Biomedical subjects

G N Rowland

Publications and source records attributed to G N Rowland.

At least 55 records · Page 3Linked to original sources

PubMedDate not supplied

Detection of in ovo-inoculated infectious bronchitis virus by immunohistochemistry and in situ hybridization with a riboprobe in epithelial cells of the lung and cloacal bursa.

In situ hybridization and immunohistochemistry were utilized to identify tissues infected in ovo with infectious bronchitis virus (IBV). Chicken embryos were inoculated in ovo (chorioallantoic sac) with the Arkansas (Ark) serotype of IBV at 18 days of age. At 24, 48, 72, and 120 hr postinfection (HPI), bursa, lung, spleen, heart, and thymus were collected, fixed in 10% neutral buffered formalin, and paraffin embedded. The digoxigenin-labeled antisense S1 riboprobe detected viral mRNA in the cytoplasm of respiratory epithelial cells in the primary bronchus at 24, 48, and 72 HPI. Viral mRNA was detected in bursa samples collected at 48 hr. Immunohistochemistry detected viral antigens in epithelial cells of the parabronchi and bursal tissues at 24 and 48 hr, respectively. No viral mRNA or antigen was detected by in situ hybridization or immunohistochemistry, respectively, in heart, thymus, or spleen at any time after inoculation. On the basis of these data, IBV apparently initially infects lung tissue, then migrates to and infects cells of the bursa. These results indicate that in situ hybridization can be useful in detection of IBV-infected chickens and in understanding the pathogenesis and virulence of IBV infection.

Animals↗

PubMedDate not supplied

Hypoglycemia spiking mortality syndrome in broilers with rickets and a subsequent investigation of feed restriction as a contributing factor.

Several cases of elevated mortality with neurologic signs in 14-to-16-day-old broilers were presented to the Poultry Diagnostic and Research Center from one local integrated company. Suspected of "spiking mortality" associated with hypoglycemia, blood glucose levels were <150 mg/dl overall, with several birds with blood glucose levels as low as 30 mg/dl. Tissues, submitted for histopathology, revealed rickets in 50% of the birds. Virus isolation and serology for reovirus and infectious bursal disease virus were negative. After evaluation of these cases, a brief investigation was conducted to determine the effects of feed restriction on the induction of rickets and resulting hypoglycemia. One-hundred 1-day-old broilers were randomly assigned to three treatment groups of: 1) ad libitum feed, 2) 25% restriction, and 3) 50% restriction. Restriction began on the fifth day of age and continued to 21 days of age. Samples collected during the course of the study included whole blood for blood glucose measurements and proximal tibiotarsus for histopathologic examination for rickets. We were unable to reproduce the clinical signs of spiking mortality, neurologic changes, or hypoglycemia experimentally. Histopathology of the growth plates of the proximal tibiotarsus did indicate mild changes consistent with rickets, but the changes were not significant between treatment groups.

Animal Feed↗

PubMedDate not supplied

Adenovirus pathogenicity in immature ostriches.

Two group I avian adenoviruses implicated as the possible cause of "fading chick syndrome" in ostriches less than 8 wk of age were isolated in primary chicken embryo liver cells. These viruses were identified by virus neutralization and further characterized by a pathogenicity trial in immature ostriches. The results showed that these isolates were noninfectious in ostrich chicks.

Adenoviridae Infections↗

PubMedDate not supplied

Poor serologic response to upper respiratory infection with Mycoplasma synoviae in turkeys.

Mycoplasma synoviae (MS) was isolated from a flock of commercial tom turkeys in which a small percentage of the birds exhibited clinical signs and lesions typical of MS synovitis. However, serologic testing of such flocks revealed poor to inconsistent reactivity by agglutination, enzyme-linked immunosorbent assay (ELISA) or hemagglutination inhibition; isolation of MS from such flocks proved to be very difficult. Turkeys were challenged with one of the isolates (K4463B) either by aerosol or systemically by a combination of intravenous, foot pad, and eyedrop routes. Turkeys challenged by the systemic route responded normally to all serologic tests, whereas those challenged by aerosol either responded very poorly on all serologic tests or were seronegative up to 6 wk postchallenge even though they were positive for MS by tracheal culture. These results suggest that turkeys may harbor an upper respiratory infection with MS while remaining serologically negative.

Agglutination Tests↗

PubMedDate not supplied

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↗

PubMedDate not supplied

Pathology of experimental vitamin D deficiency in turkeys and the effects of various vitamin D supplements.

One-day-old poults fed a vitamin D3-deficient diet were examined for clinical, biochemical, and morphological changes at 14 days of age. Changes in these parameters were compared at 15.5 and 17 days of age after one of the following vitamin D-replacement therapies was provided: water-soluble vitamin-mineral packs that contained vitamin D3; vitamin D3 in the feed; or vitamin D, 1,25-dihydroxyvitamin D3 in the feed. The vitamin D3-deficient poults were lame and had significant decreases in weight gain and in longitudinal skeletal growth. None of the therapies alleviated all these changes, but clinical lameness subsided in poults provided 1,25-dihydroxyvitamin D3. Calcium concentrations were significantly improved by all therapies. Treatment with vitamin D3 in the feed and water significantly increased 25-hydroxyvitamin D3 concentrations in vitamin D-deficient poults. The growth plate zones, with the exception of the mineralized hypertrophied zone, were all increased in length and not modified by treatment. However, the mineralized hypertrophied zones in the 1,25-dihydroxy-vitamin D3 group and the group receiving vitamin D3 in the water were comparable to that in the controls on day 15.5.

Animal Feed↗

PubMedDate not supplied

Spontaneous regression of "dermal squamous cell carcinoma" in young chickens.

Eight young chickens with lesions characteristic of those described as dermal squamous cell carcinoma were obtained before slaughter. Lesions were measured; representative lesions were biopsied and examined microscopically; and gross changes were monitored. Lesions appeared to originate as cystic, keratin-filled proliferations of the feather-follicle epithelium. These cysts progressed into raised, keratin-filled, and eventually ulcerated, nodules. Loss of the keratin core resulted in a shallow ulcer that became progressively flattened and regressed into a fibrous dermal scar. All lesions in the broilers regressed in 4 to 16 days (mean 14 days). Twenty roaster lesions completely regressed. For roasters, the mean time to regression was 20 days, with a range of 6 to 93 days. Although there was limited invasion of the dermis by atypical keratinocytes, the overall architecture and biological behavior were more consistent with a benign lesion.

Animals↗

PubMedDate not supplied

Poult malabsorption syndrome. I. Malabsorption in poult enteritis.

One-day-old poults were placed on littler on which poults had previously developed diarrhea, increased mortality, and stunting. Small intestines, pancreas, and liver were evaluated histologically. Morphometric evaluations were conducted to determine villous length and crypt depth. Poults were evaluated for malabsorption utilizing D-xylose and lipid absorption tests. Compared with controls, the gastrointestinal tract of affected birds was grossly distended, was fluid-filled, and had thin, flaccid walls on days 5 and 8. Ceca were distended with brown watery fluid and gas on days 5, 8, and 12. No histologic lesions were present in the liver, pancreas, or pancreatic ducts, and only mild inflammatory changes were present in the small intestine. Villous atrophy and crypt hypertrophy were present in the small intestine on days 5, 8, 12, 16, and 21. Morphometry revealed significant decreases in villous lengths and increases in crypt depth throughout the trial. D-Xylose and lipid absorption were significantly decreased on days 8 and 11. Intestinal epithelial damage by infectious agents with subsequent villous atrophy is postulated to have produced malabsorptive diarrhea.

Animals↗

PubMedDate not supplied

Poult malabsorption syndrome. II. Pathogenesis of skeletal lesions.

One-day-old poults were placed on litter on which poults had previously developed diarrhea, increased mortality, stunting, and malabsorption. Gross, microscopic, and morphometric evaluations of the proximal tibiotarsal growth plate, along with analysis of plasma calcium, phosphorus, and 25-hydroxyvitamin D3 concentrations, were conducted for 3 weeks to determine the development and character of skeletal lesions. Poults developed enteritis with diarrhea and dehydration. Body weights and shank lengths were significantly decreased. Plasma 25-hydroxyvitamin D3 concentrations were significantly decreased. Plasma calcium was significantly decreased on day 8. Plasma phosphorus concentrations were significantly increased on day 8 and were significantly decreased on days 15, 18, and 22. Growth plates narrowed on days 8 and 11 and expanded on days 15, 18, and 22. The proliferating-prehypertrophy zone significantly decreased in length on days 11, 18, and 22, and significantly increased in length on day 15. The unmineralized hypertrophy zone was significantly increased in length on days 15, 18, and 22. The mineralized hypertrophy zone was significantly decreased in length on all days. Skeletal lesions during the poult malabsorption syndrome evolved from an early osteoporotic lesion associated with hypocalcemia to a rachitic lesion associated with depleted vitamin D and hypophosphatemia.

