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Journal articles on the topic 'Necrotic enteritis'

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Published: 4 June 2021

Last updated: 19 February 2022

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1

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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2

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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3

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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4

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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5

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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6

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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7

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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8

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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9

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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10

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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11

Wobeser, G., and D. J. Rainnie. "EPIZOOTIC NECROTIC ENTERITIS IN WILD GEESE." Journal of Wildlife Diseases 23, no. 3 (July 1987): 376–85. http://dx.doi.org/10.7589/0090-3558-23.3.376.

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12

Antonissen, Gunther, Venessa Eeckhaut, Karolien Van Driessche, Lonneke Onrust, Freddy Haesebrouck, Richard Ducatelle, Robert J. Moore, and Filip Van Immerseel. "Microbial shifts associated with necrotic enteritis." Avian Pathology 45, no. 3 (May 3, 2016): 308–12. http://dx.doi.org/10.1080/03079457.2016.1152625.

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13

Shane, S. M., J. E. Gyimah, K. S. Harrington, and T. G. Snider. "Etiology and pathogenesis of necrotic enteritis." Veterinary Research Communications 9, no. 1 (December 1985): 269–87. http://dx.doi.org/10.1007/bf02215151.

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14

Jezdimirovic, Nemanja, Branislav Kureljusic, Vojin Ivetic, Jasna Kureljusic, Dj Cvetojevic, Danka Maslic-Strizak, O. Radanovic, and Milanka Jezdimirovic. "Haemorrhagic-necrotic enteritis in heavy breeds broilers." Veterinarski glasnik 68, no. 3-4 (2014): 265–73. http://dx.doi.org/10.2298/vetgl1404265j.

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The aim of the investigation was to determine the influence of Clostridium perfringens type A on the development of pathomorphological substrate, its intensity and distribution in fifteen weeks old heavy breeds broilers. The investigation was carried out on corpses of 8 hens and 7 roosters of heavy breeds of provenance COBB 500. After the completion of the autopsy, samples of altered parts of jejunum and liver were taken for histopathological examination, and jejunum intestinal contents for bacteriological examination. In all the corpses, in open pleuroperitoneal cavity, even in situ, an altered part of jejunum can be noticed. It was extremely dilated the entire length, and its wall was bluish-gray with disseminated subserous punctiform blood extravasates. When opened, semi-liquid content with blood coagulums and patches of necrotic mucosa went out of it. By microscopic examination of small intestine tissue cuttings, colored by HE method, there was observed a diffuse necrosis of intestinal villi. They were desroyed and replaced by eosinophilic structureless mass. Furthermore, there could be noticed submucose oedema, capillary congestion and blood extravasates in mucosa, as well as infiltration of neutrophilic granulocytes in lamina propria. These microscopic alterations reflect hemorrhagic necrotic enteritis. By microscopic examining of small intestine cuttings colored according to Brown & Brenn method, colonies of bacteria in distal parts of the submucosa were found out. Using bacteriological tests in anaerobic conditions, there was isolated a culture identified as Clostridium perfringens. After applying of multiplex PCR, the obtained isolate was genotyped as Clostridium perfringens type A. On the basis of pathomorphological, bacteriological and molecular examinations, it can be concluded that the infection of heavy breeds with Clostridium perfringens type A is manifested by appearance of haemorrhagic-necrotic jejunitis, that the causer penetrates deeply into jejunum tissue and that wheat and wheat bran were a favoring factor for proliferation of the etiological agent.

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15

Barbara, Angelique J., Hien T. Trinh, Robert D. Glock, and J. Glenn Songer. "Necrotic enteritis-producing strains of Clostridium perfringens displace non-necrotic enteritis strains from the gut of chicks." Veterinary Microbiology 126, no. 4 (January 2008): 377–82. http://dx.doi.org/10.1016/j.vetmic.2007.07.019.

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16

Paiva, Diego, and Audrey McElroy. "Necrotic enteritis: Applications for the poultry industry." Journal of Applied Poultry Research 23, no. 3 (September 2014): 557–66. http://dx.doi.org/10.3382/japr.2013-00925.

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17

Rimoldi, Guillermo, Francisco Uzal, R. P. Chin, Enzo A. Palombo, Milena Awad, Dena Lyras, and H. L. Shivaprasad. "Necrotic Enteritis in Chickens Associated withClostridium sordellii." Avian Diseases 59, no. 3 (September 2015): 447–51. http://dx.doi.org/10.1637/11077-033115-case.1.

