Avian Pathogenic Escherichia Coli O78 Research Articles

DNA microarray-mediated transcriptional profiling of avian pathogenic Escherichia coli O2 strain E058 during its infection of chicken

Avian pathogenic Escherichia coli (APEC) cause typical extraintestinal infections in poultry, including acute fatal septicemia, subacute pericarditis, and airsacculitis. These bacteria most often infect chickens, turkeys, ducks, and other avian species, and therefore pose a significant economic burden on the poultry industry worldwide. Few studies have analyzed the genome-wide transcriptional profile of APEC during infection in vivo. In this study, we examined the genome-wide transcriptional response of APEC O2 strain E058 in an in vivo chicken infection model to better understand the factors necessary for APEC colonization, growth, and survival in vivo. An Affymetrix multigenome DNA microarray, which contains most of the genomic open reading frames of E. coli K-12 strain MG1655, uropathogenic E. coli strain CFT073, and E. coli O157:H7 strain EDL 933, was used to profile the gene expression in APEC E058. We identified the in vivo transcriptional response of APEC E058 bacteria collected directly from the blood of infected chickens. Significant differences in expression levels were detected between the in vivo expression profile and the in vitro expression profile in LB medium. The genes highly expressed during infection were involved in metabolism, iron acquisition or transport, virulence, response to stress, and biological regulation. The reliability of the microarray data was confirmed by performing quantitative real-time PCR on 12 representative genes. Moreover, several significantly upregulated genes, including yjiY, sodA, phoB and spy, were selected to study their role in APEC pathogenesis. The data will help to better understand the mechanisms of APEC pathogenesis.

A cyclophosphamide-sensitive cell compartment is essential for homologous protection conferred by licensed vaccines for the control of avian pathogenic Escherichia coli in chickens

Avian pathogenic Escherichia coli (APEC) exert substantial economic costs on poultry producers worldwide. Vaccination is an attractive method of control, but the immunological basis of protection is poorly understood. Here, we examine the effect of intramuscular injection of cyclophosphamide or saline on homologous protection induced by licensed inactivated or live-attenuated APEC O78 vaccines in chickens. In saline-treated birds, both vaccines induced significant APEC-specific IgY and protection against homologous challenge, as evidenced by enumeration of tissue-associated bacteria and analysis of pathology. In cyclophosphamide-treated birds, B cells were severely depleted whereas percentages of circulating CD4- and CD8-positive T cells were normal as detected by flow cytometry. Further, such birds did not produce APEC-specific IgY and were as susceptible to challenge as age-matched unvaccinated controls. The data indicate that homologous protection conferred by licensed APEC vaccines strictly requires a cyclophosphamide-sensitive cell population that includes B cells.

Immune responses associated with homologous protection conferred by commercial vaccines for control of avian pathogenic Escherichia coli in turkeys.

Avian pathogenic Escherichia coli (APEC) infections are a serious impediment to sustainable poultry production worldwide. Licensed vaccines are available, but the immunological basis of protection is ill-defined and a need exists to extend cross-serotype efficacy. Here, we analysed innate and adaptive responses induced by commercial vaccines in turkeys. Both a live-attenuated APEC O78 ΔaroA vaccine (Poulvac® E. coli) and a formalin-inactivated APEC O78 bacterin conferred significant protection against homologous intra-airsac challenge in a model of acute colibacillosis. Analysis of expression levels of signature cytokine mRNAs indicated that both vaccines induced a predominantly Th2 response in the spleen. Both vaccines resulted in increased levels of serum O78-specific IgY detected by ELISA and significant splenocyte recall responses to soluble APEC antigens at post-vaccination and post-challenge periods. Supplementing a non-adjuvanted inactivated vaccine with Th2-biasing (Titermax® Gold or aluminium hydroxide) or Th1-biasing (CASAC or CpG motifs) adjuvants, suggested that Th2-biasing adjuvants may give more protection. However, all adjuvants tested augmented humoral responses and protection relative to controls. Our data highlight the importance of both cell-mediated and antibody responses in APEC vaccine-mediated protection toward the control of a key avian endemic disease.

Genomic avenue to avian colisepticemia.

