Rickets in turkey poults

Fifteen outbreaks of rickets were diagnosed in turkey poults in Saskatchewan between 1978 and 1981. No relationship to farm, source of poults, or source of feed was apparent. Most outbreaks started when the poults were between 10 and 14 days of age, and they had recovered by 28 days of age. Losses varied from 1% to 14% of poults started. Skeletal lesions were characteristic of a vitamin D or calcium deficiency. On the basis of chemical analyses, adequate levels of calcium and phosphorus and proper amounts of vitamin premixes were present in the feed, but in five outbreaks biological feed tests implicated feed as a causative factor. The severity of rickets in poults fed defective feeds was markedly reduced by providing the poults with extra vitamin D in the drinking water or by injection. Two premixes used in different feeds contained adequate available vitamin D on the basis of biological testing. In some of the outbreaks, the rickets may have resulted from inadequate distribution of vitamin D in the feed, destruction of vitamin D during feed processing, or some unknown factor in the feed interfering with vitamin D utilization.     

Pathogenicity of Listeria monocytogenes Scott A after oral and oculonasal challenges of day-old turkey poults

Listeria monocytogenes is a ubiquitous, environmental pathogen that has contaminated poultry ready-to-eat products resulting in large-scale recalls. Research is needed to determine the source of product and processing plant contamination with L. monocytogenes. The purpose of this study was to compare the oral and oculonasal routes of infection on the pathogenicity of L. monocytogenes in turkey poults under different housing conditions. One-day-old turkey poults were challenged by either route with the Scott A strain of L. monocytogenes and placed either in paper-lined battery-brooder cages for 1 wk or in floor pens on fresh pine-shaving litter. On day 7, birds challenged in battery cages were transferred to floor pens. Challenge by the oculonasal route resulted in higher mortality (P = 0.05) and lower body weights (P < 0.0001) compared with both nonchallenged controls and those challenged by the oral route. Birds contained in battery cages for 1 wk had higher mortality (P = 0.002) and higher body weights (P < 0.0001) compared with floor-pen-reared birds. Using direct plating, the challenge strain was isolated from the gall bladder, brain, and knee joint of only one dead poult challenged by the oculonasal route. These results suggest that day-old turkey poults may be more susceptible to an oculonasal challenge with L. monocytogenes than to an oral challenge and that containment in battery cages for the first week increased contact exposure to the challenge.     

Salt poisoning in turkey poults

A 4% mortality in 5-to-11-day-old turkey poults was attributed to 1.85% sodium chloride in the feed. The syndrome included peracute respiratory distress, ascites, and sudden death that resembled peracute heart failure. Clinical signs were observed only in the final phase of the toxicity, but progressive histologic lesions were found. Live, apparently unaffected poults showed increases in intracellular glycogen and cytoplasmic granularity, loss of striation, and early mild intercellular myocardial edema; similar but more severe histologic lesions were seen in live, ascites-affected poults. The ascites-affected poults had hydropericardium and hydrothorax which seemed to develop just minutes before death. Ultrastructurally, focal areas of myocardial cells exhibited myofibrillar disarray, lysis of myofilaments, widened Z-bands, and dilation of sarcoplasmic reticulum.     

Furazolidone toxicity in neomycin-treated turkey poults

Furazolidone (FZ) toxicity was evaluated in turkey poults treated with neomycin at a dose of 20 mg/kg body weight for 5, 10, or 26 days. Neomycin treatment had no effect on FZ-induced anorexia, delayed the onset of altered electrocardiographic patterns by approximately 1 week, and did not significantly affect the development of FZ-induced cardiomyopathy. Data indicated that FZ toxicity is not significantly altered by the gut microflora.     

Enteric viruses in diarrheic turkey poults

Thirty-three intestinal samples from 10-to-21-day-old diarrheic turkey poults were examined for the presence of enteric viruses by electron microscopy. Samples originated from 32 flocks in six commercial operations located in six states. Mortality in these flocks ranged from 3 to 15%, and birds from recovered flocks varied greatly in size. Rotavirus-like agents (RVLA) were the most common viruses associated with diarrhea outbreaks in the flocks examined, occurring in five out of six operations. Other viruses detected either singly or in combination, in order of prevalence, were astroviruses, reoviruses, rotaviruses, enteroviruses, and adenoviruses. With the exception of RVLA and rotaviruses, the other viruses were identified solely on the basis of morphology. Salmonellae were isolated from only one of the intestinal samples. By electron microscopy, RVLA were morphologically indistinguishable from rotaviruses, occurring as both 55-nm single-shelled and 70-nm double-shelled particles. However, immune electron microscopy was useful for antigenic differentiation of these two viruses. Turkey rotaviruses reacted with antisera to porcine and bovine rotaviruses, whereas turkey RVLA did not. Neither turkey rotaviruses nor RVLA reacted with antisera to porcine para-rotavirus or an antigenically distinct bovine rotavirus (bovine rotavirus-like agent). Similarly, convalescent anti-turkey RVLA serum (from recovered specific-pathogen-free poults) reacted with homologous virus but did not react with mammalian or avian rotaviruses or reoviruses. Further, RVLA were found to possess RNA electrophoretic migration patterns unlike those of conventional rotaviruses or reoviruses. This trait was used as an additional means of differentiating these viruses.     

