Changes in hematological, blood gas, and serum biochemical variables in broilers during exposure to simulated high altitude.

One-day-old broilers were reared until 35 days of age at both natural low (100 m) and simulated high altitude (2133 m) to assess the incidence and development of ascites syndrome. Clinical measurements were conducted at 7, 14, 21, 28, and 35 days of age. Birds reared at 2133 meters exhibited significantly (P less than or equal to 0.05) reduced body weights at 7 through 28 days of age. Total serum calcium and biochemical enzyme activities were found to be altered at 35 days of age. In addition, the high-altitude group had significantly (P less than or equal to 0.05) higher erythrocyte counts, hematocrits, and hemoglobin at 14, 21, 28, and 35 days of age and higher serum inorganic phosphorus at each weekly sample time than birds at the low altitude. Total mortality was 20.3% at 2133 meters and 4.6% at 100 meters. The incidence of ascites syndrome in the high-altitude group ranged from 16.6% to 61.1% during the 5-week experimental period.

Effects of a hydrated sodium calcium aluminosilicate on growing turkey poults during aflatoxicosis.

Effects of adding .5% of a hydrated sodium calcium aluminosilicate (HSCAS) to diets containing 1 or .5 mg aflatoxin (AF)/kg were determined in male turkey poults from 1 day to 3 wk of age. Body weight gains were significantly reduced by 51 and 19% in turkey poults fed 1 and .5 mg AF/kg, respectively; efficiency of feed utilization was not affected. There were no deaths in poults fed .5 mg AF/kg; however, the mortality rate was 88% in poults fed 1 mg AF/kg. The addition of .5% dietary HSCAS resulted in a 68% decrease in mortality to 28% for the 3-wk experimental period. Treatment-related changes in relative organ weights, hematological values, serum biochemical values, and enzyme activities were observed. The HSCAS in the absence of AF did not alter any of the parameters measured. The HSCAS diminished the adverse effects of AF on body weight gains, most relative organ weights, hematological values, serum biochemical values, and enzyme activities associated with .5 mg AF/kg, but not 1 mg AF/kg. These findings indicate that HSCAS may diminish many of the adverse effects of AF in an AF-sensitive species, the turkey.

The individual and combined toxicity of kojic acid and aflatoxin in broiler chickens.

The individual and combined effects of kojic acid and aflatoxin were studied in male broiler chicks (Peterson x Hubbard). The experiment had a two by two factorial arrangement of treatments with dietary treatments of 0 and 2,500 mg kojic acid/kg feed and 0 and 2.5 mg aflatoxin/kg feed. The broilers were obtained at 1 day of age and housed in electrically heated batteries with feed and water available for ad libitum intake until they reached 3 wk of age. The toxicity of kojic acid was characterized by significant (P less than .05) reductions in body weight, the relative weight of the bursa of Fabricius, serum cholesterol concentration, and serum alkaline phosphatase activity, and by significant (P less than .05) increases in the relative weight of the pancreas, proventriculus, and gizzard, and serum concentrations of uric acid and triglycerides. Aflatoxicosis was characterized by significant (P less than .05) reductions in body weight, serum concentrations of total protein, albumin, cholesterol, and inorganic phosphorus, serum glutamic oxalacetic transaminase activity, and mean corpuscular volume, mean corpuscular hemoglobin, and mean corpuscular hemoglobin concentration. Significant (P less than .05) increases in the relative weight of the liver, kidney, spleen, pancreas, proventriculus, and heart, and the serum pyruvic transaminase activity were also caused by aflatoxin alone. The only significant (P less than .05) interaction between kojic acid and aflatoxin, which can best be described as antagonistic, was seen through an increase in mean corpuscular hemoglobin and mean corpuscular hemoglobin concentration. These data indicate that kojic acid is not an aflatoxin synergist at the levels used in the present study.

Toxic effects of kojic acid in the diet of male broilers.