ABSTRACTHere we present an extensive genomic and genetic analysis of Escherichia coli strains of serotype O78 that represent the major cause of avian colisepticemia, an invasive infection caused by avian pathogenic Escherichia coli (APEC) strains. It is associated with high mortality and morbidity, resulting in significant economic consequences for the poultry industry. To understand the genetic basis of the virulence of avian septicemic E. coli, we sequenced the entire genome of a clinical isolate of serotype O78—O78:H19 ST88 isolate 789 (O78-9)—and compared it with three publicly available APEC O78 sequences and one complete genome of APEC serotype O1 strain. Although there was a large variability in genome content between the APEC strains, several genes were conserved, which are potentially critical for colisepticemia. Some of these genes are present in multiple copies per genome or code for gene products with overlapping function, signifying their importance. A systematic deletion of each of these virulence-related genes identified three systems that are conserved in all septicemic strains examined and are critical for serum survival, a prerequisite for septicemia. These are the plasmid-encoded protein, the defective ETT2 (E. coli type 3 secretion system 2) type 3 secretion system ETT2sepsis, and iron uptake systems. Strain O78-9 is the only APEC O78 strain that also carried the regulon coding for yersiniabactin, the iron binding system of the Yersinia high-pathogenicity island. Interestingly, this system is the only one that cannot be complemented by other iron uptake systems under iron limitation and in serum.

The avian pathogenic Escherichia coli O2 strain E058 carrying the defined aerobactin-defective iucD or iucDiutA mutation is less virulent in the chicken

The expression of aerobactin accounts for much of the pathogenesis of avian pathogenic Escherichia coli (APEC). iucA, iucB, iucC and iucD are involved in aerobactin synthesis and iutA is responsible for the expression of a specific outer membrane receptor protein for ferric aerobactin. Knockout mutants of iucD and iucDiutA in the APEC O2 strain E058 were constructed and named E058ΔiucD and E058ΔiucDΔiutA, respectively. To evaluate the pathogenicity of these mutants, we used multiple approaches to assess the effects of mutations on the virulence of APEC E058. Aerobactin-defective mutants E058ΔiucD and E058ΔiucDΔiutA showed significantly decreased pathogenicity compared with the wild-type strain E058, evidenced by the low extent of colonization in selected organs or being outcompeted by E058 in vivo. Chickens challenged with APEC E058 exhibited typical signs and lesions of avian colibacillosis, while those inoculated with the mutants E058ΔiucD or E058ΔiucDΔiutA showed moderate airsacculitis, mild pericarditis and perihepatitis. However, no significant differences in resistance to specific-pathogen-free chicken serum, ingestion by HD-11 cells, and growth rates in LB were observed between the mutants and the wild-type strain. These results indicated that the IucD- and IutA-related virulence factors play a significant role in the pathogenesis of the APEC strain E058.

Development of an allele-specific PCR assay for simultaneous sero-typing of avian pathogenic Escherichia coli predominant O1, O2, O18 and O78 strains.

Systemic infections by avian pathogenic Escherichia coli (APEC) are economically devastating to poultry industries worldwide. E. coli strains belonging to serotypes O1, O2, O18 and O78 are preferentially associated with avian colibacillosis. The rfb gene cluster controlling O antigen synthesis is usually various among different E. coli serotypes. In present study, the rfb gene clusters of E. coli serotypes O1, O2, O18 and O78 were characterized and compared. Based on the serotype-specific genes in rfb gene cluster, an allele-specific polymerase chain reaction (PCR) assay was developed. This PCR assay was highly specific and reliable for sero-typing of APEC O1, O2, O18 and O78 strains. The sensitivity of the assay was determined as 10 pg DNA or 10 colony forming units (CFUs) bacteria for serotypes O2 and O18 strains, and 500 pg DNA or 1,000 CFUs bacteria for serotypes O1 and O78 strains. Using this PCR system, APEC isolates and the infected tissue samples were categorized successfully. Furthermore, it was able to differentiate the serotypes for the samples with multi-agglutination in the traditional serum agglutination assay. Therefore, the allele-specific PCR is more simple, rapid and accurate assay for APEC diagnosis, epidemiologic study and vaccine development.

