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At least 19 recordsLinked to original sources

Enterococci with glycopeptide resistance in turkeys, turkey farmers, turkey slaughterers, and (sub)urban residents in the south of The Netherlands: evidence for transmission of vancomycin resistance from animals to humans?

The number of vancomycin-resistant enterococci (VRE) relative to the total number of enterococci was determined in fecal samples from turkeys and three human populations in 1996, each with a different level of contact with turkeys, i.e., turkey farmers, turkey slaughterers, and (sub)urban residents. The percentage of VRE relative to the total enterococcal population (i.e., the degree of resistance) was low (2 to 4%) in all groups (except in six samples). No difference was observed between farmers who used avoparcin and those who did not. The pulsed-field gel electrophoresis (PFGE) patterns of the VRE isolates from the different populations were quite heterogeneous, but isolates with the same PFGE pattern were found among animal and human isolates, in addition to the isolates which were described previously (A. E. van den Bogaard, L. B. Jensen, and E. E. Stobberingh, N. Engl. J. Med. 337:1558-1559, 1997). Detailed molecular characterization of vanA-containing transposons from different isolates showed, that in addition to a previously reported strain, similar transposons were present in VRE isolates from turkeys and turkey farmers. Moreover, similar VanA elements were found not only in isolates with the same PFGE pattern but also in other strains from both humans and animals.

Animals↗

[Analytical study of the locomotion of the meat turkey cock. Comparison between sound turkeys and turkeys with locomotor problems].

A comparative locomotion analysis of healthy and lame male commercial turkeys was carried out. Walking turkeys were filmed from both right and left lateral views. Video films were analysed. The coordination and the succession of hind limb movements were studied with time and space components. The gait of healthy turkeys was a walk with perfectly symmetrical and repeatable hind limb movements. All lame turkeys' movements showed abnormalities in space-time coordination. These abnormalities were bilateral but non-symmetrical, intermittent, and non-systematic. Their intensity increased with increase in the degree of clinical handicap. However, in all lame turkeys, the degree of an abnormal tibial movement was observed, ie a shorter amplitude of forward movement with variable intensity.

Animals↗

Multiplex real-time reverse transcription-polymerase chain reaction for the detection of three viruses associated with poult enteritis complex: turkey astrovirus, turkey coronavirus, and turkey reovirus.

Poult enteritis complex (PEC) is an economically important disease of young turkeys characterized by diarrhea, poor weight gain, and, in some cases, high mortality. Although PEC is considered to be a polymicrobial disease, numerous viruses, including turkey coronavirus (TCV), turkey astrovirus type 2 (TAstV-2), and avian reoviruses (ARVs), have been associated with PEC-like disease. Real-time reverse transcription-polymerase chain reaction (RRT-PCR), a highly sensitive and specific detection method for viral RNA, was developed in a multiplex format for the simultaneous detection of TAstV-2 and TCV and for the detection of two genetic types of ARV. Assay sensitivity was determined using in vitro transcribed RNA and varied by target between 150 gene copies for TAstV-2 alone and 2200 gene copies for TCV when multiplexed. Virus detection was evaluated with samples collected from poults inoculated at 1 day of age with each of the viruses. Cloacal swabs and intestinal samples were obtained at 1, 2, 3, 4, 6, 9, 14, 17, and 21 days after inoculation, processed, and tested for virus detection by RRT-PCR Cloacal swabs from TAstV-2- and TCV-infected poults were shown to have sensitivity for virus detection similar to that of intestinal samples when compared directly. ARV detection by RRT-PCR was compared with virus isolation and had similar sensitivity.

Animals↗

Metabolism of lipid labeled very low density lipoprotein from laying turkey hens in laying turkey hens and immature turkeys.

