Respiratory infection of turkeys with Listeria monocytogenes Scott A.

The pathogenesis of L. monocytogenes strain Scott A was studied by challenging day-old male turkey poults by air sac inoculation with tryptose phosphate broth containing 10(0) cfu (control), 10(4), 10(5), and 10(6) cfu (low challenge), or 10(7) and 10(8) cfu (high challenge) of the Scott A (serotype 4b) strain of L. monocytogenes. Mortality at 2 wk postinfection (PI) ranged from 25% for low challenge to 100% for high challenge (P= 0.0001). Gross and histopathological lesions were observed in heart, liver, spleen, lung, and bursa of Fabricius of mortalities at 4 days PI. Listeria monocytogenes challenge resulted in significantly decreased relative weight of the bursa of Fabricius and increased relative weight of the spleen, and L. monocytogenes was isolated by direct plating of liver, pericardium, brain, and both left and right stifle joint synovium (knee) cultures, as well as gall bladder, yolk sac, and cecal tonsil from transfer swabs onto Listeria-selective agar. Isolates were confirmed as positive using Gram stain, biochemical tests, and the Biolog system. High challenge resulted in confirmed L. monocytogenes isolation from 48% of left knee and 59% of right knee cultures. Low challenge resulted in isolation of L. monocytogenes from 11% of both left and right knee cultures. These results suggest that L. monocytogenes Scott A colonization of turkey knee synovial tissue can initiate in day-of-age poults and that L. monocytogenes Scott A can be invasive through air sac infection.

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.

Studies on the pathogenesis of hemorrhagic enteritis of turkeys.

The infectivity of turkey hemorrhagic enteritis (HE) virus was studied in poults with no detectable maternal antibody and in turkeys bursectomized or injected with killed-virus preparations. Poults less than three weeks old were not infected by hemorrhagic enteritis virus, and survivors were susceptible to challenge at the age of eight weeks. Three- and four-week-old poults were susceptible to HE, and survivors resisted challenge. Bursectomy partially interfered with the immune response but did not alter the course of the disease, and survivors were resistant to challenge. Injections of spleen suspension containing 1% formalin produced antibody in only two of six turkeys. Three of the four poults without detectable antibody resisted challenge.

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.

Broiler chicken with a duplicated lower intestinal tract.

A case is described of a duplicated lower intestinal tract in a broiler chicken. The ileum branched to form two lower intestinal tracts. The ileum of the malformed branch was swollen and attached to paired ceca that were grossly enlarged, and the rectum was a swollen blind sac, disconnected from the exterior of the bird.

The development of dermatitis (scabby-hip) on the hip and thigh of broiler chickens.

Broiler chicks grown on litter or in cages at high bird density developed skin lesions on the thigh and hip. Changes in bird denisty markedly influenced lesion incidence (100% at 0.0185 sq m of floor space per bird). The dermatitis was characterized by crusted dry "scabs" at the base of feather follicles and between follicles. The lesions often coalesced to cover wide areas. The scab consisted of a mass of pyknotic nuclei and cellular debris, and when the epidermis was intact there was little inflammatory reaction in the dermis or subcutaneous tissue. The epidermis was destroyed in some lesions, with heterophils penetrating into the subcutaneous tissue. Colonies of gram-positive cocci were present in the lesions.

The efficacy of a temperature-sensitive mutant vaccine against Northwest Arkansas isolates of Alcaligenes faecalis.

The efficacy of a commercially produced temperature-sensitive mutant Alcaligenes faecalis vaccine was evaluated in turkeys contact-challenged with one of three strains of A. faecalis. In the vaccinated control group, the vaccine strain of A. faecalis colonized the nasal turbinates but not the trachea, caused no clinical signs of turkey coryza, and induced humoral antibodies. In the vaccinated challenged groups, the vaccine reduced both the severity of lesions and the number of birds exhibiting lesions compared with unvaccinated challenged groups, but it did not prevent colonization of challenge strains of A. faecalis.

An outbreak of histomoniasis in turkeys infected with a moderate level of Ascaridia dissimilis but no Heterakis gallinarum.

