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Identification of Bordetella avium antigens recognized after experimental inoculation in turkeys.

Sera and tracheal washings (TW) were used to identify antigens of Bordetella avium recognized during experimentally induced bordetellosis in young turkeys. Pooled sera and TW were examined for antibody by a microtitration agglutination test and by western immunoblotting. In addition, comparable samples collected from 1-day-old turkeys and uninoculated control turkeys also were examined. At least 8 outer membrane proteins of B avium were recognized in immunoblots of sera and TW from infected turkeys. Reactivity of TW in immunoblots was qualitatively similar but less intense, compared with reactivity of corresponding sera collected on postinoculation (PI) weeks 2, 3, and 4. Molecular weights of the major outer membrane proteins of B avium recognized by sera and TW at PI week 4 were 100,000, 97,000, 36,000, 31,000, 21,000, 18,000, 14,000, and less than 14,000. A protein with a molecular weight of 55,000 reacted nonspecifically in all samples tested. Antibody, detectable by microtitration agglutination, was in sera of 1-day-old turkeys and in sera and TW of B avium-infected turkeys during PI weeks 2 to 4.

Agglutination Tests↗

Effect of antibodies to type 1 fimbriae on clearance of fimbriated Escherichia coli from the bloodstream of turkeys.

Young turkeys (n = 20) were inoculated IV with fimbriated, virulent Escherichia coli ECl (O78:K80: H9:F1). Blood samples were collected for bacterial quantitation at postinoculation minutes (PIM) 10, 20, 30, 40, 50, and 60. Immediately after the PIM 30 sampling, the turkeys were allotted into 4 groups (5 turkeys/group) and were injected IV with 1 of the following antisera: group 1, antibodies to F1 fimbriae (AF); group 2, antibodies to E coli O78 antigen (AO); group 3, antibodies to live, fimbriated (F1+) homologous E coli (ALEC); or group 4, normal turkey serum (NTS) collected from a healthy turkey. Compared with NTS, ALEC and AO caused a significant reduction in blood-borne E coli, whereas AF did not reduce bacterial numbers. In addition, 2 groups of 10 turkeys were inoculated IV with live, F1+ or nonfimbriated (F1-) E coli ECl. Numbers of viable bacteria were determined in blood samples and liver specimens collected 2 minutes after inoculation. Compared with F1- bacteria, significantly more F1+ bacteria were found in liver specimens and significantly fewer F1+ bacteria were found in blood samples. Results indicated that antibodies to F1 fimbriae do not enhance clearance of F1+ E coli from the bloodstream of turkeys probably because F1+ bacteria are selectively cleared by the liver, even without antibody.

Animals↗

Influence of Bordetella avium infection on association of Escherichia coli with turkey trachea.

Four-week-old Bordetella avium-infected and B avium-free turkeys were inoculated intratracheally with a suspension of fimbriated or nonfimbriated Escherichia coli. Numbers of E coli associated with tracheal sections were determined at postinoculation hour (PIH) 1 or 6. Significantly (P less than 0.05) greater numbers of E coli were isolated from the tracheas of B avium-infected turkeys compared with numbers in B avium-free turkeys. In B avium-free turkeys, tracheal associated E coli were 90% less at PIH 6 compared with that at PIH 1. However, in B avium-infected turkeys, numbers of E coli were not affected by postinoculation time. Seemingly, B avium-infected turkeys had reduced capacity to clear E coli from the trachea.

Animals↗

Pathogenesis of rotavirus infection in various age groups of chickens and turkeys: clinical signs and virology.

