Dysbiosis not observed in Canadian horse with free fecal liquid (FFL) using 16S rRNA sequencing.

Free Fecal Liquid (FFL), also termed Fecal Water Syndrome (FWS), is an ailment in horses characterized by variable solid and liquid (water) phases at defecation. The liquid phase can be excreted before, during, or after the solid defecation phase. While the underlying causes of FFL are unknown, hindgut dysbiosis is suggested to be associated with FFL. Three European studies investigated dysbiosis in horses with FFL using 16S rRNA sequencing and reported results that conflicted between each other. In the present study, we also used 16S rRNA sequencing to study the fecal microbial composition in 14 Canadian horses with FFL, and 11 healthy stable mate controls. We found no significant difference in fecal microbial composition between FFL and healthy horses, which further supports that dysbiosis is not associated with FFL.

Evaluation of the relationship between plasma glucagon-like peptide-2 and gastrointestinal dysbiosis in canine chronic enteropathies.

Chronic enteropathies are a common cause of morbidity in dogs and are associated with disruption of the normal gastrointestinal mucosal barrier. The objective of this prospective study was to determine the association between measures of gastrointestinal dysbiosis and plasma concentrations of glucagon-like peptide-2, a hormone responsible for normal mucosal structure, in dogs with chronic enteropathies. Fecal 16S V4 rRNA gene sequencing and quantitative PCR via the dysbiosis index was performed on 16 healthy controls and 18 dogs with chronic enteropathy prior to and 1 month after initiation of individualized therapy. Fasting and post-prandial plasma GLP-2 concentrations were measured via ELISA in healthy dogs and chronic enteropathy dogs at both time points. Alpha and beta diversity indices, as well as bacterial population abundances were compared between groups and time-points. Principal component analysis combined with least squares regression was used to identify taxa contributing to glucagon-like peptide-2 variance among groups. While the dysbiosis index did not differ between healthy dogs and dogs with chronic enteropathy, 16S V4 genomic sequencing identified 47 operational taxonomic units that differed between the groups, all but 2 of which resolved following chronic enteropathy treatment. Principal component analysis identified 6 families and 19 genera that contributed to differences in glucagon-like peptide-2 concentrations between groups. Dysbiosis associated with chronic enteropathies in dogs may contribute to the observed lower plasma glucagon-like peptide-2 concentrations. Further research into mechanisms of microbiota impact on the enteroendocrine system is needed. Association between glucagon-like peptide-2 secretion and microbiome indices may help to guide research into future treatment strategies for dogs with chronic enteropathy.

White feces syndrome in shrimp: Comprehensive understanding of immune system responses.

White feces syndrome (WFS) is a multifactorial disease that affects global shrimp production. The diagnostic approach to identify WFS involves traditional and molecular scientific methods by examining histopathology, bioassays, PCR (polymerase chain reaction), and calorimetric estimation. The pathogenesis of WFS is closely associated with Vibrio spp., intestinal microbiota (IM) dysbiosis, and Enterocytozoon hepatopenaei (EHP). It also has caused over 10-15 % loss in the aquaculture industry and is also known to cause retardation, lethargy and slowly leading to high mortality in shrimp farms. Therefore, it is necessary to understand the molecular mechanisms processed under the association of IM dysbiosis, Vibrio spp., and EHP to analyze the impact of disease on the innate immune system of shrimp. However, only very few reviews have described the molecular pathways involved in WFS. Hence, this review aims to elucidate an in-depth analysis of molecular pathways involved in the innate immune system of shrimp and their response to pathogens. The analysis and understanding of the impact of shrimp's innate immune system on WFS would help in developing treatments to prevent the spread of disease, thereby improving the economic condition of shrimp farms worldwide.

Microbiome in cancer: A comparative analysis between humans and dogs.

