Relevant bibliographies by topics / Canine babesiosis

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  1. Journal articles
  2. Dissertations / Theses
  3. Book chapters
  4. Conference papers

Academic literature on the topic 'Canine babesiosis'

Author: Grafiati
Published: 4 June 2021
Last updated: 6 February 2022

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Journal articles on the topic "Canine babesiosis"

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MYLONAKIS (Μ.Ε. ΜΥΛΩΝΑΚΗΣ), M. E., C. BILLINIS (Χ. ΜΠΙΛΛΙΝΗΣ), C. KOUTINAS (X. ΚΟΥΤΙΝΑΣ), and A. F. KOUTINAS (Α. Φ. ΚΟΥΤΙΝΑΣ). "Canine babesiosis." Journal of the Hellenic Veterinary Medical Society 52, no. 3 (January 31, 2018): 225. http://dx.doi.org/10.12681/jhvms.15451.

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The causative agents of canine babesiosis are Babesia canis and B. gibsoni which are transmitted by various hard tick species and blood transfusions. In the hyperacute form of the disease hypothermia, shock, severe metabolic acidosis and disseminated intravascular coagulation usually precede the death of the dog occuring in less than 24 hours. Severe anemia, icterus, splenomegaly and peripheral lymphadenopathy characterize the acute form of the disease. Intermittent fever and progressive loss of body weight may be noticed in the chronic form of babesiosis, while its many atypical clinical manifestations (e.g. ascites, gastrointestinal signs, CNS disease, subcutaneous edema, masticatory myositis) often cause diagnostic confusion. The organism detection on RBC in thin blood smears made from the buffy coat is a must for definitive diagnosis. The IFA test is a good choice for screening large numbers of dogs for detecting the asymptomatic carriers. Complete parasitological cure can be obtained with imidocarb dipropionate, pentamidine isethionate or diminazene aceturate, while metronidazole and clindamycin have been recently suggested as good alternatives. Supportive care is considered crucial for the survival of the severely affected animals. While effective tick control is the mainstay of prevention, doxycycline and imidocarb may also play a significant role to that goal. The effectiveness of a killed vaccine is still a matter of controversy.
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Boozer, A. Lindsay, and Douglass K. Macintire. "Canine babesiosis." Veterinary Clinics of North America: Small Animal Practice 33, no. 4 (July 2003): 885–904. http://dx.doi.org/10.1016/s0195-5616(03)00039-1.

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YAMASAKI, Masahiro. "Canine babesiosis." Journal of the Japan Veterinary Medical Association 68, no. 4 (2015): 245–52. http://dx.doi.org/10.12935/jvma.68.245.

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Irwin, Peter J. "Canine Babesiosis." Veterinary Clinics of North America: Small Animal Practice 40, no. 6 (November 2010): 1141–56. http://dx.doi.org/10.1016/j.cvsm.2010.08.001.

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Bourdoiseau, Gilles. "Canine babesiosis in France." Veterinary Parasitology 138, no. 1-2 (May 2006): 118–25. http://dx.doi.org/10.1016/j.vetpar.2006.01.046.

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Schetters, Theo. "Vaccination against canine babesiosis." Trends in Parasitology 21, no. 4 (April 2005): 179–84. http://dx.doi.org/10.1016/j.pt.2005.02.006.

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Dhliwayo, Solomon, Brighton Chihambakwe, Knowledge Taonezvi, Silvester M. Chikerema, Musavengana T. Tivapasi, and Davies M. Pfukenyi. "Seroprevalence of Canine Ehrlichiosis and Microscopic Screening for Canine Babesiosis in Dogs in Harare, Zimbabwe, 2016-2017." Veterinary Medicine International 2019 (December 1, 2019): 1–7. http://dx.doi.org/10.1155/2019/4130210.