The toxicological effects induced by the administration of kojic acid were characterized in young male broiler chickens (Hubbard x Peterson). The experimental design consisted of six dietary treatments of kojic acid (0, .5, 1, 2, 4, and 8 g/kg feed) and four replicates of 10 broilers per replicate. Kojic acid significantly (P less than .05) decreased growth rates at concentrations greater than 2 g basic acid/kg feed. Kojic acid in higher concentrations also significantly increased the relative weights of the proventriculus, gizzard, pancreas, and liver, and significantly decreased the relative weight of the bursa of Fabricius at necropsy (Day 21). Hematological changes included a significant increase in the number of red blood cells, a significant increase in packed-cell volume, and a significant decrease in mean corpuscular volume. Also occurring was a significant increase in the serum concentrations of total protein, albumin, cholesterol, and triglycerides. Hepatotoxicity of dietary kojic acid was evident through a significant increase in the activities of serum glutamic oxalacetic transaminase and creatine kinase and a significant decrease in the activity of alkaline phosphatase. A significant increase in serum uric acid concentration was indicative of nephrotoxicity, and a significant increase in serum glucose concentration was indicative of pancreatic toxicity. A significant decrease in colonic temperature was also observed. Because the toxic effects of kojic acid were only observed at concentrations greater than 2 g kojic acid/kg feed, this mycotoxin alone does not appear to pose a serious economic threat to the poultry industry.

Ascites in growing broilers: a research model.

A method was developed to experimentally produce ascites in broiler chickens. High-altitude simulation (treatment group) was conducted to study the development of ascites in broiler chickens. In each of three experiments, 15 male broiler chicks (1 wk old) were placed in a hypobaric chamber (principal groups) for 5 wk and 15 other chicks were reared in batteries (control groups). Ascites occurred among chicks in the principal groups recorded at 13, 27, and 80% at simulated altitudes of 1,980, 2,438, and 2,896 m, respectively. No ascites were observed in the controls at 100 m (the altitude at College Station, Texas). Body weight was significantly (P less than .05) reduced for broilers in the principal groups versus the controls-especially at 2,896 m, where the principals weighed 500 g less than the controls. The counts for hematocrit, hemoglobin, and red blood cells were significantly (P less than .05) increased in all treatment groups; while at 2,438 and 2,896 m, corticosterone was significantly reduced. Histopathology indicated consistent, mild, cardiopulmonary lesions similar to those observed in the spontaneous ascites of broiler chickens. The high-altitude simulation model will be useful in studying the etiological factors and interactions causing ascites.

Microsomal activation of constituents of white snakeroot (Eupatorium rugosum Houtt) to form toxic products.

Components of white snakeroot, a plant toxic to livestock and human beings, were activated by Aroclor 1254-induced rat liver microsomes. The toxic products of microsomal activation were evaluated in murine melanoma (B16F1) cell cultures. Toxic products in white snakeroot were inactive in cell culture systems without microsomal activation. This activation system revealed that at least 2 fractions of white snakeroot were metabolically activated to cytotoxic agents. The autocatalytic inactivator of cytochrome P-450, 1-aminobenzotriazole, inhibited activation of white snakeroot constituents by rat liver microsomes.

Effects of deoxynivalenol in a wheat ration fed to growing lambs.

A wheat diet containing deoxynivalenol (vomitoxin) at 15.6 mg/kg was fed to crossbred lambs for 28 days. Feed consumption, weight gain, and feed efficiency of deoxynivalenol-treated lambs did not differ (P less than 0.05) from those values of controls. Group differences were not noted for hematologic or serum biochemical variables, and gross or microscopic lesions were not observed in treated lambs.

[14C]monensin balance in bile-fistulated ponies.

