Runting and stunting syndrome in turkeys

A syndrome resulting in increased early deaths, runting and stunting in turkeys is described in 14 flocks at six sites in Ireland. Pathological lesions included bursal and thymic atrophy and mild degenerative changes in the pancreas of the affected poults. Entero-like virus, rotavirus, reovirus and adenovirus were detected in the affected poults and there was strong circumstantial evidence of lateral transmission of an infectious agent. Depopulation and thorough disinfection of affected houses appeared to eliminate the problem.     

乌鸡、火鸡实验性组织滴虫病病理学比较

以组织滴虫病疫区鸡异刺线虫虫卵实验诱发火鸡、乌鸡组织滴虫病，分别在潜伏期、症状明显期、转归期对盲肠、肝脏等组织器官进行病理学比较观察，结果显示：盲肠卡他（乌鸡13/20；火鸡8/29）和纤维素性坏死（火鸡19/27，乌鸡7/20）。肝脏脂肪变性（火鸡8/27；乌鸡11/20）及局灶性坏死（火鸡19/27；乌鸡4/20）。此外，火鸡肝脏与盲肠见典型传染性肉芽肿。     

Electron microscopic findings of cells with inclusion bodies in experimental hemorrhagic enteritis of turkeys.

The spleen, liver, bone marrow and intestines of two turkeys in which hemorrhagic enteritis of turkeys was experimentally reproduced were examined electron-microscopically. Intranuclear inclusion bodies as described in a previous report were found in all the tissues examined. These occupied most of the area in affected nuclei and were composed of viral particles with morphological characteristics of an adenovirus. The cells with the inclusions were divided into two types of cells, immature and reticular cells. There was some variety in the stage of differentiation of the former cells. As the viral particles developed the cells degenerated and disintegrated. A few particles had been released into the cytoplasm of the degenerated cells but no particles were present in intercellular spaces.     

Inclusion body hepatitis in bobwhite quail (Colinus virginianus)

Farm-reared bobwhite quails less than 3 weeks of age experienced high mortality (250 of 400). At necropsy, these birds had multiple 1-to-2-mm pale foci throughout their livers. Histologically, these foci varied from acute hepatocellular necrosis without an inflammatory response to necrosis with infiltrates of mononuclear inflammatory cells and some heterophils. Hepatocytes adjacent to affected areas had large basophilic intranuclear inclusions. A group I avian adenovirus was isolated from affected livers.     

Interaction of ionophore and vitamin E in knockdown syndrome of turkeys

Monensin and vitamin E concentrations, as well as histopathology of skeletal muscles and myocardium, were evaluated in broad-breasted white turkeys kept in commercial facilities. Turkeys with knockdown syndrome had myopathy of skeletal muscles, but no lesions in the myocardium. Generally, concentration of monensin in serum was highest in turkeys diagnosed with knockdown syndrome given more than 90 mg/kg of monensin in the diet, followed by turkeys diagnosed with knockdown syndrome given <90 mg/kg of monensin in the diet, healthy turkeys fed a diet that contained <90 mg/kg of monensin, and finally healthy turkeys fed a diet free of monensin (not detectable). However, the concentration of monensin was highly variable within each group, and the median was lower than the average. Vitamin E concentrations in the livers varied from low-normal to below normal and were statistically higher in healthy turkeys fed a diet free of monensin than in the livers of birds from the 3 groups exposed to monensin. This suggests that the concentration of monensin in serum positively correlates to the severity of clinical signs and pathology and to the amount of monensin in the feed. Although the methodology developed to detect serum monensin concentrations is beneficial and accurate for case investigations, it is recommended that several samples from each flock be evaluated because of variation within a flock. The current study also suggests that monensin in the feed could induce lower concentrations of vitamin E in the liver of turkeys and can predispose the turkeys to knockdown syndrome.     

