This study was carried out at the Department of Large Animal Internal Medicine, Faculty of Veterinary Medicine, Ghent University, Belgium.
Acute and Long-Term Cardiomyopathy and Delayed Neurotoxicity after Accidental Lasalocid Poisoning in Horses
Article first published online: 21 APR 2012
Copyright © 2012 by the American College of Veterinary Internal Medicine
Journal of Veterinary Internal Medicine
Volume 26, Issue 4, pages 1005–1011, July-August 2012
How to Cite
Decloedt, A., Verheyen, T., De Clercq, D., Sys, S., Vercauteren, G., Ducatelle, R., Delahaut, P. and van Loon, G. (2012), Acute and Long-Term Cardiomyopathy and Delayed Neurotoxicity after Accidental Lasalocid Poisoning in Horses. Journal of Veterinary Internal Medicine, 26: 1005–1011. doi: 10.1111/j.1939-1676.2012.00933.x
- Issue published online: 13 JUL 2012
- Article first published online: 21 APR 2012
- Manuscript Accepted: 10 MAR 2012
- Manuscript Revised: 23 FEB 2012
- Manuscript Received: 15 NOV 2011
- Cardiac troponin I;
Horses are extremely susceptible to ionophore intoxication. Although numerous reports are available regarding monensin, little is known about lasalocid toxicity.
To describe accidental lasalocid poisoning on a farm in Belgium.
Eighty-one horses, of which 14 demonstrated clinical signs from day 0–21 after being fed a new concentrate batch. One horse died on day 20 and another on day 27.
The most severe cases (n = 7), admitted to the clinic on day 29–46, underwent cardiac examination and blood biochemical analysis, including determination of plasma cardiac troponin I (cTnI) at admission and during follow-up. On day 57–70, cardiac examination, cTnI determination or both were undertaken on 72 remaining horses.
Short-term effects of lasalocid intoxication included inappetance, lethargy, sweating, and muscular weakness. All 7 horses admitted to the clinic demonstrated signs of myocardial degeneration such as increased cTnI, dysrhythmia and reduced myocardial contractility. Four horses developed ataxia on day 40–50. Five horses died or were euthanized on day 30–370, 2 horses recovered fully and returned to previous athletic use. None of the 72 remaining horses exhibited clinical signs between day 57–70, but 34 had dysrhythmia and 13 had increased cTnI concentrations. After a period of rest, all horses returned to their previous work. Lasalocid was detected in hepatic tissue of 2 necropsied horses.
Conclusions and Clinical Importance
Lasalocid intoxication induced myocardial and neurological damage. Although uncommon, this should be included as differential diagnosis for unexplained inappetance, signs of depression, cardiomyopathy, and ataxia in horses.
atrial premature depolarization
beats per minute
cardiac troponin I
single oral median lethal dose
parts per billion
ventricular premature depolarization
Ionophores are a group of polyether antibiotics used as feed additives in poultry and ruminants. Their biological activity is exerted by the formation of lipid-soluble complexes with cations, thereby facilitating transmembrane ion transport. They can be classified based on their affinity for different cation types. Monovalent ionophores such as monensin primarily bind Na+ and K+, whereas divalent ionophores such as lasalocid have a high affinity for Ca2+ and Mg2+.
Ionophore intoxication has been described in many species and may occur because of overdosage in target species. In nontarget species, intoxication can be caused by accidental mixing in feed or malicious intent. Toxicity is caused by the disruption of transmembrane ion concentration gradients and electrical potentials, which results in an overload of the active cation efflux channels, leading to ATP depletion. Furthermore, the increased Ca2+ influx results in excess mitochondrial uptake, causing mitochondrial damage and lack of cellular energy production. Ca2+ also interferes with the cellular enzyme systems. These mechanisms eventually result in cell death. The influx of Ca2+ is especially detrimental in excitable cells such as those in myocardium, skeletal muscles, and nervous tissue.
