Canine visceral leishmaniasis’de p dalgadispersiyonu ve kardiyak troponin I konsantrasyonu

Canine Visseral Leishmanisis (CVL), Eski Dünya ülkelerinde Leishmania infantum'dan (L. infantum) kaynaklanan ölümcül, kronik sistemik bir hastalıktır. Enfeksiyonda köpekler ev sahibi ve rezervuar rolünü oynar. Bu bağlamda, bulaşmış köpekler hem insanlara hem de diğer köpeklere yönelik bir tehdittir. L. infantum ile enfekte olan köpeklerde güncel literatürde diğer etkilenen organlara ve sistemlere ek olarak kardiyak tutulum da bildirilmektedir. Bu çalışmada, bilgisayarlı elektrokardiyografi ile atriyal iletim süresinin ölçülmesi yoluylaPd'nin kullanımı ve bununla birlikte kardiyak troponin I (CTnI) seviyesinde belirlenen değişikliklerin, CVL'li köpeklerin evrelerine göre muhtemel kalp hasarının klinik olarak değerlendirilmesi amaçlanmıştır. Hipertrikozis, perioküler alopesi, kilo kaybı, onikogripozis, lenfadenopati, hepatosplenomegali ve deri lezyonları (şiddetli kabuklanma, alopesi ile uyumlu eksfoliatif dermatitis) ve / veya anoreksiya gibi bir veya daha fazla klinik bulgunun bulunduğu her iki cinsiyetten ve çeşitli yaştan toplam 24 köpek, karşılaştırma için sağlıklı kontrol grubunda ve kardiyak hasarın varlığı, niteliği ve seviyesini belirlemek için CVL'li köpeklerde, bilgisayarlı 12 uçlu EKG cihazı [dinlenme ve 50 mm / sn'de 1 mV / cm amplitüd] ( Pd ölçümü)] ve serum CTnI konsantrasyonları, türe özgü ticari test kiti kullanılarak ölçüldü. Farklı klinik işareti olan / olmayan CVL (IFAT pozitif) ile enfekte 18 köpek, üç farklı gruba (n = 6) alındı; yukarıda bahsedilen klinik belirtiden, tek klinik belirtiyle (oligosemptomatik) I grubuna dahil olanlar; iki veya çok sayıda klinik bulguları olan (polisemptomatik) II. grupta ve asemptomatik köpeklere III. grup dahil edildi. Herhangi bir hastalığı olmayan CVL negatif sağlıklı köpekler IV. gruba dahil edildi. CVL ile enfekte 18 köpekten 10'unda tüm polimerik semptomları olan köpeklerle yüksek düzeyde cTnI konsantrasyonu tespit edildi. Kontrol grubunun tüm vakalarında cTnI seviyeleri referans aralık [<0.03 ng / dL] idi. Her bir grubun karşılaştırılmasında bile, CVL pozitif ve kontrol köpekleri arasında istatistiksel olarak anlamlı bir fark bulunamamıştır (p> 0.05). Pd değerlerinin ortalama ± standart sapması sırasıyla kontrol grubu, asemptomatik grup, oligosemptomatik grup ve polisemptomatik grupta 22.76 ± 3.12, 22.03 ± 0.80, 22.73 ± 0.80 ve 25.67 ± 1.41 idi. Gruplar arasında karşılaştırıldığında, polisemptomatik grup kontrol grubundan (p = 0.026), asemptomatik (p = 0.012) ve oligosemptomatik (p = 0.027) gruptan anlamlı farklılık gösterdi. Bu çalışmada CVL pozitif ve kontrol olgular arasında istatistiksel olarak anlamlı fark bulunmasa da, bireysel artışın hastalığa bağlı olarak miyokardit ile ilişkili olabileceğinigöstermnektedir. Ayrıca, özellikle polisemptomatik köpeklerde saptanan ortalama Pd değerlerinin kontrol grubuna göre daha yüksek olduğu iddia edilebilirken bu durum sağlıklı köpeklerde bildirilen ortalama Pd değerlerine dayalı referans aralıklarında kabul edilebilmekıtedir. Ancak, enfekte köpeklerin her bir grupta 6 adet olduğu düşünülürse, daha fazla sayıdaki olgunun araştırılmasının garanti altına alınabileceği iddia edilebilir.

