Hi All,
Welcome to topic 6 for 624EHS - Contemporary Issues in Equine Science.
This topic is all about sycamore poisoning. Make sure you watch the launch video (recording of the hangout) which has been posted in the Classroom. You all have from now until 2pm on Wednesday 22nd April to contribute to this blog, to debate the issues surrounding sycamore poisoning. Ensure you can also evidence your opinions and remember that you are also required to submit a reference list (word document emailed to module leader) by 2pm on Wednesday 22nd April. You will be graded on the quality and quantity of both your blog contributions and your reference list. Remember, the point of this is to debate the issues, so you should be replying to each others posts. I will be keeping an eye on the blog, but if you have any issues, you should email me.
Rosa
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ReplyDeleteHorses are at risk of poisoning from plants in their surrounding environments. Poisoning may also be seasonal depending on the plant involved (Bates, 2017). During the autumn months, atypical myopathy from repeated ingestion of sycamore seeds is the most significant hazard (Bates, 2019).
ReplyDeleteTo add to this, Atypical Myopathy (Sycamore Poisoning) is a disease that has been seen more commonly within the past decade as a greater number of cases have been diagnosed. The cause of the increase of cases could be due to the result of greater awareness among both vets and horse owners (Rendle, 2016). The disease has only been identified in association with exposure to seeds of either the common sycamore in Europe or the box elder in the US. In the US, presence of hypoglycin A was confirmed in seeds from box elder trees collected at outbreaks of atypical myopathy (Valberg et al, 2013). In Europe, the presence of high concentrations of methylene cyclopropyl acetic acid-carnitine in serum from horses with atypical myopathy, but not controls, again indicated hypoglycin A toxicity (Rendle, 2016).
DeleteResearchers have been able to identify that Atypical Myopathy (AM) is caused by ingestion of the toxin hypoglycin A (HGA) found in not only the seeds but the leaves and seedlings of the sycamore tree. As stated above, this disease most commonly occurs during the autumn months and can occasionally occur during the spring. Typically this disease follows periods of wet and windy weather (Naylor, 2017).
DeleteDiagnosis requires an analysis of plasma acylcarnitines or urinary samples, to confirm any metabolic disturbances (Naylor, 2017). With this information it becomes easier to identify the disease quicker. Previous studies revealed increased prevalence of Atypical Myopathy in mares, potentially due to the more frequent exposure to pastures compared to male horses (Votion et al,. 2007). The prevalence in young horses was speculated due to fact, younger horses spend more time on pastures until horse owners start to break them in (Votion et al,. 2007). It was also speculated that horses being provided with sufficient forage would be less likely to ingest the sycamore seeds, nevertheless, horses that obtained additional foodstuffs such as hay and hard feed and horses that had less access to the pastures, still ingested enough HGA to be poisoned (Bochnia et al,. 2015).
Because of the increase in cases, a number of pasture management strategies such as Mowing and herbicidal spraying have been proposed to avoid hypoglycin A (HGA) intoxication in horses, but their efficacy has never been fully investigated. The removal of toxic material from affected pastures is the optimal preventative measure when trying to minimise risk of intoxication however, this is not always practical, particularly in the spring (González‐Medina et al,. 2019). González‐Medina et al,. In 2019 found that neither mowing nor herbicidal spraying, reduced HGA concentration in sycamore seedlings. They also found that cross contamination was possible between grass and sycamore seedlings when mowed together (González‐Medina et al,. 2019).
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DeleteSupportive therapy is the only way to help a horse with atypical myopathy, as there is no specific treatment available. However, supportive therapy is still often unsuccessful, meaning that prevention of this condition is important (Harris, 2009). One kind of prevention I found was based around pasture and grazing of equids. In early autumn, it is recommended that owners/ yard workers identify any areas of contamination in pastures they use for grazing. The removal of seeds may help in prevention (Votion, 2016). However, this may not always be possible due to the seeds being able to travel up to three times the height of the tree and up to 100m in severe weather (Baise et al, 2015).
DeleteDuring high risk periods (Autumn and Spring), pasture time should be limited to less than six hours a day, especially in adverse weather conditions, due to any horse of any age must be considered at risk. When feeding forage, it is also important to ensure that there are no remnants of seeds and that it is toxin-free. Outbreaks at pasture can be decreased by avoiding contact with toxic plant material and by favouring low-risk pasture during spring and autumn when cases increase These preventative measures should be put in place for a period of three moths and done twice yearly; March-May for Spring cases and October-December for Autumn cases (Votion et al, 2020).
