A comparison of the intratracheal, intravenous and intratonsillar routes of inoculation of goats with Pasteurella haemolytica.
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Animals↗
Biomedical subjects
K A Brogden
Publications and source records attributed to K A Brogden.
Ovine pulmonary surfactant induces killing of Pasteurella haemolytica, Escherichia coli, and Klebsiella pneumoniae by normal serum.
Pulmonary surfactant has been shown to play an increasingly important role in bacterial clearance at the alveolar surface in the lung. This study describes a bactericidal mechanism in which ovine pulmonary surfactant induces killing of Pasteurella haemolytica by normal serum. To demonstrate killing, six bacterial species were incubated first with pulmonary surfactant for 60 min at 37 degrees C and then with serum for an additional 60 min at 37 degrees C. P. haemolytica type A1 strains 82-25 and L101, a P. haemolytica type 2 strain, Escherichia coli, and Klebsiella pneumoniae were susceptible and Pasteurella multocida, Serratia marcescens, and Pseudomonas aeruginosa were not susceptible to killing by ovine pulmonary surfactant and normal serum. No bacteria incubated with bovine pulmonary surfactant were killed by normal serum. Although the species origin of pulmonary surfactant was selective, the species origin of serum was not. P. haemolytica incubated with ovine pulmonary surfactant was killed by fetal calf serum, gnotobiotic calf serum, pooled normal sheep serum, pooled normal rabbit serum, and pooled guinea pig serum. Ultrastructurally, killed P. haemolytica suspensions contained dead cells and cells distorted with vacuoles between the cytoplasmic membrane and the cytoplasm. The mechanism of killing did not correlate with concentrations of complement or lysozyme or titers of residual antibody in either the pulmonary surfactant or the serum, and killing was reduced by preincubation of surfactant with P. haemolytica lipopolysaccharide. Preliminary characterization of both surfactant and serum implicate a low-molecular-weight proteinaceous component in the surfactant and serum albumin in the serum. This mechanism may help clear certain gram-negative bacteria from the lungs of sheep as a part of the pulmonary innate defense system.
Animals↗
Agglutination of lung surfactant with glucan.
Respirable cotton dust, implicated in the pathogenesis of byssinosis, contains a number of bioactive compounds. These include lipopolysaccharide (LPS), tannins, bacterial peptides, byssinosin, iacinilene C, and 1,3-beta-D-glucan. The exact aetiological agent of byssinosis in such dust has not been definitively identified nor has its mechanism of action on lower lung surfaces been determined. In the present study 1,3-beta-D-glucan, Enterobacter agglomerans LPS, and ovine pulmonary surfactant were mixed in varying combinations. After incubation, their characteristics were determined by sucrose density centrifugation, TLC, and carbohydrate analysis. Precipitates were found in mixtures containing surfactant-glucan and surfactant-glucan-LPS, but not in surfactant-LPS. Precipitates were not seen in the surfactant, LPS, and glucan controls. The formation of a precipitate did not increase the density of the surfactant glucan mixture when compared by density gradient centrifugation with the surfactant control. The interaction between surfactant and glucan was analysed by molecular modelling. The energy of a surfactant-glucan complex (60.07 kcal/mol) was calculated to be much lower than the sum of glucan (47.09 kcal/mol) and surfactant (30.98 kcal/mol) when added separately. The results indicate that 1,3-beta-D-glucan does interact with surfactant and this complex may play a part in the pathogenesis of byssinosis by altering lung physiology maintained by pulmonary surfactant.
Agglutination↗
Chronic proliferative rhinitis associated with Salmonella arizonae in sheep.
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Animals↗
Changes in pulmonary surfactant during bacterial pneumonia.