Anahtar Kelimeler:

Canine visceral leishmaniasis, Kardiyak Troponin I, Köpek, P dalgadispersiyonu

P wave dispersion and cardiac troponin i concentration in canine visceral leishmaniasis*

Canine Visceral Leishmanisis (CVL) is mostly fatal chronic systemic disease caused by Leishmaniainfantum (L. infantum) in the Old World countries. In infection, dogs plays both host and reservoir role. By this context, infected dogs are a threat to both people and other dogs. In dogs infected with L. infantum, cardiac involvement in addition to the other affected organs and systems were also reported in the updated literatures. In the present study, the aim was to clinically evaluate the probable cardiac damage in dogs with CVL according to its stage via measuring atrial conduction time by use of Pd determined within computerized electrocardiography and cardiac troponin I (CTnI) level. A total of 24 dogs, of both sexes and various ages, referred with one or more of the clinical findings such as hypertrichosis, periocular alopecia, weight loss, onychogryphosis, skin lesions (severe scaling, exfoliative dermatitis compatible with alopecia) and/or anorexia, lymphadenopathy, hepatosplenomegaly. In the healthy control group for comparison and in dogs with CVL to determine presence, nature and level of cardiac damage, the evaluations were performed with computerized 12-lead ECG device [(1 mV/cm amplitude in resting and 50 mm/sec) (Pd measurement)] and serum CTnI concentrations were measured by using species specific commercial test kit.Eighteen dogs infected with CVL (IFAT positive) with/without different clinical sign were enrolled into three different groups (n=6); of the above mentioned clinical sign, to those of which with single clinical sign (oligosymptomatic) were included in the group I; those with multiple or several clinical signs (polysymptomatic) were included in the group II; and asymptomatic dogs were included group III. CVL-negative healthy dogs without any disease were left in group IV.High levels of cTnI concentration were detected in 10 of 18 dogs infected CVL with all polysymptomatic dogs. In all cases of the control group, cTnI levels were in the reference range [<0.03 ng/dL]. Even the comparison of each groups, no statistically significance (p>0.05) was found between CVL positive and control dogs. Mean ± standard deviation of Pd values were 22.76±3.12, 22.03±0.80, 22.73±0.80 and 25.67±1.41 in the control group, asymptomatic group, oligosymptomatic group, and polysymptomatic group, respectively. In comparison between groups, polysymptomatic group was significantly different than control (p = 0.026), asymptomatic (p = 0.012) and oligosymptomatic (p = 0.027) groups. Although a statistically significant difference was not found between CVL positive and control dogs in the present study, it was suggested that the individual increase may be associated with myocarditis due to disease. Besides, it may be claimed that the mean Pd values determined in especially polysymptomatic dogs was higher compared to the control group, whereas this may be accepted in the reference ranges based on mean Pd values reported in healthy dogs. However considering infected dogs population as 6 in each group, it may be safely claimed that further investigations regarding greater number of cases the may be warranted.