Pulmonary congestion and edema (marble spleen disease) of chickens produced by group II avian adenovirus

"Marble spleen disease" of chickens was diagnosed in 22-week-old chickens. Total mortality was 8.9%. Deaths occurred over a period of 2 months. Gross lesions included pulmonary congestion, splenomegaly, hepatomegaly, and congestion of egg follicles. Microscopic lesions included pulmonary congestion and edema, and reticuloendothelial cell hyperplasia of the spleen with concurrent white-pulp necrosis and lymphocyte depletion. The pulmonary lesions were of sufficient intensity to have caused the death of fatally affected birds. Many of the hyperplastic reticuloendothelial cells contained basophilic intranuclear inclusions similar to those that characterize hemorrhagic enteritis of turkeys, marble spleen disease of pheasants, and adenovirus group II splenomegaly of chickens. These characteristic lesions, plus serologic identification of the causal virus, indicate that "marble spleen disease" caused by avian group II adenovirus was affecting the flock under study. This appears to be the first report of death of chickens due to pulmonary congestion and edema caused by spontaneous infection with avian group II adenovirus.     

Staphylococcosis of turkeys. 1. Portal of entry and tissue colonization

Staphylococcus aureus and various coagulase-negative staphylococci were isolated from turkeys with staphylococcosis. Virulent S. aureus adhered well (averaged more than 100 bacteria per tissue cell) in vitro to cells from tissues of the respiratory tract but did not adhere well (averaged fewer than 12 bacteria per tissue cell) to cells from tissues of the alimentary tract. Some avirulent coagulase-negative staphylococci also adhered well to cells from the respiratory tissues. Lungs and livers of turkeys became colonized with virulent S. aureus following experimental aerosol exposure. Tracheas, livers, and hock joints of some market-age turkeys were naturally colonized with S. aureus and various species of coagulase-negative staphylococci.     

Comparative effects of fumonisins on sphingolipid metabolism and toxicity in ducks and turkeys

Fumonisins (FBs) are mycotoxins that are found worldwide in maize and maize products. Their main toxic effects have been well characterized in poultry, but differences between species have been demonstrated. Ducks appeared very sensitive to toxicity, whereas turkeys are more resistant. At the same time, alterations of sphingolipid metabolism, with an increase of the concentration of the free sphinganine (Sa) in serum and liver, have been demonstrated in the two species, but the link between the toxicity of FBs and Sa accumulation remains difficult to interpret. The aim of the present work was to compare the effects of FBs (10 mg FB1 + FB2/kg body weight) on sphingolipid metabolism in ducks and turkeys. Growth, feed consumption, and serum biochemistry were also investigated to evaluate toxicity. The main results showed that FBs increased Sa concentrations in liver and serum in ducks and turkeys, but these accumulations were not directly correlated with toxicity. Sa accumulation was higher in the livers of turkeys than in ducks, whereas Sa levels were higher in the sera of ducks than in turkeys. Hepatic toxicity was more pronounced in ducks than in turkeys and accompanied a decrease of body weight and an increase of serum biochemistry in ducks but not in turkeys. So, although FBs increase Sa concentration in the livers of both species, this effect is not directly proportional to toxicity. The mechanisms of FB toxicity and/or the mechanisms of protection of ducks and turkeys to the Sa accumulation within the liver remain to be established.     

Relationship of osteomyelitis and associated soft-tissue lesions with green liver discoloration in tom turkeys

Tom turkey carcasses with partial green discolored livers (n = 191) or normal livers (n = 198) were examined for osteomyelitis and/or associated soft-tissue lesions. Seventy-nine turkeys with green discolored livers had osteomyelitis and/or associated soft-tissue lesions (41.4%), including 53 with just osteomyelitis (27.7%), while 112 (59.6%) had no osteomyelitis and/or soft-tissue lesions. Only five turkeys (2.5%) with normal livers had osteomyelitis. Discolored livers were significantly heavier, but carcasses with discolored livers weighed significantly less than carcasses with normal livers. Bacteria were isolated from 54 of 61 osteomyelitis lesions (88.5%); most frequently staphylococci (50.8%) followed by Escherichia coli (14.8%), Streptococcus sp. (13.1%), and occasional other organisms. Most associated soft-tissue lesions and livers were sterile (74.7%). These finding indicate that although turkey carcasses with green discolored livers are more likely to have osteomyelitis and/or associated soft-tissue lesions than turkey carcasses with normal livers, there is also an approximately equal chance they will not have these lesions.     