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18

Moore, Robert J. "Necrotic enteritis predisposing factors in broiler chickens." Avian Pathology 45, no. 3 (May 3, 2016): 275–81. http://dx.doi.org/10.1080/03079457.2016.1150587.

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19

Dierick, E., O. P. Hirvonen, F. Haesebrouck, R. Ducatelle, F. Van Immerseel, and E. Goossens. "Rapid growth predisposes broilers to necrotic enteritis." Avian Pathology 48, no. 5 (June 9, 2019): 416–22. http://dx.doi.org/10.1080/03079457.2019.1614147.

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20

El-Sergany, Elham, El-Helw Hamed, Hala El-Sawy, Taha Medhat, and Abdalla Yasser. "Preparation of Necrotic Enteritis Vaccine for Turkey." Journal of World's Poultry Research 9, no. 2 (June 25, 2019): 109–16. http://dx.doi.org/10.36380/jwpr.2019.13.

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21

Keyburn, Anthony L, Scott A. Sheedy, Mark E. Ford, Mark M. Williamson, Milena M. Awad, Julian I. Rood, and Robert J. Moore. "Alpha-Toxin of Clostridium perfringens Is Not an Essential Virulence Factor in Necrotic Enteritis in Chickens." Infection and Immunity 74, no. 11 (August 21, 2006): 6496–500. http://dx.doi.org/10.1128/iai.00806-06.

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ABSTRACT The Clostridium perfringens alpha-toxin has previously been implicated as the major virulence factor in necrotic enteritis in chickens, although definitive proof has not been reported. In this study an alpha-toxin mutant was constructed in a virulent chicken isolate and shown to retain full virulence in a chicken disease model. These results demonstrated that alpha-toxin is not an essential virulence factor in the pathogenesis of necrotic enteritis in chickens.

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22

Abubakar, A., H. B. Aliyu, L. Sa idu, and S. G. Usman. "Necrotic enteritis and its management in 13-week old commercial pullets in Katsina, Nigeria." Sokoto Journal of Veterinary Sciences 18, no. 2 (September 9, 2020): 104–7. http://dx.doi.org/10.4314/sokjvs.v18i2.7.

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Necrotic enteritis is rarely reported because it is often misdiagnosed as coccidiosis due to similarity in clinical and pathological features. A field outbreak of necrotic enteritis in a flock of 13 weeks old 4,500 commercial pullets was investigated, the onset of the disease, morbidity and mortality rates were recorded. Post mortem examinations were conducted and gross lesions were documented. Tissues were collected and fixed in 10 % neutral buffered formalin and processed for histopathological examinations. Clinical signs observed were ruffled feathers, weakness, somnolence, loss of weight and diarrhoea; while the gross lesions observed were emaciated carcasses, lean abdominal fat, enlarged, pale and haemorrhagic liver; enlarged, mottled and congested spleen; mucus and diphtheritic membrane on the jejunal mucosa and enlarged kidneys. The histopathological findings of the intestine were diffused necrotic epithelial cells with marked mononuclear cells infiltration in the mucosa with severe oedema fluid. The necrotic enteritis was diagnosed based on clinical signs, pathology as well as isolation and identification of Clostridium perfringes. Triplesulfa® (sulfadimidine sodium, sulfadiazine sodium and sulfamerazine sodium); Tridox® L.A (20% Oxytetracycline long acting) and Enterocillin® (Amoxycillintrihydrate and Colistin sulphate) were ineffective, while copper sulphate at 1g/5L of drinking water was found to be effective for the treatment of the disease. The haematological values indicated lymphocytosis due to damage of the tissue caused by C. perfringes and the toxins produced. Keywords: Necrotic enteritis, Commercial pullets, Copper sulphate, Clostridium perfringens

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23

Matsushita, S., and T. Matsumoto. "Spontaneous necrotic enteritis in young RFM/Ms mice." Laboratory Animals 20, no. 2 (April 1, 1986): 114–17. http://dx.doi.org/10.1258/002367786780865124.

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Fatal necrotic enteritis was observed in mice 24-52 days old in the RFM/Ms breeding colony maintained in a clean conventional condition in the National Institute of Radiological Sciences. Gross lesions included hyperaemia, petechiae, erosion and the occasional formation of pseudomembranes in the mucosa of the ileum and caecum. Histologically, there was necrotic enteritis with numerous Gram-positive bacilli-forming spores but no inflammatory cell reaction. Non-type-A Clostridium perfringens was isolated from the intestinal contents. This disease cleared after the addition of chlortetracycline hydrochloride (11 mg/I) to the drinking water.

