Enterococcus cecorum is an emerging avian pathogen, particularly in chickens, but can be found in both diseased (clinical) and healthy (non-clinical) poultry. To better define differences between E. cecorum from the two groups, whole-genome sequencing (WGS) was used to identify and compare antimicrobial resistance genes as well as the pan-genome among the isolates. Eighteen strains selected from our previous study were subjected to WGS using Illumina MiSeq and comparatively analyzed. Assembled contigs were analyzed for resistance genes using ARG-ANNOT. Resistance to erythromycin was mediated by ermB, ermG, and mefA, in clinical isolates and ermB and mefA, in non-clinical isolates. Lincomycin resistance genes were identified as linB, lnuB, lnuC, and lnuD with lnuD found only in non-clinical E. cecorum; however, lnuB and linB were found in only one clinical isolate. For both groups of isolates, kanamycin resistance was mediated by aph3-III, while tetracycline resistance was conferred by tetM, tetO, and tetL. No mutations or known resistance genes were found for isolates resistant to either linezolid or chloramphenicol, suggesting possible new mechanisms of resistance to these drugs. A comparison of WGS results confirmed that non-clinical isolates contained more resistance genes than clinical isolates. The pan-genome of clinical and non-clinical isolates resulted in 3651 and 4950 gene families, respectively, whereas the core gene sets were comprised of 1559 and 1534 gene families in clinical and non-clinical isolates, respectively. Unique genes were found more frequently in non-clinical isolates than clinical. Phylogenetic analysis of the isolates and all the available complete and draft genomes showed no correlation between healthy and diseased poultry. Additional genomic comparison is required to elucidate genetic factors in E. cecorum that contribute to disease in poultry.

Non-typhoidal Salmonella (NTS) infections in poultry, particularly in commercial-layer chickens, pose a critical risk to food safety and public health worldwide. NTS bacteria can remain undetected in poultry flocks, contaminating products and potentially leading to gastroenteritis in humans. This review examines pre-harvest control strategies for NTS in layer chickens, including biosecurity protocols, vaccinations, feed additives, genetic selection, and environmental management. These strategies have substantially reduced Salmonella colonization and product contamination rates in the commercial layer industry. By evaluating these strategies, this review highlights the importance of integrated control measures to limit NTS colonization, reduce antimicrobial resistance, and improve poultry health. This review aims to provide producers, researchers, and policymakers with insights into effective practices to minimize Salmonella contamination and enhance both animal and human health outcomes.

Salmonella Enteritidis (SE) is one of the most common causes of bacterial food-borne illnesses in the world. Despite the SE’s ability to colonize and infect a wide-range of host, the most common source of infection continues to be the consumption of contaminated shell eggs and egg-based products. To date, the role of the source of SE infection has not been studied as it relates to SE pathogenesis and resulting disease. Using a streptomycin-treated mouse model of human colitis, this study examined the virulence of SE grown in egg yolk and Luria Bertani (LB) broth, and mouse feces collected from mice experimentally infected with SEE1 (SEE1 passed through mice). Primary observations revealed that the mice infected with SE grown in egg yolk displayed greater illness and disease markers than those infected with SE passed through mice or grown in LB broth. Furthermore, the SE grown in egg yolk achieved higher rates of colonization in the mouse intestines and extra-intestinal organs of infected mice than the SE from LB broth or mouse feces. Our results here indicate that the source of SE infection may contribute to the overall pathogenesis of SE in a second host. These results also suggest that reservoir-pathogen dynamics may be critical for SE’s ability to establish colonization and priming for virulence potential.

