Histologic study of hepatic lesions in two turkey flocks.

Hepatic lesions were studied in two turkey flocks by euthanatizing 50 birds a week from the ages of 1 through 15 wk. Samples of liver that contained lesions and samples of duodenum, pancreas, ileum, and cecal tonsil were examined histologically. Lymphocytic infiltrations made up 82% and 75% of the hepatic lesions, and granulomas occurred in 18% and 25% of the livers. Nematode larvae were present in 12% and 15% of the hepatic lesions.

Antigenic characterization of an Arkansas isolate of infectious bursal disease virus.

The s977 strain of infectious bursal disease virus (IBDV) was isolated in northwest Arkansas in 1977 from the bursae of young broilers with high maternal antibody titers to the Moulthrop strain of IBDV (BursaVac). The comparison of a plaque-purified isolate of s977 with other IBDV serotype 1 and serotype 2 strains using virus neutralization indicates that s977 is a subtype of serotype 1 vaccine viruses and the MD variant strain of IBDV and has no relatedness to the Delaware Variant A (VarA) virus. In vivo cross-protection studies in specific-pathogen-free white leghorn chickens showed that an inactivated vaccine using s977 antigen was 2.5 times more protective against challenge with s977 than was an inactivated IBDV Variant E (VarE) vaccine. The vaccination of maternally immune broiler chicks with live s977 did not provide protection against subsequent challenge, indicating that s977 does not have enough antigenic difference to break through maternal immunity. Analysis of denatured viral polypeptides using polyacrylamide gel electrophoresis showed that s977 and two reported variant strains, 51 and VarE, share three protein bands, 90 kD (VP1), 40 kD (VP2), and 31 kD (VP3), that were not observed in BursaVac. BursaVac and s977 shared a 74 kD precursor band that was absent or very faint in the VarE and 51 strains. The most unique characteristic of s977 was the relative abundance of a wide, 56-63 kD band that contained two distinct immunoreactive bands when blotted with antiserum to s977. BursaVac contained a 56 kD band that failed to react with s977 antiserum. Analysis of polypeptide bands using laser densitometry indicated the presence of a number of bands between 20 kD and 25 kD in the s977, 51, and VarE preparations but only a 25 kD band in BursaVac. The number of bands decreased with the degree of relatedness to standard vaccine strains. It appears that, antigenically, S977 may hold an intermediate position between the classic virus strains and the more recently reported serotype 1 variants.

A survey of two commercial turkey farms experiencing high levels of liver foci.

Two turkey farms that had previously experienced high levels of liver condemnations at slaughter were monitored through one complete growout cycle. Liver foci appeared at both farms by week 2. More than 80% of the liver foci sampled did not have any aerobic or facultative bacteria isolated from the lesions. Low numbers of Ascaridia dissimilis larvae were found on both farms by week 3 in the growout. The patterns for the ascaridiasis at both farms were similar, although one of the farms had a higher number of ascarids earlier than the other. Neither farm had high levels of adult ascarids present, although the average larval burden was high. Piperazine was administered at both farms on multiple occasions, but there were no significant decreases in the level of adult ascarids following administration. There was no apparent development of immunity, since all stages of the life cycle remained stable, even late in the growout. The simultaneous appearance of the liver foci and the A. dissimilis indicate that the ascarids may be responsible for the hepatic pathology.

Age-related changes in the incidence of tibial dyschondroplasia in turkeys.

Age-related changes in the incidence and severity of tibial dyschondroplasia (TD) and its relationship to body weight and other bone pathologies were studied in turkeys from ages 2 through 15 wk. A steady increase in the incidence and severity of TD was observed from 11 wk onwards. Whereas there was no correlation between the body weight and TD in early ages, during Weeks 14 and 15 the turkeys with severe TD had significantly higher body weight relative to those without or with mild lesions. Starting from Week 13, hemorrhage was evident in the base of TD-affected growth plates of many turkeys, which increased linearly during the following weeks. Histological examination of these areas revealed mild necrosis with erosion in TD tissues accompanied by occasional bone formations, fibrosis, and the presence of multinucleate chondroclasts and large number of erythrocytes adjacent to lesions. Sporadic rod-like bacterial colonies were discernible in TD tissues and cartilage canals. These studies show 1) whereas the onset of TD may have an independent etiology, the severity of the disease may be influenced by a higher body weight; and 2) subepiphyseal hemorrhages possibly facilitate a healing-type response that leads to replacement of TD tissue by way of resorption, bone formation, and fibrosis, but simultaneously makes the tissue accessible to bacteria.

