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Biomedical subjects

M D Lairmore

Publications and source records attributed to M D Lairmore.

85 records · Page 5Linked to original sources
PubMed1989

Guidelines for the prevention of simian immunodeficiency virus infection in laboratory workers and animal handlers.

The authors are members of a working group that formulated guidelines to minimize transmission of simian immunodeficiency virus (SIV) infection to man. Biosafety level (BSL) 2 standards are recommended for handling of clinical specimens and housing of SIV inoculated animals. Manipulation of SIV preparations may be performed in a BSL 2 facility with additional BSL 3 practices and equipment; for large volume or concentrated preparations of SIV BSL 3 containment is necessary. Written policies regarding management and testing of workers exposed to SIV are recommended.

Animals↗
PubMed1988

Spontaneous interferon production by pulmonary leukocytes is associated with lentivirus-induced lymphoid interstitial pneumonia.

Ovine lentiviruses share genome sequence, structural features, and replicative mechanisms with HIV, the etiologic agent of AIDS. A lamb model of lentivirus-induced lymphoid interstitial pneumonia, comparable to lymphoid interstitial pneumonia associated with pediatric AIDS, was used to investigate production of leukocyte-soluble mediators. Lentivirus-infected lambs and adult sheep with severe lymphoid interstitial pneumonia had significantly elevated levels of spontaneous interferon (IFN) production from pulmonary leukocytes compared with ovine lentiviruses-infected animals with mild or no lesions of lymphoid interstitial pneumonia or non-infected controls. However, peripheral blood mononuclear cells from lentivirus-infected lambs did not spontaneously release significant amounts of IFN. IFN production by pulmonary lymph node lymphocytes was enhanced in the presence of lentivirus-infected alveolar macrophages. Animals with lentivirus-induced disease and spontaneous IFN production had enhanced virus replication within tissues. The ovine lentiviruses-induced IFN had a m.w. of between 25,000 and 35,000 and was resistant to freeze/thawing procedures. The IFN activity was sensitive to trypsin and stable to low pH and heat. IFN with similar physical and biochemical properties was produced when ovine lentiviruses was added to control leukocyte cultures. IL-2 and PGE2 production and responses to mitogen by pulmonary lymph node lymphocytes of lentivirus-diseased lambs were not statistically different from control animals. Increased local production of IFN in lentivirus-infected host tissues may serve to accelerate the entry of leukocytes into virus-induced lesions promoting cell-mediated tissue damage and also provide increased numbers of cells for virus replication.

Animals↗
PubMed1988

The etiology and pathogenesis of ovine pulmonary carcinoma (sheep pulmonary adenomatosis).

Ovine pulmonary carcinoma (OPC, sheep pulmonary adenomatosis, jaagsiekte) occurs naturally as a contagious bronchioloalveolar carcinoma of sheep in the Americas, Europe, Africa and Asia. The disease is endemic and economically important in Peru and apparently more common than previously suspected in the U.S.A. The tumor is a result of transformation of type II alveolar epithelial cells or non-ciliated bronchiolar cells of the lung. Clinically affected sheep develop dyspnea, tachypnea and often a watery nasal discharge that originates from tumor secretions. The course is progressive and death usually occurs within a few weeks. To study the viral etiology and pathogenesis of OPC in the U.S.A., the disease was experimentally transmitted to neonatal or young lambs with a success rate of 69%. Ovine lentivirus (OvLV), present in the inocula, was concurrently transmitted and induced lymphoid interstitial pneumonia in most animals. While morphological, immunological and other studies implicate a type D or type B retrovirus as the etiologic agent of OPC, this virus has not yet been cultured and the role of ovine lentivirus in the disease remains unknown.

Animals↗
PubMed1988

Lesions and retroviruses associated with naturally occurring ovine pulmonary carcinoma (sheep pulmonary adenomatosis).

