PubMed Health⌕ Search

Biomedical subjects

H J Olander

Publications and source records attributed to H J Olander.

At least 37 records · Page 2Linked to original sources
PubMed1987

Synergistic hemolysis-inhibition titers associated with caseous lymphadenitis in a slaughterhouse survey of goats and sheep in Northeastern Brazil.

A survey of caseous lymphadenitis was conducted at a goat and sheep slaughterhouse in Northeastern Brazil One hundred and fifty-eight goats and 43 sheep were examined for the presence of abscesses, with bacterial culturing of purulent material to define the etiological agent. Blood was collected simultaneously for determination of serological titer via the synergistic hemolysis-inhibition test which measures antibodies to an exotoxin of Corynebacterium pseudotuberculosis. Thirteen and nine-tenths percent of the goats had abscesses, with a high proportion having mediastinal or pulmonary lesions (9.5%). Two sheep had abscesses, both with internal organ involvement. Corynebacterium pseudotuberculosis was the most frequently isolated organism. Of 22 goats with abscesses, 20 were positive via the synergistic hemolysis-inhibition test. Both of the sheep with abscesses had positive synergistic hemolysis-inhibition titers. The proportion of serological reactors was greater than the proportion of animals with abscesses. The synergistic hemolysis-inhibition test may be detecting subclinically infected animals.

Abattoirs↗
PubMed1986

Mechanisms involved in protection provided by immunization against core lipopolysaccharides of Escherichia coli J5 from lethal Haemophilus pleuropneumoniae infections in swine.

In an investigation of the potential protective effects of immunity against common lipopolysaccharide core antigens of gram-negative bacteria during a severe gram-negative infection in the natural host, we induced Haemophilus pleuropneumoniae infections in weanling pigs immunized with a vaccine of an Rc mutant of Escherichia coli (strain J5). To help define the mechanism involved in J5-mediated protection, we compared the clinical, hematologic, bacteriologic, and serologic responses following an H. pleuropneumoniae infection in J5-immunized pigs with those following an H. pleuropneumoniae infection in nonimmunized control animals. As a result of an intranasal inoculation, all of the control animals and the J5-immunized animals were infected with H. pleuropneumoniae. However, while 80% (4 of 5) of the nonimmunized pigs died within 24 h as a result of the infection, no deaths occurred in the J5-immunized animals. In the immunized group, J5 titers dropped during the acute stages of the infection and rebounded to well above the prechallenge levels during convalescence. The J5 titer also increased in the single surviving control animal. These findings suggest that antibodies against common subsurface components of gram-negative bacterial cell walls correlate with protection from an otherwise lethal challenge of H. pleuropneumoniae but do not prevent infection. Important growth-phase-dependent antigenic changes have been recognized to occur during the growth of H. pleuropneumoniae in cultures (R. Nielson, Nord. Veterinaermed. 28:337-348, 1976). In a study of these changes and during an inquiry into the mechanism of J5 antibody-mediated protection, measured quantities of H. pleuropneumoniae were removed from a broth culture at hourly intervals and used to absorb hyperimmune equine J5 antiserum. Significantly greater amounts of J5-specific antibodies were absorbed during the log phase of bacterial growth than during the early or late phase. The availability of epitopes recognized by J5 antibodies appears to be closely related to the rate of bacterial multiplication. The results of these experiments suggest a mechanism of protection provided by increased immunity to E. coli J5 during gram-negative infections.

Animals↗
PubMed1986

Resistance of C3H/HeJ mice to the effects of Haemophilus pleuropneumoniae.