In pneumonia, bacteria induce changes in pulmonary surfactant. These changes are mediated by bacteria directly on secreted surfactant or indirectly through pulmonary type II epithelial cells. The bacterial component most likely responsible is endotoxin since gram-negative bacteria more often induce these changes than gram-positive bacteria. Also, endotoxin and gram-negative bacteria induce similar changes in surfactant. The interaction of bacteria or endotoxin with secreted surfactant results in changes in the physical (i.e. density and surface tension) properties of surfactant. In addition, gram-negative bacteria or endotoxin can injure type II epithelial cells causing them to produce abnormal quantities of surfactant, abnormal concentrations of phospholipids in surfactant, and abnormal compositions (i.e. type and saturation of fatty acids) of PC. The L/S ratio, the concentration of PG, and the amount of palmitic acid in PC are all significantly lower. The changes in surfactant have a deleterious effect on lung function characterized by significant decreases in total lung capacity, static compliance, diffusing capacity, and arterial PO2 and a significant increase in mean pulmonary arterial pressure. Also decreased concentrations of surfactant or an altered surfactant composition can result in the anatomic changes commonly seen in pneumonia such as pulmonary edema, hemorrhage, and atelectasis.
Animals↗
Biophysical alteration of lung surfactant by extracts of cotton dust.
Byssinosis, a lung disease that can affect cotton mill workers, may be caused in part by lipopolysaccharides (LPS) from Gram negative bacteria. In vitro, LPS complexes with sheep lung surfactant (SLS). To determine whether LPS in extracts of cotton dust alters the biophysical characteristics of lung surfactant, aqueous extracts (1.0% w:v) of sterile surgical cotton (SSC) and a bulk raw cotton dust (1182DB) were prepared. Aliquots of the soluble extracts were incubated with SLS and studied by sucrose gradient centrifugation, surface tension analysis, and high pressure liquid chromatography (HPLC). The chromatography was employed to analyse for 3-hydroxymyristate (3-HM), a fatty acid indicating LPS. Also, purified Enterobacter agglomerans LPS and 3-HM as controls and as mixtures with SLS, were studied by HPLC. Sucrose gradient centrifugation showed that SLS-SSC, SLS-1182DB, and the SLS control had similar densities that differed from the remaining controls. The SLS-1182DB exhibited a floccule absent in the other samples. Surface tension values of SLS-SSC and SLS-1182DB differed significantly from all controls but only slightly from one another. 3-Hydroxymyristate was detected by HPLC in the 3-HM control, EA-LPS, SLS-EA-LPS, and SLS-1182DB, but not in SLS-SSC or the remaining controls. Apparently, 3-HM was below the HPLC detection range in SSC. The data indicate that LPS in the 1182DB, SSC and EA-LPS samples complexed with SLS. Floccule development in SLS-1182DB but not in SLS-EA-LPS suggests a further component(s) present in the bulk raw cotton dust, as well as LPS, which complexes with SLS. The data suggest that biophysical alterations to lung surfactant may play a part in the pathogenesis of byssinosis.
Animals↗
A field trial to evaluate a whole cell vaccine for the prevention of caseous lymphadenitis in sheep and goat flocks.
A field trial to evaluate a whole cell vaccine for the prevention of caseous lymphadenitis (CLA) in sheep and goats was performed in one goat herd and one sheep flock over a period of three years. In goats, there was a nonstatistically significant trend for fewer cases of CLA in the vaccinated animals compared to the controls. In sheep, from six months to 36 months postinitial vaccination, the proportion of vaccinated sheep that developed CLA was significantly less (p less than 0.05) than in the control sheep. The antibody titers to Corynebacterium pseudotuberculosis as detected by microagglutination assay were significantly different (p less than 0.0001) at all times except at the initial vaccination. Swellings occurred at the vaccination site at an incidence level of 29.6% in goats and 34.1% in sheep. The vaccine appeared to be efficacious in reducing the proportion of sheep that developed CLA when challenged naturally in a field situation.
Agglutination Tests↗
Seroprevalence of ovine progressive pneumonia virus in various domestic and wild animal species, and species susceptibility to the virus.
Ovine progressive pneumonia is caused by a lentivirus of known infectivity only for sheep and goats. Virus susceptibility of 11 other species of animals was examined. Species included cattle, chickens, deer, dogs, goats, hamsters, horses, mice, pigs, rabbits, and rats. Of these species, only goats and rabbits could be experimentally infected with the virus. The infection in rabbits was acute, and virus did not persist or induce antibody production as it does in sheep and goats. Sera obtained from several people working in close contact with the virus and from several wild species, with unknown exposure history, were tested for antibodies to viral antigens. All results were negative. Knowledge of the host range of this virus is important for scientific studies and for virus eradication programs.
