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Botanicals, phytogenic feed additives, and essential oils may have potential benefits in swine production for their health, immunity, and growth promoting effects. Therefore, the objective of this study was to investigate the effects of dietary botanical supplementation on blood profiles and intestinal morphology of weaned piglets experimentally infected with a pathogenic F18 Escherichia coli (E. coli). Sixty weaned piglets (around 21 days old; 7.15 ± 0.97 kg) were individually housed and randomly allotted to one of five dietary treatments (n = 12): negative control (NC), positive control (PC), high dose of botanicals blend 1 (BB1, 100 mg/kg), and low or high dose of botanicals blend 2 (BB2, 50 mg/kg and 100 mg/kg). Both botanical blends were comprised of capsicum oleoresin but different garlic extract varieties. The experiment lasted 28 days from day -7 to +21 relative to E. coli inoculation. All piglets except the NC group were orally inoculated with F18 E. coli (1010 cfu per dose, 3 doses) for 3 consecutive days. Growth performance and diarrhea scores were recorded throughout the experiment. Blood samples were collected on d 0, 5, 14, and 21 post-inoculation (PI) for complete blood count test. Intestinal segments were collected on d 5 and 21 PI for intestinal morphology analysis. Data were analyzed by ANOVA in PROC MIXED of SAS with a randomized complete block design. E. coli infection reduced (P < 0.05) pig body weight and growth rate throughout the experiment and reduced (P < 0.05) neutrophils and lymphocytes but increased (P < 0.05) monocytes on d 4 PI. No differences in weight gain or average daily gain were observed among the botanical blend treatments compared with the control. Supplementation of high dose BB1 or BB2 reduced (P < 0.05) frequency and severity of diarrhea of challenged pigs during the experimental period. Pigs supplemented with 100 mg/kg of BB2 had less (P < 0.05) lymphocytes than pigs in PC on d 4 PI. Pigs fed with 50 mg/kg of BB2 had lower (P < 0.05) lymphocytes and monocytes than pigs in PC on d 21 PI. Pigs supplemented with 100 mg/kg of BB2 had the greatest (P < 0.05) duodenal villi width, jejunum villi height and area, and colon crypt depth than pigs in PC on d 5 PI. In conclusion, dietary supplementation of botanicals reduced diarrhea and tended to affect systemic immunity and enhance intestinal morphology of weaned pigs infected with E. coli.

Escherichia coli infections can result in lung injury, which may be closely linked to the induction of interferon secretion. The Janus kinase (JAK)/signal transducer and activator of transcription (STAT) pathway is one of most important pathways that regulate interferon production. Thus, the present study aimed to dissect whether E. coli infections can regulate interferon production and the underlying mechanisms. For this aim, two lung cell lines, a human bronchial epithelial cell line transformed with Ad12-SV40 2B (BEAS-2b) and a human fetal lung fibroblast (HFL1) cell line, were used. The effects of E. coli infections on interferon production were studied using qRT-PCR, Western blot, and siRNA knockdown assays. E. coli infections remarkably promoted the expression levels of IFN-α, IFN-β, and ISGs. Major components of the JAK/STAT pathway, including JAK1, STAT1, and STAT2, were demonstrated to be regulated by E. coli infections. Importantly, knockdown of JAK1, STAT1, and STAT2 abolished the induction of IFN-α, IFN-β, and ISGs by E. coli. Therefore, experiments in the present study demonstrated that E. coli infections remarkably promoted interferon production in lung cells, which was closely regulated by the JAK/STAT signaling pathway. The findings in the present study are useful for further understanding the pathogenesis of E. coli infections in the lung and finding novel therapies to treat E. coli-induced lung injury.

Background Escherichia coli is the most common Gram-negative bacterium causing meningitis, and E. coli meningitis is associated with high mortality and morbidity throughout the world. Our previous study showed that E. coli can colonize the brain and cause neuroinflammation. Increasing evidence supports the involvement of miRNAs as key regulators of neuroinflammation. However, it is not clear whether these molecules participate in the regulation of meningitic E. coli-mediated neuroinflammation. Methods The levels of miR-155 and miR-146a, as well as their precursors, in E. coli-infected astrocytes were measured using quantitative real-time PCR (qPCR). Overexpression and knockdown studies of miR-155 and miR-146a were performed to observe the effects on bacterial loads, cytokines, chemokines, and NF-κB signaling pathways. Bioinformatics methods were utilized to predict the target genes, and these target genes were validated using qPCR, Western blotting, and luciferase reporter system. In vivo knockdown of miR-155 and miR-146a was carried out to observe the effects on bacterial loads, inflammatory genes, astrocyte activation, microglia activation, and survival in a mouse model. Results The levels of miR-155, miR-146a, and their precursors were significantly increased in astrocytes during E. coli infection. miR-155 and miR-146a were induced by the NF-κB-p65 signaling pathway upon infection. Overexpressing and inhibiting miR-155 and miR-146a in astrocytes did not affect the bacterial loads. Further, the in vitro overexpression of miR-155 and miR-146a suppressed the E. coli-induced inflammatory response, whereas the inhibition of miR-155 and miR-146a enhanced it. Mechanistically, miR-155 inhibited TAB2, and miR-146a targeted IRAK1 and TRAF6; therefore, they functioned collaboratively to modulate TLR-mediated NF-κB signaling. In addition, both miR-155 and miR-146a could regulate the EGFR–NF-κB signaling pathway. Finally, the in vivo suppression of E. coli-induced miR-155 and miR-146a further promoted the production of inflammatory cytokines, aggravated astrocyte and microglia activation, and decreased mouse survival time, without affecting the bacterial loads in the blood and brain. Conclusions E. coli infection induced miR-155 and miR-146a, which collectively regulated bacteria-triggered neuroinflammatory responses through negative feedback regulation involving the TLR-mediated NF-κB and EGFR–NF-κB signaling pathways, thus protecting the central nervous system from further neuroinflammatory damage.

