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Biomedical subjects

W J Hadlow

Publications and source records attributed to W J Hadlow.

At least 37 records · Page 2Linked to original sources
PubMed1986

Interferon response in normal and Aleutian disease virus-infected mink.

Studies were done to determine whether differences in interferon production are responsible for the resistance of pastel mink to Aleutian disease. The abilities of normal pastel and sapphire mink to produce interferon when inoculated with either Newcastle disease virus or a synthetic polyribonucleotide, poly (I):poly (C), were identical, even to the production of a novel, acid-labile interferon. The resistance of pastel mink to Aleutian disease did not correlate with interferon production, because neither sapphire nor pastel mink produced detectable amounts of interferon when infected with either the Pullman strain of Aleutian disease virus (ADV) or the highly virulent Utah I strain. Sapphire mink infected with the Pullman strain responded normally to poly (I):poly (C) early in the course of the disease, but interferon production was impaired late, when the mink were hypergammaglobulinemic and had renal, vascular, and hepatic lesions. These data suggest that ADV Pullman neither stimulates nor interferes with interferon production in infected mink and may represent a mechanism whereby ADV can more readily establish infection.

Aleutian Mink Disease↗
PubMed1986

Carotid body tumor: an incidental finding in older ranch mink.

Carotid body tumors were found incidentally at necropsy in 15 ranch mink (Mustela vision), mostly royal pastels, kept for studies on slow viral diseases. The mink, five males and ten females, were 77 to 135 months old (mean age 107 months). Loosely or firmly attached at the bifurcation of the common carotid artery, and 11 larger tumors were smooth-surfaced, discrete, pale brown, globoid masses that varied from 2.5 to 16 mm in diameter. Four tumors of microscopic size occurred in otherwise normal-looking carotid bodies. All were composed of densely packed polygonal cells disposed in sheets and cords or arranged in clusters by a reticulin meshwork rich in blood vessels. Always unilateral, the tumors had not invaded locally or metastasized. As seen in the smallest tumors, the neoplastic cells usually arose centrally in the carotid body and formed an expansive growth that replaced much of the normal parenchyma without necessarily enlarging the organ beyond normal limits. The cause of the tumors was not apparent. All tumor-bearing mink had lived at an elevation of 1,100 meters, and none had suffered from any obvious chronic cardiopulmonary disease.

Animals↗
PubMed1986

Cerebrocortical degeneration in goats inoculated with mink-passaged scrapie virus.

Widespread spongiform degeneration of the cerebral cortex occurred in four African pygmy goats that became affected with scrapie after intracerebral inoculation with scrapie virus (Suffolk sheep brain origin) that had been passed three times in ranch mink. The occurrence of such cerebrocortical degeneration was a distinct departure from the topographic pattern of neuropathologic changes that characterizes scrapie in sheep and goats. But the cortical lesion was identical to the one found in goats that became affected with a disease otherwise indistinguishable from scrapie after intracerebral inoculation with transmissible mink encephalopathy (TME) virus that had been passed twice in mink. If TME originated from infection with wild scrapie virus, as is generally thought, then the viruses used in these two instances would be equivalent in their passage history in this aberrant host. Given this similarity, the common occurrence of the cortical lesion is thought to be consistent with the view that TME virus almost certainly is scrapie virus whose biologic properties became altered by chance passage in ranch mink.

Animals↗
PubMed1985

Temporal replication of the Pullman strain of Aleutian disease virus in royal pastel mink.

Information was sought on the temporal replication of Aleutian disease virus in 27 royal pastel mink. Groups of three were examined 8 to 126 days after they were inoculated subcutaneously with 10(3) 50% lethal doses of the Pullman strain. Much individual variation was noted in the onset of infection, occurrence of viremia, and extent of virus replication in the tissues. Thus, virus was detected in lymph nodes regional to the site of inoculation in only some mink during the first 14 days after inoculation. During this period, virus was often present as well in the mesenteric lymph node and spleen. First detected on day 10, viremia was present in all mink examined on day 28 but occurred irregularly thereafter, even when virus was widespread in the tissues. Except in five mink succumbing to the disease, the tissue distribution of virus after day 28 tended to be more limited, and the titers were generally lower than they had been earlier. Even though present in the lymph nodes and spleen, virus was often absent from the kidney, liver, and intestine after day 28. Specific antibody was detected on day 28 and was present in all mink thereafter, ostensibly without any adverse effect on virus replication. In most mink, the infection was considered subclinical, for it was usually not accompanied by a rise in serum gamma globulin or by morphologic evidence of the disease. The virologic findings in this study have a bearing on the relationship of subclinical infections to both horizontal and vertical transmission of the virus.

