O. J. Fletcher

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.

Studies on interferon induction by infectious bursal disease virus (IBDV). II. Interferon production in White Leghorn chickens infected with an attenuated or pathogenic isolant of IBDV.

Infectious bursal disease virus (IBDV) isolants that differed in virulence for chickens, were compared as to: 1) induction of interferon in serum and tissues; and 2) stimulation of IBDV serum antibody. Specific-pathogen-free chickens were infected at one day and four weeks of age by the subcutaneous and intranasal routes of inoculation. The pathogenic isolant induced a more generalized interferon response than the attenuated isolant, independent of age or route of inoculation. Pathogenic IBDV stimulated interferon in serum, kidney, lung, thymus, spleen, and bursa of Fabricius. The attenuated virus induced interferon only in the bursa. The serum interferon response was greater following inoculation with pathogenic IBDV than with the attenuated virus. Serum interferon titers peaked 2-3 1/2 days after inoculation. The pathogenic and attenuated viruses stimulated similar IBDV-neutralizing antibody responses, which occurred after peak serum interferon activity.

The individual and combined effects of citrinin and ochratoxin A on renal ultrastructure in layer chicks.

Layer chicks fed 3.0 micrograms of ochratoxin A (OA) and 300 micrograms of citrinin (CTN) per gram of feed, alone and in combination, were evaluated for changes in renal ultrastructure. Feeding OA from 0 to 21 days of age was associated with proximal tubular intranuclear membrane-bound inclusions, elongated tortuous and ring-shaped mitochondria, enlarged mitochondrial matrix granules with hyaline centers, and an increase in number and size of peroxisomes and secondary lysosomes. Birds fed OA from 0 to 7 days and then given untreated ration had similar changes but to a lesser degree. Feeding CTN from 0 to 21 days of age was associated with similar proximal tubular nuclear inclusions, elongated tortuous and ring-shaped mitochondria, and an increase in size and number of peroxisomes and secondary lysosomes. Hyalinized mitochondrial matrix granules were not present, and some proximal tubular cells had cytoplasmic aggregates of smooth endoplasmic reticulum. Birds fed CTN from 0 to 7 days had similar but milder changes. Birds fed CTN + OA for 21 days had changes similar to those fed OA alone and also had cytoplasmic aggregates of smooth endoplasmic reticulum similar to those of CTN-fed birds. Again, changes in birds fed CTN + OA for 7 days were similar but milder.

The Individual and Combined Effects of Citrinin and Ochratoxin A in Broiler Chicks

Citrinin (CTN) and ochratoxin A (OA) were fed alone and in combination to broilers from day of hatch until 3 weeks of age. Dietary concentrations of 300 micrograms CTN/g and 3.0 micrograms OA/g were used. Birds fed CTN had significantly (P less than or equal to 0.05) lower body weights than controls on days 14 and 21 and increased water consumption on days 7, 14, and 21. Birds fed OA had significantly lower body weights than controls on days 7, 14, and 21 and increased water consumption on day 14. Birds fed CTN and OA in combination had lower body weights than controls and increased water consumption during the experiment, but the alterations were intermediate in severity when compared with those in birds fed CTN or OA alone. Birds fed OA alone or combined with CTN had higher liver and kidney weights than controls, but birds fed CTN alone had only higher kidney weights. Birds fed both CTN and OA had concentrations of serum constituents similar to those in birds fed OA alone, except the levels of cholesterol and triglycerides were not significantly different from those in the controls. Histological evaluation of the kidney indicated no lesions in birds fed CTN alone, but birds fed OA, alone or in combination with CTN, had increased tubular casts and tubular hyperplasia compared with controls. These data suggest that there were no additive or synergistic toxic interactions when 300 micrograms CTN/g and 3.0 micrograms OA/g were fed simultaneously to broiler chicks for 3 weeks. However, the severe growth depression resulting from OA and the increased water consumption associated with CTN toxicosis were ameliorated when CTN and OA were fed in combination. These data may be useful in diagnosing field cases of mycotoxicosis where both CTN and OA are involved.

Comparative study of experimental inclusion body hepatitis of chickens caused by two serotypes of avian adenovirus.

