Viktor Szatmári

Epidemiology: Prevalence of intestinal parasites in dogs in some urban and rural areas of Hungary

Summary A total of 490 canine faecal specimens collected in the eastern and northern regions of Hungary were examined for helminth eggs. From the results it appears that more than 50% of the dogs were infected with at least one parasite species. The prevalence of eggs (%) in the two regions was as follows: Toxocara canis (24.3–30.1); Trichuris vulpis (20.4–23.3); Ancylostomatidae (8.1–13.1); Capillaria spp. (0–7.3); Toxascaris leonina (2.1–0); Taeniaaninum type (2.8–2.4); Dipylidium caninum (0.4–1); coccidia (3.5–3.4). Of the positive dogs 8.5–18.1% harboured two or more species of parasites. The prevalence of parasitic infection was also evaluated ccording to the maintenance, feeding, and age of the animals. The significance of zoonotic diseases (echin coccosis, toxocarosis, ancylostomatidosis) caused by intestinal helminths makes it necessary to know the infection status of domestic dogs and to take measures for control.

WSAVA Standards for Clinical and Histological Diagnosis of Canine and Feline Liver Diseases

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Effect of Pimobendan in Dogs with Preclinical Myxomatous Mitral Valve Disease and Cardiomegaly: The EPIC Study—A Randomized Clinical Trial

Background Pimobendan is effective in treatment of dogs with congestive heart failure (CHF) secondary to myxomatous mitral valve disease (MMVD). Its effect on dogs before the onset of CHF is unknown. Hypothesis/Objectives Administration of pimobendan (0.4–0.6 mg/kg/d in divided doses) to dogs with increased heart size secondary to preclinical MMVD, not receiving other cardiovascular medications, will delay the onset of signs of CHF, cardiac‐related death, or euthanasia. Animals 360 client‐owned dogs with MMVD with left atrial‐to‐aortic ratio ≥1.6, normalized left ventricular internal diameter in diastole ≥1.7, and vertebral heart sum >10.5. Methods Prospective, randomized, placebo‐controlled, blinded, multicenter clinical trial. Primary outcome variable was time to a composite of the onset of CHF, cardiac‐related death, or euthanasia. Results Median time to primary endpoint was 1228 days (95% CI: 856–NA) in the pimobendan group and 766 days (95% CI: 667–875) in the placebo group (P = .0038). Hazard ratio for the pimobendan group was 0.64 (95% CI: 0.47–0.87) compared with the placebo group. The benefit persisted after adjustment for other variables. Adverse events were not different between treatment groups. Dogs in the pimobendan group lived longer (median survival time was 1059 days (95% CI: 952–NA) in the pimobendan group and 902 days (95% CI: 747–1061) in the placebo group) (P = .012). Conclusions and Clinical Importance Administration of pimobendan to dogs with MMVD and echocardiographic and radiographic evidence of cardiomegaly results in prolongation of preclinical period and is safe and well tolerated. Prolongation of preclinical period by approximately 15 months represents substantial clinical benefit.

Reversible pulmonary hypertension associated with lungworm infection in a young cat

Two ten-week-old kittens presented with dyspnea. Two weeks later dyspnea had worsened and both kittens had developed a heart murmur. One kitten died and necropsy showed severe granulomatous pneumonia and moderate bronchi(oli)tis and peribronchi(oli)tis caused by Aelurostrongylus abstrusus. The results from echocardiography, thoracic radiography and the other kittens fecal examination were interpreted as severe parasitic pneumonia caused by A. abstrusus infection with pulmonary hypertension. Repeated administration of milbemycine-oxime and praziquantel resulted in cessation of larvae shedding and resolution of clinical, radiographic and echocardiographic signs of bronchopneumonia and pulmonary hypertension.

Ultrasonographic evaluation of partially attenuated congenital extrahepatic portosystemic shunts in 14 dogs

Doppler ultrasonography was used to evaluate the portal vein in 14 dogs before, immediately after and four weeks after a partial ligation of a congenital extrahepatic portocaval shunt. By four weeks after the operation, the hepatofugal or zero flow in the portal vein segment cranial to the shunt origin had become a hepatopetal flow in 13 of the dogs, which became clinically healthy. The other dog continued to have a hepatofugal flow in the portal vein cranial to the origin of the shunt and continued to show clinical signs of hepatic encephalopathy. The shunt remained functional in six of the dogs, and three of them developed portosystemic collaterals in addition. In the other eight dogs the patent shunt was non-functional, because a hepatopetal flow was detected in the shunt adjacent to the portal vein. This flow was the result of the splenic vein entering the shunt, and the splenic blood dividing; some flowed via the shunt towards the portal vein, preventing the portal blood from shunting, and the rest flowed via the attenuated shunt segment to the caudal vena cava. Shunting of the splenic venous blood was clinically insignificant.

Doppler-ultrasonographic detection of retrograde pulsatile flow in the caudal vena cava of a puppy with cor triatriatum dexter.

A three-month-old puppy had ascites, but its heart was normal by auscultation. Abdominal ultrasonography revealed an enlarged liver, distended hepatic veins and a distended caudal vena cava. Doppler ultrasonography detected retrograde flow in the caudal vena cava and abnormally pulsatile flow in the hepatic veins and caudal vena cava. A non-selective venogram was used to detect the path of the blood from the caudal vena cava. A postmortem examination showed that the puppy had cor triatriatum dexter and a defect in the atrial septum.

