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Biomedical subjects

A Shlosberg

Publications and source records attributed to A Shlosberg.

53 records · Page 3Linked to original sources

Mass poisoning in cattle, palm doves and mink caused by the coccidiostat dibutyltin dilaurate.

Poisoning caused by dibutyltin dilaurate (DBTD) was diagnosed in cattle, mink, and palm doves. The accidental addition of a DBTD premix to calf concentrates at levels up to 25000 ppm on 18 farms caused poisoning in 1000 cattle, of which 171 died and 287 were slaughtered. High concentrations of tin were found in the cattle tissues and precluded their consumption by humans. Palm doves ingesting concentrates containing 12500 ppm DBTD on one farm were also poisoned and had high concentrations of tin in tissues. Mink were inadvertently fed a vitamin-mineral supplement containing about 1700 ppm DBTD. They appeared the most suceptible of the three species to this compound.

Animal Feed↗

Poisoning of palm doves with dibutyltin dilaurate.

Dibutyltin dilaurate was inadvertently introduced into dairy feed which was consumed by wild palm doves (Streptopelia senegaleniss). About 150 dead and dying doves were found within several days. Extremely high concentrations of tin were found in samples of liver and skeletal muscle in these birds. A sample of the feed, which was found to contain about 2,500 ppm tin, was fed exclusively to 2 normal palm doves. On the 8th day of feeding, one dove died and the other was moribund. High concentrations of tin (27 to 141 ppm) were found in the livers of poisoned birds. Signs of poisoning in both the naturally occurring and experimentally induced poisonings were severe depression and yellow diarrhea.

Animal Feed↗

Treatment of monocrotophos-poisoned birds of prey with pralidoxime iodide.

Monocrotophos, and organophosphorus insecticide, was sprayed by farmers to control a plague of levant voles in alfalfa fields. Large numbers of birds of prey attracted by the dying and dead voles developed secondary poisoning after eating the voles. Paralysis of skeletal muscles was the principal clinical finding in these birds. Many of the birds died but some were treated with pralidoxime iodide, 100 mg/kg of body weight, given by intramuscular injection. All treated birds recovered, some in a very short time.

Animals↗

Histology of the iris in geese and ducks photosensitized by ingestion of Ammi majus seeds.

Geese and ducks were photosensitized by the ingestion of Ammi majus seeds, and exposure to sunlight. Mydriasis was a characteristic clinical feature of this syndrome in both species. Histologically the iris of the affected birds showed vacuolisation and varying degrees of atrophy of the muscle of the sphincter pupillae. The effect of pilocarpine and physostigmine on the normal and mydriatic eyes was studied. The possible mode of action of photosensitization and the significance of these findings in the light of the use of psoralens in human medicine is discussed.

Animals↗

Fluoroacetamide (1081) oisoning in wild birds.

An outbreak of poisoning in four greylag geese (Anser anser) and 35-45 teal (Anas crecca) is described. Laboratory findings led to the conclusion that a wheat bait containing the rodenticide fluoracetamide (1081) caused the poisoning. Circumstantial evidence incriminated fluoracetamide as the cause of death in white-fronted geese (Anser albifrons), mallards (Anas platyrhynchos), and chukars (Alectoris chukar).

Acetamides↗

Relationship between broiler chicken haematocrit-selected parents and their progeny, with regard to haematocrit, mortality from ascites and bodyweight.

A previous work of this group demonstrated that the relative haematocrit value of broilers is inherited and may serve as an indicator to susceptibility to the ascites syndrome in cold-stressed broilers. In this study, a full-pedigreed population was produced from male and female grandparent breeding stock that was selected by haematocrit and by normal selection parameters. Matings were made between low (L), medium (M) and high (H) haematocrit parents: L x L, M x M, and H x H. In their progeny, both before and after cold exposure, there was a statistically linear relationship between actual haematocrit and their H, M and L grouping (P<0.0001); heritability of the haematocrit was high (0.46-0.81). Both the low haematocrit parent and progeny groups showed an increased bodyweight. Exposure of the progeny from all the parental groups to an ascites-predisposing cold environment caused similar losses from ascites in the progeny of all three groups. Although this finding was not the same as in the previous trial where the H haematocrit group was associated with high ascites mortality, it is hypothesized that other factors, such as arterial blood saturation with oxygen, interacted in these birds at genetic or environmental levels.

Animals↗

Chronic lesions in geese photosensitized by Ammi majus.