The single oral median lethal dose (LD50) of ionophores varies largely between species. Horses are more sensitive to the toxic effects of ionophores than cattle or poultry. Monensin toxicosis in horses is well documented in the literature as this is the most widely used ionophore antibiotic.[5-8] The main toxic effects of monensin result from myocardial and muscular damage. Acute intoxication causes anorexia, sweating, ataxia, tachydysrhythmia, and possibly death. Long-term effects have also been described and include cardiac failure, poor performance, or muscular weakness and stiffness.[9, 10] Horses are also susceptible to intoxication by other ionophores such as salinomycin or lasalocid.[3, 11] Although lasalocid toxicosis has been described in several animal species, the short- and long-term consequences of accidental lasalocid intoxication in horses have not previously been reported.[12-15]
The aims of this study were to describe accidental lasalocid poisoning on a Belgian farm with 81 horses and to describe the presence of acute and chronic myocardial and neurological damage caused by lasalocid intoxication.
Materials and Methods
The study population consisted of 81 horses on a Belgian farm. Breeds included warmblood horses (n = 50), riding ponies (n = 25), Shetland ponies (n = 4), and Norwegian Fjord horses (n = 2). Mean height was 151 ± 20 cm and mean age was 12 ± 5 years. Sex distribution was 44 mares, 33 geldings, and 4 stallions. All horses were vaccinated against influenza and tetanus.1 The next day, a new batch of concentrate was delivered. This day will be referred to as day 0.
Biochemical examination of horses admitted to the clinic of Large Animal Internal Medicine (Ghent University) between day 29 and 46 was performed at admission and during follow-up examination and included electrolyte concentrations, serum activities of creatine kinase, and plasma cardiac troponin I (cTnI) concentration. In the remaining horses at the farm, only cTnI was measured on day 37 and during follow-up. After blood was collected in lithium heparin tubes, the samples were centrifuged as quickly as possible. Maximum time between sample collection and centrifugation was 6 hours. The samples were then immediately stored at −18°C and cTnI concentration was determined within 1 week by a validated immunoassay.2
The cardiologic examination (performed between day 30 and 490) included an echocardiogram, resting and exercising ECG. Echocardiography was performed using an ultrasound unit3 with phased array transducer.4 Left ventricular (LV) contractility was assessed by M-mode, tissue Doppler imaging, and two-dimensional speckle tracking.5 LV fractional shortening was calculated as the conventional measurement of myocardial contractility.
ECGs were recorded at rest and during a lunging exercise test with a telemetric recording system.6 The test consisted of a 5 minute walk, 10 minute trot, 4 minute canter, and 1 minute gallop. The test was discontinued if horses demonstrated signs of fatigue or if pathological ECG abnormalities were detected, such as polymorphic ventricular premature depolarizations (VPDs) or ventricular tachycardia (VT).
Gross pathological and histopathological lesions were identified and recorded. Toxicological analysis of the liver was performed in 2 horses that died on day 30 and 37. Samples were analyzed by liquid chromatography coupled to tandem mass spectrometry. The extraction of target coccidiostats was based on liquid extraction with an organic solvent (acetonitrile). This method allows quantification and confirmation of 10 coccidiostatics (maduramycin, narasin, lasalocid, monensin, salinomycin, halofuginone, robenidin, nicarbazin, diclazuril, and decoquinate), with a detection limit of 0.5 parts per billion (ppb) for most compounds. Quantification was performed with a quality control (QC) sample, analyzed with each sample batch. This sample is a matrix sample spiked with target coccidiostatics, at a level corresponding to the detection limit. Retention time of the chromatography as well as ion ratios (ie, relative intensities of the 2 product ions) are used as identification criterion, as stated by Decision 2002/657/EC.
Samples of the concentrate present at the farm on day 30 were analyzed for the presence of ionophores. Because a new batch was delivered every 2 weeks, the concentrate supply fed at day 0 was no longer available. Samples taken during the production process of the batches delivered on day 0 and 15 were provided by the manufacturer. In addition, analyses were performed on dust accumulated in the dust pipe of the silo used to store feed at the farm. The presence and concentration of ionophores in concentrate and dust were assessed by the same method as the liver samples.
Data Analysis and Statistics
Data are reported as median and range.
Between day 0 and 21, 14 horses demonstrated inappetance (n = 11), lethargy (n = 9), swelling of the neck at the vaccination site (n = 7), diffuse sweating (n = 2), increased body temperature (n = 3), or hind limb weakness (n = 3). These clinical signs were assumed to be because of vaccination and horses were treated with antibiotics and nonsteroidal anti-inflammatory drugs for several days to weeks. One horse was treated with trimethoprim and sulfadiazine administered PO during 10 days. Two ponies were referred to a private referral practice on day 17. Despite intensive treatment, both ponies suddenly became recumbent and died on day 20 and 27.