To measure absorption of monensin or its metabolites and its elimination from the body, [14C]monensin sodium was given orally (1 mg/kg body wt) to two bile-fistulated ponies and iv (8.7 mg) to one bile-fistulated pony. For one orally-dosed pony, 4.7% of the 14C was eliminated in bile, 52% in feces, .7% in urine and 33% remained in the gastrointestinal (GI) tract after 3 d. Total 14C recovery was 90%. For the other orally-dosed pony, 18.3% of the 14C was eliminated in bile, 69% in feces, 1.7% in urine and 7% remained in the GI tract after 4 d. Total 14C recovery was 98%. For the iv-dosed pony, 72% of the 14C was eliminated in bile, .5% in feces, 4.9% in urine and 15% remained in the GI tract after 23 h. Total 14C recovery was 96%. Maximum rate of 14C elimination in feces from the orally-dosed ponies occurred on the third and fourth days, and the maximum rate of biliary elimination occurred between 16 and 24 h for one pony and 48 and 56 h for the other. For the iv-dosed pony, 14C became immeasurable in plasma within 12 h after dosing and appeared in bile within 30 min, with maximum biliary concentration occurring at about 1 h. Monensin accounted for a minimum of 19% of the 14C in a 56- to 72-h sample of feces for one orally-dosed pony and a minimum of 25% of the 14C in feces from the same time period for the other.(ABSTRACT TRUNCATED AT 250 WORDS)

Toxicity of ochratoxin A and vanadium to growing chicks.

The effects of ochratoxin A (OA) and vanadium (V), singly and in combination, were determined in male Leghorn chicks from 1 to 28 days of age. The chicks were fed a control diet containing the following additives: A) none; B) 2.5 mg OA/kg; C) 50 mg V/kg; D) 2.5 mg OA plus 50 mg V/kg. These data show that body weight gains were significantly reduced by OA and V singly, and a toxicity-enhancing synergism exists between OA and V, which caused a further reduction in performance. The OA-V combination caused a significant increase in the relative weights of the liver, kidney, gizzard, and proventriculus and a significant decrease in the relative weights of the bursa of Fabricius. This decrease in bursal weight was due to atrophy of lymphoid follicles as indicated by the increase in the histologic lesion score. Uric acid in serum was increased, and albumin, calcium, and phosphorus were decreased in the OA-V combination group. There were also small but significant changes in the hematological parameters measured. Distribution of OA to the liver and kidney was not altered, nor was the distribution of V to the liver, kidney, or muscle tissue. Histologic lesions in kidneys were mild but were more prevalent in chicks in the OA-V combination group.

Effect of monensin on the morphology of mitochondria in rodent and equine striated muscle.

Heart, diaphragm, and rear limb muscle from ponies and rats treated with monensin were examined by light and electron microscopy. In both species, mitochondrial aberrations were observed in selected muscle cells. The aberrations consisted of loss of matrix substance (vacuolization) usually accompanied by swelling. Vacuolated mitochondria were characterized by an almost total loss of matrix substance with retention of the rudimentary cristae form. In ponies, most vacuolated mitochondria were observed in heart muscle though some also were found in the diaphragm. In rats, most vacuolated mitochondria were observed in the diaphragm with lesser numbers in rear limb and heart muscles. Red and white muscle fibers were identified in the rat diaphragm based upon fiber size and mitochondrial content. About equal numbers of vacuolated mitochondria were seen in each type of fiber when the total number of vacuolated mitochondria was small. However, when large numbers of mitochondria were vacuolated, the majority of affected mitochondria were seen in white muscle fibers. The form and distribution of vacuolated mitochondria seem sufficiently characteristic to be useful as indicators of monensin poisoning. Mitochondrial vacuolation may be a secondary effect of monensin toxicity since mitochondrial vacuolation does not occur either in cultured cells (plant or animal) or in root plants exposed directly to monensin.

Toxicity of ochratoxin A and tannic acid to growing chicks.

