Biomedical subjects
Publications and source records attributed to O J Fletcher.
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.
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Susceptible 3-week-old chicks were inoculated with cells of an avian transplantable lymphoid tumor (TLT) and then treated with serum from immune chickens, serum from control chickens, or balanced salt solution. Progressive tumor growth was observed in chickens of all 3 treatment groups. Tumor growth was followed by regression only in chicks treated with immune serum. Regression was characterized by necrosis of tumor cells, muscle regeneration, and lymphocyte and plasma cell infiltration.
A micromethod was modified to quantitate intestinal D-xylose absorption in young and extremely small birds. This test was performed in control and cloned-reovirus-inoculated turkey poults to investigate intestinal absorptive function. Absorption peaks and curves for control poults closely resembled those observed in normal humans. Poult groups absorbed significantly less D-xylose at 24 and 72 hours (P less than 0.0001 and P less than 0.0008, respectively) but not at 120 hours (P = 0.3178) after receiving a single oral dose of cloned reovirus. The modified D-xylose absorption test is suitable for experimental and clinical determination of absorptive function of the small intestine in the fowl.
Inoculation of 6-day-old and 4-week-old chickens with pathogenic or attenuated avian reovirus resulted in an inapparent infection. The virus had a greater tissue distribution and persisted longer in tissues of 6-day-old chickens. Interferon was detected in only the serum and lung of infected chickens and appeared to be related to route of inoculation. Titers of interferon were greater and appeared sooner in the tissues of older chickens. Reovirus-neutralizing antibody was not detected in the serum of chickens of either age 120 days postinfection.
Chickens vaccinated at one and 14 days of age with a live vaccine containing the Massachusetts and Connecticut strains of infectious bronchitis virus were protected against challenge with a Massachusetts strain administered at 5 weeks of age. The virus recovery method in which tracheal swabs taken 4 days post-challenge were used to inoculate chicken embryos was compared with the method based on ciliary activity in tracheal explants. The results showed that evaluation of ciliary activity effectively measured immunity to infectious bronchitis virus. Serological results obtained in a microneutralization test using chicken embryo kidney cells correlated with the immune status of the birds as well as with the alpha neutralization results obtained using chicken embryos.
Nine groups of 10 one-day-old broiler chicks were vaccinated by eye-drop, coarse spray, or intratracheal instillation with combined Newcastle disease-infectious bronchitis live vaccines containing the Massachusetts (Mass) 41, Holland 120, or Connecticut 46 strain of infectious bronchitis virus (IBV). Chickens vaccinated with Mass-41 or Holland 120 were protected against challenge with a Mass strain administered at 4 weeks of age. When immunity to the disease was evaluated by virus recovery, detection of IBV by fluorescent antibody, evaluation of ciliary activity, histopathology, and virus-neutralization titers, the group vaccinated with Connecticut 46 did not show protection. Vaccination at 1 day of age resulted in an antibody response and increased resistance to challenge with Mass-41, regardless of vaccination route.
Severe mortality occurred in a flock of 16,000 turkey poults after fresh litter consisting of poplar, oak, sweetgum, and pine shavings was added to the brooder house. Signs and lesions seen were consistent with aspergillosis. Mortality for the first 21 days of brooding was 305 poults. New litter was added on day 21; 6,041 poults died during the next 24 days. Mold counts were done on the original litter and added litter. The mold counts for the original litter was 1.0 X 10(5) organisms per gram of litter. The mold count for the added litter was 2.5 X 10(6) organisms per gram of litter. After the added litter had been treated with nystatin and copper sulfate, the mold count dropped to less than 1 X 10(4) organisms per gram of litter. Mortality was also reduced but not to pre-infection levels. Rales, mucus rhinitis, and airsacculitis due to Escherichia coli developed. Despite treatment, performance of the flock remained poor.
A disease syndrome of broiler chickens is described. Affected birds exhibited poor pigmentation of the shanks, decreased weight gains, elevated feed conversions, poor feathering, enlargement of the proventriculus, and a decrease in the size of the gizzard. Reoviruses were isolated from affected chickens from several farms. Signs and lesions similar to those seen in chickens with the field syndrome were reproduced when these isolates were inoculated into day-old chicks with low levels of maternal antibody against viral arthritis. The pathogenicity of the viral isolates was variable. The incidence of lameness was much higher in those groups of chicks injected with these viruses than in the control groups.
Two viruses serologically related to the tenosynovitis virus of chickens were isolated from two flocks of turkeys experiencing outbreaks of tenosynovitis. Both viruses produced a tenosynovitis when injected into the foot pad of young turkeys. Staphylococcus aureus was not isolated from either flock, nor was there any evidence of Mycoplasma synoviae antibody in either flock.
