Early clinical and morphologic alterations in the pathogenesis of furazolidone-induced toxicosis in ducklings

Clinical and pathologic alterations during the development of furazolidone-induced toxicosis were investigated in a group of 35 newly hatched male Pekin ducklings fed a ration containing 700 mg of furazolidone/kg of feed for 27 days. A control group (n = 25) was fed the same ration without added furazolidone. Every 3 days, ducklings were weighted and palpated for ascites and 3 were chosen at random for euthanasia to determine the severity of lesions and to obtain hearts for gross measurements and ultrastructural study. Clinical alterations in treated ducklings consisted of decreased feed consumption with lower weight gain and nervous signs. Gross pathologic alterations included cardiomegaly with dilatation of all chambers and thinning of the myocardium, pericardial effusion, pulmonary edema and congestion, ascites, and testicular enlargement. Gross lesions were not observed before day 8. The earliest lesion (day 9) was cardiac chamber dilatation, with the left ventricle and left atrium most commonly and most severely dilated. Hearts from ducklings euthanatized on days 6, 12, 18, 24, and 27 were examined ultrastructurally. Myofibrillar lysis was first observed on day 12 in 1 duckling (of 3) and in at least 1 duckling from subsequent euthanasia periods. Myofibrillar lysis did not appear to be uniform among the cardiac chambers.     

Serum chemistry alterations, including creatine kinase isoenzymes, in furazolidone toxicosis of ducklings: preliminary findings.

Furazolidone induces a cardiotoxicosis when fed in toxic concentrations to newly hatched ducklings. This preliminary experiment was designed to determine if creatine kinase (CK) isoenzymic activities or other serum analytes would be useful as indicators of these cardiac alterations. Sera from 12 ducklings (six fed a control ration and six fed the control ration with 700 mg furazolidone added per kg of feed [700 ppm] for 28 days) were analyzed for CK isoenzymic activities, electrolytes, nitrogenous metabolites, hepatic enzymic activities, bilirubin, and glucose. Statistically significant differences between control and treated groups were detected for creatine kinase MB (CK-MB, cardiac muscle origin) isoenzymic activity and bilirubin, potassium, calcium, and total carbon dioxide concentrations. Differences other than CK-MB isoenzymic activity were generally explained by factors related to the toxicosis or sample handling. These findings suggest that CK-MB isoenzymic activity may be useful to detect and monitor the progress of cardiac injury in furazolidone toxicosis, thereby increasing the usefulness of this model of dilated cardiomyopathy. Our findings, analyzed on the Kodak Ektachem 700 Dry Chemistry Analyzer, are compared with serum chemistry values reported in the literature.     

Furazolidone-associated cardiomyopathy in two Indiana flocks of ducklings

Furazolidone (FZ)-induced congestive cardiomyopathy was diagnosed as the cause of high mortality and unthriftiness in two flocks of white pekin ducklings. Cumulative mortality at 7 weeks of age was 10.0-14.4%. Samples of FZ-supplemented feeds fed to flocks 1 and 2 from day 1 to day 14 had 140 and 150 mg FZ/kg, respectively. Both flocks had various degrees of water restriction. Clinically, the ducklings had dyspnea, incoordination, and abdominal distention. Necropsy findings included pulmonary edema and congestion, ascites, atrophic congested livers covered with sheets of fibrin, and cardiac enlargement with biventricular dilatation. Cardiac alterations were minimal by light microscopy. Ultrastructurally, scattered myocytes had myofibrillar lysis. These outbreaks occurred following intake of FZ at therapeutic dosages and emphasize the high susceptibility of young ducklings to FZ cardiotoxicity.     

Influence of exogenous T4 on body weight, feed consumption, T4 levels, and myocardial glycogen in furazolidone-fed turkey poults.

Ten turkey poults each were placed in one of four groups: control, thyroxine (T4), furazolidone (FZ), and FZ + T4. Thyroxine (T4), at a concentration of 1 ppm, was included in the ration of poults fed T4 and FZ + T4, and furazolidone (FZ), at a concentration of 700 ppm, was included in the ration of poults fed FZ and FZ + T4 from 2 to 5 weeks of age. Levels of plasma T4 decreased significantly (P less than or equal to 0.05) between 2 and 5 weeks in control and FZ poults. At 5 weeks, plasma T4 levels were significantly (P less than or equal to 0.05) lower in FZ poults than in control poults and significantly (P less than or equal to 0.05) lower in the FZ + T4 poults than in the T4 poults. Exogenous administration of T4 had no effect on development of the round heart syndrome or on body weight, but significantly increased feed consumption in FZ-fed poults during weeks 4 (P less than or equal to 0.05) and 5 (P less than or equal to 0.01). Inclusion of T4 in the ration increased plasma levels of the hormone 12x in both T4 and FZ + T4 poults and significantly (P less than or equal to 0.05) increased myocardial glycogen content in T4 poults but not in FZ + T4 poults.     