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A cross-sectional study was done to determine ehrlichiosis seroprevalence and babesiosis prevalence in dogs that were presented to selected veterinary clinics in Harare. Sera from randomly selected dogs were tested for antibodies to Ehrlichia spp. using an enzyme-linked immunosorbent assay while microscopy of peripheral blood smears was used to confirm babesiosis. Overall, 75.2% (88/117, 95% CI: 66.2–82.5) of sera samples tested were positive to Ehrlichia spp. antibodies while the prevalence of canine babesiosis was 47.9% (56/117, 95% CI: 38.6–57.3). Age, breed, and sex were found not to be associated with the two disease conditions p>0.05. Most of the dogs with babesiosis (82.1%, 46/56) were also positive to Ehrlichia spp. antibodies. Hypoalbuminaemia (53.8%, 63/117), anaemia (53.0%, 62/117) and thrombocytopaenia (40.2%, 47/117) were the most common laboratory findings. Thrombocytopaenia and hypoalbuminaemia was more pronounced in dogs with babesiosis only while anaemia was more marked in dogs with babesiosis and positive to Ehrlichia spp. antibodies.
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Petra, Bilić, Kuleš Josipa, Barić Rafaj Renata, and Mrljak Vladimir. "Canine Babesiosis: Where Do We Stand?" Acta Veterinaria 68, no. 2 (June 1, 2018): 127–60. http://dx.doi.org/10.2478/acve-2018-0011.

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Abstract Canine babesiosis is a tick-borne disease caused by protozoal haemoparasites of different Babesia species. Babesiosis is one of the most important globally extended and quickly spreading tick-borne infections of dogs. This comprehensive review gives an in-depth overview of Babesia species currently identified in dogs together with relevant vector tick species and their geographical distribution, life cycle and transmission of parasite. The main mechanisms in the pathogenesis of babesiosis are described and elucidated by recent literature overview. As Babesia infection causes a disease with very variable clinical manifestations, special attention is given to clinical signs, laboratory features and clinicopathological findings. The diagnosis of canine babesiosis by microscopy, serological and molecular methods is reviewed, together with recent advances in mass spectrometry based assays. Accurate detection and species recognition are important for the selection of the appropriate therapy, monitoring and prediction of the outcome of the disease. Finally, guidelines for the treatment and prevention of canine babesiosis are given.
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Kostro, Krzysztof, Krzysztof Stojecki, Maciej Grzybek, and Krzysztof Tomczuk. "Characteristics, immunological events, and diagnostics of Babesia spp. infection, with emphasis on Babesia canis." Bulletin of the Veterinary Institute in Pulawy 59, no. 4 (December 1, 2015): 495–504. http://dx.doi.org/10.1515/bvip-2015-0074.

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AbstractVector-borne infection constitutes a significant health issue in dogs worldwide. Recent reports point to an increasing number of canine vector-borne disease cases in European countries, including Poland. Canine babesiosis caused by various Babesia species is a protozoal tick-borne disease with worldwide distribution and significant veterinary importance. The development and application of molecular methods have increased our knowledge about canine babesiosis, its prevalence, and clinical and pathological aspects of the infection. Parasitologists and veterinary surgeons need an accurate description of the species responsible for canine babesiosis to improve diagnostic and therapeutic methods, as well as predictions for the course of the disease. Therefore, we decided to summarise recent knowledge concerning Babesia species and B. canis.
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Bano, Sajida, and Chandan Lodh. "EPIDEMIOLOGICAL STUDIES ON CANINE BABESIOSIS." Indian Journal of Canine Practice 11, no. 1 (June 1, 2019): 090. http://dx.doi.org/10.29005/ijcp.2019.11.1.090-093.

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Dissertations / Theses on the topic "Canine babesiosis"

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Nel, Mirinda. "Serum lactate in canine babesiosis." Diss., University of Pretoria, 2005. http://hdl.handle.net/2263/22944.