Animals↗
Changes in ovine erythrocyte morphology due to sphingomyelin degradation by Corynebacterium pseudotuberculosis phospholipase D.
Corynebacterium pseudotuberculosis produces a sphingomyelin-specific phospholipase D exotoxin that is a major determinant in the pathogenesis of caseous lymphadenitis. We assessed the changes induced in the morphology and sphingomyelin concentration of ovine erythrocytes after incubation with broth culture filtrates or purified exotoxin. Sphingomyelin was hydrolysed nearly in parallel with shape change. Morphologically, spherostomatocytes were seen initially, and later these contained numerous vacuoles at the periphery. Vacuoles seen in thin sections with transmission electron microscopy appeared as pits with scanning electron microscopy. Pitting became progressively worse with time, leading to extensive scalloping of the membrane surface. Chemically, significant decreases (P less than or equal to 0.05) in erythrocyte membrane sphingomyelin content and significant increases (P less than or equal to 0.05) in the content of glycerophospholipids (i.e. phosphatidylglycerol) were observed in erythrocytes incubated with broth culture filtrates or purified exotoxin. These alterations may contribute to the pathophysiology of acute infections induced by C. pseudotuberculosis.
Animals↗
Effect of muramyl dipeptide on immunogenicity of Corynebacterium pseudotuberculosis whole-cell vaccines in mice and lambs.
Colostrum-deprived lambs and CF1 mice were vaccinated with water-in-oil emulsion vaccines containing nonviable whole cells (WC) of Corynebacterium pseudotuberculosis with and without muramyl dipeptide (MDP). Efficacy of vaccines was determined from the survival of mice and lesions in lambs after IV injection of 10(4) colony-forming units of C pseudotuberculosis. In mice, protection was related to the concentration of WC in the vaccine. At 50, 100, or 150 micrograms of WC, protection was good (78.8%). At 10 or 25 micrograms of WC, protection was considerably less (54.7%). At high WC concentrations, protection could only be moderately increased to 82.3% with high (50 and 100 micrograms) concentrations of MDP or increased to 90% protection with low (5 and 10 micrograms) concentrations of MDP. At low WC concentrations, protection significantly decreased to 32% (P less than 0.025) with high concentrations of MDP, but significantly increased to 72.5% (P less than 0.025) with low concentrations of MDP. Therefore, the amount of protection with lower concentrations of WC and MDP was comparable with the amount of protection with higher concentrations of WC without MDP. In lambs, high prechallenge antibody titers (geometric mean titers from 5.1 to 5.4 by day 35) were observed after vaccination with WC. Protection and vaccination site abscesses in lambs were related to the concentration of WC and MDP. Pulmonary or vaccination site abscesses were not observed in 4 of 4 lambs vaccinated with 1 mg of WC + 50 micrograms of MDP.
Acetylmuramyl-Alanyl-Isoglutamine↗
Alterations in the phospholipid composition and morphology of ovine erythrocytes after intravenous inoculation of Corynebacterium pseudotuberculosis.
Corynebacterium pseudotuberculosis produces a sphingomyelin-specific phospholipase D exotoxin that is a major determinant in the pathogenesis of caseous lymphadenitis. The effect of this exotoxin on erythrocytes was assessed during experimentally induced infection of sheep. Blood was drawn at timed intervals, and the phospholipid composition of erythrocytes was determined by use of high-performance liquid chromatographic analysis of membrane extracts. Erythrocyte morphology was determined by use of transmission electron microscopy. Significant (P less than or equal to 0.05) decreases in erythrocyte membrane sphingomyelin content and significant (P less than or equal to 0.05) increases in phosphatidylglycerol content were observed 30 minutes after IV inoculation of C pseudotuberculosis. The concentration of other phospholipids remained unchanged. Initially, spherostomatocytes were formed that later became pitted at the cell surface. These pits or invaginations appeared as numerous vacuoles at the periphery of thin-sectioned cells. Pitting became progressively worse, leading to an extensive scalloped cell surface. Alterations in the phospholipid composition and morphology of ovine erythrocytes may contribute to pathophysiologic findings in sheep with acute infection induced by C pseudotuberculosis.
Animals↗
Clinical and microbiologic findings in lambs inoculated with Pasteurella haemolytica after infection with ovine adenovirus type 6.
