Persistent hypoglycemia is induced by tolbutamide administration in broiler chickens fed a low-carbohydrate diet

With a view to gaining an insight into the regulatory mechanism of blood glucose concentrations specific to the chicken, an experimental induction of hypoglycemia was conducted by single or sequential administration of tolbutamide in broiler chickens fed a standard or low-carbohydrate diet. A single dosing of tolbutamide at levels of 25-200 mg/kg body weight decreased plasma glucose concentrations for 2 to 8 h after the dosing in chickens fed either diet. No significant rise in plasma insulin concentration was observed for 2 to 24 h after the single dosing of tolbutamide in chickens on either diet, with the exception of a significant rise when chickens on the standard diet received 100 mg tolbutamide. However, a transient increase of plasma insulin concentration was observed only in the 20 min immediately after the single dosing. Persistent hypoglycemia that was sustained for 5 days, with no significant changes in plasma insulin concentration, was induced by sequential dosing (3 times per day for 5 days, every 8 h) of tolbutamide (100 and 200 mg/kg body weight) in chickens fed the low-carbohydrate diet. In these chickens, the consistently low concentration of plasma glucose, with small diurnal variations, was evidenced by the determination of plasma glucose every 3 h in day 4/5 of the tolbutamide dosing. In chickens fed the standard diet, on the other hand, the low plasma glucose concentrations for 5 days were accompanied by significant diurnal fluctuations. Chickens with persistent hypoglycemia showed slight decreases in plasma non-esterified fatty acids (NEFA) concentration and only slight changes in blood D-3-hydroxybutyrate (3HB) concentration. The present study shows that the persistent hypoglycemia with normoinsulinemia, in the main, is induced by tolbutamide dosing in chickens fed a low-carbohydrate diet, and that the blood concentrations of NEFA and 3HB, alternatives of energy source in animals, are only slightly changed or not at all in hypoglycemic chickens.     

The effect of continuous ultraviolet irradiation on broiler chickens.

1.Continuous ultraviolet irradiation (10.45 muW/cm2) did not affect the growth or food conversion efficiency of broilers. 2. The cornea of the eye was roughened by the treatment and there was a loss of the regular arrangement of the corneal cells: vision was not significantly affected after 49 d exposure.     

福美双诱发肉鸡胫骨软骨发育不良的组织病理学变化

120羽1日龄健康AA肉鸡预饲1周后随机分为2组,对照组饲以基础日粮,试验组饲以基础日粮添加100mg/kg福美双,进行了肉鸡胫骨长度、生长板厚度、肉鸡胫骨软骨发育不良(TD)指数及TD发病率等指标的检测,并进行了形态学和组织病理学观察。结果显示,患病鸡胫骨长度、生长板厚度和TD指数均有显著变化(P<0.01),TD发病率显著上升(P<0.05);病鸡胫骨近端的纵切面有玉白色楔状软骨团块深入干骺端甚至骨髓腔,呈现典型的胫骨软骨发育不良病理学变化。结果提示,100 mg/kg福美双可显著提高AA肉鸡TD发病率,并引起相应的组织病理学变化,为TD分子机理的研究提供了一个理想的实验动物模型。     

维拉帕米对高盐诱发肉鸡腹水综合征的预防作用

将150只8日龄商品代AA雄性肉仔鸡随机分为对照组、高盐组（饮水中添加3．0g／L氯化钠）和高盐维拉帕米组（饮水中添加3．0g／L氯化钠及0．1g／L雏拉帕米）。分别于15、22、29、36、43、50日龄测定各组鸡肺动脉压（PAP）、红细胞比客（PCV）和腹水心脏指数（AHI），并统计腹水发生率。结果显示，50日龄时，高盐组腹水发生率极显著高于对照组和高盐维拉帕米组；15日龄时，高盐组和高盐维拉帕米组PAP极显著高于对照组，36、43、50日龄时，高盐组PAP显著或极显著高于对照组和高盐维拉帕米组；整个试验期间，高盐组PCV显著或极显著高于同日龄对照组和高盐维拉帕米组；29至50日龄，高盐组AHI显著或极显著高于同日龄对照组和高盐维拉帕米组。表明，雏拉帕米对高盐诱发的肺动脉高压、右心肥大和PCV的升高有抑制作用，能够降低腹水发生率，有效预防高盐诱发的肉鸡腹水综合征。     

