Letters to the Editor Wil J.M. LandmanJo H. H. van Eck Source: Avian Diseases, 58(3):343-344. Published By: American Association of Avian Pathologists DOI: http://dx.doi.org/10.1637/0005-2086-58.3.343 URL: http://www.bioone.org/doi/full/10.1637/0005-2086-58.3.343
BioOne (www.bioone.org) is a nonprofit, online aggregation of core research in the biological, ecological, and environmental sciences. BioOne provides a sustainable online platform for over 170 journals and books published by nonprofit societies, associations, museums, institutions, and presses. Your use of this PDF, the BioOne Web site, and all posted and associated content indicates your acceptance of BioOne’s Terms of Use, available at www.bioone.org/page/terms_of_use. Usage of BioOne content is strictly limited to personal, educational, and non-commercial use. Commercial inquiries or rights and permissions requests should be directed to the individual publisher as copyright holder.
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AVIAN DISEASES 58:343–344, 2014
Letters to the Editor— Dear Sir, It is with great interest that we have read the manuscript of Atul A. Chaudhari and Subhashinie Kariyawasam titled ‘‘An Experimental Infection Model for Escherichia coli Egg Peritonitis in Layer Chickens’’ published in Avian Diseases, 58(1):25–33. 2014. However, we have encountered a number of worrisome shortcomings, which we will address next. 1. The study seems to be a repetition of the work published earlier by Gross and Siegel (Avian Diseases 1959, 3, 370–373). This is in itself not illegitimate in our opinion as long as it is made clear to the readers. However, in view of what the authors state in the discussion, we cannot come to any other conclusion than that the non-originality of the presented study, has been clouded. The text of concern which can be found on page 31 of the manuscript is: ‘‘Previously, Gross and Siegel (11) reported that IP inoculation of egg yolk was beneficial for producing peritonitis when the infection was introduced intraperitoneally. However, an IP route is a direct route of infection and cannot be considered as a natural route of infection. The present study also indicated that the presence of egg yolk in the peritoneal cavity acts as a prerequisite factor to development of egg peritonitis. In addition, the present study utilized a possible natural route of infection to produce egg peritonitis.’’ However, Gross and Siegel certainly inoculated birds via a natural route, namely the intravaginal route, inducing successfully peritonitis in birds, which were also injected with egg yolk. 2. Due to the sigmoid shape of the vagina, intrauterine inoculation via the vagina is only possible if a complete prolapse of the
vagina has been induced (Landman et al., 2013, Avian Pathology, Vol. 42, No. 1, 55–59). Since this was not done in the study of concern, it is almost sure that inoculations were not performed intrauterinely, but intravaginally. 3. In laying hens with colibacillosis two forms prevail: salpingitis/ peritonitis/salpingoperitonitis (SPS), also commonly named ‘‘egg peritonitis’’ and the Escherichia coli peritonitis syndrome (EPS). EPS can easily be discriminated from coliform SPS, which forms a substantial proportion of the ‘‘normal’’ mortality in flocks of layer hens based on its acute and septicemic character, its high mortality rates, and the rare occurrence of salpingitis. Although the title of the manuscript suggests that ‘‘egg peritonitis’’’ was induced, in the text both terminologies are intermingled making it unclear what the real purpose of the study was. If the intention was to induce SPS, then the study was a repetition of the work of Gross and Siegel (see point 1). In case the intention was to reproduce EPS, the work would not have been novel either as this was published already in 2013 (Landman et al., 2013, Avian Pathology, Vol. 42, No. 2, 157– 162). Kind regards, Wil J. M. Landman, GD Animal Health, Deventer, the Netherlands and Jo H. H. van Eck, Department of Farm Animal Health, Faculty of Veterinary Medicine, Utrecht University, Utrecht, the Netherlands
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Response to the Editor— Dear Sir, We are pleased that Wil J. M. Landman and Jo H. H. van Eck found interest in our recent publication entitled ‘‘An Experimental Infection Model for Escherichia coli Egg Peritonitis in Layer Chickens.’’ However, they have raised some concerns with this article in their letter to you. We considered the letter seriously and below is our response. We apologize for the matters which might have been overlooked at the time of preparing the manuscript. Some of your concerns are valid but there are some key differences in our study and others: 1) an experimental infection model specifically for E. coli egg peritonitis; 2) the route of inoculation of E. coli was intrauterine (IU); 3) the bacterial suspension was re-suspended in egg yolk before inoculation via IU route; 4) APECO78 was an isolate from a hen that died exclusively of egg peritonitis without any septicemia; and 5) a detailed clinical signs/lesion scoring system to assess the severity of infection. Here are the clarifications to each of your concerns: Concern #1: Earlier publication by Gross and Siegel (Avian Diseases 1959, 3, 370–373). We sincerely apologize if our description looks