الفهرس 
AcknowledgmentOnly 14 pages are availabe for public view
 |  | from | 253 |  |  |
| | | from | 253 | | |
Abstract
In this study some enteritis causes in cattle and buffaloes were detected. A total of 100 animals (39 cattle and 61 buffaloes) of different ages, sexes and breeds were examined during a period of 25 months from March 2014 to April 2016. The survey included either necropsied recently died cattle at dairy farms of Dakahlia province with a history of enteritis and diarrhea or those slaughtered at the regional slaughter houses and showed lesions of enteritis. Ages of the animals ranged from 1 day up to 6 years. Tissue specimens were collected from small intestine and mesenteric lymph nodes of slaughtered and necropsied cattle and buffalo showing gross lesion of enteritis and lymphadenitis. Each tissue specimen was divided into two portions. The first portion was immediately fixed in 10% neutral buffered formalin for histopathological examination. The second portion was held at -4 °C for bacterial isolation to identify the causative agents. Blood samples were collected from suspected cattle to be infected with john’s disease to be examined by ELISA for detection of antibodies against MAP. Results: Out of one hundred cattle affected with enteritis, 65 cases (65%) revealed bacterial infection (7 cases of them caused by MAP and 58 cases caused by other bacteria). 19 animals were infected by mixed bacteria. Infection with E.coli + proteus was found in 12 cases (12%), E.coli + klebsiella was found in 4 cases (4%) and E.coli + salmonella was found in 3 cases (3%), 1 case (1%) showed viral infection and the remaining 34 cases (34%) revealed parasitic and protozoal infestation.The main microscopic lesions seen in MAP infection were of granulomatous enteritis in the intestinal mucosa and submucosa with marked cellular infiltrations. By using ZN stain, acid-fast rods were seen scattered within the cytoplasm of the macrophages. In cases of salmonella infection the main microscopic lesions were atrophied, blunted and fused of villi, extensive necrosis of the surface epithelium of villi and exfoliation in the intestinal lumen admixed with minute hemorrhages, fibrin and variable numbers of neutrophils, macrophages, and lymphocytes. In cases of E. coli infection the lesions detected were classified according to the ages of infected cases into two categories cases infected with E.coli and less than 3 weeks old and cases more than 3 weeks old. The main microscopic lesions were expanded lamina propria by large number of inflammatory cells and the mildly atrophied intestinal villi. In mixed bacterial infection the similar macroscopic and microscopic lesions were noticed as in E. coli and salmonella infection with different severity. The cases with Cl. perfringens infection microscopically showed marked diffuse, coagulative necrosis in intestinal villi. Multifocal loss of villi and crypts was seen, and lamina propria was multifocally denuded. The lamina propria was expanded by large number of inflammatory cells. On other hand, in BVD infection the main lesions demonstrated were destruction of the epithelial lining of the crypts of Lieberkühn with presence of necrotic debris and desquamated epithelium in the crypt lumen, also other crypts revealed hyperplasia and hypertrophy of lining epithelium. In Eimeria spp. infection the detected microscopic lesions were markedly distorted lining epithelium of intestinal villi and crypts of Lieberkühn by abundant intracellular Eimeria spp. in varying stages of development in the enterocytes. Occasionally, most enterocytes were parasitized by gametes.In Cryptosporidia infected cases the microscopic lesions were observed in the small intestine, large intestine, and cecum. Microscopically, the intestinal mucosa exhibited moderate villous atrophy characterized by blunting and fusion of villi. Meanwhile, crypts of Lieberkühn revealed hyperplasia and hypertrophy of lining epithelium. Occasionally, crypt abscesses were seen. Variable numbers of amphophilic to basophilic; round cryptosporidium protozoa were seen in the microvillus border of cells on the villi. T. vitlorum infected cases had adult T. vitlorum in intestinal lumen The small intestinal villi were fused and blunted or had diffuse coagulative necrosis. In some cases the intestinal villi were lost.