The effects of ochratoxin A (OA) and tannic acid (TA) on growing chicks were determined. One-day-old male broiler chicks were fed a diet containing the following additives for 26 days: A) none; B) 3.0 ppm OA; C) 1.5% TA; D) 3.0 ppm OA plus 1.5% TA. When compared to the controls, body weights and feed efficiencies were significantly depressed in the OA and TA groups. There was a further depression in body weights and a dramatic depression of feed efficiency in the OA-TA combination group. Pigmentation, as measured by visual shank scores, was reduced in chicks fed OA singly or in combination with TA but was not affected by feeding TA singly. There were no consistent treatment differences in the relative weights of the kidney, gizzard, proventriculus, liver, bursa, or pancreas, although there was a trend toward an elevated relative kidney weight in the groups receiving OA. Serum uric acid levels were significantly elevated in the OA and the OA-TA combination group indicating impaired renal excretory function attributable to OA. Total serum protein levels were significantly depressed in the groups receiving OA, and serum calcium levels were depressed in all treatment groups. Serum phosphorus levels were decreased in the OA and OA-TA groups but were only decreased significantly in the OA group. There were no consistent treatment differences in the hematology and other blood chemistry and mineral values.

Somatosensory-evoked response of ataxic Angora goats in suspected haloxon-delayed neurotoxicity.

Somatosensory-evoked responses (SER) were recorded in 3 Angora goats with moderate posterior paresis. The cause of posterior paresis was unknown. The goats had recently been given haloxon and had also been grazing in a pasture with carpetweed (Kallstroemia hirsutissima). Haloxon and carpetweed have each been reported to cause posterior paresis in livestock. An electrical stimulus applied subcutaneously in the pelvic limb of the affected goats failed to evoke an SER at the cerebral cortex. Electrical stimulation in the thoracic limb evoked a normal-appearing SER. The absence of SER from pelvic limb stimulation indicated a functional impairment of the somatosensory pathways.

Acute toxicity of tri-ortho-cresyl phosphate in sheep and swine.

Tri-ortho-cresyl phosphate (TOCP) was given orally or by subcutaneous (SC) injection to sheep and swine. Sheep given oral doses of 100, 200, or 400 mg of TOCP/kg of body weight developed an acute intoxication characterized by diarrhea dehydration, metabolic acidosis, and death within 6 days. Daily SC injections of TOCP in sheep caused either death or delayed neurotoxicosis depending upon the dosage. Increase of aspartate aminotransferase activity approximately 24 hours before the animal died and histopathologic changes confirmed that liver injury had occurred. Swine dosed with 100 to 1,600 mg of TOCP/kg had minimal signs of acute toxicosis, but developed severe delayed neurotoxicosis in approximately 15 days. Those given a 800 mg/kg dose by the oral route or SC injection had severely decreased serum acetylcholinesterase activity. In the swine which were euthanatized at 7 days after treatment, histopathologic examinations revealed no lesions (although the nervous system was not examined, because clinical neurologic signs were normal).

High pressure liquid chromatographic determination of penicillic acid in chicken tissues.

Penicillic acid (PA) is a mycotoxin with reported cytotoxic, cardiotoxic, and carcinogenic activity and it can occur in high concentration in corn. The occurrence of PA in contaminated poultry feed represents a potential public health hazard. A reverse phase high pressure liquid chromatographic (HPLC) method is proposed for determining PA residues in chicken tissues. Optimization of chromatography was achieved for PA using a mobile phase consisting of acetonitrile: H2O. PA was detected by ultraviolet absorption at 254 nm, identified by retention time, and quantitated by peak area integration. Blood, parenchymal tissues, muscle, and alimentary tract contents were homogenized, sonicated, and acid treated followed by extraction with ethyl acetate and analysis by HPLC. Acute oral dosing of chickens with PA over a range of 50 to 550 mg/kg body weight resulted in detectable levels of the mycotoxin (confirmed by gas liquid chromatography) in gizzard muscle and contents, liver, kidney, heart, and intestinal contents. This method should prove useful both for the rapid and sensitive detection of PA residues in poultry and in further studies on the distribution and metabolism of this mycotoxin.

