Showing papers in "Avian Diseases in 1979"
TL;DR: It is suggested that CAA may be a new viruslike agent inducing anemia in chicks from chickens in the field, which is resistant to treatment with chloroform or ether, and to heating at 80 C for 15 minutes.
Abstract: SUMMARY A transmissible agent inducing anemia in chicks (chicken anemia agent; CAA) was isolated in specific-pathogen-free chicks from chickens in the field. Chicks were inoculated intramuscularly with CAA (about 1040 CID5o/chick) at 1 day old. By 14 days postinoculation they had severe anemia, with a hematocrit value below 20%, a red-blood-cell count below 1,000,000/mm3, and a white-blood-cell count below 5,000/mm3. Morbidity was 100%, and mortality reached about 50% by 28 days postinoculation. Gross lesions found in the affected chicks were watery blood, yellow to white bone marrow, marked atrophy of the thymus and bursa of Fabricius, swelling and discoloration of the liver, and sometimes hemorrhage throughout the body. CAA was resistant to treatment with chloroform or ether, and to heating at 80 C for 15 minutes. It passed through a membrane filter of 25-nm pore size. It produced no cytopathic effect in chicken kidney cell cultures or had no fatal effect on embryonating chicken eggs. Specific antibody was produced in chickens inoculated with CAA. These findings suggest that CAA may be a new viruslike agent
339Â citations
TL;DR: The ELISA is a rapid and convenient alternative to the DCF test for identifying infected chickens in eradication programs, because virus-rich sources such as meconia and blood that are unsuitable for DCF can be tested directly.
Abstract: SUMMARY Immunoglobulins from antiserum raised against chromatographically purified avian myeloblastosis virus (AMV) group-specific (gs) antigens were used in an enzyme-linked immunosorbent assay (ELISA). Readily discernible color was produced with 2-3 ng of AMV protein in microplate wells coated with 4 jtg of salt-precipitated immunoglobulins. When a biological assay, i.e., phenotypic mixing (PM), was the criterion for the infectious status of specimens, the ELISA consistently identified a greater percentage of virus-positive specimens than direct complement-fixation (DCF) tests. Over 95% concordance was obtained between the! ELISA and PM bioassays when meconia and whole-blood samples were tested. Moreover, three DCF(-) egg albumens from one virus shedder hen were positive by the direct ELISA. Complete agreement was found between a biological assay for endogenous virus and the ELISA when blood and albumens from inbred chickens were tested. The ELISA is a rapid and convenient alternative to the DCF test for identifying infected chickens in eradication programs, because virus-rich sources such as meconia and blood that are unsuitable for DCF can be tested directly.
168Â citations
TL;DR: Two groups of White Leghorn hens, one vaccinated at 2 weeks against infectious bursal disease (IBD), and the other free of antibodies against IBD virus ( IBDV), were vaccinated at 16 weeks old with a suspension or a multiple emulsion of killed IBDV.
Abstract: Two groups of White Leghorn hens, one vaccinated at 2 weeks against infectious bursal disease (IBD), and the other free of antibodies against IBD virus (IBDV), were vaccinated at 16 weeks old with a suspension or a multiple emulsion of killed IBDV. Untreated hens from each flock were kept as controls. All birds were bled periodically for 50 weeks after vaccination. Twenty-five weeks after vaccination fertile eggs were collected. Antibody levels in the yolk were determined. Chickens hatched from the fertile eggs were bled and challenged with IBDV at weekly intervals to determine the persistence of serum antibodies and resistance to bursal atrophy. Hens revaccinated with the emulsified vaccine and the chickens derived from them had the highest neutralizing and most uniform titers, and complete protection in the chickens lasted to 4 weeks. Two of five chickens were still protected against challenge at five weeks of age. In chickens derived from hens revaccinated with a suspension of killed virus, protection was always partial, being in close relation with age; four of five chicks were protected in the first week of age and the rate of protection diminished to only 1 out of 5 by five weeks of age. Chickens obtained from unrevaccinated hens were protected only during the first week of life.
122Â citations
TL;DR: A cell-culture-adapted infectious bursal disease virus (IBDV) was as effective as a commercial vaccine in protecting against challenge and showed less effect on the bursa than chickens vaccinated with the commercial vaccine.
