Relevant bibliographies by topics / Necrotic enteritis

Academic literature on the topic 'Necrotic enteritis'

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Published: 4 June 2021
Last updated: 19 February 2022

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Journal articles on the topic "Necrotic enteritis"

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Wiedosari, Ening, and Y. Sani. "Coccidiosis as A Predisposition Factor for Necrotic Enteritis in Poultry and Their Prevention." Indonesian Bulletin of Animal and Veterinary Sciences 30, no. 3 (September 30, 2020): 139. http://dx.doi.org/10.14334/wartazoa.v30i3.2504.

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<p>Coccidiosis and necrotic enteritis are both affecting the digestive tract of chicken and both are major enteric disease that mainly affect poultry. Among the enteric diseases, necrotic enteritis is a major problem. Coccidiosis is caused by the protozoan of Eimeria sp, and is commonly found as a predisposition factor for necrotic enteritis caused by Clostridum perfringens. Both diseases are commonly shown similar pathological change namely necrosis of epthelial cells in the intestinal mucosa. The diseases have great economic impact in poultry productions, due to the increased mortality, decreased performance and medication costs. Control of these diseases are commonly treated with antibiotics and ionophores. However, an intensive use of these drugs in feed may cause the emergence of drug-resistance against some strains of Eimeria sp.and Cl. Perfringens and an increased chance of contamination in animal products for human consumption. The paper is discussing the occurrence of necrotic enteritis especially due to the coccidian as a major predisposition factor and the development of alternative control strategies for avian coccidiosis and necrotic enteritis, by modulating intestinal health.</p>
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Laishevtsev, A. I., A. V. Kapustin, E. A. Yakimova, A. V. Danilyuk, A. M. Gulyukin, and V. V. Belimenko. "Necrotic enteritis of birds." IOP Conference Series: Earth and Environmental Science 315 (August 23, 2019): 022075. http://dx.doi.org/10.1088/1755-1315/315/2/022075.

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Gazdzinski, P., and R. J. Julian. "Necrotic Enteritis in Turkeys." Avian Diseases 36, no. 3 (July 1992): 792. http://dx.doi.org/10.2307/1591787.

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GEETHA, M., and K. M. PALANIVEL. "Necrotic enteritis in layer chicken." VETERINARY SCIENCE RESEARCH JOURNAL 8, no. 1 and 2 (October 15, 2017): 73–76. http://dx.doi.org/10.15740/has/vsrj/8.1and2/73-76.

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Morris, Winston E., Agustín J. Venzano, Ana Elizondo, Daniel A. Vilte, Elsa C. Mercado, and Mariano E. Fernandez-Miyakawa. "Necrotic Enteritis in Young Calves." Journal of Veterinary Diagnostic Investigation 23, no. 2 (March 2011): 254–59. http://dx.doi.org/10.1177/104063871102300209.

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Penny, C., L. Murray, and P. Scott. "Necrotic enteritis in suckled calves." Veterinary Record 128, no. 24 (June 15, 1991): 575. http://dx.doi.org/10.1136/vr.128.24.575-b.

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Umar, Sajid, Muhammad Younus, Muhammad Shahzad, Kiran Aqil, Rizwan Qayyum, Aqsa Mushtaq, Muhammad Ali Abdullah Shah, and Muhammad Tanveer Munir. "Role of Wheat Based Diet on the Pathology of Necrotic Enteritis in Turkeys." Scientifica 2016 (2016): 1–8. http://dx.doi.org/10.1155/2016/4381067.

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The study was conducted to investigate the effects of wheat based diet on the pathology of necrotic enteritis in turkeys. Turkeys were divided into four groups. Groups A and B were kept as noninoculated and fed normal commercial diet while groups C and D were challenged orally withC. perfringensand fed wheat based diet to promote the development of experimental disease. Infected turkeys showed clinical signs of depression, ruffled feathers, and dark yellowish faeces showing the most prominent disease signs in turkeys of group D with 30% mortality. Similarly, turkeys of group D showed more striking gross and histopathologic lesions as compared to turkeys of group C. The most severe gross lesions comprised intestinal distension, small necrotic spots and haemorrhages on intestine, fragile intestinal wall, and gas bubble formation in the small intestine. Histologically, inoculated turkeys showed patchy necrosis, desquamation of intestinal epithelium, and intense leukocyte infiltration in the intestine. Microscopic examination showed significant decrease in the height of intestinal villi of inoculated birds. Haematological studies showed significant influence of necrotic enteritis on the blood profile of turkeys in group D. The findings revealed that simultaneous feeding of wheat enhanced the pathology of necrotic enteritis in turkeys.
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Zlotowski, Priscila, André Mendes Ribeiro Corrêa, David Emílio Santos Neves de Barcellos, Marisa Ribeiro de Itapema Cardoso, Anílton Cesar Vasconcelos, Luiza Amaral de Castro, and David Driemeier. "Necrotic enterocolitis in pigs naturally infected by porcine circovirus type 2." Ciência Rural 39, no. 6 (June 19, 2009): 1801–7. http://dx.doi.org/10.1590/s0103-84782009005000115.