Labeled very low density lipoprotein of laying turkey hens (VLDL-L) was prepared by injecting 1-14C-palmitate abd subsequently isolating the VLDL-L by ultracentrifugation at d=1.006. The isolated VLDL-L then was injected into recipient laying hens, immature males, or immature females. Size exclusion chromatography of recipient laying hen plasma showed no remnant particles of smaller size or greater density than the injected VLDL-L up to 400 min postinjection. In the immature birds of either sex, remnant particles of greater density and smaller size than the injected VLDL-L were present when blood samples were withdrawn at 5 (males) or 1 (females) min postinjection. In laying females, both VLDL-L-triglyceride (VLDL-L-TG) and phospholipids (VLDL-L-PL) had identical fractional clearance rates of .00253 min-1 and had parallel rates of disappearance. The irreversible loss of VLDL-L-TG was 12.8 g/day while it was 4.8 g/day for VLDL-L-PL. Thirty-one percent of the injected radioactivity was isolated in ovarian follicles undergoing rapid development. VLDL-L-TG decayed with a single exponential decay component in both immature males and females, but decayed more rapidly in the males; it also decayed more rapidly in the immature birds of both sexes than in laying females. There was also an increase in triglyceride (TG) radioactivity in lipoproteins of d greater than 1.006. The VLDL-L-PL decayed in a more complex pattern in the immature birds, showing more than a single exponential decay component. There was also an increase in phospholipid (PL) radioactivity in lipoproteins of d greater than 1.006. THe VLDL-TG and PL radioactivities did not decay in a parallel pattern in immature birds where remnant particles of d greater than 1.006 were present soon after lipid labeled VLDL-L injection.

Animals↗

Enhancement of enteropathogenic Escherichia coli pathogenicity in young turkeys by concurrent turkey coronavirus infection.

In a previous study, turkey coronavirus (TCV) and enteropathogenic Escherichia coli (EPEC) were shown to synergistically interact in young turkeys coinfected with these agents. In that study, inapparent or mild disease was observed in turkeys inoculated with only TCV or EPEC, whereas severe growth depression and high mortality were observed in dually inoculated turkeys. The purpose of the present study was to further evaluate the pathogenesis of combined TCV/EPEC infection in young turkeys and determine the role of these agents in the observed synergistic interaction. Experiments were conducted to determine 1) effect of EPEC dose, with and without concurrent TCV infection, and 2) effect of TCV exposure, before and after EPEC exposure, on development of clinical disease. Additionally, the effect of combined infection on TCV and EPEC shedding was determined. No clinical sign of disease and no attaching and effacing (AE) lesions characteristic of EPEC were observed in turkeys inoculated with only EPEC isolate R98/5, even when turkeys were inoculated with 10(10) colony forming units (CFU) EPEC (high dose exposure). Only mild growth depression was observed in turkeys inoculated with only TCV; however, turkeys inoculated with both TCV and 10(4) CFU EPEC (low dose exposure) developed severe disease characterized by high mortality, marked growth depression, and AE lesions. Inoculation of turkeys with TCV 7 days prior to EPEC inoculation produced more severe disease (numerically greater mortality, significantly lower survival probability [P < 0.05], increased frequency of AE lesions) than that observed in turkeys inoculated with EPEC prior to TCV or simultaneously inoculated with these agents. Coinfection of turkeys with TCV and EPEC resulted in significantly increased (P < 0.05) shedding of EPEC, but not TCV, in intestinal contents of turkeys. These findings indicate that TCV infection predisposes young turkeys to secondary EPEC infection and potentiates the expression of EPEC pathogenicity in young turkeys.

Animals↗

The turkey transcription factor Pit-1/GHF-1 can activate the turkey prolactin and growth hormone gene promoters in vitro but is not detectable in lactotrophs in vivo.

The transcription factor Pit-1/GHF-1 plays an important role in regulating the prolactin (Prl) and growth hormone (GH) genes in mammals. In this study, the role that Pit-1 plays in regulating the prolactin and growth hormone genes in avian species was examined by cotransfection assays and immunofluorescence staining of pituitary sections. In cotransfection assays, turkey Pit-1 activated the turkey Prl, turkey GH, and rat Prl promoters 3.8-, 3.7-, and 12.5-fold, respectively. This activation was comparable to rat Pit-1 activation of these same promoters. A point mutation in the turkey Pit-1 cDNA, which changed leu-219 to ser-219, resulted in a 2-, 2-, and 10-fold reduction in the activation of the turkey Prl, turkey GH, and rat Prl promoters, respectively. Unexpectedly, coexpression of tPit-1 (leu-219) and tPit-1(ser-219) activated turkey Prl and rat Prl promoters 9.4- and 35.9-fold, respectively, but had no effect on the turkey GH promoter. Dual-label immunofluorescence analysis of turkey pituitary sections revealed that Pit-1 was not detectable in prolactin-staining cells but was detectable in GH-staining cells. Taken together, these data indicate that in the domestic turkey, Pit-1 can activate the turkey Prl promoter in vitro, but does not appear to play a role in regulating Prl gene expression in vivo. Pit-1, however, still likely plays a role in regulating GH gene expression.

