ABSTRACT
Weaning is a critical event in the pig's life cycle, frequently associated with severe enteric infections and overuse of antibiotics; this raises serious economic and public health concerns. In this review, we explain why gut microbiota dysbiosis, induced by abrupt changes in the diet and environment of piglets, emerges as a leading cause of post-weaning diarrhea, even if the exact underlying mechanisms remain unclear. Then, we focus on nonantimicrobial alternatives, such as zinc oxide, essential oils, and prebiotics or probiotics, which are currently evaluated to restore intestinal balance and allow a better management of the crucial weaning transition. Finally, we discuss how in vitro models of the piglet gut could be advantageously used as a complement to ex vivo and in vivo studies for the development and testing of new feed additives.
Subject(s)
Dysbiosis/microbiology , Dysbiosis/physiopathology , Gastrointestinal Microbiome/physiology , Swine/microbiology , Swine/physiology , Animals , Diet/methods , Intestines/microbiology , Intestines/physiology , Microbiota/physiology , Probiotics/administration & dosage , WeaningABSTRACT
For ethical, technical, regulatory, and cost reasons, in vitro methods are increasingly used as an alternative to in vivo experimentations. The aim of the present study was to validate, according to in vivo data in living animals, a new in vitro model of the piglet colon, the PigutIVM, under both control conditions and antibiotic disturbance by the widely used colistin. The PigutIVM reproduces the main biotic and abiotic parameters of the piglet colon: temperature, pH, retention time, supply of ileal effluents, complex, and metabolically active microbiota and self-maintained anaerobiosis. Under both control and antibiotic-treated conditions, qPCR analyses showed that the main bacterial populations of piglet gut microbiota were similar in vitro and in vivo, with Pearson correlation coefficient higher than 0.9. During colistin administration, both in piglets and in the in vitro model, a significant decrease in Escherichia coli populations was observed together with changes in microbial composition of subdominant populations. SCFA concentrations were similar in vitro and in vivo and were not modified by colistin. Interestingly, the administration of the probiotic Saccharomyces cerevisiae var. boulardii CNCM I-1079 led in vitro to a decrease in E. coli levels, as previously observed when the antibiotic treatment was applied. This new in vitro model of the piglet colon provides a flexible, reproducible, and cost-effective tool for the screening of drugs or new dietary compounds, such as pre- or probiotics. It will be helpful for researchers, feed producers, or veterinarians when developing innovative non-antibiotic strategies.
Subject(s)
Bioreactors , Diffusion Chambers, Culture , Gastrointestinal Microbiome/drug effects , Microbial Consortia/drug effects , Probiotics/pharmacology , Anaerobiosis , Animals , Anti-Bacterial Agents/pharmacology , Colistin/pharmacology , Colon/drug effects , Colon/microbiology , Escherichia coli/drug effects , Escherichia coli/growth & development , Feces/microbiology , Gastrointestinal Microbiome/physiology , Hydrogen-Ion Concentration , Ileum/drug effects , Ileum/microbiology , Microbial Consortia/physiology , Models, Biological , Saccharomyces boulardii/drug effects , Saccharomyces boulardii/growth & development , Swine , TemperatureABSTRACT
Resistance to extended-spectrum cephalosporins (ESCs) is a matter of considerable concern for public health. Here, we studied the spontaneous loss of an extended-spectrum beta-lactamase (ESBL)-encoding plasmid from a rifampin-resistant Escherichia coli isolate orally inoculated into pigs under controlled conditions. Fecal samples were collected and cultured on rifampin-supplemented medium, and the resistance of the E. coli isolates to ESCs was studied by phenotypic tests, PCR detection of plasmid genes, and complete sequencing. The results showed that only 3 out of 353 rifampin-resistant E. coli isolates were ESC susceptible, and PCR and bioinformatics analysis confirmed the loss of the plasmid. These in vivo experiments indicate that the loss of an ESBL-encoding plasmid seems a rare event in gut microbiota.
Subject(s)
Base Sequence , Drug Resistance, Multiple, Bacterial/genetics , Gastrointestinal Microbiome/genetics , Plasmids/chemistry , Sequence Deletion , Animals , Anti-Bacterial Agents/pharmacology , Chromosome Mapping , Chromosomes, Bacterial/chemistry , Feces/microbiology , Gastrointestinal Microbiome/drug effects , Gene Expression , High-Throughput Nucleotide Sequencing , Polymerase Chain Reaction , Rifampin/pharmacology , Swine , beta-Lactamases/genetics , beta-Lactamases/metabolismABSTRACT
Colistin is a cyclic decapeptide bound to a fatty acid chain. It is active against many Gram-negative bacteria by destabilising the bacterial outer membrane. Bacteria can become resistant to colistin by modification of their lipopolysaccharide, thereby reducing the affinity of polymyxins. Colistin is often administered orally in poultry and pig production to control colibacillosis. Resistant isolates are sometimes recovered from pathological cases, particularly in piglets. However, in Europe the percentage of resistance to colistin in Escherichia coli strains isolated from the digestive tract microbiota of healthy animals remains <1%.
