R. K. Page

Malabsorption syndrome in broiler chickens.

A disease syndrome of broiler chickens is described. Affected birds exhibited poor pigmentation of the shanks, decreased weight gains, elevated feed conversions, poor feathering, enlargement of the proventriculus, and a decrease in the size of the gizzard. Reoviruses were isolated from affected chickens from several farms. Signs and lesions similar to those seen in chickens with the field syndrome were reproduced when these isolates were inoculated into day-old chicks with low levels of maternal antibody against viral arthritis. The pathogenicity of the viral isolates was variable. The incidence of lameness was much higher in those groups of chicks injected with these viruses than in the control groups.

Tissue residues of dietary cadmium in wood ducks

One-week-old wood ducks were fed cadmium in diets containing 18 or 30% protein for a period of three months. Seven drakes from each group were sacrificed, and blood, brain, muscle, kidney, liver, and wing feather tissues were collected and analyzed for cadmium. Highest cadmium concentrations were found in the kidney, liver, and feather tissues; blood, muscle, and brain cadmium residue levels were undetectable. Except in the kidney tissue, protein level of the diet did not affect cadmium residue levels. For birds that were changed to a cadmium-free, high-protein ration at 13 weeks of age, regression analysis indicated a significant decrease in cadmium residue levels for the kidney tissue only. Growth, as measured by body weight at 13 weeks of age, was not affected by the various cadmium treatment levels. Histopathological examination revealed lesions in the kidney tissues of the 100 ppm cadmium treatment groups, which were more severe in those birds receiving the 18% protein diet. Vacuolation of the pancreatic acinar cells was observed in all groups, but tended to occur more frequently in the higher cadmium level groups.

Influence of low levels of ochratoxin A on egg production, egg-shell stains, and serum uric-acid levels in leghorn-type hens.

Ochratoxin A, when fed at 0.0, 0.5, or 1.0 PPM to adult white Leghorn chickens, produced significant reduction in egg production and an increase in serum uric-acid levels, with a concomitant increase in egg-shell stains. These egg-shell stains were clinically similar to those described in the case report.

Infectious tenosynovitis in young turkeys.

Two viruses serologically related to the tenosynovitis virus of chickens were isolated from two flocks of turkeys experiencing outbreaks of tenosynovitis. Both viruses produced a tenosynovitis when injected into the foot pad of young turkeys. Staphylococcus aureus was not isolated from either flock, nor was there any evidence of Mycoplasma synoviae antibody in either flock.

Focal Failures of Endochondral Ossification in the Broiler

Two types of cartilaginous lesions were observed in a flock of 400 broilers separated into four groups and fed diets containing different energy and NH4Cl contents. The lesions appeared morphologically, histologically, and etiologically different. One lesion found in the vertebrae of 10 birds consisted of focal thickenings and necrosis of growth cartilages. Affected birds were predominantly faster-growing broilers fed diets without supplemental NH4Cl. The vertebral lesions were similar to osteochondrosis as described in mammals. A second lesion consisting of cones of retained cartilage was present in various long bones of 27.5% of all birds examined. The peak incidence of these dyschondroplastic lesions occurred in the slowest-growing group of 4-week-old birds fed diets containing 3% NH4Cl: 70% of these birds had dyschondroplasia. No positive correlation was found between the incidence of the vertebral lesions of osteochondrosis and the appendicular lesions of dyschondroplasia.

Studies on Orthoreoviruses Isolated from Young Turkeys. III. Pathogenic Effects in Chicken Embryos, Chicks, Poults, and Suckling Mice

The pathogenicity of four clone-purified reoviruses (81-51, 81-68, 81-311, and 82-88) was studied in experimentally infected specific-pathogen-free (SPF) chicken embryos and chicks. SPF and specific-antigen-and-antibody-negative (SAAN) turkey poults, and suckling mice. In SPF embryos, all four viruses caused death or lesions characteristic for avian reoviruses. SPF chicks inoculated orally with isolate 81-68 showed no signs of overt disease but did develop antibodies to reovirus. In some experiments, poults inoculated orally with isolate 81-68 exhibited increased mortality, abnormal feather development, lower body weight gain, and pasted vents. Body tremors, uncoordinated motor movement, and oily hair coats were seen in suckling mice inoculated intracerebrally with isolates 81-51, 81-68, and 82-88. Mice inoculated intracerebrally with isolates 81-68 and 82-88 exhibited retarded growth.

