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.     

Toxicoses associated with administration of mitoxantrone to dogs with malignant tumors

One hundred twenty-nine dogs with histologically confirmed malignant tumors were used in a prospective study to determine the toxicity of the new dihydroxyquinone derivative of anthracene, mitoxantrone, which was administered IV at 21-day intervals at dosages ranging from 2.5 to 5 mg/m2 body surface area. Each dog was evaluated for signs of toxicosis for 3 weeks after each dose was administered or until the dog died, whichever came first. The number of dogs in each evaluation period were as follows: 1 dose (n = 129), 2 doses (n = 82), 3 doses (n = 43), 4 doses (n = 26), 5 doses (n = 19), 6 doses (n = 9), 7 doses (n = 6), 8 doses (n = 5), 9 doses (n = 3), and 10 doses (n = 1). The most common signs of toxicosis were vomiting, diarrhea, anorexia, and sepsis secondary to myelosuppression. None of the dogs died of complications resulting from mitoxantrone treatment. Dogs with signs of toxicosis during the 21-day interval from administration of the first dose of mitoxantrone were 95 times (P = 0.003) more likely to develop signs of toxicosis during the 21-day interval from the second dose of mitoxantrone. Similarly, dogs that developed signs of toxicosis during the 21-day interval from the administration of the second dose were 34 times (P less than 0.001) more likely to develop signs of toxicosis during the 21-day interval from the administration of the third dose. With each 1 mg/m2 increase in mitoxantrone, the odds of developing signs of toxicosis increased by 5.9 fold (P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)     

Clinical management of potential ibuprofen toxicosis in a South American red-footed tortoise (Geochelone carbonaria).

This article describes the clinical management of potential ibuprofen toxicosis in South American red-footed tortoise (Geochelone carbonaria). A 2.5-year-old, 0.78-kg Geochelone carbonaria tortoise was presented to the emergency clinic after ingesting solubilized ibuprofen (200 mg) in a gelatin capsule. Treatment on initial presentation consisted of esophagostomy tube placement for gastric lavage and activated charcoal administration, intravenous and intraosseous fluid therapy, and administration of gastrointestinal protectants (sucralfate and famotidine). The tortoise was discharged to the owners. Although follow-up diagnostic monitoring was minimal because of owner compliance, the patient was noted to be alive and in reasonable health 1 year after initial presentation. This is the first report on the management of potential nonsteroidal anti-inflammatory drug toxicosis in any chelonian species.     

Fatal propylene glycol toxicosis in a horse

Toxicosis attributable to propylene glycol (1,2-propanediol) was suspected in an 8-year-old 450- to 500-kg male Quarter Horse. Clinical signs of toxicosis developed within 15 minutes of the accidental iatrogenic oral administration of 3.8 L of propylene glycol. Clinical signs of toxicosis included salivation, sweating, ataxia, and signs of pain. Additionally, at 24 hours after propylene glycol ingestion, the horse became increasingly atactic, had an abnormal breath odor, developed rapid shallow breathing, and was cyanotic. The horse died of apparent respiratory arrest 28 hours after the propylene glycol ingestion. Analysis of serum and combined urine and blood from the kidneys confirmed the presence of propylene glycol. Propylene glycol is used for the treatment and prevention of bovine ketosis, and is similar in appearance to mineral oil. The accidental administration of propylene glycol to horses may result in fatal poisoning.     

Phase I clinical trial of the use of zinc phthalocyanine tetrasulfonate as a photosensitizer for photodynamic therapy in dogs

OBJECTIVE: To determine the threshold for acute toxicosis of parenterally administered zinc phthalocyanine tetrasulfonate (ZnPcS(4)), a candidate second-generation photosensitizer, in mice and evaluate the compound's safety in a phase I clinical trial of ZnPcS(4)-based photodynamic therapy (PDT) in pet dogs with naturally occurring tumors. ANIMALS: Male Swiss-Webster mice and client-owned dogs with naturally occurring neoplasms. PROCEDURES: For the study of acute toxicosis, mice were given graded doses of ZnPcS(4). To determine safety, a rapid-titration phase I clinical trial of ZnPcS(4)-based PDT in tumor-bearing dogs was conducted. RESULTS: In mice, administration of >or= 100 mg of ZnPcS(4)/kg resulted in renal tubular necrosis 24 hours after IP injection. In tumor-bearing dogs, ZnPcS(4) doses 相似文献   