Objective: In this case report, we have investigated the infectious bronchitis (IB) virus (IBV) out¬break with the co-infection of Escherichia coli in 2833-day-old broiler chickens in Malaysia. Materials and Methods: A farmer complained that Cobb 500 chickens, raised in the open house, were having bloody diarrhea, open mouth breathing, non-uniform growth, and ruffled feathers. The mortality was about 100 birds (from about 7000 birds) per day. The sick birds were isolated and subjected to physical examination, postmortem, and histopathological analyses. Gross lesions were observed and recorded. The lung samples have proceeded with histopathological evalua¬tions. The lungs, kidneys, trachea, air sac, and heart samples were collected to isolate bacteria and fungi through a series of conventional cultural methods, followed by molecular confirmation of the IBV. Results: Postmortem examination revealed air sacculitis, hemorrhagic tracheitis, pulmonary con¬gestion, fibrin deposition in the liver and air sac, hemorrhagic enteritis, and renomegaly. The bacterial culture and biochemical tests revealed E. coli in the lungs, trachea, liver, intestine, and kidney samples. However, no fungus could be isolated from those samples. Histological evalua¬tion of lung samples demonstrated infiltration of inflammatory cells in the pulmonary tissues. Apart from this, reverse transcription-polymerase chain reaction confirmed the presence of avian coronavirus responsible for infectious bronchitis (IB). Conclusion: The chickens were diagnosed with IB concurrent with E.coli. The chickens exhibited typical nephropathogenic strain of IBV infection, causing high mortality. [J Adv Vet Anim Res 2021; 8(1.000): 101-104]

We characterized the antimicrobial resistance of 70 Escherichia coli isolates obtained from patients with a urinary tract infection (UTI) from 8 public hospitals in Peru. Resistance profiles were identified using the automated MicroScan® system. A standard polymerase chain reaction was used for the detection of the bla TEM, bla CTX-M, bla SHV and bla PER genes. The 65.7% (46/70) of the isolates presented a multidrug-resistant phenotype and 55.7% (39/70) were extended-spectrum beta-lactamases producers. High levels of resistance were detected for ampicillin (77,1%), ciprofloxacin (74,3%), trimethoprim/sulfamethoxazole (62,9%), cefepime (57,1%), and cefuroxime (57,1%). The bla TEM gene was the most frequent (31,4%), followed by bla CTX-M (18,6%) and bla SHV (2,9%) genes. These results show high resistance levels to antimicrobials of clinical use in E. coli isolates from hospital UTI patients in Peru.Se caracterizó la resistencia antimicrobiana de 70 aislados de Escherichia coli obtenidos de pacientes con infección del tracto urinario (ITU) provenientes de ocho hospitales públicos en el Perú. Los perfiles de resistencia fueron identificados mediante el uso del sistema automatizado MicroScan®. Se utilizó una reacción en cadena de la polimerasa convencional para la detección de los genes bla TEM, bla CTX-M, bla SHV y bla PER. El 65,7% (46/70) de los aislados presentó un fenotipo multidrogorresistente y el 55,7% (39/70) fue identificado como productores de betalactamasas de espectro extendido. Se detectaron altos niveles de resistencia para ampicilina (77,1%), ciprofloxacina (74,3%), trimetoprim/sulfametoxazol (62,9%), cefepime (57,1%) y cefuroxima (57,1%). El gen bla TEM fue el más frecuente con un 31,4%, seguido por bla CTX-M (18,6%) y bla SHV (2,9%). Los resultados evidencian altos niveles de resistencia a antimicrobianos de importancia clínica en aislados de E. coli de pacientes con ITU en el Perú.

Aim: To investigate the mRNAs and noncoding RNAs (ncRNAs) expression in astrocytes upon meningitic- Escherichia coli infection. Materials & methods: The transcription of mRNAs and ncRNAs were fully investigated and profiled by whole transcriptome sequencing and bioinformatic approaches. Whole transcriptome differences between the infected astrocytes and brain microvascular endothelial cells were further compared and characterized. Results: A total of 2045 mRNAs, 74 long noncoding RNAs, 27 miRNAs and 418 circular RNAs were differentially transcribed in astrocytes upon infection. Competing endogenous RNAs regulatory networks were constructed and preliminary validated. Transcriptomic differences between astrocyte and brain microvascular endothelial cells revealed the cell-specific responses against the infection. Conclusion: Our study comprehensively characterized the ncRNAs and mRNAs profiles in astrocytes upon meningitic- E. coli infection, which will facilitate future functional studies.

This study aimed to prove the potential of Lactobacillus casei and Lactobacillus acidophilus probiotics as alternative substitutes of antibiotic growth promoters in laying hens challenged by Escherichia coli infection in order to enhance their growth performance and hen day production. The study used a total of 120 laying hens aged 25 weeks, divided into 3×2 treatments with each comprising 4 replications, and each replication consisted of 5 hens. The study used a completely randomised factorial design; factor a was the feed additive (control, antibiotics growth promoters /AGP, probiotic), whereas factor b was the E. coli infection (non-infection and E. coli infection). The results showed that there were significant differences (p

Formyl peptide receptors (FPRs, mouse Fprs) belong to the G protein–coupled receptor superfamily and mediate phagocyte migration in response to bacteria- and host-derived chemoattractants; however, knowledge about their in vivo roles in bacterial pathogenesis is limited. In this study, we investigated the role of Fpr1 and Fpr2 in host defense against Escherichia coli infection. In vitro, we found that supernatants from E. coli cultures induced chemotaxis of wild-type (WT) mouse bone marrow–derived neutrophils and that the activity was significantly reduced in cells genetically deficient in either Fpr1 or Fpr2 and was almost absent in cells lacking both receptors. Consistent with this, E. coli supernatants induced chemotaxis and MAPK phosphorylation in HEK293 cells expressing either recombinant Fpr1 or Fpr2 but not untransfected parental cells. WT bone marrow –derived neutrophils could actively phagocytose and kill E. coli, whereas both activities were diminished in cells lacking Fpr1 or Fpr2; again, an additive effect was observed in cells lacking both receptors. In vivo, Fpr1 and Fpr2 deficiency resulted in reduced recruitment of neutrophils in the liver and peritoneal cavity of mice infected with inactivated E. coli. Moreover, Fpr1−/− and Fpr2−/− mice had significantly increased mortality compared with WT mice after i.p. challenge with a virulent E. coli clinical isolate. These results indicate a critical role of Fprs in host defense against E. coli infection.

Macrophages are the cells of the first-line defense system, which protect the body from foreign invaders such as bacteria. However, Gram-negative bacteria have always been the major challenge for macrophages due to the presence of lipopolysaccharides on their outer cell membrane. In the present study, we evaluated the effect of phloretin, a flavonoid commonly found in apple, on the protection of macrophages from Escherichia coli infection. RAW 264.7 cells infected with standard E. coli, or virulent E. coli K1 strain were treated with phloretin in a dose-dependent manner to examine its efficacy in protection of macrophages. Our results revealed that phloretin treatment reduced the production of nitric oxide (NO) and generation of reactive oxygen species along with reducing the secretion of proinflammatory cytokines induced by the E. coli and E. coli K1 strains in a concentration-dependent manner. Additionally, treatment of phloretin downregulated the expression of E. coli-induced major inflammatory markers i.e. cyclooxygenase-2 (COX-2) and hemeoxygenase-1 (HO-1), in a concentration dependent manner. Moreover, the TLR4-mediated NF-κB pathway was activated in E. coli-infected macrophages but was potentially downregulated by phloretin at the transcriptional and translational levels. Collectively, our data suggest that phloretin treatment protects macrophages from infection of virulent E. coli K1 strain by downregulating the TLR4-mediated signaling pathway and inhibiting NO and cytokine production, eventually protecting macrophages from E. coli-induced inflammation.

