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.

Molecular characterization of Mycoplasma gallisepticum isolates from turkeys.

Mycoplasma gallisepticum was isolated from several turkey flocks at different locations in the United States that were clinically affected with respiratory disease. Five of these isolates from four series of outbreaks had patterns similar to the 6/85 vaccine strain of M. gallisepticum by random amplified polymorphic DNA (RAPD) analysis using three different primer sets, whereas with a fourth primer set (OPA13 and OPA14), only two of the isolates were similar to 6/85. Results obtained by sequencing portions of the pvpA, gapA, and mgc2 genes and an uncharacterized surface lipoprotein gene indicated that the field isolates had DNA sequences that ranged from 97.6% to 100%, similar to the 6/85 results. In some of the outbreaks there was an indirect association with the presence of commercial layers in the area that had been vaccinated with this vaccine strain, but there was no known close association with vaccinated birds in any of the outbreaks. Turkeys were challenged with two of the field isolates and with 6/85 vaccine strain. Turkeys challenged with the field isolates developed respiratory disease with airsacculitis and a typical M. gallisepticum antibody response, whereas birds challenged with 6/85 developed no respiratory signs or lesions and developed only a weak antibody response. Although these isolates were very similar to the 6/85 vaccine strain, it was not possible to prove that they originated from the vaccine strain-it is possible that they could be naturally occurring field isolates.

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.

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.

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.

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.

Subcutaneous feather tract denervation does not alter feather retention force ante- and postmortem in broilers.

To determine whether feather retention force (FRF) in 6-wk-old commercial broilers was influenced by the presence or absence of cutaneous innervation, nerve trunks for the pectoral and sternal feather tracts were severed unilaterally (left side) in Trial 1. In Trial 2, the sternal subcutaneous nerve trunk was severed either unilaterally (left or right side) or bilaterally. Four days postdenervation, FRF was determined bilaterally either antemortem (immediately prior to stunning) or 2 min after stunning and bleeding (postmortem). In Trial 1, the pectoral feather tract ante- and postmortem FRF values did not differ significantly for innervated or denervated tracts. In this trial, the sternal feather tract ante- and postmortem FRF values were 13% higher (44 g) for the denervated (left side) than for the innervated (right side) treatments. Partitioning this difference into the effects of sample side or innervation could not be attained because only the left side was denervated (left-denervation or right-innervated) in Trial 1. In Trial 2, both the left and right sternal feather tracts were represented in equal numbers for the innervated and denervated treatments, and there were no significant differences in FRF related to innervation, left and right side, or ante- and postmortem sample times. The presence or absence of cutaneous nerve innervation does not appear to influence FRF ante- or postmortem. This finding indicates that treatments disabling the central nervous system antemortem may lower FRF indirectly by altering cutaneous metabolism and therefore have been consistently unsuccessful in substantially altering postmortem FRF.

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.

Influence of time off feed on broiler viscera weight, diameter, and shear.

The influence of time off feed on broiler viscera weight, intestinal diameter, and shear was studied by subjecting market-age male broilers (42, 44, or 48 d) to incremental feed withdrawal periods (0, 6, 12, 18, or 24 h). Body weight was determined prior to feed withdrawal and at the time of processing. After slaughter, scalding, and defeathering, the abdominal cavity was opened. Diameter and shear of the proventriculus-ventriculus junction, jejunum, and ileum segments were measured, as were gallbladder length and width. Thoracic and abdominal viscera, liver, and ventriculus weights were determined, and liver surface color was measured. Percentage body weight loss increased with longer feed withdrawal periods, as viscera, liver, and ventriculus weights decreased. Gallbladder length increased with time off feed, whereas its width did not change. Diameter of the proventriculus-ventriculus junction, jejunum, and ileum decreased with longer feed withdrawal periods. Shear values for the proventriculus-ventriculus junction, jejunum, and ileum were not influenced by time off feed. Positive correlations (P < 0.05 and r > 0.4) between viscera weight and intestinal diameter were detected. Correlations between all measured parameters and shear values were not significant. Liver color measurements indicated that longer feed withdrawal periods resulted in significant linear decreases in L* (lightness), +a* (redness), and +b* (yellowness). Longer feed withdrawal periods decreased viscera weight and intestinal diameter, which would lower the potential for cutting the intestine during automated evisceration. However, the resulting greater gallbladder length (5 mm) would increase the possibility of bile contamination during evisceration.

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.

Feather retention force in broilers ante-, peri-, and post-mortem as influenced by carcass orientation, angle of extraction, and slaughter method.

