Permethrin toxicosis in cats

A retrospective analysis of all adverse experience reports received by the Australian Pesticides and Veterinary Medicines Authority's Adverse Experience Reporting Program for veterinary medicines since 1995, showed that permethrin toxicity in cats usually occurred after the owner applied a canine permethrin-containing product, typically a spot-on. Cats are also at risk from grooming or being in direct contact with recently treated dogs. This paper reviews permethrin toxicosis and its treatment in cats, incorporating information from the Australian and selected overseas veterinary pharmacovigilance programs.     

Methionine toxicosis in cats

Cats given DL-methionine (1 g/kg of body weight/day) developed severe hemolytic anemia with marked increase of methemoglobin (MetHb) concentration and Heinz-body formation at treatment-day 6 to 10. Cats fed 0.5 g of methionine/kg for 52 days had a moderate Heinz-body hemolytic anemia with methemoglobinemia at treatment days 17 to 31, but thereafter recovered from the anemia despite continuation of methionine feeding, indicating an adaptation of the cats. In vitro, significant (P less than 0.01) increases of MetHb concentration and Heinz-body formation were observed when RBC were incubated with plasma from cats fed (1 g of methionine/kg) or with 10 mM 3-methylthiopropionate, a product of methionine catabolism. However, these increases were not observed when RBC were incubated with 10 mM methionine. Seemingly, excessive methionine intake leads to production of an intermediate of the methionine catabolism that may affect RBC directly as an intensive oxidizing agent, resulting in an excessive oxidation of hemoglobin to MetHb and Heinz-body formation.     

Succimer for treatment of lead toxicosis in two cats.

Two cats from a single household were examined because of neurologic abnormalities suggestive of central vestibular disease. The owner had been renovating her 150-year-old house for the preceding 3 months, and renovations included chipping and sanding of old paint from windowsills and stair railings. Lead toxicosis was diagnosed on the basis of history and concentrations of lead in blood and urine. Both cats were treated with succimer. Treatment was not associated with any adverse effects, and both cats recovered completely. Ingestion of old paint from house renovations is the most common source of lead exposure in cats. Owners of cats with gastrointestinal tract or neurologic abnormalities should be questioned specifically about house renovations.     

Systemic toxicosis associated with azathioprine administration in domestic cats.

Five cats were treated with an azathioprine suspension (2.2 mg/kg of body weight on alternate days) and 2 cats were given vehicle (controls) for 9 weeks. Complete blood and platelet counts and serum biochemistry variables were monitored weekly. Bone marrow aspirates were evaluated every 3 weeks, and core bone marrow biopsy was performed at the end of the study. Profound neutropenia (less than 600 cells/microliters) was observed in all treated cats, and 1 cat developed pancytopenia. Treatment was discontinued if the WBC count was less than 3,000 cells/microliters. Four weeks after discontinuation of azathioprine, 1 treated cat again was given azathioprine at a lower dosage (1.1 mg of azathioprine/kg on alternate days) and neutropenia recurred within 2 weeks. During treatment, 3 cats developed thrombocytosis, and 2 developed thrombocytopenia. In 4 of 5 cats, neutropenia and thrombocytopenia resolved when azathioprine was discontinued. Bone marrow cytologic examination during treatment revealed reduction of the neutrophil line, with relative increase in monocytes. Core bone marrow biopsy at the completion of the study revealed hypocellular marrow with marked decrease in the myeloid series in cats given azathioprine. One of the cats that was treated with azathioprine had a hypercellular marrow with increased numbers of mature granulocytes and precursors; however, azathioprine had been discontinued 3 weeks prior to biopsy. Alterations in serum biochemical variables were not associated with azathioprine. Two cats that were treated with azathioprine developed respiratory tract infections, and 1 of them was euthanatized during the study.     

