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Biomedical subjects

O J Fletcher

Publications and source records attributed to O J Fletcher.

At least 73 records · Page 4Linked to original sources

Influence of infectious bursal disease on the development of immunity to Eimeria tenella.

Specific-pathogen-free (SPF) chicks infected with infectious bursal disease (IBDV) virus at one day of age or midway (7 days) through a two-week immunization program for Eimeria tenella showed significantly less (P less than or equal to 0.05) protection against coccidal challenge as measured by lesion scores than chicks given IBDV after 14 days of coccidial immunization. The chicks showed complete protection to later coccidial challenge administered on Day 21. Bursae were markedly smaller from IBDV-infected chicks than from uninfected controls, and pathological changes were extensive. Virus-neutralization tests demonstrated that titers to IBD were higher in chicks exposed to the virus than in unexposed controls.

Animals↗

Serologic and pathogenicity studies of avian adenovirus isolated from chickens with inclusion body hepatitis.

A virus initially thought to be inclusion body hepatitis virus (IBHV), Tipton strain, was classified as an avian adenovirus (AAV) and shown to be antigenically related to 2 serotypes of AAV, 764 and YR36. The virus was antigenically unrelated to AAV serotype TR-22, which included IBHV, Tipton strain. Inoculating specific-pathogen-free chickens with the virus produced hepatitis with basophilic and eosinophilic staining intranuclear inclusion bodies.

Adenoviridae↗

Experimental infection of turkeys with infectious bursal disease virus.

Commercial turkey poults 3 to 6 weeks old were infected experimentally by eyedrop with an infectious bursal disease virus (IBDV) inoculum obtained from chickens experiencing clinical IBD. The IBDV was passed 6 successive times in poults in an attempt to increase its pathogenicity for turkeys. Regardless of passage level, the IBDV infection in poults was subclinical, with no morbidity, mortality, or gross lesions observed. The bursae of Fabricius from infected poults, however, displayed various degrees of microscopic degeneration and IBDV specific fluorescence at 3, 4, and 5 days postinfection (PI). Infected turkeys also developed low levels of virus-neutralizing antibodies against IBDV at 12 days PI. Uninoculated poults kept in the same unit with infected poults also displayed microscopic changes and IBDV specific fluorescence 7 days after their appearance in inoculated poults. The IBDV was isolated from infected poults only after 5 successive passages of bursal material from infected poults in 9-day-old chick embryos. The IBDV from infected embryos was inoculated into susceptible 3-week-old chickens and 5-week-old poults and produced IBDV fluorescence and microscopic pathology in the bursae of infected poults and clinical IBD in infected chickens.

Animals↗

Rhinotracheitis in turkey poults.

A severe upper respiratory disease of young turkeys is described that resulted in high morbidity and mortality. Death was due to asphyxiation produced by occlusion of the trachea or nostrils. The postmortem lesions were tracheitis, pulmonary edema, swollen livers and spleens, and a drastic reduction in bursa size. Bursal necrosis and loss of tracheal epithelium were found in tissue sections from clinically affected birds. Antibody to infectious bursal disease was found by agar-gel precipitin and virus-neutralization tests of serum samples from affected flocks. A geometric mean titer of 31.5 for Newcastle disease was found in unvaccinated flocks of five-week-old turkeys.

Animals↗

Characteristics of Salmonella spp. and Escherichia coli isolated from broiler flocks classified as "good" or "poor" producers.

Cecal samples from 100 broiler flocks were cultured for Escherichia coli and Salmonella. Samples were selected from flocks classified as either "good" or "poor" producers by a production formula. In an attempt to identify predictors of flock productivity, isolates were studied for differences in antibiotic resistances, hemagglutination of erythrocytes, production of colicins, production of siderophores, type of hemolysis, resistance to host complement, and presence of plasmids. S. typhimurium (copenhagen) was isolated from one poor producing flock and three good producers. Salmonella isolates showed no significant differences in the parameters studied. The E. coli isolates showed significant differences only for the presence of plasmids. These data indicate that differences in host intestinal E. coli from good and poor producing flocks do not predict flock productivity.

Animals↗

Airsacculitis induced in broilers with a combination of Mycoplasma gallinarum and respiratory viruses.