LuxS contributes to virulence in avian pathogenic Escherichia coli O78:K80:H9

Avian pathogenic Escherichia coli (APEC) cause avian colibacillosis, a poultry disease characterized by multiple organ infections resulting in significant economic loss in the poultry industry. Several virulence factors are important for disease manifestation in APEC of which, role of quorum sensing has not been investigated. Quorum sensing is a population dependent cell–cell signaling system which modulates numerous physiological processes such as biofilm formation and virulence in multiple species. LuxS, a well-known controller in the QS, plays a role in regulating virulence in various bacterial species. Here we investigated the role of LuxS in regulating virulence in APEC O78:K80:H9. Mutation of luxS resulted in a significant reduction of virulence in APEC O78:K80:H9, evidenced by both in vivo and in vitro assays such as decreased invasion of internal organs in chicken embryo, reduced lethality in chicken embryo lethality assay, and altered lipopolysaccharide (LPS) profile. In addition, the abilities of the knockout strain to survive in chicken macrophage cell lines and to invade in chicken embryo fibroblast cells were significantly diminished. Further, structure and expression level of the LPS profile was significantly altered in the knockout strain, which may be one of the contributing factors for the persistence and virulence of APEC. Complementation of luxS gene in trans restored the virulence of the knockout strain to the level of wild-type bacteria. Taken together, these results show that LuxS contributes to the virulence in APEC O78:K80:H9 strain and partly explain the role played by LuxS in the pathogenesis of APEC strains.

Role of the lpxM lipid A biosynthesis pathway gene in pathogenicity of avian pathogenic Escherichia coli strain E058 in a chicken infection model

Lipopolysaccharide (LPS) is a major surface component of avian pathogenic Escherichia coli (APEC), and is a possible virulence factor in avian infections caused by this organism. The contribution of the lpxM gene, which encodes a myristoyl transferase that catalyzes the final step in lipid A biosynthesis, to the pathogenicity of APEC has not previously been assessed. In this study, an isogenic lpxM mutant, E058ΔlpxM, was constructed in APEC O2 strain E058 and then characterized. Structural analysis of lipid A from the parental strain and derived mutant showed that E058ΔlpxM lacked one myristoyl (C14:0) on its lipid A molecules. No differences were observed between the mutant and wild-type in a series of tests including growth rate in different broths and ability to survive in specific-pathogen-free chicken serum. However, the mutant showed significantly reduced invasion and intracellular survival in the avian macrophage HD11 cell line (P<0.05). Nitric oxide production reduction (P<0.05) and cytokine gene expression downregulation (P<0.05 or P<0.01) also showed in HD11 treated with E058ΔlpxM-derived LPS compared with that in cells treated with E058-derived LPS at different times. Compared to the parental strain E058, E058ΔlpxM had a significant reduction in bacterial load in heart (P<0.01), liver (P<0.01), spleen (P<0.01), lung (P<0.05), and kidney (P<0.05) tissues. The histopathological lesions in visceral organs of birds challenged with the wild-type strain were more severe than in birds infected with the mutant. However, the E058ΔlpxM mutant showed a similar sensitivity pattern to the parental strain following exposure to several hydrophobic reagents. These results indicate that the lpxM gene is important for the pathogenicity and biological activity of APEC strain E058.

Transcriptome Analysis of Avian Pathogenic Escherichia coli O1 in Chicken Serum Reveals Adaptive Responses to Systemic Infection

Infections of avian pathogenic Escherichia coli (APEC) result in annual multimillion-dollar losses to the poultry industry. Despite this, little is known about the mechanisms by which APEC survives and grows in the bloodstream. Thus, the aim of this study was to identify molecular mechanisms enabling APEC to survive and grow in this critical host environment. To do so, we compared the transcriptome of APEC O1 during growth in Luria-Bertani broth and chicken serum. Several categories of genes, predicted to contribute to adaptation and growth in the avian host, were identified. These included several known virulence genes and genes involved in adaptive metabolism, protein transport, biosynthesis pathways, stress resistance, and virulence regulation. Several genes with unknown function, which were localized to pathogenicity islands or APEC O1's large virulence plasmid, pAPEC-O1-ColBM, were also identified, suggesting that they too contribute to survival in serum. The significantly upregulated genes dnaK, dnaJ, phoP, and ybtA were subsequently subjected to mutational analysis to confirm their role in conferring a competitive advantage during infection. This genome-wide analysis provides novel insight into processes that are important to the pathogenesis of APEC O1.