Use of virulent hemorrhagic enteritis virus for the induction of colibacillosis in turkeys.

Three hundred fifty 1-day-old large white turkeys were reared in brooding batteries to 10 days of age, after which they were moved to floor pens on litter. At 7 weeks of age, poults were allotted into four treatment groups as follows: 1) virulent hemorrhagic enteritis virus (HEV) alone (100 turkeys), 2) Escherichia coli alone (100 turkeys), 3) HEV + E. coli (100 turkeys), and 4) negative controls (50 turkeys). HEV was given orally at 7 weeks of age, followed by E. coli challenge in the drinking water 2 days later for 10 consecutive days. All groups were observed daily for mortality, both during and after challenge. Turkeys that died or were moribund were necropsied, and cultures were taken from the liver and bone marrow for bacterial isolation. Total mortality rates were 23% in the HEV + E. coli group, 10% in the HEV-only group, 3% in the E. coli-only group, and 0% in the negative control group. Cumulative mortality values were significantly different from those of the negative controls (P < or = 0.05) for HEV only and the HEV + E. coli group. E. coli was isolated from the liver and bone marrow of almost all turkeys that died.

Effect of age of maternal flock and strain on the incidence of tibial dyschondroplasia in growing chicks.

Two experiments were conducted to study the effects of age of the maternal flock (27 vs. 57 weeks of age at time the eggs were set) and strain of broiler chicks (Cobb 500, Ross, Arbor Acres, and Avian) on the incidence of tibial dyschondroplasia (TD) in broiler cockerels grown to 3 weeks of age. The chicks were fed a corn/soybean meal-based diet containing 3145 kcal metabolizable energy corrected for nitrogen retention (MEn)/kg, 24% protein, and 0.50% available phosphorus. Each treatment was replicated four times with eight chicks per pen. In Expt. 1, chicks from the old parent flock had significantly higher body weights (P < or = 0.05) than those from the young parent flock. There were no significant differences in feed efficiency or incidence of TD. In Expt. 2, body weights, feed efficiency, and TD were unaffected by strain.

Investigation of a chronic feed-passage problem on a broiler farm in northwest Arkansas.

A commercial broiler farm with a history of poor feed conversion and chronic feed-passage problems was chosen for investigation. Chickens were taken from the broiler flock at specified intervals during growout and tested by virus isolation and enzyme-linked immunosorbent assay (ELISA) for avian reovirus. Abnormal tissue pathology was first seen in the broilers at 9 days of age and continued sporadically throughout the growout period. Antireovirus antibody levels began to increase at 24 days of age. Avian reovirus and avian adenovirus was recovered at different intervals starting at 17 and 31 days of age, respectively. One-day-old specific-pathogen-free chicks housed in filtered-air positive-pressure isolation units were inoculated with two inocula recovered from the field study. Avian reovirus was recovered from the tissues of both treatment groups using chick kidney cells. Significant weight differences were seen in one of the two treatment groups. This avian reovirus was given the name SS-412.

Efficacy of thiabendazole (Mertect 340-F) in controlling mold in turkey confinement housing.

Mertect 340-F (thiabendazole) was evaluated as a mold inhibitor for litter in turkey confinement housing using green oak wood shavings heavily contaminated with mold spores. One day before the addition of shavings, two environmentally controlled rooms were sprayed with Mertect 340-F at a rate of 51.0 ml in 11.37 liters of water (16 fl. oz./6000 sq. ft.). After the litter was added, it was treated with Mertect 340-F at a rate of 33.0 ml in 75.8 liters of water (32 fl. oz./6000 sq. ft.). The litter was treated again at 6 and 12 weeks. Mertect 340-F-treated litter had significantly lower mold spore counts than water-treated litter. Turkeys reared on Mertect 340-F-treated litter displayed no adverse effects. No obvious differences between groups were noted post mortem. Microscopically, however, lungs from turkeys on water-treated litter had a higher incidence of granulomas and mycelia than lungs from birds on Mertect 340-F-treated litter.