Stunning and slaughter trials were conducted to evaluate the influence of carcass orientation (inverted or supine), angle of feather extraction (parallel or perpendicular to the carcass surface), and slaughter method (exsanguination without or with spinal cord transection) on feather retention force (FRF) in commercial broilers sampled ante-, peri-, and post-mortem. The pectoral, sternal, and femoral feather tracts were sampled before and after stunning contralaterally, with a maximum indicating force gauge, from broilers suspended on a shackle (inverted) or laying on a table (supine). For all trials and sample periods FRF was consistently greater in the femoral area (547 to 679 g) than in the pectoral area (273 to 391 g), with the sternal feather tract requiring the least force at 246 to 343 g. Feathers extracted parallel to the carcass resulted in consistently greater FRF (9 to 29%) than feathers extracted at a perpendicular angle, at all sample periods. Broilers suspended on shackles ante- and peri-mortem had higher FRF values (5 to 30%) than those restrained in shackles in a supine position on a table. Other parameters resulted in minor and inconsistent alterations in FRF. Electrical stunning, when not followed by bleeding, resulted in small reductions in FRF (up to 7%). Bleeding after stunning without or with spinal cord transection resulted in variable peri-mortem FRF changes (+7 to -11% and +11 to -11%, respectively). Only in the pectoral feather tract was there a significant increase (5 to 6%) in FRF as broilers went from the ante- to peri-mortem state. At 2 and 6 min after stunning and initiation of exsanguination, post-mortem FRF was unaffected by carcass orientation for the pectoral and femoral tracts.

Feather retention force in broilers ante-, peri-, and post-mortem as influenced by electrical and carbon dioxide stunning.

Stunning and slaughter trials were conducted to evaluate the influence of stunning method (electrical 50 V alternating current, CO2 gas: 0 to 40% for 90 s or 40 to 60% for 30 s) on feather retention force (FRF) in commercial broilers. Feathers from the pectoral, sternal, and femoral feather tracts were sampled with a force gauge before stunning (ante-mortem) and contralaterally either after stunning (peri-mortem from 0.5 to 4 min) or after stunning and bleeding (post-mortem from 2 to 6 min). Prior to stunning, ante-mortem FRF values varied among assigned stunning methods only for the pectoral (7%) feather tract. After stunning, peri-mortem FRF values were higher only for the sternal tract (11% for 40 to 60% CO2 for 30 s); whereas after stunning and bleeding, post-mortem FRF values were lower than ante- or peri-mortem only for the sternal tract (10% lower for 40 to 60% CO2 for 30 s). Peri- and post-mortem FRF values did not differ among stunning methods for the pectoral and femoral feather tracts. Small changes in FRF values occurred from ante-mortem to peri-mortem (-1 to +12%), and from ante-mortem to post-mortem (-2 to +8%) across stunning methods. A significant increase was determined for only the pectoral tract (7%) from ante- to peri-mortem across stunning methods. Electrically stunned broilers that were not bled gained weight in excess of the 36 feathers removed (0.16%), apparently due to body surface water pickup during the brine-stunning process, whereas CO2-stunned broilers lost weight due to excretion of cloacal contents (-0.31 to -0.98%). The change in body weight among stunning methods was significant (P < 0.0233). Peri- and post-mortem FRF, in addition to bleed-out body weight loss, were not substantially influenced by electrical or CO2 stunning methods, and, therefore, carcass defeathering efficiency may not differ after scalding.

Adenovirus-induced inclusion body hepatitis in four-day-old broiler breeders.

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.

Expression of growth factors in chicken growth plate with special reference to tibial dyschondroplasia.

Immunoreactive growth factors were identified in chick embryonic cartilage and bone, and in the growth plate of normal tibiotarsi and tibiotarsi affected with tibial dyschondroplasia (TD). A specific pattern of temporal and spatial expression was observed for each growth factor. Transforming growth factor beta and alpha (TGF beta and TGF alpha) and epidermal growth factor (EGF) were briefly expressed in chondrocytes of early chick embryos. Immunolabelling for TGF beta then gradually shifted into cartilaginous matrix and was not observed in cytoplasm of hypertrophic chondrocytes until the late embryonic and post-hatch stages. The distribution and intensity of TGF beta labelling was the same in chondrocytes of the TD and normal growth plate. Insulin-like growth factor I (IGF-I) labelling persisted from the early embryonic stage to the end of the mid-stage and then disappeared from chondrocytes. IGF-I appeared again in chondrocytes 1-2 days before hatching. After hatching, the labelling intensified in prehypertrophic and hypertrophic chondrocytes. TD lesions displayed IGF-I in the distal region, mainly in chondrocytes around small blood vessels. EGF reappeared in proliferative and hypertrophic chondrocytes of the mid-embryonic stage. By day 18 after hatching, EGF was present mainly in prehypertrophic and hypertrophic chondrocytes. EGF was demonstrated only in distal proliferative and early prehypertrophic chondrocytes of the dyschondroplastic growth plate. TGF alpha was identified in hypertrophic chondrocytes adjacent to the periosteum and in the distal tip of the mid-embryonic growth plate. With progressing ossification, TGF alpha labeling intensified in the embryonic hypertrophic chondrocytes. In the TD growth plate at day 18 after hatching, TGF alpha expression was limited to 1-3 concentric layers of chondrocytes surrounding blood vessels.