Comparisons were made in the mortality associated with an inhaled dose of viable Haemophilus pleuropneumoniae type 5, strain J45, between adult C3H/HeN and C3H/HeJ mice. Mice of both strains were also challenged with Escherichia coli strains O111:B4 and J5. The 50% lethal dose (LD50) of H. pleuropneumoniae in C3H/HeN mice was calculated to be 10(6.5) CFU. At a mean dose of 10(6.7) CFU a 46% mortality rate occurred in C3H/HeN mice, whereas only 10% of the C3H/HeJ mice died (P less than 0.01). Deaths occurred significantly earlier in C3H/HeN mice (P less than 0.01). No deaths occurred later than 12 h postinfection in either group. Pulmonary lesions in the mice that died were similar to those in pigs that die during the acute phase of H. pleuropneumoniae infection. In surviving mice of both strains, a mild resolving interstitial and bronchopneumonia was present which was not typical of subacute H. pleuropneumoniae infections in swine. Quantitative bacterial isolations from the lungs, liver, and spleen indicate that H. pleuropneumoniae did not multiply in the lungs, was rapidly cleared, and did not become systemic. No deaths occurred in the mice inoculated with E. coli J5 or O111:B4 at mean doses of 10(6.3), 10(7.2), and 10(8.5) CFU, and 10(6.4), 10(7.5), and 10(8.2) CFU, respectively. The difference in the mortality rate between the C3H/HeN and C3H/HeJ mice suggests that endotoxin may be involved in acute deaths in pigs infected with H. pleuropneumonia. As indicated by the E. coli challenge, however, other factors are also likely to be involved. Because of the differences in the pathology and microbiology following H. pleuropneumoniae pulmonary infections in mice and pigs, mice do not appear to be an accurate model of the overall disease in swine.

Animals↗
PubMed1986

Clinicopathologic study of horses surviving pyrrolizidine alkaloid (Senecio vulgaris) toxicosis.

Twenty horses of various ages had inadvertently ingested alfalfa hay contaminated with Senecio vulgaris. Among them, 4 died of liver disease. Blood was collected from affected horses at monthly intervals for 7 months and at the 9th and 14th months. The following serum enzymes and chemical items were assayed: aspartate aminotransferase, lactate dehydrogenase, alkaline phosphatase, gamma-glutamyl transferase, sorbitol dehydrogenase, total bilirubin, BUN, glucose, cholesterol, inorganic phosphate, calcium, total protein, and albumin. Amino acid profiles, conjugated bile acids, sulfobromophthalein clearance times, and liver histopathologic changes via serial biopsies were also monitored. Liver histopathologic changes revealed lesions progressively increasing in severity. Aspartate aminotransferase and plasma amino acid ratios indicated chronic liver degeneration (0.05 level of significance). gamma-Glutamyl transferase and lactate dehydrogenase as well as BUN values fluctuated, but returned to within reference values. Horses appeared clinically normal 14 months after intoxication, but were unable to tolerate stress of exercise.

Amino Acids↗
PubMed1986

Studies on the pathogenesis of Salmonella typhimurium and Salmonella choleraesuis var kunzendorf infection in weanling pigs.

Twenty-six 4-week-old pigs were randomly allotted to 4 groups: group 1--orally inoculated with Salmonella typhimurium; group 2--orally dosed with S choleraesuis; and groups 3 and 4, with surgically constructed intestinal loops--loops inoculated with either S typhimurium or S choleraesuis. One pig each from groups 1 and 2 was killed at 8, 12, 24, 48, 72, 96, and 120 hours after inoculation. One pig each from groups 3 and 4 was killed at 2, 4, 6, 8, 12, and 24 hours after intestinal loop inoculation. Inoculation of S typhimurium resulted in acute enterocolitis of variable severity, whereas inoculation of S choleraesuis resulted initially in septicemia followed by formation of large necrotic and ulcerative lesions in the colonic mucosa. The most consistent systemic lesion of S choleraesuis infection was interstitial pneumonia and multifocal hepatic necrosis. Salmonella typhimurium and S choleraesuis were ultrastructurally within enterocytes of ligated ileal loops. Intracellular bacteria were morphologically intact, occurred free in the cytoplasm and membrane bound, and caused no detectable cytotoxic effect to the cell. Both S typhimurium and S choleraesuis penetrated the intestinal mucosa and were isolated from mesenteric lymph nodes at 2 hours after inoculation.

Animals↗
PubMed1986

Use of a toxoid vaccine to protect goats against intradermal challenge exposure to Corynebacterium pseudotuberculosis.