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Samples of intestine with necrotic enteritis from 63 pigs naturally infected with porcine circovirus type 2 (PCV2) were studied. Colon was the main target of PCV2 associated necrotic enteritis in 60 cases. Immunohistological investigations were carried out to detect the presence of PCV2 in necrotic lesions and to identify the type of cells infected by the virus. Crypt epithelial cells had positive labelling for PCV2 in 17 cases. Depletion of goblet cells occurred in 10 cases. In 24 necrotic enteritis cases, co-infection of PCV2 and Salmonella was identified. An increased rate of apoptosis in the crypt epithelial cells of the large intestine from PCV2 of naturally infected pigs was observed. Immunohistochemical findings confirmed the presence of PCV2 within cells from necrotic intestinal tissue, suggesting that PCV2 may play a role in the development of those lesions. Diagnosis of necrotic enteritis associated with PCV2 should be based on the detection of PCV2 antigen or DNA in the necrotizing lesions. However, bacteriological examination should be performed to rule out the presence of bacterial agents, since co-infections are likely to occur in PCV2 affected pigs.
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Cowen, B. S., L. D. Schwartz, R. A. Wilson, and S. I. Ambrus. "Experimentally Induced Necrotic Enteritis in Chickens." Avian Diseases 31, no. 4 (October 1987): 904. http://dx.doi.org/10.2307/1591050.

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Droual, R., H. L. Shivaprasad, and R. P. Chin. "Coccidiosis and Necrotic Enteritis in Turkeys." Avian Diseases 38, no. 1 (January 1994): 177. http://dx.doi.org/10.2307/1591854.

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Dissertations / Theses on the topic "Necrotic enteritis"

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Cooper, Kerry Kevin. "Necrotic Enteritis in Broiler Chickens: Studies in Disease Reproduction and Pathogenesis." Diss., The University of Arizona, 2007. http://hdl.handle.net/10150/195545.

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Necrotic enteritis in poultry is caused by Clostridium perfringens type A, and is estimated to cost the worldwide poultry industry approximately $2 billion dollars a year, due to increased mortality and decreased feed conversion and weight gain. Very little is known about the pathogenesis of this disease due to the lack of a consistently reproducible experimental model. This dissertation outlines the development of an effective and consistent experimental model for necrotic enteritis in broiler chickens. It was also found that in vivo passage through the chicken's intestinal tract let to increased virulence; we increased the proportion of birds developing disease from 34.6% to 81.4%. Researchers have proposed that alpha toxin (CPA) is believed to be the critical virulence factor of the disease. All type A isolates have the potential to produce CPA, thus we challenged birds with numerous type A isolates that are virulent in other animal hosts. However, we found that they did not produce necrotic enteritis in broiler chickens. In addition, challenge with culture supernatant alone failed to produce gross lesions in the birds, although challenging with washed whole cell cultures did do so. Vaccinating birds with HIS-tagged recombinant CPA provided partial protection against disease; there was a 42.0% decrease in lesion development. The conclusion of this doctoral research is that CPA does have a role in the pathogenesis of necrotic enteritis in broiler chickens, but there are apparently other critical virulence factors involved in the development of disease.
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Johansson, Anders. "Clostridium perfringens the causal agent of necrotic enteritis in poultry /." Uppsala : Department of Biomedical Sciences and Veterinary Public Health, Swedish University of Agricultural Sciences, 2006. http://epsilon.slu.se/200634.pdf.

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Stringfellow, Kendre Duaron. "Evaluation of agricultural disinfectants and necrotic enteritis preventatives in broiler chickens." [College Station, Tex. : Texas A&M University, 2008. http://hdl.handle.net/1969.1/ETD-TAMU-3237.

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Paiva, Diego Moreira. "Effects of Calcium and Enzyme Supplementation on the Occurrence of Necrotic Enteritis." Diss., Virginia Tech, 2013. http://hdl.handle.net/10919/49595.