Age-related susceptibility patterns of turkeys, broilers, and specific pathogen-free (SPF) White Leghorn chickens to experimentally induced infection with turkey or chicken rotavirus isolates were compared. The following determinants were evaluated: clinical signs, onset and duration of virus production, viral titers, involvement of intestinal villi in the replication of the virus, and the development of antibodies against the virus. Older turkeys and chickens were more susceptible than were their younger counterparts, turkeys were more susceptible than were broiler and White Leghorn chickens (regardless of age), and broiler chickens were slightly more susceptible than were age-matched White Leghorn chickens. Turkeys developed diarrhea, accompanied by high viral titers within 1 day after inoculation with virus. Viral antigen was found in the epithelial cells of the intestinal villi throughout the intestinal tract and some cells of the cecal tonsils. Antibodies could be detected as early as 4 to 5 days after inoculation. These findings were more pronounced in turkeys inoculated at 112 days of age than in birds inoculated at a younger age. Age-related susceptibility patterns were similar in White Leghorn and broiler chickens. Infection was subclinical in birds less than 56 days old, whereas older birds developed soft feces. Egg production in the White Leghorn chickens decreased after being inoculated with virus at 350 days of age.

Age Factors↗

Effects of bursectomy, irradiation, and cyclophosphamide on turkeys vaccinated with CU cholera strain.

Turkeys surgically bursectomized, irradiated, and/or injected with cyclophosphamide at 1 day were vaccinated with the live Clemson University (CU) strain of Pasteurella multocida. Bursectomized turkeys vaccinated via drinking water or wing-web puncture at 7 weeks and challenged at 11 weeks had a significantly (P less than 0.05) lower survival rate after challenge than unbursectomized controls. Bursectomized and unbursectomized turkeys vaccinated via drinking water at 7 weeks, revaccinated via the auditory tube at 11 weeks, and challenged at 15 weeks had similar survival rates. The vaccinated bursectomized turkeys had significantly (P less than 0.05) lower levels of serum anti-P. multocida antibody than vaccinated unbursectomized controls. Radiation had no immunosuppressive effect. The immunosuppressive effect of cyclophosphamide was dosage-dependent. Bursectomy and injection of cyclophosphamide in the same turkey were complementary. It was concluded that in young turkeys, the development of immunity to the avirulent CU vaccine is highly dependent upon the bursa of Fabricius, but that as they grow older the bursa is of less importance, particularly if they were vaccinated via a parenteral route, such as in the air spaces of the head.

Animals↗

Tracheal mucus transport rate and bacterial clearance in turkeys exposed by aerosol to La Sota strain of Newcastle disease virus.

Tracheal mucus transport rate (TMTR) and quantitative clearance of aerosolized Escherichia coli from the trachea, lung, and air sac were measured in healthy unanesthetized turkeys and in turkeys exposed by aerosol to a La Sota vaccine strain of Newcastle disease virus (NDV). The TMTR of uninfected turkeys was 42.4 +/- 14.7 cm/min. The TMTR of NDV-infected turkeys was depressed on days 3 through 7 postexposure (PE); depression was significant (P less than or equal to 0.05) on day 7 PE. Tracheal E. coli clearance in NDV-infected turkeys was reduced on days 4 through 9 PE, significantly so on day 5 PE (P less than or equal to 0.01). Depression of TMTR and tracheal E. coli clearance were associated histologically with replacement of normal pseudostratified columnar epithelium by 3 to 8 layers of immature nonciliated cells. E. coli clearance by the lung and air sac of NDV-infected turkeys was depressed on days 5 through 9 PE.

Air Sacs↗

Airsacculitis in turkeys exposed to Mycoplasma synoviae membranes.

In studies to investigate the pathogenesis of mycoplasmal airsacculitis, exudative lesions were produced in turkeys by intra-air-sac inoculation with Mycoplasma synoviae cell membranes and viable organisms. Membrane inocula containing 5 mg of protein produced more severe lesions than inocula containing either 2.5 mg or 1 mg protein. Turkeys exposed to 5 mg of membrane protein developed moderately severe airsacculitis; those exposed to viable organisms developed markedly severe airsacculitis. Microscopic examinations revealed that membrane-induced lesions were generally similar to those resulting from infection but were less severe. At the termination of the study, 8 days after exposure, M. synoviae was isolated from respiratory tract tissues of all turkeys exposed to live organisms, but it was not isolated from any of those exposed to membranes or from unexposed control turkeys. Antibody against M. synoviae was demonstrated with the tube agglutination test in sera from turkeys exposed to membranes and those exposed to live organisms, but it was not demonstrated in sera from unexposed control turkeys.