Abstract: A cell-culture-adapted infectious bursal disease virus (IBDV) was as effective as a commercial vaccine in protecting against challenge. Chickens immunized with the cell-culture-adapted IBDV showed less effect on the bursa than chickens vaccinated with the commercial vaccine. The cell-culture-adapted virus produced effective immunity after oral or subcutaneous inoculation. The minimum immunizing dose in one-day-old chicks was between 4,000 and 40,000 plaqueforming units (PFU) when given by subcutaneous injection. Most chicks responded to a dose of 4,000 PFU. Ninety percent of maternally immune chickens were effectively vaccinated at two weeks of age when the geometric mean titer for virus-neutralizing antibody (GMT-VN) was about 1:78. Birds from this same group could not be immunized at one week of age when the GMT-VN was 1:466.
88Â citations
TL;DR: The rectal content of an apparently normal 1-week-old broiler chick yielded an unclassified cy topathogenic virus with cytopathic effects of the round type that was distinguished from avian encephalomyelitis virus by the neutralization test.
Abstract: The rectal content of an apparently normal 1-week-old broiler chick yielded an unclassified cytopathogenic virus with cytopathic effects of the round type. It was identified as a picornavirus from the following: ribonucleic acid in the viral core; virus growth in the cytoplasm; a particle about 30 nm in diameter; resistance to ethyl ether, chloroform, trypsin, and acid; relative heat-lability; and partial stabilization to molar magnesium chloride. The virus was stable under freezing and thawing, and sonication. It was distinguished from avian encephalomyelitis virus by the neutralization test.
84Â citations
TL;DR: A small gram-negative motile bacillus was isolated from laboratory poults affected by acute respiratory disease (rhinotracheitis) of turkeys and it is concluded that it is a primary etiologic agent for acute respiratory Disease of turkey poult.
Abstract: SUMMARY A small gram-negative motile bacillus was isolated from laboratory poults affected by acute respiratory disease (rhinotracheitis) of turkeys. The bacterium was inoculated intranasally into susceptible day-old poults; the poults developed typical clinical signs of acute respiratory disease, and the bacterium was reisolated. This same bacterium was isolated from commercial poults with typical signs of acute respiratory disease but not from poults of similar age which were clinically normal. The bacterium has not been identified taxonomically. We conclude that it is a primary etiologic agent for acute respiratory disease of turkey poults.
82Â citations
TL;DR: Intestinal microflora from mourning doves was at least partially effective in protecting chicks against a naladixic-acid-resistant strain of Salmonella infantis and the growth rate of chicks in the absence of salmonellae was significantly improved.
Abstract: SUMMARY A native intestinal microflora of chickens which is protective against salmonella readily transferred to penmates and apparently to birds in adjacent pens. The microflora not only minimized infection resulting from exposure following colonization of the gut with microflora, but significantly abbreviated the period of infection when introduced after a salmonella infection was established in chicks. A microflora with undiminished protective activity, sensitive to only a few commonly used antibacterials, was established in a SPF-Cofal/Marek-negative population. Intestinal microflora from mourning doves was at least partially effective in protecting chicks against a naladixic-acid-resistant strain of Salmonella infantis. In limited tests with 2 of 3 sources of protective microflora, the growth rate of chicks in the absence of salmonellae was significantly improved. A hypothesis involving specificity of attachment between the glycocalyces of the protective microflora and of the intestinal mucosa is offered as the likely mechanism of protection.
82Â citations
TL;DR: The in vitro isolation, propagation, and characterization of duck hepatitis virus Type III (DHV-III), which is serologically distinct from the classical (Type I) DHV, replicated in liver and kidney cell cultures of duck origin and was grown successfully in embryonating eggs of ducks, but not of chickens.
Abstract: The in vitro isolation, propagation, and characterization of duck hepatitis virus Type III (DHV-III), is described. This virus, which is serologically distinct from the classical (Type I) DHV, replicated in liver and kidney cell cultures of duck origin. Replication was limited in chicken and quail kidney and duck embryo fibroblast cultures. It did not replicate in a variety of other cell cultures of avian or mammalian origin. The virus was grown successfully in embryonating eggs of ducks, but not of chickens. DHV-III passed through a 50-nm membrane filter, was stable at pH 3.0 and resisted treatment with 5% chloroform. Virus growth was not inhibited by treatment with 5-iodo-2-deoxyuridine. Electron-microscope examination revealed crystalline arrays in the cytoplasm; virus particles had cubic symmetry, and were about 30 nm in diameter. By these properties, this virus can be classified as a member of the picornavirus group.
