Haemorrhagic-necrotic enteritis in heavy breeds broilers

Abstract

Ispitivanja su imala za cilj da se utvrdi uticaj Clostridium perfringens tip A na razvoj patomorfološkog supstrata, njegov intenzitet i distribuciju kod teških roditelja uzrasta petnaest nedelja. Ispitivanje je obavljeno na leševima 8 koka i 7 petlova teških roditelja provenijencije COBB 500. Posle izvršene obdukcije, za histopatološko ispitivanje uzeti su uzorci promenjenih delova jejunuma i jetre, a za bakteriološko i molekularno ispitivanje crevni sadržaj jejunuma. Kod svih leševa u otvorenoj pleuroperitonealnoj šupljini, već in situ, uočava se promenjeni deo jejunuma. On je bio izrazito dilatiran celom dužinom, a njegov zid plavičasto-sive boje sa diseminiranim subseroznim punktiformnim krvnim ekstravazatima. Njegovim otvaranjem iz lumena je izlazio polutečni sadržaj u kojem plivaju krvni koagulumi i krpičasti delovi nekrotične mukoze. Mikroskopskim pregledom isečaka tkiva tankih creva bojenih HE metodom zapažena je difuzna nekroza crevnih resica. One su destruisane i zamenjene eozinofilnom bestrukturnom masom. Pored toga, uočava se edem submukoze, kongestija kapilara i krvni ekstravazati u mukozi, kao i infiltracija neutrofilnih granulocita u lamini propriji. Navedene mikroskopske alteracije oslikavaju hemoragično-nekrotični enteritis. Mikroskopskim pregledom isečka tankih creva bojenih Brown & Brenn metodom ustanovljene su kolonije bakterija u distalnim delovima submukoze. Bakteriološkim ispitivanjem u anaerobnim uslovima, izolovana kultura je identifikovana kao Clostridium perfringens. Primenom multiplex PCR dobijeni izolat je genotipiziran kao Clostridium perfringens tip A. Na osnovu patomorfoloških, bakterioloških i molekularnih ispitivanja može da se zaključi da infekcija teških roditelja Clostridium perfringens tipa A protiče sa slikom difuznog hemoragično-nekrotičnog jejunitisa, da uzročnik duboko penetrira u tkivo jejunuma i da su pšenica i pšenične mekinje činili favorizujući faktor za proliferaciju etiološkog agensa.

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.