Effect of ferric ammonium citrate in feedlot diets with varying dried distillers' grains inclusion on ruminal hydrogen sulfide concentrations and steer growth.

Angus-cross steers ( = 128) were used to examine the effects of supplementing ferric ammonium citrate (FAC; 300 mg ferric Fe/kg DM) to diets of 20, 40, or 60% dried distillers' grains plus solubles (DDGS) on growth performance, liver mineral and ruminal hydrogen sulfide (HS) concentrations, and carcass traits of finishing steers. Steers were blocked by initial BW (436 ± 10.6 kg) into pens of 4 and randomly assigned to 1 of 6 treatments ( = 5 or 6 pens per treatment) including a 20, 40, or 60% DDGS inclusion diet with (+) or without (-) 300 mg Fe/kg DM from FAC. Liver biopsies (d -9/-10 and 96) and HS measures (d 0, 7, 14, 21, and 95) were determined from 1 steer/pen. Steers were harvested on d 102 and carcass data were collected. A treatment × month effect ( ≤ 0.006) was noted for ADG and G:F, in which the 20-FAC ADG and feed efficiency were greater ( ≤ 0.02) between d 0 to 28 but lesser ( ≤ 0.04) from d 29 to 56 than that of the 20+FAC steers. Final BW linearly decreased ( < 0.01) as DDGS inclusion increased. Final BW tended to be greater ( = 0.10) in the 60+FAC steers than in the 60-FAC steers, whereas final BW was not different ( ≥ 0.32) due to FAC supplementation in the 20 or 40% DDGS diets. A quadratic effect was noted for DMI ( = 0.02), where 60% DDGS decreased DMI. Within the 20% DDGS diet FAC+ improved DMI ( = 0.03) but had no effect within 40 or 60% DDGS inclusion. Ruminal HS concentrations were not affected ( ≥ 0.25) by FAC, but increasing DDGS linearly increased ( < 0.01) ruminal HS values. Liver Cu was decreased ( < 0.01) by FAC across all DDGS inclusions and tended to linearly decrease ( = 0.06) with increasing DDGS inclusion, whereas liver Fe, Mn, and Zn were not altered ( ≥ 0.11) by DDGS inclusion. Liver Zn concentrations tended to be ( = 0.08) or were ( = 0.03) decreased by FAC supplementation within 20 and 40% DDGS, respectively. Increasing the inclusion of DDGS linearly decreased ( = 0.04) HCW and quadratically affected marbling score where the 40% DDGS had the greatest ( = 0.02) marbling scores. Supplementation of FAC within 60% DDGS improved ( ≤ 0.03) HCW and LM area. Marbling scores were greater ( ≤ 0.04) in 20+FAC and 40+FAC compared with 20-FAC and 40-FAC, respectively. In conclusion, although ruminal HS concentrations were not affected by FAC under the conditions of this study, supplementing FAC to diets containing 60% DDGS improved HCW and LM area, suggesting that FAC may be beneficial when dietary S concentrations exceed 0.5%.

Toxic equine parkinsonism: an immunohistochemical study of 10 horses with nigropallidal encephalomalacia.

Chronic ingestion of yellow star thistle (Centaurea solstitialis) or Russian knapweed (Acroptilon repens) causes nigropallidal encephalomalacia (NPE) in horses with an abrupt onset of neurologic signs characterized by dystonia of lips and tongue, inability to prehend food, depression, and locomotor deficits. The objectives of this study were to reexamine the pathologic alterations of NPE and to conduct an immunohistochemistry study using antibodies to tyrosine hydroxylase and α-synuclein, to determine whether NPE brains show histopathologic features resembling those in human Parkinson disease. Results confirm that the NPE lesions are located within the substantia nigra pars reticulata, sparing the cell bodies of the dopaminergic neurons in the substantia nigra pars compacta, and in the rostral portion of the globus pallidus, with partial disruption of dopaminergic (tyrosine hydroxylase-positive) fibers passing through the globus pallidus. No abnormal cytoplasmic inclusions like the Lewy bodies of human Parkinson disease were seen in these NPE brains. These findings indicate that equine NPE may serve as a large animal model of environmentally acquired toxic parkinsonism, with clinical phenotype directly attributable to lesions in globus pallidus and substantia nigra pars reticulata rather than to the destruction of dopaminergic neurons.