Cystic testicular degeneration in furazolidone toxicosis of sexually immature ducks

Cystic testicular tubular dilatation was seen in ducklings fed a ration containing furazolidone at 250, 400, 550, or 700 ppm for 28 days. Gross evidence of cystic testicular dilatation was observed at necropsy in 16% (32/203) of the ducklings that survived to the end of the study. Gross testicular lesions consisted of various degrees of enlargement with increased translucency in moderately to severely enlarged testicles. Histological evidence of cystic testicular dilatation was present in 45% (41/91) of the testicles examined. Histologically, the tubules were in various states of dilatation with attenuation of the seminiferous epithelium proportional to the severity of dilatation. In the most severely affected testicles, tubules were greatly dilated, distorted, and fluid-filled, with extensively flattened epithelium visible on the inner margin of the tubule as a thin rim of cytoplasm with a protuberant nucleus. Interstitial tissues were compressed to thin septa between the dilated tubules.     

Serum Profiles of Luteinizing Hormone,Oestradiol and Cholesterol and Ovarian Functions in Layer Poultry Birds (Gallus domesticus) Fed Diets Containing Furazolidone

This study was carried out to assess the serum profiles of luteinizing hormone (LH), oestradiol, cholesterol and ovarian functions in layer poultry birds (Rhode Island Red: Gallus domesticus) fed a diet containing various concentrations of furazolidone (FZ). A total of 40 birds were randomly assigned to receive FZ 0, 200, 400 or 800 mg/kg feed (ppm) daily during the pre-laying age, i.e. 13-18 weeks (for 5 weeks). Blood samples were collected at weekly intervals. Concentrations of LH and oestradiol in serum were estimated at alternate weeks using radioimmunoassays. Serum cholesterol levels were analysed by an enzymatic calorimetric method. Furazolidone administration was terminated at the 18th week of age. The birds were sacrificed at 22nd week of age and ovarian tissues were processed for morphometric studies. Serum LH, oestradiol and cholesterol levels were affected by age (p < 0.001) and FZ dose (p < 0.001). Serum LH and oestradiol levels were lower (p < 0.05) in birds receiving FZ 800 mg/kg feed daily compared with the controls, whereas serum cholesterol profiles were lower (p < 0.05) in all FZ-administered groups than in the control group. The mean weight of ovaries having no yolky follicles observed in the group receiving FZ 400 or 800 mg/kg feed per day was reduced (p < 0.05) compared with the control group. Dosing FZ at 800 mg/kg feed per day reduced (p < 0.05) the mean volume of ovaries having no yolky follicles compared with the control group. In birds receiving FZ 800 mg/kg feed per day, the mean length of the oviduct was reduced (p < 0.05) as compared with the control group. Morphometric studies revealed that the mean number of oocytes with diameter in the range 401-800 microm decreased (p < 0.05) in birds fed FZ 400 or 800 mg/kg feed per day. Initial egg production was affected by age (p < 0.001) and dose (p < 0.001) of FZ. The mean number of eggs laid by different groups revealed that egg production was reduced (p < 0.05) in birds receiving FZ 800 mg/kg feed per day as compared with the controls. The present data suggest that FZ causes suppression in serum profiles of LH, oestradiol, cholesterol and ovarian functions in Rhode Island Red layer poultry birds. Therefore, great care must be taken with use of FZ in layer poultry birds (Gallius domesticus) with regard to dosage and duration of administration.     

Multisystemic granulomatous inflammation in a horse

A one-year-old Thoroughbred filly was examined because of poor body condition and reluctance to move its neck. Complete blood count revealed leukocytosis (15,700 WBC/microliters) and hyperproteinemia (8 g/dl). Radiography of the cervical vertebrae revealed multifocal lesions of bone lysis surrounded by zones of sclerosis. The horse was euthanatized and necropsied. Granulomatous lesions were identified in the heart, spleen, lungs, bones, and lymph nodes. The multifocal granulomatous inflammatory lesions in this horse were suggestive of mycobacteriosis.     

Efficacy of a feed-additive antibacterial combination for improving feedlot cattle performance and health.