Aleutian Mink Disease Virus↗
PubMed1985

Carcinoma of the anal sac glands in ranch mink.

During a 14-year period, carcinoma of the anal sac apocrine glands was found in 52 pastel and 8 sapphire mink (Mustela vison) kept for studies on slow viral diseases. The pastel mink varied in age from 72 to 135 months (mean age 108 months), the sapphire mink from 63 to 100 months (mean age 81 months). All but one pastel mink were females. The primary tumor varied in size from masses that caused bulges in the perineum to those that were found only after microscopic examination of the anal sac glands. Although the primary tumor grew mainly by expansion with little local infiltration, 41 of the 60 tumors had metastasized to the regional lymph nodes and sometimes also to more distant sites. The striking propensity of the carcinoma to metastasize while still small, even microscopic, often resulted in massive secondary growths, notably in the iliac lymph nodes. Hypercalcemia did not accompany the carcinoma. Its varied microscopic appearance included solid, glandular, squamous cell, and spindle or round cell components. Combinations of them formed mixed or complex histologic patterns, no doubt largely attributable to neoplastic proliferation of myoepithelial cells and squamous metaplasia of the apocrine gland epithelium. Although its cause remains obscure, the carcinoma appeared to arise from small foci of hyperplastic apocrine glands, sometimes in relation to both anal sacs. The tumor is a common and distinctive expression of neoplasia in older ranch mink.

Age Factors↗
PubMed1984

Royal pastel mink respond variously to inoculation with Aleutian disease virus of low virulence.

Information was sought on the varied responses of royal pastel mink (a non-Aleutian genotype) to Aleutian disease virus of low virulence. Thus, of 20 yearling female pastel mink inoculated subcutaneously with a large amount of the Pullman strain of Aleutian disease virus, only 3 succumbed to the disease. Of the other 17 mink, 3 had neither viremia nor a rise in level of serum gamma globulin during the 24 weeks after inoculation. The other 14 mink were viremic for variable periods during the first 12 weeks. In only five mink was the viremia accompanied by elevated levels of serum gamma globulin, usually from week 8 on. Of the 16 subclinically infected mink that did not succumb to intercurrent disease and otherwise remained healthy, 9 were examined at 19 to 31 months for persisting virus. In only one mink, small amounts were detected in the mesenteric lymph node and spleen nearly 28 months after inoculation. The other seven mink that survived the infection were not protected when challenged 31 months later with a small amount of the highly virulent Utah-1 strain. Even though still poorly understood, these varied responses of the royal pastel mink to infection with Aleutian disease virus of low virulence have important pathogenetic and epidemiological implications.

Aleutian Mink Disease↗
PubMed1984

Immunoenzyme Western blotting analysis of antibody specificity in Aleutian disease of mink, a parvovirus infection.

Aleutian disease virus (ADV), an autonomous parvovirus, persistently infects mink and induces very high levels of virus-specific antibody. All strains of ADV infect all mink, but only highly virulent strains cause progressive disease in non-Aleutian mink. The development of antibody to individual ADV proteins was evaluated by Western blotting by using the sera of 22 uninfected mink and 163 naturally or experimentally infected mink. ADV has virion proteins of 86,000 and 78,000 daltons that are closely related. A new, possibly nonvirion protein of 143,000 daltons was observed, as well as a known nonvirion protein of 71,000 daltons. Sera from mink experimentally or naturally infected with ADV of high or low virulence generally reacted about equally with all four proteins. The only exceptions noted were that 8 of 15 sera of mink infected transplacentally preferentially reacted with the two virion proteins and sera from mink with the monoclonal gammopathy of Aleutian disease reacted preferentially with either virion (10 of 12) or nonvirion (2 of 12) proteins.

Animals↗
PubMed1984

Progressive retinal degeneration in ranch mink.

Retinal degeneration was prevalent in a large group of sapphire and pastel mink (Mustela vison) kept for studies on slow viral diseases. Nearly 78% of those two to eight years old were affected. The retinopathy was equally common in both sexes but more frequent in sapphires (85%) than in pastels (63%), and it was severe more often in sapphires than in pastels. By light microscopy, the primary change appeared to be progressive degeneration of fully developed photoreceptors, beginning in their outer segments. In many mink, including some younger ones, the rods and cones and outer nuclear layer had disappeared from all but the far periphery of the fundus. The inner retinal layers were spared until late in the disease, and the pigment epithelium remained essentially unchanged. The cause of the retinopathy was not established. It may represent an abiotrophy in which the structural integrity of the photoreceptors began to wane in many mink after they reached two years of age. Apart from reducing visual acuity, the retinopathy has implications for the photoperiodic control of fur growth and reproduction in this highly light-sensitive carnivore.

