PubMed Health⌕ Search

Biomedical subjects

R J Eckroade

Publications and source records attributed to R J Eckroade.

At least 19 recordsLinked to original sources

A review of the 1996-98 nonpathogenic H7N2 avian influenza outbreak in Pennsylvania.

The nonpathogenic avian influenza (AI) outbreak in Pennsylvania began in December 1996 when there was a trace back from a New York live bird market to a dealer's flock. A total of 18 commercial layer flocks, two commercial layer pullet flocks, and a commercial meat turkey flock were diagnosed with nonpathogenic AI (H7N2) viral infection with an economic loss estimated at between 3 and 4 million dollars. Clinical histories of flocks infected with the disease included respiratory disease, elevated morbidity and mortality throughout the house, egg production drops, depression, and lethargy. A unique gross lesion in the commercial layers was a severe, transmural oviduct edema with white to gray flocculent purulent material in the lumen. Layer flocks on two separate premises were quarantined but permitted to remain in the facilities until cessation of virus shed was determined through virus isolation. Several months later, clinical AI appeared again in these flocks. It is not known whether the recurrence of disease in these cases is due to persistence of the organism in the birds or the environment. In addition to serologic testing and virologic testing by chicken embryo inoculation, an antigen capture enzyme immunoassay was evaluated as a diagnostic tool for AI. Research projects related to disinfection, burial pits, and geographical system technology were developed because of questions raised concerning transmission, diagnosis, and control of nonpathogenic AI (H7N2).

Animals↗

Economic analysis of an outbreak of avian influenza, 1997-1998.

OBJECTIVE: To determine economic losses associated with an outbreak of avian influenza in flocks in Pennsylvania during 1997 and 1998. SAMPLE POPULATION: 5 premises containing avian influenza-infected layer, pullet, and turkey flocks. PROCEDURE: Losses incurred before depopulation, those incurred at the time of depopulation, and those that were attributable to depopulation (unrealized loss of income) were evaluated. Results were extrapolated to provide values for all infected flocks. RESULTS: Extrapolating the costs determined on the basis of age and number of birds from the 5 sample flocks to all other flocks infected with nonpathogenic avian influenza H7N2 yielded an estimated total cost to the Pennsylvania poultry industry of $3.5 million. CLINICAL IMPLICATIONS: The H7N2 virus is not highly pathogenic. If the pathogenicity of the virus does not change, then the poultry industry and state and federal governments will not have severe economic losses for the 1997-1998 outbreak similar to those for the 1983-1984 avian influenza outbreak in Pennsylvania. To decrease the potential for financial losses that could result from future outbreaks of avian influenza, it is essential that the commercial industry and livebird market system be separated via increased use of biosecurity measures.

Animals↗

Salmonella enteritidis colonization of the reproductive tract and forming and freshly laid eggs of chickens.

Salmonella enteritidis colonizes the tissues of the chicken ovary and oviduct, presumably contaminating eggs and thereby contributing to human outbreaks of salmonellosis. In this study, commercial adult laying hens were given an oral inoculation of 10(8) S. enteritidis organisms. Tissues from various organs, the intestines, and the reproductive tract, including freshly laid eggs, were collected daily for up to 40 days postinoculation (p.i.). Within 2 days p.i. S. enteritidis was detected by culture in pools of the spleen, liver, heart, and gallbladder tissues, in intestinal tissues of all infected birds, and in various sections of the ovary and oviduct. Detection of organisms by immunohistochemical staining was rare for most tissues in spite of their culture-positive status, suggesting a low level of tissue colonization. However, S. enteritidis could be detected by immunohistochemical staining in oviduct tissues associated with four forming eggs, indicating the possibility of a heavier colonization in the egg during its development. In two subsequent experiments, forming eggs taken from the oviduct with their associated tissue, were found to be culture positive for S. enteritidis at a rate of 27.1 and 31.4%, while freshly laid eggs in these experiments were culture positive at the rate of 0 and 0.6%. These observations suggest that while forming eggs are significantly colonized in the reproductive tract, factors within the eggs may control the pathogen before the eggs are laid. The data show that prior to egg deposition, forming eggs are subject to descending infections from colonized ovarian tissue, ascending infections from colonized vaginal and cloacal tissues, and lateral infections from colonized upper oviduct tissues. The data are consistent with an ascending infection of freshly laid eggs from the cloaca, as the incidence of positive eggs in experiments 1 and 3 coincided with heavily contaminated cloacal tissues (50.7 and 80%, respectively), while no positive eggs were detected in experiment 2 when cloacal colonization was low (8.3%). The data do not support the possibility of egg invasion by bacterial translocation from the peritoneal cavity.

Animals↗

Characterization of avian retroviruses carrying activated transforming human c-src genes and of steps involved in expression of activated src-PKases in vitro.

We have isolated four activated transforming human c-src mutants derived spontaneously from viruses carrying the normal human c-src (SRC) genes in the form of Rous sarcoma virus. These mutants induced transformed cell morphology distinguishable from each other in vitro as well as tumors in chicks, whereas normal SRC-carrying viruses did not. Analyses of the transforming SRC proteins together with the normal SRC protein showed that levels of the carboxy-terminal Tyr-phosphorylation were negatively correlated with both transforming ability and protein kinase (PKase) activity as determined by in vitro autophosphorylation. It was observed that two cell lysis methods, that is, NP-40 and RIPA, yielded two different phosphorylated forms of transforming SRC proteins: one possessed low levels of phosphorylation at the autophosphorylation site and the other possessed high levels of phosphorylation at this site. Using the two types of transforming SRC preparations, we have studied in vitro SRC-PKase reactions in relation to in vivo and in vitro autophosphorylation and in vitro phosphorylation of an exogenous substrate. A possible functional relationship between autophosphorylation and SRC-PKase expression is discussed.

Animals↗

Lesions in broiler and layer chickens in an outbreak of highly pathogenic avian influenza virus infection.

Fifteen chickens, five broilers and ten layers, from the Pennsylvania 1983 outbreak of highly pathogenic avian influenza virus infection, were examined. Gross lesions in the broilers were limited to serosal petechiae and dehydration. In the layers there was comb edema, vesiculation, and necrosis. Microscopic lesions were mild to severe diffuse nonsuppurative encephalitis, very mild to severe diffuse necrotizing pancreatitis, and very mild to severe subacute necrotizing myositis involving numerous skeletal muscles and most severe in the external ocular muscles and limbs. While many of these lesions have been seen in experimental infections of chickens with influenza viruses, the pattern of organs involved in this group of chickens is distinctive.

Animals↗

A comparative pathogenesis of two Mareks disease virus isolates.

The pathogenesis of the JM and GA isolates of Marek's disease virus (MDV) infection was compared by studying the sequential tissue distribution of MDV associated antigens with gross and microscopic lesions in infected chickens. With both MDV isolates the initial sites of viral replication were the lymphoid organs, skin, and featers. Both the GA and JM isolates were viscerotropic as demonstrated by the presence of MDV antigens with gross and microscopic changes occurring in several visceral organs. The JM isolate was more neurotropic and had a greater affinity for the gonads than the GA isolates as evidenced by an early detection of MDV antigens and severe pathology in the peripheral nerves and gonads.

Animals↗

Susceptibility of mink to sheep scrapie.

A progressive, fatal spongiform polioencephalopathy was induced in mink intracerebrally inoculated with a suspension of brain from a Suffolk sheep with naturally acquired scrapie. The clinical signs and pathological lesions of the experimental disease were indistinguishable from transmissible mink encephalopathy, a disease of undetermined origin that occurs in mink.

Animals↗

Transmissible mink encephalopathy: experimental transmission to the squirrel monkey.

A progressive, fatal spongiform encephalopathy developed in three squirrel monkeys 11 months after inoculation with primate-passaged transmissible mink encephalopathy agent. The clinical symptoms and histopathologic and electron microscopic findings suggest that this naturally occurring disease of mink has been transmitted experimentally to squirrel monkeys.

Animals↗

Nephropathogenic infectious bronchitis in Pennsylvania chickens 1997-2000.

Nephropathogenic infectious bronchitis (NIB) was diagnosed in 28 infectious bronchitis virus (IBV)-vaccinated commercial chicken flocks in Pennsylvania from December 1997 to July 2000. Early dinical signs were increased flock mortality and urinary water loss (polyuria and pollakiuria) leading to wet litter. Daily mortality ranged from 0.01% in layers to 2.45% in broilers, with total broiler mortality as high as 23%. Severe renal swelling and accumulation of urates in the tubules were commonly seen. Visceral gout and urolithiasis were less frequently observed. Histopathologic changes included characteristic tubular epithelial degeneration and sloughing with lymphoplasmacytic interstitial nephritis. Minimal respiratory disease signs were noted in broilers. Egg production and shell quality declined in layers. Confirmatory diagnosis of NIB was made by IBV antigen-specific immunohistochemical staining of the renal tubular epithelium and virus isolation. Sequencing of the S1 subunit gene of 21 IBV isolates showed the NIB outbreak to be associated with two unique genotypes, PA/Wolgemuth/98 and PA/171/99. The cases from which the genotypes were isolated were clinically indistinguishable. The NIB viruses were unrelated to previously recognized endemic strains in Pennsylvania and were also dissimilar to each other. Genotype PA/Wolgemuth/98 was isolated almost exclusively during the first 14 mo of the outbreak, whereas PA/171/99 was recovered during the final 18 mo. The reason for the apparent replacement of PA/Wolgemuth/98 by PA/171/99 is not known.

Animals↗

Characteristics of H7N2 (nonpathogenic) avian influenza virus infections in commercial layers, in Pennsylvania, 1997-98.

Between January 1997 and March 1998, 11 cases of H7N2 avian influenza (nonpathogenic) were diagnosed at the Laboratory of Avian Medicine and Pathology, Kenneth Square, PA. These cases involved either commercial leghorn laying hens or leghorn pullets raised in Pennsylvania. Grossly and histologically, the most striking lesion associated with disease was salpingitis, usually with edema and occasionally with oviduct necrosis. Fluid, fibrinous, and egg yolk material in the peritoneum (egg yolk peritonitis) as well as pulmonary congestion and pulmonary edema were also frequently seen. Oviduct lesions have rarely been described in association with avian influenza infections in previous outbreaks. Mortality in affected houses was mild to moderate (less than 4% total mortality during the outbreak), with concurrent mild to moderate egg production declines (2%-4% at the time of disease onset).

Animals↗