Cantharidin Toxicosis in Horses

Cantharidin toxicosis in horses has become an increasing problem in certain regions of the United States. Toxicosis occurs when horses ingest alfalfa hay or products that are contaminated with "blister" beetles. Clinical signs may vary from depression to severe shock and death, depending upon the amount of toxin ingested. The most frequently observed signs include varying degrees of abdominal pain, anorexia, depression, and signs suggestive of oral irritation. Many horses make frequent attempts to void urine. Less commonly observed signs include synchronous diaphragmatic flutter and erosions of the oral mucosal surfaces. Clinical laboratory abnormalities suggestive of cantharidin toxicosis include persistent hypocalcemia and hypomagnesemia, development of hypoproteinemia, microscopic hematuria, and mild azotemia with inappropriate urine specific gravity. Chemical analysis for cantharidin is accomplished by evaluation of urine or stomach contents. Treatment of cantharidin toxicosis is symptomatic, but must include removal of toxin source. Gastrointestinal protectants, laxative, intravenous fluids, analgesics, diuretics, calcium gluconate, and magnesium are all included in the treatment regimen. Early and vigorous therapy is imperative if it is to be successful. In horses that remain alive for several days, persistence of elevated heart and respiratory rates and increasing serum creatine kinase concentration are associated with a deteriorating condition. Prevention is aimed at timely harvesting of alfalfa hay. Hay fields should be inspected for the presence of beetle clusters before harvesting. Involved areas of the field should not be harvested.     

Liver failure attributable to pyrrolizidine alkaloid toxicosis and associated with inspiratory dyspnea in ponies: three cases (1982-1988)

Of 41 equids referred to a veterinary teaching hospital in the Pacific northwest because of dyspnea and inspiratory noise, 3 ponies were diagnosed as having liver failure, most likely attributable to pyrrolizidine alkaloid toxicosis. Dyspnea appeared to be caused by laryngeal and/or pharyngeal paralysis. It is proposed that this paralysis was a manifestation of hepatic encephalopathy. Although these clinical signs are not common for pyrrolizidine toxicosis, practitioners should be aware of the possibility so that misdiagnosis of other causes of inspiratory dyspnea may not be made.     

Metal toxicosis in horses.

The ubiquity and stability of metals in the environment make them unique as a pollutant or an essential dietary component. Metals are neither created nor destroyed by chemical processes but are redistributed in the environment. In combination with other elements, metal compounds and alloys are essential materials of the contemporary world. Inappropriate use or distribution in the environment leads to adverse health effects on all biologic systems, including horses. Gastrointestinal upset is a common feature of acute toxicosis with metals in general. Among the metals discussed, arsenic and inorganic mercury have a propensity to do severe damage to the gut. Deposition of cadmium on forage is the source most likely to intoxicate horses. This subchronic to chronic problem in horses is manifest as disease of the musculoskeletal system and kidneys. Iron-containing hematinics are widely used in racetrack horses and occasionally result in hepatopathy when excessive doses are administered. Lead continues to be recognized as the most significant environmental metal pollutant. Poisoning is encountered routinely in humans and animals. Of the animal species of veterinary concern, lead-poisoned horses are not a frequent encounter. Lead-intoxicated horses show signs of peripheral neuropathy (laryngeal hemiplegia), intermittent colic, and mild anemia. Acute mercury poisoning sometimes occurs from the common use of mercury-containing blistering agents, with most clinical findings related to acute renal failure. Chronic excessive intake of zinc by horses is uncommon but devastating in rapidly growing foals. The mechanism of chronic zinc toxicosis is coupled to the induced copper deficiency. The condition is a disease of cartilage in the articular and growth physes.     

Tryptamine alkaloid toxicosis in feedlot sheep

Tryptamine alkaloid toxicosis (Phalaris staggers) was diagnosed in feedlot sheep. Clinical signs of toxicosis, which were exacerbated by excitement, included gait abnormalities, muscular tremors, nystagmus, and convulsions. An estimated 8% of the most severely affected lambs had clinical signs of toxicosis. Gross lesions detected in the brain of affected lambs consisted of focal gray-green discoloration in the brain stem and thalamus; these areas had microscopic evidence of intraneuronal pigment accumulation. Brain specimens obtained at slaughter indicated that 60% of the lambs had lesions consistent with tryptamine alkaloid toxicosis. Tryptamine alkaloids were found in low concentrations in the feed. Lambs exposed to these feeds had higher death losses than those that were not exposed to the feeds. Cobalt concentration in the feed was higher than that previously reported to be associated with Phalaris staggers.     