Two groups of male, 9-week-old goats (5 goats/group) were vaccinated subcutaneously with formalized exotoxin of Corynebacterium pseudotuberculosis, with Freund's incomplete adjuvant. Each goat was given 2 vaccinations, 2 weeks apart. At each vaccination, each group 1 goat was given 0.5 ml of toxoid, and each group 2 goat was given 1 ml of toxoid. Twenty days after the 2nd vaccination, vaccinated goats and 5 nonvaccinated 12-week-old goats (controls) were inoculated intradermally (challenge exposed) with live C pseudotuberculosis, monitored for 13 weeks, and euthanatized. At necropsy, 5 of the 10 vaccinated goats did not have C pseudotuberculosis lesions, 3 had abscesses limited to the inoculation site and draining lymph node, and 2 had disseminated bacterial lesions. Of the 5 nonvaccinated controls, 4 had disseminated abscesses and 1 had a single abscess in an internal node. Serologically, 9 of the 10 vaccinated goats developed positive (greater than or equal to 1:8) antibody titers against the exotoxin within 1 week after inoculation; the 10th goat seroconverted 2 weeks after inoculation, whereas control goats required 3 weeks to develop a positive antibody response. Therefore, early during an infection with C pseudotuberculosis, antibodies against the exotoxin may protect a goat against spread of the organism. All goats were injected intradermally before challenge exposure, 10 days after challenge exposure, and at 4, 8, and 12 weeks after challenge exposure with a skin-test reagent composed of fragmented bacterial cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Isolation and biological characterization of two lipopolysaccharides and a capsular-enriched polysaccharide preparation from Haemophilus pleuropneumoniae.

A smooth-type lipopolysaccharide (HpS-LPS), a rough-type lipopolysaccharide (HpR-LPS), and a capsular-enriched polysaccharide preparation (HpC-PS) were extracted and purified from Haemophilus pleuropneumoniae serotype 5, strain J45, by the use of phenol-water (HpS-LPS) and phenol-chloroform-petroleum-ether (HpR-LPS) techniques. Chemical analysis of the HpS-LPS and HpR-LPS indicated that they contained 0.7% and 4.4% (w/w) 2-keto-3-deoxyoctonate, 11.8% and 10.4% phosphate, 0.8% and 0.8% nucleic acid, and 0.8% and 1.1% protein, respectively. The HpC-PS contained 0.3% 2-keto-3-deoxyoctonate, 1.4% phosphate, 0.2% nucleic acid, and 0.8% protein. With sodium dodecyl sulfate-polyacrylamide-gel electrophoresis, the HpS-LPS banded as a smooth-type LPS and the HpR-LPS banded as a rough-type LPS. Electrophoresis of HpC-PS indicated the presence of a broad high molecular weight band. Gelation of Limulus amoebocyte lysate developed at a minimum concentration of 8 ng/ml of HpS-LPS, 0.3 ng/ml of HpR-LPS, and 35 ng/ml of HpC-PS. The lipopolysaccharide preparations provoked a positive dermal Shwartzman reaction in rabbits and swine, a biphasic febrile response in rabbits, and a monophasic response in swine. Responses were typical of endotoxic activity with swine having greater sensitivity than rabbits. The chick embryo 50% lethal dose was calculated to be 7.3 ng for HpS-LPS, 1.6 ng for HpR-LPS, 5.1 ng for the lipopolysaccharide of Escherichia coli 0111:B4; and the HpC-PS was not toxic. In all assays, HpR-LPS was significantly more toxic than was HpS-LPS. The HpC-PS preparation was not toxic, even at high concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Serodiagnosis of inapparent caseous lymphadenitis in goats and sheep, using the synergistic hemolysis-inhibition test.

The synergistic hemolysis-inhibition (SHI) test, a serologic test for the detection of infection with Corynebacterium pseudotuberculosis, was applied to serum samples from 196 goats and 76 sheep, including animals both with and without C pseudotuberculosis abscesses. Fifty-one of 52 (98%) goats and 27 of 28 (96%) sheep with abscesses caused by C pseudotuberculosis had seropositive titers. Seropositivity continued on subsequent samplings, even after superficial lesions were completely healed. The SHI test may detect subclinically infected animals, as well as animals with clinically recognizable lesions. Of the animals without abscesses, 53 of 186 (28%) goats and 4 of 41 (10%) sheep were seropositive. Either the SHI test is lacking in specificity or these titers are a reflection of a past or a current infection without any grossly visible abscesses.

Animals↗
PubMed1986

Electron microscopic studies on the interaction between normal mice peritoneal phagocytes and Treponema hyodysenteriae, Treponema innocens and Bacteroides vulgatus.