Keywords:

Canine Visceral Leishmaniasis, Cardiac Troponin I, Dog, P Wave Dispersion,

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REFERENCES 1. Alvar J, Canavate C, Molina R, Moreno J, Nieto J. Canine leishmaniasis. Adv Parasitol, 2004; 57: 1–88. 2. Baneth G, Koutinas AF, Solano–Gallego L, Bourdeau P, Ferrer L. Canine leishmaniosis new concepts and insights on an expanding zoonosis: Part one. Trends Parasitol, 2008; 24: 324–330. 3. Font A, Durall N, Domingo M, Closa JM, Mascort J, Ferrer L. Cardiac tamponade in a dog with visceral leishmaniosis. J Am Anim Hosp Assoc. 1993; 29: 95–100. 4. Zabala EE, Ramírez OJ, Bermúdez V. Leishmaniasis visceral em um canino. Rev Fac Cienc Vet Univ Cent Venez. 2005; 46: 43-50. 5. Torrent E, Leiva M, Segalés J, Franch J, Peña T, Cabrera B, Pastor J. Myocarditis and generalised vasculitis associated with leishmaniosis in a dog. J Small Anim Pract. 2005; 46: 549–552. 6. Lopez-Pena M, Aleman N, Munoz F, Fondevila D, Suarez ML, Goicoa A, Nieto JM. Visceral leishmaniasis with cardiac involvement in a dog a case report. Acta Vet Scand. 2009; 51: 20. 7. Alves GBB, Pinho FA, Silva SMMS, Cruz MSP, Costa FAL. Cardiac and pulmonary alterations in symptomatic and asymptomatic dogs infected naturally with Leishmania chagasi. Braz J Med Biol Res. 2010; 43: 310-315. 8. Rosa FA, Leite JHAC, Braga ET, Moreira PRR, Baltazar FH, Biondo AW, Padua PPM, Vasconcelos RO, Camacho AA, Ferreira WL, Machado GF, Marcondes M. Cardiac Lesions in 30 Dogs Naturally Infected With Leishmania infantum chagasi. Vet Pathol. 2014; 51(3): 603-606. 9. Dos Santos FP, Pascon JPE, Pereira DTP, Anjos BL, Mistieri MLA, Silveira ID, Porciuncula ML. Clinical and histopathological features of myocarditis in dogs with visceral leishmaniasis. Arq Bras Med Vet Zootec. 2015; 67(6): 1519-1527. 10. Abranches P, Santos-Gomes G, Rachamım N, Campıno L, Schnur Lf, Jaffe Cl. An experimental model for canine visceral leishmaniasis. Parasit Immunol. 1991; 13(5): 537-550. 11. Assis J, Queiroz NM, Silveira RC, Nunes CM, Oliveira TM, Junior AC, Neves MF, Machado RZ, Buzetti WA. Estudocomparativo dos métodosdiagnósticos para leishmaniose visceral emcãesoriundos de IlhaSolteira, SP. Rev Bras Parasitol Vet. 2010; 19: 17-25. 12. de Queiroz NM, Assis JD, Oliveira TM, Machado RZ, Nunes CM, Starke-Buzetti WA. Canine visceral leishmaniasis diagnosis by immunohistochemistry and PCR in skin tissues in association with RIFI and ELISA-test. Rev Bras Parasitol Vet. 2010; 19(1): 32-38. 13. de Queiroz NMGP, da Silveira RCV, de Noronha ACF, Oliveira TMFS, Machado RZ, Starke-Buzetti WA. Detection of Leishmania (L.) chagasi in canine skin. VetParasitol. 2011; 178(1): 1-8. 14. Ciaramella P, Oliva G, De luna R, Grandoni L, Ambrosio R, Cortese L, Scalone A, Persechıno A. A retrospective clinical study of canine leishmaniasis in 150 dogs naturally infected by Leishmania infantum. Vet Rec. 1997; 141: 539–543. 15. Moreira M, Luvizotto M, Garcia J, Corbett C, Laurenti M. Comparison of parasitological, immunological and molecular methods for the diagnosis of leishmaniasis in dogs with different clinical signs. VetParasitol. 2007; 145: 245–252. 