Dataset Information

Molecular and phenotypic characterization of avian pathogenic Escherichia coli isolated from commercial broilers and native chickens.

ABSTRACT: Many studies have examined avian pathogenic Escherichia coli (APEC) from commercial broilers but few have examined isolates from native chickens. This study compared APEC isolates from commercial broilers and native chickens in regard to the phylogenetic group and the phenotypic and genotypic antimicrobial resistance profiles. From 100 suspect colibacillosis cases in both commercial broilers and native chickens, a total of 90 broiler isolates and 42 native chicken isolates were identified as E. coli by biochemical tests. Phylogenetic grouping revealed that 90 broiler APEC isolates belonged to A group (5.56%), B1 group (22.22%), B2 group (31.11%), and D group (41.11%). The 42 native chicken APEC isolates belonged to A group (35.71%), B1 group (26.19%), B2 group (30.95%), and D group (7.14%). The difference in the allocation to groups A and D of the 2 isolate types was significant (P < 0.05). The APEC broiler isolates had a significantly higher multidrug-resistant (MDR) rate (80%) than the native chicken isolates (14.29%) (P < 0.05). The APEC broiler isolates demonstrated significantly higher resistance rates than the native chicken isolates for amoxicillin (98.89%; 78.57% respectively), chloramphenicol (42.2%; 9.5%), enrofloxacin (68.9%; 7.1%), gentamicin (11.1%; 0%), nalidixic acid (72.2%; 7.1%), sulfamethoxazole + trimethoprim (45.6%; 2.4%), and tetracycline (88.9%; 76.2%) (P < 0.05). The APEC broiler isolates had a significantly higher presence compared with the native chicken isolates of the following resistance genes:- by bla_TEM (43.3%; 21.4%, respectively), cml-A (34.4%; 2.4%), tetA (76.7%; 40.5%), tetB (26.7%; 0%), sul2 (23.3%; 14.3%), and dhfrI (13.3%; 0%) (P < 0.05). The qnrB and qnrS genes were detected (12.16%; 72.97% respectively), in the APEC broiler isolates resistant to nalidixic acid and/or enrofloxacin while only qnrS genes was detected in all 3 APEC native chicken isolates. Regarding the point mutations of gyrA and parC, all isolates were positive to gyrA83S, gyrA87D, gyrA87L, gyrA87NY, parC80S and parC80I except that gyrA83S was not present in 20 APEC broiler isolates. Antimicrobial stewardship programs should be targeted at the backyard poultry sector as well as the commercial poultry sector.

SUBMITTER: Thomrongsuwannakij T

PROVIDER: S-EPMC8627976 | biostudies-literature |

REPOSITORIES: biostudies-literature

ACCESS DATA

Similar Datasets

Project description:Purpose: This study is to more comprehensively understand the genome-wide host response to avian pathogen E. coli (APEC). Methods: Male broiler chicks were challenged with APEC (or mock-challenged as controls), and bone marrow was harvested at 1 and 5 days post-infection (dpi). Based upon necropsy-scored lesions on liver, pericardium, and air sacs, the challenged birds were assigned to mild or severe pathology categories, representing resistant and susceptible phenotypes, respectively. RNA sequence data were first analyzed using the R package EdgeR to identify differentially expressed genes.GO and pathway analysis using the R package GOseq identified many immune-related pathways. Results: RNA sequencing resulted in 11 to 40 million single-end raw reads of 100 bp per sample. After alignment, an average of 80 % of the reads, with 5 % representing multiple mapping, were mapped to the chicken reference transcriptome. Among these detected unique transcripts, there were 2,404 novel genes mainly distributed on chromosomes 1, 2, 4, 3, Z, 5 in decreasing number. Genes were detected as differentially expressed (DE) between treatments (susceptible, resistant, and mock-challenged) at a given time point, or DE between 1 and 5 dpi within the same treatment group. Compared to mock-challenged birds on 5 dpi, susceptible birds exhibited extensive enhancement of their T cell and B cell development, as well as innate and adaptive immune response. However, for the 1 dpi group, susceptible birds exhibited a decreased gene expression of T and B cell development. The differences between the two phenotypes, susceptible and resistant birds, at 5 dpi showed that susceptible birds had increased gene expression of B-cell development and adaptive immune response. Conclusions: This is the first report to our knowledge examining the role of bone marrow cells in responding to APEC infection in broilers. This transcriptome study provides insight and global overview into the response of genes involved in the earliest phases of the immune response to APEC infection. Our data indicate a dynamic interaction between the innate and adaptive immune responses to APEC infection in susceptible birds, providing flexibility and redundancy in the host’s induction of cytokines and chemokines. Additionally, B cell and T cell development are also extensively affected by APEC infection for susceptible birds, resulting in drastic host impairment in early response to infection. The findings of present study shed light on the underlying chicken immune modulation against APEC infection. Also, this study will build a solid foundation for identifying host genetic variation that may be manipulated to enhance resistance to infection and may be useful as colibacillosis control targets.