Suspected toxicosis after topical administration of minoxidil in 2 cats

Objective: To discuss the clinical presentation and necropsy findings of 2 cats after topical administration of a minoxidil solution. Additionally, a potential management plan is offered for future cases. Case summary: Two cats with dermal exposure to topical minoxidil solution were identified from the ASPCA Animal Poison Control Center (APCC) files. Both cats were presented with lethargy and dyspnea within 36 hours of exposure. The cats were hypothermic, and had pulmonary edema and pleural effusion present on thoracic radiography. Both cats died despite supportive care. Necropsy of both cats confirmed pleural effusion and pulmonary edema and indicated cardiac compromise. New or unique information provided: Topical administration of minoxidil solution may cause life‐threatening pulmonary edema, pleural effusion, and cardiac dysfunction in the cat.     

Efficacy and toxicosis of VELCAP-C treatment of lymphoma in cats

Background: Lymphoma is the most common malignancy affecting cats. A protocol employing vincristine, l -asparaginase, cyclophosphamide, doxorubicin, and prednisone (VELCAP-S) is effective and well tolerated in dogs with lymphoma. A 24-week variation of this protocol (VELCAP-C) was developed for treatment of cats.
Hypothesis: That VELCAP-C will result in survival times for cats with lymphoma that are similar to those obtained when cats are treated with a protocol that includes fewer chemotherapy agents.
Animals: Sixty-one cats with lymphoma.
Methods: Retrospective study. Outcomes evaluated were response to VELCAP-C therapy, toxicosis, and survival time. The effect of signalment, staging, CBC, and serum chemistry profile and dosage on these outcomes was examined.
Results: Six cats (10%) completed the protocol with a median survival of 1189 days. Forty-three percent (23 of 61) of the cats achieved complete response (CR) with a median survival time of 62 days. Cats that required a dose reduction of any drug during induction were more likely to achieve CR. Weight loss and hepatomegaly at diagnosis were negatively associated with response to treatment. Increased lactate dehydrogenase (LDH) serum activity at the time of initial treatment correlated with decreased survival times.
Conclusions and Clinical Importance: This multi agent protocol did not provide improved survival over historical data using protocols with fewer agents. Serum LDH activity levels might provide useful prognostic information for cats with lymphoma.     

Fenvalerate/N,N-diethyl-m-toluamide (Deet) toxicosis in two cats

Toxicosis attributable to fenvalerate and N,N-diethyl-m-toluamide (Deet) exposure was suspected in 2 cats. Clinical signs of toxicosis developed within 4 to 6 hours of dermal application of the pesticide. Clinical signs of toxicosis seen in both cats included hypersalivation, ataxia, and depression. In addition, seizures were seen in 1 cat. Both cats died. Analysis of skin, kidney/urine, liver, and brain tissues confirmed the presence of fenvalerate and Deet. The pyrethroid fenvalerate and the insect repellent Deet are used for the control of fleas and ticks on cats. Suspected fenvalerate/Deet toxicosis in cats is associated with tremors, hypersalivation, ataxia, vomiting, depression, and seizures.     

Effects of various antidotal treatments on acetaminophen toxicosis and biotransformation in cats

Oral N-acetylcysteine (NAC), IV NAC, and IV sodium sulfate were evaluated as treatments for cats dosed orally with toxic sublethal doses of acetaminophen (APAP). Six cats were given single oral doses of 120 mg of APAP/kg of body weight and the respective antidote at 4.5, 8.5, and 12.5 hours after APAP dosing in 3 separate trials. The cats were given each antidotal treatment in random order with at least 3 weeks separating the individual APAP-treated trials. Clinical signs, plasma APAP half-lives, clinical chemical values, and APAP urinary excretion and metabolites were studied. Results were compared (P less than 0.05) with each other and with those of a control group of 6 cats given identical APAP doses, but given no antidotal treatment. At the dosage levels used, oral NAC, IV NAC, and IV sodium sulfate were equally effective antidotes, as measured by decreased methemoglobinemia, increased whole blood reduced glutathione, decreased APAP half-lives, and increased urinary excretion of the APAP-sulfate conjugate. All the antidotal treatments produced results significantly different from those in the control cats.     

