Liver of a healthy chinchilla (left) compared with the enlarged and lighter colored liver of a chinchilla that died of acute aflatoxicosis (right). Bar 5 2 cm.  

Liver of a healthy chinchilla (left) compared with the enlarged and lighter colored liver of a chinchilla that died of acute aflatoxicosis (right). Bar 5 2 cm.  

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Chinchillas (Chinehilla lanigera) are known to be very sensitive to aflatoxins, and often a large number of animals die if toxicosis occurs. An outbreak of acute aflatoxicosis on a chinchilla farm in Argentina is described in the present study. A commercial feed suspected of causing the death of 200 animals was sampled. Livers from 9 dead chinchill...

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... In one report, the death of 200 chinchillas was attributed to high concentrations of aflatoxin B-1 in the feed. 30 The liver is the primary target organ of aflatoxin; in affected animals, it is enlarged, pale yellow, and friable. In the described cases, histopathologic analyses of hepatic parenchyma showed severe, diffuse cytoplasmic vacuolation of hepatocytes. ...
Chapter
Chinchillas are becoming increasingly popular as companion animals due to their long life span, hardiness, and simple husbandry requirements. Dental disease, including coronal elongation, gingival hyperplasia, periodontal disease, and tooth resorption, is the most common reason chinchillas get evaluated by veterinarians. Other common disorders include parasitic enteritis and diarrhea, conjunctivitis, otitis media, and penile disorders.
... The following references appear in the Supplemental Information: Bovet, 1984;Bovet and Oertli, 1974;Busch et al., 2000;Clarke, 1983;Gattermann et al., 2008;Gonzá lez Pereyra et al., 2008;Grizzell, 1955;Hayes, 1976;Hicks, 1949;Jimé nez, 1996;Latham and Mason, 2004;Link et al., 2012;Lord, 1991;Macdonald, 1981;Meagher et al., 2000;Morris and Kendeigh, 1981;Rado et al., 1993;Randall and Thiessen, 1980;Riccio and Goldman, 2000;Rood, 1972;Snyder, 1982;Steele, 1998;Taylor, 1978;Thompson, 1977;Woods;1973. Hasty, P., Campisi, J., Hoeijmakers, J., van Steeg, H., andVijg, J. (2003 Anti-H3K18ac Abcam Cat#ab1191 ...
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DNA repair has been hypothesized to be a longevity determinant, but the evidence for it is based largely on accelerated aging phenotypes of DNA repair mutants. Here, using a panel of 18 rodent species with diverse lifespans, we show that more robust DNA double-strand break (DSB) repair, but not nucleotide excision repair (NER), coevolves with longevity. Evolution of NER, unlike DSB, is shaped primarily by sunlight exposure. We further show that the capacity of the SIRT6 protein to promote DSB repair accounts for a major part of the variation in DSB repair efficacy between short- and long-lived species. We dissected the molecular differences between a weak (mouse) and a strong (beaver) SIRT6 protein and identified five amino acid residues that are fully responsible for their differential activities. Our findings demonstrate that DSB repair and SIRT6 have been optimized during the evolution of longevity, which provides new targets for anti-aging interventions.
... AFs are also reported to be associated with reduced growth in children and disorders of the immune system [10]. Several hundred deaths of calves, chinchilla and buffaloes in Australia, Argentina and Pakistan respectively, provide examples of acute aflatoxicosis as a potential threat to animals [11][12][13]. Chronic exposure may lead to impaired production and reproduction and increased mortality rates in animals. Lactating animals and humans consuming AFs secrete AFM1 in their milk. ...