The effectiveness of a feed-additive antimicrobial combination for improving feedlot performance and health was tested using 4325 high-risk feeder calves randomly allocated to a control group or an experimental group. The experimental group received the conventional ration plus a feed additive containing 700 mg per head/day of chlortetracycline and sulfamethazine from arrival at the feedlot to day 56 of the feeding period. The inclusion of the feed additive to the ration significantly improved average daily gain for days 0-28 (P = 0.0163) and 0-56 (P = 0.0001), and the feed conversion for days 0-28 (P = 0.0061) and 0-56 (P = 0.0004). Additionally, the use of the feed additive significantly reduced the rate of bovine respiratory disease morbidity for days 0-28 (P = 0.0014) and 0-56 (P = 0.0001), the rate of relapses and mortality for days 0-56 (P = 0.0151 and P = 0.0209, respectively), and the rate of animals diagnosed with chronic respiratory disease for days 0-28 and 0-56 (P = 0.0009 and P = 0.0002, respectively). Performance and health improvements produced by the use of the feed additive were cost-effective.     

Hepatitis, cardiomyopathy and hemodynamics in furazolidone-induced round heart disease of turkeys.

Twenty-five large broad-breasted white turkeys were fed a 22% protein diet supplemented with 500 ppm furazolidone from day 1 to 3.5 weeks of age and the same diet supplemented with 700 ppm furazolidone until 9.5 weeks of age. Following the development of round heart disease as indicated by altered electrocardiograms the 25 turkeys were sacrificed. In the livers of turkeys with biventricular dilatation (72% of cases) there was bile duct hyperlasia, portal fibrosis and intracytoplasmic globules in the hepatocytes. Globules stained pink with hematoxylin-eosin, deep red with PAS and variable with Massons trichrome stains in paraffin-embedded liver sections. Clear intracytoplasmic vacuoles demonstrable in hepatocytes of PAS stained liver sections embedded in paraffin did not stain as lipid in frozen sections but did contain sparse flocculent material in 1 micrometer sections of liver embedded in epoxy resin and stained with toluidine blue. At the subcellular level, the intracytoplasmic globules in hepatocytes were surrounded by a single membrane, contained flocculent material and had enzymatic properties characteristic of lysosomes. Blood pressure, heart rate, dp/dt max, total plasma proteins and plasma trypsin inhibitory capacity of turkeys with round heart disease were lower than corresponding values for control turkeys. Control turkeys did not exhibit the characteristic gross or microscopic lesions of round heart disease.     

Individual and combined effects of Fusarium moniliforme culture material, containing known levels of fumonisin B1, and Salmonella gallinarum infection on liver of Japanese quail

Three hundred day-old Japanese quail (Coturnix coturnix japonica) were divided into two groups with 150 quail in each group. One group was maintained on quail mash alone, while Fusarium moniliforme culture material was added to quail mash in the second group from day 5 of age and was supplied at a rate of 150 ppm fumonisin B1 (FB1)/kg mash. At day 21, each group was further subdivided into two groups, yielding four groups with 75 birds apiece, which served as the control (group CX), the Salmonella Gallinarum alone group (group CS), the FB1 alone group (group FX), and the group fed FB1 and infected with Salmonella Gallinarum (group FS). An oral challenge with Salmonella Gallinarum organisms (2 x 10(4) colony-forming units/ml) was given to groups CS and FS at 21 days of age. Three quail each were necropsied on day 21 (0 day interval) from groups CX and FX only. At subsequent intervals (i.e., 1, 2, 3, 5, 7, 10, 14, and 21 days postinfection [DPI]), three quail were euthanatized from all four groups (CX, CS, FX, and FS). The gross and microscopic lesions were recorded in both mortality and euthanatized birds at the above intervals. The ultrastructural studies were done at 5 DPI. Mild to moderate hepatomegaly and pale discoloration of liver were observed in group FX, while congestion, hemorrhages, necrosis, and mild to severe hepatomegaly were the predominant gross lesions in both infected groups (CS and FS). The gross lesions in quail inoculated with Salmonella Gallinarum alone (group CS) generally developed slowly, appeared more widely scattered, and involved comparatively less surface area in contrast to the rapidly progressive and frequently confluent lesions in the combination group (FS), especially in the first 5 days of infection. Mild to marked hepatocellular swelling, multifocal hepatic necrosis, and hepatocellular and bile duct hyperplasia were the characteristic microscopic changes in the FX group. Microscopic lesions in quail of group CS comprised congestion, vacuolar changes, and focal necrosis in early stages, followed by granulomatous lesions at later intervals. Similar but more severe lesions were observed in the combination group (FS). Based on transmission electron microscopy, the maximum effect of FB1 toxicity was observed on mitochondria and endoplasmic reticulum. In general, the mitochondriae showed diverse form and structure, some of which appeared to lose their intact outer membrane, and the mitochondrial cristae were disoriented. The deformity in the cisternae structure of rough endoplasmic reticulum, with their rearrangement into round or tubular forms either bearing granular surface or leading to accumulation of smooth endoplasmic reticulum, was evident only in groups FX and FS. We conclude that the continuous presence of fumonisins in the diets of young quail might increase their susceptibility to or the severity of Salmonella Gallinarum infection.     