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Canine babesiosis typically causes a haemolytic anemia and results in hypoxia and sepsis, which can eventually result in multiple organ dysfunction. Human patients with severe injury or disease such as shock, sepsis and malaria often have persistent hyperlactataemia, and there is a correlation between blood lactate and survival rate. There are various similarities between human malaria and canine babesiosis, eg. anaemia, renal failure, cerebral forms, coagulopathy, hepatopathy, pulmonary oedema, and shock. In severe malaria, lactate levels in blood rise in direct proportion to the severity of the disease. Venous lactate concentrations measured at 4 hours after admission appears to be the best prognostic indicator in severe malaria. In dogs blood lactate has been shown to be of prognostic value in patients with gastric dilatationvolvulus and in dogs admitted to intensive care units. Blood lactate has also been shown to be of prognostic value in equine colic. Blood lactate was determined in ninety dogs with naturally occurring canine babesiosis. Forty-five dogs (50%) presented with hyperlactataemia (blood lactate > 2.5mmol/L) and 20 (22.2%) with hypoglycaemia (blood glucose < 3.3 mmol/L). Measurements significantly associated with mortality were hypoglycaemia on admission, blood lactate > 5mmol/L on admission, blood lactate > 2.5 mmol/L at 8, 16 and 24 hours after admission, and increase or < 50% decrease in blood lactate within 8 and 16 hours after admission. Blood lactate persistently > 4.4 mmol/L indicated a very poor prognosis. The study concluded that serial blood lactate measurements are useful in predicting survival in dogs with severe and complicated canine babesiosis.
Dissertation (MMed Vet (Med))--University of Pretoria, 2004.
Companion Animal Clinical Studies
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Birkenheuer, Adam Joseph. "Canine Babesiosis: Epidemiological, Molecular and Therapeutic Investigations." NCSU, 2004. http://www.lib.ncsu.edu/theses/available/etd-04192004-164025/.

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Canine babesiosis is an emerging infectious disease in the United States (US). An epidemic of Babesia gibsoni infections in the US was identified. An association between dog breed and B. gibsoni infections was detected. Babesia gibsoni-infected dogs were more likely to be American pit bull terriers and B. canis vogeli infected dogs were more likely to be greyhounds. An association between a recent dog bite and B. gibsoni infection was detected, implicating direct dog-to-dog transmission as a route of infection in the US. Several genes from canine Babesia spp. were characterized, including 18S ribosomal RNA (rRNA), internal transcribed spacer regions (ITS), cytochrome B (cytB), and rhoptry-associated protein-1 (RAP-1). These genetic data were used to develop a sensitive and specific diagnostic semi-nested polymerase chain reaction (PCR) test for canine babesiosis. Using this assay, a novel large Babesia organism was identified in a blood sample obtained from a clinical patient. Molecular and phylogenetic characterization of this large Babesia spp. determined that it was most closely related to B. bigemina. Lastly, an atovaquone and azithromycin drug combination was shown to be the first treatment to clear canine B. gibsoni infections.
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Pardini, Anne Dale. "The pathology and pathogenesis of canine cerebral babesiosis." Diss., University of Pretoria, 2000. http://hdl.handle.net/2263/27842.