While it is agreeable that pasture time limits could have an impact on the prevalence of cases, practical implementation would be a cause for concern here, particularly with horses who live out on pasture 24/7. Additionally, the practice of limiting turn out during adverse weather is contradictory to the common practice of turning horses out during storms, a topic in which Falkingham (2019) discusses in depth.
DeleteHowever, the suggestion that forage be of good quality and free from toxins is a welcomed idea, and while it is a notion that should, in theory, be practiced regularly, it could be argued that owners/carers may find themselves restricted by economical or demographic factors. It should be noted here that further investigation into the factors contributing to the decisions made when purchasing feeds and forage is needed to support this statement.
To further extend on Niamh's explanation of sycamore disease, the term sycamore poisoning is derived from the common source of the illness, the Acer pseudoplatanus, the sycamore maple tree. The seedlings contain hypoglicn A. Ingestion of hypoglicn A often leads to equine atypical myopathy (EAM). Atypical myopathy occurs when there is a diminishing amount of Acyl-COA dehydrogenase (MADD) present in the body, thus a reduced output of mitochondrial aerobic metabolism. (Rendle, 2016). Energy supplies to type 1 muscle fibres are depleted. EAM is a toxic rhabdomyolysis, which results in muscular weakness, stiffness, myoglobinuria, and within 72 hours at least 75% of cases will end in death (González-Medina, 2017: Votion, 2016; Witkowska-Piłaszewicz et al, 2019).
DeleteWhile it is important to consider preventative techniques, it is also important to consider other areas of prevention. One area which could be explored and is available to horse owners is the idea of testing plants within a horse's environment. The Royal Veterinary College has developed tests that can be carried out within their comparative neuromuscular diseases laboratory, that tests for the toxin hypoglycin A, which is known to cause atypical myopathy (RVC, 2020). Tests require horse owners to submit samples of the plants which reside within the horse’s environment. Samples are easy to obtain and send off for testing, making it user friendly for all horse owners. However, some owners may be hesitant to carry out sampling, due to the high cost of £90 per sample. This price is then increased if testing more than one paddock; more than one area of the paddock; or more than one tree. This may put off a large number of horse owners willing to carry out testing. Another issue raised with this form of testing is the time it takes for the results to be received by the horse owner. Normal testing takes between two to three weeks for the results to become available. For suspected cases it simply takes too long, and treatment should be carried out if atypical myopathy is suspected. There is the option for owners to receive results quicker with a two to three day turn around, this comes at an increased price. This would be more beneficial for suspected cases which are undergoing treatment, to enable the owner to identify where the source of the toxin is and allow them to take action to prevent the ingestion of toxins for other horses.
DeleteThe ability to discriminate between affected and unaffected horses is vital when cases of atypical myopathy are present within large herds, allowing testing of all horses to identify which horses require immediate treatment and which ones do not. Hypoglycin A levels in blood and urine can be tested to allow for the identification of affected horses (Bochnia et al., 2015).
DeleteAtypical myopathy is a distressing condition with a high fatality rate. Outbreaks are common and horses displaying clinical signs should be hospitalised so they can receive 24 hour care and multimodal analgesia (Rendle, 2016).
ReplyDeleteThe increase in case reports and interests, has been associated with increased understanding of the disease. It is now appreciated European atypical myopathy and US seasonal pasture myopathy are the same condition (Rendle, 2016).
A case report from Germany last year provided further evidence that ingestion of sycamore seeds containing hypoglycin A was the cause of disease. In the US, presence of hypoglycin A was confirmed in seeds from box elder (Acer negundo) trees (Valberg, et al,. 2013). In Europe, the presence of high concentrations of carnitine in serum from horses with atypical myopathy, but not controls, again indicated hypoglycin A toxicity. (Zuraw et al,. 2015).
To add to this, I found that the survival rate of atypical myopathy was previously estimated to be from 3%-15% (Brandt et al, 1997; Votion et al, 2004; Puyalto-Moussu et al, 2004), however, the study by van Galen et al (2012) reported a 26% survival rate. The survivors in this study were mostly cases that had a high suspicion of atypical myopathy based on history, clinical signs and presence of myoglobinuria (van Galen et al, 2012).
