Biomedical subjects

D E Swayne

Publications and source records attributed to D E Swayne.

At least 73 records · Page 4Linked to original sources

PubMedDate not supplied

Nephrotropic properties demonstrated by A/chicken/Alabama/75 (H4N8) following intravenous challenge of chickens.

Tissue tropism properties of A/chicken/Alabama/75 (H4N8) were examined after intravenous inoculation of 5-week-old specific-pathogen-free chickens. From 14 clinically normal chickens euthanatized on days 1-20 postinoculation, the frequencies of virus recovery were highest for cloacal swabs (86%), bursal swabs (64%), and kidney tissues (64%) and lowest for tracheal swabs (14%), thymus tissues (14%), bone-marrow swabs (7%), and brain tissues (0%). Evidence that the high frequency of virus recovery from kidney tissues was associated with virus replication in the kidney tissues was provided by high virus titers, ranging up to 10(9.5) mean embryo infectious dose per gram of kidney tissue, and by identification of intranuclear and intracytoplasmic type A influenza nucleoprotein in kidney cells using immunohistochemistry. Virus-recovery and virus titer results from three chickens that died on days 4 and 5 postinoculation paralleled the results from the clinically normal chickens. These findings indicate that A/chicken/Alabama/75 has nephrotropic properties similar to nephrotropic properties previously reported for waterfowl-origin type A influenza viruses and provide evidence that kidney lesions could be manifestations of systemic influenza infections in commercial laying chickens.

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Evaluation of the kidney as a potential site of avian influenza virus persistence in chickens.

One-day-old chickens were inoculated intravenously with one of three low-pathogenicity avian-origin influenza isolates. On day 5 postinoculation (PI), the frequency of influenza virus isolation from cloacal swabs following challenge with each isolate ranged from 83% to 100% for clinically normal euthanatized chickens. Influenza virus was also frequently isolated from kidneys of these chickens (47%) and from chickens that died (100%). Kidneys positive for virus isolation had lesions of nephrosis and/or acute nephritis, and influenza viral nucleoprotein was demonstrated in nuclei and cytoplasm of necrotic renal tubule epithelium. On sampling days 28 and 45/60 PI, influenza virus was neither isolated from nor immunohistochemically demonstrated in kidneys (0/125); however, the kidneys (47%) did have chronic histologic lesions that suggested previous influenza virus infection of the kidneys. Influenza virus was isolated from cloacal swabs of two of 44 chickens on day 28 PI, but all cloacal swabs were negative for virus recovery on sampling day 45/60 PI (0/81). These results indicate that replication of influenza virus in renal tubule epithelial cells did not result in persistence of type A influenza virus in this immunologically privileged site.

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Necrotizing typhlocolitis associated with a spirochete in rheas (Rhea americana).

Necrotizing typhlocolitis was diagnosed in 13 juvenile common rheas (Rhea americana) from three separate of geographically isolated Ohio flocks, with mortality ranging from 25% to 80%. At postmortem examination, a diphtheritic membrane covered ulcerated cecal mucosa. Histologically, cecal sections showed necrosis and granulomatous-to-suppurative inflammation that extended into the submucosa and often surrounded large eosinophilic colonies of bacteria. Warthin-Starry staining showed these colonies to be composed of entangled spirochetes that invaded the submucosa and frequently were present transmurally. Similar organisms were identified by Warthin-Starry staining in the cecum of a juvenile rhea from a fourth flock that histologically had mild lymphocytic typhlitis. Scanning and transmission electron microscopy demonstrated the presence of a spirochete in the ceca. Anaerobic culture yielded a gram-negative, beta-hemolytic spirochete. Coccidia, histomonads, and Salmonella spp. were consistently absent.

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Assessing pathogenicity potential of waterfowl-origin type A influenza viruses in chickens.

Intravenous pathogenicity index (IVPI) tests on 29 wild duck-origin type A influenza viruses, two turkey-origin type A influenza viruses, and one chicken-origin type A influenza virus resulted in indices ranging from 0.0 to 0.49. Most of the wild duck-origin viruses and the two turkey-origin viruses had indices of 0.0, indicating they are not pathogenic. Six of the duck-origin viruses had indices ranging from 0.25 to 0.49, and the IVPI for A/chicken/Alabama/75 (H4N8) was 0.49, indicating they had low pathogenic potential. An IVPI of 1.25 up to the maximum score of 3.0 is necessary for a type A influenza virus to be classified as highly pathogenic. Gross lesions observed in chickens dying following intravenous viral challenge included kidney swelling with more prominent lobular patterns, but visceral urate deposits were not present. The usefulness of the IVPI test in evaluating the pathogenicity potential of nonpathogenic and low-pathogenic strains of avian influenza virus may be limited.