Cataracts and optic nerve hypoplasia in turkey poults

Newly hatched commercial turkey poults culled because of grossly visible cataracts were studied. A total of 43 affected and 23 unaffected control poults at various ages were necropsied, and the ocular changes in affected poults were compared with those of aged-matched controls. Affected poults had consistent cataracts coupled with a marked depletion in retinal inner plexiform, ganglion cell, and optic nerve fiber layers, with a resultant reduction in the size of the optic nerves. Lesions were seen in 1-day-old poults. Lens changes included microphakia and lens fiber degeneration throughout the lens, with nuclear liquefaction. The depletion in the numbers of retinal ganglion cells did not appear to progress over several weeks time. The ganglion cell depletion was not uniform within the retina. The cause for these ocular changes is unknown.     

Specific mucosal IgA immunity in turkey poults infected with turkey coronavirus

The objective of this study was to elucidate the kinetics and magnitudes of specific IgA antibody responses in intestines of turkey poults infected with turkey coronavirus (TCV). Turkey poults were orally inoculated with TCV at 10 days of age. Intestinal segment cultures were administered for duodenum, jejunum, and ileum and the IgA antibody responses were analyzed at 1, 2, 3, 4, 6, or 9 weeks post-infection (PI) in two different experiments. The kinetics of virus-specific IgA antibody responses in duodenum, jejunum, and ileum were similar: gradually increased from 1 week PI, reached the peak at 3 or 4 weeks PI, and declined afterward. The virus-specific IgA antibody responses in duodenum, jejunum, and ileum showed negative correlation with duration of TCV antigen in the corresponding locations of intestine with Spearman's correlation coefficient of -0.85 (p=0.034), -0.74 (p=0.096), and -0.75 (p=0.084), respectively. Moreover, the virus-specific IgA antibody responses in serum were positively correlated with that of duodenum (coefficient=0.829, p=0.042), jejunum (coefficient=0.829, p=0.042), and ileum (coefficient=0.771, p=0.072) segment cultures, suggesting that the induction of specific IgA response in serum was predictive of an IgA response in intestine. The results indicate that intestinal mucosal IgA antibodies to TCV are elicited in turkeys following infection with TCV. The local mucosal antibodies may provide protective immunity for infected turkeys to recover from TCV infection.     

Vitamin A deficiency in turkey poults.

Vitamin A deficiency was diagnosed in a commercial flock of 13,000 4-6-week-old turkey poults in the summer of 2004. The birds were initially submitted for examination because of a 3% increase in the reported daily mortality of the flock. Clinically, affected birds had stunted growth and ruffled feathers, showed signs of incoordination, and were depressed. At necropsy, pale white pseudomembranous to mucoid material was observed on the mucosal surface of the tongue, oral cavity, portions of the esophagus, and the crop of some birds. Histologically, there was squamous metaplasia of the mucosal epithelium of the oral mucosa, esophagus, sinuses, nasal glands, bronchi, proventriculus, and the bursa of Fabricius. Vitamin A was not detected in the feed sample at a detection limit of 0.5 mg/kg. Serum vitamin A concentrations in 7 birds were very low and ranged from 0.05 to 0.1 mg/L. Vitamin A concentrations in livers were extremely low (0.1 mg/kg wet weight, 1/7 poults) or undetectable (< 0.1 mg/kg wet weight, 6/7 poults). A diagnosis of vitamin A deficiency was made based on gross and microscopic lesions and vitamin A concentrations in serum, liver, and feed. To the authors' knowledge, this is the first documented case of vitamin A deficiency in poults submitted from a commercial meat turkey producer comparatively depicting the gross and microscopic lesions with those found in other species of birds and mammals.     

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.     

Experimental bovine coronavirus in turkey poults and young chickens

The DB2 calf strain of bovine coronavirus (BCV) was used to inoculate 1-day-old specific-pathogen-free (SPF) turkey poults in three trials. In all trials, the birds developed clinical signs of enteritis at 48-72 hr postinoculation. Birds euthanatized at 3, 5, and 7 days postinoculation (DPI) had flaccid, pale intestines with watery contents, and the ceca were markedly enlarged with frothy contents. Coronavirus particles were detected by immune electron microscopy with BCV antibodies from the intestinal contents of birds killed at 3, 5, 7, and 12 DPI. Body weights of inoculated poults killed at 3, 5, and 7 DPI were significantly reduced as compared with controls. Hemagglutinating antibodies were detected in sera of convalescent birds at 12 DPI. However, experimental inoculation of 1-day-old SPF chicks in two trials with the same virus resulted in no clinical signs or macroscopic or microscopic lesions. No coronaviruses were detected from intestinal contents, and there were no significant differences in body weights of inoculated and noninoculated control chicks.     

Efficacy of a commercial turkey coryza vaccine (Art-Vax) in turkey poults

Four laboratory experiments were designed to study the efficacy of the only available commercial vaccine for turkey coryza, Art-Vax. Poults were vaccinated either once or twice at different ages and challenged with pathogenic Alcaligenes faecalis. In another study, commercial turkeys vaccinated at 1 and 12 days of age on a commercial farm were brought to the laboratory for challenge with pathogenic A. faecalis. Both the laboratory- and field-vaccinated poults were given the manufacturer's recommended dosage of the vaccine strain. Regardless of the vaccine schedule or source of poults, the vaccine was not effective in protecting challenged turkeys from infection. Furthermore, the vaccine was not effective in protecting poults less than 3 weeks of age from disease, but it was effective in protecting poults more than 3 weeks of age from disease. These results indicate that although vaccinated turkeys older than 3 weeks of age were not susceptible to disease, they were susceptible to infection and could act as carriers of field strains of A. faecalis, thus perpetuating the risk of infection to flocks subsequently raised in the same buildings.