Mycoplasma gallinarum was isolated from tracheas and air-sac lesions from broilers in flocks having higher than normal condemnations due to airsacculitis. A representative M. gallinarum isolant, given by aerosol or by air-sac inoculation, produced air-sac lesions in young chickens when given in combination with a vaccine combining Newcastle disease and infectious bronchitis or with a field strain of infectious bronchitis virus.

Agglutination Tests↗

The relationship of Cryptosporidium sp. infection of the bursa of Fabricius, intestinal tract, and respiratory system of chickens in Georgia, 1974-1988.

During 1974-1984, cryptosporidiosis was diagnosed in slightly more than 1% (63/6050 = 1.04%) of histopathology reports on chickens and turkeys made at two Georgia diagnostic laboratories. During 1985-1988, cryptosporidiosis was diagnosed in almost 6% (157/2622 = 5.99%) of histopathology reports on chickens and turkeys made at the two laboratories. Intestinal and respiratory Cryptosporidium sp. infections have increased significantly (p less than 0.01) with time. During the same period, there was no statistical pattern for bursa of Fabricius Cryptosporidium sp. infections, and there was no relationship between the incidence of bursal infections and the incidence of either respiratory or intestinal infections.

Animals↗

Infectious bursal disease viral infections. II. The relationship of age, complement levels, virus-neutralizing antibody, clotting, and lesions.

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.

Aging↗

Infectious bursal disease viral infections. I. Complement and virus-neutralizing antibody response following infection of susceptible chickens.

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.

Animals↗

Studies on interferon induction by infectious bursal disease virus (IBDV). II. Interferon production in White Leghorn chickens infected with an attenuated or pathogenic isolant of IBDV.

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.

Animals↗

Isolation, identification, and pathogenicity of two field strains of infectious bursal disease virus.

Using a sentinel bird approach, two field isolates of infectious bursal disease virus (IBDV) were isolated from broiler farms in two major broiler-producing areas of the state of Georgia. These farms had a history of subclinical IBD associated with respiratory problems and poor performance. Isolates designated as U-28 and 3212 were isolated using specific-pathogen-free chicken embryos and chicken embryo bursal cells. These isolates were identified by means of agar gel precipitation and virus-neutralization tests, direct immunofluorescence, histopathology, and electron microscopy. Isolates U-28 and 3212 appear to differ in antigenicity and pathogenicity from previously known serotype I IBDV isolates. In evaluating the extent of bursal damage caused by these field isolates, an association was found between the bursa of Fabricius/body weight index, histopathology scoring of atrophy, and morphometric analysis of the total follicle area.

Animals↗

Immunosuppressive potential and pathogenicity of a recent isolate of infectious bursal disease virus in commercial broiler chickens.

At 15 days of age and in the presence of measurable levels of maternal antibody against infectious bursal disease virus serotype I (1:170 virus-neutralization geometric mean titer), a recent isolate (U-28) and a prototype virulent isolate (Edgar) of the same virus caused subclinical infections in commercial broiler chickens. Isolate U-28 caused a significant reduction in the size of the bursa of Fabricius, whereas the Edgar isolate produced splenomegaly. Both isolates reduced the serological response to Newcastle disease virus. The experimental immunosuppressive potential and pathogenicity of isolate U-28 in broiler chickens confirms the role of this virus in recent infectious bursal disease outbreaks.

Animals↗

Pathogenicity of recent isolates of infectious bursal disease virus in specific-pathogen-free chickens: protection conferred by an intermediate vaccine strain.

The pathogenicity of recent isolates of infectious bursal disease virus and the protection conferred against them by a commercial vaccine strain of intermediate virulence were examined in specific-pathogen-free chickens. Based on clinical signs, mortality, and macroscopic lesions in susceptible chickens, the isolates designated as A-Delmarva and U-28 were distinct from a previously known serotype I virulent isolate (Edgar). Histopathological analysis of the bursa of Fabricius did not establish differences between the field isolates. Although the vaccine strain produced some degree of bursal damage in antibody-free chickens, it was significantly less severe than the damage caused by the field isolates. The active immune response induced by vaccination was cross-protective against the pathological effects produced by the different isolates used in this study.

Animals↗

Characteristics of fowl cholera outbreaks in turkeys in Georgia in 1986.