misleading to the readers. The intention of the description was to highlight the fact about the IP route (Statement: However, an IP route is a direct route of infection and cannot be considered as a natural route of infection). It was not intended to hide any valuable information reported by previous researchers or to take any personal advantage of this. Again, we apologize for not mentioning about the intravaginal route of infection used by Gross and Seigel in our paper. We would also like to highlight that the peritonitis model developed by Gross and Seigel used an isolate which possessed serological similarities with periocarditis isolates. We understand that serotyping of E. coli cannot differentiate between various forms of avian colibacillosis. However, as discussed in our article with suitable references, when peritonitis occurs alone without any reproductive lesions, the origin for infection is usually respiratory. Therefore, the coliform peritonitis model developed by Gross and Seigel could be either for ‘‘E. coli peritonitis syndrome’’ (‘‘EPS’’) or ‘‘egg peritonitis’’ as the E. coli used was isolated from the peritoneal cavities of chickens. However, the reference cited and the description of the isolate (‘‘These isolates proved to be of the same serological types as those associated with pericarditis’’) suggest that these E. coli were isolated from the cases of EPS syndrome but not from SPS. Gross and Siegel have not mentioned if their model is specific for EPS or egg peritonitis, and to consider it a model for egg peritonitis is a mere speculation. 2. Concern #2: Intra-uterine inoculation of E. coli. We appreciate the comments by Landman and van Eck regarding the intrauterine route. Their article entitled ‘‘Success Rates of Intrauterine Inoculations of Layers via the Vagina’’ is very interesting and provides useful and valuable information about intrauterine route of
infection. We completed this study in 2011—long before your publication became on-line in 2013. As a proof, we presented our work at the Annual Meeting of American Association of Avian Pathologists in (AAAP) 2012 in San Diego, CA (August 4–7, 2012, abstract deadline December 1, 2011). We wish that your publication was available before we performed the experiment in 2011, so that we could have used it as a strong reference. We are extremely familiar with chicken infection models, and possess the technical skills, experience and knowledge to determine the accuracy of intra-uterine inoculations. We have performed IU inoculations on chickens previously, and proved the inoculations were done accurately by performing post-inoculation assessments. As such, we are certain that the inoculations were made right into the uterus. We have tried several different methods, and inoculation with a tuberculin syringe resulted in the best outcome. Concern #3: Two forms of colibacillosis prevail in laying hens: egg peritonitis or salpingitis/peritonitis/salpingoperitonitis (SPS) and the Escherichia coli peritonitis syndrome (EPS). We are aware of the two forms of peritonitis in laying hens. As the manuscript title clearly states, the intention of our study was to develop an experimental infection model to reproduce egg peritonitis caused by E. coli. For this purpose, we used an E. coli isolated from the reproductive tract of a hen that had died of egg peritonitis. This hen did not show septicemic lesions, but had lesions of oophoritis, salpingitis, and peritonitis. As we have mentioned above, we presented our results in 2012 at the AAAP Annual Meeting. This clearly demonstrates that we did not copy your study. Upon completion of the work, we submitted the manuscript to Veterinary Research before submitting it to Avian Diseases. As the manuscript did not match with the journal scope, it was returned without being reviewed. We later on submitted it to Avian Diseases after formatting the article to match the style of the journal. It was then sent back to us for corrections and took some time to bring the article online. Considering the amount of time and experiments (thorough investigation of bacterial recovery, signs and macroscopic lesions, histopathology, PEGF confirmation, and developing scoring system) dedicated to develop the model, one can easily understand that the experiments were carried out until the satisfactory results were obtained. In any case, our study thoroughly investigated the validity of the infection model and provided a successful experimental approach to develop egg peritonitis induced by E. coli in laying hens. Thank you. Yours sincerely, Subhashinie Kariyawasam, BVSc, PhD, ACVM, ACPV and Atul Chaudhari, BVSc, MSc, PhD
BioOne (www.bioone.org) is a nonprofit, online aggregation of core research in the biological, ecological, and environmental sciences. BioOne provides a sustainable online platform for over 170 journals and books published by nonprofit societies, associations, museums, institutions, and presses. Your use of this PDF, the BioOne Web site, and all posted and associated content indicates your acceptance of BioOne’s Terms of Use, available at www.bioone.org/page/terms_of_use. Usage of BioOne content is strictly limited to personal, educational, and non-commercial use. Commercial inquiries or rights and permissions requests should be directed to the individual publisher as copyright holder.