Analysis of environmental chemical residues in products of emerging aquaculture industry in Uganda as case study for Sub-Saharan Africa.

A study was conducted to analyse market-regulated heavy metals (lead, mercury and cadmium), organochlorine pesticides and total polychlorinated biphenyls (PCBs) in samples of 38 farmed fish comprising Nile tilapia (Oreochromis niloticus) (20 samples) and African catfish (Clarias gariepinus) (18 samples) from ten selected fish farms in Uganda. The goal of this case study was to understand the safety of aquaculture products from Sub-Saharan Africa. Lead was detected in all the 38 samples (maximum = 1.08 mg kg(-1) (dry weight)), mercury in 31 out of 38 samples (maximum = 0.35 mg kg(-1) (dry weight)), and cadmium in two samples (maximum = 0.03 mg kg(-1) (dry weight)). Total levels of PCBs were below the limit of detection of 0.02 mg kg(-1) (wet weight) in all the samples. Traces of 4,4'-dichloro-diphenyldichloroethylene (DDE) were detected in ten out of 38 samples (maximum = 0.01 mg kg(-1) (wet weight)) making it the most prevalent organochlorine pesticide. Other pesticides detected were: 4,4'-dichloro-diphenyl-trichloroethane (DDT) and endosulfan sulphate, which were found in one fish sample (both 0.002 mg kg(-1) (wet weight)). There was no statistically significant difference between the levels of lead and mercury in catfish and tilapia (t-test at p = 0.05). More catfish samples (eight) contained DDE as compared with tilapia (two). Cadmium, DDT and endosufan sulphate were only detected in catfish implying that catfish is more prone to contamination than tilapia. The levels of contaminants were below the US Food and Drug Administration (USFDA) action levels and European Union maximum residue limits (MRLs), indicating that such fish have the potential for export to these markets.

A retrospective study on the disappearance of blood lead in cattle with accidental lead toxicosis.

Lead poisoning in cattle and other food animals is of public health significance because of the potential for human exposure to lead through ingestion of contaminated meat and milk products derived from lead-poisoned animals. In Michigan, lead poisoning in livestock is a reportable disease, and positive cattle are quarantined until they test negative (<0.05 ppm blood lead). There is surprisingly little information on blood lead kinetics in cattle. The half-life has been variably reported as 9 weeks and 1-2 months. Because these data did not fit those obtained from cases received at the Michigan State University Animal Health Diagnostic Laboratory, a retrospective study was conducted to review all cases of accidental lead poisoning in cattle between 1990 and 1998. This information is needed to estimate when quarantined lead-poisoned cattle can be released. The results showed that the half-life of blood lead was quite variable and ranged from 48 to 2,507 days. The shortest half-lives (48, 56, and 57 days) were found in a lactating herd of 20-month-old heifers. The longest half-life, 2,507 days, was found in a 9-month-old castrated bull, which ingested a discarded automobile battery. Of the 24 animals monitored, only 8/24 (33%) had half-lives between 6 and 14 weeks. In conclusion, the half-life of blood lead is difficult to predict in accidental cases of cattle poisoning.

Opportunities and challenges of strengthening veterinary toxicology in Africa in the 21st century.

Veterinary toxicology is the specialty of veterinary medicine dealing with the study, diagnosis and treatment of effects of natural and man-made chemicals, forms of energy, and gasses in the animal kingdom. Historically, veterinary toxicology has been narrowly defined as the diagnosis and treatment of poisoning in domesticated animals and poultry, but the profession has grown to include food safety and environmental toxicology. Veterinary toxicology is most well-developed and recognized as a specialty in North America where professional societies and specialty board certification exist. In many parts of Africa, perhaps with the exception of South Africa, veterinary toxicology has not evolved in more than 40 years. The importance of veterinary toxicology in the modern era can not be over emphasized. This report examines the status of veterinary toxicology in Africa at the beginning of the 21st century and offers arguments why it is important for African governments to devote more resources to strengthen it.

Augmentation of mercury-induced nephrotoxicity by endotoxin in the mouse.

