Effects of dietary sulfur concentrations on the incidence and pathology of polioencephalomalicia in weaned beef calves.

Fourteen heifer calves weighing 174.5+/-17.7 kg were used to evaluate the effects of 3 levels of dietary sulfur. Sodium sulfate added to basal diet made treatments designated moderate (3860 ppm sulfur), moderatey high (5540 ppm sulfur) and high (7010 ppm sulfur). Clinical polioencephalomalacia occurred in all calves assigned to the moderately high and high treatments. The calves did not acclimate to the dietary sulfur as polioencephalomalacia occurred in 4 animals on d 35 and in 1 calf on d 37. Microscopic lesions confirmed polioencephalomalacia in the calves on moderately high and high diets. Microscopic lesions also were present in 4 moderate diet calves although clinical signs were not seen. High dietary sulfur did not limit feed intake. Diets containing sulfur levels >4000 ppm sulfur produced polioencephalomalacia in 10 calves and sub-clinical brain lesions occurred in 4 calves consuming <4000 ppm sulfur.

Mercury and selenium concentrations in livers and eggs of common loons (Gavia immer) from Minnesota.

Mercury and selenium act as mutual antagonists in mature birds, but their toxicity is additive or synergistic in avian embryos and immature birds. Twenty eggs and livers from 18 mature and 9 immature common loon carcasses found in Minnesota were collected. Livers and eggs were analyzed for mercury and selenium by atomic emission and atomic absorption spectroscopy. Liver mercury concentrations were significantly higher in mature loons compared to those of immature loons and eggs. Liver selenium concentrations were significantly higher in mature loons than those of immature loons, and selenium concentrations in immature loon livers were significantly higher than levels in eggs. There was a significant positive correlation between mercury and selenium in loon livers. There was a negative correlation between mercury and selenium in eggs.

Sulfur-induced polioencephalomalacia in stocker calves.

Calves from 3 farms exhibited blindness, head pressing, and circling before death. Brain lesions confirmed polioencephalomalacia. Excess sulfur was found in the diets on all 3 farms in corn by-products or molasses based supplements. Corn gluten feed and corn steep liquor (by-products of the refinement of corn for ethanol), corn syrup, corn gluten, corn oil, and corn starch have gained popularity as livestock feeds due to their low prices. With this increased usage as livestock feed, increasing number of cases of polioencephalomalacia have been seen.

Malicious paraquat poisoning in Oklahoma dogs.

Paraquat is a restricted use herbicide which is extremely toxic to companion animals when ingested. This report details one incident of malicious poisoning involving 6 dogs. All dogs were from the same geographic area, and 5 had pulmonary and renal lesions consistent with paraquat toxicosis. Diagnosis was initiated by a modified dithionite spot test on vomitus from 1 dog. Subsequent tissue paraquat levels ranged from non-detectable to 1 ppm.

Methamphetamine poisoning in three Oklahoma dogs.

Methamphetamine is an amphetamine derivative and a category II controlled substance. It is uncommonly prescribed by physicians, but is more often used illegally as a stimulant. In this case study, 3 dogs were believed maliciously poisoned. Methamphetamine was detected in the stomach contents of 1 dog. One died and 2 recovered after gastrointestinal decontamination and supportive care. The recommended treatment protocol of methamphetamine toxicosis should also include urine acidification and alpha-adrenergic blocking agents.

Clinical features of blister beetle poisoning in equids: 70 cases (1983-1996).

OBJECTIVE: To document clinical signs and gross pathologic changes associated with naturally acquired cantharidiasis (blister beetle poisoning) in equids. DESIGN: Retrospective study. ANIMALS: 70 equids with laboratory-confirmed blister beetle poisoning. PROCEDURE: Medical records were reviewed to obtain history, physical examination findings, feeding practices, and diagnostic test and necropsy results. RESULTS: 32 horses and 2 donkeys died from exposure to cantharidin, whereas 36 horses survived. Diet content varied, but alfalfa hay was the common component. Onset of signs of disease was rapid. Most equids had signs of gastrointestinal tract distress. Six horses had nonspecific neurologic signs. All equids dying from cantharidiasis were in shock terminally, with duration of clinical signs ranging from 3 to 18 hours. Six horses that died had no gross lesions, whereas 14 had mild to moderate erythema of gastric, small intestinal, or colonic mucosa. Only 2 horses had gastric or duodenal ulceration, and 2 had hemorrhage of the urinary bladder mucosa. One horse had cardiac muscle necrosis. Clinicopathologic data available on 10 horses included hypocalcemia, hypomagnesemia, and azotemia. Cantharidin concentrations in urine or pooled gastric-cecal contents did not always correlate with severity of disease. CLINICAL IMPLICATIONS: Blister beetle poisoning is not universally fatal in equids. Clinical signs are related to the amount of cantharidin ingested. Every horse that survived was treated aggressively. In fatal poisonings, gross lesions may be minimal or inapparent, and diagnosis must be confirmed by chemical detection of cantharidin in urine, blood, or stomach or cecal contents.