BioOne sees sustainable scholarly publishing as an inherently collaborative enterprise connecting authors, nonprofit publishers, academic institutions, research libraries, and research funders in the common goal of maximizing access to critical research.
AVIAN DISEASES 58:343–344, 2014
Letters to the Editor— Dear Sir, It is with great interest that we have read the manuscript of Atul A. Chaudhari and Subhashinie Kariyawasam titled ‘‘An Experimental Infection Model for Escherichia coli Egg Peritonitis in Layer Chickens’’ published in Avian Diseases, 58(1):25–33. 2014. However, we have encountered a number of worrisome shortcomings, which we will address next. 1. The study seems to be a repetition of the work published earlier by Gross and Siegel (Avian Diseases 1959, 3, 370–373). This is in itself not illegitimate in our opinion as long as it is made clear to the readers. However, in view of what the authors state in the discussion, we cannot come to any other conclusion than that the non-originality of the presented study, has been clouded. The text of concern which can be found on page 31 of the manuscript is: ‘‘Previously, Gross and Siegel (11) reported that IP inoculation of egg yolk was beneficial for producing peritonitis when the infection was introduced intraperitoneally. However, an IP route is a direct route of infection and cannot be considered as a natural route of infection. The present study also indicated that the presence of egg yolk in the peritoneal cavity acts as a prerequisite factor to development of egg peritonitis. In addition, the present study utilized a possible natural route of infection to produce egg peritonitis.’’ However, Gross and Siegel certainly inoculated birds via a natural route, namely the intravaginal route, inducing successfully peritonitis in birds, which were also injected with egg yolk. 2. Due to the sigmoid shape of the vagina, intrauterine inoculation via the vagina is only possible if a complete prolapse of the
vagina has been induced (Landman et al., 2013, Avian Pathology, Vol. 42, No. 1, 55–59). Since this was not done in the study of concern, it is almost sure that inoculations were not performed intrauterinely, but intravaginally. 3. In laying hens with colibacillosis two forms prevail: salpingitis/ peritonitis/salpingoperitonitis (SPS), also commonly named ‘‘egg peritonitis’’ and the Escherichia coli peritonitis syndrome (EPS). EPS can easily be discriminated from coliform SPS, which forms a substantial proportion of the ‘‘normal’’ mortality in flocks of layer hens based on its acute and septicemic character, its high mortality rates, and the rare occurrence of salpingitis. Although the title of the manuscript suggests that ‘‘egg peritonitis’’’ was induced, in the text both terminologies are intermingled making it unclear what the real purpose of the study was. If the intention was to induce SPS, then the study was a repetition of the work of Gross and Siegel (see point 1). In case the intention was to reproduce EPS, the work would not have been novel either as this was published already in 2013 (Landman et al., 2013, Avian Pathology, Vol. 42, No. 2, 157– 162). Kind regards, Wil J. M. Landman, GD Animal Health, Deventer, the Netherlands and Jo H. H. van Eck, Department of Farm Animal Health, Faculty of Veterinary Medicine, Utrecht University, Utrecht, the Netherlands
343
344
Letters to the Editor
Response to the Editor— Dear Sir, We are pleased that Wil J. M. Landman and Jo H. H. van Eck found interest in our recent publication entitled ‘‘An Experimental Infection Model for Escherichia coli Egg Peritonitis in Layer Chickens.’’ However, they have raised some concerns with this article in their letter to you. We considered the letter seriously and below is our response. We apologize for the matters which might have been overlooked at the time of preparing the manuscript. Some of your concerns are valid but there are some key differences in our study and others: 1) an experimental infection model specifically for E. coli egg peritonitis; 2) the route of inoculation of E. coli was intrauterine (IU); 3) the bacterial suspension was re-suspended in egg yolk before inoculation via IU route; 4) APECO78 was an isolate from a hen that died exclusively of egg peritonitis without any septicemia; and 5) a detailed clinical signs/lesion scoring system to assess the severity of infection. Here are the clarifications to each of your concerns: Concern #1: Earlier publication by Gross and Siegel (Avian Diseases 1959, 3, 370–373). We sincerely apologize if our description looks misleading to the readers. The intention of