Journal of Veterinary Cardiology, Vol.6, No. 1, May 2004
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Electrocardiographic changes and cardiac pathology in canine babesiosis
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Eran Dvir1; Remo G Lobetti2; Linda S Jacobson3; Joyce Pearson4; Piet J Becker5
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Abstract The main purpose of this study was to describe electrocardiographic (ECG) changes in canine babesiosis, and to relate these to clinical severity, outcome and cardiac pathology. Four groups of dogs with babesiosis were studied: mild to moderate anemia, severe anemia, concurrent autoagglutination and concurrent complications. Lead II ECG was recorded at admission for 1 minute in all dogs (121). A six lead ECG was recorded in 88 dogs. Full necropsy was performed on 16 dogs (5 died on arrival, 11 had ECG recording). The following ECG changes were recorded in relatively high prevalence: sinoatrial blocks or sinus arrest (7%), ventricular premature complexes (7%), low R-amplitude (23%), prominent Q (13%), axis deviations (40%), prolonged QRS (32%), ST depression and coving (28%), large T (42%), and notched R (28%). Differences between groups were minor. There was a significantly higher prevalence of sinus bradycardia and irregular rhythm in the non-survivors. Gross pathological changes were pericardial effusion and hemorrhages. Histological changes were hemorrhages, necrosis, inflammation and fibrin microthrombi. The only correlation between pathology and ECG was low Ramplitude and pericardial effusion. The ECG changes were similar to the pattern described for myocarditis and myocardial ischemia, and together with the histopathological findings indicated that the heart suffers from the same pathological processes described in other organs in canine babesiosis, namely inflammation and
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hypoxia. As the clinical application of the ECG changes found in this study was limited, cardiovascular assessment should be based on functional monitoring rather than ECG.
Key words: Sinoatrial block - Low R-amplitude Myocardial necrosis - Pericardial effusion Babesiosis.
Introduction Canine babesiosis is a tick-borne disease caused, in southern Africa, by the virulent hemoprotozoan parasite, Babesia canis rossi.1 Babesiosis primarily affects erythrocytes causing intra-erythrocytic parasitemia, which results in hemolytic anemia, but the disease can take myriad forms.2,3 Cardiac lesions have rarely been reported in canine babesiosis and include subepicardial and subendocardial hemorrhages,4 hydropericardium, hemopericardium,4-6 fibrin microthrombi,4 necrosis and secondary inflammation,6 as well as dilated and congested cardiac microvasculature containing considerable numbers of infected erythrocytes and free parasites.5,7 High plasma levels of cardiac troponins that were found in dogs with babesiosis from this study, indicate myocardial damage.8 Electrocardiographic (ECG) changes have not been reported in babesiosis before this study. There were a number of reasons to suspect that such changes might occur in this disease. The myocardial lesions that have been reported in babesiosis can cause numerous ECG abnormalities in both humans and dogs.9-12 Myocardial infarction can result from immune-mediated hemolytic anemia (IMHA),13,14 a common complication of babesiosis.2,3 A number of disorders that have been described in canine babesiosis, namely anemia,2,3 hypotension,15
DVM. 2,3,4 BVSc. 5 PhD. From the Departments of Companion Animal Clinical Studies (Dvir, Lobetti, Jacobson) and Pathology (Pearson), Faculty of Veterinary Science, University of Pretoria, Private Bag X04, Onderstepoort 0110, South Africa, and the Department of Biostatistics (Becker), Medical Research Council, Private Bag X385, Pretoria 0001, South Africa. All work reported in this manuscript was completed at the Onderstepoort Veterinary Academic Hospital, Faculty of Veterinary Science, University of Pretoria This study was fully funded by the Canine Babesiosis Research Fund, Faculty of Veterinary Science, University of Pretoria. The paper was presented as a poster at the 19th ACVIM Forum, Denver, CO, May 23-26, 2001. Corresponding author: Dr E Dvir, D-Pharm Ltd., Kiryat Weizmann Science Park, Bldg. 7, P.O.Box 2313, Rehovot 76123, Israel. Email:
[email protected]
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Eran Dvir; Remo G Lobetti; Linda S Jacobson; Joyce Pearson; Piet J Becker hypokalemia,16,17 hyperkalemia,18 metabolic acidosis,16,17 hypoxemia,17 and uremia,2 may induce ECG changes.19,20 Various ECG changes have been described for septic conditions,20-22 and babesiosis is a form of “protozoal septicaemia”, according to the redefinition of sepsis in the human literature.23 Cardiac lesions in malaria, a disease that shares many similarities with babesiosis,3,7,24 are similar to those described in babesiosis,25-32 and non-specific ECG changes have been described.26,29,30,33 Electrocardiographic changes in acute malaria were reported in 23-36% of cases.26,34 The aims of this study were: (1) to describe the nature and prevalence of ECG changes in canine babesiosis; (2) to assess their clinical importance; (3) to compare ECGs between groups of differing severity; (4) to compare admission and 24-hour ECGs; (5) to describe cardiac pathology in fatal cases of babesiosis; and (6) to relate the pathological findings to the ECG changes.
Animals, materials and methods Animals Client-owned dogs with babesiosis were prospectively included in the study, subject to the owners’ informed consent. Babesiosis was diagnosed using light-microscopy on a thin capillary blood smear, stained with Cams Quick staina. Exclusion criteria were: body weight 8 months, toy/small breeds ≤10kg, large breeds ≥25kg and giant breeds ≥45kg.