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The pathology of canine cerebral babesiosis was examined at the gross, histological and ultrastructural levels. Gross lesions could be categorised as either global or regional. Congestive brain swelling , diffuse cerebral congestion and diffuse cerebral pallor were classified as global lesions. Multifocal haemorrhage and malacia were classified as regional lesions. Oedema was inconsistently present and could be either focal or diffuse. The majority of histological changes were observed in both cerebral babesiosis and control cases. Regional lesions were unique to cerebral babesiosis and had specific histological features. Highly localised endothelial injury was the primary lesion. Early lesions were multifocal and strictly associated with the microvasculature. Intermediate lesions, with perivascular haemorrhage and neutrophil infiltration, were suggestive of reperfusion injury. Advanced lesions were locally extensive and similar in appearance to haemorrhagic infarction. It is likely that the pathogenesis of regional lesions is by a process of microvascular infarction, as venous thrombosis could not be demonstrated. Ultrastructural evidence for adherent contact between erythrocytes and capillary endothelium was demonstrated. Endothelial cell necrosis occurred early in the development of lesions, before neuronal and glial injury. It is postulated that endothelial injury is the primary event in the development of regional lesions and secondary lesions develop as a consequence of microvascular infarction.
Die patologie van die serebrale vorm van bosluiskoors in honde is ondersoek. Die letsels is makroskopies, histologies en elektronmikroskopies beskryf. Letsels kon makroskopies in twee groepe verdeel word: Globale letsels en gelokaliseerde letsels. Kongestiewe brein swelling, diffuse serebrale kongestie en serebrale anemie kom voor as globale letsels in serebrale babesiose. Multifokale bloeding en nekrose kom voor as gelokaliseerde letsels. Edeem was nie konsekwent teenwoordig nie, en was algemeen of verspreid. Die meeste algemene histologiese veranderinge was in beide serebrale en kontrole gevalle teenwoordig. Gelokaliseerde letsels waarin spesifieke hisotpatologiese veranderinge voorgekom het, was kenmerkend van serebrale babesiose. Die primere letsel is hoogs gelokaliseerde beskadiging van endoteelselle. Beskadiging van die kapillere bloedvate ontstaan vroeg in die ontwikkeling van letsels. Verdere ontwikkeling van die letsel word gekenmerk deur peri-vaskulere bloeding en neutrofiel infiltrasie wat aanduidend is van reperfusie beskadiging. Volontwikkelde letsels is plaaslik-ekstensief en het die voorkoms van hemoragiese infarkte Dit is waarskynlik dat mikrovaskulere infarksie 'n rol speel in die patogenese van die letsels, aangesien veneuse trombose nie ontstaan nie. Noue kontak tussen rooibloedselle en kapillere endoteel is elektronmikroskopies bevestig. Endoteelselnekrose ontstaan voordat tekens van beskadiging geidentifiseer kan word in neurone of gliaselle. Dit blyk dat kapillere endoteelselbeskadiging die primere letsel by die ontstaan van gelokaliseerde lese Is is, en dat sekondere lesels ontwikkel as gevolg van mikrovaskulere infarksie.
Dissertation (MSc)--University of Pretoria, 2000.
Paraclinical Sciences
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Dvir, Eran. "Cardiac histopathology and electrocardiographic changes in canine babesiosis." Diss., University of Pretoria, 2001. http://hdl.handle.net/2263/23548.

