Effects of ketamine, xylazine, and a combination of ketamine and xylazine were studied in 12 male Pekin ducks (7 to 12 weeks old; mean [+/- SD] body weight, 3.1 +/- 0.3 kg). After venous and arterial catheterization and fixation of a temperature probe in the cloaca, each awake duck was confined, but not restrained, in an open box in a dimly lit room. Blood pressure and lead-II ECG were recorded. Three arterial blood samples were collected every 15 minutes over a 45-minute period (control period) and were analyzed for pHa, Paco2 and Pao2. After the control period, each duck was assigned at random to 1 of 3 drug groups: (1) ketamine (KET; 20 mg/kg of body weight, IV), (2) xylazine (XYL; 1 mg/kg, IV), and (3) KET + XYL (KET 20 mg/kg and XYL, 1 mg/kg; IV). Measurements were made at 1, 5, 10, 15, 30, 45, 60, and 90 minutes after drug administration. All ducks survived the drug study. Cloacal temperature was significantly (P less than or equal to 0.05) increased above control cloacal temperature at 90 minutes after the administration of ketamine, and from 10 through 90 minutes after administration of ketamine plus xylazine. In ducks of the KET group, pHa, Paco2, and Pao2, remained unchanged after administration of the drug. In ducks of the XYL group, pHa and Pao2 decreased significantly (P less than or equal to 0.05) from control values for all time points up to and including 15 minutes after drug administration. In ducks of the KET + XYL group, pHa and Pa02 were significantly (P less than or equal to 0.05) decreased at all time points up to and including 45 and 15 minutes, respectively, after administration of the drugs. In ducks of the XYL group, Paco2 increased significantly (P less than 0.05) during the first 15 min. after drug administration, and for 45 min. after administration of KET + XYL. Results indicated that ketamine when given alone to ducks, was not associated with pulmonary depression.

A total of 65 Pasteurella multocida were isolated and identified from various animal’s samples received by Veterinary Research Institute (VRI) during the period of 2014 to 2016. These animals comprises of cattle, goat, pig, chicken, duck and rabbit. The serogroup of Pasteurella multocida were carried out using designation system of Carter’s capsular typing and molecular serogrouping method. Based on cases submitted to VRI, the prevalence of pasteurellosis in Malaysia ranging from 1.0% to 3.2% (2014 to 2016). It is low compared to previous reports and the pattern of predominant serogroups and animal hosts were found to be changing every year. In 2014, 80% (12/15) of the isolates were Pasteurella multocida Carter’s type D where all were isolated from goats. In 2015, the predominant serogroup changed to Pasteurella multocida Carter’s type A with a prevalence rate of 40.6% (13/32) which were mostly isolated from duck and cattle. While for Pasteurella multocida Carter’s type D, the prevalence in 2015 reduced to 21.9% (7/32) compared to the previous year and it was isolated from various animal species. Interestingly, in 2015 there was one isolate of Pasteurella multocida Carter’s type B isolated from goat with no reported history of outbreak. In 2016, the prevalence of Pasteurella multocida Carter’s type A increased to 72.2% (13/18), with a high percentage (92.3%) infection in young calves showing clinical signs with high mortality and morbidity in infected farms. Furthermore, during these 3 years of study, 3 isolates of Pasteurella multocida serogroup F were also identified each from pig, goat and chicken, respectively. In conclusion, this study revealed that pasteurellosis had become sporadic in Malaysia and the distribution of serogroups were diverse in all species of animal with no definitive host.