DeleteMost of the non-survivors died or were euthanised within three days of clinical signs appearing, however, some remained alive for up to 10 days before dying. Cases will often deteriorate over 48-72 hours; therefore, it is important for the horse to be hospitalised as soon as hypoglycin toxicity has been identified. If affected animals survive longer than five days from the onset of clinical signs, the prognosis significantly improves. There also is no reported evidence that hypoglycin will cause any long-lasting effects, meaning that surviving animals will be able to return to their previous level of health and athleticism (Rendle, 2016).
The survival rate is already dramatically low; however, horses do not develop protective immunity, due to reports of horses suffering from the disease for a second time (van Galen et al, 2012; Votion et al, 2007).
As previously identified treatment involves fluid administration, vitamins, non-steroidal anti-inflammatories and sometimes L-Carnitine. A study identified horses with access to a salt block and vitamins had a better prognosis than those without (González-Medina.S.et al, 2017). At present there is no specific treatment for EMA. Prevention prevails, it is advised horses are removed from the paddock where sycamore seedlings are present. Horses should have access to suitable supplementary forage in the paddock to prevent them from eating the sycamore seeds. Box elder should also be removed. Inevitably complete prevention of sycamore seedlings or any tree seedling that contains hypoglicn is almost impossible. Seedlings can be blown in the wind and carried by birds, the methods of transports allow the seeds to become available for ingestion even when there are no obvious trees in the nearby area (Witkowska-Piłaszewicz et al, 2019). Complete protection and prevention from ingestion of hypoglicn is not achievable. A treatment specific to EMA is required to reduce fatalities caused by injection of hypoglicn. As previously stated, the current treatment is inadequate and provides a very poor prognosis.
DeleteIn regards to the prevalence of EAM the disease is not limited to the UK. EAM is a worldwide concern. EAM has been identified in most commonly found in Eastern Europe due to the plentiful presence of the tree species Acer pseudopatnus. EAM has also been identified in New Zealand and the United States of America (USA). The EAM has been linked to Box Elder in New Zealand and the USA. The Box elder contains Hypoglicn, similarly to the sycamore tree in Europe (González-Medina.S.et al, 2017; Hunt et al, 2017: Votion et al, 2020).
DeleteRisk factors for atypical myopathy have been investigated in cases between2006 and 2009 (Van Galen et al, 2012). The most commonly identified factors were related to the presence of trees on or around the pasture, fallen leaves, fallen dead-wood and sparse pasture. Sloping ground was also identified as a risk factor. In previous studies an absence of sunshine (Votion et al, 2007) stormy or windy weather (Valberg et al, 2013; Votion et al, 2007; Finno et al, 2006) were concluded as being associated with the development of the disease, due to an increase in seed dispersal. It was also found that cases after the first frost reduced, which may be a reflection of the changing seasons and reduced exposure to seeds, however hypoglycin A can still cause problems due to not being destroyed by freezing. The study by Van Galen et al (2012) found that 93% of cases observed occurred in Autumn, with a small number of cases being reported year-round.
ReplyDeleteIt has also been suggested that flowers falling from sycamore trees after heavy rainfall and/or wind could be an additional cause of intoxication to the horse (Votion et al, 2019). Depending on weather conditions, it has been noted that sycamore leaves and seeds can spread for several hundred metres (Katul et al, 2005), meaning that pasture contamination is not always associated with the presence of the tree in the pasture.
DeleteValberg et al,. in 2012 discovered in his study that the maximum wind speed and maximum wind gusts for the 5 days preceding illness were significantly higher in the period before horses became ill compared to the samples of the same days in 2010. There was no difference in daily precipitation between the 5 days preceding horses becoming ill and the 2010 data. There was no difference in minimum daily temperature and maximum daily temperature between the dates preceding horses becoming ill. The year 2010 had significantly warmer temperatures than the historical averages over time and than the same dates preceding the horse's illness (Valberg et al,. 2012).
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DeleteThere are a number of environmental risk factors which have been identified including the presence of trees in and around the pasture, fallen leaves, fallen dead wood, sparse pasture and sloping ground.
The absence of sunshine (van GALEN et al., 2012) as well as stormy or windy weather (Finno, Valberg, Wünschmann and Murphy, 2006; Votion et al., 2007; Valberg et al., 2012) are associated risk factors. This is likely due to increased ability for seed dispersal.
