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Biomedical subjects

R K Page

Publications and source records attributed to R K Page.

At least 37 records · Page 2Linked to original sources

A comparison of the efficacy against Marek's disease of cell-free and cell-associated turkey herpesvirus vaccine.

One-day-old White Leghorn and broiler chicks with maternal antibody to turkey herpesvirus (HVT) were vaccinated with 300 or 1,000 plaque-forming units (PFU) of cell-free or cell-associated HVT vaccine and challenged with virulent Marek's disease virus (MDV) by contact exposure. Broiler chicks receiving 300 PFU of cell-associated HVT had a 3.3% incidence of MD lesions, whereas only 2.0% of those receiving 1,000 PFU had macroscopic lesions. Broiler chicks vaccinated with 300 PFU of cell-free vaccine had 6.8% gross lesions, and 0.67% of the birds receiving 1,000 PFU had MD lesions. Unvaccinated broiler chickens had a 28.3% incidence of MD lesions. Unvaccinated White Leghorn chickens had a 48.9% incidence of macroscopic lesions, whereas 5.4% of the birds receiving 300 PFU of cell-associated HVT had gross lesions, and 8.3% of the birds vaccinated with 1,000 PFU had lesions. In contrast, 6.7% of the chicks vaccinated with 300 PFU of cell-free HVT had MD lesions, and only 4.0% of those receiving 1,000 PFU of cell-free HVT had macroscopic lesions.

Animals↗

Cryptosporidiosis of the bursa of Fabricius of chickens.

Light-microscope and electron-microscope studies of a coccidial organism found in the bursa of Fabricius from 3 chickens clearly established the parasite as belonging to the family Cryptosporiidae. Hyperplasia and heterophil infiltration were associated with the presence of organisms attached to the microvillus border of epithelial cells lining the plicae of the bursa of Fabricius. Although there were no clinical signs or gross lesions common to the 3 cases described, all had similar histologic lesions in the epithelium lining the bursa of Fabricius.

Animals↗

Interaction of aflatoxin with Eimeria tenella infection and monensin in young broiler chickens.

Young broiler chicks inoculated with Eimeria tenella and given a diet containing 2.5 mug aflatoxin/g had significantly higher mortality than birds with aflatoxicosis or coccidiosis alone or uninoculated controls. This effect was seen even when a light coccidial infection alone did not increase mortality or cause weight depression. In addition this higher mortality with the combination began earleir and occurred at a higher rate than did mortality from aflatoxin or cecal coccidiosis alone. Dietary monensin sodium (99 umg/g) did not completely prevent mortality and weight depression when aflatoxin and E. tenella were in combination. Aflatoxin and E. tenella singly significantly depressed three-week body weights; however, the depression was most severe when the two were in combination. Both dietary aflatoxin and E. tenella significantly reduced hemoglobin, packed cell volume, and plasma pigmentation, and in combination resulted in more severely reduced hemoglobin, packed cell volume, and plasma pigmentation. Coccidial lesion scores were significantly less for the combination of E. tenella and aflatoxicosis than for coccidiosis alone. This atypical response of the ceca to E. tenella in the presence of dietary aflatoxin was characterized by less distended ceca, very little coagulated blood in the ceca, and apparently more profuse cecal hemorrhage.

Aflatoxins↗

Myopathy of the deep pectoral muscle in broiler breeder hens.

Myopathy of the pectoralis profundus and ambiens muscles was found in chickens from 5 flocks of broiler breeder hens. Histological lesions in the muscles varied from steatosis to loss of striations, fragmentation of fibers, and mineral deposition. A clinical response followed oral medication with vitamin E and selenium although analysis showed that selenium and vitamin E levels in the feed were normal. The possible relation between myopathy and Cassia seed in the feed is discussed.

Animals↗

Experimental exposure of broiler chickens to boric acid to assess clinical signs and lesions of toxicosis.

One-day-old broiler chicks were housed on litter treated with 0, 0.9, 3.6, or 7.2 kg of boric acid per 9.3 m2 of floor space. After 15 days, average body weights were 340.7 g, 278.1 g, and 213.2 g for chickens exposed to 0, 3.6, and 7.2 kg boric acid/9.3 m2, respectively (P < or = 0.05). Feed conversion was 1.68 and 2.29 in chickens exposed to 0 and 7.2 kg boric acid/9.3 m2 (P < or = 0.05). In a second experiment, after birds ingested feed treated with 2500 and 5000 ppm of boric acid for 2 weeks, body weights were 254.8 g and 149.6 g, respectively. The chickens in the control group weighed an average of 285.0 g (P < or = 0.05). The 5000 ppm treatment group had a feed conversion of 1.70, vs. 1.45 in the controls (P < or = 0.05). A dose-related feathering abnormality was evident in treated chickens. No significant histopathologic changes were observed. Livability, weight gain, and feed conversion were not adversely affected in broilers as a result of exposure to litter treated with boric acid at recommended levels of 0.4-0.9 kg/9.3 m2.

Animals↗

Acute toxicity of boric acid and boron tissue residues after chronic exposure in broiler chickens.

The acute oral mean lethal dose of boric acid in 1-day-old chickens was found to be 2.95 +/- 0.35 g/kg of body weight, which classifies this product as only slightly toxic to chickens. One-day-old broiler chicks were housed in floor pens in which litter had been treated with 0, 0.9, 3.6, or 7.2 kg of boric acid per 9.9 m2 of floor space. Boron residue levels in brain, kidney, liver, and white muscle were not statistically elevated following a 15-day exposure period. Boron residue levels in the same types of tissue were not significantly elevated in chicks fed 500 ppm or 1250 ppm boric acid in feed ad libitum for 3 weeks; however, residues were significantly higher in chicks fed 2500 ppm or 5000 ppm boric acid. These data indicate that broilers grown on boric acid-treated litter do not consume enough boric acid to cause elevated boron levels in tissues.

