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.     

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.     

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.     

Pathological lesions following an experimental intoxication with aflatoxin B1 in broiler chickens

A follow-up of chickens dosed orally over 21 days with 0.2 and 3 micrograms of aflatoxin B1 (AFB1) g-1 of bodyweight daily and their subsequent recovery 10 days after withdrawal of contaminated food was conducted. Vacuolation of liver cells during the initial days of the intoxication and cellular depletion in the follicle medulla of the bursa of Fabricius were the lesions which appeared first and persisted during the recovery phase in both groups of intoxicated animals. The intensity of these lesions and their persistence was related to the dose of aflatoxin ingested. A significant reduction in the bodyweight and absolute weights of liver, bursa of Fabricius spleen and thyroid was observed in the higher dose group.     

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.     

Pharmacokinetics of tylosin in broiler chickens

Biological availability and pharmacokinetic properties of tylosin were determined in broiler chickens after oral (p.o.) and intravenous (i.v.) administration at a dose of 10 mg/kg. The calculated bioavailability--F%, by comparing AUC values--p.o. and AUC--i.v., ranged from 30%-34%. After intravenous injection tylosin was rapidly distributed in the organism, showing elimination half-life (t1/2 beta) values of 0.52 h and distribution volume (Vd) of 0.69 L/kg, at a clearance rate (Cl) of 5.30 +/- 0.59 ml/min/kg. After oral administration, tylosin has a similar distribution volume (Vd = 0.85 L/kg), while the elimination half-life t1/2 beta of 2.07 h was four times bigger than after i.v. administration at Cl = 4.40 +/- 0.27 ml/min/kg. The obtained value tmax = 1.5 h for tylosin after oral administration indicates that using this antibiotic with drinking water in broiler chickens is the method of choice. However, a relatively low value Cmax = 1.2 micrograms/ml after oral administration of tylosin shows that dosing of this antibiotic in broiler chickens should be higher than in other food producing animals.     

Experimental biliary cryptosporidiosis in broiler chickens

Biliary cryptosporidiosis was studied by inoculation of 2 x 10(5) Cryptosporidium baileyi oocysts (AU-B1 isolate) into the gall bladders of ten 6-day-old broiler chickens. Clinical signs of disease were not seen. Three of the 10 chickens developed biliary tract infections, based on histologic examination of tissue sections. Lesions seen in the gall bladders of these birds included epithelial hyperplasia and infiltration of the underlying connective tissue with mononuclear leukocytes. One of these birds also had involvement of the hepatic bile ducts. The bile ducts were mildly dilated and contained lesions similar to those seen in the gall bladder. Few to many cryptosporidia were present in the gall bladders and bile ducts of infected birds. Chickens may be of use in the study of biliary cryptosporidiosis, a common sequel to enteric infection in humans with human immunodeficiency virus infection.     

Pharmacokinetics of butorphanol in broiler chickens

Butorphanol tartrate (2 mg/kg) was injected intravenously in 18 healthy broiler chickens to study its pharmacokinetics. Plasma samples were analysed by a highly sensitive high-performance liquid chromatography with diode-array detection method and pharmacokinetic parameters were calculated from the mean pooled data. With non-compartmental analysis, the terminal half-life (T(1/2.z)) was 71.3 minutes, clearance was 67.6 ml/minute/kg and the apparent volume of distribution was 6.9 l/kg. The concentration-time curve was also fitted to a two-compartmental model. In this analysis, elimination half-life (T(1/2β)) was 69.3 minutes, clearance was 74.6 ml/minute/kg and volume of distribution at steady state was 5.6 l/kg. The micro rate constants k(21), k(12) and k(10) were 0.034, 0.050 and 0.029, respectively. Butorphanol was well distributed in the chickens with rapid clearance. It remained above the minimum effective concentration for analgesia in mammals for approximately two hours in the chickens.     

Silicon in broiler drinking water promotes bone development in broiler chickens

1. Skeletal abnormalities, bone deformities and fractures cause significant losses in broiler production during both rearing and processing. Silicon is an essential mineral for bone and connective tissue synthesis and for calcium absorption during the early stages of bone formation.

2. Performance was not affected by the addition of silicon. However, broilers receiving silicon showed a significant increase of phosphorus, zinc, copper, manganese and ash in the tibia.

3. In conclusion, broiler performance was not impaired by adding the tested silicon product to the drinking water. In addition, bone development improved, as demonstrated by higher mineral and ash content.

4. Further studies are required to determine the optimal concentration of silicon, including heat stress simulations, to better understand the effects of silicon on bone development.

     

Feeding dihydroquercetin to broiler chickens

1. A total of 80 male Ross 308 broilers were used in a study to investigate the effect of dietary dihydroquercetin (DHQ) on growth performance variables, gastrointestinal tract (GIT) and immune organ development, glutathione peroxidase (GPx) and haemoglobin in blood, hepatic vitamin E content, dietary N-corrected metabolisable energy (AMEn) and nutrient retention coefficients when fed to broiler chickens from 7 to 35 d of age.

2. Two treatments were used in this study: control (C) and C + 0.5 g/kg extract of Siberian Larch (Larix sibirica) per kg feed, containing 85% DHQ. The diets were fed over 2 feeding phases, a grower phase from 7 to 28 d of age and a finisher phase from 28 to 35 d of age. The birds were reared under the breeder’s recommended conditions.

3. In general, there were no effects of DHQ on growth performance of broiler chickens. However, the results of this experiment showed that there can be changes in the redness colour of the breast meat when DQH is fed. No negative effects of feeding DHQ at 0.5 g/kg diet were observed in this study.

4. Supplementation of poultry diets with DHQ under standard industry-rearing conditions did not improve the performance or any of the studied variables, except an increase of redness index of the breast fillets. Feeding DHQ at different doses and/or under more challenging conditions, e.g. heat stress, may, however, bring positive responses.