Suspected Pokeweed (Phytolacca americana L.) Poisoning As the Cause of Progressive Cachexia in a Shetland Pony
Emanuela Valle*, Diana Vergano, Carlo Nebbia
Department of Veterinary Sciences, University of Turin, Grugliasco, Italy.
*Corresponding author at: Emanuela Valle, Department of Veterinary Sciences, University of Turin, Largo Paolo Braccini 2, 10095 Grugliasco, Turin, Italy.
E-mail address: emanuela.valle@unito.it (E. Valle) 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27
Abstract
The case of a six-year-old gelding Shetland pony in a cachectic state with progressive apathy, diarrhoea, difficulties in feed prehension and a slow rate of ingestion is discussed. The pony showed small hyperaemic areas on the buccal mucosa, signs of gastritis, a decrease in the plasma total protein, anaemia and depressive attitude. The pony was kept in a small dirt paddock in a semi-humid zone where it was evident that many pokeweed (Phytolacca americana L.) plants had been eaten. Based on the pony’s history, its clinical signs and the results of laboratory investigations, a presumptive diagnosis of pokeweed poisoning was made. The pony’s recovery was slow and only after a 5-month period did the pony start to exhibit normal appetite, regular food consumption and more active behaviour. Cases of pokeweed poisoning could become more common as recent changes in environmental conditions favour the growth of this plant and its dispersal by frugivorous birds. No specific therapy is currently available for pokeweed poisoning in horses, thus supportive therapies are recommended. Eliminating the source of intoxication is crucial for recovery, since pokeweed poisoning can be fatal.
Keywords: pony, pokeweed, poisoning, diarrhoea, cachexia 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54
1. Introduction
Phytolacca americana L (synonym Phytolacca decandra L.), commonly known as “pokeweed”, is a fleshy perennial plant belonging to the family Phytolaccaceae [1]. Pokeweed is native to North America, but it has become an invasive alien plant common across Europe. It was probably first introduced into Europe during the 17th century [2] and is now present across the Mediterranean area [3]. Very little literature is available about pokeweed toxicity syndromes, the cytotoxic consequences at the cellular level or recommended therapies in animals and a lot of what is available is published in non-peer reviewed papers or on websites. The first known description of pokeweed poisoning in animals was in relation to cattle, made by White [4]. Since then, toxicity has been reported in other animals, including turkey poults [5], dairy cows [6], boer goats [7], sheep [8]. and pigs [9]. A single report is available describing acute intoxication in horses caused by
accidental feed contamination [10]; the animals displaying severe gastrointestinal symptoms, resulting in the fatal outcome in two out of the four affected. No reports are available on
intoxication in horses due to the voluntary consumption of pokeweed. The present article describes a toxic syndrome in a Shetland pony that had continuous access to pokeweed plants for at least three months.
2. Case history
At the beginning of the autumn of 2014, a six-year-old gelding Shetland pony used for riding school lessons showing a marked decrease in body weight, dull and long hair coat, apathy and diarrhoea was presented to the nutritional consultancy service of the Veterinary Hospital of the University of Turin (Italy) (Fig. 1A-1B). The animal had an adequate vaccination and deworming history. The pony was reported by its owner to have shown progressive apathy and "laziness" and occasional episodes of diarrhoea for several days; if diarrhoea was not present, faeces had cowpat consistency and the production of free faecal water was almost constant. Over the three weeks prior to the consultation, the pony had also shown a marked decrease in appetite (hypophagia) with 55 56 57 58 59 60 61 62 63 64 65 66 67 68 69 70 71 72 73 74 75 76 77 78 79 80
prepharyngeal dysphagia. The animal showed difficulties in food prehension (dysprehension) and dysmastication [11]; feed would drop from the month in a semi-chewed state (quidding). The rate of ingestion and transfer of feed from the mouth to the pharynx was also very slow. No colic signs were apparent. Due to the progressive loss of weight and apathy, the pony was put at rest and referred to our department via his regular veterinary.
2.2. Clinical findings
Physical examination revealed the pony to have a Body Condition Score of 2.5 on a nine point scale[12] and a body weight of 110 kg. The pony appeared calm butwith depressive attitude; body temperature was normal (37.5°C), his respiratory rate was 16 breaths/min and heart rate was 36 beats/min. No physical signs of dehydration were noted. Mucous membranes were slightly pale with a normal capillary refill time, however, some small hyperaemic areas on the buccal mucosa were present.