Between day 29 and 46, 7 horses with persistent anorexia and lethargy were admitted to the Department of Large Animal Internal Medicine, Ghent University. These horses were treated according to their clinical status by intravenous administration of crystalloid fluids, flunixin (IV), oral or intravenous supplementation of magnesium and potassium, and oral supplementation of vitamin E. Two horses had sustained polymorphic VT and were treated by a lidocaine bolus (IV) followed by a constant rate infusion. In horse 1, VT progressed to development of ventricular fibrillation (VF) and death of the horse within 24 hours despite antidysrhythmic treatment. In horse 4, treatment initially effectively suppressed ectopy but after 1 week, this animal was euthanized because of severe weakness, increased respiratory effort, and collapse. The 5 other horses also had signs of mild to severe myocardial damage such as dysrhythmia, increased plasma cTnI concentrations, myocardial hypocontractility or all three. In addition, four of them developed weakness, ataxia, or paresis between day 40 and 50. These horses were additionally supplemented with thiamine (10 mg/kg, PO, q1d). In horse 6, mild ataxia was present which resolved fully after 3 months. However, horse 3 and 5 were euthanized on day 55 and 56 because of severe ataxia, decubitus, and excitation. Horse 2 showed severe ataxia of the hind limbs and paresis of the front limbs, but recovered at the 9-month re-evaluation period.
Feeding of the concentrate batch present at the farm was immediately discontinued from day 30 onward. The 72 remaining horses were rested and their plasma cTnI concentration was determined on day 37. Between day 57 and 70, 60 of the 72 horses underwent a full cardiac examination. Five of these horses had shown clinical signs between day 0 and 21, but clinical examination between day 57 and 70 revealed no abnormalities.
The 7 horses initially admitted to the clinic were hypokalemic, hypocalcemic, and hypomagnesemic. Despite electrolyte supplementation, these plasma electrolyte disturbances remained in some horses up to 3 weeks after admission. Serum activities of creatine kinase were increased in 6 horses (median 341.5 mU/mL, range 214–1564 mU/mL; reference range 10–146 mU/mL). Plasma cTnI concentrations were increased above reference values in all 7 horses with a median peak value of 88.78 ng/mL (1.39–816 ng/mL, reference range 0–0.10 ng/mL). Thirteen of the 72 remaining horses had increased cTnI concentrations on day 37 or during follow-up. The median peak cTnI concentration was 0.19 ng/mL (0.11–2.01 ng/mL).
Plasma cTnI concentrations generally decreased throughout the period of follow-up, but remained increased for months in several horses (Fig 1A–B). In 8/13 horses at the premises the cTnI concentration was slightly increased at one or more sampling dates during follow-up.
Ventricular dysrhythmia was detected in all 7 horses initially admitted to the clinic. By echocardiography, anechogenic fluid could be demonstrated in the pericardial space of 3 horses. Five horses showed severe LV hypocontractility (FS < 25%). The median FS of these horses was 19% (range 5–24%; reference range 29.4–44.7). Horse 1 and 4 died within 1 week, but long-term follow-up could be performed in 3 horses. Horse 3 had reduced contractility and polymorphic paroxysmal VT at admission. Contractility had improved 1 week before it had to be euthanized because of neurological abnormalities. Horse 2 also had severely reduced contractility and polymorphic paroxysmal VT at admission, but FS returned to normal values after 4 months. Horse 7 had LV hypocontractility (FS = 24%), severe myocardial fibrosis demonstrated by hyperechoic regions in the LV walls, and frequent ventricular premature depolarizations (VPDs) at admission. At repeated follow-up until day 370, myocardial fibrosis, multiple VPDs, and paroxysmal VT persisted and the horse was euthanized at the owner's request. The other 2 horses showed normal LV contractility, but the ECG revealed occasional atrial premature depolarizations (APDs) and VPDs.
