Chronic copper toxicity in a dairy herd

The addition of excessive copper to a commercially prepared dairy ration caused chronic copper toxicity in a dairy herd. A formulation error by a feed company resulted in copper levels of 800 to 1,000 mg/kg in the “as fed concentrate,” amounting to about 400-500 mg copper/kg of the whole ration. Five animals died with typical signs of acute copper toxicity, including intravascular hemolysis and methemoglobinemia. A further 39 cows died on the farm from a combination of debilitation and secondary infectious causes, and 215 were sent to slaughter because of debilitation and poor milk production. The mortality of calves born to dams that had been fed the toxic concentrate was approximately 50%.

We postulate that dairy cows, particularly pregnant cows, may be more susceptible to copper toxicity than other cattle, and suggest reexamination of the presently allowable maximum levels of copper supplementation of diets for dairy cattle.

     

Unusual history and initial clinical signs of Mycoplasma bovis mastitis and arthritis in first-lactation cows in a closed commercial dairy herd

CASE DESCRIPTION: 9 first-lactation dairy cows in a closed dairy herd had swelling in the forelimbs and forelimb lameness. Mycoplasmal arthritis and mastitis were diagnosed. CLINICAL FINDINGS: Swelling of the carpal joint, diffuse subcutaneous edema from the carpal to metacarpophalangeal joints, and forelimb lameness were evident in 9 first-lactation cows 7 to 21 days after parturition. Diagnostic testing revealed that 3 of 3 bulk-tank milk samples, 3 milk samples from cows with clinical mastitis, 2 fluid samples obtained from arthritic joints, and samples from the lungs and spleen of a cow that had died yielded positive results for Mycoplasma spp. Nucleic acid sequence analysis performed by use of a PCR assay on the joint fluid and lung tissues confirmed infection with Mycoplasma bovis. TREATMENT AND OUTCOME: Affected cows were treated by IM administration of flunixin meglumine and dexamethasone for 3 days. All cows were nonresponsive to treatment (3 cows died, and the other 6 were culled). Follow-up culture for Mycoplasma spp of milk samples from the bulk tank and from all lactating cows was recommended to screen for chronic subclinical carriers. CLINICAL RELEVANCE: Mycoplasmal infections may cause unusual initial clinical signs or an atypical history. When dairy cattle, including those residing in closed herds, have lameness, swelling of the carpal or metacarpophalangeal joints, edema of the distal portions of the forelimbs, or polyarthritis, infection with Mycoplasma spp should be investigated. Delay in diagnosis of mycoplasmal infections in dairy herds can result in substantial financial loss and the establishment of chronic subclinical carriers.     

High mortality in a herd with signs of jejunal hemorrhage syndrome

Eleven cows from a herd of 80 dairy cows (14%) died over a 7-month period. Death occurred within 12-24 hours of the onset of the first clinical signs, namely, dullness and a decrease (mean 25%) in milk production. Within 12 hours the cows were unable to rise, felt cold, and were restless. Examined mucous membranes were pale. Two of three cows examined at necropsy had blood in the jejunum and high counts of Clostridium perfringens. Jejunal hemorrhage syndrome was diagnosed in these two cows on the basis of the clinical signs and postmortem findings.     

Absorption and distribution patterns of aflatoxicol and aflatoxins B1 and M1 in blood and milk of cows given aflatoxin B1

Two 600-kg lactating cows were each given a single oral dose (0.5 mg/kg of body weight) of aflatoxin B1 (B1). Samples were obtained at postdosing hours 0, 1, 2, 3, 4, 6, 8, 10, and 12 and thereafter every 12 hours for 10 days. Aflatoxicol (Ro), B1, and aflatoxin M1 (M1) were found in the milk, plasma, and RBC of both cows at postdosing hour 1. Maximum concentrations of the toxins were observed at 12 and 60 hours. The ratio of the concentrations for Ro, B1, and M1 was approximately 1:10:100. Both cows had clinical signs of distress at 24 hours; 1 cow died at 60 hours and the other cow recovered within 4 days. In the samples of liver, kidney, urine, bile, and rumen contents of the cow that died, the B1 concentrations were 5.1, 3.3, 4.1, 1.6, and 320 ng/g, respectively, and the M1 concentrations were 4.3, 20, 37, 16, and 8.6 ng/g. The Ro concentrations in the kidney were approximately equal to that of B1; however, liver, urine, bile, and rumen contents concentrations were 0.88, 0.10, 0.36, and 4.9 ng/g, respectively.     