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24

Keerqin, C., N. K. Morgan, S. B. Wu, B. Svihus, and M. Choct. "Reintroduction of microflora from necrotic enteritis-resistant chickens reduces gross lesions and improves performance of necrotic enteritis-challenged broilers." Journal of Applied Poultry Research 26, no. 3 (September 2017): 449–57. http://dx.doi.org/10.3382/japr/pfx015.

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25

Asaduzzaman, M., MS Miah, A. Siddika, N. Popy, and MM Hossain. "EXPERIMENTAL PRODUCTION OF NECROTIC ENTERITIS IN BROILER CHICKENS." Bangladesh Journal of Veterinary Medicine 9, no. 1 (July 12, 2012): 33–41. http://dx.doi.org/10.3329/bjvm.v9i1.11207.

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The present study was conducted to isolate and identify the Clostridium perfringens, the etiology of necrotic enteritis (NE) from broiler chickens and experimental production of NE with this isolate. A total of 50 samples were collected from jejunum of necropsied birds for isolation and identification of Cl. perfringens. Out of 50 samples, only 4 isolates of Cl. perfringens were isolated and identified (prevalence 8%). In experimental NE, the birds of group A (orally administered with only 0.1 ml (1x103 sporulated Eimeria acervulina oocysts/bird) showed dullness, ruffled feather, vent feather soiled with bloody faeces after 1 week of coccidial challenge. The birds of group B (orally administered 1x103 sporulated Eimeria acervulina oocysts/bird and 1 ml of 2 days old broth culture of Cl. perfringens) showed severe depression, ruffled feathers, bloody faeces with fibrinous cast with 80% prevalence rate and 30% mortality in experimental NE. The birds of group C (orally inoculated with 1 ml of 2 days old broth culture of Cl. perfringens) showed no striking clinical, gross and histopathological lesions. Postmortem changes in small intestine (duodenum) were congestion and haemorrhages specially for birds of group A. The most severe gross lesions comprised of ascites, enlarged liver and heart, intestinal distension, profuse haemorrhage, fibrinous cast, fragile intestinal wall and gas bubble formation in the small intestine (duodenum, jejunum and ileum) of birds of group B. Histologically, birds of group B showed hemorrhage and congestion in liver, heart and intestine, desquamation of intestinal epithelium and intense leukocytic infiltration in intestine, liver and heart. The findings obtained from this study showed that simultaneous coccidial infection enhanced the pathological lesions of NE. DOI = http://dx.doi.org/10.3329/bjvm.v9i1.11207Bangl. J. Vet. Med. (2011). 9(1): 3341

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26

Aoyama, Hiroki, Norihiro Yuasa, Eiji Takeuchi, Yasutomo Goto, Hideo Miyake, Hidemasa Nagai, Masaoki Hattori, Kanji Miyata, and Masahiko Fujino. "Repeated Necrotic Ischemic Enteritis with Portal Venous Gas." Japanese Journal of Gastroenterological Surgery 48, no. 1 (2015): 38–45. http://dx.doi.org/10.5833/jjgs.2014.0071.

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27

Broom, L. J. "Necrotic enteritis; current knowledge and diet-related mitigation." World's Poultry Science Journal 73, no. 2 (June 1, 2017): 281–92. http://dx.doi.org/10.1017/s0043933917000058.

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28

Simpson, V., M. Cranwell, C. Johnson, D. Dyson, and J. Gibbens. "Necrotic enteritis of unknown aetiology in suckler calves." Veterinary Record 134, no. 18 (April 30, 1994): 479. http://dx.doi.org/10.1136/vr.134.18.479.

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29

Lovland, Atle, Magne Kaldhusdal, Keith Redhead, Eystein Skjerve, and Atle Lillehaug. "Maternal vaccination against subclinical necrotic enteritis in broilers." Avian Pathology 33, no. 1 (February 2004): 81–90. http://dx.doi.org/10.1080/0379450310001636255.

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30

Knap, I., B. Lund, A. B. Kehlet, C. Hofacre, and G. Mathis. "Bacillus licheniformis Prevents Necrotic Enteritis in Broiler Chickens." Avian Diseases 54, no. 2 (June 2010): 931–35. http://dx.doi.org/10.1637/9106-101509-resnote.1.

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31

Knap, I., B. Lund, A. B. Kehlet, C. Hofacre, and G. Mathis. "Bacillus licheniformis Prevents Necrotic Enteritis in Broiler Chickens." Avian Diseases Digest 5, no. 2 (June 2010): e45-e45. http://dx.doi.org/10.1637/9355-910610-digest.1.

