Characterization of turkey coronavirus from turkey poults with acute enteritis.

The present study was to characterize turkey coronavirus associated with turkey poult enteritis and mortality. Intestinal contents or intestines from affected turkey poults and inoculated turkey embryos contained coronaviruses as revealed by electron microscopy or were positive for turkey coronavirus by immunofluorescent antibody assay. Sucrose density gradient ultracentrifugation of the virus-containing intestinal homogenate yielded two opalescent bands corresponding to the buoyant densities of 1.14-1.15 and 1.18-1.20 g/ml, respectively. Coronaviral particles from intestinal contents or the sucrose density gradient preparation were mainly spherical in shape and had envelope and central depression. They were surrounded by a fringe of regularly spaced petal-shaped projections attached to the particles by a short stalk. Purified viruses hemagglutinated rabbit erythrocytes with a titer of 16. Major protein bands of purified viruses analyzed by SDS-PAGE were located at 200, 100-110, 50-60, and 30-35 kDa. The patterns of protein bands were consistent with those of Minnesota or Quebec turkey coronavirus isolates. A 568 bp nucleotide fragment of turkey coronavirus spike protein gene was amplified from RNA of inoculated turkey embryo intestine or purified virus. Sequence analysis of the 568 bp PCR product revealed high degree of identity with the corresponding spike protein gene sequence of human and bovine coronaviruses. The results indicated that turkey coronavirus was associated with turkey poults with acute enteritis.     

Elimination of sulfamethazine residues from swine.

Tissue concentrations of sulfamethazine in swine fed the drug at the rate of 500 g/ton of ration (550 g/1,000 kg) for a 30-day period depleted to 0.1 ppm or less within 4 to 10 days after withdrawal of medicated feed. Depletion from the tissues and plasma of treated pigs showed a linear relationship with time when the concentrations were plotted on a semilogarithmic graph. Six untreated pigs that were placed on bedding in pens formerly occupied by the treated group developed tissue residues at or above 0.1 ppm sulfamethazine; the mean plasma concentration of sulfamethazine reached 2.8 ppm by day 15.     

Poliomyelomalacia, pancreatic necrosis, and cerebellar malacia in turkey poults

Two-to-5-week-old turkey poults from three large Minnesota flocks exhibited ataxia, flaccid paralysis, and up to 5% mortality as unexpected death. The major post-mortem finding was cerebellar hemorrhage and softening detected in 22 of 89 clinically affected poults. Histologic findings were severe focal or multifocal poliomyelomalacia in the lumbosacral intumescentia of the spinal cord, cerebellar malacia, and single-cell or multifocal coagulative necrosis of pancreatic acinar cells. Thirty of 32 clinically affected poults examined had microscopic spinal cord lesions, 12 of 48 had cerebellar lesions, and 26 of 47 had pancreatic lesions. Gross and microscopic cerebellar lesions resembled those of vitamin E deficiency in chicks. Hepatic selenium levels were approximately twice normal expected levels for poults.     

Toxicity of Fusarium moniliforme var. subglutinans for chicks, ducklings, and turkey poults

Corn-based diets contaminated with various concentrations of a moniliformin-producing isolate of Fusarium moniliforme var. subglutinans were found to be lethal for chicks, ducklings, and turkey poults. Ducklings appeared to be the most sensitive to the lethal effects of the toxic feed. Gross lesions were ascites, hydropericardium, and myocardial pallor. Microscopic lesions were limited to the heart and liver, and they consisted of degeneration and necrosis of the myocardium and degeneration of hepatocytes. Cardiotoxicosis was the apparent cause of death.     

Culturing anomalies associated with Mycoplasma recovered from the tissues of chicks and turkey poults experimentally infected with Mycoplasma gallisepticum or Mycoplasma gallinarum.

Tissues of mycoplasma infected chicks and turkey poults were cultured and subcultured on mycoplasma agar. Usually, colonies which grew on the agar initially inoculated could be subcultured, but sometimes they could not. At other times, colonies were not seen on the agar initially inoculated but appeared on the subcultured plate.     