Five sheep with ovine pulmonary carcinoma were markedly dyspneic and had sporadic coughing; two had copious watery nasal exudate. In four, lesions consisted of multifocal nodules of neoplastic cuboidal epithelial cells in acinar or papillary patterns. Electron microscopically, cells had microvilli, tight junctions, and cytoplasmic lamellar bodies typical of alveolar type II cells. One sheep had a single lung tumor of nonciliated bronchiolar epithelial cells. Vacuolated alveolar macrophages surrounded adenomatous foci. One sheep had a metastatic lesion in the caudal mediastinal lymph node. All sheep had histologic lesions of lymphoid interstitial pneumonia (LIP, ovine progressive pneumonia) consisting of peribronchiolar and interstitial lymphoid hyperplasia, and fibromuscular proliferation; all had serum precipitating antibodies to ovine lentivirus. Lung fluids or tumor homogenates contained a 26-kd peptide that crossreacted with a primate-derived type D retrovirus as detected by immunoblotting or interspecies competition radioimmunoassay. Ovine lentivirus was isolated from concentrated lung fluids or tumor tissues of four sheep tested and from tumor cell DNA of one animal transfected into ovine muscle cells. These studies document the presence of type D-related retrovirus antigen in ovine pulmonary carcinoma (OPC) in the United States and indicate that lentivirus-induced LIP is a lesion frequently associated with this disease.

Animals↗
PubMed1988

Retrovirus-associated ovine pulmonary carcinoma (sheep pulmonary adenomatosis) and lymphoid interstitial pneumonia. I. Lesion development and age susceptibility.

To determine the lesion development of retrovirus-induced ovine pulmonary carcinoma (OPC), ten neonatal lambs were inoculated intratracheally with either 1) lung fluid preparations derived from a sheep with Type D retrovirus-associated OPC and concurrent ovine lentivirus (OvLV)-associated lymphoid interstitial pneumonia (LIP) (n = 8); or 2) lung fluid from a sheep with only OvLV-LIP (n = 2). Seven of eight neonates that received Type D retrovirus-associated OPC/OvLV-LIP lung fluid developed both OPC and LIP lesions between 9 and 32 weeks after inoculation. Mild OPC lesions consisted of foci of type II alveolar epithelial cells lining alveoli surrounded by minimal alveolar macrophage infiltrates. More severe OPC lesions consisted of multifocal aggregates of cuboidal to columnar neoplastic cells forming acini or masses associated with abundant alveolar macrophage infiltrates. Lesions of LIP consisted of peribronchiolar and perivascular lymphoid hyperplasia and heterogeneous interstitial leukocytic infiltrates. The two neonates that received OvLV-LIP lung fluid developed rapid and severe LIP, but not OPC lesions. Two lambs (inoculated as neonates with virus-free lung fluid) and three lambs (uninoculated contacts) served as controls and did not develop OPC. To investigate age susceptibility for development of OPC, 20 additional lambs within defined age groups (neonates, 2 weeks old, 5 weeks old, and 10 weeks old) received ultracentrifuged tumor homogenate. Neonatal to 5-week-old lambs inoculated with Type D retrovirus-associated OPC/OvLV-LIP tumor homogenate were equally likely to develop OPC, but lambs inoculated at 10 weeks of age were more refractory to tumor development.(ABSTRACT TRUNCATED AT 250 WORDS)

Age Factors↗
PubMed1988

Lentivirus-induced lymphoproliferative disease. Comparative pathogenicity of phenotypically distinct ovine lentivirus strains.