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Electrocardiographic (ECG) changes have never been reported in canine babesiosis. Based on the metabolic, electrolyte, and myocardial alterations described for the disease, such changes are to be expected. The purpose of this study was to describe ECG changes in canine babesiosis, and to correlate those changes to clinical severity, outcome and cardiac histopathological changes. Four groups of dogs with babesiosis were studied: mild to moderate anaemia (n=40), severe anaemia (n=35), concurrent immune-mediated haemolytic anaemia (n=18) and complicated (n=28). Lead II ECG was recorded at admission for 1 minute in all dogs, and repeated after 24 hours in admitted dogs (groups II – IV). Six lead ECG was recorded in 88 dogs. Full necropsy was performed between 30-60 minutes after death on 16 dogs (5 died on arrival, 11 had ECG recording). Gross cardiac pathology was recorded and histopathology of myocardial sections from ventricles, atria, apex and interventricular septa was evaluated, using a scoring system for haemorrhages, necrosis, inflammatory infiltrate and fibrin microthrombi. The following ECG changes were recorded: sinoatrial (7%) and atrioventricular blocks (4%), ventricular premature complexes (7%), low R-amplitude (23%), prominent Q (33%), axis deviations (40%), prolonged QRS (32%), ST depression and coving (28%), large T (42%), and notched R (28%). Differences between groups were minor and inconsistent. Gross pathological changes were pericardial effusion (25%) and subepicardial (56%) and subendocardial haemorrhages (63%). Histological changes were haemorrhages (69%), necrosis (50%), inflammation (63%) and fibrin microthrombi (75%). The only correlation between pathology and ECG was low R-amplitude and pericardial effusion. There was a significantly higher prevalence of sinus bradycardia and irregular sinus rhythm in the non-survivors. Both ECG and pathological changes were non-specific, but there were similarities to the pattern of changes that have been described for myocarditis and myocardial ischaemia. Antiarrhythmic treatment was only required in 1 dog. Thus, the clinical application of the ECG changes found in this study was limited. It was concluded that the heart suffers from the same pathological processes described in other organs in canine babesiosis, namely inflammation and hypoxia. Cardiovascular management, if necessary, should be based on functional monitoring rather than ECG.
Dissertation (MMedVet (Med))--University of Pretoria, 2001.
Companion Animal Clinical Studies
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Scheepers, Elrien. "The haematological kinetics of canine babesiosis in South Africa." Diss., Electronic thesis, 2008. http://upetd.up.ac.za/thesis/available/etd-07162008-132522/.

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Keller, Ninette. "Hypoglycaemia in virulent canine babesiosis prevalence and risk factors /." Diss., University of Pretoria, 2004. http://upetd.up.ac.za/thesis/available/etd-03082005-092252/.

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Liebenberg, Cherrildine Elizabeth. "Thromboelastographic evaluation of haemostatic abnormalities in uncomplicated canine babesiosis." Diss., University of Pretoria, 2011. http://hdl.handle.net/2263/24851.