Serum amyloid A and TNF alpha in serum and milk during experimental endotoxin mastitis

A cross-over study was conducted to investigate the effect of intramammarily infused lipopolysaccharide (LPS) on the acute phase reaction in early (EL) and in late (LL) lactation. Nine cows received intramammary injections of 100 microg of Escherichia coli 0111:B4 LPS during EL and LL. The severity of each cows systemic and local signs and change in milk appearance were recorded and scored throughout the experiment. Systemic and local signs were found to be more serious in EL cows. Tumor necrosis factor alpha (TNF alpha) was detected in milk but not in serum. Serum amyloid A (SAA) concentrations increased both in serum and in milk. The milk TNF alpha concentrations peaked at 8 h post-challenge (PC). SAA concentrations started to increase at 8 h PC, and peak concentrations were seen at 32 and 48 h PC in milk and serum, respectively. The milk TNF alpha and SAA seemed to be correlated, being on average higher in EL. Serum SAA concentration was not correlated with milk TNF alpha or SAA, nor with the severity of local or systemic signs, but was correlated with changes in milk appearance.     

Etiology of ammoniated hay toxicosis

Some animals consuming hay treated with anhydrous ammonia have developed neurological signs including hyperexcitability, circling and convulsions. A series of experiments was conducted to identify tentatively the toxin and determine its mode of action. Three out of four sheep fed ammoniated orchardgrass hay (approximately 4% ammonia on a dry basis) developed convulsions. Two of the three sheep died within 18 h of the onset of signs. The concentrations of blood lactate and pyruvate were elevated in the symptomatic sheep (P less than .05). A proposed toxin, 4-methyl imidazole, did not induce the syndrome when 750 mg/d (approximately 10 times the dietary amount) were administered orally. Four out of five calves that received milk from cows fed ammoniated oat hay (approximately 5% ammonia on dry basis) displayed hyperexcitability and circling. Concentrations of blood lactate and pyruvate were also elevated in the calves. The crude alkaloid fraction of the toxic milk produced neurological signs similar to those of the calves when injected into mice. A fluorescent compound was found in the alkaloid fraction of toxic milk and ammoniated hay, but not in control milk or untreated hay. The fluorescent compound was quite labile; hence, characterization has been unsuccessful thus far.     

Copper poisoning in a dairy herd fed a mineral supplement

Copper poisoning in a dairy herd resulted in the death of 9 of 63 (14%) adult Holstein cows. Clinical signs were acute anorexia, weakness, mental dullness, poor pupillary light reflexes, and scant nasal discharge. These were followed by recumbency, chocolate-colored blood, jaundice, and death. Four animals exhibited signs of hyperesthesia and/or rumen stasis prior to death. At necropsy there was generalized icterus of body tissues, with the liver appearing orange and the kidneys dark blue. Histologically, there was accumulation of hemosiderin in Kupffer cells, and severe to moderate hepatocellular necrosis in all cases. Ammonium molybdate added to the ration, combined with the cessation of mineral supplementation, arrested the outbreak.

These cases illustrate significant mortality, due to copper poisoning, in adult cattle fed a low-dose mineral dietary supplement for over two years. Dietary copper intake of the herd (on a dry matter basis) was 37.5 mg/kg for lactating cows and 22.6 mg/kg for dry cows.

     

奶牛日粮中添加富硒酵母对乳硒和血清硒含量的影响

通过日粮添加富硒酵母研究有机硒对泌乳奶牛乳硒含量和血清硒含量的影响。试验选择24头胎次相同,泌乳日龄、产奶量和体重相近的荷斯坦奶牛,随机分为2组,对照组和处理组均饲喂相同的TMR基础日粮,TMR基础日粮硒含量为0.33 mg/kg,处理组另补充富硒酵母,源于富硒酵母的硒为0.78 mg/kg DM,整个试验期56 d。试验结果表明,添加富硒酵母后对奶牛干物质采食量、产奶量、乳常规和乳常规产量没有显著影响,但显著提高了血清和牛奶中硒含量,分别为123.1和97.7 μg/L,与对照组相比,血清硒含量和牛奶硒含量分别提高了60.5%和194.3%。同时,在整个试验期内,血清硒含量呈上升趋势,而牛奶硒很快达到了稳定状态。     

