Retrospective study of toxic metal analyses requested at a veterinary diagnostic toxicology laboratory in Ontario (1990-1995).

During the 5-year period from January 1, 1990, to December 31, 1995, 887 diagnoses of metal toxicosis in domestic animals and wild birds were documented at the Veterinary Laboratory Services Branch of the Ontario Ministry of Agriculture, Food and Rural Affairs. Most of these cases involved cattle, sheep, and birds. Lead toxicosis was diagnosed in 399 cases, copper toxicosis in 387, zinc toxicosis in 49, mercury toxicosis in 44, iron toxicosis in 4, and selenium in 4 cases. Trends in species affected and sources of metals are discussed.     

Pesticide toxicosis in the horse.

Toxicosis from pesticides rarely occurs in horses and is usually the result of inappropriate pesticide use or handling by humans. Organophosphorus and carbamate insecticides inhibit acetylcholinesterase and are the insecticide class most frequently associated with toxicosis in domestic animals. Metaldehyde is a molluscicide, and zinc phosphide is a rodenticide, both of which have caused toxicosis in horses. All three of these pesticides affect the nervous system of horses and can be fatal if not treated promptly.     

Industrial chemicals and the horse.

Poisoning resulting from exposure to a wide variety of industrial chemicals is not a common occurrence in horses, but it does happen on occasion. A wide range of toxicosis can occur from a wide range of industrial pollutants, such as dioxin, carbon tetrachloride, and tetrachloroethylene, to heavy metals, such as cadmium and zinc. The equine practitioner must consider industrial chemical toxicosis in differential diagnoses and work with a reputable veterinary diagnostic laboratory to confirm or rule out industrial chemical poisoning.     

Mycotoxins.

Horses consume feed grains and forages that can produce a range of mycotoxins resulting from mold invasion. Toxicosis of horses often occurs from fumonisins or aflatoxin in grains, from the tremorgenic mycotoxins in dallis grass, or from slaframine in red clover. Fumonisin toxicosis often is severe and fatal, and aflatoxin can be acute or chronic and debilitating. Other mycotoxins reported in horses may cause moderate to mild signs that regress when the contaminated feedstuff is removed. Overall, horses appear to have a relatively low prevalence of reported mycotoxicoses among domestic animals, but they are extremely sensitive to the fumonisins. Since there are no good therapies for mycotoxin poisoning, attention to providing high quality grains and forages to prevent mycotoxicoses is the most effective means for reducing the risk of mycotoxins in horses.     

Toxicosis from agricultural chemicals

Most agricultural chemicals that horses are exposed to are pesticides. Toxicosis from pesticides is infrequent in horses and is usually the result of inappropriate use, handling, or storage. Most herbicides have low toxicity in mammals, especially if the dilution rate, application rate, and re-entry times are observed. However, some herbicides can alter the toxicity of poisonous plants. Herbicides that contain arsenic or chlorates are the most toxic. Pentachlorophenol is a fungicide and wood preservative that can be contaminated with dioxins. Horses develop a chronic wasting syndrome and significant skin lesions. Some pesticides are marketed in a pelleted form that may contain grains, which are readily consumed by horses. Metaldehyde is a molluscicide that affects the nervous system. Strychnine also affects the nervous system. Zinc phosphide is a rodenticide that is converted into a toxic gas in the horse's stomach and can be toxic to humans as well. The organophosphorus and carbamate insecticides are acetylcholinesterase inhibitors, the insecticide class most frequently associated with toxicosis. The most recognizable signs of toxicosis are the “SLUD” signs, but some of these insecticides, as well as the organochlorine insecticides, can cause seizures.     