Cancer is a major cause of death in humans and animals worldwide. While cancer survival rates have increased over recent decades, further research to identify risk factors for the onset and progression of disease, and safe and highly efficacious treatments, is needed. Spontaneous tumours in pets represent an excellent model for neoplastic disease in humans. In this regard, dogs are an interesting species, as the divergence between the dog and human genome is low, humans and dogs have important similarities in the development and functioning of the immune system, and both species often share the same physical environment. There is also a higher homology between the canine and human microbiome than murine model. This review aims to describe and organize recently published information on canine microbiome assemblages and their relationship with the onset and progression of colorectal cancer, breast cancer and lymphoma, and to compare this with human disease. In both species, dysbiosis can induce variations in the gut microbiota that strongly influence shifts in status between health and disease. This can produce an inflammatory state, potentially leading to neoplasia, especially in the intestine, thus supporting canine studies in comparative oncology. Intestinal dysbiosis can also alter the efficacy and side effects of cancer treatments. Fewer published studies are available on changes in the relevant microbiomes in canine lymphoma and mammary cancer, and further research in this area could improve our understanding of the role of microbiota in the development of these cancers.

LTA and PGN from Bacillus siamensis can alleviate soybean meal-induced enteritis and microbiota dysbiosis in Lateolabrax maculatus.

An eight-week feeding trial was designed to assess which component of commensal Bacillus siamensis LF4 can mitigate SBM-induced enteritis and microbiota dysbiosis in spotted seabass (Lateolabrax maculatus) based on TLRs-MAPKs/NF-кB signaling pathways. Fish continuously fed low SBM (containing 16 % SBM) and high SBM (containing 40 % SBM) diets were used as positive (FM group) and negative (SBM group) control, respectively. After feeding high SBM diet for 28 days, fish were supplemented with B. siamensis LF4-derived whole cell wall (CW), cell wall protein (CWP), lipoteichoic acid (LTA) or peptidoglycan (PGN) until 56 days. The results showed that a high inclusion of SBM in the diet caused enteritis, characterized with significantly (P < 0.05) decreased muscular thickness, villus height, villus width, atrophied and loosely arranged microvillus. Moreover, high SBM inclusion induced an up-regulation of pro-inflammatory cytokines and a down-regulation of occludin, E-cadherin, anti-inflammatory cytokines, apoptosis related genes and antimicrobial peptides. However, dietary supplementation with CW, LTA, and PGN of B. siamensis LF4 could effectively alleviate enteritis caused by a high level of dietary SBM. Additionally, CWP and PGN administration increased beneficial Cetobacterium and decreased pathogenic Plesiomonas and Brevinema, while dietary LTA decreased Plesiomonas and Brevinema, suggesting that CWP, LTA and PGN positively modulated intestinal microbiota in spotted seabass. Furthermore, CW, LTA, and PGN application significantly stimulated TLR2, TLR5 and MyD88 expressions, and inhibited the downstream p38 and NF-κB signaling. Taken together, these results suggest that LTA and PGN from B. siamensis LF4 could alleviate soybean meal-induced enteritis and microbiota dysbiosis in L. maculatus, and p38 MAPK/NF-κB pathways might be involved in those processes.

Safety profile and effects on the peripheral immune response of fecal microbiota transplantation in clinically healthy dogs.

BACKGROUND: Fecal microbiota transplantation (FMT) is increasingly used for gastrointestinal and extra-gastrointestinal diseases in veterinary medicine. However, its effects on immune responses and possible adverse events have not been systematically investigated. HYPOTHESIS/OBJECTIVES: Determine the short-term safety profile and changes in the peripheral immune system after a single FMT administration in healthy dogs. ANIMALS: Ten client-owned, clinically healthy dogs as FMT recipients, and 2 client-owned clinically healthy dogs as FMT donors. METHODS: Prospective non-randomized clinical trial. A single rectal enema of 5 g/kg was given to clinically healthy canine recipients. During the 28 days after FMT administration, owners self-reported adverse events and fecal scores. On Days 0 (baseline), 1, 4, 10, and 28 after FMT, fecal and blood samples were collected. The canine fecal dysbiosis index (DI) was calculated using qPCR. RESULTS: No significant changes were found in the following variables: CBC, serum biochemistry, C-reactive protein, serum cytokines (interleukins [IL]-2, -6, -8, tumor necrosis factor [TNF]-α), peripheral leukocytes (B cells, T cells, cluster of differentiation [CD]4+ T cells, CD8+ T cells, T regulatory cells), and the canine DI. Mild vomiting (n = 3), diarrhea (n = 4), decreased activity (n = 2), and inappetence (n = 1) were reported, and resolved without intervention. CONCLUSIONS AND CLINICAL IMPORTANCE: Fecal microbiota transplantation did not significantly alter the evaluated variables and recipients experienced minimal adverse events associated with FMT administration. Fecal microbiota transplantation was not associated with serious adverse events, changes in peripheral immunologic variables, or the canine DI in the short-term.