Information was gathered from 64 cases of fowl cholera (FC) in turkey flocks through diagnostic case records, flock records, and telephone and mail surveys. Forty-five cases came from flocks of commercial turkeys, of which 15 were presented twice, and four came from mature breeder flocks. The prevalence of FC was 18.0% of commercial flocks and 14.7% of breeder flocks at risk. The average age at first diagnosis of FC was 90 days in commercial turkey flocks and 32 weeks 5 days in breeder flocks. Acute mortality was the most common presenting complaint, with a 0.37% average mortality in commercial flocks on the day of first presentation, 0.80% in commercial flocks presented a second time, and 0.43% in breeder flocks. Pasteurella multocida was cultured from 69.8% of the 361 tissue samples submitted from these cases. Novobiocin, penicillin, and chlortetracycline (CTC) had the greatest in vitro activity against isolates. Serotype 3-cross-4 was found in all 18 commercial flocks from which isolates were typed. All breeder flocks and 88.6% of commercial flocks were vaccinated before disease onset. Flocks were treated for an average of 14.3 days, most commonly with high levels of sulfadimethoxine and/or CTC. Body weights of affected birds were comparable to those of birds in unaffected flocks, but mortality and feed efficiency were worse.

Animals↗

Comparison of serological tests for antibodies against Newcastle disease virus and infectious bronchitis virus using ImmunoComb solid-phase immunoassay, a commercial enzyme-linked immunosorbent assay, and the hemagglutination-inhibition assay.

COMBSCORES determined using the ImmunoComb solid-phase immunoassay were compared with hemagglutination-inhibition (HI) titers specific for Newcastle disease virus (NDV) and infectious bronchitis virus (IBV) and with mean enzyme-linked immunosorbent assay (ELISA) titers determined using Agritech Systems, Inc., ELISA. COMBSCORES for NDV and IBV increased proportionately in a stepwise manner as HI titers increased. The ImmunoComb solid-phase immunoassay was ablt to produce endpoint titers on sera with NDV-HI titers of 0 through 320 and IBV-HI titers of 0 through 1024 without reaching the maximum S-value. The ImmunoComb showed good correlation with the HI assay and the Agritech ELISA and should prove to be a useful tool for serological profiling, either alone or in conjunction with the HI test or commercial ELISA.

Animals↗

Comparative study of the pathogenicity of avian reoviruses.

Reovirus strains CO8 and 81-5, isolated from chickens with malabsorption syndrome, and reovirus strain 176, isolated from chickens with tenosynovitis, were each individually inoculated into 1-day-old specific-pathogen-free chicks. Strain CO8 caused tenosynovitis and pericarditis following footpad inoculation, but it was of low pathogenicity when given by either oral or subcutaneous route. In contrast, strains 81-5 and 176 were highly pathogenic and caused severe mortality following subcutaneous inoculation. Lesions included hepatic necrosis, bursal atrophy, thymitis, and splenic hyperplasia; strain 81-5 also caused pericarditis and myocarditis. Although strain 176 caused higher mortality than strain 81-5, these two strains differed little in the severity and distribution of the lesions they caused. No signs or lesions of typical malabsorption syndrome were observed.

Animals↗

The effect on newborn chicks of oral inoculation of reovirus isolated from chickens with tenosynovitis.

Reovirus strain 176, isolated from chickens with tenosynovitis, was highly pathogenic following oral inoculation of 1-day-old specific-pathogen-free chicks. Disseminated lesions including hepatic necrosis, splenic lymphostromal cell hyperplasia, and bursal atrophy occurred on day 3 postinoculation (PI), followed by myocarditis on day 6 PI and by pericarditis and tenosynovitis on day 9 PI. Reovirus was isolated from the liver as early as day 1 PI, whereas significant neutralizing antibody was detected on day 13 PI. Mortality occurred from day 4 to day 7 PI, and the death of birds was associated with the severity of hepatic necrosis. The occurrence of tenosynovitis in virus-inoculated birds was subclinical.

Animals↗

Application of the avidin-biotin-peroxidase complex (ABC) technique for detecting avian reovirus in chickens.

An immunoperoxidase technique, avidin-biotin-peroxidase complex (ABC), was used for detecting avian reovirus in glutaraldehyde-formalin-fixed, paraffin-embedded tissues. A peroxidase-positive reaction, characterized by the presence of dark brown granules in the cytoplasm of affected cells, was found in the liver (Kupffer cells, macrophages, and hepatocytes) and bursa of Fabricius (epithelial cells, stromal cells, and/or macrophages). The early presence of peroxidase activity in the bursa of Fabricius supports our previous idea that the bursa of Fabricius may serve as a primary site of replication for natural reovirus infection.

Animals↗