16. Coelho EA, Ramírez L, Costa MA, Coelho VT, Martins VT, Chávez-Fumagalli MA, Abánades DR. Specific serodiagnosis of canine visceral leishmaniasis using Leishmania species ribosomal protein extracts. ClinVacImmunol. 2009; 16(12): 1774-1780. 17. Noszczyk-Nowak A, Szałas A, Pasławska U, Nicpoń J. Comparison of P-wave dispersion in healthy dogs, dogs with chronic valvular disease and dogs with disturbances of supraventricular conduction. Acta Vet Scand. 2011; 53(1): 18. 18. Kraus MS, Moise NS, Rashniw M, Dykes N, Erb HN. Morphology of ventricular arrhythmias in the boxer as measured by 12-lead electrocardiography with pace-mapping comparison. J VetIntMed. 2002; 16: 153-158. 19. Dilaveris PE, Färbom P, Batchvarov V, Ghuran A, Malik M. Circadian Behavior of P‐Wave Duration, P‐Wave Area, and PR Interval in Healthy Subjects. Ann Noninvasive Electrocardiol. 2001; 6(2): 92-97. 20. Noszczyk-Nowak A, Pasławska U, Szałas A, Nicpoń J. P-wave dispersion in healthy dogs. A preliminary study. Bull Vet Inst Pulawy. 2008; 52: 683–688. 21. Villani GQ, Piepoli M, Rosi A, Capucci A. P-wave dispersion index: a marker of patients with paroxysmal atria fibrillation. Int J Cardiol. 1996; 55: 169-175. 22. Dilaveris PE, Gialafos EJ, Andrikopoulos GK, Richter DJ, Papanikolaou V, Poralis K, Gialafos JE. Clinical and electrocardiographic predictors of recurrent atrial fibrillation. Pacing Clin Electrophysiol. 2000; 23: 352-358. 23. Noszczyk-Nowak A, Szałas A, Pasławska U, Nicpon J. Comparison of P-wave dispersion in healthy dogs, dogs with chronic valvular disease, and dogs with disturbances of supraventricular conduction. Acta VetScand. 2010; 53: 18. 24. Noszczyk-Nowak A. P-wave dispersion in prediction of maintenance of sinus rhythm after an electrical cardioversion of atrial fibrillation in dogs. Bull Vet Inst Pulawy. 2012; 56: 99-102. 25. Sousa MG, Carareto R, Silva JG, Oliveira J. Assessment of the electrocardiogram in dogs with visceral leishmaniasis. Pesqui Vet Bras. 2013; 33(5): 643-647. 26. Luciani A, Sconza S, Civitella C, Guglielmini C. Evaluation of the cardiac toxicity of N-methyl-glucamine antimoniate in dogs with naturally occurring leishmaniasis. Vet J. 2013; 196: 119-121. 27. Ural K, Nakipoğlu D, Balıkçı C. Canine visceral leishmaniasis’te P dalga dispersiyonu. X. Ulusal Veteriner İç Hastalıkları Kongresi Kapadokya, Nevşehir Türkiye 27 – 30 Haziran. 2013, poster bildirisi. 28. Silvestrini P, Piviani M, Alberola J, Rodrigues-Cortes A, Planellas M, Roura X, O’Brein PJ, Pastor J. Serum cardiac troponin I concentrations in dogs with leishmaniasis: correlation with age and clinicopathologic abnormalities. Vet ClinPathol. 2012; 41(4): 568-574. 29. Mendes RS, GurjãoI TA, Oliveira LM, Santana VL, Tafuri WL, Santos JRS, Dantas AFM, Souza AP. Chronic myocarditis in a dog naturally infected by Leishmania infantum chagasi: clinical and pathological aspects. ArqBras Med Vet Zootec. 2014; 66(1): 79-84. 30. Xenoulis PG, Saridomichelakis MN, Chatzis MK, Kasabalis D, Petanides T, Suchodolski JS, Steiner JM. Prospective evaluation of serum pancreatic lipase immunoreactivity and troponin I concentrations in Leishmania infantum-infected dogs treated with meglumine antimonate. Vet Parasitol. 2014; 203(3-4): 326-330.