Importance of Escherichia coli infection in ascites in broiler chickens shown by experimental production.

Common commercial strain male broilers aged 14 days were intratracheally inoculated with 0.2 ml of 1.2 x 10(6) colony-forming units of Escherichia coli in nutrient broth and kept in a cool environment during the experiment. Ascites was produced in five surviving and two dead birds out of 50 but not in 50 mock-infected control birds. Among the 40 survivors that were infected, the erythrocyte packed cell volume (PCV) of the 10 birds with pericarditis was the same as in 21 grossly normal birds, although that of the four birds with enlarged right ventricle (RV) was high. The pericarditis caused by E. coli septicemia was not the primary cause of ascites. However, the PCV was high in some of the survivors with an enlarged RV without pericarditis, indicating overload due to the lung lesion. These data suggested that some of the birds with an enlarged RV, caused by supplying blood that was insufficiently oxygenated for the body size, suffered from ascites.

The use of feed restriction for mortality control of chickens in broiler farms.

Feed restriction was attempted for the control of mortality at broiler farms. Respiratory signs were observed in both restricted-feed flocks and fully fed flocks, but they were less severe in the restricted-feed flocks. The death rate in the fully fed flocks began to rise at the age of 4 wk but did not do so in the restricted-feed flocks. Mortality in the restricted-feed flocks was significantly lower than in the fully fed flocks aged from 3 to 7 wk. The economic performance with restriction feeding was better than that with full feeding as a result of improvements in viability and feed conversion rates. Feed restriction appeared to be beneficial in decreasing the death losses.

Experimental production of ascites in broiler chickens using infectious bronchitis virus and Escherichia coli.

Common commercial strain male broilers were intratracheally inoculated with 0.3 ml of fluid containing 10(3.7) embryo infective doses of infectious bronchitis virus (IBV) at 14 days of age and 7.5 x 10(6) colony-forming units of Escherichia coli at 18 days of age. Ascites was detected in 15 out of 100 infected birds, which was significantly higher than in a control group of 100 mock-infected birds (P < 0.01). Some parabronchi were blocked by copious exudate containing heterophils and fibrin in the infected birds at 22 days of age although these findings were not seen in the infected birds at 35 days of age or in birds with ascites. The erythrocyte packed cell volume and right ventricle/total ventricle (RV/TV) ratio of birds with ascites were higher than in birds without ascites. The RV/TV weight ratio for the infected group at the age of 35 days was higher than that of the control group. No IBV or E. coli were recovered from the ascitic birds. These findings suggest that these infectious agents induce ascites in the broilers, and then disappear until the birds suffer from ascites.

Liver capsule thickening characterized by mesothelial cell proliferation with vascularization in broilers ascites syndrome.

Thickened liver serosal membranes in 24 8-week-old male young broiler chickens with the ascitic syndrome were pathologically examined. Gross changes included inflammation of liver capsules (15/24 cases), right ventricular dilation (24/24 cases), pericarditis (5/24 cases), peritonitis (9/24 cases) and air sacculitis (7/24 cases). Histopathology revealed liver capsule thickening and focal hepatitis in all 24 cases, peri- and epi-carditis in 19 and myocarditis 11 cases. The thickened liver capsules consisted of spindle shaped-cells which reacted with anti-keratin rabbit serum and anti-vimentin monoclonal antibody, and formed cysts of varying size containing clear yellow fluid as ascitic fluid. The volume of sub-capsular fluid may have been responsible for the development of the cysts. The spindle-shaped cells were located perpendicular to the surface with thin bridges from the serosa together with a little collagen and vascularization. These changes were not observed in other serosal membranes in abdominal air sac or pericardium. We have therefore shown that the liver capsule thickening in the broilers ascites syndrome is characterized by mesothelial cell proliferation with vascularization.

Ulcerative enteritis in broiler chickens caused by Clostridium colinum and in vitro activity of 19 antimicrobial agents in tests on isolates.

Ulcerative enteritis in broiler chickens occurred at five poultry farms in Kagoshima Prefecture, southern Japan, in February and March, 1987. This is the first incidence of this disease reported for chickens in Japan. The mortality rate was estimated to be 1 to 5%. Ulcerative enteritis in the intestines, and necrosis in the liver and spleen, were observed mainly in autopsied broilers. Identification involving tests of biochemical properties and production of metabolic endproducts using gas-liquid chromatography were consistent with an identification of Clostridium colinum. Antimicrobial agent susceptibility tests on the isolates showed that all were highly sensitive to the agents, with the exception of aminoglycoside antibiotics. Minimum inhibitory concentrations of penicillin-G and ampicillin ranged from .025 microgram/mL to .05 microgram/mL. No resistant strains were isolated.