5' Flanking Region↗

Characterization of turkey coronavirus from turkey poults with acute enteritis.

The present study was to characterize turkey coronavirus associated with turkey poult enteritis and mortality. Intestinal contents or intestines from affected turkey poults and inoculated turkey embryos contained coronaviruses as revealed by electron microscopy or were positive for turkey coronavirus by immunofluorescent antibody assay. Sucrose density gradient ultracentrifugation of the virus-containing intestinal homogenate yielded two opalescent bands corresponding to the buoyant densities of 1.14-1.15 and 1.18-1.20 g/ml, respectively. Coronaviral particles from intestinal contents or the sucrose density gradient preparation were mainly spherical in shape and had envelope and central depression. They were surrounded by a fringe of regularly spaced petal-shaped projections attached to the particles by a short stalk. Purified viruses hemagglutinated rabbit erythrocytes with a titer of 16. Major protein bands of purified viruses analyzed by SDS-PAGE were located at 200, 100-110, 50-60, and 30-35 kDa. The patterns of protein bands were consistent with those of Minnesota or Quebec turkey coronavirus isolates. A 568 bp nucleotide fragment of turkey coronavirus spike protein gene was amplified from RNA of inoculated turkey embryo intestine or purified virus. Sequence analysis of the 568 bp PCR product revealed high degree of identity with the corresponding spike protein gene sequence of human and bovine coronaviruses. The results indicated that turkey coronavirus was associated with turkey poults with acute enteritis.

Acute Disease↗

Efficacy of Salmonella enteritidis (SE)-immune lymphokines from chickens and turkeys on SE liver invasion in one-day-old chicks and turkey poults.

We have shown previously that increased resistance to Salmonella enteritidis (SE) organ infectivity in 1-day-old chicks was conferred by the immunoprophylactic administration of SE-immune lymphokines (SEILK). These lymphokines have been found to be present in the cell culture media of concanavalin A-stimulated splenic lymphocytes obtained from SE-immunized chickens. In the present study we evaluated whether turkeys also produced SEILK and whether these lymphokines could protect 1-day-old chicks and turkey poults against SE liver invasion. In addition, we tested the ability of our original chicken SEILK to reduce SE liver invasion in turkey poults. Day-of-hatch chicks and turkey poults were injected intraperitoneally with immune lymphokines of either chicken or turkey origin. One hour later the birds were challenged per os with SE, and 20 hours later their livers were examined by bacteriological methods for the presence of SE. We found that SEILK induced from the splenic lymphocytes of SE-immunized turkeys reduced SE liver invasion in both chicks and turkey poults. Conversely, we also determined that SEILK produced by chicken splenic lymphocytes conferred protection against invasion by SE in turkey poults. This research is the first report of the production of SEILK in turkeys and also the first report on the cross-species activity of these effector molecules in chickens and turkeys.

Animals↗

The effect of immunosuppression on protective immunity of turkey poults against infection with turkey coronavirus.

The objective of the present study was to evaluate the protective effect of humoral and cellular immunities on turkeys infected with turkey coronavirus (TCV). Two trials were conducted with two separate hatches of turkey poults. Turkey's were experimentally immunosuppressed with cyclosporin A (CsA) or cyclophosphamide (CY) and infected with TCV. Prior to infection, treatment with CsA selectively suppressed T cell activity as revealed by 2-3 fold decreased (p < 0.1) lymphocyte proliferation responses to a T cell mitogen, concanavalin A (Con A). Treatment with CY mainly induced B cell deficiency as indicated by significant reductions (p < 0.05) in antibody responses to sheep erythrocytes 7 days after injection. Body weight gain of turkeys treated with CY was significantly lower (p < 0.05) than that of untreated turkeys at 9 days post-infection (PI). Turkeys treated with CY had 1-2 fold higher immunofluorescent antibody assay (IFA) scores for TCV antigens (p < 0.05) in the intestine than untreated turkeys at 9 or 14 days PI. These results suggested that humoral immunity against TCV infection may be important in turkeys.