We have previously shown that Mkp-1–deficient mice produce elevated TNF-α, IL-6, and IL-10 following systemic Escherichia coli infection, and they exhibited increased mortality, elevated bacterial burden, and profound metabolic alterations. To understand the function of Mkp-1 during bacterial infection, we performed RNA-sequencing analysis to compare the global gene expression between E. coli–infected wild-type and Mkp-1−/− mice. A large number of IFN-stimulated genes were more robustly expressed in E. coli–infected Mkp-1−/− mice than in wild-type mice. Multiplex analysis of the serum cytokine levels revealed profound increases in IFN-β, IFN-γ, TNF-α, IL-1α and β, IL-6, IL-10, IL-17A, IL-27, and GMSF levels in E. coli–infected Mkp-1−/− mice relative to wild-type mice. Administration of a neutralizing Ab against the receptor for type I IFN to Mkp-1−/− mice prior to E. coli infection augmented mortality and disease severity. Mkp-1−/− bone marrow–derived macrophages (BMDM) produced higher levels of IFN-β mRNA and protein than did wild-type BMDM upon treatment with LPS, E. coli, polyinosinic:polycytidylic acid, and herring sperm DNA. Augmented IFN-β induction in Mkp-1−/− BMDM was blocked by a p38 inhibitor but not by an JNK inhibitor. Enhanced Mkp-1 expression abolished IFN-β induction by both LPS and E. coli but had little effect on the IFN-β promoter activity in LPS-stimulated RAW264.7 cells. Mkp-1 deficiency did not have an overt effect on IRF3/7 phosphorylation or IKK activation but modestly enhanced IFN-β mRNA stability in LPS-stimulated BMDM. Our results suggest that Mkp-1 regulates IFN-β production primarily through a p38-mediated mechanism and that IFN-β plays a beneficial role in E. coli–induced sepsis.

Chorioamnionitis is an acute inflammation of the membranes and chorion of the placenta typically due to ascending polymicrobial infection in the setting of membrane rupture. It is a common complication of pregnancy associated with significant maternal, perinatal, and long‐term adverse outcomes. We present a case of placental infection leading to preterm delivery, severe neonatal sepsis, maternal wound infection, postnatal readmission, and prolonged hospital stay. This virulent infection was caused by multidrug–resistant extended‐spectrum beta‐lactamase (ESBL)‐producing Escherichia Coli (E. Coli), which represent a major worldwide threat according to the Centre for Disease Control and Prevention (CDC). It was managed with appropriate antibiotic therapy, patient‐centered approach, and multidisciplinary team involvement that led to favourable maternal and neonatal outcome., Chorioamnionitis is a fetomaternal condition that can be caused by ESBL‐producing E. coli which pose challenging infection control issues and are a serious global threat. Screening strategies to monitor them could be useful in women from endemic areas to prevent perinatal transmission and introduction of multiresistant strains to the maternity wards.

Infections of the thyroid gland are rare. Its innate resistance to infections can be attributed to its unique anatomical features and rich blood supply. High clinical suspicion is required as a delay in diagnosis can lead to significant morbidity and mortality. Major pathogens include the Gram-positive Staphylococcus aureus and Streptococcus species; however, Gram-negative organisms have been found especially in immunocompromised hosts. We present a rare case of acute suppurative thyroiditis (AST) secondary to Escherichia coli (E. coli) infection in a woman known to be infected with human immunodeficiency virus (HIV). LEARNING POINTS Thyroid abscesses are rare and can be confused with more common pathologies involving the neck such as a goitre, adenoma, intracystic haemorrhage, pharyngeal abscess and subacute thyroiditis. A high index of suspicion for a thyroid abscess is required for patients who present with an anterior neck swelling to avoid a late diagnosis, which is associated with significant morbidity and mortality. Acute suppurative thyroiditis is more commonly caused by Gram-positive organisms. Gram-negative organisms such as E. coli remain a rare cause. However, if a thyroid abscess is suspected clinically, broad-spectrum antibiotics can be lifesaving before definite culture and sensitivity results are available.

The exploration of multiplexed bacterial virulence factors is a major problem in the early stages of Escherichia coli infection therapy. Traditional methods for detecting Escherichia coli (E. coli), such as serological experiments, immunoassays, polymerase chain reaction, and isothermal microcalorimetry have some drawbacks. As a result, detecting E. coli in a timely, cost-effective, and sensitive manner is critical for various areas of human safety and health. Intelligent devices based on nanotechnology are paving the way for fast and early detection of E. coli at the point of care. Due to their specific optical, magnetic, and electrical capabilities, nanostructures can play an important role in bacterial sensors. Another one of the applications involved use of nanomaterials in fighting microbial infections, including E. coli mediated infections. Various types of nanomaterials, either used directly as an antibacterial agent such as metallic nanoparticles (NPs) (silver, gold, zinc, etc.), or as a nanocarrier to deliver and target the antibiotic to the E. coli and its infected area. Among different types, polymeric NPs, lipidic nanocarriers, metallic nanocarriers, nanomicelles, nanoemulsion/ nanosuspension, dendrimers, graphene, etc. proved to be effective vehicles to deliver the drug in a controlled fashion at the targeted site with lower off-site drug leakage and side effects.

This study examined the protective effects of citrulline enriched-fermented milk with live Lactobacillus helveticus ASCC 511 (LH511) on intestinal epithelial barrier function and inflammatory response in IPEC-J2 cells caused by pathogenic Escherichia coli. Five percent (v/v) of fermented milk with live LH511 and 4 mM citrulline (5%LHFM_Cit-4mM) significantly stimulated the population of IPEC-J2 cells by 36% as determined by MTT assay. Adhesion level of LH511 was significantly increased by 9.2% when incubated with 5%LHFM_Cit-4mM and 5%LHFM_Cit-4mM reduced the adhesion of enterohemorrhagic (EHEC) and entero-invasive (EIEC) E. coli in IPEC-J2 cells by 35.79% and 42.74%, respectively. Treatment with 5%LHFM_Cit-4mM ameliorated lipopolysaccharide (LPS) from E. coli O55:B5 induced activated inflammatory cytokines expression (TNF-α, IL-6 and IL-8) and concentration (IL-6 and IL-8) and early apoptosis. It restored the transepithelial electrical resistance (TEER) and regulated the expression and distribution of tight junction (TJ) proteins (zonula occluden-1 (ZO-1), occludin and claudin-1), toll-like receptors (TLRs) (TLR2 and TLR4) and negative regulators of TLRs signalling pathway (A20 and IRAK-M). In conclusion, our findings suggested that 5%LHFM_Cit-4mM might have the positive effects on improving and maintaining the intestinal epithelial cell integrity and inflammatory response under both normal and pathogenic LPS-stimulated conditions.