Endotoxin (lipopolysaccharide; LPS) and mercury are compounds of food safety concern. Endotoxin is a product of cell walls of gram negative bacteria. Humans are constantly exposed to LPS through infection plus translocation into circulation from the gastrointestinal tract. Food is the major source of mercury in humans. The toxic interaction between LPS and mercury has not been well investigated. In a previous study, we demonstrated that LPS potentiated mercury-induced nephrotoxicity in the rat. Whether this observation was species specific was not clear. In this study we tested the hypothesis that LPS enhances mercuric chloride (HgCl(2))-induced nephrotoxicity in mice. In a 2x2 factorial design, mice received either Escherichia coli 0128:B12 endotoxin (2.0 mg/kg body weight) or 200 microliter of 0.9% sodium chloride (saline), and this was followed 4 h later by either mercury (1.75 mg mercuric chloride per kg body weight) or 200 microliter of saline. Mice were monitored for 48 h. Monitored end-points included body and renal weights, urine volume, renal histology and ultrastructural pathology, serum urea nitrogen and creatinine, selected serum and urine cytokines, and renal mercury concentrations. Endotoxin by itself was not nephrotoxic at the dose used in this study. Overall, mice given LPS plus mercury were the most severely affected. Mice given LPS and mercury also had significantly greater renal mercury concentration than those given mercury alone (P

The postmortem diagnosis of cholecalciferol toxicosis: a novel approach and differentiation from ethylene glycol toxicosis.

The objectives of this study were to develop a novel approach to postmortem diagnosis of cholecalciferol (CCF) toxicosis in dogs using kidney, bile, and urine samples, and to differentiate CCF from ethylene glycol (EG) toxicosis. To achieve these objectives, specimens collected from 2 previous laboratory studies in which dogs were given a single oral toxic dose of CCF (8.0 mg/kg) were used. For EG toxicosis, historical data from the previous 13 years (1985-1998) were reviewed and confirmed cases of EG toxicosis were selected. The historical data were used to compare trace mineral concentrations, specifically of calcium and phosphorus to differentiate between intoxications caused by CCF from that caused by EG in dogs. Kidneys, bile, and urine from dogs that died of CCF toxicosis were analyzed for 25 monohydroxy vitamin D3 (25(OH)D3) and 1,25 dihydroxy vitamin D3 (1,25(OH)2D3) and compared to known control unexposed dogs. Results of this study show that biliary and renal 25(OH)D3 concentrations and renal calcium to phosphorus ratio are of diagnostic value in dogs exposed to toxic concentrations of CCF. The renal calcium to phosphorus ratio was <0.1 in normal dogs, 0.4-0.9 in dogs that died of CCF toxicosis, and >2.5 in dogs that died of EG toxicosis.

Potentiation of mercury-induced nephrotoxicity by endotoxin in the Sprague-Dawley rat.

Endotoxin (lipopolysaccharide; LPS) and mercury are nephrotoxic compounds of food safety concern. Endotoxin is a product of cell walls of gram negative bacteria. Humans are constantly exposed to LPS through food, water and air. Food is the main source of mercury exposure for humans. Endotoxin potentiates the toxicity of a number of xenobiotics, but its interaction with nephrotoxic heavy metals has not been investigated. We tested the hypothesis that endotoxin enhances mercury-induced nephrotoxicity. Thirty-two, 41-43-day-old, male Sprague-Dawley rats were allocated randomly to four groups of eight rats each as follows: group I received 0.9% sodium chloride, group II received 2.0 mg of Escherichia coli 0128:B12 LPS kg(-1) once, group III received 0.5 mg mercuric chloride kg(-1) once, and group IV received 2.0 mg E. Coli 0128:B12 LPS kg(-1) once 4 h before receiving 0.5 mg mercury chloride kg(-1) once. Mercury, LPS and 0.9% sodium chloride were all injected IV through the tail vein. Rats were monitored for 48 h after mercury injection. Serum creatinine, urea nitrogen, and polyuria were significantly increased in rats given LPS plus mercury relative to those given either agent alone or saline (P

Use of pamidronate disodium to reduce cholecalciferol-induced toxicosis in dogs.