Air Sacs↗

Staphylococcosis of turkeys. 3. Bacterial interference as a possible means of control.

Two Staphylococcus epidermidis isolates from turkeys were used as interfering agents to help control staphylococcosis. Both isolates adhered to tissues of the turkeys' respiratory tract, interfered with attachment of virulent S. aureus, produced bacteriocins bacteriocidal to S. aureus, and were avirulent for turkeys. About 200,000 turkeys in commercial flocks were exposed to aerosols of these interfering isolates between 1 and 6 weeks of age, and many became colonized with these bacteria. The aerosol-treated turkeys had lower levels of colonization with S. aureus and had a 3% higher gross survival rate than untreated control turkeys.

Animals↗

Serologic evidence of infectious bursal disease virus infection in Iowa turkeys.

Two infectious bursal disease viruses (IBDVs)--a cell-culture-adapted chicken strain designated Edgar strain and a recent isolate from turkeys in Missouri--were used to assay sera from 10 Iowa turkey flocks collected between 1 and 16 weeks of age. The two viruses were serologically distinct in cross-neutralization tests. For all flocks, a similar serologic pattern was found consisting of (1) low maternal antibody titers to turkey IBDV and occasionally to Edgar strain IBDV between 1 and 3 weeks of age, (2) a period of very low or no detectable titers between 3 and 7 weeks of age, and (3) sharply rising high titers to turkey IBDV with low titers to Edgar IBDV beginning at 5 to 8 weeks of age. These findings indicate that infection with IBDV of the serotype represented in this study by the turkey isolate is common in Iowa turkey flocks, whereas infection with IBDV represented by Edgar strain is uncommon. Infection occurred between 3 and 7 weeks of age during the late brooding period or after birds had been moved to an intermediate growing facility. All flocks developed complicated respiratory disease with excessive mortality caused by Escherichia coli septicemia, typically between 3 and 6 weeks of age. Although there was a temporal relationship between IBDV infection and respiratory disease, the possible role of IBDV in the process is unknown.

Animals↗

The organization of c-rel in chicken and turkey DNAS.

The process of transduction of a proto-oncogene involves the loss of intervening sequences, the loss of 3' mRNA terminal sequences, and possible base changes. It is not possible to know how similar the c-rel sequences we studied are to sequences from which v-rel arose. If one of the alleles we studied is identical to progenitor sequences of v-rel, then base changes must have occurred during the process of transduction. Alternatively, there may exist an allele of c-rel which did not need to undergo base changes to give rise to v-rel. The polymorphism of c-rel within a turkey population and between chicken and turkey shows clear evidence in c-rel coding sequences have not been detected within a turkey population. There is an EcoRI site in c-rel from turkey which is not in v-rel. There are unequal length substitutions in c-rel within the turkey population and between chicken and turkey. Unequal length substitutions can be explained if there has been a combination of two events, for example, insertion or deletion with extensive base changes, or two insertions or deletions. Two events occurring in a short evolutionary time span might occur if c-rel is diverging at a relatively fast rate. c-rel is much less conserved across species lines, in nucleic acid hybridization to v-rel (Chen et al. 1981; Wong and Lai 1981) than other proto-oncogenes, consistent with it diverging at a relatively fast rate. Since the evolutionary changes that have been seen for c-rel are in noncoding sequences, it is most likely that v-rel arose by transduction of a somatic mutation generated variant of c-rel or by transduction which involves sequence changes or later mutations.

Animals↗

Transmission of Chlamydiae from grackles to turkeys.

