Submitted by Johnny Rodrigues (johnnyrodrigues@ufcg.edu.br) on 2018-09-04T22:56:45Z No. of bitstreams: 1 AMÉLIA LIZZIANE LEITE DUARTE - TESE PPGMV 2012..pdf: 637832 bytes, checksum: 8a08b402027d942419996459bd5d8dfd (MD5) / Made available in DSpace on 2018-09-04T22:56:45Z (GMT). No. of bitstreams: 1 AMÉLIA LIZZIANE LEITE DUARTE - TESE PPGMV 2012..pdf: 637832 bytes, checksum: 8a08b402027d942419996459bd5d8dfd (MD5) Previous issue date: 2012 / Capes / Esta tese inclui três artigos sobre plantas tóxicas que causam ou são suspeitas de causarem morte súbita associada ao exercício em animais domésticos, intoxicação que se caracteriza por evolução superaguda, sem alterações cardíacas morfológicas significativas. O primeiro capítulo é uma revisão bibliográfica, detalhando recentes mudanças que ocorreram na identificação das diferentes espécies tóxicas de Amorimia (anteriormente referidas como Mascagnia) encontradas no Brasil e diferenciando-as quanto à epidemiologia e toxicidade. São descritos, também, os sinais clínicos, achados de necropsia e histológicos, diagnóstico e medidas de prevenção e/ou controle das intoxicações por Amorimia spp. No segundo capítulo é descrita, em caprinos, a indução de resistência à intoxicação por Amorimia septentrionalis, mediante administração repetida de doses não-tóxicas desta planta, e a transmissão da resistência de caprinos resistentes para caprinos susceptíveis através da transfaunação de líquido ruminal. Neste estudo, observou-se que os caprinos que recebiam doses não tóxicas e os que receberam a transfaunação foram mais resistentes que os que nunca ingeriram a planta previamente ou apenas coabitavam com os resistentes. O terceiro capítulo é uma comunicação científica que avaliou, experimentalmente, a toxicidade de Callaeum psilophyllum (sinônimo Mascagnia psilophylla) em coelhos e caprinos, assim como a possibilidade da ocorrência de intoxicação espontânea por esta planta em ruminantes. Foi comprovado que, em coelhos, C. psilophyllum causa um quadro clínico semelhante aos das plantas que causam morte súbita; no entanto, em caprinos, causa sinais digestivos, principalmente diarreia. Não há evidências de que C. psilophyllum cause intoxicações espontâneas em ruminantes. / This thesis includes three papers on toxic plants that cause or are suspected of causing sudden death associated with exercise in domestic animals, poisoning characterized by a per acute course without significant morphological heart changes. The first chapter is a literature review, detailing recent changes that have occurred in the identification of different species of toxic Amorimia (formerly referred as Mascagnia) found in Brazil. We also report the epidemiology, toxicity, clinical signs, necropsy and histologic findings, diagnosis, and prevention and control of the poisoning by Amorimia spp. The second chapter reports the induction of resistance to poisoning by Amorimia septentrionalis by the repeated administration of non toxic doses, and also by transfaunation of ruminal contents from resistant to susceptible goats. In this study, we observed that animals receiving non-toxic doses and transfaunation of ruminal content were more resistant than goats that never ingested the plant. The third chapter is a short communication that evaluated experimentally the toxicity of Callaeum psilophyllum (synonym Mascagnia psilophylla) in rabbits and goats, as well as the possibility of the occurrence of poisoning by this plant in ruminants. It was demonstrated that, in rabbits, this plant causes similar clinical signs than those caused by plants causing sudden death; however, in goats, C. psilophyllum causes digestive signs, mainly diarrhea. There is no evidence that C. psilophyllum causes spontaneous poisoning in ruminants.