Polymyxin B has been re‐applied to the clinic as the final choice for the treatment of multidrug‐resistant gram‐negative pathogenic infections, but the use of polymyxin B has been re‐assessed because of the emergence and spread of the plasmid‐mediated mcr‐1 gene. The purpose of this study was to search for an MCR inhibitor synergistically acting with polymyxin to treat the infection caused by this pathogen. In this study, we used the broth microdilution checkerboard method to evaluate the synergistic effect of isoalantolactone (IAL) and polymyxin B on mcr‐1‐positive Enterobacteriaceae. Growth curve analysis, time‐killing assays and a combined disc test were used to further verify the efficacy of the combined drug. Colonization of the thigh muscle in mice, survival experiments and lung tissue section observations was used to determine the effect of synergy in vivo after Klebsiella pneumoniae and Escherichia coli infection. We screened a natural compound, IAL, which can enhance the sensitivity of polymyxin B to mcr‐1‐positive Enterobacteriaceae. The results showed that the combined use of polymyxin B and IAL has a synergistic effect on mcr‐1‐positive Enterobacteriaceae, such as K pneumoniae and E coli, not only in vitro but also in vivo. Our results indicate that IAL is a natural compound with broad application prospects that can prolong the service life of polymyxin B and make outstanding contributions to the treatment of gram‐negative Enterobacteriaceae infections resistant to polymyxin B.

In recent years, effective microorganisms (EMs) have been administered to humans and domestic animals, and their usefulness has been recognized for promoting health and enhancing immunity. For example, the preventative effects against flu are enhanced by ingestion of Lactobacillus by humans, and symptom relief of atopic dermatitis has been reported, with EMs actually used in commercial products. In addition, EM preparations are being used in livestock to prevent infections (e.g. Salmonella and Escherichia coli infection). In poultry, avian influenza and Newcastle disease are terrible and fatal infectious diseases that cause significant economic damage. Furthermore, countries designated as contaminated with these pathogens can experience major trade problems. Given the above, how to protect livestock from infections safely and at low cost without using disinfectants, antibiotics and vaccines is a major issue. In the present study, we examined whether or not Newcastle disease could be suppressed by feeding chickens BX-1 as an EM feed. A field strain of Newcastle virus was cloned from cloaca swabs of large numbers of dying chickens in a poultry farm in Indonesia by polymerase chain reaction (PCR) and hemaggregation assays. Chicken kidney cells and embryonated eggs were highly sensitive to this virus, and high titers of virus were able to be collected. The experimental viral inoculated to chickens showed a high mortality rate, with high pathogenicity in birds. Conventional chickens were also raised on a diet supplemented with BX-1 and directly infected with the Newcastle virus. The mortality was decreased in these infected birds. Even the low dose of BX-1 had an inhibitory effect on the lethality of the infection. These results suggest that BX-1 intake through an EM diet is effective in controlling Newcastle disease.

Urinary tract infections caused by the bacterium Escherichia coli are among the most frequently encountered infections and are a common reason for antimicrobial prescriptions. Resistance to fluoroquinolone antimicrobial agents, particularly ciprofloxacin, has increased in recent decades. It is intuitive that variation in fluoroquinolone resistance is driven by changes in antimicrobial use, but careful study of this association requires the use of time-series methods. Between April 2010 and December 2014, we studied seasonal variation in resistance to ciprofloxacin, trimethoprim-sulfamethoxazole, and ampicillin in community-acquired urinary E. coli isolates in Montreal, Quebec, Canada. Using dynamic linear models, we investigated whether seasonal variation in resistance could be explained by seasonal variation in community antimicrobial use. We found a positive association between total fluoroquinolone use lagged by 1 and 2 months and the proportion of isolates resistant to ciprofloxacin. Our results suggest that resistance to ciprofloxacin is responsive to short-term variation in antimicrobial use. Thus, antimicrobial stewardship campaigns to reduce fluoroquinolone use, particularly in the winter when use is highest, are likely to be a valuable tool in the struggle against antimicrobial resistance.

Bacterial infection causes nutrient malabsorption in small intestine. KR-32, a kind of synthetic antimicrobial peptide, has the bacteriostatic effect. In the present study, 2 experiments were designed to analyze the effects of KR-32 on fat absorption of piglets with or without Escherichia coli infection. In Exp. 1, 12 weaning piglets (21 d old) were allocated to 2 groups: piglets with an intraperitoneal (i.p.) injection of antimicrobial peptide KR-32 (APK) and piglets with an i.p. injection of an equivalent volume (1 mL) of phosphate-buffered saline (PBS) (CON-1). Results showed that after 7 d of growth, KR-32 did not significantly change growth performance and apparent total tract digestibility (ATTD) of feed nutrients of normal pigs. To confirm whether KR-32 affects those of enterotoxigenic Escherichia coli (ETEC) K88-challenged pigs, we performed Exp. 2, in which 18 piglets (28 d old) were divided into the following 3 groups: 1) piglets orally challenged with 1 × 1010 cfu ETEC K88 on day 1 followed by an i.p. injection of 0.6 mg/kg KR-32 (K88 + APK); 2) piglets orally challenged with 1 × 1010 cfu ETEC K88 on day 1 followed by an i.p. injection of an equivalent volume (1 mL) of PBS (K88); and 3) piglets with an oral administration of fresh Luria-Bertani broth (50 mL) followed by an i.p. injection of an equivalent volume of PBS (CON-2). Results showed that ETEC K88 challenge led to poor ADFI, ADG, and G:F in piglets; decreased ATTD of feed nutrients, especially CP and ether extract (EE); and intestinal morphology disorder. After i.p. injection of KR-32, ADG and ATTD of CP and EE were greatly increased, G:F was significantly reduced (P < 0.05), and, especially, ATTD of EE returned to a normal level compared with group CON-2. Fatty acid absorption also highly increased after KR-32 injection. Then we focused on fat digestion and fatty acid uptake. The pH in the intestine and pancreas lipase showed no difference among the 3 treatment groups, whereas fatty acid transporter protein 4 (FATP4) expression was remarkably improved (P < 0.05) and the epithelial barrier was recovered after i.p. injection of KR-32. In conclusion, KR-32, given to ETEC K88-challenged piglets, improved growth performance, ATTD of EE, fatty acid absorption, and intestinal morphology, which indicated that KR-32 was likely to improve the expression of FATP4 and by repairing the epithelial barrier, thereby alleviating fatty acid malabsorption.