For investigation of the pathogenicity of lentivirus strains, which have distinctly different cytopathic phenotypes in synovial membrane cell culture, plaque-purified, lytic, and nonlytic ovine lentivirus (OvLV) isolates were inoculated intratracheally into two groups of neonatal lambs. Twelve lambs were inoculated with a lytic OvLV isolate and 3 lambs each with two nonlytic OvLV isolates. Five control lambs were inoculated with either virus-free medium or were left uninoculated. In 8 of 12 lambs inoculated with a lytic OvLV isolate mild to severe lesions of lymphoid interstitial pneumonia (LIP) and pulmonary lymphoid hyperplasia developed, 6 of 12 lambs had lesions of pulmonary lymph node follicular hyperplasia, 3 of 9 female lambs had lesions of lymphoproliferative mastitis, 3 of 10 lambs had lesions of lymphocytic/plasmacytic synovitis, and 3 lambs had no lesions. In 3 of 6 lambs inoculated with nonlytic OvLV isolates only mild LIP lesions developed, without concurrent mammary gland or joint lesions. Bronchoalveolar lavage samples from OvLV-diseased lambs contained on average 1.5-fold more numbers of total leukocytes, and 4-fold more numbers of lymphocytes, compared with bronchoalveolar lavage samples of normal lambs. Monoclonal antibodies to ovine lymphocyte surface markers showed that the SBU-T8+ lymphocyte (CD 8 equivalent) was the predominant lymphocyte subset (mean of 65% of total lavaged lymphocytes) in bronchoalveolar lavage samples of 3 diseased lambs. Ovine lentivirus was reisolated from multiple tissues of both groups of OvLV-inoculated lambs, but the percentage of individual tissues infected was greater in lambs inoculated with the lytic viral isolate. Control lambs had no lesions and failed to produce OvLV-specific antibodies or yield OvLV from tissues. All OvLV-inoculated lambs produced either low or undetectable serum virus neutralizing antibodies. In contrast, lambs inoculated with either lytic or nonlytic OvLV produced precipitating antibodies to OvLV glycoprotein and group-specific protein. However, initial detection of precipitating antibodies to OvLV glycoprotein was earlier (mean, 5.8 weeks after inoculation) in OvLV-infected lambs in which severe lymphoproliferative disease developed and delayed (mean, 10.2 weeks after inoculation) in OvLV-infected lambs with mild or no lesions. Together, these results suggest that lentivirus isolates produced disease in a virus strain-dependent manner and suggest that humoral immune responses against OvLV failed to prevent lesion development in lentivirus-infected lambs.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1987

Three primary neoplasms in a goat: hepatocellular carcinoma, phaeochromocytoma and leiomyoma.

A ten-year-old male nubian goat with no previous medical history was found recumbent. Clinical examination revealed an underweight, dehydrated, very depressed and unresponsive animal. At necropsy, the liver contained multiple, well-demarcated hepatocellular carcinomas. The right adrenal gland contained a solitary phaeochromocytoma. Multiple leiomyomas were present within the urinary bladder. The three primary neoplasms reported in this goat have been reported separately in other species; their simultaneous occurrence in one animal is uncommon.

Adrenal Gland Neoplasms↗
PubMed1987

Replication and cytopathic effects of ovine lentivirus strains in alveolar macrophages correlate with in vivo pathogenicity.

Ruminant lentiviruses share genomic sequences and biologic properties with human immunodeficiency viruses. Four ovine lentivirus strains were assessed for cytopathic effects and virus replication. Lentivirus isolate H/24 produced high virus titers and lysis of synovial cells but replicated slowly and caused no fusion of alveolar macrophages. Lentivirus isolates 84/28 and 85/14 produced low virus titers, less syncytia, and limited or no cell lysis in synovial cells and macrophages. In contrast, ovine lentivirus isolate 85/34 produced early peak virus titers and caused rapid fusion and lysis of both macrophages and synovial cells. Ovine lentivirus isolates which were cytopathic for macrophages induced lymphoproliferative disease when inoculated into lambs.

Animals↗
PubMed1987

Experimental coinduction of type D retrovirus-associated pulmonary carcinoma and lentivirus-associated lymphoid interstitial pneumonia in lambs.

Two retrovirus-associated pulmonary diseases of sheep [ovine pulmonary carcinoma (OPC); sheep pulmonary adenomatosis], a bronchoalveolar carcinoma, and lymphoid interstitial pneumonia (LIP) were induced simultaneously in 9 of 9 neonatal lambs. The lambs were killed 8-28 weeks after intratracheal injection of lung tumor homogenate or lung fluid derived from sheep with naturally occurring OPC and ovine lentivirus (OvLV) infection. The inoculated lambs developed multifocal neoplasms of alveolar type II cells or nonciliated bronchiolar epithelial cells, LIP, and pulmonary lymph node hyperplasia, and all produced antibody to OvLV. OvLV was isolated from 6 to 7 lambs tested, and infectious center assay of pulmonary lavage cells from 3 lambs revealed that approximately 1 in 1,000 pulmonary lavage cells contained infectious lentivirus. Neither contact control lambs nor control lambs that received ultrafiltered lung fluid developed evidence of either disease or of OvLV infection. Lung fluid or tumor tissue of lambs with OPC contained a 26,000-dalton protein that cross-reacted with antiserum to p27 to Mason-Pfizer monkey virus, a type D retrovirus. The fact that no antigenic cross-reaction between OvLV and type D retroviruses has been demonstrated supports the presence of two retroviruses in sheep with OPC. Although the contributions of each agent to oncogenesis in this model are difficult to evaluate, the rapid development of two retrovirus-induced pulmonary diseases in experimentally inoculated lambs suggests an etiologic or pathogenetic synergism between these two members of the family Retroviridae.