Hepatic disease associated with administration of tetanus antitoxin in eight horses.

Seven horses developed clinical or subclinical hepatitis 48 to 87 days after administration of tetanus antitoxin. One horse had mildly high hepatic enzyme activity 120 days after inoculation with tetanus antitoxin. The first horse developed signs of depression, lethargy, and anorexia. During hospitalization, signs of hepatoencephalopathy were noticed, and laboratory data were consistent with hepatic disease. Another horse that was found dead had gross and histologic lesions compatible with serum hepatitis. Screening of serum gamma-glutamyltransferase (GGT) and aspartate transaminase activities were used to investigate the remaining horses in the herd. High GGT activities (71 to 206 IU/L) were detected in 5 additional herd members. These horses appeared clinically normal, apart from 2 reports of nasal photosensitization and an aborted fetus. In 3 horses, high serum GGT activity persisted over a 44-day testing period. All affected horses had been given tetanus antitoxin within 12 hours of parturition, and a common source of vaccine was identified for 7 horses. Findings in this group of horses indicate that clinical and subclinical serum hepatitis can develop after administration of tetanus antitoxin.

Mercury toxicosis caused by ingestion of a blistering compound in a horse.

Mercury toxicosis by ingestion was diagnosed in a 3-year-old Quarter Horse mare with a history of anorexia and signs of abdominal discomfort. Ten and 9 days prior to admission, an inorganic mercuric blistering agent has been applied for topical treatment of dorsal metacarpal disease. At referral, signs of depression, dependent edema, pollakiuria, nonproductive cough, and oral ulceration were noticed. Laboratory data were consistent with renal dysfunction. Mercury content of blood and urine was high, confirming the diagnosis. The horse responded to intensive care, consisting primarily of IV fluid treatment, and mercury-chelating agents. However, acute laminitis developed, and the owners elected to euthanatize the horse 18 days after mercury exposure. Necropsy findings included renal tubulonephrosis and ulcerative colitis and enteritis. Mercury concentration was highest in kidney and liver tissues. The potential for mercury toxicosis in horses currently exists, and although the prognosis is grave, some horses may recover with appropriate treatment and long-term supportive medical care.

Laboratory diagnosis of zinc phosphide poisoning.

Zinc phosphide, a readily-available rodenticide, poses a significant risk for intoxication in animals. Animals have been poisoned by ingesting treated bait or the carcasses of poisoned rodents. Toxicity is due to the liberation of phosphine gas in the stomach. Clinical signs include central nervous system excitation, depression and vomition. Similarities of clinical signs with other central nervous system toxicants make the diagnosis difficult without a specific diagnostic test. The procedure outlined in this paper detects phosphine liberated from zinc phosphide by the addition of hydrochloric acid as well as the phosphine previously generated by contact with stomach acid.

Aortic rupture in ostrich associated with copper deficiency.

Four cases of aortic rupture in ostrich associated with deficient levels of copper in the liver are presented. The aortic lesions are consistent with vascular lesions described in turkeys and chickens with copper deficiency.

The pig as a potential organ donor for man. A study of potentially transferable disease from donor pig to recipient man.

Ten pigs, reared in an unmodified laboratory animal house environment, have been investigated to ascertain the incidence of diseases or disorders, including infection, neoplasia, or metabolic abnormalities, that might preclude the transplantation of major organs from the pig to man. Noninvasive studies were performed in the second month of life (study 1) and repeated after an interval that varied between 3 and 5 1/2 months (study 2). Necropsy was then performed as a means of assessing the accuracy of the 2 screening examinations. A total of 150 tests were performed on each pig. At both studies the feces contained cysts and/or trophozoites of several parasites, all of which were considered commensals. No other organisms potentially infective for man were identified either at study or at necropsy. Neither congenital anomalies nor malignant neoplasia was found at necropsy. However, in 2 pigs a vasculitis of uncertain etiology was present in the kidneys on microscopic examination, and in one of these the same condition affected the heart. This pathology was suspected neither from the screening examinations nor from the macroscopic appearance of these organs. Biopsy and microscopic examination would therefore appear to be essential before any organ is transplanted into a human.