Figure 1 - Electrocardiogram (lead II, 50mm/s, 1cm/1mV) from a 4-year-old, female, 15 kg, Bull Terrier with SA block or sinus arrest and a ventricular escape complex. The dog was euthanized after a diagnosis of babesiosis complicated with severe icterus. No macro- or microscopic cardiac lesions were found on histopathology.
Eran Dvir; Remo G Lobetti; Linda S Jacobson; Joyce Pearson; Piet J Becker hypokalemia,16,17 hyperkalemia,18 metabolic acidosis,16,17 hypoxemia,17 and uremia,2 may induce ECG changes.19,20 Various ECG changes have been described for septic conditions,20-22 and babesiosis is a form of “protozoal septicaemia”, according to the redefinition of sepsis in the human literature.23 Cardiac lesions in malaria, a disease that shares many similarities with babesiosis,3,7,24 are similar to those described in babesiosis,25-32 and non-specific ECG changes have been described.26,29,30,33 Electrocardiographic changes in acute malaria were reported in 23-36% of cases.26,34 The aims of this study were: (1) to describe the nature and prevalence of ECG changes in canine babesiosis; (2) to assess their clinical importance; (3) to compare ECGs between groups of differing severity; (4) to compare admission and 24-hour ECGs; (5) to describe cardiac pathology in fatal cases of babesiosis; and (6) to relate the pathological findings to the ECG changes.
Animals, materials and methods Animals Client-owned dogs with babesiosis were prospectively included in the study, subject to the owners’ informed consent. Babesiosis was diagnosed using light-microscopy on a thin capillary blood smear, stained with Cams Quick staina. Exclusion criteria were: body weight 8 months, toy/small breeds ≤10kg, large breeds ≥25kg and giant breeds ≥45kg.
Figure 1 - Electrocardiogram (lead II, 50mm/s, 1cm/1mV) from a 4-year-old, female, 15 kg, Bull Terrier with SA block or sinus arrest and a ventricular escape complex. The dog was euthanized after a diagnosis of babesiosis complicated with severe icterus. No macro- or microscopic cardiac lesions were found on histopathology.
Journal of Veterinary Cardiology, Vol.6, No. 1, May 2004 Pathology Samples were collected within 30-60 minutes of death. The pericardium was examined for hemorrhage and effusion (>5ml). The heart was opened in standard fashion, and evaluated macroscopically by the principal investigator for hemorrhages (size and location) and gross infarcts. Histological samples were taken from the following sites:
Figure 2 - Heart of a 5-month-old, male, 7 kg, Chow Chow, showing extensive multifocal hemorrhages of the subepicardium, mostly limited to the left ventricle (LV). The dog died of severe lung edema 3 hours after the ECG recording. Hemorrhages were also present in the brain. On histology myocardial inflammatory infiltrate, hemorrhages and fibrin microthrombi were present in 3 sites. The ECG showed low R-amplitude.
Figure 3 - Histologic section of subepicardial myocardium (hematoxylin-eosin, x200) from a 6-month-old, female, 4 kg, mongrel dog with sinus bradycardia as the only ECG abnormality. The dog died of cerebral babesiosis, 8 hours after the ECG recording. The micrograph shows a blood vessel (BV) containing a fibrin microthrombus surrounded by severe myocardial necrosis (arrow) and mixed inflammatory infiltrate composed of neutrophils (arrowhead) and macrophages (fat short arrow). Note the hemorrhage at the bottom left corner.
papillary muscles of the left and right ventricles, interventricular septum, left and right atrium, and apex. Full thickness (from epi- to endocardium), 5 - 7mm thick sections were taken and placed separately in 10% buffered formalin. Additional samples were taken from macroscopic hemorrhages. Samples were wax embedded, sectioned at 5µm, and stained with hematoxylin and eosin and modified Martius Scarlet blue for fibrin. The same pathologist (JP), who was blind to the ECG results, evaluated all sections. Twenty 400x, adjacent, but not overlapping fields, 10 from the subendocardium and 10 from the subepicardium of each site, were examined. Abnormalities recorded were fibrin microthrombi, hemorrhage, necrosis and inflammatory infiltrates. The location of lesions within the myocardium (subepicardial, mid-myocardial or subendocardial), their distribution within each site (focal, multifocal, diffuse) and inflammatory cell type were noted. Distribution within the myocardium was classified as discrete if lesions were limited to one area (e.g. subepicardium) and scattered if they occurred in several areas. Necrosis and inflammation were classified as follows: (1) Necrosis: ≥6 necrotic fibers in any field; (2) Severe necrosis: >20 necrotic fibers in any field; (3) Inflammation: ≥6 inflammatory cells in any field; (4) Severe inflammation: >20 inflammatory cells in any field. Statistical analysis Statistical analysis was performed using Stata version 6.c Each ECG parameter was analyzed for the prevalence of abnormal (low and/or high) and normal observations and was tested against the expected normal distribution with the binomial test (95% within the normal range and 5% outside this range). Fisher’s exact test was used to compare the prevalence of abnormal observations between different groups. To evaluate whether the change between the first and the second ECG was consistent in the population, the paired t-test was used for numerical parameters (Wilcoxon matched pairs signed-ranks test was used for less than 15 observations) and the McNemar’s test for symmetry was used for categorical parameters. To evaluate the difference between groups with respect to changes between first and second ECG, one-way analysis of variance was used. The association between cardiac pathology and ECG findings was assessed by the one sided t-test, correlating the presence of any pathology in each cardiac site with the categorical ECG parameters. The same test was used to assess the association between specific abnormalities and the ECG parameters. In all tests the level of significance was P