Dietary inclusion of a Saccharomyces cerevisiae metabolite improved reproductive performance but did not affect intestinal permeability in two chicken meat breeder lines.

Gastrointestinal dysbiosis is a disturbance in mucosal homeostasis, producing low-grade chronic intestinal inflammation and impaired intestinal barrier function. It is induced by several factors, including nutrition and stress, which are both significant factors when considering current broiler breeder practices. A great grandparent (GGP) chicken meat line was identified displaying clinical signs characteristic of potential dysbiosis, including wet droppings and litter, in addition to reduced reproductive performance when compared to a consistently high performing line. This study aimed to determine whether the reduced reproductive performance observed in these hens was a result of dysbiosis and whether dietary supplementation with a Saccharomyces cerevisiae (SC) fermentation product would alleviate clinical signs. Dietary inclusion of SC did not influence intestinal permeability, WBC differentials, or corticosterone concentration in either the wet litter (WL) or high-performing (HP) breeder lines. Compared to hens from the HP line, WL line hens had a significant increase in intestinal permeability at 26 wk (onset of lay). WL hen heterophil counts were increased markedly at week 26 before declining. At weeks 26, 32, and 37 there were also significant increases in monocytes. Higher plasma corticosterone was also observed in WL hens at 37 wk. No significant differences in heterophil to lymphocyte (H:L) ratios or feather corticosterone were observed between lines. Dietary inclusion of SC supplementation to breeder diets had some benefit in regards to reducing hen mortality, improving egg production and hatchability but only in the WL line. Results from this study did not indicate that hens from the wet litter line were experiencing gut dysbiosis. Chronic intestinal inflammation may be a possible reason for the increase in intestinal permeability. These results do indicate that both breeder lines may be exhibiting physiological stress. Future investigation into the physiology and behavior around point of lay is required to find novel strategies to alleviate this stress and in turn, potentially improve welfare and production outcomes.

The intestinal commensal fungus Wallemia mellicola enhances asthma in mice through Dectin-2.

Overgrowth of the fungus Wallemia mellicola in the intestines of mice enhances the severity of asthma. Wallemia mellicola interacts with the immune system through Dectin-2 expressed on the surface of myeloid and intestinal epithelial cells. Using Dectin-2-deficient mice, we show that the interaction of W. mellicola with Dectin-2 is essential for the gut-lung pathways, enhancing the severity of asthma in mice with W. mellicola intestinal dysbiosis. These findings offer better insight into dysbiosis-associated inflammation and highlight the role pattern recognition receptors have in immune recognition of commensal fungi in the gut, leading to alterations in immune function in the lungs.

Effects of inhaled fine particulate matter on the lung injury as well as gut microbiota in broilers.