Comparison of two heavy metal chelators for treatment of lead toxicosis in cockatiels

OBJECTIVE: To compare efficacy and safety of meso-2,3-dimercaptosuccinic acid (DMSA) and Ca EDTA for treatment of experimentally induced lead toxicosis in cockatiels (Nymphicus hollandicus). ANIMALS: 137 (69 females, 68 males) healthy cockatiels between 6 months and 8 years old. PROCEDURE: Lead toxicosis was induced by placing lead shot in the gastrointestinal tract. Treatment with Ca EDTA (40 mg/kg of body weight, IM, q 12 h), DMSA (40 or 80 mg/kg, PO, q 12 h), and sodium sulfate salts (SSS; 0.5 mg/kg, PO, q 48 h) was initiated 4 days after induction of lead toxicosis. Blood lead concentrations were determined, using atomic absorption spectrophotometry. Number of birds surviving and blood lead concentrations were compared among groups. RESULTS: In Phase II of the study, administration of DMSA and Ca EDTA significantly decreased blood lead concentrations when used alone or in combination in birds with lead toxicosis. Addition of SSS did not result in further decreases in lead concentrations. Eight of 12 (66.7%) birds without lead toxicosis given 80 mg of DMSA/kg did not survive to the end of the study. Lesions related to treatment with chelating agents were not detected during necropsy. CONCLUSIONS AND CLINICAL RELEVANCE: DMSA and Ca EDTA are effective chelating agents in cockatiels. Because DMSA is administered orally, it may be easier than other chelating agents for bird owners to administer at home. However, the narrow margin of safety of DMSA indicates that this agent should be used with caution.     

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.     

Acute and short-term toxicoses associated with the administration of doxorubicin to dogs with malignant tumors

One hundred eighty-five dogs with histologically confirmed, measurable malignant tumors were used in a study to determine the toxicity of the anthracycline antitumor antibiotic, doxorubicin, which was administered once or twice (at a 21-day interval) at the rate of 30 mg/m2 of body surface area, iv. During this study, 7 dogs died as a direct result of doxorubicin-induced toxicosis and 16 died as a direct result of the malignant neoplastic disease. Each dog was evaluated for signs of toxicosis for 3 weeks after the last dose was administered (15 dogs received 1 dose, 170 dogs received 2 doses) or until the dog died, whichever came first. The most common signs of toxicosis were vomiting, diarrhea, colitis, anorexia, and pruritus. The probability of doxorubicin-induced toxicosis decreased significantly (P less than 0.0001) in inverse relationship to body weight. Dogs with signs of toxicosis during the 21-day interval from administration of the first dose of doxorubicin were 17.2 times (P less than 0.01; 95% confidence interval; 5.5, 54.2) more likely to develop signs of toxicosis during the 21-day interval from the second dose of doxorubicin. The performance status of each dog was evaluated using a modified Karnofsky performance scheme; the only time the performance status was adversely affected to a significant extent by doxorubicin-induced toxicosis was during the 21-day period, starting with the second dose (P less than 0.0001).     

