Effects in Food-Producing Animals CHAPTER 5 CHAPTER Summary Ergot Alkaloids

chapter 5. Effects in food-producing animals CHAPTER 5 CHAPTER Summary ergot alkaloids. In all cases the effect possible involvement of a mycotoxin of mycotoxins on animal performance in an animal production problem. Unexplained disease outbreaks in is potentially a major problem for In conjunction with the information farm and domestic animals have farmers regardless of their scale provided in the other chapters, this suggested the likely presence of of operation. Reduced growth, information will assist farmers in mycotoxins in feeds for many years. decreased egg and milk production, making decisions that will minimize The manifestations of mycotoxicoses lower reproductive efficiency, and losses due to diseases induced by in the field are frequently nondescript increased susceptibility to stress are all mycotoxins. and potentially have many contrib- potentially devastating consequences uting factors, which are often of mycotoxin exposure. Thus, being 1. Introduction difficult to define. Nevertheless, aware of the outward signs that might toxigenic moulds were implicated signal the involvement of a mycotoxin In this chapter, we discuss the in, and sometimes proven to be the in an animal performance problem is effects in farm and domestic animals cause of, animal disease in field the first step to minimizing potential of the most economically important outbreaks long before the toxins adverse impacts. The target organ feedborne mycotoxins. The chapter were discovered. The development affected can provide important clues begins with a summary of field of methods for the chemical analysis to involvement of a specific mycotoxin, outbreaks, followed by sections of mycotoxins in feeds and animal in which case understanding the that describe the toxicokinetics tissues has contributed to an toxicokinetics and toxicology will assist and metabolism of each mycotoxin improved understanding of the dose– in minimizing the cost and maximizing or group of mycotoxins. Of the response relationships of farm animal the effectiveness of interventions. trichothecenes, only deoxynivalenol diseases associated with exposure The primary objective of this chapter is covered in depth; however, it should to aflatoxins, fumonisins, ochratoxin is to provide information that will be recognized that the predominant A, deoxynivalenol, zearalenone, and aid in the field identification of the trichothecene encountered in con- Chapter 5. Effects in food-producing animals 59 taminated feeds may differ in different to cause animal disease. A major the case for aflatoxins, fumonisins, geographical locations (Starkey et al., problem for the veterinarian in the field deoxynivalenol, zearalenone, and 2007; Miller, 2008; Sugita-Konishi and is that disease expression is seldom ergot alkaloids, where mould- Nakajima, 2010). pathognomonic, i.e. with a sign or contaminated feed was associated Additional information relevant symptom that is so characteristic of a with disease outbreaks before the to the toxicology in animals can be disease as to be diagnostic. Instead, toxins were identified. For example, found in Chapter 6, which focuses multiple interacting factors often in the 1960s the outbreak of a on effects and toxicology in humans. occur that can modify the expression disease known as turkey “X” disease Potential interventions to prevent field of toxicity. Thus, the manifestations led to the discovery of aflatoxins. outbreaks or minimize their adverse of mycotoxicoses in the field are However, before this disease was effects are described in Chapter 9. frequently nondescript and have reported, outbreaks of liver cancer Numerous extensive review articles many potential contributing factors, in farm-raised rainbow trout fed diets and monographs provide additional which are often difficult to define. containing cottonseed (Butler, 1974) information on effects in farm An attempt to apply Koch’s and of liver toxicity in pigs and cattle fed animals (WHO, 2001, 2011; CAST, postulates to demonstrate causality maize contaminated with Aspergillus 2003; Cousin et al., 2005; Roberts requires a bioassay that reproduces flavus were documented in 1935 and et al., 2005; Fink-Gremmels and the disease when a pure compound 1953, respectively (Raisbeck et al., Malekinejad, 2007; Morgavi and is used. Unfortunately, reproducing 1991). Equine leukoencephalomalacia Riley, 2007a, 2007b; Voss et al., the exact conditions that existed (ELEM) was first linked to mouldy 2007; Fribourg et al., 2009; Pestka, in the field is confounded by the maize in 1891 (Haliburton and Buck, 2010a, 2010b; Eaton et al., 2010). potential presence of multiple 1986). ELEM is now known to be To aid in the field identification of the contributing factors. These include, caused by fumonisins. Effects