Age Factors↗
PubMed1984

Experimental infection of fetal and newborn Suffolk sheep with scrapie virus.

Fetal (n = 21) and newborn (n = 7) Suffolk sheep were inoculated with scrapie virus isolated from other Suffolk sheep. Twenty fetuses, 76 to 109 days of gestational age, were inoculated IM in the neck through the uterine wall and were examined for virus 47 to 322 days later by mouse inoculation. Scrapie virus was not detected before 254 days of age; only traces of virus were detected in 3 of 7 lambs examined thereafter (2 at 254 days of age and 1 at 322 days of age). Virus was limited to the supra-pharyngeal, prescapular, and mesenteric lymph nodes. Seven lambs were inoculated into the palatine tonsils with scrapie virus as newborns (3 to 12 days old) and were examined for virus when they were 147 to 210 days old. Virus was not detected in the lymphoreticular tissues or terminal portion of ileum of any lamb. Failure to find scrapie virus in these lambs and in most lambs inoculated as fetuses might indicate few had became infected. However, if most lambs and fetuses had become infected, the long zero phase of the infection could have accounted for failure to find scrapie virus in many of them examined too soon after inoculation. The limited findings of this study indicate that efforts to demonstrate prenatal or neonatal transmission of scrapie by detecting virus are hampered by the slowness of its replication.

Animals↗
PubMed1983

Comparative pathogenicity of four strains of Aleutian disease virus for pastel and sapphire mink.

Information was sought on the comparative pathogenicity of four North American strains (isolates) of Aleutian disease virus for royal pastel (a non-Aleutian genotype) and sapphire (an Aleutian genotype) mink. The four strains (Utah-1, Ontario [Canada], Montana, and Pullman [Washington]), all of mink origin, were inoculated intraperitoneally and intranasally in serial 10-fold dilutions. As indicated by the appearance of specific antibody (counterimmunoelectrophoresis test), all strains readily infected both color phases of mink, and all strains were equally pathogenic for sapphire mink. Not all strains, however, regularly caused Aleutian disease in pastel mink. Infection of pastel mink with the Utah-1 strain invariably led to fatal disease. Infection with the Ontario strain caused fatal disease nearly as often. The Pullman strain, by contrast, almost never caused disease in infected pastel mink. The pathogenicity of the Montana strain for this color phase was between these extremes. These findings emphasize the need to distinguish between infection and disease when mink are exposed to Aleutian disease virus. The distinction has important implications for understanding the natural history of Aleutian disease virus infection in ranch mink.

Aleutian Mink Disease↗
PubMed1982

Natural infection of Suffolk sheep with scrapie virus.

A better understanding of the infectious process in scrapie was sought by studying the temporal distribution of virus in naturally infected Suffolk sheep. Virus was detected (by mouse inoculation) first in lymphatic tissues and intestine of clinically normal lambs (age, 10-14 months). Titers were generally low. Infection of the central nervous system was first detected in a 25-month-old clinically normal sheep whose nonneural tissues had moderate amounts of virus. In sheep affected with scrapie, similar amounts in nonneural tissues accompanied high concentrations in the central nervous system, notably in sites of severest neurohistologic changes. No virus was found in clinically normal high-risk sheep 54 to 104 months old. The early appearance of virus in tonsil, retropharyngeal and mesenteric-portal lymph nodes, and intestine suggests that primary infection occurs by way of the alimentary tract, either prenatally from virus in amniotic fluid or postnatally from virus in a contaminated environment.

Animals↗
PubMed1982

Ocular lesions in mink affected with Aleutian disease.

Uveitis, characterized by infiltrates of lymphocytes and plasma cells, was the principal ocular lesion in 122 sapphire and pastel mink affected with experimental Aleutian disease. It was present to various degrees in all but five mink examined five to 164 weeks after inoculation (intraperitoneal or intranasal) with any of four North American strains of Aleutian disease virus. The uveitis, mostly iridocyclitis, was accompanied often by protein-rich fluid in the anterior chamber and less often by fibrin and cells in the vitreous body. Cellular infiltration of the limbus, seldom pronounced, also occurred in about 20% of the mink. In 11 mink with moderate or severe uveitis, the retina was detached by pools of protein-rich fluid. Infiltrates of lymphocytes, plasma cells, and a few histiocytes often were found in the orbital soft tissues, occasionally in association with retrobulbar arteritis. In general, the ocular lesions were more severe in sapphire than in pastel mink. The uveitis accompanies glomerulonephritis, the principal lesion of Aleutian disease, much more regularly than do several other lesions of the disease. Like the glomerulonephritis, it probably results from the deposition of circulating immune complexes.