74Â citations
TL;DR: Healthy waterfowl were found to be carriers of duck plague (DP) virus and all ducks with lesions proved to shed DP virus, although not necessarily at the time they had the lesion.
Abstract: Healthy waterfowl were found to be carriers of duck plague (DP) virus. Black ducks (Anas rubripes) and Canada geese (Branta canadensis) surviving a natural outbreak of DP at Coloma, Wisconsin, in 1973 yielded DP virus in cloacal swabs taken four years postinfection. Experimental infection of previously unexposed mallard ducks (Anas platyrhynochos) with the Coloma strain of DP virus CO-WI (73) also produced cloacal virus shedding for up to four years after infection. A second DP virus strain, LA-SD (73) from the Lake Andes, South Dakota, epornitic, was detected from cloacal swabs of pintail ducks (Anas acuta), gadwall ducks (Anas strepera), wood ducks (Aix sponsa), and Canada geese infected experimentally one year before. The frequency of swabs positive for DP virus varied between individuals within each of the tested species. The amount of detectable DP virus shed was about 100 plaqueforming units of virus percloacal swab. Oral erosions were present in all species tested except Canada geese and gadwall ducks. Erosions occurred at the openings of the sublingual salivary gland ducts. DP virus was isolated from erosions. All ducks with lesions proved to shed DP virus, although not necessarily at the time they had the lesion.
73Â citations
TL;DR: Inclusion of avoparcin at 20 ppm in feed prevented necrotic enteritis in one group, but 10 ppm was only marginally effective in another group, and Bacitracin at 110 ppm also prevented the disease.
Abstract: Four groups of about seventy 2-week-old broiler chickens were challenged with a Clostridium perfringens Type A isolate. Inclusion of avoparcin at 20 ppm in feed prevented necrotic enteritis in one group, but 10 ppm was only marginally effective. Bacitracin at 110 ppm also prevented the disease. Necrotic enteritis was successfully reproduced in untreated control birds.
63Â citations
TL;DR: Differences in antibody titers, blood protein, and weight gains between controls and birds fed 80 ppm of deoxycorticosterone could be demonstrated only with adapted birds.
Abstract: SUMMARY Chickens were adapted to their handler before the experiment. Adapted birds produced more antibody, had more blood protein, gained more weight, and were more resistant to Mycoplasma gallisepticum than unadapted birds. The antibody response to sheep red blood cells was not reduced by fasting for 48 hours in adapted birds but was in unadapted birds. Differences in antibody titers, blood protein, and weight gains between controls and birds fed 80 ppm of deoxycorticosterone could be demonstrated only with adapted birds.
TL;DR: In a chronological study on the distribution of the virus in organs, the virus was recovered from various organs, exclusive of the brain and trachea, and the virus titer was higher in the kidneys, jejunum, rectum, and bursa of Fabricius than in any other organ.
Abstract: The pathogenicity of the G-4260 strain of picornavirus for day-old chicks was studied by intraperitoneal inoculation. No clinical signs were observed. A mild yellowish-tan discoloration of the kidneys was noticed in necropsy 7 to 21 days after inoculation. Mean body weight was significantly lower (P less than 0.01) in inoculated groups than in control groups 7 days after inoculation. In a chronological study on the distribution of the virus in organs, the virus was recovered from various organs, exclusive of the brain and trachea. The virus titer was higher in the kidneys, jejunum, rectum, and bursa of Fabricius than in any other organ. Fluorescent antigens were seen predominantly in the epithelia of the renal tubules.
TL;DR: The dissociation concept was a useful thesis but the precise separation of the immune system into antibodyand cell-mediated responses is no longer valid since, for example, thymic-derived (T) and bursalderived (B) lymphocytes are known to interact in antibodymediated immunity.