An outbreak of dictyocaulosis in lactating cows on a dairy farm

CASE DESCRIPTION: The owner of a herd of 74 Holstein-Friesian cattle reported decreased milk production, weight loss, and coughing among lactating cows. Owner-initiated antimicrobial treatment was unsuccessful; 1 lactating cow died, and 50% of the lactating cows had clinical signs of respiratory distress, such as tachypnea and coughing. CLINICAL FINDINGS: On the basis of history, physical examination findings, and fecal examination results, affected animals were determined to have Dictyocaulus viviparus (lungworm) infestation. The disease history suggested that the herd contained cows with subclinical patent lungworm infestations; after introduction of susceptible heifers, the pastures had become heavily infested with D viviparus and clinical problems subsequently developed in both newly introduced and resident cows. TREATMENT AND OUTCOME: Affected and unaffected heifers and adult cows were treated with a pour-on formulation of eprinomectin (0.5 mg/kg [0.23 mg/lb]). One animal died, but 2 weeks after treatment, clinical signs among affected cattle were markedly improved. Ten weeks after treatment, milk production improved from 23 kg/cow/d (51 lb/cow/d) to 28 kg/cow/d (62 lb/cow/d). CLINICAL RELEVANCE: The outbreak provides additional evidence that dictyocaulosis is becoming more common among adult dairy cattle, rather than almost exclusively affecting young stock. This may be attributable to anthelmintic use and management practices on dairy farms. Combined with anecdotal reports of an increase in the incidence of dictyocaulosis among adult cattle in North America, D viviparus infestation should be included as a differential diagnosis for decreased milk production, weight loss, and coughing among adult dairy cattle.     

利用乳汁体细胞研究共轭亚油酸钙对奶牛乳腺基因表达的作用

8头泌乳中期的奶牛被随机分为2组，分别是对照组（每头牛：基础日粮＋棕榈酸钙200g／d）和试验组（每头牛：基础日粮＋共轭亚油酸钙200g／d），试验期14d，检测了奶产量、乳成分，分析奶牛的血液变化，并采用荧光定量PCR对乳汁体细胞中脂蛋白脂酶（LPL）、乙酰辅酶A羧化酶（ACACA）的基因表达进行检测。结果显示，与对照组相比，试验组奶牛的乳产量、乳蛋白、乳糖和乳汁体细胞含量没有显著影响，但是显著降低了乳脂肪含量（P〈0．05），对照组和试验组奶牛乳脂肪含量分别为0．0326g／mL和0．0244g／mL。检测血液指标发现，共轭亚油酸钙显著升高了奶牛血液中高密度脂蛋白的含量（P〈0．05）。基因分析发现，试验组奶牛乳汁体细胞中LPL、ACA—CA的基因表达显著下调，表明共轭亚油酸钙抑制了奶牛乳腺细胞脂肪酸合成酶的基因表达。     

The efficacy of bovine lactoferrin in the treatment of cows with experimentally induced Escherichia coli mastitis

The effect of bovine lactoferrin (Lf) was studied in experimental Escherichia coli mastitis, using enrofloxacin as a comparator. Mastitis was induced in six clinically healthy primiparous dairy cows by infusing 1500 colony-forming units of E. coli into a single udder quarter. The challenge was repeated into a contralateral quarter of the same cows 3 weeks later. At the first challenge, three cows were treated with 1.5 g of bovine lactoferrin intramammarily three times (12, 20 and 36 h postchallenge, PC), and the other three cows received 5 mg/kg of enrofloxacin (Baytril) parenterally (12, 36 and 60 h PC). Flunixin meglumine (2.2 mg/kg) was administered to all cows twice at 24-h intervals. During the second challenge, the treatments for the two groups were reversed. Intramammary challenge with E. coli produced clinical mastitis in all cows, but the severity of the disease varied markedly. No statistically significant differences between treatment groups were observed in clinical signs such as rectal temperature, rumen motility and general attitude. Milk somatic cell count, daily milk yield and bacterial counts in cows treated with Lf and those receiving enrofloxacin also did not differ significantly. However, a trend for a more rapid elimination of bacteria was seen in the cows treated with enrofloxacin. Milk NAGase activity also decreased significantly faster in the group treated with enrofloxacin. The concentration of lipopolysaccharide in milk compared with the number of bacteria was significantly lower in Lf than in enrofloxacin-treated cows (20 h PC).     