Fowl cholera immunity induced by various vaccines in broiler minibreeder chickens determined by enzyme-linked immunosorbent assay

Broiler minibreeder hens were vaccinated for protection against fowl cholera at 12 and 21 weeks of age using several vaccination schemes, which included a live Pasteurella multocida (CU strain) vaccine, two commercial polyvalent fowl cholera oil-based bacterins, and two experimentally prepared polyvalent oil-based bacterins. Some treatment groups received only live or killed vaccines, whereas others received a live vaccine at 12 weeks followed by a killed product at 21 weeks. At 42 weeks of age, all birds that received the live CU vaccine twice or once followed by a bacterin survived challenge. Birds that received killed vaccines only were significantly less protected but still showed a respectable survival rate of 86%. All unvaccinated controls died within 72 hr after challenge. At 72 weeks of age, overall protection was lower than that at 42 weeks, regardless of vaccination treatment. Antibody titers were usually higher in birds that received bacterins than in those receiving live vaccines, yet overall protection was still greater in those birds that received the live cholera vaccine twice.     

Campylobacter succession in broiler chickens

The competitive ability of Campylobacter coli OR12 over C. jejuni OR1 has been examined in experimental broiler chickens following the observation that C. coli replaced an established C. jejuni intestinal colonisation within commercial chicken flocks reared outdoors [El-Shibiny, A., Connerton, P.L., Connerton, I.F., 2005. Enumeration and diversity of campylobacters and bacteriophages isolated during the rearing cycles of free-range and organic chickens. Appl. Environ. Microbiol. 71, 1259-1266]. Co-cultures of C. coli OR12 with C. jejuni OR1, revealed that the two species were able to grow together at similar growth rates in exponential growth phase but if the disparity of the inoculum ratios were >log(10)4 in favour of C. coli OR12, C. jejuni OR1 was observed to prematurely enter decline phase. Chickens were pre-colonised with C. jejuni OR1 at 21-days-old to examine succession in vivo. The birds were inoculated between 2 and 12 days later with C. coli OR12, to determine if the second isolate could efficiently colonise and compete with an established C. jejuni strain. C. coli OR12 were able to co-colonise before replacing C. jejuni OR1 as the dominant species when the birds were more than 27 days of age at the time of administration over a 4-day period. If these criteria were met C. coli OR12 became the dominant isolate otherwise co-colonisation occurred until they were met. C. coli OR12 was also found to displace three alternative C. jejuni strains from pre-colonised chickens challenged with C. coli OR12 at 30 days of age and tested at 40 days. These data raise the possibility of manipulating populations of Campylobacter colonising chickens through competition.     

Swollen-head syndrome in broiler chickens

Swollen-head syndrome is a disease seen in broiler chickens between 4 and 6 weeks of age in Southern Africa. It appears to be caused by a mixed coronavirus and Escherichia coli infection. The coronavirus appears to be of a hitherto unrecorded serotype. The disease is controlled by an attenuated live-virus vaccine and antibacterial medication.     

Salt poisoning in broiler chickens

The clinical signs of salt poisoning in young chickens are thirst, diarrhoea and weakness. When 13 500 broilers are simultaneously affected, the deterioration that occurs in their physical condition and in the litter beneath their feet is dramatic. Two flocks of meat chickens on a small unit in North Otago were affected in this way.     

Salt poisoning in broiler chickens

The incident occurred on a small, owner-operated broiler unit that used home-mixed feed. Two flocks of broilers, one aged 6 weeks and one aged 6 days, developed signs of watery diarrhoea, thirst and weakness. Over 3 days the mortality increased considerably and many birds were noticed to show laboured breathing. The majority of dead birds had an excess of clear fluid in the pericardial sac, oedematous lungs and pale swollen kidneys. Cystic dilation of the testes was conspicuous in several birds from the younger flock killed at 12 days of age. This lesion is a specific indication of sodium toxicity in young broilers. Histological lesions were those associated with cardiovascular collapse and hypoxia. Liver levels of sodium chloride were 4 g/kg of wet weight. Broiler feed samples contained more than 7% sodium chloride whereas the nutritional specifications were for 0.4%. The rations had been correctly mixed and the problem was traced to a faulty batch of meatmeal that had been contaminated by salt used for curing hides.     