Abstract: In 1956, we reported that removal of the bursa of Fabricius during the early part of its rapid growth period (16) would markedly compromise antibody production in the chicken (23). Other investigators later demonstrated that removal of the avian thymus would prevent the normal elimination of skin grafts (3) but would not interfere with the production of immunoglobulins (the antibody molecule) or plasma cells which produce antibody (12). Those latter experiments were convincing proof of an earlier thesis (60) that a dissociation of the immune response exists in the chicken. The bursa of Fabricius was believed to control antibody-mediated immunity, which includes the level of circulating immunoglobulin (Ig), production of antibody, and presence of plasma cells; and the thymus was responsible for cell-mediated immunity, which includes cell responses to foreign agents, e.g., skin-graft rejection (allograft) and the ability of lymphocytes to produce a graft-vs.-host response (13,19). The dissociation concept was a useful thesis. However, the precise separation of the immune system into antibodyand cell-mediated responses is no longer valid since, for example, thymic-derived (T) and bursalderived (B) lymphocytes are known to interact in antibodymediated immunity. This review discusses briefly: 1) the development of the BF; 2) identification of B and T cells; 3) ontogeny of B cells and Ig synthesis; 4) sites of Ig and antibody production; and 5) subpopulations of T cells. Bursa of Fabricius development. Hieronymus Fabricius described the location of the bursa in the late 16th century. The bursa is a diverticulum of the proctadael region of the cloaca and is round or oval in the chicken and elongated in the duck. Basophilic stem cells appear to migrate to the bursa earlier than 9 days of embryonic development (31,40). These stem cells, under the influence
TL;DR: Results strongly suggest that B-cells are the target for IBD virus infection in chicks infected as embryos or at 1 day old.
Abstract: Chickens were infected with infectious bursal disease (IBD) virus in ovo or at different times posthatching to 6 weeks of age. The B- and T-cell responses in the lymphoid tissues and blood were examined sequentially to 8 weeks of age by using indirect immunofluorescence. The proportion of B-cells was consistently lower in infected birds than in controls, especially in chicks infected as embryos or at 1 day old. The proportion of T-cells increased following these early infections but was slightly lower in spleen and blood of birds infected at 1, 4, and-6 weeks of age. Serum IgM levels dropped significantly after infection, regardless of the time of infection. IgG levels decreased following early infection but increased after infection at 1 week old or more. The results strongly suggest that B-cells are the target for IBD virus infection.
TL;DR: The results suggest that the mortality and many of the clinical signs seen with infectious bursal disease are associated with: 1) a depletion in circulating levels of hemolytic C from the formation of immune complexes at sites of viral replication; and/or 2)A depletion in some clotting factor which results in hemorrhage.
Abstract: SUMMARY Complement (C) titers were decreased at 3 days postinfection, and virus-neutralizing (VN) antibody was detectable at 3 or 4 days postinfection in chickens with infectious bursal disease virus (IBDV). Clotting times were prolonged in all groups tested during the acute phase of the disease. Mortality appeared to be associated with the severity of decrease in C titer. The results suggest that the mortality and many of the clinical signs seen with infectious bursal disease are associated with: 1) a depletion in circulating levels of hemolytic C from the formation of immune complexes at sites of viral replication; and/or 2) a depletion in some clotting factor which results in hemorrhage.
TL;DR: Large doses of purified lipopolysaccharide purified from Escherichia coli induced clinical signs but no mortality in chicks and attempts to produce a generalized Shwartzman-like reaction with two intravenous inoculations of LPS failed.
Abstract: Large doses of purified lipopolysaccharide (LPS) purified from Escherichia coli induced clinical signs but no mortality in chicks. Five chicks survived a mean dose of 517 mg/kg. One individual that received LPS at 577 mg/kg recovered from clinical manifestations within two days. Attempts failed to produce a generalized Shwartzman-like reaction with two intravenous inoculations of LPS at about 24-hour intervals. Prior injection of uric acid did not protect chicks from LPS by intravenous exposure.
TL;DR: The Salmonella status of 15 different farm flocks was assessed at the farm level and at processing plants, and culture of 6-weeks litter in particular would be a good indicator of carcass contamination atprocessing plants.
Abstract: The Salmonella status of 15 different farm flocks was assessed at the farm level and at processing plants. Bacteriological examination for Salmonella was made of litter, dust, feed, 5-day-old culled chicks, and chicken carcasses. Fresh straw litter was found contaminated with Salmonella and may be a source of flock infection. Culture of floor litter can be a practical method for detecting flock infection, and culture of 6-weeks litter in particular would be a good indicator of carcass contamination at processing plants. Properly pelleted feed did not contain Salmonella. Processing did not render carcasses free of Salmonella.