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32

Broussard, C. T., C. L. Hofacre, R. K. Page, and O. J. Fletcher. "Necrotic Enteritis in Cage-Reared Commercial Layer Pullets." Avian Diseases 30, no. 3 (July 1986): 617. http://dx.doi.org/10.2307/1590433.

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33

Rood, Julian I., Anthony L. Keyburn, and Robert J. Moore. "NetB and necrotic enteritis: the hole movable story." Avian Pathology 45, no. 3 (May 3, 2016): 295–301. http://dx.doi.org/10.1080/03079457.2016.1158781.

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34

Milanov, Dubravka, Nevenka Aleksić, Milica Živkov Baloš, Marko Pajić, and Slobodan Knežević. "CURRENTLY UNKNOWN ASPECTS OF POULTRY NECROTIC ENTERITIS PATHOGENESIS." Archives of Veterinary Medicine 12, no. 1 (September 12, 2019): 55–69. http://dx.doi.org/10.46784/e-avm.v12i1.38.

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Necrotic enteritis (NE) or poultry clostridiosis is a disease which poses enormous health problems and makes tremendous economic losses to intensive poultry production worldwide. Despite having been targeted in extensive research for decades, a number of aspects of its pathogenesis remain unknown. For more than 30 years alfa-toxin has been considered to be the main virulence factor of the causative agent, but experimental research using a mutant Clostridium perfringens strain lacking the gene coding for this confirmed that alpha-toxin is not necessary for pathogenesis. Since the 1980s, NetB toxin has been the main suspected virulence factor. However, recently it has been discovered that the large clostridial cytotoxin named TpeL also contributes to the pathogenesis of NE. In spite of that, the prevalence of the genes which code for these toxins vary between the isolates of C. perfringens from the intestines of diseased poultry, which made clear that further investigation into their roles is necessary. It has been agreed that specific intestinal environmental conditions, which favour the growth and multiplication of C. perfringens, are key factors to the emergence of disease. Given that a battery of non-specific factors contributes to pathogenesis, as well as that it is impossible to eliminate them in intensive poultry production, not much hope remains that NE can be controlled. In this short review, the current knowledge on the pathogenesis of NE has been summarized.

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35

Bansal, Mohit, Tahrir Alenezi, Ying Fu, Ayidh Almansour, Hong Wang, Anamika Gupta, Rohana Liyanage, Danielle B. Graham, Billy M. Hargis, and Xiaolun Sun. "Specific Secondary Bile Acids Control Chicken Necrotic Enteritis." Pathogens 10, no. 8 (August 17, 2021): 1041. http://dx.doi.org/10.3390/pathogens10081041.

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Necrotic enteritis (NE), mainly induced by the pathogens of Clostridium perfringens and coccidia, causes huge economic losses with limited intervention options in the poultry industry. This study investigated the role of specific bile acids on NE development. Day-old broiler chicks were assigned to six groups: noninfected, NE, and NE with four bile diets of 0.32% chicken bile, 0.15% commercial ox bile, 0.15% lithocholic acid (LCA), or 0.15% deoxycholic acid (DCA). The birds were infected with Eimeria maxima at day 18 and C. perfringens at day 23 and 24. The infected birds developed clinical NE signs. The NE birds suffered severe ileitis with villus blunting, crypt hyperplasia, epithelial line disintegration, and massive immune cell infiltration, while DCA and LCA prevented the ileitis histopathology. NE induced severe body weight gain (BWG) loss, while only DCA prevented NE-induced BWG loss. Notably, DCA reduced the NE-induced inflammatory response and the colonization and invasion of C. perfringens compared to NE birds. Consistently, NE reduced the total bile acids in the ileal digesta, while dietary DCA and commercial bile restored it. Together, this study showed that DCA and LCA reduced NE histopathology, suggesting that secondary bile acids, but not total bile acid levels, play an essential role in controlling the enteritis.

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36

Cravens, R. L., G. R. Goss, F. Chi, E. D. De Boer, S. W. Davis, S. M. Hendrix, J. A. Richardson, and S. L. Johnston. "The effects of necrotic enteritis, aflatoxin B1, and virginiamycin on growth performance, necrotic enteritis lesion scores, and mortality in young broilers." Poultry Science 92, no. 8 (August 2013): 1997–2004. http://dx.doi.org/10.3382/ps.2013-03011.