Twenty 1-day-old specific-pathogen-free chickens each were given an intraabdominal inoculation of either a type-8 avian adenovirus, [AMG 5 (2a)], or a type-5 avian adenovirus, inclusion body hepatitis virus (IBHV). The diseases produced were similar. High (60–100%) mortality and statistically significant depression of body weights occurred in both infections. There were necrotizing hepatitis and pancreatitis, lymphoid depletion in the spleen, bursa of Fabricius and thymus, hydropericardium, nephritis and enteritis. Intranuclear inclusions occurred in affected organs. Fluorescent-antibody staining, the Feulgen reaction for deoxyribonucleic acid and electron microscopic studies, as well as studies from the literature, indicated that basophilic inclusions consisted of assembled adenovirions.

Immunosuppressive potential and pathogenicity of a recent isolate of infectious bursal disease virus in commercial broiler chickens.

At 15 days of age and in the presence of measurable levels of maternal antibody against infectious bursal disease virus serotype I (1:170 virus-neutralization geometric mean titer), a recent isolate (U-28) and a prototype virulent isolate (Edgar) of the same virus caused subclinical infections in commercial broiler chickens. Isolate U-28 caused a significant reduction in the size of the bursa of Fabricius, whereas the Edgar isolate produced splenomegaly. Both isolates reduced the serological response to Newcastle disease virus. The experimental immunosuppressive potential and pathogenicity of isolate U-28 in broiler chickens confirms the role of this virus in recent infectious bursal disease outbreaks.

Marek's disease virus-induced transient paralysis in chickens. 1. Time course association between clinical signs and histological brain lesions.

Association between Mareks disease virus (MDV)-induced clinical signs of transient paralysis (TP) and brain. histological lesions (vasogenic oedema and perivascular mononuclear cell cuffs) were evaluated in TP-susceptible line G-B2 chickens in a time sequence study. The most consistent histological lesions were seen in the cerebellum. Leakage of albumin and vacuolation were parallel in development with clinical signs, but preceded the clinical signs by 6 to 12 h. During resolution of signs, a parallel decline in vacuolation, but not in extra-vascular albumin content was observed. The extravascular albumin shifted from an extracellular to intracellular location. No association was seen between the IgG leakage and vasogenic oedema or clinical signs. Perivascular mononuclear cell cuffing was statistically associated with clinical signs, but evaluation of plotted data indicated the slope for the cuffs was less than the slope for corresponding clinical signs. In addition, cuffing began 2 days prior to clinical signs. Thus, perivascular mononuclear cell cuffing was not causally associated with the TP syndrome.

Microscopic and Ultrastructural Renal Pathology of Oosporein-Induced Toxicosis in Broiler Chicks

Kidneys from broiler chicks receiving 300 micrograms of oosporein K salt per gram of feed continuously from 0 to 21 days of age were examined by light and electron microscopy. Chicks that died at 3 days had nephrosis of initial proximal tubular segments with an early pyogranulomatous interstitial response. Macula densa cells had cytoplasmic accumulations of periodic-acid-Schiff-positive granules. Kidneys from chicks surviving 21 days had hypercellular or atrophic glomeruli and hyperplastic dilated proximal tubules. Centrilobular distal tubules were dilated and filled with hyaline basophilic casts. Interstitial fibrosis was prominent in cortical and medullary zones. These findings indicate that oral oosporein is a severe nephrotoxin which can cause visceral urate deposition and severe nephrosis of initial proximal tubular segments. The histopathology of this mycotoxicosis was compared with those of infectious-bronchitis-induced nephrosis and avian urolithiasis syndrome.

Histology of Air Sac Lesions Induced in Chickens by Contact Exposure to Mycoplasma synoviae

Chickens were housed when 1 day old with chickens experimentally infected with Mycoplasma synoviae. Air sacs from 16 of the 2-week-old and eight of the 3-week-old contact-exposed chickens were given gross lesion scores and embedded in glycol methacrylate for slide preparation. Histologic lesions in air sacs with gross scores of 0–2 were mild edema resulting in a two to eightfold increase in air sac thickness, capillary proliferation, and exudate consisting largely of heterophils and necrotic debris. Histologic lesions in air sacs with gross scores of 3 and 4 were marked hyperplasia of epithelial cells and diffuse infiltration of the air sac connective tissue by mononuclear cells. Nine of 10 air sacs with gross scores of 0 had no histologic evidence of inflammation. The most severe histologic lesions were in those air sacs with gross scores of 4. The glycol methacrylate procedure resulted in 2-μm sections with excellent cellular detail.