Colostrum-deprived lambs (10 to 20 days old) were inoculated with either ovine adenovirus type 6 (OAV-6; n = 6), Pasteurella haemolytica type A1 (n = 6), or OAV-6 followed by P haemolytica 5 days later (n = 10). Another group (n = 3) served as sham-inoculated controls. Lambs inoculated with OAV-6 or P haemolytica developed mild and moderate respiratory tract disease of 6 and 3 days' duration, respectively. Lambs inoculated with virus and bacteria developed clinical signs of respiratory tract disease of greater intensity and duration (9 days) than with either agent alone. Within 3 hours of bacterial inoculation, all lambs that received P haemolytica were anorectic, listless, and febrile, and had hyperpnea and dyspnea. Ovine adenovirus type 6 was isolated from all virus-inoculated lambs. Although P haemolytica was not recovered from all bacteria-inoculated lambs, it was recovered for a longer period in the group that received both agents. Antibody to OAV-6 was detected in virus-inoculated lambs as early as day 6 after inoculation. The control lambs remained clinically normal and neither virus nor bacteria were recovered at necropsy.
Adenoviridae↗
Effect of Pasteurella haemolytica (A1) capsular polysaccharide on sheep lung in vivo and on pulmonary surfactant in vitro.
Capsular polysaccharide (CP) of Pasteurella haemolytica (type A1) was first deposited by fiberoptic bronchoscopy into the lungs of sheep to examine lesions and changes in bronchoalveolar lavage cell populations and, later, was mixed with pulmonary surfactant to investigate alterations in physical properties or surface tension. At 22 hours after deposition, minimal lesions were seen in the lungs only at and contiguous to the site of CP deposition in 2 of 4 sheep. Microscopically, alveoli and interlobular septa were filled with edema fluid. Terminal airways and alveoli contained a moderate amount of neutrophils that varied between sheep. Significant differences in number or type of bronchoalveolar lavage cells were not observed in the weekly lavages between each group or among sheep within each group, either before or after deposition of CP or physiologic saline solution. After 6 hours of incubation at 37 C, CP-surfactant mixtures were examined with a surface tensiometer and centrifuged in sucrose gradients. The CP bound to surfactant, resulting in formation of a precipitate with a surface tension of 31.6 +/- 0.1 dynes/cm and a density of 1.07 to 1.08 g/ml. Lipopolysaccharide of P haemolytica, used as a control, also bound to surfactant, resulting in a complex with a surface tension of 57.7 +/- 0.4 dynes/cm and a density of 1.06 to 1.10 g/ml. Surfactant alone had a surface tension of 32.6 +/- 0.2 dynes/cm and density of 1.05 to 1.06 g/ml. The CP appears by itself not to be a direct major factor in the lung damage that develops in cases of pneumonic pasteurellosis.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Ovine progressive pneumonia (maedi-visna) in sheep.
Ovine progressive pneumonia (OPP) is a multi-systemic disease of sheep caused by a nononcogenic exogenous retrovirus belonging to the Lentiviridae subfamily. Characteristics of the disease are chronic lymphocytic pneumonitis, encephalitis, arthritis, mastitis and vasculitis associated with progressive wasting, dyspnea, lameness, indurated udder and, rarely, paralysis. Any one or all of the characteristics may be manifest. Transmission of the virus is predominantly through the colostrum to newborn lambs, however, transmission can occur by contact and in utero. Treatment of the disease is only symptomatic and prevention of infection is only by avoiding the virus.
Animals↗
The ultrastructural morphology of endotoxins and lipopolysaccharides.