Disposition kinetics of lactoferrin in milk after intramammary administration

Disposition kinetics of lactoferrin (Lf) purified from cheese whey was studied in the milk of Finnish Ayrshire cows after intramammary administration of 1 g of Lf into one udder quarter. Intramammary administration of 1 g of Lf increased Lf concentration in milk for several hours. Mean elimination half-life of Lf was 2.2 h and a mean maximum concentration of 6.3 g/L was reached between 1 and 4 h. After 8 h of administration, Lf concentrations in milk decreased to almost the same level as before the infusion. Forty-eight hours postinfusion, the mean Lf concentration was again higher than in the milk samples taken before the infusion of Lf, being on average 1.5 g/L. Lactoferrin caused some local tissue irritation in the udder quarter. Severity of the irritation reactions varied between cows. The udder quarters of primiparous cows reacted faster than those of multiparous cows, but irritation reactions decreased more rapidly in the older cows than in primiparous cows. The cows had no general signs such as fever or anorexia. The somatic cell count returned to baseline level 4 days after the administration.     

Possible involvement of selenium in Staphylococcus aureus inhibition in cow's whey

Previous investigations have shown that selenium supplementation inhibits growth of mastitis pathogens in cow's milk. The present study was performed to clarify the role of selenium in defence mechanisms of mammary gland. We have examined the effects of selenium supplementation on Staphylococcus aureus growth inhibiting activity in whey. Six selenium-supplemented and six non-supplemented Estonian dairy cows were used for this study. Selenium-supplemented cows received 4 mg organic selenium in the form of selenium yeast in their daily diet for 8-week period. Cows from non-supplemented group received the same amount of yeast free of selenium in their diet. All cows had initially low blood glutathione peroxidase (GPx) activity (相似文献   

Sodium fluoride/copper naphthenate toxicosis in cattle.

Fourteen cattle on a Kansas pasture died from ingestion of a wood preservative compound containing sodium fluoride and copper naphthenate. Clinical signs included depression, anorexia, ataxia, diarrhea, and recumbency. Grossly visible lesions included perirenal edema, pale kidneys, and forestomach ulceration. All 3 cows that had postmortem evaluations had extensive renal cortical tubular necrosis. Tissue concentrations of fluoride were slightly elevated above expected background levels, while copper tissue concentrations were not elevated. The findings indicated that the sodium fluoride caused renal tubular necrosis leading to renal failure. Copper naphthenate may have contributed to abomasal ulceration; however, tissue copper concentrations indicated that copper from the formulation was not appreciably absorbed from the gastrointestinal tract.     

Fonofos toxicosis in dairy cows: an accidental poisoning (1977)

An accidental poisoning (in 1977) of 28 Holstein cows occurred when approximately 0.9 kg of 25% active ingredient fonofos, O-ethyl S-phenyl ethylphosphonothiolothionate, was spilled onto bulk feed in a delivery truck. Eight cows died within 2 days; the remaining 20 were necropsied 29 days later. Of the 8 fatally poisoned, 7 were being fed a high-grain diet and 1 was fed a medium-grain diet. Fonofos concentrations in feed cart and storage bin samples were 100 micrograms/g and 61 micrograms/g, respectively. Tissues from 6 animals were analyzed extensively for fonofos concentrations: 2 had died immediately; the other 4 were in the recovery state when they were necropsied. Rumen contents and liver, kidney, brain, heart, and milk samples were analyzed. Fonofos concentrations in these samples were significantly higher in the cows fatally affected than in the cows necropsied 3 weeks later. The oral acute LD50 and LD1 of fonofos in Holstein cows were calculated by the Litchfield and Wilcoxon method to be 1.30 and 0.84 mg/kg, respectively, with a 95% confidence range of +/- 0.20 mg/kg.     

An epidemiologic study of mortality in veal calves subsequent to an episode of zinc toxicosis on a California veal calf operation using zinc sulfate-supplemented milk replacer

Ninety-five 3- to 6-month old male Holstein veal calves were evaluated after an episode of zinc toxicosis, to describe clinical signs and to identify management and/or host-related factors that may have contributed to death. Clinical signs appeared 23 days after feeding of milk replacer commenced. Of 85 calves examined, 64 had pneumonia (75.5%), 62 had ocular signs (72.9%), 46 had diarrhea (54.1%), 34 were anorectic (40.0%), 15 were bloated (17.6%), 8 had cardiac arrhythmias (9.4%), 3 had convulsions (3.5%), and 3 were polydipsic/polyphagic (3.5%). Clinical signs began to appear when calves each were being fed approximately 1.5 to 2.0 g of zinc/day and exposed to a cumulative zinc intake of 42 to 70 g, from a milk replacer containing 706 micrograms of elemental zinc/g of milk replacer. Of 95 calves studied, 1 died before zinc was supplemented, 16 died during the episode, 12 were euthanatized, 1 was lost to follow-up evaluation, 1 was culled, and 64 were slaughtered. Deaths attributable to zinc toxicosis were observed between 25 and 53 days after the milk replacer was supplemented with zinc. Calves died while being exposed cumulatively to 30 to 66 g of zinc. The factors of previous pneumonia severity, age, cumulative daily exposure to zinc, and calf location within a bay were examined for possible associations with mortality, using stepwise logistic regression. Though younger calves tended to have a higher mortality than older calves, neither age category nor severity of pneumonia, before zinc supplementation, accounted for a significant mortality.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of copper supplementation on the copper status of peripartum beef cows and their calves