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Renal pathology in specific-pathogen-free chickens inoculated with a waterfowl-origin type A influenza virus.

Five-week-old specific-pathogen-free chickens inoculated intravenously with a waterfowl-origin type A influenza virus (A/mallard/Ohio/184/86) had swollen and mottled kidneys on days 3, 5, and 7 postinoculation (PI) and multiple raised nodules on days 5, 10, and 20 PI. Histologically, the kidneys had multifocal heterophilic tubulointerstitial nephritis with epithelial necrosis on day 3 PI, lymphoplasmacytic tubulointerstitial nephritis on day 5 PI, and fibrosing interstitial nephritis with cortical lobular collapse, atrophic tubules, glomerular aggregates, and interstitial lymphoid follicles and aggregates on days 7, 10, and 20 PI. Heterophilic intratubular medullary-cone nephritis was present in dead or moribund chickens on days 3 and 5 PI. Furthermore, the presence of mild multifocal heterophilic tubulointerstitial nephritis on day 20 PI suggests that a waterfowl-origin strain of type A influenza virus of low pathogenicity has the potential to produce acute and chronic active nephritis in the chicken and that the kidney is a potential site for influenza viral persistence. The acute, subacute, and chronic histopathologic renal lesions of this influenza virus in chickens are similar to lesions reported for some nephropathogenic infectious bronchitis viruses and avian nephritis picornavirus.

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PubMedDate not supplied

A small round virus associated with enteritis in turkey poults.

In a natural outbreak of enteric disease in turkey poults, Salmonella, group D rotavirus, astrovirus, and a small (18-24 nm) round virus were detected in the gut contents. Except for the small virus, the pathogenic potential of the other agents is recognized. In experiments, the small round virus was shown to be transmissible and pathogenic in specific-pathogen-free turkey poults.

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Enteric disease in specific-pathogen-free turkey poults inoculated with a small round turkey-origin enteric virus.

Four- and 5-day-old specific-pathogen-free turkey poults were inoculated orally or by contact exposure to a small round turkey-origin enteric virus. At days 4 and 8 postinoculation (PI), the orally inoculated poults had significantly lower body weight gains than control poults. Poults at day 4 (orally inoculated) and 5 (contact-exposed) PI had watery droppings, dilated thin-walled ceca filled with yellow foamy fluid, catarrhal small intestinal secretions, pale intestinal serosa, and mild lymphocytic enteritis. In addition, at day 4 PI, poults were lymphopenic, had intracytoplasmic crystalline arrays of 17.1 +/- 1.1 nm viral particles in the jejunal villar enterocytes, and had an 18-to-24-nm virus in intestinal contents. Analysis of morphometric data revealed mild shortening of villi in the duodenum and elongation of crypts in the duodenum and ileum during the late stage of the syndrome (day 8 PI). These findings suggest that the 18-to-24-nm virus can produce an enteric disease syndrome and that the acute clinical manifestation of this syndrome is not the result of morphologic change such as intestinal villus atrophy. The definitive identity of this 18-to-24-nm virus is not known; however, based on size and intracytoplasmic arrays of virus, it is most probably an enterovirus.

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PubMedDate not supplied

Replication of a waterfowl-origin influenza virus in the kidney and intestine of chickens.

Intravenous inoculation of chickens with a waterfowl-origin type A influenza virus resulted in high titers of virus in kidney tissues and viral nucleoprotein in renal tubular epithelial cells and in intestinal mucosal epithelial cells. Virus titers in kidneys of four of eight clinically normal chickens sampled on days 3 and 5 postinoculation (PI), one dead chicken on day 3 PI, and one dead chicken on day 7 PI exceeded 10(6) mean embryo infectious dose per gram of tissue. Using immunofluorescent and immunoperoxidase staining, viral nucleoprotein was identified in the cytoplasm and nucleus of tubular epithelial cells in kidneys and in nucleus of mucosal epithelial cells lining villi in the lower small intestine. Based on the low intravenous pathogenicity index for this virus (0.3) along with the high virus titers in kidney tissues and localization of viral antigen in kidney important site for replication of avian influenza (AI) virus of low pathogenicity. Recovery of type A influenza viruses from cloacal swabs could result from viral replication in kidneys as well as in the lower intestine and/or the bursa of Fabricius.

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PubMedDate not supplied

Sudden death syndrome in turkey hens.