Cisplatin and doxorubicin toxicosis in dogs with osteosarcoma

Toxicosis associated with doxorubicin and cisplatin administration starting either 2 or 10 days after limb amputation for osteosarcoma was examined retrospectively in dogs. The purpose was to determine whether dosage and timing of chemotherapy affected rates of toxicosis after administration of the 1st treatment. Records of 100 dogs with appendicular osteosarcoma without evidence of metastases or concurrent disease were examined. Dogs received chemotherapy with doxorubicin and cisplatin every 3 weeks for 3 treatments starting 2 days (n = 51) or 10 days (n = 49) after amputation. The dosage of cisplatin was 60 mg/m2 and was given with 6-hour saline diuresis and butorphanol. Doxorubicin was given at 12.5-25 mg/ml during fluid administration. Hematologic data were collected before and weekly after treatment. Client interviews were conducted to assess gastrointestinal toxicosis during the interval between treatments. The reported toxicoses were graded on a scale of 0 to 4. Dogs receiving 25 mg/m2 of doxorubicin experienced greater rates of grade 4 toxicity (67%; n = 6) than dogs in groups receiving 12.5-20 mg/m2 of doxorubicin (< or = 25%; n = 94, P = .03). Dogs in the Day 2 group experienced greater rates (35%) of grade 4 toxicity than dogs in the Day 10 group (12%, P = .007). We concluded that chemotherapy administered 2 days after surgery produced an unacceptable level of toxicoses. except at greatly reduced dosages, and that even with a delay of treatment, 25 mg/m2 of doxorubicin, when given in combination with cisplatin at 60 mg/m2, was too toxic for routine use.     

Benzimidazole Toxicosis in Rabbits: 13 Cases (2003 to 2011)

The objective of this study was to evaluate both clinical and histologic anomalies associated with suspected benzimidazole toxicosis in rabbits. Histopathologic records were reviewed from rabbit cases that were diagnosed with suspected benzimidazole toxicosis at 2 specialty pathology services. Medical records were also solicited from veterinarians who treated rabbits with suspected benzimidazole toxicosis. In all, 13 cases were included in this retrospective study. Histologically, presumed radiomimetic lesions of benzimidazole toxicosis were noted in 3 cases. An additional 10 cases exhibited lesions suggestive of benzimidazole toxicosis. Common clinical signs observed in the study of rabbits included inappetence, lethargy, hemorrhage, and death. One rabbit with suspected benzimidazole toxicosis survived. Benzimidazoles should be used judiciously in rabbits at published doses only after the owners are knowledgeable of the potential health risks associated with this class of drugs. The prognosis for rabbits with suspected benzimidazole toxicosis is poor, but supportive care resulted in the survival of 1 suspected case in this study.     

Diazepam as a treatment for metronidazole toxicosis in dogs: a retrospective study of 21 cases

The currently recommended treatment for metronidazole toxicosis is drug discontinuation and supportive therapy. Reported recovery times are 1-2 weeks. The records of 21 dogs with metronidazole toxicosis were retrospectively analyzed to determine whether diazepam improved recovery. The dosage and duration of metronidazole therapy and the response and recovery times of 13 dogs treated with diazepam were compared to those of 8 dogs receiving only supportive care. Response time was defined as the time to resolution of the debilitating clinical signs. Recovery time was the time to resolution of all residual clinical signs. The average dosage and duration of metronidazole administration for the diazepam-treated and untreated groups were 60.3 mg/kg/d for 44.9 days and 65.1 mg/kg/d for 37.25 days. The protocol for diazepam administration consisted of an initial i.v. bolus and then diazepam PO q8h for 3 days. The average dosage of both the i.v. and PO diazepam was 0.43 mg/kg. The average response time for the diazepam-treated dogs was 13.4 hours compared to 4.25 days for the untreated group. Recovery time also was markedly shorter for the diazepam-treated dogs (38.8 hours) compared to the untreated group (11 days). Results of this study showed that dogs with metronidazole toxicosis recover faster when treated with diazepam. Although the mechanism of metronidazole toxicosis or how diazepam exerts its favorable effect is not known, it is likely related to modulation of the gamma-aminobutyric acid (GABA) receptor within the cerebellar and vestibular systems.     