Two female common grackles (Quiscalus quiscula) were inoculated intratracheally with 1.6 X 10(8) chick embryo lethal doses50 of a chlamydial organism isolated from turkeys. Eight female grackles were kept as uninoculated contacts. Six days later, two 12-week-old Broad-Breasted White turkeys (1 male and 1 female) were placed in the pen with the grackles. Chlamydiae were isolated in mice from cloacal swabs taken 14 days postinoculation from the infected grackles. Swabs from the contact grackles did not yield chlamydiae, nor did swabs taken 7 days later from all birds. Twenty-one days after being placed with the grackles, the turkeys developed signs of chlamydiosis. Cloacal swabs taken at 24 days yielded chlamydiae from only the female. Visceral organ tissues collected at 28 days from the male yielded chlamydiae. The only lesions in the turkeys at necropsy were enlarged spleens. The turkeys were serologically negative for chlamydial antibody both when placed and 15 days later, but were positive at days 24 and 28. These results indicate contact transmission of chlamydiae from infected grackles to turkeys.

Animals↗

Negative findings concerning Alcaligenes faecalis as an etiologic agent in acute respiratory disease of turkeys.

An acute respiratory disease of turkeys in Israel was first reported in November 1978. Alcaligenes faecalis was isolated from sick turkeys and from chickens not affected by the disease. Plate agglutination tests with A. faecalis antigen of 1,067 turkey and 494 chicken serum samples gave variable results: healthy turkeys gave positive reactions and sick turkeys sometimes gave negative ones. All isolated strains were highly sensitive in vitro drug sensitivity tests, but chemotherapy failed in the field. Pathogenicity trials with A. faecalis, given alone or in combination with Yucaipa virus to 8-day-old turkey poults, failed to reproduce the disease.

Alcaligenes↗

Aerosol transmission of Pasteurella multocida in turkeys.

In three incidents, uninoculated turkeys separated from Pasteurella multocida-inoculated turkeys died of fowl cholera; it was inferred that the pathogen was transmitted by aerosol through the circulating air. Uninoculated and inoculated turkeys were separated by a solid partition and wire netting, and were handled separately. Turkeys were inoculated with a highly virulent strain of P. multocida, which induced the pulmonary form of fowl cholera. In four of the five uninoculated turkeys that died, pneumonia was the principal lesion. In two of these turkeys, which were bled one day before death while still alert, the plasma corticosterone concentration had increased markedly.

Aerosols↗

[Comparative pathomorphological studies of turkeys and hens experimentally infected with Newcastle disease virus].

Comparative pathomorphologic studies were carried out with 40 birds (29 turkeys and 11 hens) infected per os with 0.5 cc embryonal fluid 10(5) ELD 50 each with two Newcastle disease virus strains (Texas -- standard and 7/5 isolated from dead hens and typed as viscerotropic). It was found that the pathoanatomical picture is negative for all birds experimentally infected with the Texas strain. Haemorrhagic necrotic modification of the glandular stomach and intestine were found in birds infected with strain 7/5. The pathoanatomical finding is better expressed in hens compared with that for turkeys. The histologic modification in birds infected with strain Texas were manifested mostly by nonsuppurative encephalitis. Haemorrhagic-diphtheroid inflammation of the alimentary tract, haemorrhages in the viscera and unreactive necrotic foci in the spleen as well as poorly manifested inflammatory changes in the central nervous system were found in birds infected with strain 7/5. No pathoanatomical modifications for Newcastle disease were found in turkeys, analogous to hens, infected with velogenic neurotropic virus. The velogenic viscerotropic strain is less pathogenic for turkeys than for hens. It causes slighter haemorrhagic necrotic modification in turkeys viscera than in hens. Nonsuppurative encephalitis established histologically in both turkeys and hens infected with neurotropic and viscerotropic Newcastle disease virus is a constant finding and may be used as a diagnostic sign of the disease.

Animals↗

Pasteurella multocida: antibody-mediated resistance to virulent challenge exposure in vaccinated turkeys.