When assessing horse risk factors the most affected horses in a study by van GALEN et al., (2012) were young adults. However, this is contradicted by other studies already commented on previously. Increased access to pasture was also a factor, with affected horses spending more than six hours per day at pasture and 86% being turned out 24/7. Neither breed nor gender have been identified as risk factors. It is thought that some horses are more at risk than others, however, it is not possible to identify those horses which may be at an increased risk.
A study conducted by van Galen et al (2012) found that over the study period (2006-2009), 600 potential cases of AM were notified from 9 European countries. France, Belgium and Germany together provided 69% of cases. The other affected European countries were: The Netherlands, the UK, Ireland, Denmark, Switzerland and Luxembourg.
ReplyDeleteIn this study, a range of breeds, as well as Donkeys (three highly probable cases), and Zebras (one confirmed case and two highly probable cases), were affected and both sexes were equally represented. This is the first known study that clinically affected donkeys and zebras, however, there is no evidence that Atypical Myopathy can affect species other than equids. In the study population, all age groups were represented, but findings reported that it was mostly younger horses that were affected. This may be due to their developing immune system to unidentified causative agents, or because of the greater likelihood that younger horses will spend more time at pasture (van Galen et al, 2012).
The first large outbreak (categorised by more than one hundred horses dying of the condition) was reported in the fall of 1995 in Northern Germany (Brandt et al, 1997). Belgium, Germany and France experience large outbreaks of atypical myopathy at regular intervals, and are the European countries with the most reported cases (van Galen et al, 2012).
DeleteRegarding the prevalence of AM in younger horses, Votion et al (2020) clarify that in 2006, <3-year-olds made up 71% of cases, however in 2020, that group makes up only 36%. Votion et al (2020) go on to suggest that the reason behind this may be because toxic pressure has increased in recent years, within the general population, as opposed to developed or acquired immunity. This may be further explained by equid overpopulation and a lack of suitable grazing, or a lack of grazing management techniques. However, further investigation in this area is required.
DeleteRegarding species affected by AM, research by Bunert et al. (2018), indicate the inclusion of deer species, in particular Père David's (Elaphurus davidianus) to the equid species already noted. Their research was carried on zoo and wildlife park animals in Germany and Austria involving 79 deer, 19 diseased and 60 healthy specimens.
DeleteIn agreement with Rebekah and Niamh, current research concurs the prevalence of AM in Western Europe and North America, with some 408 cases reported in the UK between 2006 and 2019 compared to a 3039 cases in Western Europe for the same period (Votion et al., 2020). This indicates rates of 0.05% compared with the estimated UK equine population (BETA, 2020) and a 0.07% incidence rate for Western Europe (WHW & Eurogroup for Animals, 2015).
ReplyDeleteHowever, studies also indicate that not only autumn, but also spring is a high risk period, albeit less so in comparison to autumn, for example UK cases peaked in 2014 with 154 cases in the autumn period compared to just 20 in spring 2015 (Votion et al., 2020).
Regarding the impact on welfare and management, this is high due to the high fatality rate for AM - c.75% in less than 2 days (Boemer et al., 2017), and the difficulty to identify which horse(s) are at risk since co-grazers of affected horses do not show any symptoms (Bochnia et al., 2018). This is in part due to the lack of knowledge on why some equids obtain high levels of Hypoglycin A (HGA), and are affected and pasture companions not, though young horses (< 3 years) where more likely to be affected (Bochnia et al., 2019).
Research has also shown that it is not only HGA and its derived Mehtylenecyclopropylacetyl-CoA (MCPA-CoA), but also Mehtylenecyclopropylformyl-CoA (MCPF-CoA) is also a factor indicating that other species of Sapindaceae family may contribute to the disease, as well as the current idea that animals with a greater energy consumption are at risk, due to the action of the toxins MCPA-CoA and MCPF-CoA on the β-oxidation of fatty acids (Bochnia et al., 2019). Not only seeds, seedlings and samaras are sources of HGA, but also the flowers, which due to climatic conditions can be spread over a wider area (Votion et al., 2019).
In concurrence with preventative management practices, previously mentioned, mowing, herbicidal spraying or forage production and storage does not have any impact on the levels of HGA (González-Medina et al., 2019). While other methods such as providing mains supplied water, and preventing access to natural water sources should be included considering HCA is a water-soluble toxin, with cases being linked to humid pastures as well as the accumulation of dead plant matter (Votion et al., 2020).