One hundred and twenty female mice (CF1 strain) were divided into three groups of 40. The first group was injected intraperitoneally with broth cultures of Treponema hyodysenteriae. The second group was injected with a combination of T. hyodysenteriae and Bacteroides vulgatus. The third group was injected with Treponema innocens. Peritoneal wash from four mice of each group was collected at eight time intervals postinjection, then prepared for and examined by light and electron microscopy. Peritoneal wash from one mouse at each time interval was prepared for microbiological examination. Treponema hyodysenteriae produced peritoneal macrophage aggregation, transient neutrophilia and macrophage cytolysis. Cytolysis was characterized by rarefaction of the cytoplasm, vesiculation of the endoplasmic reticulum, mild swelling of the mitochondria and disruption of the nuclear and ctyoplasmic membranes. The combination of T. hyodysenteriae and B. vulgatus produced macrophage aggregation and marked neutrophil necrosis. Peritoneal macrophages phagocytized more T. hyodysenteriae than B. vulgatus during early postinjection intervals. Treponema innocens failed to produce cytotoxicity of peritoneal macrophages but did produce macrophage aggregation and transient neutrophilia. Treponema hyodysenteriae and T. innocens did not multiply in the mice peritoneal cavity and were reisolated up to 16 hours postinjection. Bacteroides vulgatus was reisolated up to 24 hours postinjection.

Animals↗
PubMed1985

Studies on the pathogenesis of Salmonella heidelberg infection in weanling pigs.

Experiments were conducted to define the pathogenic potential of Salmonella heidelberg in weanling pigs. Oral inoculation with S heidelberg resulted in severe catarrhal enterocolitis with accumulation of large amounts of fluid in the small intestine and colon. Salmonella heidelberg was demonstrated, with fluorescence microscopy and bacteriologic cultural techniques, to colonize the ileum, to invade ileal mucosal enterocytes, and to reach mesenteric lymph nodes and extraintestinal tissues by 8 hours. In 5 pigs, intestinal loops were surgically prepared and inoculated with S heidelberg (to determine its invasiveness). Microscopically, there were atrophy of villi, erosion of enterocytes, and neutrophilic infiltration in the lamina propria. Ultrastructurally, intracellular bacteria were demonstrated in villous and cryptal enterocytes, as well as in macrophages of the lamina propria. Bacteria were morphologically intact, occurred free and membrane-bound and caused no detectable cytotoxic effect to the cell.

Animals↗
PubMed1985

Serologic response and lesions in goats experimentally infected with Corynebacterium pseudotuberculosis of caprine and equine origins.

Fifteen goat kids were experimentally inoculated with Corynebacterium pseudotuberculosis. Five were given a strain of caprine origin (nitrate-negative biotype) intradermally, 5 were given a strain of equine origin (nitrate-positive biotype) intradermally, and 5 were inoculated intranasally with the caprine-origin strain. Animals were monitored for 127 days. The goats given the inocula intradermally developed abscesses; those given caprine-origin strain had multiple lesions both peripherally and in visceral locations (primarily endothoracic abscesses), whereas those given the equine-origin strain had abscesses only at injection sites and draining nodes. The difference in extent of lesions could be due to biotypic bacterial differences or to the individual strains used. Intranasally inoculated goats did not develop abscesses and were essentially no different from controls. The cranial part of the respiratory tract may not be an important portal of entry for C pseudotuberculosis. Serum samples obtained monthly from all animals were subjected to the synergistic hemolysis-inhibition test, which measures antibodies to the exotoxin of C pseudotuberculosis. Animals with abscesses developed titers within 1 month of inoculation. Animals without abscesses remained seronegative. The synergistic hemolysis-inhibition test may be a reliable diagnostic assay for caseous lymphadenitis in goats.

Animals↗
PubMed1985

Ultrastructural characterization of colonic lesions in pigs inoculated with Treponema hyodysenteriae.

Twelve pigs were inoculated orally with pure cultures of Treponema hyodysenteriae. Pigs were necropsied at different time intervals postinoculation; colonic specimens were collected and prepared for light and electron microscopy. The earliest colonic lesion detected by electron microscopy consisted of superficial vascular congestion and dilatation, edema of the lamina propria and intercellular separation of the epithelial cells at the crypt shoulders. This lesion progressed to epithelial cell necrosis and extrusion into the lumen and extravasation of red cells. Large numbers of spirochetes were present and free, between, over and under necrotic epithelial cells whether in place or partially extruded. Spirochetal penetration of colonic enterocytes and intracytoplasmic multiplication were confirmed in this study. The spirochetes were found to invade the epithelial cells only from their lateral borders. The relationship between T. hyodysenteriae and the colonic anaerobes was not determined.

Animals↗
PubMed1984

Lesions of porcine necrotic ear syndrome.