Use of 64Copper Measurements to Diagnose Canine Copper Toxicosis

Inherited canine copper toxicosis is a serious problem in Bedlington terriers and West Highland White terriers, and may also be a problem in other less-studied breeds. Affected dogs become ill at midlife with progressive and ultimately fatal liver disease. Treatments for removal of copper and prevention of copper accumulation are available, but are most effective if begun before the dog becomes ill. Until recently diagnosis has not been available until the dog is 1 year of age, and then only by an invasive liver biopsy with determination of liver copper concentration. The authors studied the use of 64copper for early diagnosis of canine copper toxicosis. Two procedures were evaluated. The first involved measuring the concentration of 64copper in blood 24 hours after oral administration of the radioisotope. At this time, 64copper was associated primarily with ceruloplasmin secreted into the blood by the liver. This procedure is useful in the diagnosis of the human counterpart, Wilson's disease. However, the authors found it to be nondiscriminatory between affected and unaffected dogs. In contrast, the second procedure, which involved measuring 64copper excreted in stool during 48 hours after an intravenous dose of radioisotope, yielded results that differentiated most affected and unaffected dogs.     

A 24-Year Retrospective Study of Equine Abortion in Normandy (France)

The main causes of abortion in mares in France were studied from 1,822 cases submitted for necropsy. The cause of abortion was established in 74.9% of cases (n = 1,365). Fetoplacental infections (n = 869) represented 63.7% of diagnosed abortions. A noninfectious cause was found in 27.2% of cases (n = 496). Of the infectious causes of abortion, the vast majority were caused by bacteria (n = 695; 79.9%), followed by viruses (15.1%), and then fungi (1.8%). In 27 cases (3.1%), no specific pathogenic agent could be identified despite the presence of lesions. Of the noninfectious causes of abortion, umbilical cord abnormalities were the most frequent (n = 300; 60.5%). Placental villous hypoplasia represented the second most frequent cause (17.3%). This was followed by lethal congenital malformations (6.9%). The causes of placental insufficiency other than placental villous hypoplasia—twins, placental edema, placental premature separation, and body pregnancy—were less frequent. The diagnosis of equine abortion cases examined in Normandy seemed to be somewhat in agreement with the findings reported in Kentucky and the United Kingdom. In this study, about 60% of the cases were associated with a condition involving the allantochorion or the umbilical cord. Thus, to enhance diagnostic success, it is of prime importance to submit the fetal membranes along with the fetus for necropsy.     

Slaframine toxicosis in Brazilian horses causing excessive salivation

Ingestion of food contaminated with slaframine, an alkaloid produced by Rhizoctonia leguminicola, causes a mycotoxicosis, characterised by excessive salivation. Twenty‐eight horses demonstrated this clinical sign after the consumption of alfalfa hay which on inspection showed dark patches on many of the stems. The presence of slaframine (1.5 ppm) in this hay was confirmed by gas chromatography and mass spectroscopy. This is the first equine slaframine toxicosis case reported in Brazil.     

Lead toxicosis in cats-a review

Although the incidence of lead toxicosis in small animals continues to decrease, it remains a significant malady. We have reviewed the literature of the past 45 years, which revealed 70 cases involving cats. Sources, signs, diagnosis, pathology and treatment of feline lead toxicosis are reviewed. In 84% of these cases the source of lead was old paint usually from home renovation. The most common signs in cats are anorexia, vomiting, and seizures. The younger individuals seem more likely to show CNS signs. Since signs are often vague, lead toxicosis may be significantly under diagnosed in cats. The gold standard of diagnostic tests is blood lead concentration, although it does not necessarily correlate with total body burden of lead or with metabolic effects including clinical signs. Diagnostic tests including erythropoietic protoporphyrin (EPP), urine aminolevulinic acid, and others are discussed. Gross findings on necropsy are few and include a yellow-brown discoloration of the liver often with a nutmeg-like appearance. Histological examination may reveal pathognomonic inclusion bodies in liver and renal tissues. Characteristic histological changes in the CNS include neuronal necrosis and demyelination. Treatment of lead toxicosis in cats, as in any species, involves removing the exposure, decontaminating the individual and the environment, supportive care and chelation therapy. The most recently available chelator is succimer (meso 2,3-dimercaptosuccinic acid). Succimer given orally is well tolerated and has a wide margin of safety. A high index of suspicion of lead toxicosis is warranted in cats since they often present with vague and non-specific signs. With any consistent history owners need to be asked about home renovation. Early diagnosis and treatment affords a good prognosis.     

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.     