OBJECTIVE: To determine whether pamidronate disodium can reduce cholecalciferol-induced toxicosis in a dose-related manner. ANIMALS: 20 clinically normal, 8- to 12-month-old male Beagles. PROCEDURE: All dogs were given 8 mg of cholecalciferol (CCF)/kg of body weight once orally, then were randomly assigned to 4 groups of 5 dogs each. Dogs were treated with IV administration of 0.9% NaCl solution (SC group), 0.65 mg of pamidronate/kg in 0.9% NaCl solution (LP group), 1.3 mg of pamidronate/kg in 0.9% NaCl solution (MP group), or 2.0 mg of pamidronate/kg in 0.9% NaCl solution (HP group) on days 1 and 4 after administration of CCF. Dogs were observed for 14 days, and serial blood samples were collected for serum biochemical, electrolyte, and 25-hydroxyvitamin D3 analyses. Urine samples were collected for determination of specific gravity. Glomerular filtration rate (GFR) was determined by plasma iohexol clearance. Histologic examination of renal tissue was performed. RESULTS: One dog in the SC group was euthanatized 3 days after administration of CCF because of severe clinical signs of toxicosis. Dogs in the HP group had significantly higher mean GFR (day 3), serum potassium concentrations (day 14), and urine specific gravity (days 7 and 14) and significantly lower mean serum creatinine concentrations and total calcium X phosphorus concentration product (days 4 and 7) than dogs in the SC group. Dogs in the HP group had no abnormal findings on histologic examination of renal tissue, dogs in the LP and MP groups had trace to mild mineralization of renal tissue, and dogs in the SC group had moderate mineralization and cellular necrosis of proximal renal tubules. CONCLUSIONS AND CLINICAL RELEVANCE: Pamidronate disodium is a potentially useful drug to reduce CCF-induced toxicosis and other causes of hypercalcemia associated with increased bone resorption in dogs.

Use of pamidronate to reverse vitamin D3-induced toxicosis in dogs.

OBJECTIVES: To determine whether pamidronate disodium can reduce vitamin D3-induced hypercalcemia in dogs and whether combination treatment with calcitonin is more effective than treatment with pamidronate alone. ANIMALS: 20 clinically normal male Beagles. PROCEDURE: All dogs were given 8 mg of cholecalciferol (CCF)/kg of body weight once orally, then were assigned randomly to 4 groups of 5 dogs each. Dogs were given 0.9% NaCl solution IV (group 1), calcitonin SC and 0.9% NaCl solution IV (group 2), pamidronate and 0.9% NaCl solution IV (group 3), or a combination of all 3 agents (group 4). Dogs were observed for 28 days, and serial blood and urine samples were collected for determination of serum biochemical, electrolyte, and 25(OH)D3 values, CBC, and urine mineral excretion. Samples of kidney, stomach, lung, aorta, liver, duodenum, and brain were evaluated by light microscopy and quantitative mineral analysis. RESULTS: Two dogs in group 1 were euthanatized 4 days after CCF administration because of severe clinical signs of disease. Dogs in group 3 lost less weight and had significantly lower serum phosphorus, total and ionized calcium, and urinary zinc concentrations, compared with dogs in group 1. On day 4, serum urea nitrogen concentration was significantly lower in dogs of groups 3 and 4, compared with dogs in group 1. Mild to moderate mineralization of kidneys and stomach were observed in the 2 group-1 dogs euthanatized on day 4. CONCLUSIONS: Pamidronate administration effectively prevents CCF-induced hypercalcemia and mineralization of soft tissues. CLINICAL RELEVANCE: Pamidronate is a potentially useful antidote against CCF toxicosis in dogs.

Experimental murine IgA nephropathy following passive administration of vomitoxin-induced IgA monoclonal antibodies.

Oral exposure of mice to vomitoxin (VT) induces elevated levels of serum IgA, circulating IgA immune complexes (IgA-IC), mesangial IgA deposition and haematuria, which all mimic the clinical signs of human IgA nephropathy (IgAN). To further assess the effects of VT-induced IgA in the murine model, B6C3F1 and BALB/C mice were injected intraperitoneally with affinity-purified monoclonal IgA derived from Peyer's patch hybridomas of VT-exposed mice. In B6C3F1 mice, serum IgA, IgM and IgA-IC levels were increased two- to fivefold in treatment groups after 4 and 6 wk compared with controls, whereas increases in serum IgG as high as 18-fold were observed. Urinary erythrocyte counts were also significantly elevated in treatment groups after 2, 4 and 6 wk compared with controls. Concurrent increases in IgA and IgG complexes containing casein, the dietary protein source, occurred in treatment mice. Mesangial IgA, IgG, IgM and C3 deposition were significantly increased in all treatment mice after 6 wk. Electron-dense deposits occurred in the glomeruli of IgA-injected mice after 6 wk. All the above parameters were similarly affected in BALB/C mice. Injection of IgA-secreting hybridoma cells into BALB/C mice increased serum IgA, IgA-IC and IgG levels as well as elevated mesangial IgA, IgG and C3 deposition and haematuria after 2-3 weeks compared with controls. In total, these data indicate that passive administration of VT-induced IgAs can induce the hallmarks of IgA nephropathy. Casein, an antigen found in the diet used for these mice, appeared to form IC with IgA or IgG and these IC may participate in the pathogenesis of this nephropathy.