Animals↗

Pathogenicity of turkey coronavirus in turkeys and chickens.

We designed this study to compare the replication potential of turkey coronavirus (TCV) and its effect in chickens and turkeys and to study the effect of singleand combined infection of turkey poults with TCV and astrovirus. We studied the pathogenicity of TCV in experimentally inoculated turkey poults and chickens by observing the dinical signs and gross lesions. Two trials were conducted with 1-day-old and 4-wk-old specific-pathogen-free turkey poults and chickens. One-day-old turkey poults developed diarrhea at 48 hr postinoculation. Poults euthanatized at 3, 5, and 7 days postinoculation had flaccid, pale, and thin-walled intestines with watery contents. The 4-wk-old turkeys had no clinical signs or gross lesions. One-day-old and 4-wk-old chicks developed no clinical signs or gross lesions although the TCV was detected in gut contents of the birds throughout the experimental period (14 days). In another experiment, mean plasma D-xylose concentrations in 3-day-old turkey poults inoculated with TCV, turkey astrovirus, or a combination of both viruses were significantly lower than in the uninoculated controls.

Age Factors↗

High mortality and growth depression experimentally produced in young turkeys by dual infection with enteropathogenic Escherichia coli and turkey coronavirus.

Six-day-old turkeys were inoculated with turkey coronavirus (TCV) and an enteropathogenic Escherichia coli (EPEC) (isolate R98/5) that were isolated from poult enteritis and mortality syndrome (PEMS)-affected turkeys. Turkeys inoculated with only R98/5 did not develop clinically apparent disease, and only mild disease and moderate growth depression were observed in turkeys inoculated with only TCV. Turkeys dually inoculated with TCV and R98/5 developed severe enteritis with high mortality (38/48, 79%) and marked growth depression. R98/5 infection resulted in attaching/effacing (AE) intestinal lesions characteristic of EPEC: adherence of bacterial microcolonies to intestinal epithelium with degeneration and necrosis of epithelium at sites of bacterial attachment. AE lesions were more extensive and were detected for a prolonged duration in dually inoculated turkeys compared with turkeys inoculated with only R98/5. An apparent synergistic effect in dually inoculated turkeys was indicated by increased mortality, enhanced growth depression, and enhanced AE lesion development. The results suggest that TCV promoted intestinal colonization by R98/5; however, R98/5 did not appear to alter TCV infection. The present study provides a possible etiologic explanation for PEMS.

Animals↗

Humoral and cellular immune responses in turkey poults infected with turkey coronavirus.

The objective of the present study was to elucidate the kinetics of humoral and cellular immune responses of turkey poults infected with turkey coronavirus (TCV). Turkey poults were orally inoculated with TCV at 10 d of age, and the immune responses were analyzed at 1, 3, 7, 14, 21, 28, 42, and 63 d postinfection (PI) in three different experiments. Total Ig to TCV was initially detected at 7 and 14 d PI in Experiments 1 and 3. In addition, Ig gradually increased from 7 to 21 d PI and remained at 80 immunofluroescent antibody assay (IFA) titers or more thereafter. Lymphocyte proliferation responses of spleen cells to concanavalin A were higher in TCV-infected turkeys than in noninfected control turkeys with significant differences (P < 0.05) being noted at 14 and 63 d PI in Experiment 2 and at 3 and 28 d PI in Experiment 3. Strong IFA staining response to TCV antigen was observed in intestines of turkeys at 1, 3, and 7 d PI, and the response declined from 14 to 28 d PI in Experiment 3. In Experiment 3, the IgG isotype antibody response to TCV was markedly increased after 21 d PI and remained high until 63 d PI. The IgM isotype antibody response to TCV was 1.40 and 0.91 at 7 and 14 d PI, respectively. The IgA isotype antibody response to TCV was very low as detected at 7 (0.13), 14 (0.20), and 21 (0.17) d PI. Turkeys infected with TCV had significantly higher (P < 0.05) antibody response to sheep erythrocytes than noninfected controls at 7 d PI. Virus-specific lymphocyte proliferation response of spleen cells was significantly stimulated (P < 0.05) at 63 d PI in Experiment 3. The proportion of the CD4+ subpopulation of T lymphocytes was significantly increased (P < 0.05) at 1, 7, and 21 d PI in Experiment 3. The results indicate that humoral and cellular immunities to TCV are elicited in turkeys following infection with TCV.

