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Results for “POULTRY DISEASES”

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At least 559 records · Page 31Linked to original sources
PubMed1976

Isolation of a reticuloendotheliosis virus from chickens inoculated with Marek's disease vaccine.

Over a period from spring to fall in 1974, a disease with delayed growth, anemia, abnormal feathers, and leg paralysis as main symptoms broke out in flocks of chickens inoculated with Marek's disease vaccine. A virus was isolated from affected birds in the field and the same lot of Marek's disease vaccine as inoculated into these birds. It had a common antigenicity to the T strain of reticuloendotheliosis virus (REV) and could not be discriminated from this strain on the basis of morphology or property. When chicks were inoculated with it, they presented essentially the same symptoms as the birds affected in the field. Since the disease was reproduced in this manner, it was presumed to have been caused by REV contained in the vaccine as contaminant. The virus persisted in the body for long time and also induced horizontal infection.

Animals↗
PubMed1977

[Methods for the control of avian tumour virus diseases (author's transl)].

Methods developed in the Netherlands for the control of avian tumour virus diseases, Marek's disease and lymphoid leukosis, are discussed. Marek's disease is successfully kept under control by vaccination of all day-old chickens raised for egg production. Broilers are not vaccinated. During 1975 over 23 million chicks were vaccinated with cell-associated Marek's disease virus CVI 988 vaccines and about 3 million doses of HVT vaccine were administered, mostly in lyophilised form. The mechanism of the immunity conferred by the MD vaccines is discussed. Lymphoid leukosis was successfully controlled in three inbred lines of White Leghorn chickens and in a commercial grand parent flock of White Plymouth Rocks. The control method that can be applied to flocks in the field is based on three elements: From an infected flock hens are selected in whose eggs no lymphoid leukosis viruses can be detected in pooled extracts of groups of embryos. Only eggs from hens that demonstrably do not shed virus congenitally to their embryos are used for the production of progeny. The offspring are reared in isolation until two months of age at which time the age related resistance against tumour formation appears to be sufficiently developed. The chickens are subsequently inoculated intramuscularly with lymphoid leukosis viruses of subgroups A and B and transferred to a conventional chicken house. The inoculated birds become persistently viremic, resist intramuscular challenge infections or exposure by contact, but produce virus-negative eggs during the laying period. For lymphoid leukosis, congenital infection is considered the usual mode of virus transmission. Horizontal virus transmission becomes important when virus-free chickens, reared in isolation for two months, are exposed in field conditions without previous "vaccination". During the egg-laying period of these flocks, virus shedding was observed in a similar percentage as in flocks with congenitally infected birds.

Animals↗
PubMed1977

Virus-induced lysosomal enzyme dissolution of nasal turbinate cartilage.

The mechanism of laryngotracheitis virus-induced dissolution of chick nasal turbinate cartilage was studied by lysosomal enzyme histochemistry. Five-day-old chicks were infected by intranasal instillation, and changes in lysosomal enzyme distribution were followed at daily intervals through the tissue regeneration stage, Day 28. In the mucosa the lysosomes were activated beginning on Day 1, and glycerol acid phosphatase and a diffuse form of beta-glucuronidase were released concomitant with tissue cell destruction. In the chondrocytes (where glycerol acid phosphatase was absent), beginning on Day 2, particulate (lysosomal) beta-glucuronidase decreased as diffuse beta-glucuronidase increased and extended out into the matrix. The cartilage lost its metachromatic staining properties and became soft and pliable. Regeneration of the mucosa started on Day 6 and gradual reappearance of metachromatic staining of the cartilage began on Day 8 with considerable recovery of original turbinate structure by Day 12. A lysosomal membrane labilizer, vitamin A, exacerbated the cartilage pathology, whereas a stabilizer, cortisone, retarded it.

Acid Phosphatase↗
PubMedDate not supplied

Demyelinating peripheral neuropathy in a guinea hen associated with subacute lead intoxication.

In mammalian species lead acts primarily as a neurotoxin. Lead poisoning is common in avian species but lesions in the nervous system have not been associated with it. This paper describes a peripheral neuropathy with fragmentation and segmental demyelination of fibers in the sciatic nerves of an adult guinea hen (Numida meleagris) which died of lead poisoning.

Animals↗
PubMed1990

[The effect of cyadox and virginiamycin on Marek's disease in chickens].