Project description:BackgroundAvian pathogenic Escherichia coli (APEC) is a major cause of disease impacting animal health. The bone marrow is the reservoir of immature immune cells; however, it has not been examined to date for gene expression related to developmental changes (cell differentiation, maturation, programming) after APEC infection. Here, we study gene expression in the bone marrow between infected and non-infected animals, and between infected animals with mild (resistant) versus severe (susceptible) pathology, at two times post-infection.ResultsWe sequenced 24 bone marrow RNA libraries generated from the six different treatment groups with four replicates each, and obtained an average of 22 million single-end, 100-bp reads per library. Genes were detected as differentially expressed (DE) between APEC treatments (mild pathology, severe pathology, and mock-challenged) at a given time point, or DE between 1 and 5 days post-infection (dpi) within the same treatment group. Results demonstrate that many immune cells, genes and related pathways are key contributors to the different responses to APEC infection between susceptible and resistant birds and between susceptible and non-challenged birds, at both times post-infection. In susceptible birds, lymphocyte differentiation, proliferation, and maturation were greatly impaired, while the innate and adaptive immune responses, including dendritic cells, monocytes and killer cell activity, TLR- and NOD-like receptor signaling, as well as T helper cells and many cytokine activities, were markedly enhanced. The resistant birds' immune system, however, was similar to that of non-challenged birds.ConclusionThe DE genes in the immune cells and identified signaling models are representative of activation and resolution of infection in susceptible birds at both post-infection days. These novel results characterizing transcriptomic response to APEC infection reveal that there is combinatorial activity of multiple genes controlling myeloid cells, and B and T cell lymphopoiesis, as well as immune responses occurring in the bone marrow in these early stages of response to infection.

Project description:BackgroundAvian pathogenic Escherichia coli (APEC) is detrimental to poultry health and its zoonotic potential is a food safety concern. Regulation of antimicrobials in food-production animals has put greater focus on enhancing host resistance to bacterial infections through genetics. To better define effective mechanism of host resistance, global gene expression in the spleen of chickens, harvested at two times post-infection (PI) with APEC, was measured using microarray technology, in a design that will enable investigation of effects of vaccination, challenge, and pathology level.ResultsThere were 1,101 genes significantly differentially expressed between severely infected and non-infected groups on day 1 PI and 1,723 on day 5 PI. Very little difference was seen between mildly infected and non-infected groups on either time point. Between birds exhibiting mild and severe pathology, there were 2 significantly differentially expressed genes on day 1 PI and 799 on day 5 PI. Groups with greater pathology had more genes with increased expression than decreased expression levels. Several predominate immune pathways, Toll-like receptor, Jak-STAT, and cytokine signaling, were represented between challenged and non-challenged groups. Vaccination had, surprisingly, no detectible effect on gene expression, although it significantly protected the birds from observable gross lesions. Functional characterization of significantly expressed genes revealed unique gene ontology classifications during each time point, with many unique to a particular treatment or class contrast.ConclusionsMore severe pathology caused by APEC infection was associated with a high level of gene expression differences and increase in gene expression levels. Many of the significantly differentially expressed genes were unique to a particular treatment, pathology level or time point. The present study not only investigates the transcriptomic regulations of APEC infection, but also the degree of pathology associated with that infection. This study will allow for greater discovery into host mechanisms for disease resistance, providing targets for marker assisted selection and advanced drug development.

Dataset Information

Molecular and phenotypic characterization of avian pathogenic Escherichia coli isolated from commercial broilers and native chickens.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets