Hepatopathy and lymphosarcoma in a mynah bird with excessive iron storage.
Hemochromatosis and hepatic neoplasia were diagnosed in a mynah bird. Poorly differentiated cells were identified ultrastructurally as neoplastic lymphocytes.
Biomedical subjects
Publications and source records attributed to G N Rowland.
Hemochromatosis and hepatic neoplasia were diagnosed in a mynah bird. Poorly differentiated cells were identified ultrastructurally as neoplastic lymphocytes.
An incidental central nervous system tumor was found in a broiler breeder. The cellular mass was histologically similar to the normal pineal gland, but it was characterized by a decreased ratio of follicular/parafollicular cells, a relative increase in mitoses, a size three times greater than a normal pineal gland, and growth and expansion into adjacent cerebellar tissue. These characteristics warranted a diagnosis of pinealoma rather than pineal gland hyperplasia.
Supplementing a practical chick starter diet with 30 mg tetramethylthiuram disulfide per kg of diet produced tibial dyschondroplasia (TD) in single-comb white leghorn chicks without compromising growth or bone mineralization. The incidence and severity of the lesion increased over time, with the highest incidence (40%) occurring in 4-week-old chickens. Microscopically, the lesion was consistent with the description of TD in broilers. This is the first known report of TD in the layer-type chick, which heretofore was felt to be highly resistant to TD.
Severe skeletal lesions were produced in both broilers and leghorns orally administered toxic levels of vitamin A (330 or 660 IU vit. A/g body weight X day) for 21 consecutive days. Hypervitaminosis A in broilers produced an osteodystrophy characterized by abnormal thickening of the proliferative-maturation zone, metaphyseal sclerosis, hyperosteoidosis, decreased number of osteoclasts, and parathyroid gland hyperplasia. In leghorns, the osteodystrophic lesions were characterized by a thin proliferative-maturation zone, a relatively thickened hypertrophy zone, flattened spindle-shaped osteoblasts, and osteoporosis. In both broilers and leghorns given excessive vitamin A, the osteogenic layer of periosteum in all bones was thin.
This report describes an inexpensive, rapid technique for preparing 4-micron-thick undecalcified sections of avian growth plate and metaphysis using paraffin embedment, rotary microtomes, and disposable knives. Sections were stained by von Kossa's technique with a hematoxylin-and-eosin counterstain.
Day-old broiler chicks were fed a calcium-deficient diet for 30 days. Gross, microscopic, and radiographic examinations of the proximal tibiotarsus were done at 2, 3, and 4 weeks of age. In 2-week-old chicks, the growth-plate proliferating-prehypertrophied zone (P-PHZ) was variably lengthened and disorganized, cartilage columns of the degenerating hypertrophied zone and metaphyseal primary spongiosa were shortened, and bone spicules of the secondary spongiosa were bordered by increased osteoid. In 3-week-old chicks, lesions were either similar or more pronounced, with the additional finding of metaphyseal peritrabecular fibrosis. In 4-week-old chicks, the P-PHZ decreased in relative length, osteoid seams and fibrous connective tissue were less prominent, and tibial dyschondroplasia-like lesions were present. Results demonstrated that dietary calcium deficiency produced rachitic lesions, that the lesions were very different from those of phosphorus deficiency or calcium excess, and that the lesions were variable over time.
Day-old broiler chicks were fed a vitamin D-deficient diet for 30 days. Gross, microscopic, and radiographic examinations of the proximal tibiotarsus were done at 2, 3, and 4 weeks of age. In 2-week-old chicks, there was variable lengthening and disorganization of the proliferating-prehypertrophied zone (P-PHZ), resorption of cartilage spicules in the degenerating hypertrophied zone and primary spongiosa, and lengthening of bone spicules in the secondary spongiosa; many bone surfaces were lined with increased osteoid. In 3-week-old chicks, there was a tendency for the P-PHZ to decrease in relative length and for cartilage spicules to increase in length. In 4-week-old chicks, however, there was marked lengthening of the P-PHZ, resorption of cartilage spicules, and replacement of the metaphysis with irregularly oriented islands of woven bone, osteoid, and loose fibrous connective tissue.
Day-old broiler chicks were fed diets high in calcium or low in phosphorus for 30 days. Chicks in both groups had similar gross, microscopic, and radiographic lesions. At 2 weeks, the growth-plate degenerating hypertrophied zone (DHZ) and metaphyseal primary spongiosa were lengthened and decreased in radiopacity. Metaphyseal vessels extended to the growth-plate hypertrophied zone (HZ), and osteoid seams were widened. At 3 and 4 weeks, lesions were similar; however, folding fractures were common and cartilage columns of the metaphysis were thinned and replaced with increased woven bone.
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 types of cartilaginous lesions were observed in a flock of 400 broilers separated into four groups and fed diets containing different energy and NH4Cl contents. The lesions appeared morphologically, histologically, and etiologically different. One lesion found in the vertebrae of 10 birds consisted of focal thickenings and necrosis of growth cartilages. Affected birds were predominantly faster-growing broilers fed diets without supplemental NH4Cl. The vertebral lesions were similar to osteochondrosis as described in mammals. A second lesion consisting of cones of retained cartilage was present in various long bones of 27.5% of all birds examined. The peak incidence of these dyschondroplastic lesions occurred in the slowest-growing group of 4-week-old birds fed diets containing 3% NH4Cl: 70% of these birds had dyschondroplasia. No positive correlation was found between the incidence of the vertebral lesions of osteochondrosis and the appendicular lesions of dyschondroplasia.
Explore the source record for details and available documents.
Chicken embryos were exposed to formaldehyde vapors in the hatcher during the final 3 days of incubation. Measured formaldehyde levels approached 130 ppm. Tracheas collected at hatch and 5 days post-hatch were evaluated for functional and morphologic changes. Tracheal cilia motility was reduced in formaldehyde-exposed chicks. Scanning electron microscopy revealed blunted cilia and blebs occurring in the cilia surfaces. At 5 days of age, excessive tracheal mucus was present. Sloughing of the tracheal epithelium was visible by light microscopy.
Filariasis due to Pelecitus was found in the subcutaneous tissue of the neck of a domestic pigeon from Spain that died from trichomoniasis. Macroscopically, filariae were observed in the congested and hemorrhagic cervical connective tissue. Microscopically, a particular distribution of parasites with no inflammatory infiltrates was observed. Adult nematodes were located in peritracheal connective tissue and in the deep zone of the subcutaneous tissue. Microfilariae were mainly located in the superficial zone of the subcutaneous tissue. The only other changes observed were a moderate catarrhal tracheitis and congestion of the viscera.
Severe foot-pad dermatitis was diagnosed in a case of broiler hens housed on slats made of lumber pressure-treated with chromated copper arsenate. Studies were conducted in an attempt to determine whether contact with the lumber caused the lesions. Breeder pullets were housed for 17 weeks on slats made from either untreated oak or pressure-treated lumber. Cresylic acid disinfectant was applied to one set of each slat type. Foot-pad lesions were scored and tissue arsenic levels were measured. Foot pads of the hens on pressure-treated slats were the only tissue with detectable arsenic levels. All groups developed foot-pad lesions, although the lesions appeared to be most severe, and to have developed earlier, in birds on pressure-treated disinfected slats.
A normal 21-day-old British United Turkey of America had an intestinal diverticulum. The diverticulum, which affected all layers of the intestinal wall, arose on the mesenteric surface of the ileum midway between the yolk sac and the cecal tonsils. The general structure of the diverticulum resembled the normal histological appearance of the ileum, although a progressive atrophy of the wall occurred throughout the length of the diverticulum. No metaplasia, inflammation, or tumor was observed.
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.
Two separate parent broiler flocks originating from the same grandparent flock experienced mortalities of 23% and 40%, respectively, in chicks between 1 and 14 days of age. Chicks affected at 4 days of age had tremors, depression, and hypoglycemia. They had pale yellow, swollen, friable livers. Pancreata were discolored and hemorrhagic. Spleens were swollen and sightly darkened. Microscopic lesions consisted of multifocal areas of acute hepatic and pancreatic necrosis with numerous basophilic intranuclear inclusions with karyomegaly. Splenic sections had severe lymphoid depletion and reticular cell and macrophage hyperplasia. An adenovirus from affected livers was isolated in chicken embryo liver cells. Serologic evidence suggests that the grandparent flock began egg production seronegative to adenovirus antibodies, was exposed during production, and, subsequently, shed adenovirus vertically to its progeny. The clinical syndrome was reproduced by injecting the isolated adenovirus into 1-day-old antibody-negative chicks. Histologic lesions in the experimentally reproduced disease cases were identical to those in the naturally occurring cases.
A late-breaking infectious bronchitis virus (IBV)-associated respiratory disease was a chronic problem in Georgia broilers in 1995. The predominant virus isolated from diseased birds was the Arkansas (Ark) type of IBV. Because broilers in Georgia are currently vaccinated with the Arkansas serotype, there was concern that a phenotypic and/or genotypic change had occurred in the field virus so it could break through immunity conferred by commercial vaccines. The purpose of this study was to determine if a commercially available vaccine for IBV as currently used in the field still protected broilers against those viruses. We obtained 108 1-day-old broilers from a commercial source and assigned them randomly to 12 groups. One-half of the groups of birds were vaccinated at 1 day of age and again at 18 days of age with commercially available B1/Mass/Ark vaccine. One-half of both vaccinated and nonvaccinated groups of birds were challenged at 35 and 42 days of age with a recent IBV Ark field isolate. Serologic titers were evaluated by enzyme-linked immunosorbent assay at time of challenge and at the end of the trial. A necropsy was performed on birds at 56 days and pathogenicity was assessed. Seroconversion was statistically significant in all birds exposed to vaccine or challenge by 56 days of age. Gross airsacculitis was significantly more severe in broilers challenged without prior exposure to vaccine.