Porcine necrotic ear syndrome is a disease of swine characterized by large erosive lesions at the margin of the pinna(e). The gross and microscopic characteristics of the lesions were studied in 38 pigs selected from eight affected swine herds. The progression of the lesions was examined in a herd of 174 weaned pigs in a total confinement nursery. The lesions began as a superficial vesicular dermatitis associated with superficial auricular trauma and progressed to become exudative and encrusted. Localized lesions slowly healed or sporadically progressed to deep necrotic ulcers. The early lesions resembled the epidermal changes produced by Staphylococcus hyicus. Deep ulceration and necrosis was attributed to the invasion of streptococci into the dermis resulting in cellulitis, vasculitis, thrombosis, ischemia, and necrosis.

Animals↗
PubMed1981

Shedding of Treponema hyodysenteriae, transmission of disease, and agglutinin response to pigs convalescent from swine dysentery.

Fecal shedding of Treponema hyodysenteriae, transmission of disease, and humoral antibody production against the large spirochete were evaluated in pigs convalescent from experimentally induced swine dysentery. Untreated pigs (n = 21) and 5 pigs that had been treated with virginiamycin were included in the study. Treponema organisms were culturally detected in the feces of 2 untreated pigs as long as 70 and 71 days, and in the feces of 1 treated pig as long as 83 days after the last clinical evidence of disease. Of 8 convalescent pigs that intermittently discharged T hyodysenteriae in their feces, 4 transmitted clinical disease to exposed susceptible pigs. One of the convalescent animals has been free of clinical signs of disease for 57 days before introduction of the susceptible pigs. Treated and untreated convalescent pigs developed similarly elevated agglutinin titers that were maintained as long as 150 days after infection. There was no apparent correlation between the frequency or duration of fecal shedding of the spirochetes and the magnitude of the agglutinin titers of the convalescent pigs.

Agglutination Tests↗
PubMed1979

Studies on the pathogenesis of swine dysentery. I. Characterization of the lesions in colons and colonic segments inoculated with pure cultures or colonic content containing Treponema hyodysenteriae.

Swine dysentery was induced in pigs and in ligated colonic segments by inoculation of pure cultures of, or colonic contents containing, Treponema hyodysenteriae. The mildest changes, best seen in ligated segments 48 or 72 hours after inoculation, were congestion and leucocytic margination in mucosal capillaries and depletion of mucigen from goblet cells lining the base of the crypts of Lieberkühn. Superficial mucosal necrosis and crypt cell hyperplasia were later changes. Perfusion studies with India ink did not demonstrate occlusive mucosal ischemia in acute swine dysentery. Mucosa with lesions of swine dysentery contained at least 10(5) colony forming units of T. hyodysenteriae per gram. Mucosa without lesions had 10(5) or fewer T. hyodysenteriae per gram. Segments with acute swine dysentery were distended with clear mucoid fluid with electrolyte composition indicative of net colonic secretion. No increase in the concentration of volatile fatty acids was detected in content from intact colons or colonic segments with lesions of acute swine dysentery.

Animals↗
PubMed1979

Studies on the pathogenesis of swine dysentery. II. Search for a cytotoxin in spirochetal broth cultures and colon content.

Broth cultures of Treponema hyodysenteriae and colonic content from pigs with swine dysentery were tested for cytotoxicity in cell cultures, erythrocyte suspensions and in ligated segments of pig colon. Live cells of T. hyodysenteriae attached to the surface of cells in all cultures tested but did not penetrate them nor cause morphologic change detectable by light microscopy. Only live T. hyodysenteriae caused erythrolysis. Broth cultures or colonic content sterilized by filtration or by disruption with ultrasound had no visible effect on the cell cultures, erythrocyte suspensions or the mucosa of ligated colonic segments.

Animals↗
PubMed1978

Esophagogastric ulcers associated with Ascaris suum infestation in swine.

When a group of 3-month-old pigs was moved to another location, several died from internal bleeding. Two pigs that were necropsied had large esophagogastric ulcers, hepatic fibrosis with "milk spots" and swollen edematous lungs. The ulcers involved the full thickness of the gastric mucosa with pronounced eosinophilic infiltration and perivascular cuffing of the submucosal vessels. There was an acute interstitial and granulomatous pneumonia with an inflammatory exudate composed mainly of eosinophils. Ascarid larvae were recovered from the lungs. Gastric ulceration could have resulted from a second exposure to Ascaris suum infestation because pigs not removed from their original location did not develop ulcers.

Animals↗