Fumonisin exposure to Kansans through consumption of corn-based market foods.

Fumonisins are secondary metabolites of the fungus Fusarium moniliforme Sheldon, a common corn contaminant world wide. Presently 6 different fumonisins (FB1, FB2, FB3, FB4, FA1 and FA2) have been identified and characterized. In veterinary medicine fumonisins cause equine leucoencephalomalacia and swine pulmonary edema. In addition, fumonisins have been shown to be carcinogenic in laboratory animals and have been linked to human esophageal cancer in South Africa and China. In this study we examined the prevalence of FB1, FB2 and FB3 in corn-based human foods in Kansas using HPLC equipped with a fluorescent detector. All 3 fumonisins were detected in at least 1 food item. However, only 24/121 samples analyzed (20%), contained detectable (> 40 ppb) fumonisins. Corn flour was the most frequently contaminated as 13/25 items (52%) were positive for fumonisins. For all analyzed human foods, the range of fumonisins was 42-350 ppb in comparison to 765-9953 ppb found in corn meant for animal consumption. This data shows that corn flour is the item most likely to be contaminated with low concentrations of fumonisins. Corn-based foods do not appear a significant source of fumonisins for Kansans although the implications to human health of these low levels are unknown.

Comparison of N-acetylcysteine and methylene blue, alone or in combination, for treatment of acetaminophen toxicosis in cats.

Acetaminophen is widely used in human beings for analgesic purposes, but is one of the most frequent causes of poisoning in cats. Acetaminophen-poisoned cats develop methemoglobinemia and sometimes hepatic failure. To determine the benefit of using methylene blue, a treatment for methemoglobinemia, along with N-acetylcysteine (NAC), the recommended treatment for acetaminophen-poisoned cats, groups of 3 male and 3 female cats each were given methylene blue NAC, or both after administration of acetaminophen (120 mg/kg of body weight, PO). Male cats seemed more susceptible than female cats to acetaminophen toxicosis, because 3 males died of hepatic failure (2 cats given acetaminophen/methylene blue and 1 given acetaminophen/NAC/methylene blue). Although NAC alone seemed to elicit the best overall response, methylene blue, alone or in combination with NAC, may be useful in female cats.

Methylene blue can be used to treat methemoglobinemia in cats without inducing Heinz body hemolytic anemia.

Methylene blue (MB) is the drug of choice in the treatment of methemoglobinemia (MTHB) in humans and most domesticated animals, but is reported contraindicated in cats. Although prolonged treatment of cats for urologic syndromes with MB-containing antiseptics causes Heinz body (HB) hemolytic anemia, there is no evidence to suggest that single or repeated therapeutic doses of MB cause hemolytic anemia. We investigated the efficacy and safety of MB in reversing nitrite-induced MTHB in cats. Forty random-bred adult cats (20 males and 20 females) were divided as follows: Group 1, 1.5 mL saline/kg bw iv (control); Group 2, 1 dose of 1.5 mg MB/kg bw iv; Group 3, 2 doses of 1.5 mg MB/kg bw iv 4 h apart; Group 4 1 dose of 1.5 mg sodium nitrite/kg bw iv; Group 5, 1 dose of 1.5 mg sodium nitrite/kg bw iv followed by 1 dose of 1.5 mg MB/kg bw iv 1 h later; and Group 6, 1.5 mg sodium nitrite/kg bw iv followed in 2 h by 2 doses of 1.5 mg MB/kg iv 4 h apart. One iv dose of MB sufficiently and rapidly reversed MTHB in the cats without increasing circulating HB-containing red blood cells. Giving 2 iv doses of MB without or after sodium nitrite significantly increased the frequency of circulating HB-containing red blood cells. Pre-exposure to sodium nitrite potentiated the HB-inducing effect of 2 doses of MB. Hemolytic anemia was not observed or demonstrated in any of the cats groups.