Effect of Bordetella avium infection on electrocardiograms in turkey poults.

Electrocardiograms (ECGs) were recorded from turkey poults infected with the W isolate of Bordetella avium. Strip chart data (amplitudes and intervals) were measured at 7, 14, 21, and 28 days postinoculation and compared with data from uninoculated controls. B. avium infection altered P-, RS-, and T-wave amplitudes, as well as P-R and S-T intervals throughout the 4-week experimental period. Heart rates were similar over the 4-week period in control poults, while rates in the infected birds were variable. Alterations in ECGs associated with B. avium infection appeared to be the result of disturbances in the cardiovascular system and may be associated with the pathogenicity of the organism in turkey coryza.     

磺胺二甲嘧啶在黑鲪体内的药物代谢动力学和残留消除研究

在(14±1)℃水温条件下,对黑鲪单次口灌100 mg/kg体重的磺胺二甲嘧啶,进行药物代谢动力学研究。在(20±2)℃水温条件下,按照《中华人民共和国水产行业标准磺胺类药物水产养殖使用规范》推荐剂量对黑鮶连续5天口灌给予磺胺二甲嘧啶,研究其在黑鮶体内的残留消除规律。血浆、肌肉和肝脏样品采用高效液相色谱检测,DAS2.0药物代谢动力学软件对数据进行处理分析。结果表明磺胺二甲嘧啶在黑鲪血浆、肌肉和肝脏中均符合一室模型,肝脏、血液和肌肉中药物达峰时间分别为6 h,8 h和10 h;峰值浓度分别为26.45μg/g、25.57μg/g和31.15μg/g;连续多次给药后,黑鮶血液、肌肉、肝脏中药物浓度分别在给药后12d、14d、15d后小于最大残留限量要求(0.1mg/kg)。     

Protection of turkey poults from Bordetella avium infection and disease by pili and bacterins

The role of pili in protection against Bordetella avium infection in turkey poults was studied. An isolate that produced the largest number of pili under growth conditions developed in our laboratory was used for preparation of pili and bacterin and for challenge. The pili were isolated, purified, examined by electron microscopy, and tested for purity by gel electrophoresis. Poults were vaccinated with oil-adjuvant pili, formaldehyde- or merthiolate-inactivated bacterins, or a commercial bacterin. Poults were vaccinated once or twice subcutaneously at different ages and challenged intranasally with a pathogenic B. avium isolate 5 days following the last vaccination. A few vaccinated birds had very mild clinical signs. B. avium was isolated from the sinuses of a few vaccinated birds, and growth was scanty. The mean colony counts from tracheal sections was significantly higher (P less than 0.1) in unvaccinated challenged poults than in vaccinated challenged poults. It is postulated that B. avium pili are important immunogens in turkey poults.     

The toxic effects of saline drinking water on young turkey poults.

Turkey poults were offered ad libitum a diet containing 2.5 g salt/kg and tap water containing, 0, 90 or 105 mn NaCl to drink from 1 to 12 d of age. 2. High mortality with oedbema and ascites occurred mainly from 5 to 8 d in poults given the saline solutions. Mortality seemed to be related to salt and water intakes. 3. Plasma and body composition indicated abnormal retention of salt and water in poults younger than 12 d of age offered hypotonic saline. 4. In a second experiment using the same diet poults were offered hypotonic saline (105 mn NaCl in tap water) from 5, 9 or 13 d of age. High mortality with oedema and ascites was only observed when saline was given from 5 or 9 d. 5. The results suggest that from about 5 to 10 d of age there is a relative functional renal insufficiency which causes susceptibility to the toxic effects of saline water.     

In vitro cellular migration of leukocytes from turkey poults infected with Alcaligenes faecalis

The ability of peripheral blood leukocytes from young turkey poults to migrate in vitro was investigated. Migration from capillary tubes was relatively rapid and was usually complete in 2 hours. Leukocyte migration was significantly enhanced in Alcaligenes faecalis-infected turkeys compared with uninfected controls at 1, 2, 5, and 6 weeks of age.     