The use of ultrapurified bovine hemoglobin solution in the treatment of two cases of presumed red maple toxicosis in a miniature horse and a pony

Objective: To report the use of ultrapurified bovine hemoglobin (PBHg) in the treatment of red maple toxicosis in horses. Summary: The use of PBHg in a miniature horse and a pony with clinical signs of red maple toxicosis is described. Initial treatment of the horses included blood transfusion in Case 1, and intravenous crystalloid fluids, nasogastrically administered mineral oil, and activated charcoal in both cases. Both cases received PBHg (16 and 11 ml/kg, respectively) when the hematocrit dropped below 10%. Clinical stabilization of the horses (reflected by improved vital signs and mucous membrane color, increase in P_vO₂, and increase in plasma hemoglobin) was temporary, lasting 12 and 42 hours, respectively. A whole blood transfusion was given 16 hours after the infusion of PBHg in Case 1 and 42 hours after the infusion of PBHg in Case 2. The horses were discharged on days 15 and 17, respectively. Both were stable on discharge and were reported to be doing well 1 month after discharge. New information provided: Ultrapurified bovine hemoglobin is shown to be safe in the treatment of red maple toxicosis. Ultrapurified bovine hemoglobin infusion resulted in temporary improvement in oxygen (O₂) delivery as assessed by clinical and laboratory parameters. The use of PBHg may provide an ‘oxygen bridge’ in an acute hemolytic crisis in the horse. It may allow additional time in the treatment of red maple toxicity for the acute hemolysis to subside and for metabolism of the toxin to occur, thus providing a more optimal environment for an effective whole blood transfusion.     

Zinc intoxication in dogs: 19 cases (1991-2003)

OBJECTIVE: To determine physical examination findings, clinicopathologic changes, and prognosis in dogs with zinc toxicosis. DESIGN: Retrospective case series. ANIMALS: 19 dogs with zinc toxicosis. PROCEDURES: Medical records from 1991 through 2003 were searched for animals with a diagnosis of zinc toxicosis. Information concerning signalment, body weight, historical findings, initial owner complaints, physical examination findings, clinicopathologic findings, blood zinc concentrations, source of zinc, treatments given, duration of hospital stay, and outcome was collected. RESULTS: Records of 19 dogs with zinc toxicosis were reviewed.The most common historical findings were vomiting (n = 14) and pigmenturia (12). The most common clinicopathologic findings were anemia (n = 19) and hyperbilirubinemia (12). Median age was 1.3 years, and median weight was 5.6 kg (12.3 lb). The prognosis was favorable, with 17 dogs surviving after a median hospital stay of 2 days. CONCLUSIONS AND CLINICAL RELEVANCE: Hemolytic anemia as a result of zinc toxicosis appeared to affect young small-breed dogs more frequently than older large-breed dogs. The prognosis with treatment is good, and most affected dogs had a short hospital stay.     

Zinc-associated acute pancreatitis in a dog

Zinc-induced haemolytic anaemia is a common phenomenon in dogs in the USA following the ingestion of pennies minted after 1982. A case of acute pancreatitis secondary to zinc toxicosis in a dog is described. Acute pancreatitis has been reported in humans, following the ingestion of liquid zinc chloride, but zinc-associated pancreatitis has not been reported previously in the dog. The mechanism of toxicity is unknown, although the pathophysiology may relate to the role of the pancreas in zinc excretion. Acute pancreatitis as a sequela to zinc toxicosis in the dog represents a complication that may prolong hospitalisation and worsen the prognosis.     

Salinomycin toxicosis in horses

CASE DESCRIPTION: A 4-month-old American Paint filly was evaluated because of sudden onset of ataxia that progressed to recumbency. Five additional horses from the same and neighboring premises developed signs of poor performance, generalized weakness, ataxia, and recumbency; 2 of those horses were also evaluated. A new batch of a commercial feed supplement had been introduced to the horses' diet on each farm within the preceding 3 days. CLINICAL FINDINGS: Other than recumbency, findings of physical and neurologic examinations of the foal were unremarkable. The other 2 horses had generalized weakness and mild ataxia, and 1 horse also had persistent tachycardia. The foal had mild leukocytosis with neutrophilia, hyperglycemia, and mildly high serum creatine kinase activity. Results of cervical radiography, CSF analysis, and assessments of heavy metals and selenium concentrations in blood and vitamin E concentration in serum were within reference limits. Feed analysis revealed high concentrations of the ionophore antimicrobial salinomycin. TREATMENT AND OUTCOME: The 5 affected horses survived, but the foal was euthanized. At necropsy, a major histopathologic finding was severe vacuolation within neurons of the dorsal root ganglia, which was compatible with ionophore toxicosis. The surviving horses developed muscle atrophy, persistent weakness, and ataxia. CLINICAL RELEVANCE: In horses, ionophore toxicosis should be considered as a differential diagnosis for acute weakness, ataxia, recumbency, or sudden death. Furthermore, ionophore toxicosis should be considered as a cause of poor performance, weakness, muscle wasting, and cardiac arrhythmias in horses. Surviving horses may have impaired athletic performance.     