the description was to highlight the fact about the IP route (Statement: However, an IP route is a direct route of infection and cannot be considered as a natural route of infection). It was not intended to hide any valuable information reported by previous researchers or to take any personal advantage of this. Again, we apologize for not mentioning about the intravaginal route of infection used by Gross and Seigel in our paper. We would also like to highlight that the peritonitis model developed by Gross and Seigel used an isolate which possessed serological similarities with periocarditis isolates. We understand that serotyping of E. coli cannot differentiate between various forms of avian colibacillosis. However, as discussed in our article with suitable references, when peritonitis occurs alone without any reproductive lesions, the origin for infection is usually respiratory. Therefore, the coliform peritonitis model developed by Gross and Seigel could be either for ‘‘E. coli peritonitis syndrome’’ (‘‘EPS’’) or ‘‘egg peritonitis’’ as the E. coli used was isolated from the peritoneal cavities of chickens. However, the reference cited and the description of the isolate (‘‘These isolates proved to be of the same serological types as those associated with pericarditis’’) suggest that these E. coli were isolated from the cases of EPS syndrome but not from SPS. Gross and Siegel have not mentioned if their model is specific for EPS or egg peritonitis, and to consider it a model for egg peritonitis is a mere speculation. 2. Concern #2: Intra-uterine inoculation of E. coli. We appreciate the comments by Landman and van Eck regarding the intrauterine route. Their article entitled ‘‘Success Rates of Intrauterine Inoculations of Layers via the Vagina’’ is very interesting and provides useful and valuable information about intrauterine route of
infection. We completed this study in 2011—long before your publication became on-line in 2013. As a proof, we presented our work at the Annual Meeting of American Association of Avian Pathologists in (AAAP) 2012 in San Diego, CA (August 4–7, 2012, abstract deadline December 1, 2011). We wish that your publication was available before we performed the experiment in 2011, so that we could have used it as a strong reference. We are extremely familiar with chicken infection models, and possess the technical skills, experience and knowledge to determine the accuracy of intra-uterine inoculations. We have performed IU inoculations on chickens previously, and proved the inoculations were done accurately by performing post-inoculation assessments. As such, we are certain that the inoculations were made right into the uterus. We have tried several different methods, and inoculation with a tuberculin syringe resulted in the best outcome. Concern #3: Two forms of colibacillosis prevail in laying hens: egg peritonitis or salpingitis/peritonitis/salpingoperitonitis (SPS) and the Escherichia coli peritonitis syndrome (EPS). We are aware of the two forms of peritonitis in laying hens. As the manuscript title clearly states, the intention of our study was to develop an experimental infection model to reproduce egg peritonitis caused by E. coli. For this purpose, we used an E. coli isolated from the reproductive tract of a hen that had died of egg peritonitis. This hen did not show septicemic lesions, but had lesions of oophoritis, salpingitis, and peritonitis. As we have mentioned above, we presented our results in 2012 at the AAAP Annual Meeting. This clearly demonstrates that we did not copy your study. Upon completion of the work, we submitted the manuscript to Veterinary Research before submitting it to Avian Diseases. As the manuscript did not match with the journal scope, it was returned without being reviewed. We later on submitted it to Avian Diseases after formatting the article to match the style of the journal. It was then sent back to us for corrections and took some time to bring the article online. Considering the amount of time and experiments (thorough investigation of bacterial recovery, signs and macroscopic lesions, histopathology, PEGF confirmation, and developing scoring system) dedicated to develop the model, one can easily understand that the experiments were carried out until the satisfactory results were obtained. In any case, our study thoroughly investigated the validity of the infection model and provided a successful experimental approach to develop egg peritonitis induced by E. coli in laying hens. Thank you. Yours sincerely, Subhashinie Kariyawasam, BVSc, PhD, ACVM, ACPV and Atul Chaudhari, BVSc, MSc, PhD