Pathology of adenoviral infection in turkeys (Meleagris gallopavo) with respiratory disease and colisepticemia.

Nuclear inclusion bodies typical of the adenovirus group were widespread in in the spleen and other tissues of 8-week-old turkeys with severe respiratory disease and concomitant evidence of colisepticemia. Adenoviral virions were seen in affected nuclei of splenic tissue and in negatively stained preparations of ground spleen. In splenic tissue, inclusions were most prominent in reticular cells and macrophages in the periarterial lymphoid sheaths, the red pulp and the marginal zones of the periarteriolar reticular sheaths. Marked reticuloendothelial hyperplasia, lymphoid atrophy and granulocytic splenitis characterized the splenic changes. There were inclusions in the respiratory tract, intestinal tract, liver, kidney and pancreas. Inoculation of young turkeys, especially when immunosuppressed, resulted in evidence of infection and respiratory disease. The viruses produced cytopathic changes in primary turkey kidney cell cultures but did not affect embryonating chicken eggs. Concentrated viral suspensions induced precipitin lines in agar gel immunodiffusion tests with known antisera against known turkey adenoviruses but did not show an antigenic relationship to chicken adenoviruses.     

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.     

Detection of Histomonas meleagridis DNA in different organs after natural and experimental infections of meat turkeys

Histomonas meleagridis infection of turkeys is usually accompanied by a severe disease with unspecific clinical symptoms but with distinct pathological lesions in the ceca and liver. In the literature some macro- and microscopic evidence of the spread of histomonads to the other organs has been provided. The aim of the present investigations was to use real-time polymerase chain reaction (PCR) to demonstrate the dissemination of H. meleagridis DNA to different organs after natural and experimental infection of meat turkeys. Samples from several organs were collected from a meat-turkey flock, which proved to be naturally infected with histomoniasis, and examined for histomonad DNA by real-time PCR. Histomonad DNA was detected in all investigated ceca, livers, spleens, kidneys, and pooled brain swabs. Additionally it was found in 75% of investigated samples from bursae of Fabricius, in 50% of investigated duodenums, and in 40% of investigated jejunum samples. After experimental intracloacal infection of 3-wk-old turkey poults with 147,500 histomonads, similar samples were collected from all turkeys that died. After a 3-wk observation period the surviving birds, as well as the noninfected control group, were euthanatized and samples were taken. During the entire experimental period, 10 birds out the 20 infected birds died. Histomonad DNA was detected in all investigated ceca, livers, lungs, and hearts (100%) and almost all kidneys (90%) and bursae of Fabricius (80%). On the other hand, only 30% of examined spleens and 10% of brain samples revealed positive results. Surviving infected birds were euthanatized and necropsied; histomonad DNA was found in one out of 10 livers but not in any ceca. Also, histomonad DNA could not be detected in examined cecal and lung samples from the noninfected control group.     

Recurrent transient paresis in a turkey flock.

Recurring episodes of extreme leg weakness and associated mortality were documented in a turkey flock at 8 to 15 weeks of age. Flock mortality attributed to posterior paresis was approximately 12%, or 4800 of 40,000 turkeys. Four of six open-confinement units were affected. Gross and histological examinations revealed no significant lesions. Immunology and virology were uninformative. There were no significant differences in serum chemistry between clinically affected and normal turkeys. Testing of feed, water, soil, and tissues revealed no common toxicants. Isolation and supportive care for affected turkeys, both in the laboratory and in the field, frequently resulted in full recovery. Injection of a test group of affected turkeys with Type C botulism antitoxin appeared to enhance recovery. However, repeated attempts to detect botulism toxin in serum, liver, or cecal contents using mouse bioassay procedures were unsuccessful.     

Type C botulism in intensively farmed turkeys

Type C botulism in turkeys has been confirmed on several production sites by demonstrating the presence of toxin in sera from affected birds. Only male turkeys were affected, mortalities being up to 30 per cent. No source of toxin was found. Possible modes of intoxication are discussed.     