Fine particulate matter (PM2.5) has been widely regarded as an important environmental risk factor that has widely influenced health of both animals and humans. Lung injury is the main cause of PM2.5 affecting respiratory tract health. Gut microbiota participates in the development of lung injury in many pathological processes. However, there is still unknown the specific effects of PM2.5 on the gut-lung axis in broilers. Thus, we conducted a broiler model based on 3-wk-old male Arbor Acres broiler to explore the underlying mechanism. Our results showed that PM2.5 exposure triggered TLR4 signaling pathway and induced the increase of IL-6, IFN-γ, TNF-α expression as well as the decrease of IL-10 expression in the lung. Inhaled PM2.5 exposure significantly altered the gut microbiota diversity and community. Specifically, PM2.5 exposure decreased α diversity and altered ß diversity of gut microbiota, and reduced the abundance of DTU089, Oscillospirales, Staphylococcus, and increased the Escherichia-Shigella abundance, leading to the increase of gut-derived lipopolysaccharides (LPS). Moreover, PM2.5 significantly disrupted the intestinal epithelial barrier by reducing the expression of muc2 and claudin-1 to increase intestinal permeability, which possibly facilitated the LPS translocation into the blood. Spearman analysis revealed that gut microbiota dysbiosis was positively related to TLR4, TNF-α, and IFN-γ expression in the lung. In summary, our results showed that PM2.5 exposure induced lung injury by causing inflammation and triggering TLR4 signaling pathway, and also induced gut microbiota dysbiosis resulting in the overproduction of gut-derived LPS. And gut microbiota dysbiosis may be associated with lung injury. The above results provide basis data to comprehend the potential role of gut microbiota dysbiosis in the lung injury as well as providing a new regulatory target for alleviating lung injury associated with environmental pollutants.

Host-gut microbiota interactions shape parasite infections in farmed Atlantic salmon.

Animals and their associated microbiota share long evolutionary histories. However, it is not always clear how host genotype and microbiota interact to affect phenotype. We applied a hologenomic approach to explore how host-microbiota interactions shape lifetime growth and parasite infection in farmed Atlantic salmon (Salmo salar). Multi-omics data sets were generated from the guts of 460 salmon, 82% of which were naturally infected with an intestinal cestode. A single Mycoplasma bacterial strain, MAG01, dominated the gut metagenome of large, non-parasitized fish, consistent with previous studies showing high levels of Mycoplasma in the gut microbiota of healthy salmon. While small and/or parasitized salmon also had high abundance of MAG01, we observed increased alpha diversity in these individuals, driven by increased frequency of low-abundance Vibrionaceae and other Mycoplasma species that carried known virulence genes. Colonization by one of these cestode-associated Mycoplasma strains was associated with host individual genomic variation in long non-coding RNAs. Integrating the multi-omic data sets revealed coordinated changes in the salmon gut mRNA transcriptome and metabolome that correlated with shifts in the microbiota of smaller, parasitized fish. Our results suggest that the gut microbiota of small and/or parasitized fish is in a state of dysbiosis that partly depends on the host genotype, highlighting the value of using a hologenomic approach to incorporate the microbiota into the study of host-parasite dynamics.IMPORTANCEStudying host-microbiota interactions through the perspective of the hologenome is gaining interest across all life sciences. Intestinal parasite infections are a huge burden on human and animal health; however, there are few studies investigating the role of the hologenome during parasite infections. We address this gap in the largest multi-omics fish microbiota study to date using natural cestode infection of farmed Atlantic salmon. We find a clear association between cestode infection, salmon lifetime growth, and perturbation of the salmon gut microbiota. Furthermore, we provide the first evidence that the genetic background of the host may partly determine how the gut microbiota changes during parasite-associated dysbiosis. Our study therefore highlights the value of a hologenomic approach for gaining a more in-depth understanding of parasitism.

Effects of exposure to the neonicotinoid pesticide clothianidin on α-defensin secretion and gut microbiota in mice.

The mechanism by which the neonicotinoid pesticide clothianidin (CLO) disrupts the intestinal microbiota of experimental animals is unknown. We focused on α-defensins, which are regulators of the intestinal microbiota. Subchronic exposure to CLO induced dysbiosis and reduced short-chain fatty acid-producing bacteria in the intestinal microbiota of mice. Levels of cryptdin-1 (Crp1, a major α-defensin in mice) in feces and cecal contents were lower in the CLO-exposed groups than in control. In Crp1 immunostaining, Paneth cells in the jejunum and ileum of the no-observed-adverse-effect-level CLO-exposed group showed a stronger positive signal than control, likely due to the suppression of Crp1 release. Our results showed that CLO exposure suppresses α-defensin secretion from Paneth cells as part of the mechanism underlying CLO-induced dysbiosis.