Use of intralipid emulsion therapy to treat suspected oleander toxicosis in a domestic goose (Anser anser domesticus)

Ingestion of toxic substances is a common event in companion animals and livestock, especially in waterfowl. Oleander (Nerium oleander) toxicosis is rarely reported in avian species, with symptoms including cardiac, neurological and gastrointestinal manifestations. A 6-month-old domestic goose (Anser anser domesticus) was presented for depression, anorexia, permanent sternal recumbency, weakness and incoordination, and the owners witnessed the ingestion of oleander leaves. Despite the absence of evident cardiac symptoms, biochemical hematological findings showed significant increase of CPK, AST, LDH, and troponin I. Therapy was set with intravenous (IV) fluid administration, antibiotic and anti-inflammatory, oral activated charcoal, and IV lipid emulsion at 15 mL/kg/h. Clinical improvement was achieved after 2 hours. The patient was discharged 3 days after admission, with complete recovery and return to normal biochemical values 10 days after initial presentation. The present work describes a suspected case of spontaneous oleander poisoning in a domestic goose, with the first use of troponin I to diagnose cardiac injury in this species, and the first report of IV lipid emulsion to successfully treat this kind of toxicosis in veterinary practice.     

Propylene glycol toxicosis in a llama

Propylene glycol toxicosis in llamas can result from overzealous administration of propylene glycol-containing gels formulated and labeled for use in cattle. Treatment of ketosis in llamas requires re-establishment of stomach flora and stimulation of appetite.     

Acute oxalate poisoning attributable to ingestion of curly dock (Rumex crispus) in sheep

Ten of 100 mature ewes were afflicted with acute oxalate toxicosis within 40 hours after being temporarily penned in a lot that contained considerable growing Rumex crispus (curly dock). Clinical signs of toxicosis included excess salivation, tremors, ataxia, and recumbency. Affected ewes were markedly hypocalcemic and azotemic. Oxalate crystals were not observed in urine. Gross postmortem lesions were minimal and nondiagnostic in 2 ewes that died peracutely, but perirenal edema and renal tubular degeneration were clearly observable in ewes euthanatized on the third day of toxicosis. Diagnosis of oxalate toxicosis was confirmed by histopathologic findings. Samples of Rumex spp contained 6.6 to 11.1% oxalic acid on a dry-weight basis, a concentration comparable with that in other oxalate-containing plants that have caused acute oxalate toxicosis.     

Acute thallium toxicosis in a dog.

A Doberman Pinscher was evaluated for acute onset of gastroenteritis, characterized by anorexia, hematemesis, and hematochezia. The dog had ingested mole bait containing thallium 2 days prior to admission. Thallium toxicosis was confirmed by detection of thallium in the urine, using colorimetric analysis. The dog responded well to administration of antibiotics, fluids administered IV, warm-water enemas, and oral administration of activated charcoal slurries.     

Oxytetracycline pharmacokinetics, tissue depletion, and toxicity after administration of a long-acting preparation at double the label dosage

Oxytetracycline (OTC) concentration in plasma and tissues, plasma pharmacokinetics, depletion from tissue, and toxicity were studied in 30 healthy calves after IM administration of a long-acting OTC preparation (40 mg/kg of body weight) at double the label dosage (20 mg/kg). Plasma OTC concentration increased rapidly after drug administration, and by 2 hours, mean (+/- SD) values were 7.4 +/- 2.6 micrograms/ml, Peak plasma OTC concentration was 9.6 +/- 2.6 micrograms/ml, and the time to peak plasma concentration was 7.6 +/- 4.0 hours. Plasma OTC concentration decreased slowly for 168 hours (elimination phase) after drug administration, and the elimination half-life was 23.9 hours. Plasma OTC concentration exceeded 3.8 micrograms/ml at 48 hours after drug administration. From 168 to 240 hours after drug administration, plasma OTC concentration decreased at a slower rate than that seen during the elimination phase. This slower phase was termed the depletion phase, and the depletion half-life was 280.7 hours. Tissue OTC concentration was highest in kidneys and liver. Lung OTC concentration exceeded 4.4 micrograms/g of tissue and 2.0 micrograms/g of tissue at 12 and 48 hours after drug administration, respectively. The drug persisted the longest in kidneys and liver. At 42 days after drug administration, 0.1 micrograms of OTC/g of kidney was detected. At 49 days after drug administration, all OTC tissue concentrations were below the detectable limit. Reactions and toxicosis after drug administration were limited to an anaphylaxis-like reaction (n = 1) and injection site swellings (n = 2).     