Animal Feed↗

Effect of infectious bursal agent on the response of chickens to Newcastle disease and Marek's disease vaccination.

White Leghorn chickens raised from one day old in an environment contaminated by the infectious bursal agent (IBA) had lower geometric mean titers (GMT) as measured by the hemagglutination-inhibition (HI) test to the Newcastle disease virus (NDV), than control Leghorns reared in an uncontaminated environment. Immunosuppression, defined as a reduction in GMT, was most pronounced at 35-56 days old for Leghorns vaccinated with NDV at 1 and 28 days or at 28 days. In a separate trial with broilers, immunosuppression was similar at 42-56 days old. This study also demonstrated that IBA infection in chickens increased susceptibility to Marek's disease (MD). The unvaccinated control chickens infected with IBA averaged 56.3% MD lesions, whereas unvaccinated controls not exposed to IBA averaged only 18.1% macroscopic lesions. It was also found that 20.7% of the HVT-vaccinated chickens exposed to IBA had gross MD lesions, whereas those HVT-vaccinated chickens reared in an environment free of IBA had 2.99% gross MD lesions.

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↗

Necrotic enteritis in cage-reared commercial layer pullets.

Necropsy of five 12-week-old pullets from a flock of 99,300 suffering from an increased mortality rate revealed enlarged, gas-filled intestines, the mucosal surfaces of which had the "dirty turkish towel" appearance typical of necrotic enteritis. Although the pullets had been raised entirely in cages, intestinal scrapings revealed the presence of Eimeria maxima. Histopathological findings were compatible with necrotic enteritis. Clostridium perfringens was isolated by anaerobic culture from the intestines. Mortality returned to normal after bacitracin and amprolium were added to the feed.

Animal Husbandry↗

Studies on orthoreoviruses isolated from young turkeys. III. Pathogenic effects in chicken embryos, chicks, poults, and suckling mice.

The pathogenicity of four clone-purified reoviruses (81-51, 81-68, 81-311, and 82-88) was studied in experimentally infected specific-pathogen-free (SPF) chicken embryos and chicks. SPF and specific-antigen-and-antibody-negative (SAAN) turkey poults, and suckling mice. In SPF embryos, all four viruses caused death or lesions characteristic for avian reoviruses. SPF chicks inoculated orally with isolate 81-68 showed no signs of overt disease but did develop antibodies to reovirus. In some experiments, poults inoculated orally with isolate 81-68 exhibited increased mortality, abnormal feather development, lower body weight gain, and pasted vents. Body tremors, uncoordinated motor movement, and oily hair coats were seen in suckling mice inoculated intracerebrally with isolates 81-51, 81-68, and 82-88. Mice inoculated intracerebrally with isolates 81-68 and 82-88 exhibited retarded growth.

Age Factors↗

Viral arthritis in fryers related to reovirus infection in breeders.

In 1983, twenty-two outbreaks of viral arthritis/tenosynovitis were diagnosed in a 6-month period on 18 fryer farms of one commercial operation located in western Washington. The main source of the reovirus infection was traced to a breeder flock that supplied progeny chicks to all of the affected farms.

Animals↗

Subcutaneous clostridial infection in broilers.

A flock of 12,500 broilers 36 days of age experienced a sudden increase in mortality. Post-mortem lesions were emphysema, severe enteritis, and a serosanguineous fluid in the subcutaneous tissue of the breast and thighs; there was no evidence of a loss in the integrity of the skin. Clostridium perfringens and C. septicum were isolated from the affected subcutaneous tissue. Histopathological and serological examination indicated previous infection with infectious bursal disease virus. The subsequent immunosuppression and severe enteritis may have permitted the clostridia access to the circulatory system, with localization in the subcutaneous areas of the breast and thighs. Mortality returned to normal 48 hours after potassium penicillin G was administered via the drinking water.

Animals↗

Newcastle disease vaccination of broilers with high- and low-titered commercial vaccines.

The virus titers of seven commercial B1 strain Newcastle disease vaccines were evaluated. A 2 log difference in virus content was found between the vaccine with the highest titer (10(8.8) EID 50/ml) and the one with the lowest titer (10(6.8) EID 50/ml). Broiler chickens were vaccinated with the high- and low-titered vaccines to compare hemagglutination-inhibition (HI) antibody and challenge responses. The effect of vaccination at different ages on the HI titers was also examined. There were no significant differences between vaccine groups in HI antibody response or resistance to challenge. However, the high-titered vaccine may provide a margin of safety with the currently used methods of mass vaccination.

Animals↗

Studies on orthoreoviruses isolated from young turkeys. II. Virus distribution in organs and serological response of poults inoculated orally.

Day-old specific-antibody-negative turkey poults were inoculated orally with cloned turkey reovirus isolate 81-68. Virus reisolations from 11 different tissues revealed widespread distribution at 3, 5, and 7 days postinoculation (PI). Virus was isolated from the intestines until 21 days PI. Virus was isolated from tendons until day 7 PI and again at day 28 PI. Reovirus serum-neutralization antibodies appeared as early as 7 days PI. All inoculated birds showed positive VN serum titers (greater than or equal to 1:20) by day 21 PI. No reovirus was isolated from control poults, and they remained antibody-negative during the entire experiment.

Animals↗

Suspected mycotoxicosis in laying hens.

A flock of 15,000 leghorn-type hens experienced a 10% drop in egg production. Enlarged, blue combs and diarrhea were also present. Clinical signs, postmortem and histopathological lesions, and response to therapy were compatible with a diagnosis of mycotoxin intoxication. However, all feed samples submitted were negative for mycotoxins, so the diagnosis could not be confirmed.

Animals↗