Areas that need further attention include understanding the actions of the toxins in the horse, thus helping to find a suitable treatment, one promising area seems to be the supplementation of anti-oxidants such as vitamin E, which may provide an improved survival rate (Witkowska-Piłaszewicz et al., 2019).
Another aspect is to identify why co-grazing animals, even with a detectable level of HGA do not become affected with AM. The possibilities, including metabolic detoxification abilities, need to be studied, thus possibly providing a solution or further weapon in the fight against AM (Bochnia et al., 2018).
Following Simon’s comments regarding co-grazers, in-vitro studies conducted by Krägeloh et al. (2017) identified activated charcoal composition and activated charcoal as a HGA binding agent, therefore reducing intestinal absorption and limiting the risk of developing AM. These findings may have considerable inference on not only treating horses in the early stages of toxin ingestion, but preventative measures, particularly with regards to co-grazing animals.
ReplyDeletePasture management techniques in addition to those mentioned previously include testing for the presence of HGA in the pasture and reducing stock density to ensure that pastures are not overgrazed (B&W Vets, nd; RVC, 2018). Votion et al (2020) advise that favoring low-risk areas for pasture should be practiced during high-risk seasons (spring and autumn). While dated, Votion and Serteyn (2008) also highlight the importance of healthy body weight, as those on the poor end of the condition scale are more at risk of developing AM. Additionally, Votion and Serteyn (2008) go on to iterate that regular vaccination, anthelminthic treatments, and exercise are all linked with reducing the risk of AM. Spreading of manure, ie harrowing has been associated with increasing the risk of AM, so this practice should be avoided. (Votion et al, 2020)
To extend the discussion on treatment protocols, Robyn mentioned the use of two forms of activated charcoal as a binding agent in the intestinal tract (Krägeloh et al., 2018). This obviously requires early diagnosis of HGA intoxication while it is still in the digestive tract. To aid diagnosis Sander et al. (2016) tested a serum and/or urine sample test for C4 - C8 carnitines and glycines which can be done within 100 minutes by a single laboratory technician.
ReplyDeleteThis would need to be carried out at the first suspicion, or as part of the daignosis protocol to rule out other diseases, so as to be effective as an early diagnostic tool. Further research into creating a field-based version would be extremely useful considering the rapidity from initial visual symptoms to morbidity (Boemer et al., 2017).
Furthermore, treatment using Carnitine as a detoxifying agent, considering its binding effects with several acyl-CoA types which have been found in the urine of affected horses, making it indicative for this purpose. Carnitine is also known to stimulate leptin levels in plasma, which in turn assists the β-oxidation of fatty acids thus stimulating glucose uptake and metabolism. Administration is possible over longer periods with research to date being a maximum of 28 days, thus possibly acting a preventative measure (Fabius & Westermann, 2018).
Fabius & Westermann (2018) also advise not only using vitamin E but also selenium as it promotes healthy muscle tissue, and riboflavin as this is involved in the energy pathway with which MCPA-CoA interferes, as part of the treatment regime.
This area of treatment and/or prevention warrants further study to confirm the metabolic effects and possible side-effects of long-term use of carnitines in equines.
Returning to the sources of HGA toxins, other than Acer pseudoplatanus (Europe) and Acer negundo (Americas), the presence of Malvia parviflora could be included in this list, as research by Bauquier et al. (2016) has indicated a link between this plant species with equine AM and myocardial disease.
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DeleteIn Valbergs study, Hypoglycin A concentrations varied significantly from seed to seed, with the highest measurement (∼160 μg/seed) approximately 50 times greater than the lowest (∼3 μg/seed), (Valberg et al,. 2012). Further research is required to determine the lethal dose of hypoglycin A in horses, as well as factors that affect annual seed burden and hypoglycin A content in Acer species in North America and Europe (Valberg et al,. 2012).
DeleteIn a number of studies using rats, the toxic dose of hypoglycin A has been investigated. It is estimated that the ingestion of 26.5mg of hypoglycin A would be required to cause toxicity in a 500kg horse. The amount of hypoglycin in sycamore seeds varies markedly and may range from 0.7mg/seed to 821mg/seed (Valberg et al., 2012; Unger et al., 2014; Bochnia et al., 2015). Therefore, using these findings ingestion of anywhere between 32 seeds and 9,000 seeds may, therefore, be required to cause disease.