The effects of administering methylmercury in combination with ethanol in the rat.

Methylmercury (MeHg) is a potent neurotoxicant and nephrotoxicant in several animal species including humans. Although the in vivo toxicity of MeHg per se is well known, the interaction between MeHg and other pollutants and with nutritional factors is not well understood. Since ethanol (EtOH) is a widely consumed toxicant which has been shown to enhance the histopathologic effects of MeHg on renal tissues, a study was undertaken to examine the effects of the combined administration to rats of MeHg and EtOH on renal function and on mercury distribution in body tissues. Forty-eight rats were divided into 6 treatment groups of 8 rats each. Rats in groups 1, 2 and 3 were given feed ad libitum, a restricted liquid diet of 70 mL/d or distilled water orally, respectively. Rats in groups 4, 5 and 6 were given 1.5 mg MeHg/kg bw, 2.0 g EtOH/kg bw, or 1.5 mg MeHg + 2.0 g EtOH/kg bw, respectively, by oral gavage daily for 45 d. All rats except those in group 1 (ad libitum) were fed 70 mL of liquid diet/d for the entire study period. The ingestion of MeHg + EtOH in combination induced a greater increase in renal weight compared to treatment with either MeHg + EtOH alone. Only those rats given MeHg in combination with EtOH exhibited oliguria and elevated blood urea nitrogen levels. Despite this antidiuresis, urinary concentrating ability was impaired in those rats given both MeHg and EtOH. In contrast, the ingestion of MeHg by itself caused the most rapid loss of glucose in urine.(ABSTRACT TRUNCATED AT 250 WORDS)

The renal histology and ultrastructure in rats given methylmercury and ethanol in combination.

The effects of combined administration of methylmercury (MeHg) and ethanol (EtOH) on renal morphology were examined in the rat. Forty-eight male Wistar rats were divided into 6 groups of 8 rats each as follows: group 1 was given feed ad libitum with no treatment; group 2 was restricted to 70 mL of feed daily with no treatment; groups 3-6 were restricted to 70 mL of feed daily and gavaged with distilled water, MeHg alone, EtOH alone, or MeHg in combination with EtOH, respectively, daily for 45 days. The ingestion of MeHg and EtOH in combination caused severe structural renal lesions which involved the glomerulus and all segments of the uriniferous tubule. Only with this combination treatment (group 6) was glomerular pathology observed; accumulations of platelets and inflammatory cells, fibrosis and thickening of the mesangium were observed in the glomerulus. There was also severe tubulointerstitial nephritis characterized by tubular atrophy, accumulation of inflammatory cells especially neutrophils, and increased collagen deposition in the same group. In contrast, the ingestion of either MeHg or EtOH produced less severe lesions mainly in the proximal tubular epithelium. This study suggests that EtOH enhanced the nephrotoxicity of MeHg.

Combined effects of methylmercury and ethanol on renal metallothionein and mercury residues in rats fed restricted amounts of a liquid diet.

Simultaneous treatment of rats with ethanol (EtOH) and methylmercury (MeHg) increases the frequency of lesions in the rat kidney. Therefore, it was of interest to us to study the effects of simultaneous treatment of rats with MeHg and EtOH on kidney metallothionein (MT) and mercury residues levels in kidneys of rats maintained on 70% of ad libitum diet. Treatment with MeHg alone induced kidney MT the most (twice) compared to its pair-fed control. Simultaneous treatment with MeHg and EtOH also induced kidney MT but to a lesser degree than treatment with MeHg alone (by about 30%). Ethanol by itself caused a slight increase in kidney MT although starvation resulting from pair-feeding with mercury-treated animals may have contributed to this observation. Simultaneous treatment with MeHg and 2 g/kg EtOH caused a significant reduction in inorganic mercury levels in the kidney (P less than 0.05) compared to treatment with MeHg alone or in combination with 1 g/kg EtOH. Corresponding with the decrease in kidney inorganic mercury levels was a significant increase in urine inorganic mercury levels in this group compared to treatment with 1 g/kg ethanol + MeHg.