Chickens infected with highly virulent Marek's disease virus were administered in the course of 56-day fattening cyadox at a dose of 20 mg per kg feed mixture (MC group). and virginiamycin at a dose of 10 mg per kg feed mixture (MV group). The weight gains on the 56th day and dressing percentage were highest, in comparison with the control group (711.11 g and 60.62%), in the virginiamycin-treated group. An investigation into the basic chemical composition of meat revealed lower contents of dry matter and proteins in the virginiamycin-treated group (26.9% and 22.76%) if compared with the control group of chickens which were also infected with Marek's disease virus. A biometrical examination of the organs showed a statistically significant decrease in heart weight in the cyadox-treated group, increase in liver and heart weight and intestine shortening in the virginiamycin-treated group, in comparison with the control group. Pathologico-anatomical changes typical of Marek's disease were recorded in a randomly selected number of chickens in 33.3% in the control group, in 28.5% in the cyadox-treated group and in 50.0% in the virginiamycin-treated group.

Animals↗
PubMedDate not supplied

Factors affecting the development of respiratory disease complex in chickens.

Factors playing a part in the development of respiratory disease complex in chickens were investigated in a series of experiments. The experimental infection was produced by exposing chickens to Mycoplasma gallisepticum and the B1 vaccine strain of Newcastle disease virus and later exposing them to aerosols containing the O1:K1 serotype of Escherichia coli. Chickens became susceptible (pericarditis or death) to E. coli 8 days after mixed respiratory disease challenge. One day after respiratory disease challenge, lesions consisted of edema and infiltration with lymphoid cells and heterophils. At the time of susceptibility to E. coli, the lesions were strongly lymphoid with many dense follicular areas and very few heterophils. The incidence of pericarditis and death was similar when the concentration of bacteria in the aerosol inoculum ranged between 10(9)/ml and 10(5)/ml. At the time of maximum susceptibility to aerosol challenge, chickens were less susceptible to intravenously administered E. coli than were the uninfected controls. Resistance of chickens that had been selectively bred for a high (HA) or low (LA) antibody response to sheep erythrocytes was compared. HA chickens were more resistant to respiratory agents and less resistant to E. coli than LA line chickens. When the lines were exposed to respiratory disease followed by exposure to aerosols containing E. coli, the HA line had the lowest incidence of pericarditis and death.

Aerosols↗
PubMedDate not supplied

Sudden death syndrome in turkey hens.

A turkey breeder flock of 5600 31-week-old hens experienced an abrupt increase in daily mortality for a 2-day period. This higher mortality rate corresponded with the handling and moving of the hens 1 to 2 days before. No clinical illness was seen in the hens before carcasses were discovered. The four hens that were necropsied had small spleens, congested lungs, and enlarged livers. The most consistent histologic lesions were pulmonary hemorrhage and edema, and congestion of veins and capillaries in several visceral organs. One hen had subserosal hemorrhage of the oviduct and perirenal hemorrhage. The increased mortality pattern, the lack of clinical signs, and the histopathologic changes are consistent with a diagnosis of sudden death syndrome. The presence of concurrent inflammatory lesions in the lungs predisposed the hens to sudden death following the stress of handling and moving.

Animals↗
PubMed1990

[A case of cryptosporidiosis in breeding laying hens with Marek's disease].

The simultaneous occurrence of Marek's disease and cryptosporidiosis in two flocks of rearing pullets on a multi-age farm with rearing-pullets and layers, is reported. This is the first report of cryptosporidiosis in rearing pullets in the Netherlands and also the first time that the combination of this infection with Marek's disease is mentioned.

Animals↗
PubMed1990

[Tumor histogenesis and macrophage content in lymphomas in Marek's disease of chickens].

Histological and to some extent additional enzyme-histochemical studies were conducted into 28 cases of Marek's disease with minor, moderate, and intensive lymphoma formation. The investigations were undertaken with a view to differentiating T-lymphocytes and macrophages by differentiated activity on acid unspecific alpha naphthylacetate esterase. Lymphoma specimens were cytologically evaluated under semi-quantitative or quantitative aspects. Evidence was provided to the existence of correlations between intensity of Marek's disease lymphomas and their relative contribution to lymphocytes, lymphoblasts, and macrophages. The amount of lymphoblasts was found to go up along with advancing lymphoma proliferation, while the amounts of lymphocytes and macrophages went down. Moderately pronounced lymphomas contained 16 percent macrophages on average, whereas only about 8 percent were recordable from highly pronounced lymphomas. The high presence of macrophages in less developed lymphomas is considered to reflect unspecific defence reaction against neoplastic lymphatic cells in the phase of low tumour malignancy.

Animals↗
PubMed1989

Effect of adrenal blocking chemicals on viral and respiratory infections of chickens.