Examination of the digestive system showed normal dentition, but very slow mastication and little interest in feed, including treats such as apples or carrots. On auscultation, gut sounds were normal and no apparent alterations were recorded. Differential diagnoses for chronic diarrhoea were considered in accordance with Valle and co-worker [13]They included: i) faecal examination for infective causes or sand; ii) detailed anamnesis on any previous surgery, prolonged therapy with antibiotics or NSAIDS. Rectal palpation was omitted due to the small size of the pony, and
additional procedures like explorative laparotomy or rectal/liver biopsy were not performed due to the owner’s concerns. A gastroscopic exam was performed to inspect the gastric mucosa and reach the duodenum. Areas of reddening and deep mucosal ulcerations were identified in the stomach (glandular and nonglandular) with a score of 3 in relation to both number and severity, according to the scoring system proposed by MacAllister [14].
Considering the symptoms, other differential diagnoses considered were neoplasia and poisoning. Blood sampling was performed to evaluate haematological and biochemical parameters, the results 81 82 83 84 85 86 87 88 89 90 91 92 93 94 95 96 97 98 99 100 101 102 103 104 105 106
of which are reported in Table 1. Compared to the reference range values, the pony was diagnosed as anaemic due to a decrease in red blood cells, haemoglobin content and packed cell volume. A slight increase in mean corpuscular haemoglobin concentration (MCHC) was recorded. A moderate increase in serum alkaline phosphatase, a decrease in total proteins and a decrease in AST and albumin were recorded in the biochemical profile. Due to the presence of the pony’s long hair coat and the "pot belly” appearance of the abdomen, plasma ACTH was also measured to exclude the presence of
Equine Pituitary Pars Intermedia Dysfunction disease; however, all values measured were within normal ranges.
Subsequently, the feeding plan was accurately evaluated to estimate the caloric content of the diet and the feed used. According to the pony’s energy requirements and work-load, the energy provided by the feed regime should have been adequate (Table 2). However, although it was possible to calculate the total energy provided by the owner in the form of hay and hard feed, it was not possible to evaluate the exact daily amount being assumed by the pony; another small pony of the same size was cohabiting the dirt paddock, and uneaten hay and remainders from the morning meal were evident. According to the owner the total quantities given in the paddock were 5-6 kg of good quality meadow hay (6% crude protein, 30% crude fibres, 8 % ash and 0.1% crude fat) and 1 kg of cereal-based concentrate (12% of crude protein, 6% of crude fibres, 8.5 % of ash and 3% of crude fat) divided into three meals. Based on the data collected during the visit in the barn, the general body condition of the animals in the stable and the progressive cachectic state of the animal was excluded that the pony was poorly fed.
The pony’s paddock measured 7x6 metres. This small dirt paddock was in a semi-humid zone and no grass was available, but a lot of weeds were present around the fence. In particular, many examples of pokeweed were identified (Fig. 1C). The leaves and the stems had been eaten. Formal diagnosis of plant poisoning in horses was performed as outlined in Table 3. According to the owner, the plants were not present the previous year. Pokeweed plants grow quickly between the 107 108 109 110 111 112 113 114 115 116 117 118 119 120 121 122 123 124 125 126 127 128 129 130 131 132
months of April to June and the stems and the leafs slowly take on more a reddish hue. The pony had been seen to consume the plant, especially during its early growth stage; the owner had not been concerned as he had confused the plant with another species: Cornus sanguinea or
“dogwood”. Based on the pony’s history, clinical signs and the diagnostic investigations and the since the animals was observed to eat the plant even during the visit presumptive diagnosis of pokeweed poisoning was made.