Sixteen outbreaks of Senna occidentalis (coffee senna) occurring in cattle from the state of Rio Grande do Sul, Brazil, were reviewed. The great majority (75%) of the outbreaks occurred in adult cattle at pasture during the autumn and winter months with 50% occurring in May, evidencing a striking seasonality. Mortality rates varied from 4.2% to 55.2% and cattle died 2 days up to 2 weeks after showing clinical signs that included dry feces (occasionally diarrhea), muscle weakness, reluctance to move, tachypnea, instability of the hind limbs with dragging of the toes, tremors in muscles of the thighs, neck, and head, ear dropping, sternal recumbency, lateral recumbency and death. Myoglobinuria characterized by a dark red or black discolored urine was a consistent finding in cattle affected at pasture but not in those poisoned by ration contaminated with coffee senna beans. Creatine phosphokinase serum activity was markedly elevated. Main gross changes observed in 23 necropsies involved skeletal muscles of the hind limbs. These changes consisted of varying degrees of paleness of muscle groups. Subepicardial and subendocardial hemorrhages were present in the hearts of all affected cattle. Histologically a segmental degenerative myopathy of striated muscles was present in every case and had a multifocal polyphasic or monophasic character. Myocardial (3/23), hepatic (3/13), renal (3/10), and splenic (1/6) microscopic lesions were observed occasionally. Myocardial lesions were mild and consisted of vacuolation of cardiomyocytes or focal fibrosis. Hepatic changes consisted of diffuse hepatocellular vacuolation, cytosegrosomes within hepatocytes, and individual hepatocellular necrosis. Kidneys have vacuolar degeneration of tubular epithelium associated with acidophilic casts (proteinosis) within tubular lumina. In the spleen there was marked necrosis of lymphocytes of the white pulp. No histological changes were found in the brains of 13 affected cattle. The data of this study suggest that coffee senna poisoning is an important cause of death in cattle in southern Brazil. The epidemiological, clinical and pathological features described in the study shoud be useful for diagnosing the condition in the field. / Dezesseis surtos de intoxicação por Senna occidentalis (fedegoso) em bovinos do Rio Grande do sul foram revisados. A grande maioria dos surtos (75%) ocorreu em bovinos adultos em pastoreio durante o outono e inverno com 50% dos surtos ocorrendo em maio, evidenciando uma notável sazonalidade. Os coeficientes de mortalidade variaram de 4,2% a 55,2% e os bovinos morriam dois dias a duas semanas após mostrarem sinais clínicos que incluíam fezes ressecadas (ocasionalmente diarreia), fraqueza muscular, relutância em mover-se, taquipneia, instabilidade dos membros pélvicos com arrastamento das pinças, tremores nos músculos das coxas, pescoço e cabeça; orelhas caídas, decúbito esternal, decúbito lateral e morte. Mioglobinúria, caracterizada por urina vermelho-escura ou preta foi regularmente encontrada em bovinos afetados em pastoreio, mas não naqueles que se intoxicaram ingerindo ração contaminada com as sementes da planta. A atividade sérica da creatina fosfocinase estava acentuadamente elevada. As principais alterações macroscópicas observadas em 23 necropsias envolviam os músculos esqueléticos dos membros pélvicos. Essas alterações consistiam de graus variáveis de palidez em grupos musculares. Hemorragias subepicárdicas e subendocárdicas ocorreram nos corações de todos os bovinos afetados. Histologicamente, miopatia degenerativa dos músculos estriados esteve presente em todos os casos e tinha um caráter multifocal monofásico ou polifásico. Lesões microscópicas no miocárdio (3/23), fígado (3/13), rim (3/10) e baço (1/6) foram ocasionalmente observadas. As lesões miocárdicas eram discretas e consistiam de vacuolização dos cardiomiócitos ou fibrose focal. As lesões hepatocelulares consistiam de vacuolização difusa, formação de citossegrossomos e necrose individual. Nos rins havia degeneração vacuolar do epitélio tubular associada a cilindros eosinofílicos (proteinose) na luz tubular. No baço havia marcada necrose de linfócitos da polpa branca. Nenhuma alteração foi encontrada ao exame histológico do encéfalo de 13 bovinos afetados. Os dados deste estudo sugerem que a intoxicação por fedegoso é uma importante causa de morte em bovinos do sul do Brasil. Os aspectos epidemiológicos, clínicos e patológicos descritos neste estudo deverão ser úteis no diagnóstico a campo desta intoxicação.