Effects of ketamine, xylazine, and a combination of ketamine and xylazine were studied in 12 male Pekin ducks (7 to 12 weeks old; mean [+/- SD] body weight, 3.1 +/- 0.3 kg). After venous and arterial catheterization and fixation of a temperature probe in the cloaca, each awake duck was confined, but not restrained, in an open box in a dimly lit room. Blood pressure and lead-II ECG were recorded. Three arterial blood samples were collected every 15 minutes over a 45-minute period (control period) and were analyzed for pHa, Paco2 and Pao2. After the control period, each duck was assigned at random to 1 of 3 drug groups: (1) ketamine (KET; 20 mg/kg of body weight, IV), (2) xylazine (XYL; 1 mg/kg, IV), and (3) KET + XYL (KET 20 mg/kg and XYL, 1 mg/kg; IV). Measurements were made at 1, 5, 10, 15, 30, 45, 60, and 90 minutes after drug administration. All ducks survived the drug study. Cloacal temperature was significantly (P less than or equal to 0.05) increased above control cloacal temperature at 90 minutes after the administration of ketamine, and from 10 through 90 minutes after administration of ketamine plus xylazine. In ducks of the KET group, pHa, Paco2, and Pao2, remained unchanged after administration of the drug. In ducks of the XYL group, pHa and Pao2 decreased significantly (P less than or equal to 0.05) from control values for all time points up to and including 15 minutes after drug administration. In ducks of the KET + XYL group, pHa and Pa02 were significantly (P less than or equal to 0.05) decreased at all time points up to and including 45 and 15 minutes, respectively, after administration of the drugs. In ducks of the XYL group, Paco2 increased significantly (P less than 0.05) during the first 15 minutes after drug administration, and for 45 minutes after administration of KET + XYL. Results indicated that ketamine when given alone to ducks, was not associated with pulmonary depression. There was drug-associated respiratory depression after IV administration of XYL or KET + XYL.

The aim of study is provide basic data about the histological features of the liver of local Iraqi ducks and to study the glycogen content in the cytoplasm of the hepatocyte. The anatomical examination showed that liver laid cranial part of the abdominal cavity caudally and ventrally to the heart and associated to the gizzard. The liver of Mallard is divided into two undivided lobes right and left lobes (the right lobe is larger than left lobe). Histological examination revealed that the liver consist of several lobules separated from each other by thin trabeculae of connective tissue extend from delicate capsule that enclosed the liver. The basic unit of the parenchyma of liver is hepatocyte which arranged in plates or cords like that radiated around the central vein and between these cords there is sinusoids lined by alayer of fenestrated endothelial cells and Kupffer's cells. In the boundary of each lobule showed portal area which consist of hepatic artery; hepatic vein and bile duct lining by cuboidal cells. The histochemical study showed formed differ size of glycogen granules in cytoplasm of hepatocytes and in some speciment the glycogen large granules arranged around the central vein because the bird in starvation period .the liver of Mallard generally is closely similar to the liver of another avian birds and vertebrates

Furazolidone cardiotoxicosis was induced in 2 groups (FZ and FZ-CR groups) of newly hatched male Pekin ducklings (100/group) by feeding a ration containing 650 mg of furazolidone/kg of feed (ppm) for 28 days. A third group (control ration, CR group; n = 100) was fed the same ration without furazolidone. On day 28, the control ration was initiated for the FZ-CR group initially given the furazolidone-containing ration, to allow recovery from the effects of the drug, whereas ducklings of the FZ group continued to consume the furazolidone-containing ration. Biweekly, beginning with week 4, ducklings were euthanatized to assess severity of gross lesions and to obtain sections of myocardium for histologic and ultrastructural examination. Clinical evidence (increased weight gain, increased feed consumption, decreased mortality, reduced prevalence of palpable ascites) of regression of cardiotoxicosis of ducklings of the FZ-CR group was nearly complete by day 56 (28 days after cessation of furazolidone intake). Likewise, regression of gross lesions, as measured by overall prevalence of gross lesions, left ventricular volume, and ascites prevalence and severity, were also essentially complete by day 56. Myofibrillar lysis was not seen in sections from the heart (examined ultrastructurally) obtained from ducklings of the CR group that were euthanatized on day 28, 56, or 98. Myofibrillar lysis was detected in all ducklings (4/4) fed furazolidone (FZ and FZ-CR groups) and euthanatized on day 28. Myofibrillar lysis was not seen in the heart of ducklings of the FZ-CR group that were euthanatized on day 56 or 98. Myofibrillar lysis was detected in the heart from all ducklings of the FZ group that were euthanatized on day 56. Leptomeres were observed in cardiac myocytes of ducklings that had been fed furazolidone, but not in those fed only the control ration. Our clinical, gross pathologic, and ultrastructural findings indicate that regression of the cardiac lesions of furazolidone toxicosis may be essentially complete by 28 days after cessation of furazolidone intake. Our ultrastructural findings indicate that furazolidone consumption may result in cardiac dilatation by altering myofibrillar/cytoskeletal attachments of myocytes.