Molecular Typing of Avian Pathogenic Escherichia coli O78 Strains in Japan by Using Multilocus Sequence Typing and Pulsed-Field Gel Electrophoresis

Avian pathogenic Escherichia coli (APEC) serogroup O78 isolates in Japan were characterized using multilocus sequence typing (MLST) and pulsed-field gel electrophoresis (PFGE). Thirty-four of the serotype O78 isolates were clustered into 11 PFGE types with 80% similarity and were classified into 5 sequence types (STs), ST23, ST117, ST155, ST369 and 1 novel ST (ST1645). The most dominant ST was ST23 (54.3%). Fluoroquinolone-resistant strains belonged to ST23 (9 strains), ST155 (3 strains) and ST117 (1 strain). The combined findings of MLST and PFGE suggested that 1 genotype belonging to ST23 was the genotype specific to fluoroquinolone-resistant strains. These results indicate that the combination of MLST and PFGE is useful for conducting epidemiological studies on APEC O78 strains.

PapMutant of Avian Pathogenic Escherichia coli O1, an O1:K1:H7 Strain, Is AttenuatedIn Vivo

P or Pap fimbriae of avian pathogenic Escherichia coli (APEC) have previously been shown to be important in the pathogenesis of colibacillosis. However, no study has been done to ascertain the effects of deletion of the genes responsible for P fimbrial biogenesis on APEC's in vitro and/or in vivo characteristics. In the present study, all 11 genes of the pap gene cluster were deleted from APEC O1, the recently sequenced APEC strain, and the wild-type strain was compared to the mutant (ECPAP1) for changes in certain phenotypic characteristics and virulence for chickens. Both APEC O1 and ECPAP1 demonstrated mannose-sensitive agglutination of guinea pig and chicken erythrocytes, but only APEC O1 demonstrated mannose-resistant hemagglutination and P-receptor binding properties. The in vivo experiments revealed that ECPAP1 was markedly attenuated as compared to its wild-type strain APEC O1. These findings suggest that P fimbriae are involved in the virulence of APEC O1.

The conserved portion of the putative virulence region contributes to virulence of avian pathogenic Escherichia coli

Colibacillosis is a common systemic disease of worldwide economic importance in poultry, caused by Escherichia coli. E. coli are normally found in the intestines of poultry, but some strains are able to cause extraintestinal disease. Plasmid pVM01 is essential for virulence in avian pathogenic Escherichia coli (APEC) strain E3 in chickens after aerosol exposure and contains the virulence-associated genes iucA, iss and tsh in distinct regions. The determination of the complete sequence of this plasmid identified many ORFs that were highly similar to genes found in the APEC O1 plasmid, as well as many hypothetical ORFs. Truncated versions of pVM01 were constructed and introduced into avirulent APEC strain E3/2.4 and the pathogenicity of these strains was assessed by aerosol exposure. The function of the region of pVM01 that contains the genes for conjugation was confirmed. Strains carrying the truncated plasmids appeared to be of intermediate virulence compared to the wild-type APEC strain E3. The conserved portion of the putative virulence region was found to contribute to the colonization of and generation of lesions in the air sacs. Both the conserved and variable portions of the putative virulence region were shown to contribute to the colonization of the trachea, but the variable portion of the putative virulence region was not required for the strain to confer a virulent phenotype. These results reveal that deletion of the conserved portion of the putative virulence region, but not the variable portion of the putative virulence region, is associated with a decrease in virulence of APEC.

Acquisition of Avian PathogenicEscherichia coliPlasmids by a CommensalE. coliIsolate Enhances Its Abilities To Kill Chicken Embryos, Grow in Human Urine, and Colonize the Murine Kidney

We have found an avian pathogenic Escherichia coli (APEC) plasmid, pAPEC-O2-ColV, which contains many of the genes associated with APEC virulence and also shows similarity in content to a plasmid and pathogenicity island of human uropathogenic E. coli (UPEC). To test the possible role of this plasmid in virulence, it was transferred by conjugation along with a large R plasmid, pAPEC-O2-R, into a commensal avian E. coli strain. The transconjugant was compared to recipient strain NC, UPEC strain HE300, and donor strain APEC O2 using various assays, including lethality for chicken embryos, growth in human urine, and ability to cause urinary tract infection in mice. The transconjugant killed significantly more chicken embryos than did the recipient. In human urine, APEC O2 grew at a rate equivalent to that of UPEC strain HE300, and the transconjugant showed significantly increased growth compared to the recipient. The transconjugant also significantly outcompeted the recipient in colonization of the murine kidney. These findings suggest that APEC plasmids, such as pAPEC-O2-ColV, contribute to the pathogenesis of avian colibacillosis. Moreover, since avian E. coli and their plasmids may be transmitted to humans, evaluation of APEC plasmids as possible reservoirs of urovirulence genes for human UPEC may be warranted.