Cardiac auscultation of 60 horses at the farm revealed no dysrhythmias. In 2 horses, a pathological murmur was detected because of valvular regurgitation as confirmed by color flow Doppler. Conventional echocardiography showed normal LV diameters and function in all horses. However, 34 horses had a dysrhythmia (Table 1). Two horses with more than 10 VPDs during exercise were re-examined on day 134 and day 195. In both horses, VPDs were still present on both occasions. However, after 1 year all surviving horses had returned to their previous level of exercise.
|Dysrhythmia||Horses with Increased cTnI (n = 13)||Horses with Normal cTnI (n = 47)|
|Number per Horse (Median–Range)||Number of Horses (%)||Number per Horse (Median–Range)||Number of Horses (%)|
|Sinus/AV-block at > 70 bpm||1||2 (15.4)||2 (1–3)||6 (12.8)|
|APDs at rest||47 (1–92)||2 (15.4)||3 (1–31)||8 (17.0)|
|APDs during exercise||0||0 (0.0)||1 (1–19)||10 (21.3)|
|APDs rest and exercise||47 (1–92)||2 (15.4)||2 (1–50)||13 (27.7)|
|VPDs at rest||7 (1–9)||3 (23.1)||2 (1–4)||6 (12.8)|
|VPDs during exercise||23 (16–30)||2 (15.4)||1 (1–4)||15 (32.0)|
|VPDs rest and exercise||23 (1–30)||3 (23.1)||2 (1–6)||18 (38.3)|
|All dysrhythmias||6 (46.2)||28 (59.6)|
Six horses were necropsied: 1 pony that died at the referral practice on day 27 and 5 horses that died at the clinic on day 30, 37, 55, 56, and 370. Gross pathological lesions revealed signs of myocardial degeneration in all horses. These included multifocal pale areas in the myocardium, left and right cardiac dilatation and hydropericardium. Small subendocardial pale, irregular lesions were present in the interventricular septum. Horse 7 had evidence of severe myocardial fibrosis, especially in the septum. The pony that died at the referral practice, horse 1 and horse 4 had secondary signs of heart failure including pulmonary edema, hepatic venous congestion, and ascites. Horse 4 had a severe mesenteric hemorrhage.
Histopathological examination demonstrated acute to chronic myocardial degeneration, with multifocal to coalescent hyalinisation, fragmentation, and loss of striation of cardiomyocytes combined with interstitial edema, fibroblast proliferation or fibrosis and infiltration of macrophages, neutrophils, and lymphocytes. The most severe lesions were located subendocardially and subepicardially, with subendocardial deposition of mineraloid matrix in the septum. Horse 3 and 5, euthanized 8 weeks after the onset of clinical signs, also presented myocardial regeneration with mild anisokaryosis. Hepatic lesions were caused by chronic hepatic congestion, characterized by dilatation of centrolobular veins and atrophy of paracentral hepatocytes with diffuse vacuolar degeneration. Renal histopathological lesions included signs of congestion, hemorrhage, calcification, and degeneration of the tubuli. Hind limb skeletal muscles showed mild degeneration and regeneration in horse 3 and 5. The sciatic and tibial nerve of both horses demonstrated myelin sheath swelling and focal axonal degeneration, with formation of digestion chambers. In both horses, multifocal axonal swelling was detected along the spinal cord from the cervical segments to the cauda equina.
Toxicological analysis of liver tissue of horse 1 and 4 (collected on day 30 and 37) demonstrated lasalocid concentrations of 0.5 ppb lasalocid in the liver samples. No other ionophores were detected.
Samples of the feed concentrate present at the farm on day 30 contained low concentrations of lasalocid (6 ppb) and robenidin (170 ppb). Samples taken from the batches delivered on day 0 and 15 contained 1 ppb lasalocid and 80 ppb robenidin. Several ionophores were detected in the dust accumulated in the dust pipe of the silo: 1 ppb nicarbazin, 0.7 ppb monensin, 1 ppb salinomycin, 1 ppb narasin, 15 ppb lasalocid, and 100 ppb robenidin.
This study describes accidental lasalocid poisoning on a premises with 81 horses. Fourteen horses had clinical signs between day 0 and 21, including anorexia, lethargy, profuse sweating, and muscular weakness. Two horses died at a referral practice. Seven horses admitted to the clinic of Large Animal Internal Medicine demonstrated signs of myocardial damage such as increased cTnI, dysrhythmias, and myocardial hypocontractility. Four horses developed a delayed neuropathy between day 40 and 50 characterized by ataxia and paresis. Five of the 7 horses died or were euthanized and 2 horses recovered fully. None of the 72 remaining horses exhibited clinical signs between day 57 and 70, but 34 had dysrhythmias and 13 had increased cTnI concentrations. Diagnosis was confirmed by lasalocid detection in liver tissue, but not in feed.