犬猫食物性有机氟化物中毒的诊治

近年来，犬猫有机氟化物中毒较多，原临床治疗多以对症急救法：即先注射“阿托品”，解除平滑肌痉挛，抑制腺体分泌；再注射“解氟灵”，配合“胃复安”或“艾茂尔”缓解呕吐。此治疗办法往往使病情恢复很慢。笔者近年来，在宠物门诊治疗工作中，通过对犬猫中毒原因的全面分析，和对各种相对药物治疗原理的探讨后，采用“解氟灵”配合“樟脑磺酸钠”治疗犬猫氟化物中毒症，均取得见效快，无后遗症的效果。     

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.     

Evaluation of toxicosis of liposome-encapsulated cis-bis-neodecanoato-trans-R,R-1,2-diaminocyclohexane platinum (II) in clinically normal cats

OBJECTIVE: To determine adverse effects of single and multiple doses of liposome-encapsulated cis-bis-neodecanoato-trans-R,R-1,2-diaminocyclohexane platinum (II) (L-NDDP) administered IV to healthy adult cats. ANIMALS: 10 healthy adult cats. PROCEDURE: 8 cats were given a single dose of L-NDDP (at rates of 75, 100, 150, or 200 mg/m2), and 2 cats were given liposomal lipid (1,500 mg/m2). Six of the 10 cats were given doses of L-NDDP at the maximum tolerated dosage (100 mg/m2) or a lower dosage (75 mg of L-NDDP/m2) at 21-day intervals, for a total of 4 treatments. Hematologic and serum biochemical analyses, urinalyses, and physical examinations were used to monitor effects of L-NDDP. RESULTS: All cats had transient pyrexia, lethargy, vomiting (1 to 3 times/24 h), inappetence, and an acute species-specific infusion reaction that was prevented by administration of atropine-diphenhydramine. Dose-limiting toxicosis was evident as a 10-day course of lethargy, intermittent vomiting, and diarrhea. In cats given multiple doses, dose-related thrombocytopenia, cumulative myelosuppression, transient increased hepatic transaminase activity, and mild to moderate hepatic hydropic degeneration and proximal renal tubular lipidosis in excess of lipidosis expected for this species were detected. Bone marrow hypoplasia was detected in some cats that received higher doses (cumulative dosages of 300 or 400 mg of L-NDDP/m2). CONCLUSION: Cats can safely be given L-NDDP at potentially therapeutic dosages without inducing renal or pulmonary toxicoses. CLINICAL RELEVANCE: Because L-NDDP has better tumoricidal activity than cisplatin (in vivo and in vitro) and is not cross resistant, it may be similarly or more efficacious than cisplatin in humans and dogs.     

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.     

Neomycin toxicosis in calves

Calves (n = 4) were given neomycin (2.25 or 4.5 mg/kg) twice daily IM and were compared with 2 calves given penicillin IM. The 2 hallmarks of aminoglycoside toxicosis, nephrotoxicosis and ototoxicosis, were seen with both dosages of parenterally administered neomycin. Nephrotoxicosis was confirmed by abnormal findings in urinalysis (granular casts, proteinuria, low specific gravity), renal biopsy results (tubular degeneration and necrosis), and increased 24-hour amounts of urinary enzymes (alanine aminopeptidase and gamma-glutamyltranspeptidase). Azotemia, decreased creatinine clearance, polyuria, and polydipsia also were documented in calves given neomycin. Clinically, deafness was suspected in 2 calves and was documented by electrical auditory-evoked response tests. Abnormalities in partial thromboplastin times and renal residues of neomycin were seen in all 4 calves that were given neomycin, but not in calves that were given penicillin.