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Babesiosis, caused by Babesia rossi, is a common cause of morbidity and mortality of dogs in South Africa. Canine babesiosis can be classified either as uncomplicated or complicated based on the degree of anaemia and the severity of the presenting clinical signs.1,2 In uncomplicated babesiosis, the clinical signs are mostly attributable to the degree of the anaemia, whereas in complicated babesiosis the disease process is characterised by additional organ involvement.3,4 One of the most common haematological hallmarks of canine babesiosis, caused by B. rossi, is thrombocytopenia, which is not associated with clinical haemorrhage despite very low platelet counts that would normally cause inability to maintain normal primary haemostatic function.5 The aim of this study was to describe the thromboelastographic findings in uncomplicated canine babesiosis and compare them with those of normal, healthy control dogs. We hypothesised that these dogs would have a normal to hypercoagulable haemostatic capacity, despite the severe thrombocytopenia, and that this could be detected with thromboelastography (TEG), which has previously been shown to correlate well with clinical signs of haemorrhage in dogs.6 This was a prospective, cross sectional, observational study that included 20 client-owned dogs, diagnosed with uncomplicated canine babesiosis at the Onderstepoort Veterinary Academic Hospital (OVAH). Infection with B. rossi was confirmed by polymerase chain reaction (PCR) and reverse line blot (RLB) hybridisation assay. Blood samples were collected at the time of diagnosis. A group of 10 healthy control dogs were included for comparison. Antithrombin activity (AT) was measured using an automated spectrophotometric analyser (Cobas Integra 400, Roche, South Africa). D-dimer was measured using an immunometric flow-through principle (D-dimer Single test, Nycocard Reader II, Medinor A/S). Prothrombin time (PT), activated partial thromboplastin time (aPTT) and fibrinogen assays were performed on the ST art® 4 analyser (Diagnostica Stago, Roche, South Africa). TEG analysis was performed using the TEG® 5000 Thromboelastograph® Haemostasis System (Haemoscope, Pro-Gen Diagnostics (Pty) Ltd, South Africa). A complete blood count was performed on the ADVIA 2120 (Siemens, South Africa). The results of the babesiosis and control groups were compared using the Mann-Whitney U test or the Students t-test based on normality. The normality assumption for distribution of the variables in the data was evaluated using the Shapiro-Wilk test. The statistical significance was set at p<0.01. The mean haematocrit (Ht) and median platelet count was significantly lower in the babesiosis group than the controls (0.29 vs. 0.50 L/L; p<0.01 and 22.0 vs. 374.5 x 109/l; p<0.01, respectively). There was no significant difference in any of the TEG parameters between the babesiosis group and the controls. The medians for the various TEG parameters in the babesiosis group versus the controls were; R: 5.5 vs. 4.4 min (p=0.05); K: 2.5 vs. 2.0 min (p=0.08); angle: 58.3 vs. 61.1 degrees (p=0.35); MA: 47.0 vs. 57.0 mm (p=0.02); G: 4.9 vs. 6.7 dyn/cm2 (p=0.02); LY30: 0.00 vs. 0.6% (p=0.20); and LY60: 0.00 vs. 3.0% (p=0.014). The median fibrinogen concentration was significantly higher in the babesiosis group than in the control group; 5.8 g/L (5.0 – 7.0) vs. 2.9 g/L (2.5 – 3.3); (p<0.01). The mean AT activity was significantly lower in the babesiosis group than in the control group; 102.6 mg/dl (89.9 – 112.8) vs. 127.8 mg/dl (110.6 – 134.8); (p<0.01). The median D-dimer concentration was not significantly different in the babesiosis group compared to the control group; 0.3 mg/L (0.1 – 0.4) vs. 0.1 mg/L (0.1 – 0.2); (p=0.016). Median PT was not significantly different in the babesiosis group compared to the control group; 6.5 sec (6.4 – 7.2) vs. 6.8 sec (6.6 – 7.5); (p=0.14). Median aPTT was significantly prolonged in the babesiosis group compared to the control group; 13.6 sec (12.4 – 14.5) vs. 11.5 sec (10.7 – 12.2); (p<0.01). Despite the severe thrombocytopenia, dogs suffering from uncomplicated babesiosis did not have clinical signs of haemorrhage. The thromboelastograms of the babesiosis group were normal to hypercoagulable and thus correlated well with the clinical phenotype. Copyright
Dissertation (MSc)--University of Pretoria, 2011.
Companion Animal Clinical Studies
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Koma, Lee Martin Palia Koli. "Abdominal splanchnic haemodynamics in a canine normovolaemic anaemia model and uncomplicated canine babesiosis a comparative doppler study /." Thesis, University of Pretoria, 2005. http://upetd.up.ac.za/thesis/available/etd-03062006-101906/.

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Lobetti, Remo Giuseppe. "The pathophysiology of renal and cardiac changes in canine babesiosis." Pretoria : [s.n.], 2009. http://upetd.up.ac.za/thesis/available/etd-08192008-085936/.

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Lobetti, R. G. (Remo Giuseppe). "The pathophysiology of renal and cardiac changes in canine babesiosis." Thesis, University of Pretoria, 2005. http://hdl.handle.net/2263/27378.