The effects of copper supplementation on the copper status of 40 late-pregnant Aubrac beef cows grazing a copper-deficient pasture and later fed a marginally deficient diet were studied for five months. They were divided into four equal groups; the control group received no copper supplement, groups 1 and 2 received copper as copper sulphate at 10 and 30 mg/kg of diet dry matter (DM), respectively, for five months, and group 3 received 120 mg/kg of diet dry matter for 10 days. Plasma copper concentration and the activity of erythrocyte superoxide dismutase (eSOD) were measured at the beginning of the experiment, in the cows and calves during weeks 1 and 3 after calving, and in the calves before they were turned out to pasture at a mean (sd) age of 51 (26) days. In spite of the low dietary copper content (4.2 mg/kg of DM), the plasma copper concentration of the control cows increased during the winter. All the copper supplements resulted in normal and similar plasma copper concentrations in the cows after calving, but the concentration decreased slightly between weeks 1 and 3 after calving in the group supplemented for 10 days. The treatments did not affect the eSOD of the cows. The calves born to the four groups showed the same patterns of plasma copper and eSOD. Compared with the cows, the calves had low plasma copper concentrations at week 1 and values in the normal range at week 3; their eSOD was high at weeks 1 and 3 but decreased after week 3.     

Acute, fatal illness in cattle exposed to boron fertilizer

Twenty-six cows died after accidental exposure to boron fertilizer. Cows developed diarrhea, weakness, ataxia, signs of depression, and died, usually within a few hours. Seizure-like behavior was noticed in 2 cows, and 2 were suspected of aborting. High boron concentrations in tissues from affected cows confirmed ingestion of an appreciable amount of boron fertilizer. In an attempt to confirm the diagnosis of boron poisoning, boron fertilizer was administered to goats. A kid goat given 3.6 g of fertilizer/kg of body weight developed clinical signs similar to those seen in the cattle. Boron compounds such as sodium borate and boric acid have been considered generally nontoxic, and reports of livestock toxicosis are uncommon. This case report suggests that these compounds may be palatable under certain circumstances leading to ingestion of toxic quantities.     

Hemorrhagic bowel syndrome in dairy cattle: 22 cases (1997-2000)

OBJECTIVE: To determine signalment, history, and clinical, necropsy, and microbiologic findings in dairy cows with hemorrhagic bowel syndrome. DESIGN: Retrospective study. ANIMALS: 22 adult dairy cows from a single farm in Colorado. PROCEDURE: Medical records were reviewed for information on signalment, medical and reproductive history, the owner's chief complaints, results of physical examinations and ancillary diagnostic tests, treatment and response to treatment, results of microbiologic testing, and, if applicable, postmortem findings. RESULTS: Common clinical signs were acute signs of profound depression, decreased milk production, tachycardia, ruminal stasis, abdominal distention, and dark clotted blood in the feces. Rectal examination revealed distended loops of small intestine in 7 of 14 cows. Transabdominal ultrasonography revealed small intestinal ileus and distention in 12 of 12 cows and homogeneous echogenic intraluminal material compatible with intraluminal hemorrhage and clot formation in 4. Seven of 8 cows treated medically died; 9 of 13 cows that underwent surgery died or were euthanatized. Clostridium perfringens was isolated from fecal samples from 17 of 20 cows. The most common morphologic diagnosis at necropsy was severe necrohemorrhagic enteritis or jejunitis with intraluminal hemorrhage or blood clots. The most prominent histologic finding was severe, segmental submucosal hemorrhage and edema of the small intestine. CONCLUSIONS AND CLINICAL RELEVANCE: Results confirm that in adult cattle, hemorrhagic bowel syndrome is a sporadic acute intestinal disorder characterized by intraluminal hemorrhage and obstruction of the small intestine. Clostridium perfringens was consistently isolated from the feces of affected cows. The prognosis for affected cows was grave.