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37

Yang, Qing, Melanie A. Whitmore, Kelsy Robinson, Wentao Lyu, and Guolong Zhang. "Butyrate, Forskolin, and Lactose Synergistically Enhance Disease Resistance by Inducing the Expression of the Genes Involved in Innate Host Defense and Barrier Function." Antibiotics 10, no. 10 (September 27, 2021): 1175. http://dx.doi.org/10.3390/antibiotics10101175.

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The rising concern of antimicrobial resistance highlights a need for effective alternatives to antibiotics for livestock production. Butyrate, forskolin, and lactose are three natural products known to induce the synthesis of host defense peptides (HDP), which are a critical component of innate immunity. In this study, the synergy among butyrate, forskolin, and lactose in enhancing innate host defense, barrier function, and resistance to necrotic enteritis and coccidiosis was investigated. Our results indicated that the three compounds synergistically augmented the expressions of multiple HDP and barrier function genes in chicken HD11 macrophages. The compounds also showed an obvious synergy in promoting HDP gene expressions in chicken jejunal explants. Dietary supplementation of a combination of 1 g/kg sodium butyrate, 10 mg/kg forskolin-containing plant extract, and 10 g/kg lactose dramatically improved the survival of chickens from 39% to 94% (p < 0.001) in a co-infection model of necrotic enteritis. Furthermore, the three compounds largely reversed growth suppression, significantly alleviated intestinal lesions, and reduced colonization of Clostridium perfringens or Eimeria maxima in chickens with necrotic enteritis and coccidiosis (p < 0.01). Collectively, dietary supplementation of butyrate, forskolin, and lactose is a promising antibiotic alternative approach to disease control and prevention for poultry and possibly other livestock species.

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38

., Simon M. Shane. "Re-Emergence of Necrotic Enteritis in the Broiler Industry." International Journal of Poultry Science 4, no. 9 (August 15, 2005): 604–11. http://dx.doi.org/10.3923/ijps.2005.604.611.

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39

Hermans, P. G., and K. L. Morgan. "57. The epidemiology of necrotic enteritis in broiler chickens." Research in Veterinary Science 74 (2003): 19. http://dx.doi.org/10.1016/s0034-5288(03)90056-7.

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40

shanmugasamy, Malmarugan, Boobalan Adhimoolam, and Dorairajan Natarajan. "Necrotic Enteritis in Broiler and Layer Farms in Tamilnadu." International Journal for Agro Veterinary and Medical Sciences 6, no. 4 (2012): 241. http://dx.doi.org/10.5455/ijavms.126.

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41

Kurkure, N. V., S. B. Kale, R. T. Kale, S. P. Awandkar, and N. N. Joat. "Occurrence of necrotic enteritis in a commercial layer flock." Indian Journal of Veterinary Pathology 41, no. 1 (2017): 50. http://dx.doi.org/10.5958/0973-970x.2017.00011.6.

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42

Behera, Debasish, D. C. Pathak, R. K. Sharma, T. N. Upadhyaya, S. Goswami, and S. Tamuly. "Pathology and molecular diagnosis of necrotic enteritis in chicken." Indian Journal of Veterinary Pathology 44, no. 1 (2020): 22. http://dx.doi.org/10.5958/0973-970x.2020.00005.x.

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43

Mcdevitt, R. M., J. D. Brooker, T. Acamovic, and N. H. C. Sparks. "Necrotic enteritis; a continuing challenge for the poultry industry." World's Poultry Science Journal 62, no. 2 (June 1, 2006): 221–47. http://dx.doi.org/10.1079/wps200593.

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Asaoka, Yoshiji, Tokuma Yanai, Haruko Hirayama, Yumi Une, Eriko Saito, Hiroki Sakai, Masanobu Goryo, Hideto Fukushi, and Toshiaki Masegi. "Fatal necrotic enteritis associated withClostridium perfringensin wild crows (Corvusmacrorhynchos)." Avian Pathology 33, no. 1 (February 2004): 19–24. http://dx.doi.org/10.1080/03079450310001636228.

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Tsiouris, V., I. Georgopoulou, Chr Batzios, N. Pappaioannou, R. Ducatelle, and P. Fortomaris. "Temporary feed restriction partially protects broilers from necrotic enteritis." Avian Pathology 43, no. 2 (February 28, 2014): 139–45. http://dx.doi.org/10.1080/03079457.2014.889278.

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Prescott, John F., Joan A. Smyth, Bahram Shojadoost, and Andrew Vince. "Experimental reproduction of necrotic enteritis in chickens: a review." Avian Pathology 45, no. 3 (May 3, 2016): 317–22. http://dx.doi.org/10.1080/03079457.2016.1141345.