Endotoxins and LPS are constituents unique to the outer surface of gram-negative bacteria. Cell-associated endotoxins are now readily observable on the cell outer membrane with labelled monoclonal antibodies. These probes are not only more specific than those used in the past, but also easier to see. Interest in free endotoxin as a method to generate outer membrane proteins without contamination with other cell constituents is also increasing (Gamazo and Moriyon, 1987). The morphologic identification and characterization of LPS by electron microscopy has been facilitated recently by advances in chemical extraction and purification techniques. LPS, originally thought to be heterogenous, exists in forms that are dependent upon (1) the method of its extraction, (2) its chemical composition, and (3) the physical or chemical conditions of its environment. New models were proposed on the arrangement of LPS molecules in molecular aggregates (i.e. discs, vesicles or ribbons) and a schematic was presented on the dissociation from one morphologic type to another. Morphologic studies on endotoxins and LPS will continue in the future. Using molecular biological techniques, carbohydrate epitopes of LPS from one bacterial species will be expressed with increasing frequency in other bacterial species (Manning et al., 1986; Stein et al., 1988). Electron microscopy will help visualize the distribution of the 'new' LPS on the recipient cell surface. Labelled monoclonal antibodies will also differentiate host cell LPS from the recombinant LPS. As molecular model programming becomes more complex, new schematics will help visualize the arrangement of LPS in membranes to explain recombinant LPS structure as well as other characteristics (i.e. membrane permeability to various antibiotics).
Antibodies, Bacterial↗
Enterobacter agglomerans lipopolysaccharide-induced changes in pulmonary surfactant as a factor in the pathogenesis of byssinosis.
Lipopolysaccharide (LPS) from Enterobacter agglomerans and pulmonary surfactant mixtures were centrifuged in discontinuous sucrose gradients to determine whether LPS bound to surfactant and examined in a Langmuir trough with a Wilhelmy balance to determine whether LPS altered the surface activity of surfactant. The LPS was found to bind to the surfactant and altered its surface tension properties. The binding of LPS to surfactant in the lung may change the physiological properties of surfactant and be a possible mechanism for the pathogenesis of byssinosis.
Analysis of Variance↗
Isolation and identification of mycoplasmas from the nasal cavity of sheep.
Mycoplasmas isolated from the nasal cavity of sheep in a ram test station were examined to determine their identity and prevalence. Specimens were obtained for mycoplasmal culture in 1980, 1982, and 1983 from 558 sheep, and mycoplasmas were isolated from 630 specimens from 320 sheep (57.3%). The isolates were characterized and differentiated into groups on the basis of sensitivity to digitonin, fermentation of glucose, and hydrolysis of arginine. Isolates in some groups were further characterized by use of additional diagnostic media, and their identity was confirmed by agglutination or growth inhibition with antiserum prepared from reference mycoplasmas. Of the 320 sheep with mycoplasmas, 293 had Mycoplasma ovipneumoniae, 12 had M arginini, and 1 had M capricolum. Two sheep had Acholeplasma spp, and 3 sheep had unidentified Mycoplasma spp. The remaining 9 sheep had M ovipneumoniae in combination with Acholeplasma spp (n = 3), M arginini (n = 3), M capricolum (n = 2), and an unidentified Mycoplasma spp (n = 1). The biochemical reactions of the M ovipneumoniae from the 293 sheep were similar, but varied in the degree of growth and fermentation in the basal medium containing glucose. The high prevalence of M ovipneumoniae indicated that it may be commensal in the upper respiratory tract of healthy sheep.
Animals↗
Gonococci in vivo and in vitro. Further studies on the host and bacterial determinants of gonococcal resistance to killing by human serum, and by phagocytes.
A small M, heat and acid labile, host inducer(s) of gonococcal resistance to complement mediated killing by fresh human serum (-FHS), being purified from red blood cell (RBC) extracts, produced changed in lipopolysaccharide (LPS) structure, surface antigens and proteins; and acquirement of resistance related to loss of a target antigen for bactericidal IgM, possibly LPS components. A 20 kDalt. lipoprotein with a high content of glutamic acid isolated from outer membranes of a gonococcal strain selected in vivo is a determinant of gonococcal resistance to killing by human phagocytes. Sonic extracts of gonococci may contain a cytotoxin for human phagocytes. At the 4th International Pathogenic Neisseriae Conference, we reported (Parsons et al. 1985) that conditions in vivo induced phenotypic change leading to gonococcal resistance to complement-mediated killing by human serum; and, also, selected gonococcal types which showed a greater resistance to intracellular killing by human phagocytes than laboratory strains. Furthermore, evidence was presented that not only was resistance to complement mediated killing important in gonococcal pathogenesis, but also resistance to phagocytic defences. This paper describes the continuance of our studies on the determinants of induced serum resistance and of resistance to killing by phagocytes including toxicity to these cells. Each section begins by summarising previous work that was referenced in Parsons et al. (1985).
Animals↗