Ultrastructural observations in ponies after treatment with monensin.

Ultrastructural studies were made of myocardium, diaphragm, appendicular muscle, liver, and kidney of 3 ponies acutely poisoned with a single oral dose of monensin (4 mg/kg of body weight). These ponies developed severe signs of toxicosis and were killed 28 to 72 hours after treatment. Severe mitochondrial damage (swelling) and lipoidosis in myocardial tissues were observed in 2 of the 3 ponies; similar, but less severe, changes were observed in the 3rd pony. The hepatocytes of the 3 ponies were characterized by increased amounts of smooth endoplasmic reticulum, large numbers of lipid droplets, vacuoles bounded by fibrous material, and a 2-fold increase in the number of peroxisomes per cell. Some hepatocytes also contained a membrane-bounded protein-like body. The observations indicate that heart mitochondria are primary targets of monensin poisoning in ponies.

Body temperature changes in sows during the periparturient period.

Deep body temperatures were monitored with an implanted radiotelemetry device from 2 to 4 days prepartum to approximately 12 days postpartum in sows. The mean prepartum temperature of five normal sows was 38.6 degrees C, with a range of 38.3--38.9 degrees C. An increase in body temperature (1.4 degrees C) was associated with parturition. The increase in body temperature began about 12 hours before the first pig was born, peaked 1-2 hours after delivery of the last pig, and decreased during the first day postpartum but did not reach the prepartum values. Two days postpartum, the mean body temperature was about 1 degree C higher than it was during the prepartum period. The mean body temperature increased an average of 0.06 degrees C per day during the 12-day postpartum period. A diurnal pattern was evident in the body temperature variations.

Congenital stationary night blindness: an animal model.

Electroretinographic studies of myctalopic Appaloosa horses demonstrated photopic and scotopic abnormalities similar to those in humans with congenital stationary night blindness (CSNB) of the Schubert-Bornschein type. The phototopic abnormalities consisted of reduced b-wave amplitudes and slower than normal b-wave implict time. The dark-adapted ERG's consisted of a simple negative potential; the scotopic b-wave was nonrecordable. However, a normal c-wave was present in the dark-adapted response. Histologic studies demonstrated no structural abnormalities that could explain the functional defect.

Cone and rod photoreceptors in the white-tailed deer Odocoileus virginianus.

Duplicity of the white-tailed deer (Odocoileus virginianus) retina, ie, cone and rod function, was established by histologic and electrophysiologic data. The presence of cones and rods in the deer retina was shown by light and electron microscopy. Electroretinography revealed distinct photopic (bp) and scotopic (bs) components in the b-wave of the electroretinogram that are characteristic of the cone and rod activity. These findings are in contrasts to the popular belief that deer have retina composed entirely of rods.

Photosensitization in sheep fed Ammi majus (Bishop's weed) seed.

Ammi majus (bishop's weed) grows on the coastal region of southern United States and in other parts of the world. This plant causes severe photosensitization in livestock and probably contributes to the severe photosensitization outbreaks seen in Texas. Sheep were fed finely ground seed of A majus via stomach tube at dose rates of 1, 2, 4, and 8 g/kg of body weight and exposed to sunlight. The single dose of 8 g/kg produced severe clinical signs (in 24 to 48 hours): cloudy cornea, conjunctivokeratitis, photophobia, and edema of the muzzle, ears, and vulva. Daily dosing at 2 and 4 g/kg produced (in 72 to 96 hours) similar signs, whereas the smallest dose (1 g/kg) produced mild irritation of the muzzle. Pathologic changes included (1) corneal edema and marked neutrophilic infiltration of the cornea and corneal/ciliary process, (2) subacute ulcerative and exudative dermatitis of the skin of ears, muzzle, and vulva, and (3) mild focal tubular degeneration (vacuolar type) of the kidney.