Animals↗

Iron, transferrin, and acid and alkaline phosphatase in healthy turkeys and in turkeys inoculated with the lymphoproliferative disease virus.

Presented are data on iron-binding capacity determinations in the serum of turkeys infected with lymphoproliferative disease (LPD) virus and in healthy males and females (laying eggs and nonlaying) from a breeding flock. Also presented are results of serum and tissue total acid and alkaline phosphatase determinations in turkey poults infected with LPD virus and their uninfected controls and of serum enzyme levels in healthy males and females from the breeding flock. There was no significant alteration in total iron binding capacity (transferrin level) in the serum of turkeys with LPD. Turkey poults inoculated with LPD virus showed a significant decrease in serum alkaline phosphatase activity 4 and 7 weeks postinfection (pi), and a decrease in serum acid phosphatase activity 7 weeks pi. Acid and alkaline phosphatase activity determined in the spleen and pancreas (organs with pronounced tumor involvement) 7 weeks pi did not differ significantly from that of healthy controls, although there was a tendency for both enzymes to decline in the pancreas of the infected turkeys. Healthy laying female turkeys demonstrated marked elevation in serum transferrin level and in acid and alkaline phosphatase activity, as compared with males of the same age. Serum alkaline phosphatase of turkey poults was markedly higher than that of adult turkeys.

Acid Phosphatase↗

Efficacy of avirulent hemorrhagic enteritis virus propagated in turkey leukocyte cultures for vaccination against hemorrhagic enteritis in turkeys.

Avirulent hemorrhagic enteritis virus (HEV-A) propagated in turkey leukocyte cell culture was tested as a vaccine to prevent hemorrhagic enteritis (HE) in turkeys in experimental and field trials. Immunization of turkeys with live HEV-A resulted in protection against a challenge with virulent HEV (HEV-V) as measured by the serological response and the absence of clinical disease and HEV antigen in spleens. In field trials, 19 out of 20 flocks seroconverted within 21 days after vaccination with live HEV-A distributed in the drinking water. The average immune response of the turkeys in these flocks was 96%. Most importantly, neither clinical HE nor other adverse effects caused by HEV-A vaccination were observed in any of the vaccinated flocks. Because maternal antibodies can interfere with the immune response to the vaccine, the optimum time for vaccination was determined. Using an established half-life value of 4.25 days for turkey antibody, and knowing the enzyme-linked immunosorbent assay titer of the maternal antibodies and age of the turkey, the time of vaccination could be calculated taking into account that maternal antibody titers should be lower than 40 to vaccinate the turkeys successfully and induce protection. In vivo tests with HEV-A preparations confirmed the replication of the virus in turkey leukocyte cultures and the potential to pass it in culture. Furthermore, in vivo analysis showed that most infectious virus was associated with preparations of the nonadherent cell population, confirming the results obtained by in vitro analysis. The potency of HEV-A preparations was dependent on the production method and varied from an average of 570 to 8135 doses per ml.

Adenoviridae↗

Comparative investigations of Listeria monocytogenes isolated from a turkey processing plant, turkey products, and from human cases of listeriosis in Denmark.