Background Increased resistance to third-generation cephalosporin (3GC) is a serious concern for community-onset Escherichia coli infection because this resistance easily delays effective treatment. This study surveyed the current antimicrobial resistance pattern among E. coli isolates that cause community-onset bacteremia, with a special focus on the prevalence of and the risk factors for 3GC resistance, and determined factors for poor outcomes among patients with community-onset E. coli bacteremia. Methods This retrospective study was conducted at a tertiary-care teaching hospital in Taiwan. All adult patients with community-onset E. coli bacteremia between January 1, 2015, and December 31, 2015 were enrolled and were divided into two groups depending on whether the E. coli isolate was susceptible to 3GCs. Risk factors for 3GC resistance, 14-day all-cause mortality, and length of hospital stay were analyzed. Results The overall rate of 3GC resistance among E. coli isolates causing community-onset bacteremia was 19.7%, whereas it was 9.6% if only isolates causing community-acquired bacteremia were considered. Independent risk factors for 3GC-resistant community-onset E. coli bacteremia were hospitalization within the past 1 year (odds ratio: 2.4, 95% confidence interval: 1.6–3.7, P

The grey predictive mathematical model based on big data was used for analysis on the effect of Escherichia coli infection on patients with lupus nephritis (LN) in this study. Then, 156 patients diagnosed with LN infections by Wuzhong People’s Hospital’s information system (HIS) from October 30, 2017 to October 30, 2019 were selected as the experimental group, and 89 patients without LN infections were selected as the control group. Besides, the grey theory mathematical model was applied to process the integrated data, and feature analysis was employed to screen out disease-related bio-markers for the diagnosis of LN. The two groups were compared for affected organs, treatment, laboratory indicators, pathogenic bacteria, and recovery status. Multivariate logistic regression was used to analyze the related factors of patients with infections. The results showed that the specificity, sensitivity, and accuracy of the big data diagnosis based on the grey theory mathematical model were 78.9%, 87.6%, and 92.1, respectively; hormones, c-reactive protein, procalcitonin, and the daily antibiotic dose were positively correlated with concurrent infections (P

Escherichia coli constitutes an immense challenge to the poultry industry due to its devastating effect on productivity, mortality, and carcass condemnations. To aid future studies on disease mechanisms and interventions, an aerogenous infection model was established in adult broiler breeders. Hens (n = 120) were randomly allocated into six groups receiving either aerosolised E. coli or vehicle, or intratracheal E. coli or vehicle. Replication of aerosol inoculation was performed on distinct days. Alternating euthanasia time points were predetermined in order to evaluate the progression of the disease. All animals were thoroughly necropsied, and bacteriological samples were collected as well as tissues for histopathology. Birds inoculated with E. coli exhibited clinical signs and developed characteristic gross and histopathological lesions of colibacillosis, including splenic fibrinoid necrosis, folliculitis, polyserositis and impaction of parabronchi with fibrinoheterophilic exudate and necrotic debris, as well as positive in situ localisation of intralesional E. coli by immunohistochemistry. This study presents a successful development of a discriminative colibacillosis model through aerosol inoculation of adult broiler breeders. Gross and histopathological lesions characteristic of colibacillosis were established in two independent experiments.

Mastitis caused by Escherichia coli (E. coli) remains a threat to dairy animals and impacts animal welfare and causes great economic loss. Furthermore, antibiotic resistance and the lagged development of novel antibacterial drugs greatly challenge the livestock industry. Phage therapy has regained attention. In this study, three lytic phages, termed vB_EcoM_SYGD1 (SYGD1), vB_EcoP_SYGE1 (SYGE1), and vB_EcoM_SYGMH1 (SYGMH1), were isolated from sewage of dairy farm. The three phages showed a broad host range and high bacteriolytic efficiency against E. coli from different sources. Genome sequence and transmission electron microscope analysis revealed that SYGD1 and SYGMH1 belong to the Myoviridae, and SYGE1 belong to the Autographiviridae of the order Caudovirales. All three phages remained stable under a wide range of temperatures or pH and were almost unaffected in chloroform. Specially, a mastitis infected cow model, which challenged by a drug resistant E. coli, was used to evaluate the efficacy of phages. The results showed that the cocktails consists of three phages significantly reduced the number of bacteria, somatic cells, and inflammatory factors, alleviated the symptoms of mastitis in cattle, and achieved the same effect as antibiotic treatment. Overall, our study demonstrated that phage cocktail may be a promising alternative therapy against mastitis caused by drug resistant E. coli.

Summary This study aims to determine the influence of silver nanoparticles (Ag-NPs) on performance, clinical and pathological pictures, virulence gene expression, and electron microscopy of experimentally induced Escherichia coli infection (colisepticemia) in broiler chickens. One-day-old chickens (n = 120) were segregated into 4 equal groups (1–4) with 3 replicates of 10 birds each. Birds were fed mash diet in 3 phases: starter (1–14 d), grower (15–28 d), and finisher (29–35 d). Chickens of the first 3 groups (T1, T2, T3) were fed Ag-NPs in the following dietary levels: 4, 6, and 8 mg/kg diet, respectively, while chickens of the fourth group (C) were fed a basal diet. All groups were individually infected by crop gavages with 0.5 mL/bird of PBS containing 3 × 108 CFU/mL of E. coli serogroup O78 for 2 successive days. In vitro Ag-NPs had a potent inhibitory effect against E. coli growth in pure form only (2,000 mg). In vivo study revealed that treatment of colisepticemic broiler chickens at a low dose (4 mg/kg diet) improved performance, reduced both gross and histopathological lesion scores, and virulence genes. It also altered the electron microscopic profile of the inoculated E. coli in the examined liver tissue. Severe negative effect was recorded on supplementation of the higher dose of Ag-NPs (8 mg/kg diet) that resulted in major effects on all the measured parameters except the gene expression analysis. Ag-NPs treatment with a dose of 4 mg/kg diet could play an optimistic role in the impedance of colisepticemia in broiler chickens.

Background: Nicotinic acid (NA) has been used to treat different inflammatory disease with positive influence, the mechanisms by which NA exerts its anti-inflammatory effects remain largely undefined. Here we proposed a new mechanism that NA manipulated endogenous antimicrobial peptides (AMPs) which contributed to the elimination of enterotoxigenic Escherichia coli (ETEC) K88, and thus affects the alleviation of inflammation.Results: The results showed that NA alleviated the clinical symptoms of weaned piglets infected with ETEC K88. NA significantly reduced the amount of ETEC K88 in the spleen and liver (P < 0.05). The intestinal morphological damage caused by ETEC K88 infection was alleviated by NA in weaned piglets. In addition, NA significantly alleviated the expression of inflammatory cytokine (IL-6, IL-8, and TNF-α) in the serum and intestines of weaned piglets infected with ETEC K88 (P < 0.05). and increased in intestinal mucosa. NA significantly increased the content of SIgA and the expression of antimicrobial peptides (pBD2, PG1-5 and PR39) in intestines of weaned pigs. NA increased the diversity of microflora in colonic contents, while NA significantly reduced the relative abundance of Bacteroidetes, Bacteroidales and bacteroidia in weaned piglets infected with ETEC K88 (P < 0.05). Furthermore, the NA group significantly reduced the level of HDAC7 in jejunum (P < 0.05) and increased the level of SIRT1 in the colon compared with the Control group. Moreover, NA significantly increased the levels phosphorylation of histone H3 at Ser10 (pH3S10) in ileum and the levels of acetylation of lysine 9 on histone 3 (acH3K9) and acH3K27 in colon (P < 0.05) in weaned piglets infected with ETEC K88 (P < 0.05). Conclusions: NA could alleviate the clinical symptoms, the damage of intestinal morphology, and intestinal inflammation in weaned piglets infected ETEC K88 through enhancing the endogenous AMPs expression by manipulating the histone acetylation modification.