Portal hypertension in a dog due to circumscribed fibrosis of the wall of the extrahepatic portal vein

A two-and-a-half-year-old German shepherd dog with ascites and a high concentration of blood ammonia was investigated. Sonographically, its liver was normal but the portal vein was dilated and the flow of blood within it was slow. A liver biopsy showed that the liver was normal, and did not reveal any possible cause of portal hypertension or ascites. Postmortem, the cranial part of the portal vein was dilated with a crossstriped internal surface, but the caudal part looked normal; there was a stenotic ring between the normal and dilated parts. Histology of the dilated segment revealed marked hypertrophy of both the internal circular and the external longitudinal smooth muscle layers. At the site of the stenosis, the longitudinal muscular layer was replaced by connective tissue. Circumscribed fibrosis in the wall of the portal vein was responsible for the stenosis and the subsequent prehepatic portal hypertension. The cross-striped pattern in the dilated part of the vein was the result of hypertrophy of the inner circular smooth muscle layer.

Juxtaductal coarctation of both pulmonary arteries in a cat

A 4-year-old, male, neutered cat was referred because of recurrent episodes of dyspnea. Physical examination revealed a harsh systolic murmur, with the point of maximal intensity in the left heart base, with an intensity of 4 out of 6. Echocardiographic diagnosis was severe supravalvular pulmonary artery stenosis. A selective right ventricular angiocardiogram showed an absence of arterial blood flow to the left lung lobes. A balloon dilatation of the localized stenosis of the right pulmonary artery was attempted with cardiac catheterization. However, when the catheter was passed through the stenosis, the blood flow to the lungs temporarily completely ceased, which led to death. Postmortem examination revealed a circumscribed stenosis of both pulmonary arteries at the site of the bifurcation, where the ligamentum arteriosum was attached. Histopathology showed that the localized ridge-like stenosis at the pulmonary artery bifurcation was caused by connective tissue. The suspected cause of this congenital anomaly is the presence of ectopic ductal tissue in the wall of the pulmonary artery. When the ductus arteriosus closes at birth, pulmonary artery stenosis developed because of constriction of the ectopic ductal tissue.

Innocent Cardiac Murmur in Puppies: Prevalence, Correlation with Hematocrit, and Auscultation Characteristics

Background The aims of this study were to establish the prevalence of innocent cardiac murmurs in clinically healthy puppies, to investigate a possible correlation between the presence of an innocent murmur and hematocrit, and to describe the auscultation characteristics of innocent murmurs. Hypothesis Lower hematocrit contributes to the genesis of innocent murmurs. Animals Five hundred and eighty‐four client‐owned clinically healthy puppies, between 20 and 108 days old. Methods Two cross‐sectional surveys with a 1‐year (n = 389 pups) pilot and a half‐year (n = 195 pups) principal study periods. Cardiac auscultation was performed by a single, board‐certified cardiologist. Hematocrit was measured with an automatized hematology analyzer. Echocardiography was performed only on puppies with a cardiac murmur in the principal study. Results In the pilot study, 15% of the dogs had a murmur. Innocent murmur was diagnosed in 28% of the 195 dogs in the principal study. Innocent murmurs were systolic, mostly with a musical character and with a maximal intensity of 2 of 6, and mostly with the point of maximal intensity in the left cardiac base. The hematocrit was significantly lower in the group with a murmur compared to the group without (P = .023). Conclusions and Clinical Importance Innocent murmur was a common finding in puppies at the age when the first veterinary controls usually take place. Physiologic anemia contributes to the genesis of innocent murmurs in puppies. Rising hematocrit in growing puppies can explain the spontaneous disappearance of innocent murmurs with aging. Hematocrit did not differentiate innocent murmurs from abnormal murmurs.

Pulmonary alveolar proteinosis in a cat

BackgroundPulmonary alveolar proteinosis is an extremely rare lung disease in animals and humans. It is characterized by the deposition of a large amount of phospholipoproteinaceous material in the alveoli. There are several possible etiologies, both congenital and acquired. Alveolar macrophages play an important role in the clearance of surfactant. This is the first report of pulmonary alveolar proteinosis in the feline species.Case presentationPulmonary alveolar proteinosis was diagnosed in an 8-month-old cat with chronic tachypnea, failure to thrive and finally respiratory distress. The diagnosis was based on the milky appearance of the bronchoalveolar lavage fluid taken under general anesthesia after bronchoscopy. Because of the worsening respiratory distress and development of anorexia the kitten was euthanized. Histopathology of the lungs showed alveoli and bronchi filled with eosinophilic material. Electron microscopy revealed lamellated intra-alveolar bodies. As the granulocyte-macrophage colony-stimulating factor was elevated in the serum and no autoantibodies against granulocyte-macrophage colony-stimulating factor were detected, a primary hereditary pulmonary alveolar proteinosis was suspected. The underlying cause was thought to be a dysfunction of the receptor of the granulocyte-macrophage colony-stimulating factor, however, a mutation in the genes encoding the alpha and beta chains of this receptor has not been found.ConclusionThis is the first description of pulmonary alveolar protienosis in a cat. This kitten is thought to have a primary hereditary pulmonary alveolar proteinosis with a possible defect in the signalling pathway of the receptor of the granulocyte-macrophage colony-stimulating factor. The imaging and pathologic findings are similar to those of humans.