Hematological and biochemical profiles and histopathological evaluation of experimental intoxication by sodium fluoroacetate in cats

Sodium fluoroacetate (SFAC) is a potent rodenticide, largely used for rodent and domestic pest control. The toxic effects of SFAC are caused by fluoroacetate, a toxic metabolite, whose toxic action blocks the Krebs cycle and also induces the accumulation of citrate in the body, which is a serum calcium chelator. The most common clinical signs of this intoxication are the cardiac and neurological effects. However, the hematological, biochemical and histopathological findings occurring in intoxication are still unknown in different species. In the present study, 16 domestic cats were experimentally intoxicated with oral doses of fluoroacetate (0.45 mg/kg). The hematological and biochemical profiles and histopathological findings were made to look for auxiliary diagnosis methods in SFAC intoxications. The hematological profile showed transitory leucopenia and thrombocytopenia; in the biochemical profiles were detected hyperglycemia, increase of creatinequinase enzyme (CK) and creatinequinase cardiac isoenzyme (CK-MB), hypokalemia and hypophosfatemia. In the macroscopic and histopathological findings were observed lesions characteristic of degenerative and ischemic processes in heart, kidneys, liver, brain and lungs. These changes may be auxiliary to the diagnosis of intoxication by SFAC in cats, when associated with clinical signs described for the species. Thus, the complete blood count with platelet count, serum glucose, enzymes CK and CK-MB isoenzyme, as well as the electrolytes potassium and phosphorus, can facilitate the laboratory diagnosis during intoxication by SFAC, associated with the pathological findings in the case of death of the intoxicated animal.Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES

Calcium gluconate and sodium succinate for therapy of sodium fluoroacetate experimental intoxication in cats: clinical and electrocardiographic evaluation

Sodium fluoroacetate (SFAC) or Compound 1080 is a potent rodenticide, largely used after 1946 for rodent and home pest control. The toxic effects of SFAC are caused by fluorocitrate action, a toxic metabolite, which has a competitive action with aconitase enzyme, leading to citrate accumulation and resulting in interference in energy production by Krebs cycle blockade. In the present study, domestic cats were intoxicated with oral doses of fluoroacetate (0.45 mg/kg). The intoxicated animals presented emesis, diarrhea with abdominal pain posture and an abdominal palpation, tachypnea, bilateral midriasis, hypothermia, hyperexcitability and convulsions. Blood gas analysis indicated decreased pH and bicarbonate levels. Serum ionized calcium was also decreased. ECG showed non-specific changes in ventricular repolarization and ventricular arrhythmias. The survival rate was 75% in the treated group with calcium gluconate and sodium succinate and 37.5% in the non-treated group

Serologic response of SPF chickens to live vaccines and other strains of Mycoplasma gallisepticum

False positive serologic reactions and difficulties in the diagnosis of Mycoplasma gallisepticum (MG) in chickens have increased lately as a result of infection by low virulent MG strains and the use of live MG vaccines in poultry. The objective of this study was to evaluate the serologic responses of SPF chickens exposed to the three commercially available live MG vaccines, and one low virulent MG strain (MG-70), contributing to the diagnosis and monitoring of MG infection in birds. Six groups of SPF chickens were used. The control group was not infected nor challenged; one group was infected with the low virulent strain MG-70 (MG-70); three groups were immunized and named after the MG vaccine used, i.e., MG-6/85, MG-ts11, and MG-F; and finally one group was infected with the virulent MG standard strain, MGR. Random Amplification of Polymorphic DNA (RAPDPCR) was used to compare the strains to each other, to the standard MG-A5969, and to MGR. All strains were found to be genetically distinguishable from each other. Birds in the control group showed negative results throughout the experiment and showed no cross-reaction with M. synoviae in any serologic test. ELISA tests at 21 days post first exposure (P1E) and seven days after the second exposure (P2E), evidenced that 25% of the MG70 birds were positive, whereas vaccine groups yielded higher positivity rate, i.e., 57%, 43% and 29% for MG-6/85, MG-ts11 and MG-F, respectively. Serum plate agglutination (SPA) evidenced the first positive results at 35 days P1E on birds in the MG-F group at the rate of 100%; followed by 40% of birds in the MG-70 group at 63 days P1E. Chickens in MG-ts11 and MG 6/85 groups had identical behavior and yielded 100% positive SPA at 77 days P1E. In regard to hemagglutination inhibition (HI), 14 % of the birds in MG-F and MG-ts11 reacted at 42 days P1E, while MG-70 and MG-6/85 groups yielded positive results only after challenge; MG-70 birds reacted at 56 days P1E at the rate of 17% against 63 days P1E for 100% of MG-6/85 birds. The time lag for positive serologic response was monitored on a weekly basis and was statistically different among groups (p<0.05) by Analysis of Variance (ANOVA). No clinical signs or gross lesions were seen in the control, vaccinated or MG-70 infected birds. Tracheitis and airsaculitis were observed in birds in the MG-R group. MG was isolated from all studied groups