from main observations characterizing but are not limited to, environmental the consumption of maize on which exposure to a particular mycotoxin, stress, multiple toxigenic fungi Fusarium verticillioides had been Table 5.1 summarizes the expected and mycotoxins, nutrient/vitamin cultured were the first indication that toxic effects, species sensitivity, and deficiencies, infectious agents, and mouldy maize might cause porcine potentially useful biomarkers in farm pre-existing conditions. These co- pulmonary oedema (PPE) syndrome animals for each of the major groups occurring factors can influence (Kriek et al., 1981). This was of mycotoxins. the clinical signs, severity, and confirmed only after the discovery progression of the disease (CAST, of fumonisins in 1988 and after the 2. Field outbreaks 2003) in ways that can confound cause of outbreaks of PPE in the both diagnosis and replication of USA in 1989–1990 was confirmed The interest of the scientific and the observed adverse effects. Also, by inducing PPE with pure fumonisin regulatory communities in mycotoxins mycotoxins in feeds are not evenly B1 (Marasas, 2001). began in earnest when aflatoxins were distributed (see Chapter 3); therefore, Feed refusal syndrome in the USA, found to be potent carcinogens that reproducing disease at the dosages most likely caused by deoxynivalenol occurred in several important food found in feed samples analysed from and other trichothecenes, led to an and feed commodities. However, even field outbreaks can be difficult. It has embargo of United States barley by in the absence of any known causal been suggested that 100–200 kg Germany in the 1930s (Hamilton, agent, unexplained disease outbreaks or more of suspect feed should be 1982). The association between in farm and domestic animals, which saved for confirmatory studies in consumption of mouldy feed and often involved mortality or evidence of experimental animals (Osweiler, estrogenism in pigs has been known acute toxicity, served as an indicator 2000). In addition, experimental since 1928 (McNutt et al., 1928), and of the likely presence of mycotoxins in confirmation can require a large estrogenism has been attributed to foodstuffs (Forgacs and Carll, 1962). number of animals if the incidence consumption of feeds contaminated Definitively linking a disease of the disease in the suspected field with zearalenone. The biological outbreak in the field to a specific outbreak is low. activity of ergot (the sclerotia of mycotoxin is very difficult (Hamilton, Despite these difficulties, toxi- Claviceps spp.) was known in China 1982), even though a great deal genic moulds were implicated as more than 5000 years ago even of experimental evidence exists the cause of animal disease in though its involvement in animal to characterize the potential of field outbreaks long before the disease was probably not reported mycotoxins and mouldy foodstuffs toxins were discovered. This was until the Middle Ages (Christensen, 60 Table 5.1. Expected toxic effects, species sensitivity, and potentially useful biomarkers in farm animals for each of the major groups of mycotoxins Relative sensitivity of Mycotoxin Target organs and major effects Biomarkers species Aflatoxins Reduced performance, jaundice, pale liver, hepatotoxicity with Ducklings > turkeys Aflatoxin–albumin adducts fatty changes, coagulopathy, and increased susceptibility to > chicks > quail. in serum and DNA adducts internal bruising during handling. Rabbits > swine > cattle > in urine. Liver tumours in trout. sheep. Aflatoxin M1 in milk and Dogs and mink can also be urine. affected. Young animals > mature animals. Fumonisins Liver in all species and kidney in many. Brain in horses (ELEM) Horses and rabbits > pigs Fumonisin B1 in urine and and lung in pigs (PPE). and catfish > ruminants and faeces. poultry. Elevated sphinganine and Breeding animals sphinganine-1-phosphate > animals being raised for in tissues, urine, and serum slaughter. and elevated sphinganine- 1-phosphate in red blood cells. Ochratoxin A Pale and grossly enlarged kidney. Fatty liver in poultry. Pigs and dogs > poultry Ochratoxin A or its Altered performance, including decreased feed consumption, > calves. metabolites in tissues, reduced weight gain, and decreased egg production. Increased Chicks > turkeys > quail. blood, and urine. susceptibility to bruising, decreased tensile strength of the large Mature cattle are intestines, reduced pigmentation, decreased immune response, considered resistant. increased susceptibility to infection, and glycogen accumulation in the liver. Deoxynivalenol Feed refusal in swine and reduced weight gain and vomiting. Pigs > dogs and cats Deoxynivalenol and its Gastrointestinal problems, soft stools, diarrhoea, increased > cattle, sheep,

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