TL;DR: A virus indistinguishable from the causal viruses of hemorrhagic enteritis of turkeys and marble spleen disease of pheasants was isolated from enlarged spleens of chickens condemned for Marek's disease, and serum from 13 of 28 commercial broiler-breeder chicken flocks contained HE/MSD precipitin.
Abstract: A virus indistinguishable from the causal viruses of hemorrhagic enteritis (HE) of turkeys and marble spleen disease (MSD) of pheasants was isolated from enlarged spleens of chickens condemned for Marek's disease (MD). Sera from 13 of 28 commercial broiler-breeder chicken flocks contained HE/MSD precipitin. The 13 positive flocks had a mean age of 32.9 + 12.4 weeks, and the 15 negative flocks a mean age 12.8 + 7.3 weeks. Avian adenovirus group-II splenomegaly of chickens is the name proposed for this disease.
TL;DR: Antimicrobial sensitivity patterns showed all strains to be sensitive to chloromycetin, erythromycin, furoxone, gentamicin, nalidixic acid, neomycin, novobiocin, spectinomycin and tetracycline.
Abstract: The biochemical and physiological characteristics of 35 strains of avian haemophili from 7 countries were examined. All strains required V-factor but not X-factor for growth on artificial media. They produced acid in phenol-red broth containing fructose, glucose, and mannose. Acid production from other carbohydrates was variable or did not occur. Thirty-two strains were pathogenic to chickens. Pathogenicity varied with method of exposure. Hyaluronic acid was found in 9 strains. Hemagglutination of human or chicken erythrocytes was inhibited by its presence. Antimicrobial sensitivity patterns showed all strains to be sensitive to chloromycetin, erythromycin, furoxone, gentamicin, nalidixic acid, neomycin, novobiocin, spectinomycin, and tetracycline.
TL;DR: Cryptosporidiosis was diagnosed in the cloacal coprodeum of two red-lored parrots (Amazona autumnalis) and their presence was associated with loss and atrophy of microvilli.
Abstract: SUMMARY Cryptosporidiosis was diagnosed in the cloacal coprodeum of two red-lored parrots (Amazona autumnalis). The parasites were adhered to the microvillus border of epithelial cells and their presence was associated with loss and atrophy of microvilli. Merozoites, trophozoites, gametes, and oocytes were identified with light and transmission electron microscopy. The coprodeal epithelium was hyperplastic and the lamina propria was infiltrated with moderate numbers of heterophils and lymphocytes.
TL;DR: A trivalent formalin-inactivated bacterin containing Pasteurella anatipestifer serotypes 1, 2, and 5 gave no significant protection against heterologous serotype challenge, and day-old ducklings were also responsive to PA bacterin, and developed significant immunity against experimental challenge.
Abstract: Since Pasteurella anatipestifer (PA) serotypes 1, 2, and 5 gave no significant protection against heterologous serotype challenge, a trivalent formalin-inactivated bacterin containing all these serotype cells was developed and tested in the laboratory. Two inoculations of bacterin in White Pekin ducklings at 10 and 17 days of age gave highly significant protection against challenge with virulent organisms. The protection lasted only 2 weeks after the second inoculation. A third bacterin inoculation given at 31 days or exposure to an active field infection during the period of protection extended protection to market age (7 wk). Aluminum-hydroxide-gel-adsorbed bacterin gave no better protection than bacterin without adjuvant. One inoculation of multiple oil-emulsion (MOE) bacterin gave absolute protection up to market age: unfortunately, it produced noticeable tissue reactions at the site of inoculation. Day-old ducklings were also responsive to PA bacterin, and developed significant immunity against experimental challenge.
TL;DR: A comparison of breeding for resistance and susceptibility to lymphomatosis in highly inbred chickens and the adaptive value of blood group genes in chickens shows the need for further research into this topic.