2.3. Treatment and outcome
The owner quickly removed all pokeweed plants from the dirt paddock. Manual removal and digging deep into the earth to remove the entire taproot was conducted. After removing the ponies from the paddock chemicals substances were also applied to ensure that all traces of the plants were killed and would not grow back, The pony was treated for 30 days with omeprazole (Gastrogard®; 4 mg/kg body weight via the oral route for the first five days and thereafter at a dosage of 2 mg/kg)2 and received non specific supportive therapy based on the i.v. administration of fluids and treatment with a commercial preparation containing vitamins, minerals and amino acids (Metabolase®)1 for 5 days. Very slowly, over a period of 40 days, the pony started to improve, with his feed intake gradually increasing. The feeding plan was formulated as shown in Figure 2. The pony was
presented with different feeds in order to stimulate him to eat. When the first steps of the flow chart were set up, the pony’s diet comprised the ad-libitum provision of good quality meadow hay plus 0.5 kg of flaked barley (being the pony’s favourite feed), plus of 100 g soya-bean oil and a balancer containing vitamins, minerals and proteins divided into 4 meals a day. The owner guaranteed his presence for two selected meals to ensure the complete consumption of the feed concentrate. In addition, succulent foods like carrots and apples were added to stimulate the pony to eat and the pony was gradually reintroduced in a paddock with fresh grass. After three months, the pony’s body condition score had increased to 4 on a nine point scale and his body weight to 119 kg. Over a period of almost 5 months, the pony gradually started to exhibit a normal appetite, regular feeding 133 134 135 136 137 138 139 140 141 142 143 144 145 146 147 148 149 150 151 152 153 154 155 156 157 158
consumption times and more active behaviour. By the end of this period, the animal had also gained an acceptable body condition score of 5 and a body weight of 140 kg.
3. Discussion and conclusions
The examination of supposed poisoning is one of the most complex diagnostic problems for a practitioners and often no clear evidence of exposure to a toxic agent is present [15]. However since a number of plants that are toxic to equines are preset [16], plant poisoning must always be
considered in the differential diagnosis of a disease, especially when a state of progressive cachexia is present. Poisoning from voluntary consumption of pokeweed has not been previously reported in horses, most probably because pokeweed is not very palatable; however when forage is not
available, or there is competition among animals for feed resources, horses may nibble and ingest toxic amounts of the plant.
Considering its widespread distribution in Europe, pokeweed should be taken into account as a source of possible animal poisoning. The wide distribution of the plant can be attributed to seed dispersal by frugivorous birds, and when the seeds find the appropriate conditions, plant growth is fast and highly invasive [17]
To the best of our knowledge, the only published report of pokeweed poisoning in horses is that by Griess and co-workers [10], who reported an acute case of intoxication in horses ingesting carrots accidentally mixed with pokeweed root. Other studies on pokeweed toxicity in humans report symptoms that include burning sensations in the mouth, salivation, cramps, vomiting and bloody diarrhoea [18]; ruminants, like dairy cattle or goats, are also known to develop diarrhoea after the ingestion of the plant [6]; pigs present neurological symptoms in addition to those related to involvement of the gastrointestinal tract [9]
No information is available concerning the amount of the plant that needs to be consumed in order to be considered toxic for horses. Under experimental conditions, 10 to 25 g of fresh green
leaves/kg body weight has been shown to induce severe toxicosis in sheep, with the higher dosage 159 160 161 162 163 164 165 166 167 168 169 170 171 172 173 174 175 176 177 178 179 180 181 182 183 184
already fatal. Surviving individuals showed signs, not only related to gut involvement, but also increased respiratory rate, muscle tremors and neurological signs [7].
In the present case report, clinical signs were restricted to the gastroenteric apparatus and could be ascribed to the prolonged consumption of Phytolacca americana. The pony had been exposed to pokeweed for three months from the spring; with the beginning of the summer (June) the animal’s loss in body weight was noted and became a concern for its owner . However the animal continued to have access to the plant for plus an additional 2 months before it was presented to our group for investigation, at which point the pony presented a cachectic state and so the animal had been exposed to the entire life cycle of the plants. During this time, it is presumed that the pony
consumed just small amounts of the plant. It was evident that the leaves and stems had been eaten and it had been seen to nibble the plants by the owner and during the visit to the stable; this could have been the result of boredom, small enclosure with another pony and lack of access to group pastures, where free movement and social events could be guaranteed.
Many toxic compounds are found in pokeweed and different mechanisms of action have been proposed. However, according to the literature, the main toxic effects can be ascribed to saponin, oxalates and a proteinaceous mitogen [19] (Table 4). Other constituents are histamine, gamma amino butyric acid and potassium nitrate [1].
All plants in the Phytolaccaceae family are rich in triterpene saponins [20]. The triterpene saponins, like phytolaccosides, are strong irritants, but they are not significantly absorbed by the gut [1]. In the present case, they may have contributed to the onset of the ulcerative gastritis, which has previously been reported in relation to pokeweed poisoning [21]. The hyperaemic lesions in the oral mucosa are also consistent with pokeweed ingestion, which has been linked to burning sensations in the mouth, salivation and mucosal haemorrhage [18,21].