A turkey breeder flock of 5600 31-week-old hens experienced an abrupt increase in daily mortality for a 2-day period. This higher mortality rate corresponded with the handling and moving of the hens 1 to 2 days before. No clinical illness was seen in the hens before carcasses were discovered. The four hens that were necropsied had small spleens, congested lungs, and enlarged livers. The most consistent histologic lesions were pulmonary hemorrhage and edema, and congestion of veins and capillaries in several visceral organs. One hen had subserosal hemorrhage of the oviduct and perirenal hemorrhage. The increased mortality pattern, the lack of clinical signs, and the histopathologic changes are consistent with a diagnosis of sudden death syndrome. The presence of concurrent inflammatory lesions in the lungs predisposed the hens to sudden death following the stress of handling and moving.

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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.

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PubMedDate not supplied

Pinealoma in a broiler breeder.

An incidental central nervous system tumor was found in a broiler breeder. The cellular mass was histologically similar to the normal pineal gland, but it was characterized by a decreased ratio of follicular/parafollicular cells, a relative increase in mitoses, a size three times greater than a normal pineal gland, and growth and expansion into adjacent cerebellar tissue. These characteristics warranted a diagnosis of pinealoma rather than pineal gland hyperplasia.

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PubMedDate not supplied

Comparative pathology of intravenously inoculated wild duck- and turkey-origin type A influenza viruses in chickens.

Five-week-old specific-pathogen-free chickens were inoculated intravenously with one of 16 low-pathogenicity type A influenza virus isolates; 14 were of wild duck origin, and two were of turkey origin. Tubulointerstitial nephritis was the most frequent specific histopathologic change. The frequency and severity of kidney lesions were independent of the virus hemagglutinin-neuraminidase subtype or titer of the challenge virus. Influenza nucleoprotein was most frequently demonstrated in the kidney and was consistently localized to necrotic proximal and/or distal renal tubule epithelium. Common nonspecific histopathologic changes were lymphoid hyperplasia of the spleen and cecal tonsils, as well as lymphocyte depletion in the cloacal bursa. Uncommon histopathologic changes, in decreasing order of frequency, were interstitial pneumonia, lymphoid follicular hyperplasia in the myocardium, and lymphocytic tracheitis. Histopathologic changes were rare or absent in the jejunum, duodenum, pancreas, and brain. The low-pathogenicity avian-origin type A influenza virus isolates were epitheliotropic in chickens, primarily nephrotropic. Such findings were dissimilar from findings with highly pathogenic avian-origin type A influenza virus isolates both in severity and in tissue distribution of histopathologic changes and influenza viral antigen.

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PubMedDate not supplied

Acute renal failure as the cause of death in chickens following intravenous inoculation with avian influenza virus A/chicken/Alabama/7395/75 (H4N8).

One-day-old and 5-week-old commercial leghorn, specific-pathogen-free leghorn, and broiler chickens were inoculated intravenously with either avian influenza virus isolate A/chicken/Alabama/7395/75 (H4N8) (Ck/AL) or sterile diluent. Ck/AL infection resulted in a 44% mortality rate, reduced weight gains, and necrosis of proximal renal tubules and/or tubulointerstitial nephritis. The renal tubule necrosis was more severe and widespread in chickens that died than in chickens that were euthanatized. Hyperuricemia, hypercalcemia, and hyperphosphatemia were present in 5-week-old chickens at day 5 postinfection. Influenza virus isolate Ck/AL was nephropathogenic, and death was associated with acute severe renal damage and failure. Some data suggested that the pathogenicity of Ck/AL may be more severe in leghorns than broilers.

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Pathological studies of A/chicken/Alabama/7395/75 (H4N8) influenza virus in specific-pathogen-free laying hens.

Specific-pathogen-free laying hens were inoculated with avian influenza virus (AIV) A/chicken/Alabama/7395/75 (H4N8) either intratracheally (IT) or intravenously (IV). IT inoculation produced a localized infection of the upper and lower respiratory tracts with lesions of tracheitis, bronchitis, airsacculitis, and pneumonia around the secondary bronchi. IV inoculation produced a systemic infection with major lesions of nephritis, interstitial pneumonia, salpingitis, and splenic and hepatic necrosis. In IV-inoculated hens, AIV nucleo-protein was demonstrated within renal tubule epithelium, in luminal surface and glandular oviduct epithelium, and in mononuclear cells within pulmonary blood capillaries. However, no virus was recovered from internal contents of eggs laid between days 1.5 and 5 postinfection. These data indicate that A/chicken/Alabama/7395/75 has tissue tropism and pathogenicity for the respiratory and urogenital systems of reproductively active laying hens. Site and severity of lesion development are determined by the localized or systemic nature of AIV infection.