The novel virulent Siphoviridae bacteriophage swi2 was isolated from a pig farm, and its biological characteristics, genome architecture, and infection-related properties were characterized. Phage swi2 has a high titer of 1.01 × 1012 PFU/mL with good tolerance to UV rays and remains stable in the pH range of 6–10 and at temperatures less than 50°C. One-step growth analysis revealed that phage swi2 had a 25 min latent period with a large burst size (1,000 PFU/cell). The biological characteristics indicated that swi2 had good host infectivity and effective lytic activities. The genome of phage swi2 is composed of 47,611 bp with a G + C content of 46.50%. Eighty-nine orfs were predicted, and only 18 of them have known functions. No virulence genes or drug resistance genes were found in the genome. Genome sequence comparison of phage swi2 showed that there were a total of 10 homologous phages in the database with low similarity (less than 92.51% nucleotide identity and 66% query coverage). The predicted host lysis-related genes of phage swi2 consist of one holin, two endolysins, and Rz/Rz1 equivalents. Antibacterial activity assays showed that both endolysins could naturally reduce the host Escherichia coli 51 titers by -1 log unit both in vitro and in vivo, EDTA showed no obvious synergistic action, and holin had no lytic effects on the host cell. These results provide necessary information for the development of antibiotic alternatives for the treatment of multidrug-resistant Escherichia coli infection.

Escherichia coli infection is considered one of the most economically important multi-systemic diseases in poultry farms. Several nanoparticles such as silver, chitosan, and copper oxide are known to be highly toxic to several microbes. However, there are no data concerning their success against in vivo experimental E. coli infection in broilers. Therefore, the present study was designed to investigate the bactericidal effect of low doses of CuO-NPs (5 mg/kg bwt), Ag-NPs (0.5 mg/kg bwt), and Ch-Ag NPs (0.5 mg/kg bwt) against E. coli experimental infection in broilers. One hundred chicks were divided into five groups as follows: (1) control; (2) E. coli (4 × 108 CFU/ml) challenged; (3) E. coli +CuO-NPs; (4) E. coli +Ag-NPs; (5) E. coli +Ch-Ag NPs. The challenged untreated group, not NPs treated groups, recorded the lowest weight gain as well as the highest bacterial count and lesion score in all examined organs. The highest liver content of silver was observed in Ag-NPs treated group compared with the Ch-Ag NPs treated group. Our results concluded that Ch-Ag NPs not only had the best antibacterial effects but also acted as a growth promoter in broilers without leaving any residues in edible organs. We recommend using Ch-Ag NPs in broiler farms instead of antibiotics or probiotics.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

Broilers are frequently infected with Escherichia coli (E.Coli) bacteria, which often leads to the emergence of many diseases and high economic losses. Hence, the present study was performed to assess the comparative efficacy of dietary rosemary and fenugreek, under E.Coli-infection in broilers, via evaluation of growth performance, biochemical indices, immunological response and histo-morphological changes. Eighty Cobb broilers were allotted to four equal groups (n=20 chicks/group); control non-infected (CN), control infected (CI), rosemary infected (RI) and fenugreek infected (FI) groups. RI and FI groups showed a significant elevation in their body weight and body weight gain compared with CI group. Moreover, both groups revealed a significant decline in serum aspartate and alanine aminotransferase activities, as well as uric acid and creatinine levels. Significant decreases of total antioxidant capacity, catalase and superoxide dismutase activities were noted among CI chicks. Moreover, distinctly higher levels were evident in both RI and FI groups. Immunomodulatory markers assessment showed a significant increase in immunoglobulin G with a significant decline in interleukin-6 level in both RI and FI groups, with the lowest IL-6 value within FI group. Histopathological evaluations focused on the deleterious effect associated with E-Coli infection of broilers’ liver, kidney, intestine, spleen, bursa of fabricius, and thymus. A partial histological improvement was noticed among RI group, and nearly normal tissues were recorded in FI group. Overall, these findings suggest the ability of fenugreek to mitigate the adverse effects of E.Coli-infection on broiler performance and tissue pictures, through improvement of the chicken general health condition.

IMPORTANCE: Escherichia coli is a leading cause of serious infection among term and preterm newborn infants. Surveillance of antibiotic susceptibility patterns of E coli among infants admitted to neonatal intensive care units should inform empirical antibiotic administration. OBJECTIVE: To assess the epidemiologic characteristics and antibiotic susceptibility patterns of E coli in infants admitted to neonatal intensive care units in the US over time. DESIGN, SETTING, AND PARTICIPANTS: This retrospective cohort study used the Premier Health Database, a comprehensive administrative database of inpatient encounters from academic and community hospitals across the US. Participants included newborn infants admitted to centers contributing microbiology data from January 1, 2009, to December 31, 2017, with E coli isolated from blood, cerebrospinal fluid, or urine cultures. Data were collected and analyzed from December 1, 2018, to November 30, 2019. MAIN OUTCOMES AND MEASURES: Changes in annual antibiotic susceptibility of E coli during the study period. The proportion of infants with nonsusceptible organisms (resistant or intermediate susceptibility) in antibiotic categories by year, birth weight, infection source, and timing of infection and patient and center characteristics associated with neonatal E coli infection and antibiotic susceptibility were assessed. RESULTS: A total of 721 infants (434 male [60.2%]; median age at E coli infection, 14 days [interquartile range, 1-33 days]) from 69 centers had at least 1 episode of E coli infection and available susceptibility results. No significant changes were observed over time in the overall annual proportions of antibiotic nonsusceptibility to ampicillin (mean [SD], 66.8% [1.5%]; range, 63.3% to 68.6%; estimated yearly change, −0.28% [95% CI, −1.75% to 1.18%]), nonsusceptibility to aminoglycosides (mean [SD], 16.8% [4.5%]; range, 10.7% to 23.2%; estimated yearly change, −0.85% [95% CI, −1.93% to 0.23%]), or extended-spectrum β-lactamase phenotype (mean [SD], 5.0% [3.7%]; range, 0% to 11.1%; estimated yearly change, 0.46% [95% CI, −0.18% to 1.11%]). No isolates with nonsusceptibility to carbapenems were identified. Among 218 infants with early-onset infection, 22 (10.1%) had isolates with nonsusceptibility to both ampicillin and gentamicin, the antibiotics most commonly administered to newborns as empirical therapy. CONCLUSIONS AND RELEVANCE: In this cohort study, nonsusceptibility to commonly administered antibiotics was found in substantial proportions of neonatal E coli isolates, with no significant change from 2009 to 2017. These findings may inform empirical antibiotic choices for newborn infants.