Saponins can cause other negative effects, including the decrease in feed consumption, protein digestibility and micronutrient (vitamins and minerals) absorption [22]. Taken together, these effects could be related to the observed decrease in plasma total protein content, anaemic condition 185 186 187 188 189 190 191 192 193 194 195 196 197 198 199 200 201 202 203 204 205 206 207 208 209 210
and body weight loss, culminating in a state of cachexia in the affected pony. However, the results of blood analyses for small pony breeds should always be interpreted carefully since differences in reference values could exist reflecting breed, age and fitness level.
Saponins can also exert glucocorticoid-like effects [22], which could have contributed to the “pot belly" appearance and the long hair coat observed in the present case. Pokeweed also contains oxalates [20]. Oxalic acid is a common constituent of plants and occurs in two forms: soluble and insoluble [23]. Phytolacca americana contains the soluble form [24]. Oxalates can combine with calcium to form calcium oxalate that can be excreted or absorbed into the bloodstream and
precipitate in organs such as the kidney; they can irritate the digestive tract, especially in the month whilst the plant is being chewed [24]. In general, horses and non-ruminants tend to be more
sensitive to oxalate than ruminants (e.g. goats), because rumen bacteria degrade oxalate into harmless formic acid and carbon dioxide in the latter [23]
To the authors’ knowledge, this is the first report of suspected poisoning by prolonged pokeweed exposure in a pony due to voluntary consumption. It should be noted that the incidence of
pokeweed poisoning could potentially increase due to environmental conditions that favour the growth of the plant, seed dispersal by frugivorous birds and the overgrazing of pastures.
Since no specific therapy is available, supportive therapy should be performed, with particular attention being paid to identifying and removing the source of plant ingestion. Removing the source of intoxication and promoting a balanced nutritional plan can help the recovery of intoxicated animals. However, it is important to remember that pokeweed poisoning can also be fatal, thus measures should be taken to keep animals away from the plant.
Suspect poisoning could be one of the most complex diagnostic task for an equine practitioners especially when no test are available and the animals show generalized clinical signs [15]. Case reports, like the present one, could be useful for veterinarians for the diagnosis and treatment of pokeweed poisoning and for the establishment of preventive measures.
211 212 213 214 215 216 217 218 219 220 221 222 223 224 225 226 227 228 229 230 231 232 233 234 235 236
Manufacturers’ addresses
1Metabolase, Fatro S.p.A. Ozzano Emilia (Bo) Italy 2Gastrogard, Merial, Italia, USA
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Table 1
Haematological and biochemical parameters measured. 289 290 291 292 293 294 295 296 297 298 299 300 301 302 303 304 305 306 307 308 309 310 311 312 313 314 315 316 317
Parameter Results
Reference ranges according to the Veterinary Hospital of Turin University
Reference ranges for American miniature ponies [25] WBC 103/μL 9.00 4.3-14.8 7.5-12.5 RBC 106/μL 5.84 7.5-11.0 5.9-8.3 Hb g/dL 10.1 11.3-19.8 10.7-14.5 PCV % 25.9 31.1-50.5 29-39 MCV fL 44.3 35.7–53.9 42.7-54.1 MCH pg 17.3 11.9-20.3 -MCHC g/dL 39 35-38 -PLT 103/μL 139 69.9-250.8 -Neu % 43.4 52-82.8 29-45 Lymph % 45.8 19.8-58.9 50-68 Eos % 5.4 0-8.7 1-5 ALP U/L 402 86-285 128-234 AST U/L 71 138-409 156-222 GGT U/L 10 8-22 6.6-15.4 Bil tot mg/dL 0.55 0.5-3 -Azo mg/dL 8.88 11.2-22 -CREA mg/dL 1.31 1.2-1.9 0.8-1.2 TP g/dL 5.50 5.7-7.9 6-7.2 Alb g/dL 2.1 2.9-3.5 -Alb:Globulin ratio 0.62 0.6-1.4 -CK U/L 329 119-287 137-409 LDH U/L 617 520-1480
-Abbreviations: Alb , albumin; ALP , alkaline phosphatase; ALT , alanine aminotransferase; AST , aspartate transaminase; Azo , azotemia; Bil tot , bilirubin total; BUN , blood urea nitrogen; CREA , creatinine; CK , creatinkinase; Eos , eosinophyls; GGT , gamma-glutamyl transferase; HCT, hematocrit; Hb, hemoglobin; LDH , lactate dehydrogenase; Lymph , lymphocyte; MCV , mean corpuscular volume; MCH , mean corpuscolar hemoglobin; MCHC , mean corpuscolar hemoglobin content; Neu , neutrophils; PLT , platelets; PCV , packed cell volume; RBC , red blood cells; TP , total protein; WBC, white blood cells.