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This thesis showed that dogs with natural infection with B. canis had both renal and cardiac dysfunction, both of which can be classified as complications of babesiosis and would thus necessitate supportive therapy. This thesis demonstrated that RTE celluria, proteinuria, and variable enzymuria and azotaemia occur in dogs with babesiosis. However, these were all minimal changes and all could be consistent with hypoxia, reduced GFR, or reduced cardiac output This thesis showed that dogs with naturally occurring babesiosis had significant urine met-haemoglobin with no evidence of blood met-haemoglobin. The possibility would be that the urinary methaemoglobin was either produced in the kidney or possibly by oxidation of haemoglobin to met-haemoglobin in the bladder. It has been shown experimentally that met-haemoglobin can be toxic. The combination of reduced GFR, anaemic hypoxia, and met-haemoglobin can all act synergistically to cause renal damage. Renal haemodynamics are also much more likely to be abnormal when cardiac dysfunction is present Reduced renal blood flow and glomerular filtration rate are evidence of redistribution of blood flow that commonly occurs in early heart failure. An important finding in this thesis was that dogs with babesiosis had lower serum sodium than control dogs but there was no difference between mild, severe, or complicated cases of babesiosis. In addition, dogs with babesiosis had a lower fractional clearance of sodium than Clinically healthy control dogs, which can be interpreted as sodium retention by the kidneys. This sodium retention would also result in water retention , which will result in an expansion of the plasma volume. In the past heart lesions in canine babesiosis were regarded as rare complications, with the majority of lesions being reported as incidental findings at post-mortem examination of complicated babesiosis cases. This thesis has demonstrated that cardiac lesions to be common in canine babesiosis. This thesis showed that that ECG changes in babesiosis were similar to the pattern described for myocarditis and myocardial ischaemia, 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 hypoxia. As the clinical application of the ECG changes found in this thesis was limited, cardiovascular assessment should be based on functional monitoring rather than ECG. Using cardiac troponin as a marker of myocardial injury, this thesis showed that myocardial cell injury occurs with canine babesiosis. Cardiac troponins, especially troponin I, are sensitive markers of myocardial injury in canine babesiosis, and the magnitude of elevation of plasma troponin I concentrations appears to be proportional to the severity of the disease. ECG changes and serum cardiac troponin were correlated with histopathology. On cardiac histopathology from dogs that succumbed to babesiosis, haemorrhage, necrosis, inflammation and fibrin microthrombi in the myocardium were documented, all of which would have resulted in ECG changes and elevations in cardiac troponin. Myocardial infarction causes left ventricular failure, which will result in hypotension and an expansion of the plasma volume due to homeostatic mechanisms. This thesis showed that dogs with babesiosis had hypoalbuminaemia, which may be because of intravascular volume dilution due to fluid retention. In disease hypoalbuminaemia can occur as a negative acute-phase protein. In the light of the cardiac changes, hyponatraemia, and hypotension, a probable cause would be fluid retention due to myocardial disease. This thesis showed that dogs with babesiosis had left ventricular lesions, which can result in systolic heart failure.
Thesis (PhD)--University of Pretoria, 2005.
Veterinary Tropical Diseases
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Book chapters on the topic "Canine babesiosis"

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Gabrys, Beata, John L. Capinera, Jesusa C. Legaspi, Benjamin C. Legaspi, Lewis S. Long, John L. Capinera, Jamie Ellis, et al. "Canine Babesiosis." In Encyclopedia of Entomology, 710. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6359-6_476.

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Kuleš, Josipa, Vladimir Mrljak, Renata Barić Rafaj, Jelena Selanec, Richard Burchmore, and Peter D. Eckersall. "A proteomic analysis of canine serum during the course of babesiosis." In Farm animal proteomics 2013, 135–38. Wageningen: Wageningen Academic Publishers, 2013. http://dx.doi.org/10.3920/978-90-8686-776-9_36.

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Birkenheuer, Adam J. "Babesiosis." In Canine and Feline Infectious Diseases, 727–38. Elsevier, 2014. http://dx.doi.org/10.1016/b978-1-4377-0795-3.00075-2.

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Vishwakarma, Poonam, and M. K. Nandini. "Overview of Canine Babesiosis." In Veterinary Medicine and Pharmaceuticals. IntechOpen, 2020. http://dx.doi.org/10.5772/intechopen.82243.

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Irwin, Peter. "Babesiosis and cytauxzoonosis." In BSAVA Manual of Canine and Feline Haematology and Transfusion Medicine, 74–80. British Small Animal Veterinary Association, 2012. http://dx.doi.org/10.22233/9781905319732.8.