Animals↗

PubMedDate not supplied

Poult malabsorption syndrome. III. Skeletal lesions in market-age turkeys.

Skeletal deformities, a major contributing factor to economic losses in market-age turkeys, may be associated with the poult malabsorption syndrome. A study was performed to determine whether the naturally occurring malabsorption syndrome produces skeletal lesions in turkeys at market age. Poults were placed on litter on which poults had previously developed malabsorption. Exposed poults developed enteric disease with 21% mortality during the first 3 weeks. Controls had no enteric disease and no mortality. At the end of the study, 20-week-old exposed turkeys weighed 0.621 kg (5%) less than controls and had a higher incidence of angular limb deformities with significantly higher angulation scores. Exposed turkeys also had a greater incidence of rotated tibias and bowed tibias. The mechanical property of tibial shear strength was significantly lower in turkeys that had survived the earlier poult malabsorption syndrome.

Animals↗

PubMedDate not supplied

Skeletal lesions associated with a naturally occurring poult enteritis.

One-day-old poults were placed on contaminated litter on which poults previously had developed an enteric disease characterized by diarrhea, increased mortality, and stunting. These exposed birds were examined for clinical signs and pathologic changes in bone and parathyroid glands compared with controls. Intestinal and fecal samples were examined for potential pathogens. Exposed poults varied in size as early as day 8 and had significantly decreased weight gains and reduced shank lengths on days 8, 12, 16, and 21. The proximal tibial growth plate was narrowed. The mineralized hypertrophy zone was decreased in length and contained multiple non-mineralized bands on days 8, 12, 16, and 21. Metaphyseal trabeculae were reduced in amount on days 16 and 21. Parathyroid glands were hyperplastic on days 16 and 21. The bone and parathyroid gland lesions indicated that mineral homeostasis was being maintained at the expense of the skeleton during the enteric disease. A specific etiology for the enteric disease was not determined. Cryptosporidium, rotavirus, paramyxovirus, and Salmonella were identified in the exposed poults, and paramyxovirus and Salmonella were identified in the controls.

Animals↗

PubMedDate not supplied

Ultrastructure of the gastrocnemius tendon and sheath from broilers infected with reovirus.

Gastrocnemius tendon and sheath from male broilers infected with reovirus at 1 day of age were evaluated ultrastructurally at 1, 2, 3, 4, 5, 10, 15, and 20 weeks postinoculation (PI). Although virus particles were not identified, degenerative changes in sheath and tendon fibroblasts were characterized by cytoplasmic vacuolization, disruption of membranes, and loss of ribosomes from rough endoplasmic reticulum, mitochondrial degeneration, and cell disruption.

Animals↗

PubMedDate not supplied

Effects of cyclosporine A on reovirus-infected broilers.

The effect of cyclosporine A on reovirus-infected male broiler chickens was studied. Beginning at 1 or 10 days of age, 3 groups of 15 broilers were injected in the pectoral muscle with 50 mg of cyclosporine A (CSA) in oil per kg body weight every 3 days until 28 days. Controls were injected with olive oil. Two CSA-injected groups and one untreated group were orally infected with 1000 TCID50 of reovirus at 1 day of age. Cell-mediated immunity was evaluated at 17 and 24 days by a delayed-wattle-response test to injected phytohemagglutinin (PHA-M). Cyclosporine A and reovirus significantly (P less than 0.001) depressed the wattle response following the first injection of PHA-M but not the second. At necropsy 28 days postinoculation (PI), no gross lesions were apparent. Histologic lesions in birds infected with reovirus were lymphocytic pericarditis and tenosynovitis; synovial cells were hyperplastic, and heterophils and fibrin were in synovial spaces. Thymic medullary diameters were significantly (P less than 0.001) smaller in all CSA-treated birds. Although CSA suppressed cell-mediated immunity somewhat, there were no apparent differences in severity of microscopic lesions among reovirus-infected groups.

Animals↗

PubMedDate not supplied

Comparative microscopic lesions in reoviral and staphylococcal tenosynovitis.