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Marshall, R. N., R. B. Williams, R. M. La Ragione, J. A. Marshall, and J. Catchpole. "102. Experimental production of necrotic enteritis and its use for studies on the relationships between necrotic enteritis, coccidiosis and anticoccidial vaccination of chickens." Research in Veterinary Science 74 (2003): 34. http://dx.doi.org/10.1016/s0034-5288(03)90101-9.

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Wade, Ben, Anthony L. Keyburn, Volker Haring, Mark Ford, Julian I. Rood, and Robert J. Moore. "Two putative zinc metalloproteases contribute to the virulence of Clostridium perfringens strains that cause avian necrotic enteritis." Journal of Veterinary Diagnostic Investigation 32, no. 2 (January 10, 2020): 259–67. http://dx.doi.org/10.1177/1040638719898689.

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Abstract:

Two putative zinc metalloproteases encoded by Clostridium perfringens have been implicated in the pathogenesis of necrotic enteritis, an economically significant poultry disease that is caused by this anaerobic bacterium. These proteases have ~64% amino acid identity and are encoded by the zmpA and zmpB genes. We screened 83 C. perfringens isolates by PCR for the presence of these genes. The first gene, zmpB, is chromosomally located and was present in all screened strains of C. perfringens, regardless of their origin and virulence. The second gene, zmpA, is plasmid-borne and was only found in isolates derived from chickens with necrotic enteritis. We describe the generation of insertionally inactivated mutants of both zmpA and zmpB in a virulent C. perfringens isolate. For each mutant, a significant ( p < 0.001) reduction in virulence was observed in a chicken necrotic enteritis disease model. Examples of each mutant strain were characterized by whole genome sequencing, which showed that there were a few off-site mutations with the potential to affect the virulence of these strains. To confirm the importance of these genes, independently derived zmpA and zmpB mutants were constructed in different virulent C. perfringens isolates and shown to have reduced virulence in the experimental disease induction model. A zmpA–zmpB double mutant also was generated and shown to have significantly reduced virulence, to the same extent as the respective single mutants. Our results provide evidence that both putative zinc metalloproteases play an important role in disease pathogenesis.

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Das, Arunava, Yahya Mazumder, Biman Kumar Dutta, Bibek Ranjan Shome, Komal Molla Bujarbarua, and Ashok Kumar. "Clostridium perfringens Type A from Broiler Chicken with Necrotic Enteritis." International Journal of Poultry Science 7, no. 6 (May 15, 2008): 601–9. http://dx.doi.org/10.3923/ijps.2008.601.609.

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Kulkarni, R. R., V. R. Parreira, S. Sharif, and J. F. Prescott. "Immunization of Broiler Chickens against Clostridium perfringens-Induced Necrotic Enteritis." Clinical and Vaccine Immunology 14, no. 9 (July 18, 2007): 1070–77. http://dx.doi.org/10.1128/cvi.00162-07.

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ABSTRACT Necrotic enteritis (NE) in broiler chickens is caused by Clostridium perfringens. Currently, no vaccine against NE is available and immunity to NE is not well characterized. Our previous studies showed that immunity to NE followed oral infection by virulent rather than avirulent C. perfringens strains and identified immunogenic secreted proteins apparently uniquely produced by virulent C. perfringens isolates. These proteins were alpha-toxin, glyceraldehyde-3-phosphate dehydrogenase, pyruvate:ferredoxin oxidoreductase (PFOR), fructose 1,6-biphosphate aldolase, and a hypothetical protein (HP). The current study investigated the role of each of these proteins in conferring protection to broiler chickens against oral infection challenges of different severities with virulent C. perfringens. The genes encoding these proteins were cloned and purified as histidine-tagged recombinant proteins from Escherichia coli and were used to immunize broiler chickens intramuscularly. Serum and intestinal antibody responses were assessed by enzyme-linked immunosorbent assay. All proteins significantly protected broiler chickens against a relatively mild challenge. In addition, immunization with alpha-toxin, HP, and PFOR also offered significant protection against a more severe challenge. When the birds were primed with alpha-toxoid and boosted with active toxin, birds immunized with alpha-toxin were provided with the greatest protection against a severe challenge. The serum and intestinal washings from protected birds had high antigen-specific antibody titers. Thus, we conclude that there are certain secreted proteins, in addition to alpha-toxin, that are involved in immunity to NE in broiler chickens.

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