Characterization of Stg Fimbriae from an Avian Pathogenic Escherichia coli O78:K80 Strain and Assessment of Their Contribution to Colonization of the Chicken Respiratory Tract

In a previous study, ecs-3, a sequence from avian pathogenic Escherichia coli (APEC) O78:K80 strain chi7122, was found to be expressed in vivo in infected chicken tissues. The region encompassing ecs-3 carries a fimbrial gene cluster that is a putative ortholog of the stg fimbrial gene cluster of Salmonella enterica serovar Typhi. This APEC fimbrial gene cluster, which we have termed stg, is a member of a distinct group of related fimbriae that are located in the glmS-pstS intergenic region of certain E. coli and S. enterica strains. Under the control of the pBAD promoter, the production of Stg fimbriae was demonstrated by Western blotting and immunogold electron microscopy with E. coli K-12. Transcriptional fusions suggest that stg expression is influenced by the carbohydrate source and decreased by the addition of iron and that Fur plays a role in the regulation of stg expression. stg sequences were associated with APEC O78 isolates, and stg was phylogenetically distributed among E. coli reference strains and clinical isolates from human urinary tract infections. Stg fimbriae contributed to the adherence of a nonfimbriated E. coli K-12 strain to avian lung sections and human epithelial cells in vitro. Coinfection experiments with APEC strain chi7122 and an isogenic Deltastg mutant demonstrated that compared to the wild-type parent, the Deltastg mutant was less able to colonize air sacs, equally able to colonize lungs, and able to more effectively colonize tracheas of infected chickens. Stg fimbriae, together with other adhesins, may therefore contribute to the colonization of avian respiratory tissues by certain APEC strains.

Occurrence of Pathogenicity Island IAPEC-O1Genes Among Escherichia coli Implicated in Avian Colibacillosis

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 (PAls). 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.

DNA Sequence and Comparative Genomics of pAPEC-O2-R, an Avian Pathogenic Escherichia coli Transmissible R Plasmid

In this study, a 101-kb IncF plasmid from an avian pathogenic Escherichia coli (APEC) strain (APEC O2) was sequenced and analyzed, providing the first completed APEC plasmid sequence. This plasmid, pAPEC-O2-R, has functional transfer and antimicrobial resistance-encoding regions. The resistance-encoding region encodes resistance to eight groups of antimicrobial agents, including silver and other heavy metals, quaternary ammonium compounds, tetracycline, sulfonamides, aminoglycosides, trimethoprim, and beta-lactam antimicrobial agents. This region of the plasmid is unique among previously described IncF plasmids in that it possesses a class 1 integron that harbors three gene cassettes and a heavy metal resistance operon. This region spans 33 kb and is flanked by the RepFII plasmid replicon and an assortment of plasmid maintenance genes. pAPEC-O2-R also contains a 32-kb transfer region that is nearly identical to that found in the E. coli F plasmid, rendering it transferable by conjugation to plasmid-less strains of bacteria, including an APEC strain, a fecal E. coli strain from an apparently healthy bird, a Salmonella enterica serovar Typhimurium strain, and a uropathogenic E. coli strain from humans. Differences in the G+C contents of individual open reading frames suggest that various regions of pAPEC-O2-R had dissimilar origins. The presence of pAPEC-O2-R-like plasmids that encode resistance to multiple antimicrobial agents and that are readily transmissible from APEC to other bacteria suggests the possibility that such plasmids may serve as a reservoir of resistance genes for other bacteria of animal and human health significance.

