Journal of Veterinary Science & Medical Diagnosis ISSN: 2325-9590

All submissions of the EM system will be redirected to Online Manuscript Submission System. Authors are requested to submit articles directly to Online Manuscript Submission System of respective journal.

Case Report, J Vet Sci Med Diagn Vol: 4 Issue: 4

Poisoning of Cattle Feeding on Allium ampeloprasum (Egyptian kurrat)

El-Sayed YS1*, El-Okle OSM1*, Hassan SMH3 and Bakir NMA4
1Department of Veterinary Forensic Medicine and Toxicology, Faculty of Veterinary Medicine, Damanhour University, Damanhour 22511, Egypt
1Department of Veterinary Forensic Medicine and Toxicology, Faculty of Veterinary Medicine, Alexandria University, Edfina 22576, Egypt
3Department of Clinical Pathology, Alexandria Regional Lab. Animal Health Research Institute, Alexandria, Egypt
4Department of Animal Medicine and Infectious Diseases, Faculty of Veterinary Medicine, Damanhour University, Damanhour 22511, Egypt
Corresponding author : Yasser Said El-Sayed
Department of Veterinary Forensic Medicine and Toxicology, Faculty of Veterinary Medicine, Damanhour University, Damanhour 22511, Egypt
Tel: +20-100-108-5567
E-mail: [email protected], [email protected]
Received: August 07, 2015 Accepted: September 04, 2015 Published: September 08, 2015
Citation: El-Sayed YS, El-Okle OSM, Hassan SMH, Bakir NMA (2015) Poisoning of Cattle Feeding on Allium ampeloprasum (Egyptian kurrat). J Vet Sci Med Diagn 4:4. doi:10.4172/2325-9590.1000170


Poisoning of Cattle Feeding on Allium ampeloprasum (Egyptian kurrat)

Ten days after ingesting a large quantity of Allium ampeloprasum (kurrat), 10 one-year-old calves and 2 eight-year-old cows in a group of cattle were referred for voiding dark-red urine, generalized jaundice, anemic or icteric mucous membranes, lack of appetite, and lethargy. Hematologically, Heinz bodies – hemolytic anemia, polychromasia, anisocytosis and leukocytosis were detected. Biochemically, higher serum transaminases activities and bilirubin, urea and uric acid levels were detected. As well as, an induced lipid peroxidation and a perturbed antioxidant system; decreased glutathione level, and glutathione reductase and catalase activities were significantly detected. The treatment regimen of the poisoned animals included the parenteral administration of fluids, phosphorous and vitamins, and recovery occurred within one week after initiating the treatment. This is the first report describing Allium ampeloprasum toxicity in cattle with special reference to oxidative status.

Keywords: Allium ampeloprasum; Cattle; Anemia; Antioxidants; Lipid peroxidation


Allium ampeloprasum; Cattle; Anemia; Antioxidants; Lipid peroxidation


Poisonous plants cause large economic losses to the livestock industries throughout the world. This cost considered death losses and specific reproductive losses in cattle and sheep. Fewer obvious costs such as lost grazing opportunities, additional feed costs, increased health care costs, management changes, increased culling costs and lost weight gains [1]. The genus Allium includes onion, garlic, leek, kurrat, chives, shallots and scallions were previously classified in the family Alliaceae [2]. New classification of Angiosperm Phylogeny Group, Alliaceae is now the subfamily Allioideae of the family Amaryllidaceae [3]. Some of Allium species such as Allium cepa, Allium sativum, Allium ampeloprasum and Allium schoenoprasum are of toxicological importance as it contains toxic components that may damage red blood cells and provoke hemolytic anemia accompanied by the formation of Heinz bodies in the erythrocytes of animals [4]. Cats, dogs, and cattle appear to be most susceptible to the onion’s toxic effects, whereas sheep and goats appear to be most resistant. This difference in susceptibility between species may be due to differences in hemoglobin structure, as well as differences in metabolism and detoxification within the gastrointestinal tract and internal tissue organs [5].
N-propyl disulfide and sodium n-propylthiosulfate are the main organo sulfur compounds [20]. The clinical signs observed in cattle with onion toxicosis include off food, staggering, abortion [5,16]. Although body temperatures are usually normal to low, there may be fever up to 40.5°C. Death is common unless effective treatment is provided, and surviving animals require a long period of convalescence [6]. There is no specific antidote for onion toxicosis but the treatment depends on whole blood transfusion if necessary, intravenous fluids to control shock and dehydration. An empirical therapy to limit oxidant-induced damage of erythrocytes is ascorbic acid [7]. The main aim of this case report is to increase the attention of veterinarians to the possibility of facing similar cases and to prepare them for correct diagnosis and treatment, in addition to detect biochemical alteration and status of oxidative stress in the blood of affected animals.

