The proportional occurrence of bacteria and pathological lesions in the nasal sinuses and trachea of dead chickens were determined during [2008][2009]. Nasal sinus and tracheal swabs from 50 dead birds were collected in sterile nutrient broth. The histopathological samples were collected in 10% neutral buffered formalin and studied with light microscope. The isolation and identification of bacteria were performed by culture, staining and biochemical tests. The proportional occurrence of bacteria in trachea (n = 50) and nasal sinuses (n = 50) of dead chickens was Klebsiella sp.
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 (1x10 3 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 1x10 3 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.
Here, we report the draft genome sequences of two Escherichia coli strains that were isolated from raw milk samples obtained from lactating cows with mastitis in Bangladesh. One strain was assigned to a novel sequence type 13054, and the other strain belonged to sequence type 101.
The present study was conducted for the detection of toxic effects of clostridial crude toxin in experimental rats. The crude toxin of Clostridium perfringens was prepared and the rats were injected intraperitoneally (IP) 0.5 ml, 1.0 ml and 2.0 ml of crude toxin. The rats were observed for 24 hrs. The crude toxin inoculated rats showed the dose dependent clinical signs; depression, rough hair coat, respiratory distress, diarrhea and rapid heart beats, whereas PBS inoculated rats did not show any clinical sings. Necropsy changes were variable however, highly dilated and distended whole intestine with blood stained semifluid contents and gas along with congestion in all the affected rats were found dose dependently. Liver, lung and kidney were congested, hemorrhagic and swollen. More or less hydrothorax was seen during the postmortem of all affected rats. The peritoneal fat was frequently congested in all affected rats.Histopathological changes in intestine (0.5 ml inoculated rats) involved congestion, slightly swollen goblet cells and hemorrhages. The most severe lesions comprised of profuse hemorrhages in the mucosa and submucosa with complete necrosis, desquamation and intense leukocytic infiltration in 2 ml inoculated rats. Affected liver (1 ml inoculated rats) exhibited engorgement of central veins, sinusoidal spaces with blood and fatty change. The hepatocytes revealed swelling, granulation and vacuolation of cell cytoplasm, extensive hemorrhage and congestion were seen in 2 ml toxin inoculated rats. Congestion and sometimes extravasation were observed in the subepicardial region of heart. The myocardium revealed mild degenerative changes in the form of granularity of myocardial fiber. In lungs there was congestion, hemorrhage and leukocytes infiltration in the interstitial spaces around the bronchioles in both 1 and 2 ml toxin inoculated rats. Affected kidneys of different doses of crude toxin showed hemorrhage, congestion and inflammatory cells dose dependently. From the above findings, it may be concluded that clostridial crude toxin induced clinical signs, gross and histopathological lesions dose dependently in experimental rats.
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