Abstract: 26. Pink, J. R. L., A. Buder, and V. C. Miggiano. Genetic control of the response of chicken leucocytes to a T cell mitogen. Folia Biologica 23:417. 1977. 27. Schiermann, L. W., and A. W. Nordskog. Immunogenetic studies with fowl: relationship of blood groups to transplantation immunity and tolerance. Ann N.Y. Acad. Sci. 120:348-355. 1964. 28. Schiermann, L. W., D. H. Watanabe, and R. A. McBride. Genetic control of Rous sarcoma regression in chickens: linkage with the major histocompatibility complex. Immunogenetics 5:325-332. 1977. 29. Schultz, F. T., and W. E. Briles. The adaptive value of blood group genes in chickens. Genetics 38:35-50. 1953. 30. Somes, R. G. Registry of poultry genetic stocks in North America. Bulletin 437. Storrs Agr. Expt. Station, Storrs, Connecticut. 1976. 31. Stone, H. A. Use of highly inbred chickens in research. USDA Tech. Bull. 1514. pp. 22. 1975. 32. Wakeland, E. K., A. E. Benedict, and H. Abplanalp. Structural and genetic studies on chicken 7S immunoglobulin allotypes. II. Distribution in heterozygous chickens. J. Immunol. 118:401-404. 1977. 33. Waters, N. F. Breeding for resistance and susceptibility to lymphomatosis. Poultry Sci. 24:259-269. 1945. 34. Waters, N. F., and C. O. Prickett. The development of families of chickens free of lymphomatosis. Poultry Sci. 23:321-333. 1944.
TL;DR: Virus-neutralizing antibody rose rapidly following infection in both 2- and 8-week-old chickens, and Hyper-immune serum given during infection in an attempt to produce immune complexes did not increase disease severity in either 2- or 6- week-old susceptible chickens.
Abstract: Experimental infection with infectious bursal disease virus (IBDV) reduced the complement (C) titer in 8-week-old chickens on days 3, 5, and 7 postinfection. Since the C titer was much lower in normal 2-week-old chickens than in normal 8-week-old chickens it could not be determined whether there was a reduction in titer during the infection process. Virus-neutralizing antibody rose rapidly following infection in both 2- and 8-week-old chickens. Hyper-immune serum given during infection in an attempt to produce immune complexes did not increase disease severity in either 2- or 6-week-old susceptible chickens.
TL;DR: One-day-old chicks were inoculated intraperitoneally with a newly isolated picornavirus, and focal lesions were observed in the cortex of the kidneys from 3 to 21 days PI, characterized by interstitial lymphocytic infiltration and degeneration of epithelial cells of the proximal convoluted tubules.
Abstract: One-day-old chicks were inoculated intraperitoneally with a newly isolated picornavirus. The inoculated chicks showed no clinical signs until 28 days postinoculation (PI), but discoloration of the kidneys was recognized from 7 to 21 days PI at autopsy. Histologically, focal lesions were observed in the cortex of the kidneys from 3 to 21 days PI. The lesions were characterized by interstitial lymphocytic infiltration and degeneration of epithelial cells of the proximal convoluted tubules. The degenerated cells contained acidophilic granules in their cytoplasm. Electron-microscope examination of the cytoplasm revealed electron-dense amorphous areas, phagosomal areas with viral particles, and isolated crystal arrays of the virus particles, 23 to 30 nm in size. Granular antigen was also detected by fluorescent-antibody technique in the cells.
TL;DR: The conclusion is that high levels of spontaneously produced endogenous virus do not induce high levelsof neoplasms in chickens susceptible to lymphoid leukosis.
Abstract: SUMMARY A flock of 258 male and 243 female chickens of a cross of Regional Poultry Research Laboratory lines 15B and 72 were kept in a filtered-air positive-pressure house and observed for tumors from 100 to more than 729 days of age. These birds produced high titers of a subgroup E endogenous virus from the middle of the embryonic incubation period through the end of the experiment. No neoplasms were observed in the males. The females had two neoplasms indistinguishable from lymphoid leukosis and three other neoplasms not involving lymphoid cells. No evidence was found of infection with exogenous lymphoid leukosis viruses, Marek's disease virus, reticuloendotheliosis virus, or adenovirus (isolated on the isolation farm). Inoculation of another sample of this cross with a lymphoid leukosis virus of subgroup A resulted in 88% mortality with neoplasms (mostly lymphoid leukosis) by 167 days of age. The conclusion is that high levels of spontaneously produced endogenous virus do not induce high levels of neoplasms in chickens susceptible to lymphoid leukosis.
TL;DR: Pasteurella multocida grown in the turkey underwent bacteriolysis after thawing from a frozen state and did not induce cross-protection when used as vaccines whereas unfiltered lysates did.