Vitamin K3-induced renal toxicosis in the horse

Renal toxicosis attributable to vitamin K3 (menadione sodium bisulfite) was suspected in 5 young adult horses in which acute renal failure developed following parenteral administration of vitamin K3 at the manufacturers' recommended dosages. Renal disease was subsequently induced experimentally in 5 of 6 horses by administration of vitamin K3 at manufacturers' recommended dosages. Signs of renal disease in the clinical patients as well as in the horses treated experimentally included renal colic, hematuria, azotemia, and electrolyte abnormalities consistent with acute renal failure. Two clinical patients and 3 experimental horses were subsequently necropsied and found to have lesions of renal tubular nephrosis.     

Zinc toxicosis due to ingestion of a penny in a gray-headed chachalaca (Ortalis cinereiceps).

Zinc toxicosis was diagnosed in a gray-headed chachalaca (Ortalis cinereiceps) due to ingestion of a copper-plated zinc penny. Histopathological lesions were most marked in the pancreas. These lesions included apoptosis, zymogen granule depletion, and loss of normal acinar architecture. There was also severe gizzard erosion. Heavy metal analysis revealed abnormal levels of zinc and iron in the liver. Iron pigment in the liver was most concentrated in Kupffer cells. This, along with evidence of erythrophagocytosis in the spleen, suggested that extravascular hemolysis was also associated with zinc toxicosis in this case.     

Pyrrolizidine alkaloid-induced liver disease in horses: an early diagnosis

Nine adult horses were fed alfalfa hay cubes containing approximately 10% Senecio vulgaris until all horses had consumed approximately the same amount of toxic components of S vulgaris, pyrrolizidine alkaloids (PA). The amount of PA consumed was determined by the amount that induced clinical signs of PA toxicosis in 3 horses. The 6 other horses were given similar amounts per kilogram of body weight. An initial decrease of feed intake was observed when horses' diets were changed from alfalfa cubes to alfalfa/Senecio cubes, and feed intake was decreased further over 89 to 98 days. From 50 to 159 days, body weight decreased in all horses. Liver disease was induced in all 9 horses after they ate an average of 233 +/- 9.2 mg of PA/kg of body weight. Eight horses died or were euthanatized. Treatment with branched chain amino acids had no effect on mortality, but appeared to reduce neurologic problems. Clinical signs of PA-induced liver disease included ataxia, head pressing, and decreased feed intake. Other clinical signs of toxicosis were observed individual horses, but did not develop in most horses. Megalocytic hepatopathy developed. Liver abnormalities proceeded as PA was consumed and were severe in 8 of 9 horses before clinical signs of toxicosis appeared. Sulfobromophthalein sodium clearance did not decrease until PA-induced liver disease was advanced. Bile acid (BA) concentrations increased to greater than or equal to 50 mumol/L, in the 8 horses that died. One horse had hepatopathy and increased BA concentration, but survived. In this horse, BA concentration peaked at 33 mumol/L and then decreased.(ABSTRACT TRUNCATED AT 250 WORDS)     

Chlorpyrifos Toxicosis in Two Cats

Organophosphate compounds are widely employed for control of external parasites in cats and for control of insects in homes and yards. Chlorpyrifos is a long-acting organophosphate (OP) available for use as a systemically and topically acting parasiticide and insecticide in cattle. Its use on cats is not recommended, and no previous clinical cases of toxicosis have been described. Two cases of chronic chlorpyrifos toxicosis in cats are presented and pathophysiology as well as treatment are discussed. The cats had been showing signs of chronic organophosphate toxicosis before diazepam administration. Signs of acute organophosphate toxicosis were precipitated after diazepam was given. Treatment with pralidoxime chloride (2-PAM) and atropine was attempted. Response to treatment was dramatic and complete recovery was achieved with six injections of pralidoxime and atropine administration.     