Listeria monocytogenes was isolated from critical control points in a Danish turkey processing plant, from turkey products and from cases of human listeriosis. During processing in the plant the prevalence of L. monocytogenes ranged from 25.9 to 41.4%. Cleaning and disinfection decreased the prevalence to 6.4%. Isolates of L. monocytogenes were characterized by pulsed-field gel electrophoresis (PFGE) using restriction endonuclease ApaI. Identical DNA types were obtained from turkey products and the processing line even after cleaning and disinfection. Two identical DNA types were demonstrated among isolates from turkey products and human cases of listeriosis. The prevalence of L. monocytogenes in turkey products ranged from 7.3 to 17.4% for ready-to-eat products and raw products, respectively. Since none of the 27 flocks examined before slaughter sampled positive for L. monocytogenes and the prevalence increased during processing, the potential risk from turkey meat was apparently due to factory hygiene rather than intrinsic contamination of the turkeys.

Animals↗

Limited transmission of turkey coronavirus in young turkeys by adult Alphitobius diaperinus (Coleoptera: Tenebrionidae).

We examined the role of lesser mealworm, Alphitobius diaperinus (Panzer), in the transmission of an enteric disease of turkeys caused by a coronavirus. Turkey coronavirus (TCV) from two sources was studied, one isolate (NC95) was embryo propagated, the second was TCV infected material from turkeys diagnosed with poult enteritis mortality syndrome (PEMS). Beetles were fed virus-infected feces mixed with chicken feed. Transmission of virus was effectively halted by surface sterilization of the beetles. Turkey poults administered beetle homogenates infected with TCV+ PEMS that had not been surface sterilized had reduced weight gains and 50% mortality. Mortality and weight gains were not effected in the NC95 group. Virus isolation procedures were performed to determine NC95 viability at varying time intervals. Beetles were dissected and the guts removed 1, 12, and 24 h after the initial viral feeding. Whole beetles were also examined for comparison. Whole beetles and beetle guts were homogenized and injected into turkey eggs for embryo propagation. Direct immunofluorescence was used to determine the presence of TCV. A. diaperinus were capable of mechanical transmission of TCV. However, only turkey embryos receiving whole beetle and beetle gut homogenates within 1 h of feeding on the virus were positive for TCV. Laboratory studies demonstrating PEMS transmission by A. diaperinus are continuing.

Animals↗

Marek's disease in turkeys. II. Characterization of the viral glycoprotein B gene and antigen of a turkey strain of Marek's disease virus.

Marek's disease virus (MDV) causes immunosuppression and tumors in chickens. As sporadic cases of Marek's disease (MD) were recorded in turkeys, the antigenic and genomic characteristics of the MDV glycoprotein B (gB) gene and antigen of turkeys were compared to the chicken MDV gB. The whole chicken and turkey gB genes were sequenced and found identical. By immunoblotting of infected-cell culture lysates using chicken convalescent and gB monoclonal antibodies, the antigenic epitopes of the chicken and turkey viruses were found to differ. The turkey MDV had a unique epitope, compared to the chicken MDV and compared with our previous findings. While the chicken MDV had two epitope types, heat-labile but dithiothreitol (DTT)-stable and heat-stable but DTT-labile, the turkey MDV gB epitope is both heat and DTT-labile.

Animals↗

Interaction of turkey complement with Escherichia coli isolated from turkeys.

The role of turkey complement in a serum bactericidal reaction was determined using serum-sensitive and serum-resistant Escherichia coli isolated from turkeys. Inactivation of complement by heating serum (56 C for 40 minutes) or by treating serum with 10 mM EDTA eliminated bactericidal activity. Serum-sensitive E coli organisms were killed by turkey serum treated with 10 mM ethylene glycol-bis-beta-(aminoethyl ether)-N,N,N',N'-tetraacetic acid and 5 mM MgCl2. Exposure of normal turkey serum to serum-sensitive or serum-resistant E coli resulted in equivalent reductions in hemolytic activity of serum. Treatment of serum-resistant E coli with antibody rendered the bacteria sensitive to bactericidal effects of normal turkey serum. Serum-sensitive E coli organisms were readily killed by an alternative complement pathway, serum-sensitive and serum-resistant E coli activated the complement system equally well, and antibody was required for complement-mediated killing of certain serum-resistant E coli organisms from turkeys.

Animals↗