The effects of torula yeast as a protein source on apparent total tract digestibility, inflammatory markers, and fecal microbiota dysbiosis index in Labrador Retrievers with chronically poor stool quality.

This study examined the effects of varying protein sources on apparent total tract digestibility, inflammatory markers, and fecal microbiota in Labrador Retrievers with historically poor stool quality. Thirty dogs (15 male, 15 female; aged 0.93 to 11.7 yr) with stool quality scores ≤2.5 on a 5-point scale (1 representing liquid stool and 5 representing firm stool) were randomly assigned to 1 of 3 nutritionally complete diets with differing protein sources and similar macronutrient profiles: 1) chicken meal (n = 10); 2) 10% brewer's yeast (n = 10); or 3) 10% torula yeast (n = 10). Another 10 dogs (five male, five female) with normal stool quality (scores ranging from 3 to 4) received diet 1 and served as negative control (NC). All dogs were fed diet 1 for 7 days, then provided their assigned treatment diets from days 7 to 37. Daily stool scores and weekly body weights were recorded. On days 7, 21, and 36, blood serum was analyzed for c-reactive protein (CRP), and feces for calgranulin C (S100A12), α1-proteinase inhibitor (α1-PI), calprotectin, and microbiota dysbiosis index. Apparent total tract digestibility was assessed using the indicator method with 2 g titanium dioxide administered via oral capsules. Stool scores were greater in NC (P < 0.01) as designed but not affected by treatment × time interaction (P = 0.64). Body weight was greater (P = 0.01) and CRP lower (P < 0.01) in NC dogs. Dry matter and nitrogen-free extract digestibility did not differ among groups (P ≥ 0.14). Negative controls had greater fat digestibility compared to BY (94.64 ±â€…1.33% vs. 91.65 ±â€…1.25%; P = 0.02). The overall effect of treatment was significant for protein digestibility (P = 0.03), but there were no differences in individual post hoc comparisons (P ≥ 0.07). Treatment did not affect S100A12 or α1-PI (P ≥ 0.44). Calprotectin decreased at a greater rate over time in TY (P < 0.01). The dysbiosis index score for BY and TY fluctuated less over time (P = 0.01). Blautia (P = 0.03) and Clostridium hiranonis (P = 0.05) abundances were reduced in BY and TY. Dogs with chronically poor stool quality experienced reduced body weights and increased serum CRP, but TY numerically increased protein digestibility, altered the microbiome, and reduced fecal calprotectin. Torula yeast is a suitable alternative protein source in extruded canine diets, but further research is needed to understand the long-term potential for improving the plane of nutrition and modulating gut health.

Pet and human populations continue to grow and compete for nutritious, sustainable protein sources. The incorporation of alternative proteins like torula yeast can provide a solution to this problem. Torula yeast also may have additional health benefits like reducing gut inflammation. To test its effects in dogs, we fed Labrador Retrievers with chronically poor stool quality either a control diet with chicken meal, a diet with 10% brewer's yeast, or a diet with 10% torula yeast. We compared their responses to dogs with normal stool quality fed the control diet. Dogs with chronically poor stool quality had lower body weights and increased systemic inflammation compared to those with good stool quality. Calprotectin, a marker of gut inflammation, was reduced more in dogs fed torula yeast than in dogs fed chicken meal. Torula and brewer's yeast also changed the abundance of certain gut bacteria. Torula yeast may be added to dog diets with no negative effects and can alter the gut environment in Labrador Retrievers with chronically poor stool quality.

Exocrine pancreatic insufficiency in dogs and cats.