Aleutian Mink Disease↗
PubMed1981

Common occurrence of urethral cysts in older female ranch mink.

Cysts were found often in the proximal urethra of female sapphire and pastel mink, Mustela vison, examined at necropsy during studies on slow viral diseases. Their prevalence, the same in both color phases, was age-dependent. They occurred in less than 2% of females under 2 years old but in more than 60% of those over 7 years old. The cysts varied from ovoid vesicles 3 to 4 mm long to multilocular masses 10 to 15 mm across that greatly distended the proximal urethra and sometimes occluded it. Small cysts were not accompanied by clinical signs, but large ones often caused persistent urinary incontinence and occasionally, urine retention. The cysts contained fluid that varied from water-clear to dull yellow. They arose by expansion of small urethral glands normally present in female mink and destroyed much of the urethral wall by pressure atrophy. Although the cysts became larger and more prevalent as the mink aged, the stimulus that caused them to form was not apparent. They appear to have no counterpart in other animals.

Animals↗
PubMed1981

Ovine progressive pneumonia: pathologic and virologic studies on the naturally occurring disease.

Pathologic and virologic studies were conducted on 13 mature ewes with serum precipitin antibodies to progressive pneumonia virus (PPV). Pulmonary lesions of ovine progressive pneumonia were found in 4 sheep, a meningoencephalitis resembling visna in 1 sheep, chronic proliferative carpal arthritis in 2, and massive lymphoid proliferation in the mammary gland in 3. Virus producing cytopathic effect typical of PPV was isolated from the lungs, mediastinal lymph node, spleen, and choroid plexus of 4 sheep and from the carpal synovium of 2 sheep with chronic carpal arthritis. Three viral isolates selected for further study were antigenically related to visna virus by immunofluorescence and immunodiffusion, but these 3 isolates were not neutralized by antisera to reference strains of visna virus. Seemingly, infection of sheep by ovine retroviruses is common in the United States, and these viruses are capable of causing disease in more than 1 organ system.

Animals↗
PubMed1980

Brain tissue from persons dying of Creutzfeldt-Jakob disease causes scrapie-like encephalopathy in goats.

Two goats became affected with an encephalopathy indistinguishable from scrapie 43 months after they were inoculated intracerebrally with 10% suspensions of brain from two persons dying of Creutzfeldt-Jakob disease. Although this observation does not establish the common identity of Creutzfeldt-Jakob disease virus and scrapie virus, it is thought to provide strong evidence of a close etiological relationship between the two diseases.

Aged↗
PubMed1980

Experimental scrapie in the mouse: electrophoretic and sedimentation properties of the partially purified agent.

Some biochemical and biophysical properties of the scrapie agent in a partially purified fraction P5 from murine spleen are described in this communication. The agent was stable in the nonionic detergents Triton X-100 and Nonidet P40 and stable in the nondenaturing, anionic detergents sodium cholate and sodium N-lauroyl sarcosinate. In contrast, sodium dodecyl sulfate (SDS) inactivated the agent at high concentrations (1% or >) when the detergent-to-protein ration approached 1.5 g SDS/g protein. The agent was resistant to inactivation by nucleases and proteases, even in the presence of 0.1% SDS. A broad peak of infectivity was exhibited in modified colloidal silica (Percoll) density gradients. Maximal titers were found at a Percoll density of 1.10 g/cm3 in the presence and absence of 0.05% SDS. Gel electrophoresis of the agent in the presence of 0.1% SDS resulted in inactivation of > 95% of the agent loaded onto the gel. Free-flow electrophoresis showed that > 99% of the agent in fraction P5 migrated toward the anode, but not as a discrete species. Sedimentation analysis of the agent in fraction P5 in the presence of 1% lysolecithin showed that the agent has a sedimentation coefficient of < 300S but > 30S. Heating P5 preparations caused the agent to associate with cellular elements and form aggregates with sedimentation coefficients > 10,000S. Removal by differential centrifugation of the large forms of the agent produced upon heating permitted characterization of a discrete subpopulation of scrapie agent particles. Rate-zonal sucrose gradient studies showed that > 95% of the infectivity in this subpopulation sedimented as uniform particles with a sedimentation coefficient of 240S.

Animals↗