Horses are very susceptible to ionophore intoxication and accidental poisoning is well described. The LD50 of monensin in horses is estimated to be between 2 and 3 mg/kg body weight. This is very low compared with the LD50 in cattle (26 mg/kg body weight) and chickens (200 mg/kg body weight).[17, 18] Lasalocid is less toxic and the LD50 in horses has been estimated to be 21.5 mg/kg bodyweight. However, this estimate has been questioned as it is based on the data from 4 horses that died after being fed concentrate providing 15–26 mg/kg bodyweight. In the current study, the total ingested dose of lasalocid could not be determined. The feed was not withdrawn until 4 weeks after the onset of clinical signs, and at that time 2 new batches of concentrate had already been delivered. The horses could have ingested low daily doses of lasalocid over a 2-week period, resulting in a more chronic intoxication instead of a single oral dose. The short-term effects of lasalocid intoxication are similar to other ionophores. Inappetance is one of the first clinical signs and often the ingestion of concentrate is refused. Profuse sweating had not previously been reported for lasalocid, but is an acute clinical sign of monensin intoxication.[3, 16] Increased serum activities of muscle enzymes indicated muscle cell damage. The post-injection neck swelling probably resulted from mild muscular damage due the vaccination which may have been exacerbated by the ionophore. Furthermore, plasma electrolyte disturbances were present. These are caused by the ability of the ionophores to bind cations, as described in several cases of monensin intoxication.
In total, 14/81 horses (17%) showed clinical signs between day 0 and 21. Full cardiac examination between day 30 and 70 revealed abnormal findings, such as increased cTnI concentration, dysrhythmia, or myocardial hypocontractility in 48/67 horses (72%). Seven horses died or had to be euthanized whereas all other horses recovered fully. This is consistent with the large individual variations of ionophore susceptibility described in the literature. Even after experimental administration of monensin, clinical signs differ, ranging from absence of clinical abnormalities to sudden death.[16, 21, 22] In the case of accidental poisoning, variation may be larger because of different amounts of concentrates ingested, inhomogeneous partitioning of the ionophore in the feed and other components in the diet. Antioxidants, such as vitamin E, act as a protective factor against intoxication and were used in the treatment of affected animals. Vitamin E status in these horses remains unknown, but might have contributed to individual variation in clinical signs. Horse 1 in this study showed severe LV hypocontractility and ectopy, and died because of VF despite intensive anti-dysrhythmic treatment. This horse had been treated at the farm with sulfonamides, which are known to enhance lasalocid toxicity.[11, 24]
For monensin intoxication, it has been suggested that permanent cardiac damage can occur. Several studies have demonstrated LV hypocontractility and ventricular dysrhythmias 2–4 months after ingestion of feed containing monensin.[7, 9] Similarly, 2 months after the onset of clinical signs in this study, 13/72 (18%) of the remaining horses at the premises demonstrated increased cTnI concentrations and 21/60 (35%) demonstrated ventricular dysrhythmias at rest or during exercise. APDs, sinus exit block or first and second degree AV block at high heart rates were present in 22/60 (37%) horses. The higher prevalence of first and second degree AV block has been previously described in a case of salinomycin intoxication. Histopathologically, the long-term effects of intoxication include marked cardiac fibrosis, as previously reported in 6 cases within 5 months after exposure to monensin. In this study, all horses necropsied showed gross and histopathological signs of mild to severe myocardial degeneration and fibrosis.
Cardiac troponin I is a sensitive marker of myocardial injury and can be measured using human assays. This molecule is primarily bound to the contractile apparatus, although a small percentage remains free in the cytosol. Myocardial cell necrosis or membrane damage result in cTnI leakage into the circulation. The upper limit of the reference range for the assay used in this study has been estimated at 0.10 ng/mL. After experimental administration of monensin to healthy horses, the highest cTnI concentrations (>50 ng/mL) were reached in the horses that died or were euthanized because of severe cardiac disease.[21, 22] Similarly, the highest cTnI concentrations in this study were generally found in horses with the most severe echocardiographic and electrocardiographic signs. The maximal cTnI concentration was as high as 816 ng/mL in a fatal case with severe LV hypocontractility and VT. In some surviving horses, the cTnI concentration remained increased for several months, which is likely because of ongoing release from damaged myocytes. Similarly, experimentally induced monensin intoxication resulted in increased plasma cTnI up to 7 months after monensin administration. Remarkably, cTnI concentrations increased during follow-up in some of our cases. This might be explained by the fact that some owners did not put their horses at rest although this was recommended. Conversely, in the horse with severe LV fibrosis, the cTnI concentration remained high for 5 months, but had returned to normal values at the time of euthanasia after 1 year of rest.