Animals↗
PubMed1986

Ovine lentivirus lymphoid interstitial pneumonia. Rapid induction in neonatal lambs.

For examination of the characteristics of lentivirus-induced pulmonary disease in an animal model, neonatal lambs were given intratracheal injections of high-and low-passage ovine lentivirus (OvLV) isolates. In 6 of 6 lambs inoculated with low-passage OvLV or OvLV from lung lavage fluid, lesions of lymphoid interstitial pneumonia (LIP) developed. In none of 7 lambs inoculated with a high-passage OvLV or 4 control lambs inoculated with medium alone or ultrafiltered lung fluid did lung lesions develop. Systemic distribution of lentivirus was greater and development of lentivirus antibody was more rapid in lambs inoculated with low-passage OvLV, compared with lambs inoculated with high passage OvLV. The number of lymphocytes in bronchoalveolar lavage samples was increased in lambs with lymphoid interstitial pneumonia. The development of lymphoid interstitial pneumonia was markedly accelerated, in comparison with previous reports of experimentally induced lentivirus pneumonia in sheep. In lentivirus-inoculated lambs pulmonary lesions developed comparable to lymphoid interstitial pneumonia associated with the acquired immunodeficiency syndrome and other human benign lymphoid disorders of the lung. Similarities between the disease manifestations and virologic properties of OvLV and human T-cell lymphotropic virus III argue for the relevance of OvLV-induced disease as a model for human retrovirus diseases. The ability of OvLV to cause accelerated pulmonary disease in neonates may be due to age-related susceptibility factors that enhance the pathogenicity of lentiviruses.

Animal Diseases↗
PubMed1984

Oxytetracycline-associated nephrotoxicosis in feedlot calves.

Renal nephrosis and increased mortality were investigated in feedlot calves that had received excessive doses of oxytetracycline for the treatment of bronchopneumonia. Histopathologic findings included moderate to severe, cortical tubular nephrosis, and suppurative bronchopneumonia. Results of serum and peritoneal fluid analysis were consistent with severe renal disease. Renal toxicosis from the administration of excessive oxytetracycline should be considered a possible side effect in stressed calves with concurrent respiratory disease.

Animals↗
PubMed1983

Comparative biological features of a rat liver abscess model induced with three Fusobacterium necrophorum strains.

Several biological features were compared in a rat liver abscess model, using intraportal inoculations with 3 bovine strains of Fusobacterium necrophorum which varied in virulence. Serum alanine aminotransferase activities were increased significantly (P less than 0.05) in rats inoculated with F necrophorum 2101 by postinoculation hours 6, 12, and 24. Thereafter, alanine aminotransferase values returned to base line for the remainder of the experiment. Also, rats inoculated with F necrophorum 2101 had a significantly greater (P less than 0.05) weight loss than did the control rats during the first 5 postinoculation days and developed leukocytosis characterized by a neutrophilia with a left shift. The duration of the bacteremia was related directly to the virulence of the F necrophorum strain. Fusobacterium necrophorum 2101, a biotype A which was the most virulent, induced the most persistent bacteremia; F necrophorum 2035, a biotype B which was the least virulent, produced the shortest bacteremia; and F necrophorum 2030, a biotype AB which was of intermediate virulence, led to bacteremia of intermediate duration. Plasma endotoxin was demonstrated intermittently during the first 24 hours, but did not correlate with the bacteremia.

Alanine Transaminase↗