318 319 320 321 322 323 324 325 326
Table 2
Analysis of the diet provided according to the pony’s requirements [26] Abbreviations: BW , body weight.
Shetland pony 140 kg (max. intake level: 2% BW "as fed")
Maintenance (easy keeper breed with a non reactive temperament) plus moderate work-load (pony games/activities 3-5 hours a week)
Energy
(0.0303 Mcal x BW)*1.4
Crude Protein 1.08 x BW=
Animal Requirements 5.9 Mcal day 151 g day
Dietary supply Meadow hay (1.5 Mcal/Kg; 6 % CP) (1.5*3)= 4.5 Mcal/kg 210 g Cereal mix (2.8 Mcal /kg; 12%CP) (0.5*2.7)=1.4 60 g
Total: 5.9 Mcal/day 270 g/day
Balance: 0 Mcal + 119 g 327 328 329 330 331 332
Table 3
Formal diagnosis of plant poisoning in horses.
General data collection Signs Problems
Anamnesis through in-depth discussions with the animal’s owner
Geographic localization and season
Age, physiological and general health status before the problem. Evaluation of the animal’s diet and its management via inspection of all foodstuffs and the pasture available.
Evaluation of the stable/place were the horse is kept
Data collection may be difficult, and require highly specialised skills. The horse’s owner may provide only partial information as he may feel responsible and potentially be charged of negligence
Predictive factors Boredom and behavioural abnormalities are very important factors to consider. Horses in their natural surroundings would be perpetual grazers. When forage is not available, they may ingest other non edible materials. Pica or the ingestion of foreign materials should be evaluated
A veterinarian should be able to recognize these factors
according to type of horse management involved (e.g. quantities of hay given, meals provided, pasture, and
possibility to interact with other horses); this will allow subjects at low possible risk to be
distinguished from those at high risk.
Symptoms Less severe forms of poisoning mainly affect the digestive tract; more severe poisoning can result in consequences in the
nervous/cardiovascular systems.
Not all possible signs are always present. For this reason, it is important to determine when and to what extent the horse was exposed. Signs may vary according to time of exposure, dose and type of poison. Plant identification Genus and species identification,
and examination of all plant parts. Accurate search in meadows and examination of forage available.
Owner may not know that a plant is toxic. So it is necessary to inspect all the places where the horses are kept.
Diagnosis May be obvious when all other possible problems are excluded and the clinical signs and lesions are compatible with the plant identified
Laboratory confirmations are not always possible due to the lack of quick tests and the high cost of specific poison research. Plants may also contain different toxic principles that can have synergic effects
Data adapted from [27,28] 333
334
335 336 337
Table 4
Main toxic principles and effects of pokeweed poisoning.
Toxic principles Effects
Saponis (Phytolaccosides) Strong irritants of the gut; can cause decrease in feed
consumption, protein digestibility and micronutrient absorption. Glucocorticoid-like effects.
Oxalate Irritation of the digestive tract, especially in the month upon chewing. Can precipitate as calcium oxalate in the gut or in the kidney
Other constituents Histamine, gamma amino butyric acid (GABA), and potassium nitrate Data from [1,20,22,24] 338 339 340 341 342 343 344 345 346 347 348 349 350 351 352 353 354 355 356
Fig. 1. A) Wet and dirty hind limbs due to the presence of soapy diarrhoea; B) dorsal view of the pony’s body (lateral imagines are not shown since the long hair coat and the potty belly appearance mask the signs of shape; C) Phytolacca americana plant.
Fig. 2. Diet plan procedure flow diagram for the hypophagic and underweight horse; designed according to the authors’ own experience and previously published data [26,29,30,31,32]. Abbreviations: BW, Body weight; ER, energy requirement; MER, maintenance energy requirement; CP, crude protein.
a adaptedfrom Becvarova and Pleasant [33]
b only the main requirements are showed (for the complete list, please see NRC tables [26]). 357 358 359 360 361 362 363 364 365 366