Chronic lesions of the beak, footweb, and eye of geese photosensitized by the comsumption of Ammi majus (L.) are described, 7 weeks after the acute symptoms commenced. Sixty-four (48%) of the 133 birds in the flock showed various degrees of abnormality. All affected birds had stunting of the upper beak and cicatrization and thickening of the footweb. Eighty-nine percent of the affected birds showed ocular involvement, comprising chemosis, blepharoconjunctivitis, keratitis, symblepharon, ankyloblepharon, cicatricial ectropium, and mydriasis.

Animals↗

The susceptibility of young chickens, ducks, and turkeys to the photosensitizing effect of Ammi visnaga seeds.

Young chickens, ducks, and turkeys were exposed to sunlight and fed various amounts of Ammi visnaga seeds for 14 days in an attempt to induce photosensitization. In chickens, seeds at 1.25% in the diet had no effect whereas 3% induced mild signs of photosensitization within 6 to 8 days. No visible effects resulted in ducklings from 1.5, 3 and 6% in the diet, or in turkey poults from 3%. These differences appear to be due to differences between these avian species in the metabolism of the photodynamic agent.

Animals↗

Controlled early feed restriction as a potential means of reducing the incidence of ascites in broilers.

Male broiler chicks were grown at cold temperatures to enhance susceptibility to the ascites syndrome. Various feeding regimens were used to determine whether they could influence mortality due to ascites. It was found that a precisely controlled early feed-restriction regimen at the age of 6 to 11 days significantly reduced mortality from all causes and mortality due to ascites, while maintaining optimum body weight and feed conversion at marketing age.

Animal Feed↗

Salt poisoning in turkey poults.

A 4% mortality in 5-to-11-day-old turkey poults was attributed to 1.85% sodium chloride in the feed. The syndrome included peracute respiratory distress, ascites, and sudden death that resembled peracute heart failure. Clinical signs were observed only in the final phase of the toxicity, but progressive histologic lesions were found. Live, apparently unaffected poults showed increases in intracellular glycogen and cytoplasmic granularity, loss of striation, and early mild intercellular myocardial edema; similar but more severe histologic lesions were seen in live, ascites-affected poults. The ascites-affected poults had hydropericardium and hydrothorax which seemed to develop just minutes before death. Ultrastructurally, focal areas of myocardial cells exhibited myofibrillar disarray, lysis of myofilaments, widened Z-bands, and dilation of sarcoplasmic reticulum.

Animals↗

Effect of tiamulin administered by various methods and dosages on turkeys at different ages.

Healthy male turkeys not receiving monensin in their feed were treated with tiamulin by various methods and at different ages. Nine cycles of treatments were performed at the ages of 26, 40, 61, 89, 103, 117, 131, 145, and 160 days. Intramuscular of subcutaneous injections of 12.5 mg/kg tiamulin up to 145 days did not result in any signs of toxicity or impair growth rate. Administration at a dose of up to 25 mg/kg, using the drinking-water-deprivation technique, caused no effect in turkeys up to 160 days (marketing age).

Administration, Oral↗

Photosensitization in ducklings induced by seeds of Cymopterus watsonii and C. longipes.

For 14 days ducklings were fed seeds of Cymopterus watsonii or C. longipes at 100 mg, 500 mg, or 2 g/kg of body weight and exposed to sunlight. Those fed C. longipes at 500 mg showed transient photosensitization. C. watsonii at 2 g induced mild photosensitization at 8 days, with consequent beak deformity and little apparent effect on the birds' health. C. longipes at 2 g induced acute photosensitization within 3 days, with consequent severe damage to the skin of the head, beak, footwebs, and legs. These birds showed extreme stunting within 8 days of first ingesting the seeds, and several weeks later were still very retarded, with severely deformed beaks and footwebs. One bird in this group died at 22 days.

Animals↗

Efficacy of pralidoxime iodide and obidoxime dichloride as antidotes in diazinon-poisoned goslings.

The antidotal efficacy of pralidoxime iodide and obidoxime dichloride was investigated in goslings poisoned by a supralethal dose of the organophosphorus insecticide diazinon. Various doses of both drugs were administered by intramuscular injection when the poisoned birds were unable to walk. Pralidoxime at 100 mg/kg brought about a complete and speedy clinical recovery. Fifty mg/kg induced recovery in 4 of 6 poisoned goslings, and 25 mg/kg successfully trated only 1 of 6 birds. Obidoxime at 25 mg/kg showed no therapeutic properties whereas 50 and 100 mg/kg delayed the death of some birds by several hours. At 100 mg/kg, all goslings had transient signs of intoxication, which precluded the use of this compound as an antidote at higher doses. The mode of action of these antidotes in diazinon-poisoned goslings is discussed.

Animals↗