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Diet composition and nutrient balance can have a critical impact on intestinal integrity during exposure to enteric pathogens. Researchers have extensively reported benefits on nutrient availability and broiler performance as a consequence of the impact of phytase supplementation. However, the poultry industry has little information on the effects of phytase supplementation in disease settings. The objective of these studies was to evaluate phytase supplementation impact on bird performance, intestinal morphology and pH, nutrient digestibility and bone mineralization during necrotic enteritis (NE). In each experiment, Cobb 500 broilers were obtained from a commercial hatchery and housed in floor pens at the Virginia Tech Turkey Research Center. Birds were placed on used litter from a previous flock that had presented clinical signs of NE. Broilers were fed non-medicated diets formulated to meet NRC (1994) nutrient requirements, except for calcium and phosphorus. In the first experiment, birds began exhibiting clinical signs of NE on d 9, and elevated NE-associated mortality persisted until d 26. Mortality was influenced by the main effects of dietary Ca or phytase. Dietary Ca supplemented at 0.9% or 1000 FTU/kg of phytase increased mortality compared to 0.6% Ca or 0 FTU/kg phytase, respectively, from d 0 to 19. Feed intake (FI) and feed conversion (FC) were affected by Ca x P interaction. From d 0 to 19, birds fed 0.9% Ca and 0.3% available P (avP) had decreased FI and improved FC compared to birds fed 0.9% Ca and 0.45% avP, while FI and FC were similar in birds fed diets with 0.6% Ca, regardless of avP level. Calcium x P x phytase interaction influenced BW or BWG from d 0-12. In general, birds fed 0.9% Ca and 0.45% avP with phytase were heavier compared to birds fed 0.6% Ca, 0.45% avP, and phytase. Calcium at 0.9% increased gizzard (d 19) and jejunum (d 12) pH. Dietary Ca supplemented at 0.9%, avP supplemented at 0.45%, and 1,000 FTU/kg phytase significantly increased tibia ash weight compared to 0.6% Ca, 0.3% avP, and 0 FTU/kg phytase, respectively, on d 12. A 3-way interaction was observed on d 35 for tibia ash percentage; birds fed 0.9% Ca and 0.45% avP had a significant increase in tibia ash percentage, regardless of phytase supplementation. A 3-way interaction was also observed for Ca and P digestibility on d 35. Phytase supplementation significantly increased Ca digestibility regardless of Ca and P levels of the diets. In addition, diets containing 0.6% Ca and 1,000 FTU/Kg of phytase resulted in a significant increase in P digestibility, regardless of P levels. In the second experiment, birds also began exhibiting clinical signs of NE on d 9, and elevated NE-associated mortality persisted until the end of the trial (d 21). Mortality was significantly affected by an interaction between Ca source and Ca levels. Significantly higher mortality was observed when animals were fed 0.9% Ca diets formulated with calcified seaweed from d 0-21 compared to 0.6% Ca diets (regardless of Ca source). From d 0-7, birds fed 0.6% Ca in diets supplemented with phytase had heavier BW than the other treatments regardless of Ca source. From d 0-14 and 0-21, animals fed diets with calcified seaweed had significantly higher FC than animals fed diets with limestone. On d 21, the gizzard of birds fed 0.9% Ca was significantly less acidic than the gizzard of birds fed 0.6% Ca. In conclusion, reducing dietary levels of Ca associated with phytase supplementation improved bird performance and nutrient digestibility. In addition, these experiments indicate that Ca is an important dietary factor in the pathogenesis of NE.
Ph. D.
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Saleem, Gulbeena. "Necrotic enteritis, disease induction, predisposing factors and novel biochemical markers in broiler chickens." Thesis, University of Glasgow, 2013. http://theses.gla.ac.uk/4372/.