Case Presentation

History and clinical observations
In April 2015, on a property at El-Bahera Governorate, Egypt, 10 one-year-old calves and 2 eight-year old cows clinically affected in a group of 20 cattle (Bos taurus) with calves, commencing after they had been feeding kurrat for consecutive 10 days. Clinically, the affected animals exhibited signs of weakness, loss of appetite, dyspnea, lethargy, tensmus, frequent voiding of dark red urine (Figure 1), pale or icteric skin and mucus membranes (Figure 2), garlic odor on breath, and a lowered body temperature (37.2-37.6°C) with exception of one feverish cow (41.2°C). Samples of the kurrat fed to the cattle were collected and submitted for definitive botanical identification by an agronomist at the Herbarium Department in the Faculty of Agriculture, Alexandria University. The results revealed that the plant samples belonged to the family Alliaceae, and in particular, to the cultivated vegetable A. ampeloprasum; Egyptian kurrat (Figure 3).
Figure 1: (A) Normal color urine of a control cow. (B) Dark-red colored urine of a poisoned 1.5 years-old cow and (C) of a poisoned 1.5 years-old bull.
Figure 2: Heifer cow showing icteric skin and vulval mucous membrane.
Figure 3: Allium ampeloprasum (Egyptian kurrat).
Hematological and serum biochemical assays
Venous blood samples were collected from poisoned animals (ills, n=12) and non-poisoned healthy animals (controls, n=6) into plain tubes with or without anticoagulant for routine hematological and serum biochemical screening. Compared with the control animals, the poisoned animals exhibited marked microcytic hypochromic anemia, with leukocytosis, neutrophilia and lymphopenia. The microcytic hypochromic hemolytic anemia was indicated by a decreased red blood cells (RBCs) count (2.8 ± 0.48 ×106/μL), hemoglobin concentration (Hb) (6.1 ± 1.4 g%), packed cell volume (PCV) (14.3 ± 2.9%), mean corpuscular hemoglobin (MCH) (23.3 ± 3.2 pg) and mean corpuscular hemoglobin concentration (MCHC) (42.7 ± 2.5%), which were below the normal ranges (Table 1). Polychromasia, anisocytosis and Heinz bodies, in addition to a moderate increase in neutrophils (50 ± 1.5%) and a decrease in eosinophils (6 ± 0.43%), were consistent findings in the poisoned animals. With respect to serum biochemistry, the poisoned animals exhibited increased transaminases activity, particularly alanine aminotransferase (ALT) (37.2 ± 1.30 U/dL), and levels of bilirubin (11.2 ± 2.23 mg/dL), urea (58.24 ± 1.42 mg/dL) and uric acid (3.88 ± 0.31 mg/dL), which were above the normal ranges (Table 2); these findings are consistent with hepatorenal failure. No consistent changes were observed in any of the other analyzed biochemical parameters, which included total protein, albumin and globulin concentrations.
Table 1: Hematological indices in cattle ingested kurrat (A. ampeloprasum), The mean values indicated by asterisk are significantly different between groups (*p<0.05, **p<0.01). RBCs, red blood cells; Hb, hemoglobin; PCV, packed cell volume; MCV, mean corpuscles volume; MCH, mean corpuscles hemoglobin; - MCHC, mean corpuscles hemoglobin concentration; WBCs, white blood cells.
Table 2: Blood biomarkers of hepatorenal function, lipid peroxidation and antioxidant molecules in cattle ingested kurrat (A. ampeloprasum). The mean values indicated by asterisks are significantly different between groups (*p < 0.05, **p<0.01, ***P<0.0001). ALT, alanine aminotransferase; AST, aspartate aminotransferase; CAT, catalase; GPx, glutathione peroxidase; GR, glutathione reductase; GSH, reduced glutathione; MDA, malondialdhyde.
Blood antioxidants and lipoperoxidation
To evaluate antioxidant status, heparinized blood samples were collected from poisoned and control animals, and then centrifuged at 4,000 rpm for 15 min at 4°C in a cooling centrifuge. Sera were collected and utilized for spectrophotometric assays of blood malondialdehyde (MDA) [8] and GSH levels [9], and glutathione peroxidase (GPx) [10], catalase (CAT) [11], and glutathione reductase (GR) [12] enzymatic activities. Relative to the sera of the controls, the analytical findings revealed that the poisoned animals exhibited elevated MDA (65.06 ± 4.28 nmol/L), bio-indicator of lipid peroxidation. These animals also had significantly decreased GSH (1.35 ± 0.47 μmol/L) levels and GR (538.8 ± 37.2 U/mg protein) and CAT (113.1 ± 7.8 U/mg protein) enzymatic activities; these results are consistent with oxidative stressinduced hemolytic anemia. However, GPx activity (404.5 ± 20.5 U/ mg proteins) was significantly enhanced in the blood of poisoned animals.
Statistical analysis
All data are expressed as the mean ± standard deviations (SDs), and the levels of significance are cited. The SPSS statistical package version 17.0 for Windows (IBM, Armonk, NY, USA) was used for all data analyses. Differences in values were analyzed by t-test. Differences were deemed significant for p<0.05.


