Death associated with parenteral administration of copper disodium edetate in calves

Copper disodium edetate in recommended doses was apparently responsible for the deaths of one calf and clinical signs of toxicosis in 5 others on one farm, and 7 deaths and clinical signs of toxicosis in a number of others on another ranch. Signs of hyperexcitability, hypermetria, hindlimb weakness, head pressing, depression, and opisthotonos occurred 6 to 24 hours after injections and preceded death by 1 to 2 days. Necropsy and histologic examination revealed massive liver necrosis. High blood concentrations of liver enzymes in affected cattle that did not die indicated that they had liver damage. High blood concentration of iron in cattle that died indicated possible interaction of copper and iron.     

Characterization of Copper Algaecide (Copper Ethanolamine) Dissipation Rates Following Pulse Exposures

Dissipation rates of copper following algaecide treatments resulting in pulse exposures can be accurately modeled if the component dissipation rates are known. Scaled experiments (in situ, laboratory and mesocosm) were used to parse and rank dominant processes from concurrent processes affecting copper fate in pulse exposures. Copper dissipation rates were measured cumulatively in situ and in mesocosms as well as individually in laboratory experiments. Predictions of the influence of individual dissipation rates on the cumulative dissipation rate were assessed mathematically. In situ aqueous copper dissipated rapidly following an algaecide treatment, with a measured half-life of 0.03 days. Based on laboratory experiments, the most rapid copper fate process was dilution with a half-life of 0.03 days, followed by sediment sorption with a half-life of approximately 3 days. Mesocosm experiments incorporating physical characteristics of the site (i.e., dilution, sediment, algae, and site water) resulted in similar copper dissipation rates (0.02 days) relative to the in situ copper dissipation rate. Prediction of the fate of copper from algaecide treatments requires incorporation of accurate estimates of dominant fate processes that can be determined physically and mathematically.     

Discovery and characterization of a molecular marker for <Emphasis Type="Italic">Sclerotinia minor</Emphasis> (Jagger) resistance in peanut

The production of cultivated peanut, an important agronomic crop throughout the United States and the world, is consistently threatened by various diseases and pests. Sclerotinia minor Jagger (S. minor), the causal agent of Sclerotinia blight, is a major threat to peanut production in the Southwestern US, Virginia and North Carolina. Although information on the variability of morphological traits associated with Sclerotinia blight resistance is plentiful, no molecular markers associated with resistance have been reported. The identification of markers would greatly assist peanut geneticists in selecting genotypes to be used in breeding programs. The main objective of this work was to use simple sequence repeat (SSR) primers previously reported for peanut to identify a molecular marker associated with resistance to S. minor. Out of 16 primer pairs used to examine peanut genomic DNA from 39 different genotypes, one pair produced bands at approximately 145 and 100 bp, consistent with either S. minor resistance or susceptibility, respectively. Cloning and sequencing of these bands revealed the region is well conserved among all genotypes tested with the exception of the length of the SSR region, which varies with disease resistance levels. This is the first report of a molecular marker associated with resistance to Sclerotinia blight in peanut. The identification of this marker and development of a PCR-based screening method will prove to be extremely useful to peanut breeders in screening germplasm collections and segregating populations as well as in pyramiding S. minor resistance with other desirable traits into superior peanut lines.     

Een geval van noodrijpheid bij blauwmaanzaad

Summary Premature dying of seed poppies, of unknown cause, was observed in The Netherlands, in 1959, at the end of the vegetative growth period.In a spraying experiment with systox the untreated plants died prematurely and showed a 50% decrease in yield based mainly on the weight of harvested seed. This disorder may be due to sugar beet yellows virus or to aphid damage alone. One spray before flowering reduced the disease and increased the yield.The fungusPyrenophora calvescens (Fr.) Sacc., which also is supposed to cause a premature ripeness of seed poppies, was present to the same degree in both the untreated and the sprayed plots.     

Inhibition of aflatoxin M1 production by bovine hepatocytes after intervention with oltipraz

It is well known that cattle ingesting aflatoxin B1 contaminated feed commodities excrete aflatoxin M1 into their milk. As aflatoxin M1 originates from hepatic metabolism, measures to prevent aflatoxin M1 formation need to be directed to either the immobilization of aflatoxin B1 in the gastrointestinal tract or the modification of hepatic metabolism of aflatoxin B1. Here we studied the influence of oltipraz and a second dithiolthione, (1,2) dithiolo (4,3-c)-1,2-dithiole-3,6 dithione (DDD) on bovine hepatic aflatoxin B1 biotransformation. Oltipraz inhibited aflatoxin B1 metabolism as no aflatoxin M1 and no aflatoxin B1-dihydrodiol, the second metabolite found in bovine hepatocytes, was formed. DDD did not significantly inhibit aflatoxin B1 metabolism. It could be demonstrated that the inhibition of aflatoxin B1 metabolism was due to the inhibition of several cytochrome P450 enzyme activities by oltipraz. In contrast, DDD inhibited only ethoxyresorufin O-deethylation activity. These findings suggest a high efficacy of oltipraz in inhibiting aflatoxin M1 contamination of milk from dairy cows exposed to aflatoxin B1 contaminated feeds.     

Antigen quantification as in vitro alternative for potency testing of inactivated viral poultry vaccines

Routine batch control of licensed inactivated viral vaccines for poultry usually includes a potency assay as a measure of vaccine efficacy. Potency assays often consist of vaccination-challenge experiments in the target species or in laboratory animals. Instead of measuring the protection of vaccinated animals against virulent pathogens, the serological response after vaccination can be quantified for some vaccines. In vitro antigen quantification assays would be attractive alternatives for the current potency assays because the time and costs involved could be greatly reduced and animal use could be avoided. Such in vitro assays will only be acceptable when the correlation between results and efficacy or potency has been demonstrated convincingly. The results of our studies on antigen quantification assays indicate that, in principle, quantification of viral antigens from inactivated oil-adjuvanted vaccines is feasible and reproducible using specially developed antigen capture ELISAs in combination with specific software for statistical analysis of the ELISA data. We have developed methods to quantify the haemagglutination-neuraminidase (HN) and fusion (F) proteins of Newcastle disease virus (NDV), the viral protein 3 (VP3) of the infectious bursal disease virus (IBDV), and the spike-1 (S1) protein of the infectious bronchitis virus (IBV). Vaccination experiments with inactivated ND vaccines indicate that the in vitro quantified HN- or F-proteins of NDV are reliable indicators of the serological response after vaccination.     

Hostplants ofAgrobacterium gypsophilae

Symptoms obtained after either natural or artificial infection on roses, carnations and cacti byAgrobacterium gypsophilae are described, as well as a modification of the isolation method for this pathogen.