Efeito protetor da acetamida em bovinos indica monofluoroacetato como princípio tóxico de Palicourea marcgravii (Rubiaceae)

O presente trabalho teve como objetivo avaliar e comparar o efeito protetor da acetamida nas intoxicações experimentais por monofluoroacetato (MF) e por folhas frescas de Palicourea marcgravii em bovinos, no intuito de confirmar, de forma prática, que esse composto é o princípio tóxico responsável pelo quadro clínico-patológico e pela morte dos animais intoxicados por essa planta. Três bovinos receberam MF, por via oral, na dose de 0,5mg/kg e, em seguida, a dois desses animais administraram-se acetamida, por via oral, nas doses de 0,38 e 2,0g/kg. Outros dois bovinos receberam 1,0g/kg de P. marcgravii, em seguida, a um deles administrou-se 1,0 g/kg de acetamida. Acetamida, quando administrada em quantidades suficientes (maior dose), evitou o aparecimento dos sinais clínicos e a morte de todos os animais que receberam MF ou P. marcgravii. Tal efeito protetor foi, de fato, confirmado após uma semana, quando o mesmo protocolo experimental foi repetido, para cada bovino, porém sem a administração de acetamida. Todos os bovinos não tratados com acetamida manifestaram sinais clínicos e morreram subitamente. O quadro clínico-patológico manifestado pelos bovinos intoxicados por MF ou P. marcgravii foi semelhante e, caracterizou-se por "morte súbita". Os animais em geral, apresentaram taquicardia, taquipnéia, tremores musculares, jugular repleta com pulso venoso positivo, polaquiúria, instabilidade, perda de equilíbrio, por vezes, cambaleavam e apoiavam a cabeça no flanco. Na fase final, todos os animais deitavam-se e levantavam-se com maior frequencia, deitavam ou caíam em decúbito lateral, esticavam os membros, faziam movimentos de pedalagem, apresentavam respiração ofegante, arritmia, opistótono, nistagmo, mugiam e morriam. A duração da "fase dramática" variou de 2 a 26min. À necropsia verificaram-se, em geral, aurículas, jugulares, ázigos e pulmonares leve a moderadamente ingurgitadas, leve a acentuado edema da subserosa da vesícula biliar, sobretudo, na sua inserção no fígado, bem como moderada quantidade de líquido espumoso róseo na traquéia e brônquios. O exame histopatológico revelou, no rim de todos os animais, leve até acentuada degeneração hidrópico-vacuolar das células epiteliais dos túbulos uriníferos contornados distais associada à picnose nuclear; no fígado, havia leve a moderada congestão, discreta a moderada tumefação e moderada vacuolização de hepatócitos, predominantemente, centrolobular, necrose de coagulação individual ou de grupos de hepatócitos e corpúsculos de choque. Os dados obtidos neste trabalho comprovam, de forma prática, que MF é o princípio tóxico de P. marcgravii responsável pelo quadro clínico-patológico e a morte dos animais que ingerem e se intoxicam naturalmente por essa planta, uma vez que a acetamida atua como antídoto eficaz (efeito antagônico) de forma idêntica em ambas as intoxicações