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.     

Transplacental infection of porcine fetuses following experimental challenge inoculation with encephalomyocarditis virus.

Ten multiparous sows were inoculated between 46 and 50 days of gestation with a fetal swine isolate of encephalomyocarditis virus (EMCV) to investigate the ability of the virus to cause transplacental infection and fetal death. Four sows (group 1) were inoculated IM with EMCV MN-25 that had been passaged 4 times on baby hamster kidney-21 line cell monolayers. Two sows were euthanatized at postinoculation (PI) day 23, and the other 2 sows at PI day 44. An additional 6 sows (group 2) were inoculated IM with the same virus that had been passaged 5 additional times in pigs. Two sows were euthanatized at 14 days, and the remaining 4 sows at PI day 28. Clinical signs were not observed in any of the sows, whereas all sows seroconverted to EMCV. In group 1, only 2 of 50 fetuses were mummified. Virus was not recovered, although EMCV antibodies were detected in the 2 mummified fetuses. In group 2, the 2 sows that were euthanatized at PI day 14 had 26 normal fetuses and there was no evidence of fetal infection. However, in the 4 sows euthanatized at PI day 28, 20 of 48 fetuses were mummified, hemorrhagic, or edematous. Encephalomyocarditis virus was recovered from 21 of 48 fetuses. Transplacental infection and fetal deaths in pregnant sows was achieved following infection with EMCV passaged in pigs.     

Susceptibility of male white-tailed deer (Odocoileus virginianus) to Brucella ovis infection

Infection with Brucella ovis was established by conjunctival instillation in 8 male white-tailed deer (Odocoileus virginianus). Infection was transient in young bucks, but persisted in bucks that were mature when inoculated. The deer were euthanatized and necropsied at various intervals after inoculation. Brucella ovis was recovered from a mature buck at necropsy on postinoculation day 429. Four deer had gross lesions and histopathologic changes of the epididymides. A mature noninfected buck confined for 7 months with an infected buck acquired infection and developed epididymal lesions.     

植酸酶对0～3周樱桃谷鸭生长性能、钙、磷表观存留率影响

为了在负对照组 (钙、磷水平各减少 0 .1 % )日粮基础上添加植酸酶对肉鸭生长、钙、磷表观存留率的影响 ,用 64只 1日龄樱桃谷鸭进行试验 ,按体重随机分为 4组 ,代谢期 6天。试验组鸭分别添加植酸酶 30 0和 50 0PU/kg。结果表明 :添加植酸酶显著提高试鸭的日采食量、日增重、钙、磷的表观存留率 ,植酸酶可以部分替代磷酸氢钙     

北京地区鸭传染性浆膜炎的流行病学调查

１９９７ 年１０ 月～１９９８ 年１２ 月, 从北京地区３０ 个商品鸭场随机收集自然死亡鸭５６１ 只, 经过病理剖检和细菌分离鉴定, 确定２９ 个鸭场存在鸭传染性浆膜炎, ６１ ％ 的病例患有本病, 其日龄范围为７ ～４２ 日。结果说明,一年四季中, 鸭传染性浆膜炎均是引起北京地区肉鸭死亡的主要疾病, 广泛分布于该地区各养鸭场; 肉鸭日龄越小, 对本病越易感, 随着肉鸭日龄的增加, 尤其在５ ～６ 周龄后, 肉鸭对本病的抵抗力增加。从死亡鸭的脑、心血、肝脏、脾脏和胆囊均易分离到鸭疫里氏杆菌, 但从脑组织最易分离到该菌; 共分离到鸭疫里氏杆菌４２１ 株, 分别属于１ 、２ 、６ 、１０ 、１３ 、１４ 型, 其中１ 、２ 、６ 、１０ 型占总分离株的９６ ％ , 是目前主要流行的血清型。给健康鸭注射各血清型分离株的液体培养物均可复制出鸭传染性浆膜炎的临床症状和病理变化, 并引起鸭死亡。１０９ 株受试菌对红霉素、青霉素 Ｇ、新生霉素、痢特灵、氯霉素高度敏感。     