Onion-induced hemolytic anemia has been already known, and the current case has now documented a similar effect of another Allium spp.; kurrat. Similar findings were previously reported in bovines as well as in other animal species such as canines, equines and ovines that were fed a large amount of other Allium spp. (onion or garlic) [13,14]. The toxicity of Allium spp. is attributed to their contents of disulfides, n-propyl disulfate, and S-methyl and S-prop(en)yl cysteine sulfoxides (SMCOs) derived from amino acids [15]. Anaerobic bacteria play a role in increasing the toxicity of SMCOs by hydrolyzing such compounds in the rumen to thiosulfonate, which is then further metabolized to dipropyl disulfides and dipropenyl disulfides [16]. These disulfides are responsible for oxidative damage to erythrocytes [17]. SMCOs cause a marked decrease in the activity of G6PD, in turn cause an increase in the formation of methemoglobin and Heinz body count, and reduction of GSH concentration in the erythrocytes of the poisoned animals [14,18,19]. In erythrocytes, the declined GSH content was associated with elevated levels of hydrogen peroxide (H2O2) [20]. H2O2 and MDA oxidize the sulfhydryl groups of Hb, resulting in its denaturation. In the described case, a significant increase in MDA was observed after the ingestion of A. ampeloprasum, suggesting the production and/or accumulation of ROS, particularly H2O2, due to degradation by CAT and the reduction of GR [21]. Because of oxidative damage, denatured Hb would precipitate, aggregate and bind to the erythrocyte membrane [21], thereby increasing formation of Heinz bodies. In addition, lipid peroxidation is closely related to erythrocyte deformity. Hemolytic anemia resulting from Allium toxicity may be due to intravascular or extravascular hemolysis [13]. Intravascular hemolysis, as indicated by increased serum bilirubin, may occur because erythrocytes containing Heinz bodies have decreased deformability and can burst when passing through sinusoids or small capillaries [22]. Furthermore, direct oxidative damage to the erythrocyte cell membrane contributes to cell lysis [23], wherever formation of Heinz bodies and eccentrocytes increases erythrocyte fragility and extravascular hemolysis [24].
The recommended treatment for kurrat toxicosis includes restriction of access to the plant and the parenteral administration of excess fluids, phosphorus, and vitamins, particularly vitamin C for at least five consecutive days. Animals treated in this way recovered within a week after the initiation of treatment. An additional and potentially preventive recommendation is the administration of oral antibiotics, which can provide the benefit of reducing ruminal anaerobic bacteria that promote the formation of certain oxidative substances [25]. A potential alternative to the unrestricted ingestion of kurrat by ruminants might be to crush these plants and mix them with the feed at no greater than 25% of the entire diet [26]. The use of kurrat to feed ruminants is also possible in the context of a protein-rich diet. Dietary proteins are important for the synthesis of enzymes and for ensuring the availability of cofactors required for antioxidative reactions [27].


The consumption of A. ampeloprasum by ruminants resulted in poisoning. Allium toxicosis is typically diagnosed through a combination of history, clinical signs, and microscopic confirmation of oxidative Heinz body – hemolytic anemia and disturbed hepatorenal function. Restricting access to the Allium spp. and treating poisoned animals with fluids, phosphorous, and vitamin supplements induced successful recoveries.


The authors thank Vet. Dr. Mosád Zaid (Directorate of Veterinary Medicine, Damanhour, Egypt) for his invaluable assistance in consultation and for providing descriptions for poisoned animals.


  1. Panter KE, Gardner DR, Lee ST, Pfister JA, Ralphs MH, et al. (2007) Important poisonous plants of the United States. In: Gupta RC (ed) Veterinary Toxicology. Academic Press, Oxford 825-872.

  2. Friesen N, Fritsch RM, Blattner FR (2006) Phylogeny and new intrageneric classification of Allium (Alliaceae) based on nuclear ribosomal DNA ITS sequences. Aliso 22: 372-395.

  3. Bennett BC, Alarcón R2 (2015) Hunting and hallucinogens: The use psychoactive and other plants to improve the hunting ability of dogs. J Ethnopharmacol 171: 171-183.