Shiga toxin-producing Escherichia coli (STEC) are notorious foodborne pathogens, capable of causing severe diarrhea and life-threatening complications in humans. Cattle, acting as both primary reservoirs and asymptomatic carriers of STEC, predominantly harbor the pathogen in their rectoanal junction (RAJ), facilitating its transmission to humans through contaminated food sources. Despite the central role of cattle in STEC transmission, the molecular mechanisms governing STEC’s adaptation in the RAJ of the asymptomatic reservoir host and its subsequent infection of human colonic epithelial cells, resulting in diarrhea, remain largely unexplored. This study aims to uncover these complicated dynamics by focusing on the STEC O157:H7 serotype within two distinct host environments, bovine RAJ cells and human colonic epithelial cells, during initial colonization. We employed comparative transcriptomics analysis to investigate differential gene expression profiles of STEC O157:H7 during interactions with these cell types. STEC O157:H7 was cultured either with bovine RAJ cells or the human colonic epithelial cell line CCD CoN 841 to simulate STEC-epithelial cell interactions within these two host species. High-throughput RNA sequencing revealed 829 and 1939 bacterial genes expressed in RAJ and CCD CoN 841, respectively. After gene filtering, 221 E. coli O157:H7 genes were upregulated during initial adherence to CCD CoN cells and 436 with RAJ cells. Furthermore, 22 genes were uniquely expressed with human cells and 155 genes with bovine cells. Our findings revealed distinct expression patterns of STEC O157:H7 genes involved in virulence, including adherence, metal iron homeostasis, and stress response during its initial adherence (i.e., six hours post-infection) to bovine RAJ cells, as opposed to human colonic epithelial cells. Additionally, the comparative analysis highlighted the potential role of some genes in host adaptation and tissue-specific pathogenicity. These findings shed new light on the potential mechanisms of STEC O157:H7 contributing to colonize the intestinal epithelium during the first six hours of infection, leading to survival and persistence in the bovine reservoir and causing disease in humans.

Inflammatory bowel disease (IBD) is characterized by gastrointestinal inflammation comprised of Crohn’s disease and ulcerative colitis. Centers for Disease Control and Prevention report that 1.3% of the population of the United States (approximately 3 million people) were affected by the disease in 2015, and the number keeps increasing over time. IBD has a multifactorial etiology, from genetic to environmental factors. Most of the IBD treatments revolve around disease management, by reducing the inflammatory signals. We previously identified the surface layer protein A (SlpA) of Lactobacillus acidophilus that possesses anti-inflammatory properties to mitigate murine colitis. Herein, we expressed SlpA in a clinically relevant, food-grade Lactococcus lactis to further investigate and characterize the protective mechanisms of the actions of SlpA. Oral administration of SlpA-expressing L. lactis (R110) mitigated the symptoms of murine colitis. Oral delivery of R110 resulted in a higher expression of IL-27 by myeloid cells, with a synchronous increase in IL-10 and cMAF in T cells. Consistent with murine studies, human dendritic cells exposed to R110 showed exquisite differential gene regulation, including IL-27 transcription, suggesting a shared mechanism between the two species, hence positioning R110 as potentially effective at treating colitis in humans.