Neoplasms in the oviducts of turkeys.

The reproductive tracts of turkey breeder hens from five flocks were examined grossly and histologically. Hens from one flock had a normal reproductive history, but hens from the four other flocks had poor records in both egg production and hatchability. Nodular growths occurred in the oviducts of birds in all five flocks. The incidence of lesions varied from flock to flock and from bird to bird. In four flocks, lesions were small and consisted of areas of dysplasia with adenomatous change. Histologically, the lesions in some birds in the fifth flock were adenocarcinomas. No metastases were observed.

Isolation and identification of citrinin produced by Penicillium lanosum.

Penicillium lanosum, when grown on corn, produces a metabolite which increases water intake and excretion by chicks. During a 5-hr test period, chicks fed inoculated corn as the only feed began excreting water within 2 hr and excreted as much as 36 ml, whereas chicks fed untreated corn did not excrete measurable amounts. Chicks fed the inoculated corn drank more water than those fed untreated corn. The metabolite could not be extracted from oven-dried corn but was removed from air-dried corn which had been moistened with acid and extracted with chloroform and then with methanol. It was soluble in 1% sodium bicarbonate and precipitated as yellow cystals when the solution was acidified to pH 1.5. The precipitate was identified as citrinin based on the results of thin layer chromatography, ultraviolet, infrared, mass spectrometer, fluorescence excitation and emission, and nuclear magnetic resonance spectra.

Experimental infection of broiler and Leghorn chickens with virulent and avirulent isolates of hemorrhagic enteritis virus.

The effects of virulent and avirulent isolates of hemorrhagic enteritis virus were studied in Leghorn and broiler chickens. The viruses caused subclinical infections in both strains of birds. The avirulent isolate produced enlarged spleens, inclusion bodies, and antibody in all inoculated Leghorns. In broilers the avirulent virus produced infection in only half of the inoculated birds. Inclusion bodies were widely dispersed in the spleens of both types of birds. The virulent virus produced infection in all inoculated birds of both strains. Inclusion bodies were numerous in the spleens of Leghorn birds and were widely scattered in the spleens of broilers.

Transmission of transmissible venereal tumor of the dog to the coyote.

Three coyotes experimentally implanted with cells from a transmissible venereal tumor of a dog developed neoplasms. Histopathologic appearances of the tumors in the coyotes were similar to those described in the dog. Attempts to transmit the tumor to suckling mice, rats, hamsters, kittens, and opossums were not successful.

Ultrastructural characteristics of canine transmissible venereal tumor at various stages of growth and regression.

Ultrastructural study of canine transmissible tumors in developing, mature, and regressing stages from 6 dogs revealed the presence of healthy and degenerating tumor cells in all neoplasms. The total number of neoplastic cells seemed to decrease, and the number of degenerating neoplastic cells seemed to increase in mature tumors. Macrophages, lymphocytes, and plasma cells infiltrated mature and regressing tumors. Alteratons in degenerating tumor cells consisted mainly of cytoplasmic changes in early stages and of both nuclear and cytoplasmic changes in cells in which degeneration was more advanced. Amounts of endoplasmic reticulum and ribosomes were decreased. There were swelling and vacuolation of mitochondria. Nuclear chromatin was clumped along the nuclear envelope, and the perinuclear space was widened. Degenerating cells often contained membrane-bound granules and clusters. Lamellar complexes were observed in tumor cells from 2 dogs. Virus particles were not seen.

Pathological response of the chicken embryo to an agent which causes acute leukosis (Marek's disease).

A laboratory test system specific for Marek's disease was developed by using the pathological response of the chicken embryo. Chicken epidermal scales (dander) and feather calami from infected chickens contain an agent(s) which after a 3- to 4-day incubation period caused gross or microscopic pathological changes (or both) in the embryo. A cell-free inoculum was obtained from infectious dander by 5-min sonic treatment, differential centrifugation, and membrane filtering (0.45 mum). Evidence for the cell-free existence of this agent(s) was obtained when membrane filtrates of dander preparations were shown to cause Marek's disease in 10-day-old chickens and in chickens inoculated at 1 day of age.