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The present study was conducted to observe the seasonal variation in aflatoxin M1 and nutritional quality of milk along informal marketing chains. Milk samples (485) were collected from three different chains over a period of one year. The average concentrations of aflatoxin M1 during the autumn and monsoon seasons (2.60 and 2.59 ppb) were found to be significantly higher (standard error of the difference, SED = 0.21: p = 0.003) than in the summer (1.93 ppb). The percentage of added water in milk was significantly lower (SED = 1.54: p < 0.001) in summer (18.59%) than in the monsoon season (26.39%). There was a significantly different (SED = 2.38: p < 0.001) mean percentage of water added by farmers (6.23%), small collectors (14.97%), large collectors (27.96%) and retailers (34.52%). This was reflected in changes in milk quality along the marketing chain. There was no difference (p = 0.178) in concentration of aflatoxin M1 in milk collected from the farmers (2.12 ppb), small collectors (2.23 ppb), large collectors (2.36 ppb) and retailers (2.58 ppb). The high levels of contamination found in this study, which exceed the standards set by European Union (0.05 ppb) and USFDA (0.5 ppb), demand radical intervention by regulatory authorities and mass awareness of the consequences for consumer health and safety.
... The unusual intoxications by narasin and dieldrin can be considered as sporadic incidents, but mycotoxicosis is a common problem among Argentinian farms (González Pereyra et al. 2008;Greco et al. 2012). These reports demonstrated that fungi and mycotoxins were usually present in chinchilla feed, with fungal contamination exceeding the limits (up to 4.5 × 10 4 CFU g −1 ) and the co-occurrence of the five most important mycotoxigenic mould genera recovered at high concentrations. ...
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Fur ranching has been a prosperous industry for decades. Despite its worldwide distribution, little published information is available regarding the importance of the various causes of death in chinchilla (Chinchilla lanigera). In the period 1999–2013, 698 captive chinchillas from different commercial ranches were presented for necropsy at the Pathology Department (UNLP). Two-hundred and forty-four animals (35.0%) had classical enteritis, 198 (28.4%) had pneumonia, 63 (9.0%) had other infections, 40 (5.7%) had traumatic injuries, 109 (15.6%) had miscellaneous conditions, meanwhile 44 (6.3%) had no significant lesions. Although some disease processes may be underrepresented (i.e. heat stroke and the shock syndrome), the data were collected from a field wide enough and over a sufficient period to give a reliable overview of the fatal problems of this rodent in captivity.
... Hepatic lipidosis because of excessive fat mobilization and, less frequently, toxicosis is one of the most common findings in chinchillas at necropsy. 32,112 Chinchillas with hepatic lipidosis often have a history of anorexia and decreased fecal output and, in advanced cases, can be depressed and dehydrated. Hyperglycemia, pronounced ketonuria, and possible glucosuria and acidosis can develop. ...
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Chinchilla pelt is a rare and expensive fur. Therefore, breeding these animals is a profitable activity. Confirmed acute cases of aflatoxin intoxication have been reported in Argentinean farms. The aims of this study were i) to evaluate mycobiota and AFB-1producing species in chinchilla feeds ii) to investigate their natural AFB1 contamination and iii) to analyze histopathological lesions in chinchilla livers. Feed samples (A: fur, B: mother, C: lucerne cubes) were collected from a factory and a farm. Livers of sacrificed chinchilla from the farm were macroscopically and microscopically examined. Total fungal counts of feed C exceeded 1x104 CFU/g. Aspergillus, Fusarium and Penicillium were the prevalent genera, while A. flavus, A. fumigatus, F. verticillioides and F. proliferatum were the prevalent species. Fifty % of A. flavus strains from factory samples and 69.7% from farm samples were able to produce 2.78 to 8.64μg/g and 0.66 to 58.8μg/g AFB1, respectively. Aflatoxin B1 was detected only in feeds from the farm, finding the highest incidence in feed C. Toxin levels varied between 1.90 and 97.34 μg/kg AFB1. Mean levels in feed A and C exceeded 20 μg/kg. Macroscopic examination of livers revealed normal appearance, size and color. However, histopathological examination indicated 63.3% showed slight to moderate lipid degeneration with diffuse cytoplasm vacuolation, 9% intense lipid cytoplasm vacuolation and 27.3% hydropic degeneration and nuclear vacuolation in hepatocytes. A periodic monitoring of aflatoxins in feeds and their ingredients can prevent acute outbreaks and economic losses caused by chronic exposure.