猪轮状病毒概述

轮状病毒（Porcine Rotavirus，PRV）属呼肠孤病毒科（Reoviridae）轮状病毒属（Rotavirus）成员，是引起幼龄仔猪病毒性腹泻的主要病源之一。目前尚无治疗RV感染的有效药物，对于发病动物，可以对症治疗以及采取措施防止脱水和酸中毒等等。预防该病的有效方法是加强饲养管理和在准确诊断基础上的有效疫苗接种。     

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.     

Clinical toxicoses of domestic rabbits.

Toxicoses are an uncommon presentation to rabbit practitioners; however, veterinarians who accept rabbits as patients should be familiar with the basic concepts of toxicosis management and the specific syndromes associated with clinical toxicoses. The objective of this article is to present clinically relevant information for veterinarians presented with rabbits exhibiting characteristic signs of toxicosis. In addition, specific mention is made to the most common clinical toxicoses, including lead, chemicals, rodenticides, aflatoxins, and poisonous plants.     

A survey concerning the equine fescue toxicosis malady

The objective of this research was to determine the scope of equine fescue toxicosis, current procedures to control the disease, and to gain veterinary insight to possible new therapies. A survey was developed with help form experts in the area of fescue toxicosis. From a list of members of the American Veterinary Medical Association (AVMA), a sample was obtained by selecting large animal/equine veterinarians from states where fescue toxicosis is common. These states included: Alabama, Arkansas, Georgia, Illinois, Indiana, Kentucky, Missouri, Mississippi, North Carolina, Ohio, South Carolina, Tennessee, Virginia, and West Virginia. One-fifteenth of the veterinarians (515 total) were mailed questionnaires; 207 responded. Veterinarians were grouped into regions based on latitude. Region 1 included veterinarians practicing north of 39.0° latitude; Region 2 included veterinarians practicing between 36.5° and 39.0° latitude; and Region 3 included veterinarians practicing south of 36.5° latitude.A majority of horse pasture in the area of the survey is comprised of at least 50% fescue, with approximately 70% of the pasture being at least partially comprised, of fescue.Almost 50% of the brood mares in the area of the survey are exposed to endophyte-infected fescue. Many gravid brood mares in the area of the survey were suffering from acute and subacute symptoms, with over 43% warranting some kind of management technique to prevent toxicity from occurring. A large majority of veterinarians in the area of the survey feel that fescue toxicosis is, to some level, a problem. Current management techniques can be tedious and expensive. New management techniques and/or therapies are needed to handle the problems associated with equine fescue toxicosis. A large majority of veterinarians in the area of the survey feel an effective drug therapy would be valuable in treating equine fescue toxicosis. If a drug therapy were developed, a daily feed additive or an oral gel would be the most popular method of dosing with veterinarians.As a result of trends noticed in the rates of equine fescue toxicosis in different areas, statistical analyses were conducted on data generated from this survey along regions that seemed to have different infection rates. There was no difference (P>0.05) in levels of fescue in pastures, mare exposure to the endophyte, and mare expression of acute or subacute symptoms between regions 2 and 3. There was a difference (P<0.05) between region 1 and regions 2 and 3 for all of the factors tested except for number of mares seen by veterinarians.     

Pathologic features of adriamycin toxicosis in young pigs: nonskeletal lesions

In ten experiments, 53 castrated male 4- to 8-week-old weanling pigs were given adriamycin (ADR) IV at mean dosages of 0.64, 1.0, 1.6, 3.2, or 6.4 mg/kg/week at various frequencies for up to 20 weeks. Mortalities in pigs given these dosages were 0% after 112 days, 100% after 134 days (survival time was 48 to 134 days), 91% after 75 days (survival time was 5 to 75 days), 100% after 28 days (survival time was 23 to 28 days), and 100% after 14 days (survival time was 10 to 14 days), respectively. Survival time was prolonged in younger pigs and in pigs given smaller but more frequent dosages of ADR. Characteristic gross and histopathologic alterations of ADR toxicosis were observed in pigs given 1.0, 1.6, 3.2, or 6.4 mg/kg/week mean dosages. The most frequent lesions were in the alimentary tract, myeloid and lymphoid tissues, skin, and perivascular tissues at injection sites. Alimentary tract lesions were mucosal epithelial atrophy, with secondary fibrinonecrotic inflammation in the oral cavity and large intestine. Marked hypoplasia was seen in bone marrow and lymphoid tissues, with frequent terminal hemorrhagic diathesis and septicemia. Several days before death, the pigs developed severe dermatitis over the ventral portion of the abdomen and inner surfaces of the limbs. Perivascular necrosis and cellulitis produced by extravasation of ADR was a frequent complication of treatment. Terminal severe acute pneumonia occurred in most pigs. Pericarditis or cardiomyopathy (or both) developed in 14 pigs, given 0.64, 1.0, or 1.6 mg/kg each week (mean cumulative dosage 520.5 mg/m2 of body surface). Characteristic histopathologic and ultrastructural alterations in affected cardiac muscle cells were vacuolar degeneration, myocytolysis, and hyaline necrosis. Nephrotoxicosis also was in pigs with chronic ADR toxicosis. Systemic antibiotic treatment did not prolong survival of ADR-treated pigs in two experiments, but did in one other experiment.     