In a series of experiments chickens were treated with chemicals which block the production of corticosterone by the adrenal cortex prior to being challenged with respiratory disease (and other) agents in order to determine if the course of the diseases could be altered. Some chickens received a single intramuscular injection (14 mg/kg) of 1,1-dichloro-2,2-bis/p-chlorophenyl/ethane (ABC) dissolved in corn oil (20 mg/mL) at least 12 h before challenge. Other chickens received feed containing 500 mg/kg of metyrapone for at least 12 h before and during the challenge infection. Treated chickens were more resistant than the untreated controls to Newcastle disease virus, Mycoplasma gallisepticum, combined M. gallisepticum-Newcastle disease virus infection, and avian adenovirus group II infection. The feeding of erythromycin (1 g/kg of feed), one day before and during the challenge, reduced the severity of M. gallisepticum infection. The effects of feeding both metyrapone and erythromycin resulted in a further increase in resistance. Chickens which had been treated with ABC had less severe lesions and greater postchallenge weight gain than the controls in response to a secondary Escherichia coli infection.

Adenoviridae Infections↗
PubMed1989

Immunohistological identification of both infectious bursal and Marek virus antigens in the bursa of Fabricius.

Indirect Immunoperoxidase (IIP) and Avidin Biotin-Peroxidase Complex (ABC) techniques were used for the detection of Infectious Bursal Virus (IBV) and Marek Disease Virus (MDV) antigens in alcohol and formalin-fixed, paraffin-embedded lymphoid tissues from broilers. Both techniques appeared potentially useful for the diagnosis of both viral antigens in alcohol-fixed tissues, and allowed the observation of dual infection in the bursa of Fabricius of the studied animals in a natural infection.

Animals↗
PubMed1989

[The occurrence of Marek's disease in genetically different groups of chickens].

The occurrence of Marek's disease was studied under laboratory conditions in four genetically different groups of chickens (Brown Leghorn, F1 hybrids of the CB x IA inbred lines, pullets of the paternal branch of the grandparent stock of the Hybro meat type, and final hybrids of the White Hisex layer type) after infection with the Georgia strain of Marek's disease (MD) virus, used in two doses (1600 and 16,000 PFU per one bird). MD was diagnosed on the basis of the occurrence of macroscopic tumours; when these tumours were absent in birds which had died within 105 days from infection, the dead bodies were subjected to microscopic examination (peripheral nerves, gonads, skin, bursa of Fabricius, thymus, spleen). The size of the parenterally administered dose of the virus had no significant effect on mortality, occurrence of tumours and the MD virus in any of the groups of chickens tested. However, there was a time shift in the mortality curve in chickens infected with a lower dose. The significantly highest occurrence of MD was recorded in BrL chickens (100%). A somewhat lower occurrence of MD was recorded in the Hisex White chickens (87.8%) and in the CB x IA hybrids (73.8%). However, the dead CB x IA chickens had a higher occurrence of tumours (96.6%) than the Hisex White chickens (77.1%). The lowest MD occurrence was recorded in the pullets of the Hybro meat type (25.5%). The organ most frequently affected by tumours after infection of the birds with the Georgia strain was the liver (24.1%).

Animals↗
PubMedDate not supplied

Intestinal cryptosporidiosis in chickens.

In a retrospective examination of histopathology reports from Aug. 1, 1985, through Sept. 31, 1987, 10 cases of small- or large-intestinal cryptosporidiosis (not epithelial cryptosporidiosis of the bursa of Fabricius) were found in chickens. Infection was evenly distributed among young chickens. Incidence of intestinal cryptosporidiosis increased during 1987. Although all infected birds were clinically ill, signs or gross lesions of intestinal disease were not always present. In all cases, mild to marked histologic lesions were associated with Cryptosporidium sp.; however, intestinal tracts were not cultured for other infectious agents. The numbers of Cryptosporidium sp. and character of inflammatory response were not significantly correlated. A difference (P = 0.01) among intestinal segment (small vs. large) infection with Cryptosporidium was seen. Light-microscopic appearance and organ distribution of Cryptosporidium sp. suggest that in addition to C. baileyi, other Cryptosporidium species infect chickens. Until the diagnostic procedure for outbreaks of gastrointestinal disease in poultry routinely includes histopathology, fecal flotation, and virus, bacteria, and chlamydia cultures, and until species of Cryptosporidium are isolated, identified, reported, and investigated experimentally, the importance of intestinal cryptosporidiosis in chickens will remain unknown.

Animals↗