Avian pathogenic Escherichia coli transmission from broiler breeders to their progeny in an integrated poultry production chain

Early cases of colibacillosis with omphalitis, yolk sac infection and increased mortality were observed in five broiler chicken flocks (A1, A2, A3, A4 and B1) from two broiler breeder flocks A and B, respectively. Avian pathogenic Escherichia Coli (APEC) serotype O78, Fim/Tsh/Iuc pathotype, were isolated from flocks A, A1, A2, A3 and A4, and APEC serotype O139, pathotype Fim/Iuc, from flocks B and B1. APEC O78 strains isolated from broiler chicks A1, A2, A3 and A4, originating from breeder flock A, had the same antibiotic resistance pattern as APEC O139 strains isolated from broiler chicks B1 and breeder B. The random amplified polymorphic DNA technique performed on APEC strains revealed two distinct clusters of genetic similarity: cluster I consisted of some APEC O78 and cluster II of APEC O139. These results indicated that a transmission of APEC strains from adults A and B to their respective progeny could occur. Transmission d' Escherichia coli pathogène aviaire (APEC) à partir de reproducteurs de type chair à leur descendance dans une production intégrée. Les cas précoces de colibacillose avec omphalite, infection du sac vitellin, et augmentation de mortalité, ont été observés dans cinq troupeaux de poulets de chair A1, A2, A3, A4 et B1 issus de deux troupeaux de reproducteurs respectivement A et B. Des Escherichia coli pathogènes aviaires (APEC) sérotype O78, pathotype Fim/Tsh/Iuc ont été isolés des troupeaux A1, A2, A3, A4 et des APEC O139, pathotype Fim/Iuc ont été isolés des troupeaux B et B1. Les souches d'APEC O78 isolées à partir des poulets de chair A1, A2, A3 et A4 issus du troupeau de reproducteurs A, avaient le même profil de résistance aux antibiotiques que les souches de l'APEC O139 isolés des poulets de chair B1 et des reproducteurs B. Les souches d'APEC ont fait l'objet d'une analyse par RAPD qui a révélé que ces souches se répartissaient en deux groupes distincts de similarité génétique : le groupe I comprenant quelques APEC O78, et le groupe II comprenant les APEC O139. Ces résultats ont montré que la transmission des souches d'APEC des adultes A et B à leur descendance respective peut se produire. Übertragung von Escherchia coli (APEC) von Broilerelterntieren auf ihre Nachkommen innerhalb einer integrierten Geflügelproduktionskette In fünf Broilerherden (A1, A2, A3, A4 und B1) von zwei Broilerelterntierherden (A und B) wurden frühe Fälle von Colibazillose verbunden mit Omphalitis, Dottersackinfektion und erhöhter Mortalität beobachtet. Aus den Herden A, A1, A2, A3 und A4 wurden pathogene aviäre Escherichia coli (APEC)-Serotyp O78,-Pathotyp Fim/Tsh/iuc und aus den Herden B und B1 APEC-Serotyp O139, -PathotypFim/Iuc isoliert. Die O78-APEC-Stämme aus den Broilerherden A1, A2, A3 und A4, die von der Broilerelterntierherde A abstammten, wiesen das gleiche Antibiotikaresistenzmuster auf wie die O139-APEC-Stämme aus den Broilern aus Herde B1 und ihrer Elterntierherde B. Die mit den APEC-Stämmen durchgeführte RAPD-Technik ließ zwei verschiedene genetische Cluster erkennen: Cluster I beinhaltete einige der APEC O78- Stämme und Cluster II die APEC O139. Diese Ergebnisse weisen darauf hin, dass eine Übertragung von APEC-Stämmen von den Adulten der Herden A und B auf ihre Nachkommen vorkommen kann. Transmisión de Escherichia coli patógena aviar (APEC) de reproductores a su progenie en una cadena de producción avícola integrada Se observaron casos tempranos de colibacilosis con onfalitis, infección del saco vitelino y mortalidad incrementada en cinco lotes de pollos de engorde A1, A2, A3, A4 y B1 provenientes de dos lotes de reproductores, A y B respectivamente. Se aisló una Escherichia Coli patógena aviar (APEC) serotipo O78, patotipo Fim/Tsh/Iuc de los lotes A, A1, A2, A3, A4 y APEC del serotipo O139 y patotipo Fim/Iuc de los lotes B y B1. Las cepas APEC O78 aisladas de los pollitos A1, A2, A3 y A4, originarios de los lotes de reproductores A, presentaron el mismo patrón de resistencia a los antibióticos que las cepas APEC O139 aisladas de los pollitos de engorde B1 y de los reproductores B. La técnica de RAPD realizada sobre las cepas APEC reveló dos grupos distintos de similaridad genética: el grupo I consistió en algunas APEC O78 y el grupo II en APEC O139. Estos resultados indican que la transmisión de cepas APEC de adultos A y B a su progenie respectiva puede ocurrir.