Exocrine pancreatic insufficiency (EPI) is a malabsorptive syndrome caused by insufficient secretion of digestive enzymes from pancreatic acini. The most common causes of EPI in dogs and cats are pancreatic acinar atrophy and chronic pancreatitis. EPI is diagnosed by measurement of species-specific immunoassays for serum trypsin-like immunoreactivity, the concentration of which directly reflects the mass of functioning pancreatic acinar tissue. EPI is treated by pancreatic enzyme replacement therapy, nutritional management (low-residue diets with moderate fat content), and supplementation of cobalamin. Some dogs and cats have persistent clinical signs despite these treatments. Growing evidence suggests that these clinical signs may be due to enteric microbiota dysbiosis or the presence of concurrent diseases such as chronic enteropathies. Management of these abnormalities may improve outcome in dogs and cats with EPI. The long-term prognosis for dogs and cats with EPI is generally good if high-quality medical therapy is provided. Future studies are needed to further understand the causes of persistent dysbiosis in animals with EPI following initiation of pancreatic enzyme replacement therapy and assess the efficacy of treatments to ameliorate these abnormalities.

Giardiasis and diarrhea in dogs: Does the microbiome matter?

BACKGROUND: Giardia duodenalis (Gd) causes intestinal parasitosis. The involvement of the intestinal microbiome in determining the infection's clinical phenotype is unknown. OBJECTIVE: Investigate the fecal microbiome features in dogs with giardiasis. ANIMALS AND METHODS: Cross-sectional study, including fecal samples of kenneled dogs with Gd diagnosed by fecal Giardia antigen dot ELISA. The fecal microbial compositional characteristics and dysbiosis index (DI) were compared between diarrheic and nondiarrheic dogs. RESULTS: Fecal samples of 38 Gd-infected dogs (diarrheic, 21; nondiarrheic, 17) were included. No differences were found in Faith's phylogenic diversity and beta diversity (weighted UniFrac distances) and in specific taxa abundances at the phylum, genus, and species levels, as well as in alpha and beta diversities between diarrheic and nondiarrheic dogs, and also when divided by sex or age. Among diarrheic dogs, alpha diversity was higher in males than in females (pairwise Kruskal-Wallis, q = 0.01). Among males, fecal abundances of the genus Clostridium (W = 19) and Clostridium spiroforme species (W = 33) were higher in diarrheic compared to nondiarrheic dogs. In diarrheic dog fecal samples, Proteobacteria were more prevalent (W = 1), whereas Verrucomicrobia were less prevalent in dogs <1 year of age than in older dogs. The fecal sample DI of 19 diarrheic and 19 nondiarrheic dogs was similar (median, -0.2; range, -4.3 to 4.5 and median, -1.0; range, -4.3 to 5.8, respectively). CONCLUSIONS: The fecal microbial composition of symptomatic and asymptomatic dogs with giardiasis is similar. Based on fecal DI, giardiasis is not characterized by prominent dysbiosis. Other host and parasite characteristics might determine the severity of giardiasis in dogs.

Update on the skin barrier, cutaneous microbiome and host defence peptides in canine atopic dermatitis.

BACKGROUND: Canine atopic dermatitis (AD) is a complex inflammatory skin disease associated with cutaneous microbiome, immunological and skin barrier alterations. This review summarises the current evidence on skin barrier defects and on cutaneous microbiome dysfunction in canine AD. OBJECTIVE: To this aim, online citation databases, abstracts and proceedings from international meetings on skin barrier and cutaneous microbiome published between 2015 and 2023 were reviewed. RESULTS: Since the last update on the pathogenesis of canine AD, published by the International Committee on Allergic Diseases of Animals in 2015, 49 articles have been published on skin barrier function, cutaneous/aural innate immunity and the cutaneous/aural microbiome in atopic dogs. Skin barrier dysfunction and cutaneous microbial dysbiosis are essential players in the pathogenesis of canine AD. It is still unclear if such alterations are primary or secondary to cutaneous inflammation, although some evidence supports their primary involvement in the pathogenesis of canine AD. CONCLUSION AND CLINICAL RELEVANCE: Although many studies have been published since 2015, the understanding of the cutaneous host-microbe interaction is still unclear, as is the role that cutaneous dysbiosis plays in the development and/or worsening of canine AD. More studies are needed aiming to design new therapeutic approaches to restore the skin barrier, to increase and optimise the cutaneous natural defences, and to rebalance the cutaneous microbiome.

Fish gut and skin microbiota dysbiosis induced by exposure to commercial sunscreen formulations.

UV filters (organic or mineral) present in sunscreen products are emerging contaminants of coastal aquatic environments. There is an urgent need to understand marine organisms responses to these compounds. In this study, we investigated the effect of exposure to dilutions of commercial sunscreen formulations on bacterial communities of mullet (Chelon sp.). The gut and skin mucus microbial communities were characterized using a metabarcoding approach targeting the 16S rRNA gene. Our results revealed that mullets had its own bacterial communities that differ from their surrounding habitats and specific to tissue. The dilutions of commercial sunscreens modified the relative abundance of Actinobacteroita, Bacteriodota and Proteobacteria for both gut and skin microbiota. They also allowed to bacteria affiliated to Mycobacterium, Nocardia and Tenacibaculum genera, known to house pathogenic species, to colonize the epithelium which may have implications for fish host health.

Epizootic of enterocolitis and clostridial overgrowth in NSG and NSG-related mouse strains.

While the immunodeficient status of NOD.Cg-Prkdcscid Il2rgtm1Wjl/SzJ (NSG) and NSG-related mice provides utility for numerous research models, it also results in increased susceptibility to opportunistic pathogens. Over a 9-week period, a high rate of mortality was reported in a housing room of NSG and NSG-related mice. Diagnostics were performed to determine the underlying etiopathogenesis. Mice submitted for evaluation included those found deceased (n = 2), cage mates of deceased mice with or without diarrhea (n = 17), and moribund mice (n = 8). Grossly, mice exhibited small intestinal and cecal dilation with abundant gas and/or digesta (n = 18), serosal hemorrhage and congestion (n = 6), or were grossly normal (n = 3). Histologically, there was erosive to ulcerative enterocolitis (n = 7) of the distal small and large intestine or widespread individual epithelial cell death with luminal sloughing (n = 13) and varying degrees of submucosal edema and mucosal hyperplasia. Cecal dysbiosis, a reduction in typical filamentous bacteria coupled with overgrowth of bacterial rods, was identified in 18 of 24 (75%) mice. Clostridium spp. and Paeniclostridium sordellii were identified in 13 of 23 (57%) and 7 of 23 (30%) mice, respectively. Clostridium perfringens (7 of 23, 30%) was isolated most frequently. Toxinotyping of C. perfringens positive mice (n = 2) identified C. perfringens type A. Luminal immunoreactivity to several clostridial species was identified within lesioned small intestine by immunohistochemistry. Clinicopathologic findings were thus associated with overgrowth of various clostridial species, though direct causality could not be ascribed. A diet shift preceding the mortality event may have contributed to loss of intestinal homeostasis.

Gut dysbacteriosis induces expression differences in the adult head transcriptome of Spodoptera frugiperda in a sex-specific manner.

Mounting evidence indicates that the gut microbiota influences the neurodevelopment and behavior of insects through the gut-brain axis. However, it is currently unclear whether the gut microbiota affect the head profiles and immune pathway in pests. Here, we find that gut bacteria is essential for the immune and neural development of adult Spodoptera frugiperda, which is an extremely destructive agricultural pest worldwide. 16 S rRNA sequencing analysis showed that antibiotics exposure significantly disturbed the composition and diversity of gut bacteria. Further transcriptomic analysis revealed that the adult head transcripts were greatly affected by gut dysbacteriosis, and differently expression genes critical for brain and neural development including A4galt, Tret1, nsun4, Galt, Mitofilin, SLC2A3, snk, GABRB3, Oamb and SLC6A1 were substantially repressed. Interestingly, the dysbacteriosis caused sex-specific differences in immune response. The mRNA levels of pll (serine/threonine protein kinase Pelle), PGRP (peptidoglycan-sensing receptor), CECA (cecropin A) and CECB (cecropin B) involved in Toll and Imd signaling pathway were drastically decreased in treated male adults' heads but not in female adults; however, genes of HIVEP2, ZNF131, inducible zinc finger protein 1-like and zinc finger protein 99-like encoding zinc-finger antiviral protein (ZAP) involved in the interferon (IFNα/ß) pathway were significantly inhibited in treated female adults' heads. Collectively, these results demonstrate that gut microbiota may regulate head transcription and impact the S. frugiperda adults' heads through the immune pathway in a sex-specific manner. Our finding highlights the relationship between the gut microbiota and head immune systems of S. frugiperda adults, which is an astonishing similarity with the discoveries of other animals. Therefore, this is the basis for further research to understand the interactions between hosts and microorganisms via the gut-brain axis in S. frugiperda and other insects.

Effect of esomeprazole with and without a probiotic on fecal dysbiosis, intestinal inflammation, and fecal short-chain fatty acid concentrations in healthy dogs.

BACKGROUND: Proton pump inhibitors can cause diarrhea and a transient increase in fecal dysbiosis index in dogs. It is unknown if concurrent probiotic administration mitigates these effects. OBJECTIVE/HYPOTHESIS: To assess the fecal Canine Microbial Dysbiosis Index (CMDI), fecal short chain fatty acid (SCFA), and fecal calprotectin concentrations in dogs administered esomeprazole with and without a probiotic. ANIMALS: Eleven healthy dogs. METHODS: Prospective, within-subjects before and after study. All dogs received 7-day courses of esomeprazole (1 mg/kg PO q 24h) alone followed by esomeprazole with a probiotic (15 billion CFU/kg), separated by a 4-week washout period. Data were compared between phases using mixed effects ANOVA or generalized estimating equations with post-hoc Holm adjustment for 2-way comparisons. RESULTS: Compared to baseline (mean CMDI -2.66, SD 3.04), fecal CMDI was not different with esomeprazole administration alone (mean CMDI -1.48, SD 3.32, P = .08), but there was a significant increase (Diff 3.05, 95% CI [1.37, 4.74], P < .001, Effect size 2.02) when esomeprazole and a probiotic were administered concurrently (mean CMDI 0.39, SD 2.83). CMDI was significantly higher when esomeprazole was administered with a probiotic than alone (Diff 1.87, 95% CI [0.19, 1.87], P = .02, Effect size 1.24). Fecal calprotectin and SCFA concentrations did not differ between phases. The occurrence of vomiting and diarrhea was not different from baseline when esomeprazole was administered alone (36%/27%) or with a probiotic (46%/9%). CONCLUSIONS AND CLINICAL IMPORTANCE: In healthy dogs, concurrent administration of a probiotic is unlikely to lessen adverse effects associated with esomeprazole administration.

The respiratory microbiota and its impact on health and disease in dogs and cats: A One Health perspective.

Healthy lungs were long thought of as sterile, with presence of bacteria identified by culture representing contamination. Recent advances in metagenomics have refuted this belief by detecting rich, diverse, and complex microbial communities in the healthy lower airways of many species, albeit at low concentrations. Although research has only begun to investigate causality and potential mechanisms, alterations in these microbial communities (known as dysbiosis) have been described in association with inflammatory, infectious, and neoplastic respiratory diseases in humans. Similar studies in dogs and cats are scarce. The microbial communities in the respiratory tract are linked to distant microbial communities such as in the gut (ie, the gut-lung axis), allowing interplay of microbes and microbial products in health and disease. This review summarizes considerations for studying local microbial communities, key features of the respiratory microbiota and its role in the gut-lung axis, current understanding of the healthy respiratory microbiota, and examples of dysbiosis in selected respiratory diseases of dogs and cats.