  4. Salgado B, Monteiro L, Rocha N (2011) Allium species poisoning in dogs and cats. J Venom Anim Toxins incl Trop Dis 17: 4-11.

  5. Plumlee KH (2004) Plants. In: Plumlee KH (ed) Clinical Veterinary Toxicology. Mosby, Saint Louis 337-442.

  6. Radostits OM, Gay CC, Blood DC, Hinchcliff KW (2000) Veterinary Medicine: A textbook of the diseases of cattle, sheep, pigs, goats and horses, 9th edn.

  7. Beasley V (1999) Toxicants that cause hemolysis In: Beasley V Veterinary Toxicology, Urbana, IL, USA.

  8. Placer ZA, Cushman LL, Johnson BC (1966) Estimation of product of lipid peroxidation (malonyl dialdehyde) in biochemical systems. Anal Biochem 16: 359-364.

  9. Beutler E, Duron O, Kelly BM (1963) Improved method for the determination of blood glutathione. J Lab Clin Med 61: 882-888.

  10. Paglia DE, Valentine WN (1967) Studies on the quantitative and qualitative characterization of erythrocyte glutathione peroxidase. J Lab Clin Med 70: 158-169.

  11. Aebi H (1984) Catalase in vitro. Methods Enzymol 105: 121-126.

  12. Goldberg DM, Spooner RJ (1983) Methods of Enzymatic Analysis. In: Bergmeyen HV (ed)

  13. Borelli V, Lucioli J, Furlan FH, Hoepers PG, Roveda JF, et al. (2009) Fatal onion (Allium cepa) toxicosis in water buffalo (Bubalus bubalis). J Vet Diagn Invest 21: 402-405.

  14. Salgado BS, Monteiro LN, Rocha NS (2011) Allium species poisoning in dogs and cats. J Venom Anim Toxins incl Trop Dis 17: 4-11.

  15. Yamato O, Hayashi M, Kasai E, Tajima M, Yamasaki M, et al. (1999) Reduced glutathione accelerates the oxidative damage produced by sodium n-propylthiosulfate, one of the causative agents of onion-induced hemolytic anemia in dogs. Biochim Biophys Acta 1427: 175-182.

  16. Selim HM, Yamato O, Tajima M, Maede Y (1999) Rumen bacteria are involved in the onset of onion-induced hemolytic anemia in sheep. J Vet Med Sci 61: 369-374.

  17. Yamato O, Hayashi M, Kasai E, Tajima M, Yamasaki M, et al. (1999) Reduced glutathione accelerates the oxidative damage produced by sodium n-propylthiosulfate, one of the causative agents of onion-induced hemolytic anemia in dogs. Biochim Biophys Acta 1427: 175-182.

  18. Ogawa E, Akahori F, Kobayashi K (1985) In vitro studies on the breakdown of canine erythrocytes exposed to the onion extract. Nihon Juigaku Zasshi 47: 719-729.

  19. Tang X, Xia Z, Yu J (2008) An experimental study of hemolysis induced by onion (Allium cepa) poisoning in dogs. J Vet Pharmacol Ther 31: 143-149.

  20. Harvey JW (2006) Pathogenesis, laboratory diagnosis, and clinical implications of erythrocyte enzyme deficiencies in dogs, cats, and horses. Vet Clin Pathol 35: 144-156.

  21. Tang X, Xia Z, Yu J (2008) An experimental study of hemolysis induced by onion (Allium cepa) poisoning in dogs. J Vet Pharmacol Ther 31: 143-149.

  22. Mehta JR, Braund KG, Hegreberg GA, Thukral V (1991) Lipid fluidity and composition of the erythrocyte membrane from healthy dogs and Labrador retrievers with hereditary muscular dystrophy. Neurochem Res 16: 129-135.

  23. Rifkind RA, Danon D (1965) Heinz Body Anemia--An Ultrastructural Study. I. Heinz Body Formation. Blood 25: 885-896.

  24. Rifkind RA (1965) Heinz body anemia: an ultrastructural study. II. Red cell sequestration and destruction. Blood 26: 433-448.

  25. Ogawa E, Akahori F, Kobayashi K (1985) In vitro studies on the breakdown of canine erythrocytes exposed to the onion extract. Nihon Juigaku Zasshi 47: 719-729.

  26. Lincoln SD, Howell ME, Combs JJ, Hinman DD (1992) Hematologic effects and feeding performance in cattle fed cull domestic onions (Allium cepa). J Am Vet Med Assoc 200: 1090-1094.

  27. Fredrickson EL, Estell RE, Havstad KM, Shupe WL, Murray LW (1995) Potential toxicity and feed value of onions for sheep. Livest Prod Sci 42: 45-54.

Track Your Manuscript