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ReplyDeleteIt appears from the increased reporting of AM that the disorder has gone from a sporadic condition to more frequent large outbreaks throughout Europe. Climate change may have affected Acer pseudoplatanus fecundity, seed dispersal by weather or toxin concentrations in seeds. It is possible, however, that awareness of the disease has resulted in increased reporting of AM rather than an increased incidence (Votion et al,. 2014).
DeleteEAM was initially recorded in Scotland in 1939 (Bowen et al, 1942). The disease has since seen increased recordings and disconcertingly outbreaks continue to rise which suggests there is a lack of research into adequate prevention of the deadly disease. (Witkowska-Piłaszewicz et al, 2019). The link between the EAM and hypoglicn A was identified in 2006, relatively recently, therefore this could provide a partial explanation for the lack of available cures and effective treatments. It is clear there is scope for further investigation into the prevention and treatment of the disease. However, although the disease does not discriminate between the competition and leisure horse, the leisure horse is more commonly affected. Leisure horses are more likely to have increased paddock time compared to a competition horse with limited paddock turnout time. Increased time in the paddock increases the chances of ingesting hypoglicn A. The funding for research into leisure horses is reduced compared to top level, high earning racehorses, because the return from the pharmaceuticals manufactures is likely to be small in the leisure industry (BHS, 2019; Pilsworth, 2018). At Present there is no cure for EAM. Predominantly prevention is emphasised (Votion, 2016). Due to the very high mortality rate there should be an abundance of researchers aiming to develop a treatment for this disease and reduce the mortality percentage, currently are 75%. In 2017 there were 258,490 horses in the UK. 200,000 are leisure horses (Lange,2019). This source does lack some clarity of how the information was gathered, further studies would be required to ensure reliability of the figures. The majority of UK horse population are leisure horses, if a substantial number of leisure horses became a victim of Sycamore poisoning the industry would suffer financial consequences. Riding schools would struggle to cope with vet bills and the cost of purchasing new horses. The veterinary industry would have few horses to complete routine treatment if the horses have passed away due to EAM. Some vets could close. Farriers would not have horses to shoe. The equine industry could suffer great financial loss if EAM affected leisure horses. Therefore, funding for research into the treatment of EAM in leisure horses is imperative for prevention of industry collapse.
ReplyDeleteCases of atypical myopathy were first reported in the 1940s (Bowen et al, 1942), but there has been a significant increase in cases in recent years. This may partly be due to an increased awareness within the equestrian community along with increased publicity on social media platforms such as Facebook, where news of new cases has the potential to spread rapidly reaching a large number of horse owners.
DeleteAtypical myopathy or otherwise known as sycamore myopathy/poisoning is a severe and often fatal muscle disorder caused by ingesting sycamore seeds, leaves or seedlings, which contain the toxin hypoglycin A (HGA). The ingestion of this toxin causes the production of Adenosine triphosphate(ATP) within muscle cells to slow down and in some cases to stop. (RVC, 2020) Being an unusual amino acid it can be found in certain trees but not others. The function of HGA is as yet unknown, however, it is believed it plays a vital role in the tree's growth and protection from grazing animals. Research has indicated that trees belonging to the Acer family contain HGA, the most common being the sycamore tree (Rendle, 2016). There are over 25 species belonging to the Acer family, however it has been shown that not all of these species contain the toxin HGA. Distinguishing between the different species and knowing if they contain the toxin or not, is difficult and often can lead to confusion. In a study carried out in America, the presence of hypoglycin A was found in seeds from box elder (Acer negundo) trees which were collected at the location of outbreaks (Valberg et al., 2012). It was also found that high concentrations of methylene cyclopropyl acetic acid-carnitine in the serum from horses with atypical myopathy, but not in control horses. This highlights that hypoglycin A toxicity is again present in cases. In a different study the ingestion of sycamore seeds was the cause of the atypical myopathy (Żuraw et al., 2015). This was backed by evidence of fragments of sycamore seeds within the stomachs of the horses, acute rhabdomyolysis of type one muscles, accumulation of lipid within affected cells and increased urine and serum concentrations of several acylcarnitines, acylglycines and metabolites of hypoglycin A.
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