Histomoniasis was diagnosed in a commercial turkey flock. All morbidity and mortality occurred in one house. Birds exhibited lesions characteristic for histomoniasis, and the diagnosis was confirmed by histopathologic examination. Affected turkeys were infected with moderate levels of Ascaridia dissimilis but not Heterakis gallinarum. Compression smears of hepatic tissues showed typical histotrophic phase Histomonas meleagridis, whereas cecal smears exhibited large numbers of Trichomonas gallinarum. A challenge experiment was conducted in which turkey poults were placed on contaminated litter. Although histomoniasis was not reproduced in the experiment, the birds did become infected with low numbers of A. dissimilis.

Efficacy in turkeys of spray vaccination with a temperature-sensitive mutant of Bordetella avium (Art Vax).

Broad-breasted white turkeys were vaccinated with a temperature-sensitive mutant of Bordetella avium (Art Vax) at 2 and 15 days of age and challenged at 22 days of age by contact with infected birds. Necropsy was performed at 35 days of age. Two vaccination protocols (eyedrop/oral and spray cabinet/spray bottle) and two challenge isolates (Arkansas 105 and North Carolina [NC] isolates) were used. Neither the spray nor the eyedrop/oral methods of vaccination prevented infection of the anterior trachea with either of the virulent challenge strains. The spray and eyedrop/oral methods of vaccination were equally effective in reducing the severity of gross lesions in the trachea. The vaccine reduced the severity of gross lesions in the tracheas of turkeys challenged with the NC isolate to a level approximately equal to that observed in unchallenged vaccinated controls, but the vaccine only moderately reduced the severity of lesions in birds challenged with the 105 isolate.

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.

High mortality of domestic turkeys associated with Ascaridia dissimilis.

Third- and fourth-stage Ascaridia dissimilis larvae were isolated from commercial white turkey intestinal scrapings from two farms that were experiencing high mortality. Lesions consisted of a necrotic-like enteritis that was most severe in the jejunum. Subsequent bacteriological isolation yielded heavy growth of Escherichia coli and Clostridium perfringens. The rate of mortality declined rapidly when the turkeys were administered 18 ppm fenbendazole for 7 days.

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.

Use of an enzyme-linked immunosorbent assay to measure antibody levels in turkey breeder hens, eggs, and progeny following natural infection or immunization with a commercial Bordetella avium bacterin.

Twelve large white turkey hens were immunized with a commercially available Bordetella avium bacterin. Hens and eggs were tested using an enzyme-linked immunosorbent assay (ELISA) to determine the response to the bacterin. Three hundred poults were then obtained from two commercial flocks, the hens of one flock having been immunized with the same bacterin used on the group of 12 turkeys. Titers of the poults were monitored for 7 weeks, and poults were challenged by exposure to infected poults at 1, 7, 14, and 21 days post-hatch. Hens produced an antibody response following immunization, with a parallel antibody response being detected in eggs. Maternal antibodies were present in poults from immunized hens. Poult titers declined to near the level of poults from unimmunized hens by 14 days of age. Poults from immunized hens challenged at 1 and 7 days were resistant to development of clinical disease and gross lesions, whereas all poults from unimmunized hens exhibited clinical signs and gross lesions. After 14 days, the resistance of both groups to development of clinical disease, became near equal, neither group being affected as severely as the unimmunized hens challenged at days 1 and 7. Six commercial turkey breeding flocks and their progeny that had not been vaccinated for B. avium and had no history of B. avium infection were evaluated with the B. avium ELISA. There were variations between the flocks, with poult titers reflecting those found in the hens.

Identification and partial characterization of Arkansas isolates of chicken anemia virus.