International audience; Probiotics could help combat infections and reduce antibiotic use. As use of live bacteria is limited in some cases by safety or regulatory concerns, the potential of inactivated bacteria is worth investigating. We evaluated the potential of live and heat-inactivated Lactobacillus gasseri LA806 to counteract Staphylococcus aureus and Escherichia coli infection cycles in an in vitro model of bovine mastitis. We assessed the ability of live and inactivated LA806 to impair pathogen colonisation of bovine mammary epithelial cells (bMECs) and to modulate cytokine expression by pathogen-stimulated bMECs. Live LA806 induced a five-fold decrease in S. aureus adhesion and internalisation (while not affecting E. coli colonisation) and decreased pro-inflammatory cytokine expression by S. aureus-stimulated bMECs (without interfering with the immune response to E. coli). The ability of inactivated LA806 ability to diminish S. aureus colonisation was twofold lower than that of the live strain, but its anti-inflammatory properties were barely impacted. Even though LA806 effects were impaired after inactivation, both live and inactivated LA806 have barrier and immunomodulatory properties that could be useful to counteract S. aureus colonisation in the bovine mammary gland. As S. aureus is involved in various types of infection, LA806 potential would worth exploring in other contexts.

The pathogenesis of Escherichia coli-induced hemolytic uremic syndrome (eHUS) caused by infections with pathogenic Shiga toxin (Stx) producing E. coli (STEC) is centered on bacterial (e.g., Stx) and host factors (circulating cells, complement system, serum proteins) whose interaction is crucial for the immediate outcome and for the development of this life-threatening sequela. Stx2a, associated to circulating cells (early toxemia) or extracellular vesicles (late toxemia) in blood, is considered the main pathogenic factor in the development of eHUS. Recently, it was found that the functional properties of Stx2a (binding to circulating cells and complement components) change according to modifications of the structure of the toxin, i.e., after a single cleavage of the A subunit resulting in two fragments, A1 and A2, linked by a disulfide bridge. Herein, we describe a method to be used for the detection of the cleaved form of Stx2a in the serum of STEC-infected or eHUS patients. The method is based on the detection of the boosted inhibitory activity of the cleaved toxin, upon treatment with reducing agents, on a rabbit cell-free translation system reconstituted with human ribosomes. The method overcomes the technical problem caused by the presence of inhibitors of translation in human serum that have been stalled by the addition of RNAase blockers and by treatment with immobilized protein G. This method, allowing the detection of Stx2a at concentrations similar to those found by ELISA in the blood of STEC-infected patients, could be a useful tool to study the contribution of the cleaved form of Stx2a in the pathogenesis of eHUS.

This review focuses on typical hemolytic uremic syndrome (HUS), a life-threatening sequela of human infections caused, particularly in children, by Shiga toxin–producing Escherichia coli strains. Thrombotic microangiopathy of the brain and the kidney is the end point of toxin action, resulting in the hallmarks of HUS (ie, thrombocytopenia, anemia, and acute renal failure). A growing body of evidence points to the role of extracellular vesicles released in the blood of patients by toxin-challenged circulating cells (monocytes, neutrophils, and erythrocytes) and platelets, as a key factor in the pathogenesis of HUS. This review provides i) an updated description of the pathogenesis of Shiga toxin–producing E. coli infections; ii) an analysis of blood cell–derived extracellular vesicles, and of their parent cells, as triggering factors in HUS; and iii) a model explaining why Shiga toxin–containing vesicles dock preferentially to the endothelia of target organs.

Background Cefiderocol, ceftazidime-avibactam, ceftolozane-tazobactam, intravenous fosfomycin and plazomicin represent potential carbapenem sparing agents for extended-spectrum-beta-lactamase or AmpC beta-lactamase producing Escherichia coli infection. However, available data is limited in predicting the volume of carbapenem therapy which could be substituted and real-world contraindications. Methods We determined the number of carbapenem days of therapy (DOT) which could be substituted and frequent contraindications accounting for antimicrobial susceptibility and site of infection in an unselected cohort with ceftriaxone-non-susceptible E. coli bacteremia at a single health network from 2015 to 2016. Individual patient data was used to calculate DOT and substitution for each agent. Results There were 108 episodes of E. coli bacteremia resulting in 67.2 carbapenem DOT/100 patient-days of antimicrobial therapy administered. Ceftazidime-avibactam could be used to substitute 36.2 DOT/100 patient-days (54%) for inpatient definitive therapy, ceftolozane-tazobactam for 34.7 DOT/100 patient-days (52%), cefiderocol for 27.1 DOT/100 patient-days (40%), fosfomycin for 23.3 DOT /100 patient-days (35%) and plazomicin for 27.1 DOT/100 patient-days (40%). Non-urinary tract source of infection was the most frequent contraindication to fosfomycin (25), plazomicin (26) and cefiderocol (26). Use in outpatient parenteral antimicrobial therapy (OPAT) programs accounted for 40% of DOT, all of which could be substituted if stability data allowed for ceftazidime-avibactam and ceftolozane-tazobactam. Conclusions All tested agents could be used to replace a significant volume of carbapenem therapy. Establishing stability of these agents for use in OPAT is required for maximizing their use as carbapenem sparing agents while randomized clinical data is awaited for some of these agents in resistant E. coli bacteremia.

Gut microbiota serves as a critical indicator for gut health during treatment of pathogenic bacterial infection. Both Pulsatilla Decoction (abbreviated to PD, a traditional Chinese medicine compound) and Levofloxacin Hydrochloride (LVX) were known to have therapeutic effects to intestinal infectious disease. However, the changes of gut microbiota after PD or LVX treatment remain unclear. Herein, this work aimed to investigate the changes of intestinal flora after PD or LVX therapy of Escherichia coli infection in rats. Results revealed that PD exhibited a valid therapeutic approach for E. coli infection via the intestinal protection, as well as the inhibited release of IL-8 and ICAM-1. Besides, PD was beneficial to rebuild the gut microbiota via restoring Bacteroidetes spp in the composition of the gut microbiota. Comparatively, LVX treatment promoted the infection and ravaged gut microbiota by significantly decreasing Bacteroidetes and increasing Firmicutes. These findings not only highlight the mechanism of Chinese herbal formula, but extend the application of PD as veterinary medicine, feed additive and pre-mixing agent for improving the production of animal derived foods.

