Effects of activity on avian gastrocnemius tendon.

Physical activity and its relationship to animal health is a continuous concern of the food animal industry. This study investigated the relationship between broiler (meat-type chicken) activity to the structural integrity of the gastrocnemius tendon. Birds were exposed to treadmill pacing to determine if increased mobilization would increase tendon strength and improve its resistance to soft tissue injury. One hundred eighty broilers raised under normal commercial housing conditions were forced to walk on a treadmill 30 min/d, 5 d/wk for 3 wk, beginning at 3 wk of age. The treadmill treatment did affect the growth rate of the broilers. At the end of the study, the average body mass of the treatment birds was 9% less than the average body mass of the control birds, and the average length of the treatment shanks was 5% less than those from the control birds. Biomechanical parameters were measured and used to determine changes in the structural and material integrity of the tendons. The treadmill treatment did not affect tendon toughness, stiffness, relaxation behavior, and failure strength, but treatment did appear to affect tendon geometry, in which 33% of the treadmill treatment tendons had an increased amount of tissue near the bifurcation. The treadmill treatment did not affect the amount of procollagen within the tendon, and no cellular anomalies were found.

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.

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.

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.

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.

Vitamin A toxicity: comparative changes in bone of the broiler and leghorn chicks.

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.

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.

Filariasis (Pelecitus sp.) in the cervical subcutaneous tissue of a pigeon with trichomoniasis.

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.

Intestinal diverticulum in a turkey.

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.

Pinealoma in a broiler breeder.

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.

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.

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.

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.

Sodium sesquicarbonate toxicity in broiler chickens.

A case of feed misformulation resulted in the addition of sodium sesquicarbonate (SSC) into broiler chicken feed. SSC is a buffering agent used in the manufacture of high urea ruminant feeds that were also produced in this feed mill. Within 2 days of receipt of the tainted broiler feed on the farm, chickens were exhibiting polydypsia and wet droppings and had increased levels of mortality. The postmortem lesions were dehydration, fluid-filled intestines, swollen, pale kidneys, and visceral urate deposits. Histopathology of the kidneys revealed dilated tubules with a giant cell response, loss of tubular epithelium, and a few needlelike crystals. The mortality within 4 days of exposure in three severely affected houses reached 17%. An analysis of the feed revealed sodium levels ranging from 2.59% to 4.88%, with chloride levels of 0.24%-0.40%. Ten percent of the ration was thought to be SSC that contains 36% sodium. To determine if the presence of the SSC caused the problems observed, a controlled study was undertaken. One hundred fifty 3-wk-old broilers were evenly distributed into three floor pens. One group was fed a normal grower ration, a second group was fed a ration containing 5% SSC, and a third group received a ration with 10% SSC. Mortality, packed cell volumes (PCV), total serum proteins, and histopathology of the kidneys were determined. The 10% SSC group had a 6% mortality. Dehydration was evident by elevated PCV within 1 day of ingestion of either ration containing SSC. Microscopic lesions in the kidney were more severe in chickens ingesting SSC when compared with control groups.

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.

Protection by a commercial Arkansas-type infectious bronchitis virus vaccine against a field isolate of the same serotype.

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.

Intravascular cartilaginous emboli in the spinal cord of turkeys.

A flock of 15-wk-old tom turkeys experienced an acute onset of paresis and ataxia in 75% of the birds after handling. Cartilaginous emboli were found in the spinal cord vasculature from one of five turkeys at this initial presentation. Most of the flock recovered within 6 days, but 3% remained paretic. Myelomalacia was present in three turkeys that failed to recover. Two of these turkeys had cartilaginous and osseous emboli within the medullary spaces of the vertebral bodies, internal vertebral venous sinuses, and spinal cord. The third turkey had vascular and spinal cord necrosis consistent with thrombosis and resultant ischemia. These changes suggest that turkeys may be susceptible to a syndrome analogous to fibrocartilaginous embolism of the spinal cord in mammals. The articular cartilage of the vertebral body endplate may be the source of the emboli. The turkeys with emboli had articular cartilage defects consisting of matrix eosinophilia, chondrocyte loss, multicellular cluster formation, cartilage detachment, and cartilage clefts. Cartilaginous emboli in the spinal cord should be considered as a potential cause for acute paresis and ataxia, especially in flocks with preexisting abnormalities of the vertebral articular cartilage surfaces.

Tibial dyschondroplasia in single-comb White Leghorn chicks fed tetramethylthiuram disulfide (a fungicide).

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.

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.

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.