Anaphylactoid reaction caused by sodium ceftriaxone in two horses experimentally infected by Borrelia burgdorferi

BMC Veterinary Research

Antonio Queiroz Neto²  Paulo Aléscio Canola³  Natalino Hajime Yoshinari¹  Guilherme Ferraz²  Edson Giangrecco³  Gabriel Paiva Domingues do Amaral²  Talissa Camargo Mantovani de Bonis²  Lara Antoniassi Del Rio²  Gabriela Gomes Rivera³  Roberta Carvalho Basile² 

[1] Faculdade de Medicina da Universidade de São Paulo FMUSP, Departamento de Reumatologia, São Paulo, Brazil;Faculdade de Ciências Agrárias e Veterinárias, UNESP – Univ Estadual Paulista, Campus Jaboticabal, Departamento de Morfologia e Fisiologia Animal, Laboratório de Farmacologia e Fisiologia do Exercício Equino (LAFEQ), Jaboticabal 14884-900, SP, Brazil;Departamento de Clínica e Cirurgia Veterinária, Jaboticabal, Brazil

关键词: Laminitis;    Colic;    Lyme;    Hypersensitivity;   

Others  :  1224376
DOI  :  10.1186/s12917-015-0478-6

 received in 2014-09-24, accepted in 2015-07-13,  发布年份 2015

【 摘 要 】

Background

Lyme borreliosis is a disease transmitted by ticks to mammals, especially in horses and humans. Caused by a spirochete Borrelia burgdorferi, it can result in lameness, arthritis, carditis, dermatitis and neurological signs. Anaphylactoid reactions are severe responses caused by direct action of substances (drugs, toxins), which can pose risks to life. Still poorly documented in horses, these reactions are caused by the effects of inflammatory mediators such as histamine, kinins and arachidonic acid metabolites. The last two are the most clinically relevant for the species.

Case presentation

The simultaneous occurrence of anaphylactoid reaction in two horses experimentally infected by Borrelia burgdorferi undergoing intravenous treatment with ceftriaxone sodium is reported. It was administered 4.7 × 10 ⁸spirochetes intradermal and subcutaneous applications in both horses to evaluate clinical aspects of the Lyme disease, 95 days before the application of sodium ceftriaxone. During the administration, one horse (a gelding) showed immediate and severe anaphylactoid symptoms such as urticaria, dyspnea, tachycardia, and eyelid edema, which were controlled by injecting dexamethasone. After 1 day, it expressed signs of abdominal discomfort, caused by severe bloat, which was treated surgically via celiotomy. Subsequently, this gelding had piroplasmosis and severe anemia, requiring treatment with an antimicrobial and blood transfusion. Second horse (a mare) showed signs of hypotension during the application of the antibiotic, which disappeared only when the application was interrupted. Days after the event, the mare developed moderate large colon bloat, which was treated with medication only. Subsequently the mare was evolved into the prodromal phase of laminitis in one of the forelimbs, which was treated for 10 days with non-steroidal anti-inflammatory and rheology modifying drugs and cryotherapy.

Conclusions

From the two cases presented here, it does appear that sodium ceftriaxone can induce anaphylactoid reactions in horses infected by Borrelia burgdorferi, which may evolve into colic syndrome, laminitis and the occurrence of opportunistic infections. However, further evidence should be collected in order to draw definite conclusions.