The mammary immune and physiological responses to distinct mammary-pathogenic E. coli (MPEC) strains were studied. One gland in each of ten cows were challenged intra-mammary and milk composition (lactose, fat, total protein, casein), biochemical (glucose, glucose-6-phosphate (Glu6P), oxalate, malate, lactate, pyruvate and citrate, malate and lactate dehydrogenases, lactate dehydrogenase (LDH), nitrite, lactic peroxidase, catalase, albumin, lactoferrin, immunoglobulin) and clotting parameters were followed for 35 days post-challenge. Challenge lead to clinical acute mastitis, with peak bacterial counts in milk at 16–24 h post-challenge. Biochemical and clotting parameters in milk reported were partially in accord with lipopolysaccharide-induced mastitis, but increased Glu6P and LDH activity and prolonged lactate dehydrogenase and Glu6P/Glu alterations were found. Some alterations measured in milk resolved within days after challenge, while others endured for above one month, regardless of bacterial clearance, and some reflected physiological responses to mastitis such as the balance between aerobic and anaerobic metabolism (citrate to lactate ratios). The results suggest that E. coli mastitis can be divided into two stages: an acute, clinical phase, as an immediate response to bacterial infection in the mammary gland, and a chronic phase, independent of bacteria clearance, in response to tissue damage caused during the acute phase.

Heat shock protein 27 (HSP27) plays an important role in protecting cells from various stress factors. This study aimed to investigate the function of HSP27 gene and its regulatory mechanism as infected by Escherichia coli (E. coli) at the tissue and cellular levels. Real-time PCR was used to detect the differential expression of HSP27 gene in F18 resistant and sensitive Sutai pigs and the differential expression upon E. coli F18ab, F18ac, K88ac bacterial supernatant, thallus infection and LPS induction in IPEC-J2. In addition, the HSP27 gene overexpression vector was constructed to detect the effect of the HSP27 gene overexpression on the adhesion of E. coli F18 to IPEC-J2, secretion of pro-inflammatory factors, and the expression of the upstream key genes in Mitogen-activated protein kinase (MAPK) pathway. Ribosomal S6 kinase (RSK2) is an important protein in the MAPK pathway. Therefore, the RSK2 gene overexpression vector was constructed and the number of colonies was counted after co-transfection of HSP27 and RSK2 gene. Results revealed that the expression level of HSP27 gene in resistant individuals in 11 tissues was higher than sensitive type. At the cellular level, the relative expression levels of HSP27 gene were increased after F18ab, F18ac bacterial supernatant, F18ab thallus infection, and LPS induction for 4 h (P 0.01). The adhesion ability of E. coli F18ab to IPEC-J2 was significantly reduced after HSP27 gene overexpression (P 0.01), and the concentration of pro-inflammatory factors in the HSP27 gene overexpression group was significantly reduced compared with the control group after F18ab infection (P 0.05). Furthermore, the expression of RSK2 was significantly increased in HSP27 overexpression group upon F18ab infection (P 0.01). The colonies quantitative results also showed that the number of colonies was significantly reduced after co-transfection of HSP27 and RSK2 gene. We indicated that the high expression of HSP27 gene may resist the inflammatory response caused by exogenous stress and enhance the ability of IPEC-J2 to resist E. coli F18 infection. RSK2 gene in the MAPK pathway may cooperate with HSP27 gene to participate in the immune response of the organism, which provides a theoretical basis for the study of the mechanism of anti-E. coli infection in piglets.

The German cockroach, Blatella germanica (L.), is a suspected vector of several enteric bacterial pathogens, including Escherichia coli, among livestock and humans. However, little is known about the factors that influence bacterial transmission by cockroaches. Here, we orally infected B. germanica with various laboratory and field strains of E. coli and examined bacterial titers over time to shed new light on the factors that influence the dynamics of infection. Our results reveal that a laboratory strain of E. coli is largely cleared within 48 h while one field isolate can persist in a majority of cockroaches (80–100%) for longer than 3 d with minimal impact on cockroach longevity. We also find that the ability to clear some strains of E. coli is greater in cockroach nymphs than adults. Notably, no differential expression of the antimicrobial gene lysozyme was observed between nymphs and adults or in infected groups. However, clearance of E. coli was significantly reduced in gnotobiotic cockroaches that were reared in the absence of environmental bacteria, suggesting a protective role for the microbiota against exogenous bacterial pathogens. Together, these results demonstrate that the interactions between cockroaches and enteric bacterial pathogens are highly dynamic and influenced by a combination of microbial, host, and environmental parameters. Such factors may affect the disease transmission capacity of cockroaches in nature and should be further considered in both lab and field studies.

To investigate the different effects of acute pulmonary infection induced by Escherichia coli (E. coli) on lipid metabolism between diet-induced obesity (DIO, fed with high-fat diet) mice and lean mice. A total of 180 ICR mice were selected to be challenged intranasally with phosphate-buffered saline or 109 CFUs/mL of E. coli, and the body character indexes, biochemical indexes and expressions of genes and proteins involved in lipid metabolism were examined pre- and post-infection. Results revealed that, before infection, DIO mice had significantly higher body weight, adipose and liver indexes, free fatty acid and triglyceride contents than lean mice. After infection, increased free fatty acid and triglyceride contents, increased expressions of resistin, SREBP-1c, ACC1, FAS and SCD-1, and declined PPARα, CPT-1α expressions and AMPKα phosphorylation were detected in the infected group, while the change rates were more serious in the lean mice than the DIO mice. The above-mentioned findings verified that, after being infected with E. coli, hepatic lipid metabolism disorder was aggravated by activating SREBP-1c related lipid synthesis pathway and inhibiting PPARα related fatty acid oxidation pathway. However, infection-induced lipid metabolic disorders was slighter in the DIO mice than the lean mice through AMPKα pathway.

The emergence of carbapenemase-producing Enterobacteriaceae (CPE) is a critical concern worldwide. In Italy, CPE isolates are very frequent, with the KPC enzyme types strongly predominant whereas the New Delhi metallo-β-lactamase (NDM) enzymes are extremely rare. Here we report the first detection of NDM-5-producing Escherichia coli sequence type 167 (ST167) isolates from two patients with urinary tract infection (Ec001 and Ec002 from urines), including one with colonisation (Ec003 from faeces) admitted to the same hospital 2 months apart in 2017. Minimum inhibitory concentrations (MICs) were determined by broth microdilution. The carbapenemase type was identified both by phenotypic and genotypic methods. Isolate genotypes were investigated by phylogenetic typing, multilocus sequence typing (MLST) and pulsed-field gel electrophoresis (PFGE). Next-generation sequencing (NGS) was used to obtain complete sequences of plasmids. The three E. coli isolates carried the blaNDM-5 gene, shared the same resistance phenotype and belonged to ST167. By PFGE, isolates showed the same profile, suggesting that they were the same strain. NGS revealed that the blaNDM-5 gene was located on a 99-kb multireplicon plasmid (designed pNDM-5-IT) with a peculiar scaffold constituted by four replicons of the IncF type (FIA, FIB and two copies of the FII replicon). pNDM-5-IT plasmid harboured multiple resistance and virulence determinants, including the arginine deaminase (ADI) cluster never found associated with plasmids before. Since NDM-5-producing E. coli ST167 has been regarded as a successful epidemic clone in China, the emergence of such a clone carrying a plasmid associated both with multiresistance and virulence could be a public-health threat.