Delayed neurotoxicity occurred in 4 horses at 6 weeks after the onset of clinical signs. Ataxia has been described as an acute clinical sign of monensin toxicosis. Furthermore, ataxia, hind limb weakness, and muscle atrophy over a period of a week to several months have been reported in cases of accidental monensin and salinomycin poisoning.[11, 20] Delayed neuropathy because of lasalocid intoxication has not yet been described in horses. However, lasalocid induces axonal degeneration in other species. In dogs, accidental lasalocid ingestion results in tetraparesis, hyporeflexia, and hypotonia. Mental status and pain perception are not affected, indicating a generalized lower motor neuron deficit. Most dogs recover fully over 2–50 days.[15, 24, 28] The mechanism of neurotoxicity has been investigated in broiler chickens and rats. The mitochondrial energy deficit and impaired osmoregulation because of influx of Ca2+ ions lead to myelin edema and demyelination with secondary axonal degeneration. Histopathological lesions of neural tissue included axonal swelling with the presence of digestion chambers and vacuolation.[13, 29, 30] These lesions are very similar to those found in horse 3 and 5 in this study. In the 2 other affected horses, clinical signs were completely reversible.
The diagnosis of lasalocid intoxication is difficult as ionophores are not deposited in high concentrations in target tissues. Horses that survived an LD50 dose of monensin longer than 24 hours had no detectable monensin in the liver (<0.05 ppm) even though they eventually died. In this study, lasalocid could be demonstrated in the liver of 2 horses at low concentrations which confirmed exposure of these horses to lasalocid. Unfortunately, no sample was available at the premises from the concentrate batch delivered at the onset of clinical signs. A sample of this batch taken during the production process did not contain high lasalocid concentrations. However, contamination might have occurred during feed transportation. In addition, the ionophore concentration in concentrate is often nonuniform in cases of feed mixing errors. Therefore, the final diagnosis of lasalocid intoxication was primarily based on the clinical signs, histopathological lesions, and the presence of lasalocid in hepatic tissue of 2 horses. The dust collected from the silo at the farm contained several other ionophores. These might have accumulated in the dust pipe over a long period because of electrostatic adherence. However, the potential role of these ionophores could not be ruled out entirely because of the delay between ingestion and necropsy and the possible difference in pharmacokinetics between individual ionophores.
In conclusion, lasalocid intoxication induced myocardial and neurological damage, resulting in various short-term and long-term clinical signs. Although uncommon, lasalocid intoxication should be included as a differential diagnosis for unexplained inappetance, signs of depression, cardiac disease, and ataxia.
Annelies Decloedt is a PhD fellow of the Research Foundation – Flanders (FWO).
Duvaxyn IE-PLUS-T, Fort Dodge, Naarden, The Netherlands
Acces Accu-TnI, Beckman Coulter Inc, Fullerton, CA
GE Vivid 7 Dimension, GE Healthcare, Horten, Norway
3S Phased Array Transducer, GE Healthcare
Decloedt A, Verheyen T, Sys S, De Clercq D, van Loon G. Tissue Doppler imaging and 2D speckle tracking detect left ventricular hypocontractility in horses exposed to ionophores. J Vet Intern Med, submitted
Televet 100 Version 4.1.3., Kruuse, Marslev, Denmark
- 20Monensin toxicity in horses. An outbreak resulting in the deaths of ten horses. Aust Eq Vet 1991;9:4., , , et al.
- 25Salinomycin poisoning in horses: Case report. Proc 31st Ann AAEP Conv, Beltsville, Maryland December 1985;10., .
- 29Oral administration of lasalocid causes peripheral neuropathy in Sprague Dawley rats: Effect of water salinity on lasalocid-induced peripheral neuropathy. J Anim Vet Adv 2005;4:719–722., , .