Honey mesquite toxicosis in a goat

Honey mesquite (Prosopis glandulosa) is distributed across a large portion of the southwestern United States. Ingestion of young leaves, pods, or beans can cause toxicosis in cattle and goats if they comprise a substantial portion of their diet. Goats, as browsers, are most likely to develolp mesquite toxicosis. Sheep appear to be more resistant to the plant's toxic effects. Consistent clinical signs include weight loss, ptyalism, mandibular tremors, tongue protrusion, and dysphagia. Diagnosis of mesquite toxicosis is largely made on the basis of history and clinical signs with exclusion of appropriate differentials. Laboratory findings are nonspecific but may reveal a mild anemia and hypoglycemia. Postmortem findings suggestive of mesquite toxicosis are limited to fine vacuolation of neurons in the trigeminal motor nucleus. Treatment consists of an alternative diet and supportive care. The disease is treatable in cattle and sheep but has a high case fatality rate in goats.     

Nonsteroidal anti-inflammatory drug toxicosis in dogs and cats: 240 cases (1989-1990)

A search of medical records at the Georgia Animal Poison Information Center over a 19-month period revealed 240 cases of dog and cat exposure to nonsteroidal anti-inflammatory drugs (NSAID). The most common NSAID consumed were ibuprofen, acetaminophen, aspirin, and indomethacin. The most common clinical signs of toxicosis were vomiting and diarrhea, CNS depression, and circulatory manifestations. Pets are at risk from NSAID toxicosis through administration by the owners or accidental consumption of improperly stored drugs.     

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.     

Mushroom toxicosis in dogs in general practice causing gastroenteritis,ptyalism and elevated serum lipase activity

Mushroom toxicosis is rarely diagnosed in dogs and is poorly reported in the veterinary literature. This report suggests that mushroom toxicosis is a potentially under‐diagnosed condition in first opinion practice in the UK. Nine dogs with clinical signs consistent with mushroom toxicosis were identified from the records of an out‐of‐hours emergency service between August 2010 and January 2011. Four dogs were later excluded because of clinical inconsistencies. Clinical signs included acute profuse ptyalism (5/5), diarrhoea (5/5), vomiting (4/5), hypovolaemia (4/5), stuporous (3/5) or obtunded mentation (1/5), miosis (2/5) and hypothermia (2/5). Serum lipase activity was elevated in 4/4 dogs; canine‐specific pancreatic lipase was elevated in the remaining dog. Four dogs recovered with aggressive intravenous fluid therapy, analgesia and supportive care; the remaining dog was euthanased due to severe clinical signs and financial constraints. Mushroom toxicosis is an important differential diagnosis for acute gastroenteritis and one possible cause of some cases of “Seasonal Canine Illness”. Affected dogs may demonstrate elevated pancreatic enzymes and mushroom toxicosis should be considered in cases of elevated lipase or abnormal semi‐quantitative canine‐specific pancreatic lipase activities.     

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.     

Review of Pododermatitis circumscripta (ulceration of the sole) in dairy cows

Sole ulcers are among the most frequent causes of lameness in dairy cattle. They are found most commonly in the hind lateral claw, are frequently bilateral, and have a high rate of reoccurrence. The pathogenesis of sole ulceration is primarily based on mechanical injury by the 3rd phalanx to the corium, basement membrane, and basal layers of the sole epidermis as a result of failure of the suspensory apparatus in the claw. The main pathways in the failure of the suspensory system include inflammatory (dermal vascular changes followed by disruption of keratinocyte proliferation and differentiation caused by local and systemic mediators) and noninflammatory (hormonal and biochemical changes in the peripartum period resulting in alterations of connective tissue in the suspensory system) pathways. Sole ulcers tend to occur in specific locations; the most reported site is the junction of the axial heel and sole. Other locations include the apex of the toe and the heel. Varying degrees of lameness may result, and the most severe are seen with complicated cases in which ascending infection affects the deeper structures of the claw. Pathologic changes at the ulcer site include dyskeratosis and dilated horn tubules with microcracks. Vascular changes include dilatation and thrombosis of capillaries with "neocapillary formation." Areas of dyskeratosis may remain for as long as 50 days at the ulcer site. Treatment includes corrective trimming and relief of weight bearing. Complicated cases may require surgical intervention.