveillance in Africa Program.

BackgroundClearly differentiating causes of fever is challenging where diagnostic capacities are limited, resulting in poor patient management. We investigated acute febrile illness in children aged ≤15 years enrolled at healthcare facilities in Butajira, Ethiopia, during January 2012 to January 2014 for the Typhoid Fever Surveillance in Africa Program.MethodsBlood culture, malaria microscopy, and blood analyses followed by microbiological, biochemical, and antimicrobial susceptibility testing of isolates were performed. We applied a retrospectively developed scheme to classify children as malaria or acute respiratory, gastrointestinal or urinary tract infection, or other febrile infections and syndromes. Incidence rates per 100 000 population derived from the classification scheme and multivariate logistic regression to determine fever predictors were performed.ResultsWe rarely observed stunting (4/513, 0.8%), underweight (1/513, 0.2%), wasting (1/513, 0.2%), and hospitalization (21/513, 4.1%) among 513 children with mild transient fever and a mean disease severity score of 12 (95% confidence interval [CI], 11–13). Blood cultures yielded 1.6% (8/513) growth of pathogenic agents; microscopy detected 13.5% (69/513) malaria with 20 611/µL blood (95% CI, 15 352–25 870) mean parasite density. Incidences were generally higher in children aged ≤5 years than >5 to ≤15 years; annual incidences in young children were 301.3 (95% CI, 269.2–337.2) for malaria and 1860.1 (95% CI, 1778.0–1946.0) for acute respiratory and 379.9 (95% CI, 343.6–420.0) for gastrointestinal tract infections.ConclusionsWe could not detect the etiological agents in all febrile children. Our findings may prompt further investigations and the reconsideration of policies and frameworks for the management of acute febrile illness.

The relationship of preoperative estimated glomerular filtration rate and outcomes after cardiovascular surgery in patients with normal serum creatinine: a retrospective cohort study

BackgroundAlthough serum creatinine concentration has been traditionally used as an index of renal function in clinical practice, it is considered relatively inaccurate, especially in patients with mild renal dysfunction. This study investigated the usefulness of preoperative estimated glomerular filtration rate (eGFR) in predicting complications after cardiovascular surgery in patients with normal serum creatinine concentrations.MethodsThis study included 2208 adults undergoing elective cardiovascular surgery. Preoperative eGFR was calculated using Chronic Kidney Disease Epidemiology Collaboration equations. The relationships between preoperative eGFR and 90 day postoperative composite major complications were analyzed, including 90 day all-cause mortality, major adverse cardiac and cerebrovascular events, severe acute kidney injury, respiratory and gastrointestinal complications, wound infection, sepsis, and multi-organ failure.ResultsOf the 2208 included patients, 185 (8.4%) had preoperative eGFR < 60 mL/min/1.73 m2 and 328 (14.9%) experienced postoperative major complications. Multivariable logistic regression analyses showed that preoperatively decreased eGFR was independently associated with an increased risk of composite 90 day major postoperative complications (adjusted odds ratio: 1.232; 95% confidence interval [CI]: 1.148–1.322; P < 0.001). eGFR was a better discriminator of composite 90 day major postoperative complications than serum creatinine, with estimated c-statistics of 0.724 (95% CI: 0.694–0.754) for eGFR and 0.712 (95% CI: 0.680–0.744) for serum creatinine (P = 0.008).ConclusionsDecreased eGFR was significantly associated with an increased risk of major complications after cardiovascular surgery in patients with preoperatively normal serum creatinine concentrations.