Preliminary studies on bacterial interference of staphylococcosis of chickens

Previous studies indicated that Staphylococcus epidermidis strain 115 might be an effective interfering agent in reducing the rate of staphylococcosis in turkeys. In the present study, strain 115 was avirulent when administered to 3-day-old chicks by oral, aerosol, or intravenous route. Strain 115 adhered specifically to tracheal, lung, air-sac, and liver cells in vitro and interfered with subsequent colonization by virulent Staphylococcus aureus. In vivo colonization of lungs and livers of young chicks occurred following exposure to aerosols of strain 115. Strain 115 interfered with the in vivo colonization of lungs and livers by virulent S. aureus.     

Clearance of bacteria in turkeys with Bordetella avium-induced tracheitis

Quantitative clearance of aerosolized Escherichia coli from the trachea, lung, and air sacs was measured in turkeys infected with Bordetella avium. Clearance of E. coli in turkeys with B. avium-induced tracheitis was minimally affected early in infection. Sixteen to 23 days after infection with B. avium, sporadic, mild depressions in clearance of E. coli were observed in the tracheas, which had large areas of deciliated tracheal epithelium or replacement of normal epithelium by immature hyperplastic epithelium or metaplastic squamous epithelium. Clearance of E. coli from the lung and air sacs was minimally affected in turkeys infected with B. avium.     

Inclusion Body Hepatitis in Young Broiler Breeders Associated with a Serotype 2 Adenovirus in Ontario,Canada

In July 2001 in southwestern Ontario, a young broiler breeder pullet flock experienced 2.1% mortality from 10 to 14 d of age. Mortality prior to and after this period was normal. Clinical signs included depression, lateral recumbency, and death with feed present in the crop. Necropsy lesions included friable, pale yellow-white livers scattered with hemorrhages. Histological examination revealed necrotizing hepatitis with large basophilic intranuclear inclusion bodies in the hepatocytes compatible with inclusion body hepatitis (IBH). An adenovirus from livers was isolated in chicken hepatoma cells. Virus neutralization and DNA analysis based on restriction fragment length polymorphism performed on this isolate were consistent with group I fowl adenovirus serotype 2. The origin of the adenovirus involved in this outbreak of IBH could not be established with certainty.     

Differentiation of avian adenovirus type-II strains by restriction endonuclease fingerprinting

Three serologically indistinguishable viruses from the avian adenovirus type-II splenomegaly virus of chickens, marble spleen disease virus of pheasants, and hemorrhagic enteritis virus of turkeys, were analyzed by restriction endonuclease fingerprinting. The DNA from these viruses were examined with 6 restriction endonucleases (Bgl II, EcoRI, HindIII, Hha I, Xho I, and BamHI). Markedly different DNA cleavage patterns were found in these virus isolates with all the 5 enzymes, except with BamHI, suggesting genetic differences between isolates of adenovirus type II. Restriction endonuclease analyses were found to provide a method for distinguishing genetically different, and yet serologically similar, strains of avian adenovirus type II.     

Mycoplasma gallisepticum infection in wild-type turkeys living in close contact with domestic fowl

Mycoplasma gallisepticum was isolated from 2 wild-type turkeys (Meleagris gallopavo) and 1 domestic turkey living in close contact on a farm in Tehama County, California. Sinusitis was detected in 2 of 14 wild-type turkeys and in 1 of 12 feral broad-breasted bronze turkeys, but in none of several chickens on the premises. The entire mixed flock was captured, sinus aspirates were collected from affected birds, and blood samples were obtained from all birds for serologic testing. Blood samples also were obtained from 10 domestic turkeys on adjacent premises from which breeding stock had been borrowed. The M gallisepticum isolated from sinus aspirates was typed and inoculated into susceptible chickens, resulting in airsacculitis. California wild turkeys with and without histories of exposure to domestic fowl and wild turkeys shipped into California from Texas for release were tested for antibodies to M gallisepticum, using the plate agglutination test. Evidence of M gallisepticum infection was not found in wild turkeys at any location other than the original premises.