Colibacillosis caused by avian pathogenic Escherichia coli (APEC) is a leading cause of economic loss to the poultry industry worldwide. The ability of APEC to cause disease is determined by certain virulence markers, some of which are located on pathogenicity islands (PAIs). We recently described one such PAI in an APEC O1:K1 strain (APEC-O1). This PAI, termed PAI I_APEC-O1, carries the genes of the pap operon, a region similar to the tia invasion determinant of enterotoxigenic E. coli; ireA, a gene that encodes an iron-responsive element; and a novel 1.5-kb region, ORF 54. Here, the occurrence of six selected loci of PAI I_APEC-O1 (papA, papC, papG, ireA, tia, and ORF 54) among APEC and fecal E. coli strains from apparently healthy chickens (avian commensal E. coli) was determined using polymerase chain reaction (PCR) techniques. None of the commensal E. coli was positive for all six traits, whereas 7.2% of the APEC isolates were positive for all the traits. Although there was no significant difference in the occurrence of ORF 54 among APEC and commensal E. coli, tia, ireA, papC, and papG genes were predominantly present in APEC rather than in avian commensal E. coli. papA was detected in only 6.3% of APEC, perhaps because of the presence of allelic variants of the gene. Additionally, the presence of all six traits was tested with PCR in APEC isolates collected in the 1980s, and these results were compared with those obtained with the APEC isolated in the 1990s. There was no significant difference in the occurrence of tia, ireA, papC, papG, and ORF 54 between APEC isolates collected during the different decades. However, papA was more frequently present in APEC from the 1980s than it was in APEC from the 1990s. Phylogenetic group of an isolate did not correlate with pathogenicity or the presence of PAI traits, except that more APEC of the low-pathogenicity group belonged to the phylogenetic group B1. However, PAI traits occurred more frequently in isolates belonging to the intermediate- and high-pathogenicity groups than in isolates of low pathogenicity. Ocurrencia de los genes en la denominada Isla Patogénica I_APEC-O1 entre cepas de Escherichia coli implicadas en colibacilosis aviar. La colibacilosis causada por cepas patógenas de Escherichia coli aviar es una de las mayores causas de pérdidas económicas en la avicultura a nivel mundial. La capacidad de las cepas patógenas aviares de E. coli para causar enfermedad está determinada por ciertos factores de virulencia, algunos de los cuales están localizados en las denominadas islas patogénicas. Recientemente descubrimos una de estas islas patogénicas en una cepa patógena aviar de E. coli denominada O1:K1 (APEC-O1). Esta isla patogénica, identificada como isla patogénica I_APEC-O1, contiene los genes del operón pap, una región similar al determinante de invasión tia para E. coli enterotoxigénica; ireA, un gen que codifica un elemento en la respuesta al hierro, y una nueva región de 1.5 Kb, con un marco abierto de lectura (ORF por sus siglas en Inglés) 54. Aquí, la ocurrencia de los seis genes de la isla patogénica I_APEC-O1 (papA, papC, papG, ireA, tia, y ORF 54) entre las cepas patógenas aviares de E. coli y las cepas de E. coli fecal de pollos aparentemente sanos (E. coli aviar comensal) fue determinada usando la técnica de reacción en cadena de la polimerasa (PCR por sus siglas en Inglés). Ninguna de las cápsulas de los E. coli comensales fue positiva para todas las seis características, mientras que el 7.2% de los aislamientos patógenos de E. coli aviar fueron positivos para estas seis características. Aunque no hubo diferencia significativa en la ocurrencia de ORF 54 entre las cepas patógenas aviares de E. coli y las cepas de E. coli comensales, los genes, tia, ireA, papA, y papG, se presentaron predominantemente en las cepas patógenas aviares de E. coli mas que en las cepas de E. coli comensales. El gen papA fue detectado sólo en 6.3% de las cepas patógenas aviares de E. coli, posiblemente debido a la presencia de variantes alélicas en el gen. Además, la presencia de todas las seis características fue estudiada por medio de PCR en aislamientos de cepas patógenas aviares de E. coli tomados en la década de 1980, comparando estos resultados con los obtenidos de aislamientos de cepas patógenas aviares de E. coli en la década de 1990. No se encontró diferencia significativa en la incidencia de papA, papC, papG, ireA, tia, y ORF 54 entre los aislamientos de cepas patógenas aviares de E. coli de las dos décadas. No obstante, papA fue detectado mas frecuentemente en los aislamientos de cepas patógenas aviares de E. coli de la década de 1980 que en las de la década de 1990. El grupo filogenético de un aislamiento no se relacionó con la patogenicidad o con la presencia de las características de las islas patogénicas, excepto que más cepas patógenas aviares de E. coli del grupo de baja patogenicidad pertenecieron al grupo filogenético B1. Sin embargo, las características de las islas patogénicas ocurrieron más frecuentemente en aislamientos pertenecientes a los grupos de patogenicidad intermedia y alta, que de los de baja patogenicidad. Abbreviations: APEC = avian pathogenic Escherichia coli; ddH₂O = double-distilled water; ExPEC = extraintestinal pathogenic Escherichia coli; ireA = iron-responsive element; ORF = open reading frame; PAI = pathogenicity island; pap = pyelonephritis-associated pili; PCR = polymerase chain reaction; UPEC = human uropathogenic Escherichia coli