Experimental inoculation of 1-day-old male broiler chickens with avian reo-virus or Staphylococcus aureus caused tenosynovitis of the gastrocnemius and digital flexor tendons. Reovirus inoculation by either the oral or footpad route initiated a diffuse lymphocytic infiltration in the peritendineum, synovial membrane, and epitenon from 1 to 5 weeks postinoculation (PI). Heterophils were not a predominant feature of the inflammatory response, but when present they were localized with fibrin in and around synovial spaces. The prevalence of microscopic tendon lesions was less common with staphylococcal infection than with reovirus infection. With staphylococcus, lesions were localized to the synovial space and membranes and were characterized by heterophils and fibrin but few lymphocytes. Synovial cell hyperplasia and bursal atrophy were common in both groups. From 10 to 20 weeks PI, both groups developed progressive tendon fibrosis. These results indicate that tenosynovitis due to inoculation with reovirus or staphylococcus may be differentiated histologically from 1 through 5 weeks PI. After 10 weeks, this may not be possible, because diffuse fibrosis was the major lesion with both. Perhaps fibrosis predisposes older, heavier broilers to tendon failure and rupture.

Animals↗

PubMedDate not supplied

Pasteurella multocida infection in Japanese quail (Coturnix coturnix japonica).

Three flocks of Japanese quail, approximately 75,000 birds each, experienced acute high mortality beginning at 24 to 28 days of age. Gross lesions were absent or were composed of either multifocal small pale areas on livers and spleens or lungs slightly darker in color than normal. Histopathology revealed multifocal splenic and hepatic necrosis and interstitial pneumonia. Pasteurella multocida, serotype 3,4, was isolated from affected tissues. The quail were successfully treated with chlortetracycline, and the organism was apparently eliminated from the premises by thorough cleaning, disinfection, and insect and rodent control. Experimental studies showed Japanese quail to be highly susceptible to disease caused by the P. multocida isolated from the affected flocks.

Animals↗

PubMedDate not supplied

Evaluation of Pasteurella multocida mutants of low virulence. I. Development and pathogenicity.

Mutagenesis of the Clemson University (CU) vaccine strain of Pasteurella multocida with N-methyl-N-nitro-N-nitrosoguanidine resulted in temperature-sensitive mutants that grew at 37 C but not at 42 C. Seven such mutants were evaluated for immunogenicity in turkeys. From these seven, only two, PM#1 and PM#3, provided turkeys with a level of protection against challenge with a virulent serotype 3 P. multocida strain (P-1059) comparable to the protection provided by the CU strain. Intravenous (IV) inoculation of PM#1, PM#3, or CU was used to assess differences in virulence. PM#1 and PM#3 resulted in lower rates of mortality and lameness than the CU strain. Histopathological evaluation of spleens 24, 48, and 72 hours after IV inoculation demonstrated that the CU strain induced significantly more fibrinoid necrosis of the spleen than either PM#1 or PM#3.

Animals↗

PubMedDate not supplied

Exacerbative effect of vitamin A on malabsorption syndrome in chicks.

The interaction between malabsorption syndrome (MAS) and dietary vitamins A and D was studied in broiler chicks reared in floor pens for 4 weeks. The chicks were naturally infected with MAS, whereas hatchmates fed the same diets but in a separate facility (battery brooder) did not exhibit signs of MAS and, therefore, were considered controls. MAS significantly reduced body weights, bone ash, serum calcium and phosphorus concentrations, and liver lipids and increased the incidence of skeletal abnormalities (tibial dyschondroplasia and rickets). Rather than ameliorating the effects of MAS, vitamin A caused a further reduction in body weight and bone ash. A possible nutrient interaction between vitamin A and vitamin D or vitamin E in birds with MAS may account for the exacerbative effect of vitamin A.

Animals↗

PubMedDate not supplied

Skeletal and tendon lesions of male broiler-breeders reared on elevated slats.

Eighty 25-week-old male broiler-breeder chickens were placed in pens with elevated slats for 16 weeks. A similar group of birds was housed on floor pens for comparison. The coxofemoral, stifle, and tibiotarsal joints and their supporting tendons and ligaments were examined grossly. Rearing heavy broiler-breeders on elevated slats did not result in grossly apparent arthritis, tendonitis, or tendon failure. Body weights and shank lengths and diameters were not markedly different. Microscopically, the broiler-breeders reared on slats had a lymphocytic synovitis with synovial cell hyperplasia involving the gastrocnemius and digital flexor tendons. The incidence and severity of the lesion increased with time.

Animals↗