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Yves, Moreau, Martinod Serge, and Fayet Georg. "Epidemiologic And Immunoprophylactic Aspects Of Canine Babesiosis In France." In Babesiosis of Domestic Animals and Man, 191–96. CRC Press, 2018. http://dx.doi.org/10.1201/9781351070027-11.

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Conference papers on the topic "Canine babesiosis"

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Bilokur, Diana, and Victoria Gryshchenko. "AMINOTRANSFERASE ACTIVITY OF BLOOD PLASMA IN CANINE BABESIOSIS." In DÉBATS SCIENTIFIQUES ET ORIENTATIONS PROSPECTIVES DU DÉVELOPPEMENT SCIENTIFIQUE. European Scientific Platform, 2021. http://dx.doi.org/10.36074/logos-05.02.2021.v3.01.

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Degregori, Bruna, Geane Consorte, and Fernando Zorzi. "HEMOPARASITOSE EM UMA CANINA- RELATO DE CASO." In I Congresso On-line Nacional de Clínica Veterinária de Pequenos Animais. Revista Multidisciplinar em Saúde, 2021. http://dx.doi.org/10.51161/rems/1888.

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Introdução: A hemoparasitose é uma patologia de alta casuística na rotina clínica veterinária, desencadeada por bactérias, protozoários, helmintos, possuindo como principal transmissor o carrapato em períodos do ano de maior incidência de calor e umidade, tendo em vista o potencial zoonótico. A babesiose é causada pelos protozoários Babesia Canis e Babesia gibsoni transmitida pelo carrapato Rhipicephalus sanguineus, esses parasitas causam a hemólise das hemácias. Já a anaplasmose é oriunda de bactérias intracelulares Anaplasma platys ou Anaplasma phagocytophilum transmitidas pelo carrapato Rhipicephalus sanguineus, causando trombocitopenia. A rangeliose é ocasionada por um piroplasma Rangelia vitalli, transmitida por carrapatos Rhipicephalus sanguineus e Amblyomma aerolatum, se replicando nos eritrócitos. Objetivo: Relatar um caso clínico de uma canina. Relato de caso: canina castrada, sem raça definida, com 1 ano e dois meses, pesando 11,4 Kg, sendo atendida em uma clínica veterinária particular em Caxias do Sul/RS, apresentando apatia, hematoquezia, anorexia, prostração, epistaxe, sangramento em pontas de orelhas, mucosas hipocoradas com petéquias e febre. Durante o atendimento foi realizada coleta sanguínea para avaliação hematológica, esfregaço sanguíneo periférico da orelha, bioquímica sérica (creatinina, fosfatase alcalina, ureia, transaminase pirúvica) e urinálise, apresentando alterações, tais como anemia regenerativa, leucocitose por neutrofilia com desvio a esquerda, linfocitose, trombocitopenia, na urinálise houve presença de hemoglobina, leucócitos, proteinúria. No exame de esfregaço de sangue periférico apresentou-se negativo para hemoparasitas. O diagnóstico definitivo foi através da Reação em Cadeia da Polimerase (PCR), na qual evidenciou os agentes patogênicos de babesiose, rangeliose e anaplasmose. O tratamento instituído foi doxiciclina (5 mg/kg/q.12h durante 28 dias), azitromicina (10 mg/Kg/q.24h durante 10 dias), diaceturato de diminazeno (0,5ml/2Kg) repetindo em 14 dias a dose com prévia aplicação de atropina (0,044 mg/Kg), suplemento vitamínico mineral aminoácido (1 ml/q.24h). O animal se manteve bem clinicamente durante o tratamento, obtendo cura da enfermidade. Conclusão: Mesmo com o diagnóstico negativo de esfregaço sanguíneo periférico, com a suspeita clínica do animal foi solicitado PCR para confirmar a patologia, assim foi de suma importância a pesquisa de hemoparasitas pelos sinais clínicos do canino, juntamente do tratamento precoce e assertivo.
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