Fledgling budgerigars from aviaries in Georgia and Texas were reported to have high rates of mortality. Affected birds died acutely and exhibited abdominal distention and reddening of the skin. Postmortem lesions were hydropericardium, enlarged heart and liver with areas of necrosis, and swollen, congested kidneys. Histologic examination of a variety of tissues revealed cells with enlarged nuclei containing inclusions. Electron micrographs revealed the presence of viral particles 42 to 49 nm in diameter in the nuclei of epithelial cells of the renal tubule.
A virus suspected of causing high death rates in fledgling budgerigars in Georgia and Texas aviaries was isolated in budgerigar embryo fibroblasts inoculated with tissue homogenates from affected birds. Virus was most easily recovered from tissues containing many intranuclear inclusion bodies. Cytopathic effect on fibroblasts of all four isolates was characterized by a swollen nucleus followed by rounding and detachment of the affected cell from the monolayer. Properties suggesting the B-931 isolate belongs to the papovaviridae family are (1) presence of DNA; (2) insensitivity to treatment with CHCl3; and (3) presence of cubic viral particles 42 to 49 nm in diameter in the nucleus of infected chicken embryo fibroblasts. The isolate did not hemagglutinate erythrocytes of chickens, turkeys, budgerigars, guinea pigs, or type O humans and was basically stable against heating and freeze-thawing. An examination of fledgling budgerigars from infected aviaries demonstrated that sick birds carried more virus than healthy birds.
Ochratoxin A, when fed at 0.0, 0.5, or 1.0 PPM to adult white Leghorn chickens, produced significant reduction in egg production and an increase in serum uric-acid levels, with a concomitant increase in egg-shell stains. These egg-shell stains were clinically similar to those described in the case report.
Ten 3-day-old chicks were submitted from a flock experiencing high mortality. Necropsy revealed lacrimation, diarrhea, pleural effusion, hemorrhage and ulceration of the proventriculus, and swollen, hemorrhagic livers. Numerous yellow granules were present in the crop. Assayed crop contents contained 39 ppm diazinon [O,O-diethyl O-(2-isopropyl-4-methyl-6-pyrimidyl)phosphorothioate]. The insecticide had been applied to the litter to control fire ants. The high mortality abated after new litter was added on top of the old litter. Diazinon toxicosis was traced to ingestion of diazinon-impregnated granules and was reproduced experimentally.
Germ-free and conventional chickens were infected with Lactobacillus acidophilus and/or Eimeria brunetti. Germ-free chickens acquiring single infections of E. brunetti were found to have lifecycle stages of the coccidial organism in the bursa of Fabricius.
Pathologic changes and distribution of viral antigen as determined by immunohistochemistry were compared among 4-wk-old specific-pathogen-free chickens inoculated intratracheally with avian influenza virus (AIV) isolates of either low or high pathogenicity. Viruses of low pathogenicity, previously characterized as mildly pathogenic (MP), included A/chicken/Pennsylvania/21525/83 (H5N2) (MP-Penn) and A/chicken/Alabama/7395/75 (H4N8) (MP-Alab). Viruses of high pathogenicity included A/chicken/Pennsylvania/1370/83 (H5N2), A/chicken/Victoria/A185/85 (H7N7), and A/turkey/Ontario/7732/66 (H5N9). Extremely variable clinical signs ranging from mild respiratory distress to high mortality were present among chickens inoculated with these viruses. Chickens inoculated with highly pathogenic (HP) virus had histologic lesions of necrosis and inflammation in cloacal bursa, thymus, spleen, heart, pancreas, kidney, brain, trachea, lung, and skeletal muscle, whereas chickens inoculated with MP virus had histologic lesions most frequently in lung and trachea or lacked histologic lesions. Immunospecific staining for avian influenza viral proteins was most common in cells within heart, lung, kidney, brain, and pancreas of chicken inoculated with HP viruses, but immunospecific staining was present only and infrequently in trachea and lung of chickens inoculated with MP-Penn AIV. MP-Alab did not produce lesions nor have viral antigen in inoculated chickens but did produce serologic evidence of infection. The pattern of organ involvement and viral antigen distribution in chickens intratracheally inoculated with HP AIV isolates indicates a common capability to spread beyond the respiratory tract and confirms the pantrophic replicative, pathobiologic, and lethal nature of the viruses. However, variability in severity and lesion distribution exists between different HP AIVs. By contrast, MP viruses had the ability to replicate in respiratory or enteric tracts or both and produce lesions within the respiratory tract. These MP viruses exhibited a restricted ability to replicate or produce lesions or both in nonrespiratory or nonenteric tissues; such effects were associated with only sporadic deaths.