Aspects of antibody-mediated resistance to Pasteurella multocida infection in vaccinated turkeys were investigated. Pasteurella immune serum obtained from vaccinated turkeys was shown to confer temporary protection to nonvaccinated turkey poults. Recipients given immune serum were free of clinical signs of disease for at least 8 days after IM challenge exposure with virulent P multocidae 1059. All turkeys given normal serum died within 36 hours of challenge exposure. Vaccinated bursectomized turkeys were more susceptible to IM challenge exposure than were vaccinated nonbursectomized turkeys. In two of three trials, mortality also occurred earlier in the bursectomized groups when compared with mortality in the control groups. The presence of specific antibody may be an important determinant in resistance to Pasteurella infection.

Animals↗

Consumptive coagulopathy in turkeys exposed to Pasteurella multocida.

When turkeys were inoculated intramuscularly with live Pasteurella multocida, three of the four inoculated turkeys developed an increase in modified Russell's viper venom time (mRVVT) 24 hours after inoculation. This increase was followed by irregular decreases and increases in mRVVT at subsequent bleedings. When turkeys were inoculated intravenously with P. multocida, the mRVVT increased markedly after inoculation in all eight inoculated turkeys: 9 hours later, the average mRVVT was significantly (P < 0.05) higher than that of the uninoculated turkeys. No microthrombi were observed in the blood vessels of the liver, spleen, kidneys, or lungs. An increase in mRVVT was interpreted as an excessive consumption of one or more of clotting factors X, V, II, and I. These results indicate that consumptive coagulopathy could be a factor in the pathogenesis of fowl cholera in turkeys.

Animals↗

Effect of protein restriction during brooding on spontaneous turkey cardiomyopathy.

The effect of early protein restriction on poult performance and mortality due to spontaneous turkey cardiomyopathy were examined in a facility that historically had a high incidence of the condition. Two thousand male turkey poults were divided into two equal subgroups for the first 4 weeks of life: one received standard commercial rations for the first 4 weeks (high-protein subgroup), and the other received rations with a protein content approximately 70% of the first subgroup (low-protein subgroup). Rations were the same after 4 weeks of age (standard commercial rations). At 16 weeks of age, turkeys in the low-protein subgroup weighed an average of 12.32 kilograms (27.1 pounds), whereas turkeys in the high-protein subgroup weighed an average of 12.73 kilograms (28.0 pounds). Total mortality for the low-protein subgroup was 10.1%, whereas total mortality for the high-protein subgroup was 15.7%. Total mortality due to spontaneous turkey cardiomyopathy in the high-protein subgroup was greater than twice that in the low-protein subgroup (10.4% versus 4.6%). These results show that lowering the protein content of the feed in the first 4 weeks significantly reduces mortality due to spontaneous turkey cardiomyopathy, but body weight gain is also reduced.

Animals↗

Clinical Mycoplasma gallisepticum infection in multiplier breeder and meat turkeys caused by F strain: identification by sodium dodecyl sulfate-polyacrylamide gel electrophoresis, restriction endonuclease analysis, and the polymerase chain reaction.

In February 1991, a flock of North Carolina multiplier breeder turkeys experienced respiratory signs, sinusitis, airsacculitis, and increased mortality. Mycoplasma gallisepticum (MG) was isolated, and appropriate control measures were initiated. Ultimately, this outbreak involved several breeder flocks of an integrated turkey production company before the last infected flock was identified in May 1991. During this time, MG was also isolated from a flock of commercial layer-type chickens raised as pullets in close proximity to the index turkey flock. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis and restriction endonuclease analysis indicated that these isolates were identical to each other and to examples of the vaccinal F strain. Additionally, MG isolates from the affected turkey breeder and layer flocks were identified as MG F strain by use of an F strain-specific DNA probe and polymerase chain reaction. A separate outbreak of MG disease in several meat-turkey flocks of a Midwest producer/processor yielded isolates identified as F strain by the polymerase chain reaction. These studies demonstrated: 1) the utility of newer technologies for disease outbreak investigations; and 2) the potential of MG F strain to cause disease in breeder and meat turkeys under field conditions.

Animals↗