【 授权许可】

   
2015 Basile et al.

【 图 表 】

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【 参考文献 】

• [1]Butler CM, Houwers DJ, Jongejan F, Van der Kolk JH. Borrelia burgdorferi infections with special reference to horses. A review. Vet. Q. 2005; 27:146-156.
• [2]Stanek G, Wormser GP, Gray J, Strle F. Lyme borreliosis. Lancet. 2012; 379:461-473.
• [3]Voehringer D. Protective and pathological roles of mast cells and basophils. Nat. Rev. Immunol. 2013; 13:362-375.
• [4]Estelle F, Simons R. Anaphylaxis. J. Allergy Clin. Immunol. 2010; 125:s161-s181.
• [5]Eyre P. Pharmacological aspects of hypersensitivity in domestic animals: A review. Vet Res Commun. 1980; 4:83-98.
• [6]Chand N, Eyre P. Nonsteroidal anti-inflammatory drugs: A review. New applications in hypersensitivity reactions in cattle and horses. Can. J. Comp. Med. 1977; 41:233-240.
• [7]Lagopoulos V, Gigi E. Anaphylactic and anaphylactoid reactions during perioperative period. Hippokratia. 2011; 15:138-140.
• [8]Eyre P, Lewis AJ. Acute systemic anaphylaxis in the horse. Br J Pharmacol. 1973; 48:426-437.
• [9]Eyre P. Preliminary studies of pharmacological antagonism of anaphylaxis in the horse. Can. J. Comp. Med. 1976; 40:149-152.
• [10]Breukink HJ, Eysker M. Intravenous administration of Ivomec in horses. Tijdschr Diergeneeskd. 1995; 120:113-114.
• [11]Alcott CJ, Wong DM. Anaphylaxis and systemic inflammatory response syndrome induced by inadvertent intravenous administration of mare’s milk in an neonatal foal. J Vet Emerg Crit Care. 2010; 20:616-622.
• [12]Fadok VA. Update on equine allergies. Vet. Clin. N. Am. Equine Pract. 2013; 29:541-550.
• [13]Wagner B. IgE in horses: Occurrence in health and disease. Vet. Immunol. Immunopathol. 2009; 132:21-30.
• [14]Halperin JJ. Nervous system Lyme disease. Handb. Clin. Neurol. 2014; 121:1473-1483.
• [15]Gardner SY, Aucoin DP. Pharmacokinetics of ceftriaxone in mares. J Vet Pharmacol Ther. 1994; 17:155-156.
• [16]Ringger NC, Pearson EG, Gronwall R, Kolepp SJ. Pharmacokinetics of ceftriaxone in healthy horses. Equine Vet J. 1996; 28:476-479.
• [17]Ringger NC, Brown MP, Kohlepp SJ, Gronwall RR, Merritt K. Pharmacokinetics of ceftriaxone in neonatal foals. Equine Vet J. 1998; 30:163-165.
• [18]Romano A, Gaeta F, Valluzi RL, Caruso C, Rumi G, Bousquet PJ. IgE-mediated hypersensitivity to cephalosporins: Cross-reactivity and tolerability of penicilins, monobactams and carbapenems. J Allergy Clin Immunol. 2010; 126:994-999.
• [19]Pham NH, Baldo BA. Beta-lactam drug allergens. Fine structural recognition patterns of cephalosporin-reactive IgE antibodies. J Mol Recognit. 1996; 9:287-296.
• [20]Baldo BA. Penicillins and cephalosporins as allergens – structural aspects of recognition and cross-reactions. Clin. Exp. Allergy. 1999; 29:744-749.
• [21]Goudah A. Pharmacokinetic parameters of ceftriaxone after single intravenous and intramuscular administration in camels (Camelus Dromedarius). Res Vet Sci. 2008; 84:483-489.
• [22]Rebuelto M, Albarellos G, Ambros L, Kreil V, Montoya L, Bonafine R, Otero P, Hallu R. Pharmacokinetics of ceftriaxone administered by intravenous, intramuscular or subcutaneous routes in dogs. J. Vet. Pharmacol. Ther. 2002; 25:73-76.
• [23]Maradiya JJ, Goriya HV, Bhavsar SK, Patel UD, Thaker AM. Pharmacokinetics of ceftriaxone in calves. Veterinarski Arhiv. 2010; 80:1-9.
• [24]Ismail MM. Pharmacokinetics, urinary and mammary excretion of ceftriaxone in lactating goats. J Veterinary Med Ser A. 2005; 52:354-358.
• [25]Orsini JA, Divers TJ. Equine emergencies: Treatment and Procedures – Third Edition. Elseviers Saunders, St. Louis, EUA; 2013.
• [26]Swiderski CE. Hypersensitivity disorders in horses. Vet. Clin. N. Am. Equine Pract. 2000; 16:131-151.
• [27]Peters LJ, Kovacic JP. Histamine: metabolism, phisiology, and pathophysiology with applications in veterinary medicine. Journal of Emergency and Critical Care. 2009; 19:311-328.
• [28]Eyre P, Hanna CJ, Wells PW, Mcbeath DG. Equine immunology 3: Immunopharmacology – Anti-inflammatory and antihypersensitivity drugs. Equine Vet J. 1982; 14(4):277-281.
• [29]Hanna CJ, Eyre P, Wells PW, Mcbeat DG. Equine immunology 2: Immunopharmacology – Biochemical basis of hypersensitivity. Equine Vet J. 1982; 14:16-24.
• [30]Hoorn EJ, Zietse R. Severe hypokalaemia caused by flucloxacillin. J. Antimicrob. Chemother. 2008; 61(6):1396-8.
• [31]Einbinder JM, Nelson CT, Fox CL. Tissue electrolyte changes in anaphylactic shock. Am J Physiol. 1954; 179:347-352.