Marek's disease virus‐induced transient paralysis in chickens. 3. Differentiation of field cases from classical Marek's disease by central nervous system lesions

Vasculitis with intramural pseudocyst formation primarily in the cerebellar white matter, but also in nuclei of the medulla, resulted in leakage of IgG and albumin and vacuolation of the neuropil (vasogenic oedema) in brains from chickens with clinical signs of Mareks disease virus (MDV)-induced transient paralysis (TP). Demyelination was absent. Chickens that had recovered from TP had a restored blood-brain-barrier, indicated by the rarity of vasculitis and vascular intramural pseudocysts in the cerebellum. In addition, the vacuolation and protein leakage were greatly decreased. The minor vacuolation resulted primarily from intramyelinic (cytotoxic) oedema. The small quantity of extravascular protein was being removed by microglial cells and astrocytes. In one chicken which failed to fully recover from TP (TP-prolonged) there was neither vasogenic oedema, cytotoxic oedema, nor vasculitis in the cerebellum. The medulla of the TP-prolonged chicken had a severe lymphocytosis, swollen axons, neuronal degeneration, secondary demyelination and some associated serum protein leakage. All TP-affected and TP-recovered chickens, and the TP-prolonged chicken, had perivascular mononuclear cell cuffs within all brain sections. Chickens with classical Mareks disease (MD) generally lacked CNS vacuolation, perivascular mononuclear cell cuffs, vasculitis and serum protein leakage. However, in a few cases of MD with severe perivascular mononuclear cell cuffs, focal demyelinating plaques were seen. These plaques had associated vacuolation, serum protein leakage, axonal spheroids and neuronal degeneration.

Acute Toxicity of Boric Acid and Boron Tissue Residues after Chronic Exposure in Broiler Chickens

The acute oral mean lethal dose of boric acid in 1-day-old chickens was found to be 2.95 +/- 0.35 g/kg of body weight, which classifies this product as only slightly toxic to chickens. One-day-old broiler chicks were housed in floor pens in which litter had been treated with 0, 0.9, 3.6, or 7.2 kg of boric acid per 9.9 m2 of floor space. Boron residue levels in brain, kidney, liver, and white muscle were not statistically elevated following a 15-day exposure period. Boron residue levels in the same types of tissue were not significantly elevated in chicks fed 500 ppm or 1250 ppm boric acid in feed ad libitum for 3 weeks; however, residues were significantly higher in chicks fed 2500 ppm or 5000 ppm boric acid. These data indicate that broilers grown on boric acid-treated litter do not consume enough boric acid to cause elevated boron levels in tissues.

Calcium Toxicosis in Broiler Chicks

A number of food ingredients and other feed additives are used routinely in formulating poultry rations. Some of these additives are used to produce a premix which is added to the feed at a prescribed concentration level, and others are added individually at the feed mixer. Although the majority of poultry feeds are made to specifications, errors are occasionally made. Limestone and dicalcium phosphate are generally added to poultry rations as a dietary source of calcium and phosphorus. When added at the correct concentration, no harm results. High dietary calcium concentrations, however, have been implicated as a cause of nephrosis and visceral gout. Young et al. reported hyperuricemia and hypophosphatemia in pullets fed a ration containing 3.0% calcium (2). Nephrosis with renal failure and visceral gout have been produced in 16-week-old pullets consuming rations containing 3.0% calcium and 0.4% phosphorus (3). This report describes two cases in which large numbers of young chicks died after consuming feeds containing high concentrations of calcium. The first case involved 25,000 broiler chickens eleven days old. The birds were housed in a conventional broiler house with a dirt floor and Saran curtains on the side walls. The litter was pine shavings. The house was equipped with a chain feeder and 8-ft.long automatic drinkers. Feeder lids and one-gallon water jars were used to brood the chicks. Mortality began in this flock when the chicks were three days old and continued until the flock was two weeks old. Clinical signs

Experimental Exposure of Broiler Chickens to Boric Acid to Assess Clinical Signs and Lesions of Toxicosis

One-day-old broiler chicks were housed on litter treated with 0, 0.9, 3.6, or 7.2 kg of boric acid per 9.3 m2 of floor space. After 15 days, average body weights were 340.7 g, 278.1 g, and 213.2 g for chickens exposed to 0, 3.6, and 7.2 kg boric acid/9.3 m2, respectively (P < or = 0.05). Feed conversion was 1.68 and 2.29 in chickens exposed to 0 and 7.2 kg boric acid/9.3 m2 (P < or = 0.05). In a second experiment, after birds ingested feed treated with 2500 and 5000 ppm of boric acid for 2 weeks, body weights were 254.8 g and 149.6 g, respectively. The chickens in the control group weighed an average of 285.0 g (P < or = 0.05). The 5000 ppm treatment group had a feed conversion of 1.70, vs. 1.45 in the controls (P < or = 0.05). A dose-related feathering abnormality was evident in treated chickens. No significant histopathologic changes were observed. Livability, weight gain, and feed conversion were not adversely affected in broilers as a result of exposure to litter treated with boric acid at recommended levels of 0.4-0.9 kg/9.3 m2.