Suspected red maple (Acer rubrum) toxicosis with abortion in two Percheron mares.

Horses develop severe and often fatal hemolytic anemia after ingesting dried leaves from red maple (Acer rubrum) trees. Toxicosis appears related to an unknown oxidant present in the dried or wilted leaves. This case report describes 2 horses that aborted and developed fatal hemolytic anemia after consuming wilted leaves from red maple (Acer rubrum). While an absolute diagnosis was not confirmed due to lack of proper antemortem and postmortem examinations, red maple toxicosis appeared a reasonable diagnosis based on clinical signs and laboratory findings. Other differentials include equine infectious anemia, autoimmune hemolytic anemia, piroplasmosis, leptospirosis, ehrlichiosis, and other plant or chemical sources of oxidants (onion, garlic, kale, phenothiazines).

A case of monensin poisoning in ostriches.

A clinical case of monensin poisoning in ostriches is presented. Analytical results and histopathologic changes in intercostal muscles and liver supported the ionophore toxicity diagnosis.

Heavy metal poisoning in ostriches from proventricular foreign bodies.

Cases of iron, zinc, lead and copper poisoning in ostriches are discussed. Metallic proventricular foreign bodies are a potential source of heavy metal poisoning in ratites. Tissue levels of heavy metals and trace elements supporting these diagnoses are reviewed.

Investigating oiled birds from oil field waste pits.

Procedures and results of investigations concerning the oiling of inland raptors, migratory water-fowl and other birds are presented. Freon washings from the oiled birds and oil from the pits were analyzed by gas chromatography. In most instances the source of the oil could be established by chromatographic procedures. The numbers of birds involved (including many on the endangered species list) suggested the need for netting or closing oil field waste pits and mud disposal pits. Maintaining a proper chain of custody was important.

Livestock poisoning from oil field drilling fluids, muds and additives.

The use and potential toxicity of various components of oil well drilling fluids, muds and additives are presented. Many components are extremely caustic resulting in rumenitis. Solvent and petroleum hydrocarbon components may cause aspiration pneumonia and rumen dysfunction. Some additives cause methemoglobinemia. The most frequently encountered heavy metals are lead, chromium, arsenic, lithium and copper. Considerations for investigating livestock poisoning cases and several typical cases are reviewed.

Aldicarb toxicosis in a dairy herd.

Aldicarb, an extremely toxic carbamate, caused sudden death of several lactating Holstein cows. Confirmation of this toxic agent as the cause of death was hindered by its rapid breakdown in biological tissue. Therefore, aldicarb was not detected in rumen contents of some of the dead cows, and brain acetylcholinesterase values were essentially normal. The analyses were conducted 2 to 4 days after death of the cows. Rapid testing of tissue samples is necessary if a carbamate insecticide is suspected.

Sorption of sodium hydroxide by type I collagen and bovine corneas.

There are no quantitative studies on the uptake of alkali into corneal tissues. To study this phenomenon, both type I collagen and bovine corneas were incubated in sodium hydroxide (NaOH) under varying conditions for periods up to 27.5 h. The sorption (absorption or adsorption) of the alkali to protein and tissue was measured as the quantity of NaOH no longer available for titration to neutrality with hydrochloric acid. Sorption was found to be dependent on the concentration of NaOH (0.01-1 N) but independent of the incubation temperature (4-35 degrees C). In whole cornea, sorption of 1 N NaOH began immediately and increased with time up to 6 h. After 6 h, sorption decreased, together with the observed degradation and solubilization of the tissue. Stripping of the corneal endothelium alone or of the endothelium and epithelium increased sorption in a similar manner when compared to whole corneas for periods up to 4 h. These observations are compatible with ionic and nonionic bonding of hydroxide ions to collagen (including that of the cornea) and the subsequent release of hydroxide ions during hydrolysis of the protein itself. Indirect evidence also suggests the inclusion of quantities of unbound hydroxide ions in hydrated gels of glycosaminoglycans. It is proposed that in a chemical burn of the cornea, alkali is both stored in the tissue (by sorption) and reacted with it (by hydrolysis), without any net consumption of alkali taking place.