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Necrotic enteritis (NE) is an important enteric disease in poultry production that has re-emerged as a major problem following an EU wide ban on the use of in-feed antimicrobials. Although the primary aetiological agent of disease is Clostridium perfringens type A, a commensal in the gastrointestinal tract (GIT) of chickens, numerous additional influential factors have been reported that can predispose chickens to NE. These precipitating factors mainly include diet, co-infection with other pathogens particularly coccidia, as well as environmental and management factors. Despite being first described almost more than 50 years ago, a reliable, consistently reproducible experimental model for NE induction is still lacking. Here, a series of experiments were conducted to investigate the importance of the various potential predisposing factors, in isolation and in combination, that are believed to play a role in sub-clinical NE development: feed withdrawal, dietary protein sources, co- infection with coccidia, C. perfringens dose and contact with reused litter. In addition, chicken breed sensitivity to NE was assessed, and last, but not least, blood and gut tissue samples were used to identify novel biochemical markers for sub-clinical NE. Chapter 3 reports an experiment showing that feed withdrawal up to 24 hrs in experimentally challenged birds did not result in NE specific lesions. Chapter 4 shows that replacing dietary soyabean meal with potato protein concentrate or canola meal or adding synthetic trypsin inhibitor to the soyabean meal control diet did not induce sub-clinical NE in birds housed on reused litter, a natural source of C. perfringens challenge. Chapter 5 describes that in vitro growth of C. perfringens on in vitro digested grower diets was prolonged following the addition of fishmeal, suggesting that the role of fish meal as a predisposing factor for in vivo sub-clinical NE cannot be excluded. All subsequent diets therefore contained high levels of fish meal. When this was used in combination with high dose of coccidial vaccine, a repeated in-feed challenge for three days at 102 colony forming units (cfu) C. perfringens per g feed did not result in sub-clinical NE, though at 109 cfu/g resulted in 10% of challenged birds (3 out of 30) showing NE-specific lesions (Chapter 6). Further study is needed to determine if the two Ross birds with gross NE lesions compared to the one Hubbard bird (out of 15 birds each) was due to a lower level of NE resistance. 3 The failure to significantly induce sub-clinical NE in the previous experiments suggests that challenging the birds with C. perfringens in the isolated presence of suspected predisposing factors may not provide a suitable experimental model. Indeed, when birds were dosed twice daily with 108 cfu C. perfringens for three days in the presence of high levels of fishmeal, canola meal as main protein source, coccidial and IBD vaccinations, and feed withdrawal prior to challenge, 40.6% of the challenged birds developed lesions of sub-clinical NE without inducing mortality (Chapter 7). This concurred with reduced growth performance relative to the sham-infected control birds, and thus is a successful model for induction of sub-clinical NE. Finally this work has, for the first time provided novel information on potential biomarkers (Chapter 8). Whilst challenge did not impact on the expression of genes previously shown to be differentially expressed upon C. perfringens toxin exposure, the serum ceruloplasmin concentration increased, suggesting that monitoring this acute phase protein may indicate the presence of C. perfringens infection in poultry. However, as such markers generally lack specificity, further research confirming its role in response to sub-clinical NE is needed to provide a fully effective diagnostic and prognostic marker for flock health and welfare, as well as ultimately helping to gain better understanding of the pathophysiology of sub-clinical NE. Improved knowledge of the effect of different dietary components on the growth of C. perfringens may help in the formulation of broiler diets to assist in further reducing the incidence of NE particularly in the absence of antimicrobial growth promoters. It is hoped that host responses in terms of acute phase proteins, and possibley gene expression, will also provide greater insight into the pathogenesis of NE. Provided that the developed experimental sub-clinical NE model is reproducible, this will benefit the understanding of this billion dollar disease and enable further investigation of various chemical and non-chemical interventions to reduce its severity and impact on poultry production.
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McReynolds, Jackson Lee. "The effects of an experimental chlorate product on the microbial ecology in Gallus gallus var. domesticus." Diss., Texas A&M University, 2004. http://hdl.handle.net/1969.1/544.

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Previous reports have shown that some bacteria utilize a dissimilatory nitrate reductase enzyme (NR) in anaerobic environments. This enzyme reduces nitrate to nitrite and also has been shown to co-metabolize chlorate to cytotoxic chlorite. A commercially available competitive exclusion (CE) product was evaluated for its nitrate reductase activity and therefore its experimental chlorate product (ECP) sensitivity. Of the 29 constituent bacteria of the CE culture, 11 had slight utilization of NR, 3 had moderate utilization of NR; the remaining were NR negative (with slight and moderate utilization: >0.1 to < 1.0 mM and > 1.0 mM nitrate utilized within 6 h, respectively). In vivo studies utilizing CE and ECP showed significant reductions in Salmonella. Although some of the bacteria were affected by ECP, the combined effect of the CE culture and ECP were effective in reducing Salmonella. Clostridium perfringens (CP) is a pathogen in the commercial poultry industry, which is the etiologic agent of necrotic enteritis (NE). Day-of-hatch broilers were fed a wheat diet and assigned to the following groups: control, commercial coccidia vaccine, commercial bursal disease vaccine, or the combination of the two, and challenged with CP in order to develop a disease model. Broilers in each treatment group had significant increases (P≤ 0.05) in lesion scores, mortality, and CP incidence. As pressure mounts for discontinuing the use of antibiotics in the agriculture industry, it is important to develop new strategies to combat these costly enteric pathogens. In vitro investigations evaluated a mixed gut culture with CP and the ECP at 5 mM or a 10 mM concentrations, over time. By 3 h there was a reduction (P≤ 0.05) in the 5 mM ECP and 10 mM ECP treatment groups. In vivo studies showed significant reductions in the incidence of CP and populations of intrinsic E. coli in all of the chickens provided ECP in the drinking water. Birds administered ECP in the feed showed significant reductions in lesion scores, incidence of CP and also had reduced E. coli log10 values. These results show that an ECP could provide the industry with a new management tool for controlling NE.
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Eswaran, Jeyanthy. "Purification and characterisation of recombinant C. perfringens beta toxin from E. coli and B. subtilis." Thesis, University of Newcastle Upon Tyne, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.341444.