Fibrosing cholehepatitis in broiler chickens induced by bile duct ligations or inoculation of Clostridium perfringens.

The pathogenesis of fibrosing hepatitis causing condemnations in broiler chickens was investigated. Three to four week old broilers were inoculated via the hepatoenteric bile duct with saline washed suspensions of Clostridium perfringens (10(7) and 10(8) organisms). In another group of broilers, both bile ducts were ligated. The sequential development of liver and gall bladder lesions was studied at intervals ranging from 1-28 days postsurgery. The lesions were similar in both experiments in that the liver became mottled and swollen by five to seven days. Fibrinoid necrosis, heterophil and lymphocyte infiltration, bile duct hyperplasia and fibrosis with reticulin fiber proliferation occurred. By 14-17 days, the liver was enlarged, tan colored and firm with red and white foci. By 28 days, bile duct proliferation and fibrosis were massive with only a few hepatocytes remaining. The liver capsule was not involved. Jaundice was not present but the birds with ligated bile ducts excreted intensely yellow stained droppings after six to seven days. The gall bladder in inoculated birds was edematous and distended with flocculent or inspissated material. Clostridium perfringens was reisolated from gall bladder and/or liver of inoculated birds up to 28 days postsurgery. It is suggested that this organism plays a role in the pathogenesis of fibrosing cholehepatitis by inducing septic intrahepatic cholestasis.     

Campylobacter jejuni infection in broiler chickens

Day-old, straight-run broiler chickens were procured from a hatchery located in the Pacific Northwest. The chickens were subdivided individually into nine groups of 20 chickens. The chickens were tagged, housed in isolation chambers on wire, fed commercial broiler feed, and given water ad libitum. Three isolates of Campylobacter jejuni of poultry origin and one of human origin were tested in this study. Various C. jejuni cultures were inoculated into 9-day-old chickens by crop gavage. Four groups of 20 chickens were inoculated at a dose level of 0.5 ml of 1 x 10(2) colony-forming units (CFU)/ml. The other four groups were inoculated with 0.5 ml of 1 X 10(4) CFU/ml. One group of 20 chickens was kept as an uninoculated control group. Four randomly selected chickens from each of the inoculated and uninoculated groups were necropsied at 5, 12, and 19 days postinoculation (DPI). The C. jejuni was cultured and enumerated from a composite of the upper and midintestine and the cecum. Body weights of all chicken groups at 7 days of age and at 5, 12, and 19 DPI were measured and statistically analyzed. No significant differences were present in the mean body weights (MBWs) of 7-day-old, 5 DPI, and 12 DPI male and female broiler chickens inoculated with C. jejuni at both dose levels compared with uninoculated controls. Differences in MBWs of the male and female broilers at 19 DPI were observed in some of the groups. Results of the C. jejuni culture enumeration mean (CEM) of composite intestine samples at 5 DPI from all inoculated chicken groups, irrespective of the dose level, ranged from (2.5 +/- 5.0) x 10(2) to (2.8 +/- 4.8) x 10(5) CFU/g (mean +/- SD). Results of cecum C. jejuni CEM at 5 DPI inoculated at both dose levels ranged from (2.5 +/- 5.0) x 10(6) to (1 +/- 0.0) x 10(7) CFU/g in all treatment groups irrespective of the dose level. CEM results from the composite intestine samples at 12 and 19 DPI increased by 1 log unit, or sometimes more. Results of cecum C. jejuni CEM at 5 DPI inoculated at both dose levels ranged from (2.5 +/- 5.0) x 10(6) to (1 +/- 0.0) x 10(7) CFU/g in all treatment groups irrespective of the dose level. Increases of 2-5 log units in C. jejuni CEM was present in chicken groups inoculated with 1 X 10(2) CFU of C. jejuni, and a 2- to 3-log increase was present in groups inoculated with a higher dose level of C. jejuni at 12 DPI. The results of C. jejuni CEM from cecal samples at 19 DPI were similar to chicken groups at 12 DPI. Campylobacterjejuni was not isolated from the uninoculated control chickens at 5, 12, and 19 DPI. Clinical signs of illness or gross pathologic lesions were not present in any of the chicken groups during this study. No lesions were present on histopathologic evaluations in C. jejuni-inoculated chickens or uninoculated control chickens.