Dietary 1,25-dihydroxycholecalciferol has variable effects on the incidences of leg abnormalities, plasma vitamin D metabolites, and vitamin D receptors in chickens divergently selected for tibial dyschondroplasia.

Three experiments were conducted to examine the efficacy of dietary 1,25-dihydroxycholecalciferol [(1,25-(OH)2D3)] on the development of tibial dyschondroplasia (TD) in chickens divergently selected for high (HTD) and low (LTD) incidences of TD. In Experiment 1, chickens from the two lines were fed two calcium levels (0.75 and 1.0%), with and without 5 micrograms/ kg dietary 1,25-(OH)2D3. In Experiment 2, both lines were fed diets containing 1.0% calcium and 0, 5, 10, or 15 micrograms/kg 1,25-(OH)2D3. The addition of 1,25-(OH)2D3 did not reduce the overall incidence of TD in Experiment 1, but did reduce the incidence of severe TD from 69 to 48% in the chickens receiving the 0.75% calcium diet. In this experiment, LTD chickens had higher plasma phosphorus and bone ash. No line differences were noted between plasma vitamin D metabolites or intestinal vitamin D receptors. In Experiment 2, 5 micrograms/kg of 1,25-(OH)2D3 decreased the incidence of TD from 94 to 76% and number three scores from 69 to 44% (P < or = 0.001). Higher amounts of 1,25-(OH)2D3 further decreased TD, but there was a reduction in body weight above 5 micrograms/kg. Plasma 25-hydroxycholecalciferol [25-(OH)D3] and 1,25-(OH)2D3 were higher and intestinal vitamin D receptors were lower in HTD chickens than in LTD chickens. Plasma 1,25-(OH)2D3 was not affected by dietary treatment, but 25-(OH)D3 was reduced by dietary 1,25-(OH)2D3. Experiment 3 was conducted to examine effects of line and dietary 1,25-(OH)2D3 on plasma vitamin D metabolites and intestinal and growth plate receptors. No effect of genetic line or dietary 1,25-(OH)2D3 was observed for vitamin D receptors concentration or plasma 1,25-(OH)2D3 levels. Plasma 25-(OH)D3 was reduced when 1,25-(OH)2D3 was fed. These results indicate that HTD chickens are somewhat responsive to dietary 1,25-(OH)2D3, but this treatment failed to prevent the lesion in a large portion of the population.

Comparative pathology of chickens experimentally inoculated with avian influenza viruses of low and high pathogenicity.

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.

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.

Effects of dietary calcium and 1,25-dihydroxycholecalciferol on the development of tibial dyschondroplasia in broilers during the starter and grower periods.

Two experiments were conducted to determine whether dietary 1,25-dihydroxycholecalciferol [1,25-(OH)2D3] can prevent tibial dyschondroplasia in broiler chickens throughout the growing period when withdrawn from the grower diet. The birds were reared in floor pens with pine shavings to 6 wk in Experiment 1 and 5 wk of age in Experiment 2. Calcium was fed at .65 or 1.00% and 1,25-(OH)2D3 was fed at 0 or 5 micrograms/kg to 3 wk of age. Half the birds consuming 1,25-(OH)2D3 were then fed 0 microgram/kg until the end of the experiments. The higher level of calcium decreased the incidences of tibial dyschondroplasia and severe lesions and increased bone ash. Dietary 1,25-(OH)2D3 increased bone ash at both levels of calcium at 3 wk and the end of the experiments when supplemented for the duration of the studies. When 1,25-(OH)2D3 was fed, tibial dyschondroplasia was reduced in Experiment 2 only at 3 wk. Tibial dyschondroplasia was decreased at 5 wk in Experiment 2 when .65% calcium was fed with or without 1,25-(OH)2D3 from 3 to 5 wk of age. There were no treatment effects on plasma calcium, dialyzable phosphorus, or 25-hydroxycholecalciferol. Plasma 1,25-(OH)2D3 was decreased at 3 and 5 wk in Experiment 2 when 1.00% calcium was fed. The results of Experiment 2 suggest that 1,25-(OH)2D3 can prevent tibial dyschondroplasia caused by inadequate calcium when fed for only 3 wk. The bone ash observed when 1.00% dietary calcium is fed is equal to that obtained when 5 micrograms/kg 1,25-(OH)2D3 is fed with .65% calcium for the entire growout period.

Formaldehyde vaporization in the hatcher and the effect on tracheal epithelium of the chick.

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 (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.