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Cartman, Stephen Thomas. "Oral administration of 'Baciilus subtilis' spores for prophylactic control of 'Clostridium perfringens' associated necrotic enteritis in poultry." Thesis, Royal Holloway, University of London, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.434372.

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Sumners, Lindsay Hart. "Immunological Response to Clostridium perfringens in Two Genetically Divergent Lines of Chickens as Influenced by Major Histocompatibility Complex (MHC) Genotype." Thesis, Virginia Tech, 2011. http://hdl.handle.net/10919/43370.

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Chickens genetically selected for low (LA) or high (HA) antibody response to sheep red blood cells (SRBC) displayed a correlated change in major histocompatibility complex (MHC), so that LA chickens were 96% B13 and HA chickens were 96% B21. During a clinical outbreak of necrotic enteritis, B21B21 genotypes experienced significantly less mortality (6% vs. 13 %) compared to B13B13 genotypes. A study was carried out to assess immunological differences between LA and HA lines during exposure to Clostridium perfringens. In Experiment 1, chickens were orally gavaged with a low (10^7 CFU/mL) or high (10^9 CFU/mL) dose of C. perfringens. In Experiment 2, chickens were orally gavaged with live coccidia oocysts on experiment d 1, followed by 107 CFU/mL C. perfringens on d 5. Unfortunately, establishment of necrotic enteritis infection was unsuccessful in both experiments as evidenced by lack of significant intestinal lesions, as well as no negative effect on bird performance. In an ex vivo study, peripheral blood mononuclear cells (PBMCs) were isolated from each genetic line, cultured, stimulated with LPS (4 h), and exposed to varying concentrations of C. perfringens α- toxin (1, 10, 100, 1000 U/L) for 2 and 4 h. Evaluation of cellular proliferation, percent cytotoxicity and immunological gene expression was carried out in a variety of experiments. Genetic lines were found to be highly divergent in all analyses.
Master of Science
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Chasser, Kaylin M. "Impact of necrotic enteritis on the growth curve and the evaluation of test parameters for measuring coccidial infection." The Ohio State University, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=osu1523281345700585.

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Books on the topic "Necrotic enteritis"

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N. Liu, J.Q. Wang, Z.Y. Liu, Y.K. Chen, and J.P. Wang. Tetramethylpyrazine attenuates necrotic enteritis by reducing gut oxidative stress, inflammation, opportunistic bacteria and endotoxins in broilers. Verlag Eugen Ulmer, 2018. http://dx.doi.org/10.1399/eps.2018.233.

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Book chapters on the topic "Necrotic enteritis"

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Cooper, Kerry K., and J. Glenn Songer. "Necrotic Enteritis of Poultry." In Clostridial Diseases of Animals, 123–37. Hoboken, NJ: John Wiley & Sons, Inc, 2016. http://dx.doi.org/10.1002/9781118728291.ch10.

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Flores-Díaz, M., E. Barquero-Calvo, M. Ramírez, and A. Alape-Girón. "Role of Clostridium perfringens Toxins in Necrotic Enteritis in Poultry." In Microbial Toxins, 1–16. Dordrecht: Springer Netherlands, 2016. http://dx.doi.org/10.1007/978-94-007-6725-6_15-1.

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Flores-Díaz, M., E. Barquero-Calvo, M. Ramírez, and A. Alape-Girón. "Role of Clostridium perfringens Toxins in Necrotic Enteritis in Poultry." In Toxinology, 119–34. Dordrecht: Springer Netherlands, 2018. http://dx.doi.org/10.1007/978-94-007-6449-1_15.

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Reports on the topic "Necrotic enteritis"

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van Krimpen, Marinus, David Lamot, Ralph Kok, Arjan Hoekman, Marcel Hulst, Alex Bossers, Annemarie Rebel, Mari Smits, and Dirkjan Schokker. Nutritional interventions to modulate immune competence in broilers and correlation to quantitative disease phenotype after Necrotic enteritis challenge. Wageningen: Wageningen Livestock Research, 2017. http://dx.doi.org/10.18174/428321.

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