<p>Ricin je prirodni protein, toksin koji spada među najpristupačnije i najsmrtonosnije otrove. Nalazi se u biljci Ricinus (Ricinus communis), sa najvećim sadržajem u semenu (1-5 %). Ricin se smatra potencijalnim bioterorističkim oružjem i prema riziku za ljudsko zdravlje svrstan je u B kategoriju biolo&scaron;kog oružja. U novije vreme kori&scaron;ćen je za konstruisanje imunotoksina protiv tumorskih ćelija u terapiji maligniteta. Dokumentovana su mnoga trovanja ricinom, kako zadesna, tako i samoubilačka i ubilačka. U tu svrhu koristilo se intaktno seme ricinusa ili ekstrahovani ricin. Osim ricina, u semenu ricinusa je prisutan toksični alkaloid ricinin u količini 0.3-0.8 %. Ricinus je jedini poznati prirodni izvor ricinina, koji se ko-ekstrahuje sa ricinom iz semena biljke. Ricinin se jednostavno detektuje u kliničkim uzoracima metodom tečne hromatografije i masene spektrometrije i, s obzirom na komplikovanu identifikaciju ricina u biolo&scaron;kim uzorcima, smatra se biomarkerom za intoksikaciju ricinusom, odnosno ricinom. Osnovni ciljevi ovog istraživanja su da se uz pomoć HS-GC metode i patohistolo&scaron;kom&nbsp; analizom dokaže prisustvo ricinina u krvi laboratorijskih pacova u odnosu na vremenski interval koji je protekao od oralne aplikacije suspenzije do vremena žtvovanja, da se odredi distribucija i koncentracija ricinina u organima laboratorijskih pacova u različitim vremenima žrtvovanja, kao i da se utvrdi da li postoji značajna razlika u razvoju patomorfolo&scaron;kih promena na organima laboratorijskih pacova u različitim vremenima žrtvovanja. Istraživanje je bilo otvoreno, randomizirano i prospektivnog tipa. Laboratorijski pacovi su u istom vremenu oralno tretirani suspenzijom koja je sadržaja subletalnu koncentraciju ricina. Nakon žrtvovanja u precizno definisanim vremenskim intervalima uzeti su uzorci krvi i unutra&scaron;njih organa radi daljih analiza. Odgovarajući uzorci su analizirani metodom HC-GS u cilju određivanja koncentracije i distribucije ricinina, kao pouzdanog markera trovanja ricinom, u krvi i unutra&scaron;njim organima. Takođe je izvr&scaron;ena patohistolo&scaron;ka analiza uzoraka tkiva unutra&scaron;njih organa u cilju utvrđivanja promena izazvanim delovanjem ricina u odnosu na vreme proteklo od aplikacije suspenzije. Dobijeni rezultati su obrađeni odgovarajućim statističkim metodama. Rezultati istraživanja omogućavaju standardizaciju postupaka odabira reprezentativnih uzoraka prilikom sumnje na trovanje ricinusom i metode dokazivanja akutnog trovanja. Na taj način može se pouzdano i efikasno dokazati trovanje ricinusom.</p> / <p>Ricin is a naturally occurring protein, a toxin which belongs to the category of the most accessible and the most lethal poisons. It is obtained from the castor oil plant ( Ricinus communis), whose seeds contain its highest content (1-5%). Ricin is also thought to be a potential weapon of bioterrorism and taking into account the risk for human health, it is classified as a biological weapon category B. Lately it has been used for the construction of the immunotoxins against tumor cells in the therapy of malignant diseases. Numerous poisonings using ricin have been documented, not only accidental poisoning, but also in case of suicides and homicides. In those cases, intact ricin seeds or extracted ricin were used. Apart from ricin, castor oil plants also contain a toxic alkaloid ricinine (0.3-0.8%). Castor oil plants are the only known natural source of ricinine, which is co-extracted with ricin from the seeds of this plant. Ricinine is simply detected in clinical samples by using the method of liquid chromatography and mass spectrometry. Taking into account a complicated identification of ricin in biological samples, it is considered to be a biomarker for the intoxication by castor oil plant, or ricin itself. The main aim of this research is to use the HS-GC method and pathohistological analysis in proving the existence of ricinine in the blood of experimental rats in relation to the time interval between the oral application of solution of castor seeds in water and the time of sacrificing, to determine the distribution and concentration of ricinine in the organs of experimental rats, as well as to establish whether there was a significant difference in the development of pathomorphological changes on the organs of experimental rats at various points of sacrificing. The research was open, randomised and prospective. Experimental rats were simultaneously orally tested by the solution which contained sublethal concentration of ricin. After sacrificing, blood samples were taken from inner organs in specifically defined intervals of time and used for further analysis. The appropriate samples were analysed by HC-GS method in order to determine the concentration and distribution of ricinine as a reliable marker of ricin poisoning in blood and inner organs. Also, pathohistological analysis of the samples of inner organ tissues was made with the purpose of establishing the changes caused by the effects of ricinine in relation to time which passed from the application of the solution. The obtained results were processed by appropriate statistical methods. The results of this research allow for the standardisation of the actions in selecting the representative samples in case there is a possibility of ricin poisoning and the method of proving the acute poisoning. Following these steps, ricin poisoning can be proved in a reliable and an efficient way.</p>