Tolerance of young turkey poults to various combinations of dietary furazolidone and salt.

Three feeding trials were conducted to study the tolerance of young turkey poults to furazolidone and to various combinations of salt and furazolidone in the diet. Poults of mixed sexes tolerated up to 0.03% dietary furazolidone from hatch to six weeks of age without harmful effects as judged from the data on mortality rate, feed intake, body weight and plasma composition. High mortality with cardiac dilation and ascites occurred in poults fed the same basal diet containing 0.05 or 0.07% furazolidone. Mortality was positively related to levels of dietary furazolidone, and occurred mainly between two and four weeks of age. The cumulative feed intake and body weight of these poults were significantly lower than those of the control poults at six weeks of age. There was indication of decreased renal function in poults on high furazolidone intake and the mechanism of furazolidone-induced cardiac dilation is discussed. Mortality rate, incidence of cardiac dilation with ascites and heart, liver and body weights and feed efficiency were similar in poults fed diets containing 0.022% furazolidone and varying levels of salts (0.5, 1.0 or 1.5%) compared with the control fed the same basal diet containing 0.5% salt from hatch to eight weeks of age. It is concluded that a starter diet containing 0.022% furazolidone and up to 1.5% salt does not affect the performance of poults from hatch to eight weeks of age.     

Isolation of a reovirus from poult enteritis and mortality syndrome and its pathogenicity in turkey poults

Poult enteritis and mortality syndrome (PEMS) is an acute, infectious intestinal disease of turkey poults, characterized by high mortality and 100% morbidity, that decimated the turkey industry in the mid-1990s. The etiology of PEMS is not completely understood. This report describes the testing of various filtrates of fecal material from control and PEMS-affected poults by oral inoculation into poults under experimental conditions, the subsequent isolation of a reovirus, ARV-CU98, from one of the PEMS fecal filtrates, and in vivo and in vitro studies conducted to determine the pathogenicity of ARV-CU98 in turkey poults. In order to identify a filtrate fraction of fecal material containing a putative etiologic agent, poults were challenged in two independent experiments with 220- and 100-nm filtrates of fecal material from PEMS-negative and PEMS-positive poults. The 100-nm filtrate was chosen for further evaluation because poults inoculated with this filtrate exhibited mortality and significantly lower (P < or = 0.05) body weight and relative bursa weight, three clinical signs associated with PEMS. These results were confirmed in a third experiment with 100-nm fecal filtrates from a separate batch of PEMS fecal material. In Experiment 3, body weight and relative bursa and thymus weights were significantly lower (P < or = 0.05) in poults inoculated with 100-nm filtrate of PEMS fecal material as compared with poults inoculated with 100-nm filtrate of control fecal material. Subsequently, a virus was isolated from the 100-nm PEMS fecal filtrate and propagated in liver cells. This virus was identified as a reovirus on the basis of cross-reaction with antisera against avian reovirus (FDO strain) as well as by electrophoretic analysis and was designated ARV-CU98. When inoculated orally into poults reared under controlled environmental conditions in isolators, ARV-CU98 was associated with a higher incidence of thymic hemorrhaging and gaseous intestines. In addition, relative bursa and liver weights were significantly lower (P < or = 0.05) in virus-inoculated poults as compared with controls. Virus was successfully reisolated from virus-challenged poults but not from control birds. Furthermore, viral antigen was detected by immunofluorescence in liver sections from virus-challenged poults at 3 and 6 days postinfection and virus was isolated from liver at 6 days postinfection, suggesting that ARV-CU98 replicates in the liver. In addition to a decrease in liver weight, there was a functional degeneration as indicated by altered plasma alanine aminotransferase and aspartate aminotransferase activities in virus poults as compared with controls. Although this reovirus does not induce fulminating PEMS, our results demonstrated that ARV-CU98 does cause some of the clinical signs in PEMS, including intestinal alterations and significantly lower relative bursa and liver weights. ARV-CU98 may contribute directly to PEMS by affecting the intestine, bursa, and liver and may contribute indirectly by increasing susceptibility to opportunistic pathogens that facilitate development of clinical PEMS.