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Role of circulating maternal anti-rotavirus IgG in protection of intestinal mucosal surface in turkey poults.

The effect of circulating maternally transferred IgG on immunity of turkey poults to rotavirus infections was investigated. Specific-pathogen-free (SPF) turkey hens were hyperimmunized with avian group A rotavirus 2 weeks before the laying cycle. SPF poults designated positive for group A rotavirus (Rab+) and negative for such maternal antibody (Rab-) were challenged orally with the homologous virus at 2, 5, or 12 days of age (challenge Groups 1, 2, and 3, respectively). Poults were examined at 3 and 6 days postinfection (PI) for clinical signs, gross lesions, histopathological changes in the small intestine, rotavirus in intestinal contents, and D-xylose absorption as an indicator of the intestinal absorptive function. In challenge Groups 1 and 2, rotavirus titers in the intestinal contents were significantly lower in Rab+ poults than in Rab- poults at 3 days PI. Gross lesions and D-xylose absorption results were consistent with the virus-shedding data. Histopathological changes were moderate and comparable in Rab- and Rab+ poults. In challenge Group 3, however, no significant differences were observed between Rab- and Rab+ poults in any of the examined parameters. Results provided evidence that circulating maternally derived IgG has an important role in protection of the intestinal mucosa against rotavirus infection during the first week of life. It is suggested that protective immunity afforded by maternal IgG is titer-dependent.

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Effects of vitamin A deficiency on the reproductive system of mature White Leghorn hens.

Two groups of 100 white leghorn hens were fed rations either supplemented or deficient in vitamin A for 32 weeks. At the conclusion of the study, vitamin A-supplemented hens laying normally were also compared with a group of vitamin A-supplemented hens in a state of low egg production. Mean egg retinol equivalents (microgram retinol/g egg yolk), egg production, and hatchability in the vitamin A-deficient group were decreased significantly by 4, 20, and 28 weeks, respectively, after beginning treatment. The ovaries of vitamin A-deficient chickens had increased numbers of atretic follicles compared with the ovaries of vitamin A-supplemented hens (20, 24, 28, and 32 weeks), and these atretic follicles contained moderate to severe hemorrhage. Hemorrhage was located either uniformly throughout the follicle or more commonly between the detached granulosa cell layer and the theca interna. Hemorrhagic follicles were uncommon in both vitamin A-supplemented hens and low-production vitamin A-supplemented hens.

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Tissue tropism and replicative properties of waterfowl-origin influenza viruses in chickens.

Waterfowl-origin influenza (WFOI) viruses were evaluated for their tissue tropism and replicative properties in chickens. The 14 WFOI isolates used in this study represented 13 different hemagglutinin-neuraminidase combinations recovered during 1987 and 1988 and included isolates possessing the H5 and H7 hemagglutinin subtypes and one isolate possessing the H5N2 combination. Following intravenous challenge, the frequencies of virus recovery within individual experiments were generally higher for the lower digestive tract and kidney samples. Virus titers ranged up to 10(8.5) mean embryo infective doses per gram of kidney tissue in clinically normal chickens. Differences in frequencies of virus recovery and virus titers in tissues indicated that some of these uniformly nonpathogenic and low-pathogenicity WFOI virus isolates replicated more extensively in chickens than did others. This enhanced ability to replicate in chickens should be further evaluated as a potential factor associated with the threat WFOI viruses present to poultry.

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Assessment of the ability of ratite-origin influenza viruses to infect and produce disease in rheas and chickens.

Pathobiologic characteristics were determined for three mildly pathogenic (MP) ratite-origin avian influenza viruses (AIVs). Ratite-origin AIVs produced respiratory disease in rheas, and virus was reisolated from oropharyngeal and cloacal swabs on days 2-6 postinoculation. Inoculation of two ratite-origin AIVs in the upper respiratory tract of chickens resulted in viral infections, but the mean chicken infectious dose (CID50) for A/emu/Texas/39924/93 (H5N2) (Emu/Texas) virus was 500-fold lower than the CID50 for the A/rhea/North Carolina/39482/93 (H7N1) virus. In ovo and in vivo passage of the MP parent Emu/Texas isolate resulted in emergence of a highly pathogenic (HP) variant that had high plaquing efficiency in chicken embryo fibroblast cultures and was highly lethal in chicken pathotyping tests. This variant virus produced gross lesions in chickens similar to those reported for other HP AIVs. These findings demonstrated that ratite-origin AIVs can produce significant clinical disease in rheas and have a realistic potential for interspecies transmission to domestic poultry. Furthermore, HP variants can emerge from MP H5 ratite-origin AIVs if introduced and allowed to circulate in chicken populations.

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