Clinical signs of cardiovascular effects secondary to suspected pimobendan toxicosis in five dogs

The purpose of this study was to review the medical records of dogs that were either suspected or known to have ingested large doses of pimobendan and to describe the clinical signs associated with pimobendan toxicosis. The database of Pet Poison Helpline, an animal poison control center located in Minneapolis, MN, was searched for cases involving pimobendan toxicosis from Nov 2004 to Apr 2010. In total, 98 cases were identified. Of those, seven dogs that ingested between 2.6 mg/kg and 21.3 mg/kg were selected for further evaluation. Clinical signs consisted of cardiovascular abnormalities, including severe tachycardia (4/7), hypotension (2/7), and hypertension (2/7). In two dogs, no clinical signs were seen. Despite a wide safety profile, large overdoses of pimobendan may present risks for individual pets. Prompt decontamination, including emesis induction and the administration of activated charcoal, is advised in the asymptomatic patient. Symptomatic and supportive care should include the use of IV fluid therapy to treat hypotension and address hydration requirements and blood pressure and electrocardiogram monitoring with high-dose toxicosis. Practitioners should be aware of the clinical signs associated with high-dose pimobendan toxicosis. Of the dogs reported herein, all were hospitalized, responded to supportive care, and survived to discharge within 24 hr of exposure.     

Effect of yohimbine hydrochloride on serum prolactin concentration in the rat: possible antagonist for fescue toxicosis

Yohimbine hydrochloride is an indole alkaloid which blocks alpha 2-adrenergic and dopamine receptors and stimulates serotonergic receptors. Yohimbine was selected for testing as a possible antagonist in fescue toxicosis. Reduced body weight gains in cattle with chronic fescue toxicosis may be due to ergot alkaloids produced by fungi which infect the fescue grass. Ergot alkaloids stimulate dopamine receptors, antagonize serotonin, and lower serum prolactin concentrations. It was hypothesized that yohimbine may reverse or counteract the effects of the toxic fescue. Investigation was made of the treatment effects of multiple doses of yohimbine given in rats by intraperitoneal and oral routes. Given intraperitoneally once a day for 8 days, yohimbine hydrochloride increased serum prolactin concentrations. When given orally in feed for 7 days, the drug decreased the serum prolactin concentration. The effects of yohimbine on prolactin concentrations were dependent on the dosages and routes of administration. The inability of yohimbine, when given orally, to increase serum prolactin levels decreased its potential usefulness for prolonged treatment of fescue toxicosis.     

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.     

Effect of oral administration of excessive iron in adult ponies

OBJECTIVE: To evaluate the potential of excess dietary iron to cause hepatic lesions similar to those described in horses with suspected iron toxicosis or hemochromatosis. DESIGN: Prospective study. ANIMALS: 6 adult male ponies. PROCEDURE: 4 ponies received 50 mg of iron/kg (22.7 mg/lb) of body weight each day by oral administration of ferrous sulfate, which contained 20% elemental iron; 2 ponies received only the carrier (applesauce). Complete blood counts, serum biochemical analyses, and hepatic tissue biopsies were performed, and serum iron concentrations were measured. Blood and tissue samples were obtained at days 0 and 2, and at the end of weeks 1, 3, 6, and 8 after administration of iron was initiated. Treatment was discontinued after 8 weeks, and hepatic iron concentrations were measured at 28 weeks. RESULTS: Hepatic iron concentrations, serum iron concentrations, percentage saturation of transferrin, and serum ferritin concentrations were increased, compared with baseline and control concentrations, by week 8. Adverse clinical signs or histologic lesions in the liver were not detected in any ponies. At 28 weeks, hepatic iron concentrations had decreased. CONCLUSIONS AND CLINICAL RELEVANCE: Histologic lesions were not seen in the hepatic biopsy specimens obtained from the ponies treated with ferrous sulfate. It was concluded that it would be unlikely for iron toxicosis to develop in adult ponies or horses during a period of < 8 weeks when food or water contained increased amounts of iron. It is suspected that previous reports of hepatopathies in animals with hemosiderin accumulation may represent a primary hepatopathy with secondary hemosiderin accumulation, especially if the only source of iron is via oral consumption.