重庆地区雏鹅暴发鸭病毒性肝炎

鸭病毒性肝炎是一种传播迅速并对雏鸭具有高度致死性病毒病,以肝炎为其主要特征。本文报道重庆地区雏鹅暴发鸭病毒性肝炎病例。疾病发生于3～14日龄雏鹅,发病率20%～30%,死亡率20%～25%,临死前出现角弓反张及病死鹅肝脏出血。利用RT-PCR能从肝组织中检测到鸭肝炎病毒A型(DHV-A)和C型(DHV-C)的VP1基因。利用鸭胚从肝组织中分离出A型病毒CQ1株和C型病毒CQ2株,二者人工接种能引起6～7日龄雏鹅出现典型临床症状与病变。这是首次报道A型和C型鸭肝炎病毒混合感染导致雏鹅发病死亡。     

中药组方对黄曲霉毒素B1中毒雏鸭肝功能的影响

为观察黄曲霉毒素B1(AFB1)对试验雏鸭肝功能血清指标的影响及复方中药对AFB1的颉颃效应,本试验选用7日龄健康雏鸭90只,分为3组,每组30只。Ⅰ组为空白对照组,灌胃与试验组等体积二甲基亚砜;Ⅱ组、Ⅲ组为试验组。每天分别按0.1mg/kg剂量给Ⅱ组、Ⅲ组雏鸭灌胃AFB1一次,连续投药21d,试验期间给Ⅲ组雏鸭日粮中添加2%复方中药。分别在给雏鸭投药后7、14、21d,检测雏鸭肝功能部分血清指标。结果显示,Ⅱ组、Ⅲ组雏鸭丙氨酸氨基转移酶(ALT)、天冬氨酸氨基转移酶(AST)与Y-谷氨酰转肽酶(GGT)活性显著高于Ⅰ组(P<0.05),而血清总蛋白(TP)与白蛋白(ALB)含量显著下降(P<0.05);与Ⅱ组比较,在日粮中添加复方中药的Ⅲ组雏鸭各项血清指标均有显著改善(P<0.05)。说明黄曲霉毒素B1导致雏鸭肝功能发生显著的变化,而复方中药能明显改善其变化。     

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.     

Prevalence of Dirofilaria immitis infection among shelter cats

OBJECTIVE: To determine prevalence of Dirofilaria immitis infection among shelter cats. DESIGN: Cross-sectional study. ANIMALS: 239 cats euthanatized at an animal shelter in southeastern Michigan. PROCEDURE: A gross necropsy focusing on the thoracic cavity, heart, lungs, and pulmonary vessels was performed within 5 hours after cats were euthanatized. Blood was collected directly from the heart of cats found to be infected and tested, using a filter test for microfilariae. Serum was tested for D immitis antigens by use of 2 antigen detection kits and for D immitis-specific antibodies by use of 2 antibody detection kits. RESULTS: Cats ranged from approximately 4 months to 15 years old. Adult D immitis were found in 6 (2.5%) cats. Blood could not be recovered from 1 of the cats with heartworm infection. For the 5 other cats, results of the filter test were negative, and results of both antigen and both antibody tests were positive. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that cats living in an urban area in the northern part of the United States have a low prevalence of adult D immitis infection. However, this is likely to be an underestimate of the true prevalence of infection, because no attempts were made to identify cats infected with larval or juvenile stages of D immitis.     

Blood glucose and tissue glycogen levels in turkey poults with spontaneous round heart disease and furazolidone-induced cardiomyopathy.

Furazolidone (FZ) at 700 ppm was added to feed mixtures fed turkey poults two weeks posthatching to induce acute experimental cardiomyopathy. Poults in the control pen received the same ration but without FZ. Four of the control poults developed spontaneous round heart disease. From EKG data and blood samples obtained at weekly intervals, poults were selected for sacrifice at 5 weeks of age. Tissue samples from the left myocardial wall, liver, and pectoralis major and tibialis anterior muscles were analyzed for glycogen by biochemical assay. Blood glucose was determined with the Technicon autoanalyzer. Deposition of glycogen increased significantly (p less than 0.05) in the myocardium of all affected poults and in the liver of all FZ-treated poults. Glycogen levels of the pectoralis major and tibialis anterior muscles were not affected by FZ, but a significant increase (p less than 0.05) was apparent in the pectoralis major muscle of spontaneous round heart poults. It was concluded that FZ influences glycogen metabolism, probably by enzyme inhibition, and that it tends to magnify effects seen in the spontaneous round heart syndrome. Glycogen infiltration of tissues such as the heart and white skeletal muscle suggests that the round heart syndrome may be a manifestation of the glycogen storage disease, idiopathic generalized glycogenosis. Lack of significant differences in the blood serum glucose levels of all poults indicates that these levels are not a reliable clinical parameter for monitoring development of the round heart syndrome.