Chickens from both broiler and broiler breeder pullet flocks experiencing symptoms of chicken anemia virus (CAV) infection were first observed at the Poultry Health Research Laboratory at the University of Arkansas in September 1992. Flocks had experienced higher than normal mortality with subcutaneous hemorrhages on the wings, neck, and thorax. Postmortem and histopathologic evaluation revealed thymus and bursal atrophy and lesions consistent with those reported for CAV infection. Because this infection had not previously been observed by Poultry Health Research Laboratory personnel in Arkansas-grown chickens, the establishment of a definitive diagnosis was deemed important. The presence of CAV was established by infecting MSB-1 cells with pooled liver homogenates from groups of 10 specific-pathogen-free chickens that had previously been inoculated in an attempt to experimentally reproduce the disease observed in the field. Cytopathic effects in the infected MSB-1 cells were first evident following the fifth passage. Indirect fluorescent antibody technique identified infected MSB-1 cells following at least five blind passages. To further confirm the presence of CAV, a polymerase chain reaction (PCR) technique was used to amplify a specific portion of the virus genome from infected MSB-1 cells and tissue extracts from several submitted chickens. Sequence analysis of a 186-bp PCR amplification product revealed that the Arkansas isolate was very similar to the Cuxhaven-1 isolate (99.5% sequence identity).

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.

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.

A survey of sixty turkey flocks exhibiting hepatic foci taken at time of processing.

Fifty turkey flocks including 24 16-week-old male flocks and 26 20-week-old male flocks were sampled at time of processing. Hepatic foci were cultured for aerobic and anaerobic bacteria. The majority of these did not have any bacteria recovered from the lesions. Of the bacteria that were recovered, most were facultative anaerobes, with Escherichia coli and Salmonella sp. comprising the most common isolates. All of the birds examined (300 total) for parasites were infected with varying levels of Ascaridia dissimilis. The highest average worm burden was found in the 20-week-old flocks. Heterakis gallinarum were found in only a few of the younger turkeys (16 weeks old) and not in any of the older birds. An analysis of the spatial distribution of the hepatic foci performed in an additional 10 turkey flocks (500 birds) revealed that, although present on the surface of all regions of the liver, 56.12% of the lesions were found on the left hepatic lobe and 43.88% were found on the right hepatic lobe.

Pathogenicity studies of an Arkansas variant infectious bursal disease virus.

A variant infectious bursal disease virus (IBDV), IBDV-s977, was blind passaged in cell culture, plaque purified, and attenuated by serial passage at a high multiplicity of infection (MOI) in chick embryo fibroblasts (CEF). Cell culture passages of virus caused less bursal atrophy and splenomegaly than did the original isolate and retained immunogenicity; however, virus tended to persist for a longer time in the bursa and spleen of birds infected with the highest CEF passages. Antibody to both low MOI and high MOI passages of IBDV-s977 poorly neutralized virus that was isolated from bursal tissue 28 days postinfection (PI). The spleens of chickens infected with the eighteenth CEF passage were negative for virus at 3 and 7 days PI but had high titers of virus at 14 and 28 days PI. There was also more virus in the bursa of birds infected with the fifteenth and eighteenth CEF passages at 28 days PI than at 7 or 14 days PI. Defective interference (DI) was demonstrated when cell cultures were coinfected with a constant amount of low MOI virus and serial dilutions of high MOI virus. There was an increase in interference score with increased passage number in CEF, and there was more interference in virus passaged at a high MOI. There was an inverse relationship between interference score and bursal lesion score and splenomegaly at 7 days PI, indicating that DI particles may be involved in virus attenuation. There was a positive relationship between interference and viral persistence in the bursa and spleen at 28 days PI. Antiserum to s977 was shown to enhance the nonlytic replication of s977 in CEF, presumably within macrophages, providing a possible mechanism for the pathotypic variation seen in emerging strains of IBDV.

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.

Digestion of feed by chicks with pale bird syndrome.

Unaffected chicks (normal) and chicks with pale bird syndrome (pale) were fed a control diet or a test diet obtained from the broiler house containing the pale chicks. Pale birds digested less (P less than 0.05) dry matter and ether extract than normal chicks, and the nitrogen content in their feces was greater. The chicks from both sources digested more (P less than 0.05) dry matter from the test feed but also excreted more (P less than 0.05) nitrogen than those fed the control diet. Neither diet resulted in differences in the digestion of ether extract. The cause of pale bird syndrome was related more to source of chicks rather than source of feed. Depigmentation may have resulted from decreased pigment absorption because of reduced absorption of dietary components, including ether extract.