生猪不同养殖阶段粪便中金属残留及富集分析

为探究集约化生猪养殖过程中不同养殖阶段粪便中金属残留量及其对环境的影响效应.试验选取正常饲养条件下保育、育肥、后备、妊娠和泌乳5个阶段的猪饲料及粪便样品进行了铜、锌、镉、铅、铬、汞和砷等7种常见超标元素的检测和分析.试验表明:不同养殖阶段猪粪便样品中铜、锌含量差异较大,所有样品中均未检出铅、铬、汞、砷等元素,仅在后备和...     

Serum Protein Concentrations in Horses With Severe Liver Disease: A Retrospective Study and Review of the Literature

The present retrospective study was undertaken to determine the frequency of hypoproteinemia and hypoalbuminemia in horses with natural occurring severe liver disease. The study represents a review of case records and laboratory data of 84 horses presented with acute or chronic liver disease to the University of California Veterinary Medical Teaching Hospital between 1973 and 1991. Forty horses (48%) had serum protein concentrations above the maximum reference value (7.7 g/dL). The increase in serum protein concentration was associated with hyperglobulinemia ( P = .00005, R ² = .80). Only 13% (11/84) of the horses had serum albumin concentrations below the minimum reference range (2.5 g/dL), and hypoproteinemia was found in only 1 of these horses. Of these, 18% (9/51) of the horses with chronic liver disease and 6% (2/33) of the horses with acute liver disease had albumin concentrations below the minimum reference value. Globulin concentrations in 64% of the horses (54/84) were above the maximum reference value (4.0 g/dL). The present study indicates that hypoproteinemia and hypoalbuminemia are not common features in horses with severe liver disease.     

Leptospirosis: An important infectious disease in North American horses

North American horses are commonly exposed to Leptospira organisms. Leptospira Bratislava is the most common infecting serovar but this serovar has not been confirmed to cause clinical disease in North American horses. Leptospira Pomona type kennewicki is responsible for most of the clinical diseases (leptospirosis) in North American horses. Leptospirosis is most commonly associated with diseases of the placenta and fetus, the kidneys and the eyes in horses. In-utero infections in pregnant mares may result in abortion, neonatal illness or birth of an antibody positive healthy foal. Acute renal failure in younger horses and recurrent uveitis in adult horses are other well documented clinical syndromes of leptospirosis. Abortions, neonatal disease and acute renal failure are caused by a subacute infection, while horses with Leptospira associated recurrent uveitis develop ocular disease months or years after the initial Leptospira infection. Diagnosis of Leptospirosis is made by a combination of antigen or antibody testing methods. Mares that abort following Leptospira infection have no additional clinical signs at the time of abortion but may shed the offending Leptospira spp. in the urine for several weeks. Antibiotic treatments are sometimes used in hopes of decreasing Leptospira shedding in infected horses or prophylactically in exposed pregnant mares but documentation of efficacy is lacking. Horses with Leptospira - associated acute renal failure can be successfully treated with antibiotics and supportive care. Recurrent uveitis is commonly associated with leptospirosis in North American horses and although horses may have chronic intraocular infection triggering an immune disease, systemic antimicrobial therapy has not been effective in eliminating the organism from the eye. An equine approved Leptospira Pomona type kennewicki vaccine is now available in North America.     