Abstract: Crude liver homogenates from turkeys that died of fowl cholera produced by serotype 1 or 3 Pasteurella multocida induced cross-protection. Pasteurella multocida harvested from the blood of infected turkeys by a centrifugal technique were as immunogenic as the liver homogenates. Neither bacterial cell-free blood plasma nor washed P. multocida from infected turkeys induced significant cross-protection. Blood plasma containing P. multocida induced significant cross-protection. Pasteurella multocida grown in the turkey underwent bacteriolysis after thawing from a frozen state. Filtered lysates did not induce cross-protection when used as vaccines whereas unfiltered lysates did. Membrane filters impeded passage of immunogenic material.
TL;DR: Protection was only partial in passively immune chickens vaccinated with KVME after passive antibodies were no longer protective to unvaccinated and KVS-vaccinated chicks, and evidence of virus was found in immune chickens inoculated IB with modified IBDV.
Abstract: Modified infectious bursal disease virus (IBDV) administered ocularly to either susceptible or passively immune chicks did not induce protection against bursal atrophy by wild IBDV, while intramuscular (IM) or intrabursal (IB) injection protected susceptible chickens. No protection was obtained in passively immune chickens vaccinated IM or IB. Susceptible and passively immune chickens vaccinated with a single dose of killed-virus suspension (KVS) did not become resistant to wild IBDV challenge. A killed-virus multiple emulsion (KVME) induced partial protection (3/5) against challenge 28 days after subcutaneous vaccination of three-day-old susceptible chickens. At 35 and 42 days old, all susceptible chickens were protected by KVME. Protection by passive antibodies was observed in unvaccinated, KVS-, and KVME-vaccinated chickens challenged at 10 and 17 days of age. Protection was only partial in passively immune chickens vaccinated with KVME after passive antibodies were no longer protective to unvaccinated and KVS-vaccinated chicks. Modified IBDV was detected two days post-IB inoculation only in the bursa of Fabricius of susceptible chickens, while wild IBDV was found also in the thymus, spleen, and blood. No evidence of virus was found in immune chickens inoculated IB with modified IBDV. The growth of wild IBDV was limited to the bursa of Fabricius in immune chickens. Furthermore, the intensity of fluorescence, as well as the number of positive bursa cells, was low when compared with fluorescence in the bursa of susceptible chickens infected with wild IBDV.
TL;DR: Acute respiratory disease in turkeys appears to be of an infectious nature, and the infectious agent(s) probably exist in the heavily contaminated environment used to house young commercial turkey poults.
Abstract: Clinical signs of acute respiratory disease of turkeys were transmitted to susceptible day-old poults by direct contact, litter contact, and drinking water. Attempts failed to transmit the disease by air (cage-to-cage) or by oral and nasal inoculation with feces, nasal exudates, or nasal turbinate extracts. The disease was not transmitted by inoculation with white blood cells. Chicks were not affected by the disease, but young quail developed signs of respiratory disease when exposed to contaminated drinking water. Thus, acute respiratory disease in turkeys appears to be of an infectious nature, and the infectious agent(s) probably exist in the heavily contaminated environment used to house young commercial turkey poults.
TL;DR: The pathogenic and attenuated viruses stimulated similar IBDV-neutralizing antibody responses, which occurred after peak serum interferon activity, which was greater following inoculation with pathogenic I BDV than with the attenuated virus.
Abstract: Infectious bursal disease virus (IBDV) isolants that differed in virulence for chickens, were compared as to: 1) induction of interferon in serum and tissues; and 2) stimulation of IBDV serum antibody. Specific-pathogen-free chickens were infected at one day and four weeks of age by the subcutaneous and intranasal routes of inoculation. The pathogenic isolant induced a more generalized interferon response than the attenuated isolant, independent of age or route of inoculation. Pathogenic IBDV stimulated interferon in serum, kidney, lung, thymus, spleen, and bursa of Fabricius. The attenuated virus induced interferon only in the bursa. The serum interferon response was greater following inoculation with pathogenic IBDV than with the attenuated virus. Serum interferon titers peaked 2-3 1/2 days after inoculation. The pathogenic and attenuated viruses stimulated similar IBDV-neutralizing antibody responses, which occurred after peak serum interferon activity.