... Detection of lipid structures in tissues from plant, animal, and human beings Aliscioni et al. (2009); Murabayashi et al. (1999); Kim et al. (2005); Tsuchiya et al. (2007), Gonzalez Pereyra et al. (2008); Kitoh et al. (2008); Neri et al. (2010); Obikane et al. (2010) Sudan II and IV Interactions of the dyes with lecithin liposomes and live E. coli 90 and 95% of the dyes that penetrated the cells remained within the plasmatic membrane. ...
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... Em 16 casos esta era a lesão predominante ou única lesão observada. Anteriormente, lipidose hepática havia sido descrita como altamente sugestiva de aalatoxicose aguda, observado em uma mortandade de chinchilas na Argentina após ingestão de ração contendo 208ppm de aalatoxinas (González 2008). Porém, em estudo experimental as chinchilas demonstraram ser resistentes a aalatoxinas na dose de 200 ppm por até oito semanas de ingestão ( Cepeda et al. 2011). ...
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... Aflatoxin is a liver toxin in several animal species (International Agency for Research on Cancer 2002). It causes liver enlargement in broiler chickens (Kumar and Balachandran 2009;Mani et al. 2000) and in animals suffering aflatoxicosis (Gonzalez Pereyra et al. 2008;Osman et al. 2004). To our knowledge there are no previous reports of chronic HM occurrence in chronically exposed humans. ...
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... Na nossa experiência, vacuolização hepática é também observada em associação a várias doenças de chinchilas e mesmo em chinchilas mantidas em restrição alimentar antes do abate (dados não publicados). Em razão disso lipidose hepática, mesmo acentuada, não deve ser considerada característica de aflatoxicose como foi anteriormente sugerido (Pereyra et al. 2008) nem de qualquer intoxicação específica. ...
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Quatro surtos de intoxicação por salinomicina são descrito em chinchilas de três municípios do Estado do Rio Grande do Sul. Uma semana após a ingestão de ração contendo 37 ppm de salinomicina, aproximadamente duas mil chinchilas de quatro fazendas expostas diminuíram o consumo da ração. Quatrocentos e vinte sete chinchilas demonstraram apatia. Dessas, duzentos e setenta e sete desenvolveram decúbito esternal e lateral, dispneia e coma, seguidos de morte. As primeiras mortes ocorreram oito dias após a ingestão da ração. A evolução dos sinais clínicos até a morte ou eutanásia foi de 2-5 dias. Os exames bioquímicos do soro sanguíneo em quatro chinchilas revelaram níveis aumentados da alanina aminotransferase, aspartato transaminase, fosfatase alcalina, creatina cinase, glicose, triglicerídeos e colesterol total. Quarenta e cinco chinchilas foram submetidas à necropsia. Os achados macroscópicos consistiam de marcada lipidose hepática em todas as chinchilas necropsiadas; fetos em estado de decomposição em doze chinchilas que estavam prenhes. Microscopicamente, múltiplas fibras musculares esqueléticas estavam hipereosinofílicas, tumefeitas e com perda das estriações. Nas chinchilas que sobreviveram por mais dias era possível observar segmentos fragmentados de miofibras afetadas (necrose flocular) e regeneração de miofibras. No fígado foi observada marcada degeneração gordurosa. Não foram observadas anormalidades microscópicas nos demais órgãos analisados. Análises à procura de aflatoxinas, resíduos de pesticidas e isolamento bacteriano foram negativos. A análise da ração por cromatografia líquida revelou 37ppm de salinomicina na ração. A ração suspeita foi administrada a 12 chinchilas, três das quais (25%) morreram apresentando lesões semelhantes às observadas nas chinchilas com a doença natural. O diagnóstico de intoxicação por salinomicina foi baseado na epidemiologia, lesões histológicas características e na presença de salinomicina na ração administrada nas quatro criações envolvidas.