Concentrations of trace minerals in the spinal cord of horses with equine motor neuron disease

OBJECTIVE: To compare concentrations of trace minerals in the spinal cord of horses with equine motor neuron disease (EMND) with those of horses without neurologic disease (control horses). ANIMALS: 24 horses with EMND and 22 control horses. PROCEDURE: Spinal cord trace mineral concentrations in horses with EMND and control horses were analyzed by use of inductively coupled plasma atomic emission spectroscopy (calcium, phosphorus, sodium, potassium, magnesium, copper, iron, manganese, nickel, zinc, aluminum, cobalt, and chromium), atomic absorption spectrophotometry (lead and cadmium), flameless atomic absorption (mercury), and fluorometry (selenium). RESULTS: Copper concentration was significantly higher in the spinal cord of horses with EMND, compared with control horses; spinal cord concentrations of all other trace minerals were similar between groups. CONCLUSION AND CLINICAL RELEVANCE: Among spinal cord trace minerals investigated in the study, only copper concentrations were significantly different between horses with EMND and horses without neurologic disease, which suggests that copper may be involved in the pathogenesis of EMND. An hypothesis of oxidative injury in this disease is supported by the finding of increased copper concentrations in the spinal cord and by low vitamin E concentrations reported by other researchers.     

Concentration of Selenium in Liver in Relation to Copper Level in Normal and Copper-Poisoned Sheep

Copper absorption, liver accumulation and development of copper toxicosis in sheep are influenced by a variety of other elements, in particular molybdenum, sulphur and zinc (Underwood 1977). In a previous study on liver concentrations of copper, molybdenum and zinc in normal and copper-poisoned sheep, no direct correlation was found between the concentrations of the three metals, but molybdenum was significantly lower in the livers from sheep dead from chronic copper poisoning than in normal animals (Frøslie & Norheim 1976).     

Red maple (Acer rubrum) leaf toxicosis in horses: a retrospective study of 32 cases

BACKGROUND: Ingestion of wilted red maple leaves by horses can result in severe hemolytic anemia and methemoglobinemia. Little is known about what factors influence the outcome of red maple leaf toxicosis in horses. HYPOTHESIS: Our hypothesis was that physical examination findings, clinicopathologic variables or therapeutic modalities may predict outcome in horses with red maple leaf toxicity. ANIMALS: Horses with red maple leaf toxicosis presented to referral hospitals in the southeast region of the United States. METHODS: A multi-institutional retrospective study was designed to identify factors that predict mortality in horses with red maple toxicosis. RESULTS: Thirty-two horses with red maple toxicosis were identified, 19 of which died. Twenty-nine horses presented with anemia and 24 had clinicopathologic evidence of systemic inflammation. Renal insufficiency was identified in 12/30 (41%) horses. Laminitis (9/28) and colic (13/30) also were identified in horses with red maple toxicosis, but development of these 2 conditions did not have a negative effect on short-term survival. Horses with red maple toxicosis that survived to discharge were likely to have developed pyrexia during hospitalization (P = .030). Horses that were treated with a corticosteroid had a significantly increased likelihood of death (P = .045). There was no significant relationship between initial serum hemoglobin concentration, methemoglobin concentration, or percentage methemoglobin and mortality in this horse series. CONCLUSIONS AND CLINICAL IMPORTANCE: This study suggests that information obtained on initial examination cannot be used to accurately predict survival in horses with red maple toxicosis, but horses that receive corticosteroids are unlikely to survive.     

Equine recurrent uveitis: A clinical manifestation of leptospirosis

Leptospirosis is a zoonosis of worldwide distribution affecting domestic animals, wildlife and man. The bacterial disease is caused by pathogenic Leptospira spp., which are transmitted from reservoir hosts to accidental hosts. Horses are accidental hosts and can become susceptible to leptospiral infections. Widespread exposure to leptospires exists and is significantly more common than clinical disease. Leptospirosis can have different clinical manifestations including abortion, still birth, systemic disease with hepatic or renal dysfunction, and equine recurrent uveitis (ERU). ERU is the most frequently encountered clinical manifestation and this article will focus on the review of leptospira‐associated ERU. Equine recurrent uveitis is the most common cause of vision impairment and blindness in horses. The pathogenesis of leptospira‐associated ERU involves direct bacterial effects and immune‐mediated responses. Clinical signs vary between the acute and chronic phases of the disease and progress over time. The diagnosis of leptospira‐associated ERU can be difficult and usually requires a combination of diagnostic tests. Medical and surgical treatments have been described with varying outcomes. The prognosis for sight is usually poor, although core vitrectomy may improve the outcome. Avoidance of leptospiral exposure of horses is the only reliable prevention of leptospira‐associated disease.