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Biomedical subjects

S Krakowka

Publications and source records attributed to S Krakowka.

At least 19 recordsLinked to original sources
PubMed1992

Chronic active gastritis due to Helicobacter pylori in immunized gnotobiotic piglets.

In gnotobiotic piglets, parenteral vaccination with formalin-killed Helicobacter pylori and oral vaccination with live bacteria induced H. pylori-specific serum immunoglobulins G, M, and A. Vaccination reduced but did not prevent infection by subsequent challenge with viable H. pylori. Oral vaccination with killed bacteria was less effective in inducing serum antibody and had no effect on bacterial colonization. Immunization status influenced the histologic response of piglets to challenge by H. pylori. Lymphoplasmacytic gastritis was more severe in parenterally vaccinated piglets than in the other groups. In addition, neutrophilic infiltrates and neutrophilic gland abscesses in the gastric mucosa were present in 5 of 7 parenterally immunized piglets, none of the orally immunized piglets, and only 1 of 8 infected nonimmune control piglets. Furthermore, there was a positive correlation between immunoglobulin G, M, and A titer at challenge and severity of both neutrophilic and lymphocytic inflammation. These results suggest that although vaccination does not prevent infection by H. pylori, infection of an immune host leads to increased severity and activity of gastritis.

Administration, Oral↗
PubMed1992

Motility as a factor in the colonisation of gnotobiotic piglets by Helicobacter pylori.

Non-motile variants of Helicobacter pylori (strain 26695) occurred with a frequency of 1.6 (SD 0.4) x 10(-4) variants/cell/division cycle, and reversion to the motile form occurred with a frequency of less than 10(-7) variants/cell/division cycle. The two forms remained greater than 90% pure for up to 50 cell divisions and differed only in the presence or absence of motility and flagella. Bacteria were recovered from nine of 10 gnotobiotic piglets inoculated orally with motile H. pylori, but from only two of eight inoculated with the non-motile variant. The motile form survived for 21 days in infected piglets, but the non-motile variant survived for only 6 days. Bacteria recovered from piglets inoculated with the non-motile variant were non-motile. These data support the hypothesis that motility is a colonisation factor for H. pylori.

Animals↗
PubMed1992

Ultrastructural study of Helicobacter pylori adherence properties in gnotobiotic piglets.

Ultrastructural examination of gastric mucosa from Helicobacter pylori-infected gnotobiotic piglets identified four general adherence patterns comparable to those observed in human patients. Intimate associations between the bacterial and mucosal cell membranes, including cuplike invaginations and adherence pedestals, were present and were accompanied by alterations to microvilli and cell membrane morphology.

Animals↗
PubMed1992

Role of Helicobacter felis in chronic canine gastritis.

Five gnotobiotic Beagle dogs were orally inoculated with a pure culture of Helicobacter felis. The remaining two littermates served as contact controls. Thirty days after infection, all animals were euthanatized and specimens were collected for evaluation. In infected dogs, H. felis was recovered from all areas of the stomach. Colonization was heaviest in the fundus and antrum. H. felis was not cultured from any segment of the gastrointestinal tract distal to the duodenum. Two weeks after infection, all five infected dogs had detectable IgM and IgG serum antibody to H. felis, whereas control dogs had no measurable H. felis serum antibody throughout the study. Histopathologic changes in the stomachs of infected dogs included large numbers of lymphoid nodules throughout all regions of the gastric mucosa and were most numerous in the fundus and body. A mild, diffuse lymphocytic infiltrate with small numbers of plasma cells and eosinophils was also present in the subglandular region of all portions of the gastric mucosa. Electron microscopic examination revealed large numbers of spiral-shaped H. felis in gastric mucus adjacent to or superimposed over the areas of inflammation. Occasionally, however, H. felis was observed within the canaliculi of gastric parietal cells. Histopathologic changes in the stomachs of the contact control dogs were limited to focal infiltrates of eosinophils and small aggregates of lymphocytes in the subglandular portions of the gastric mucosa in one animal. Infection with H. felis is a likely cause of naturally occurring lymphofollicular gastritis.

Animals↗
PubMed1991

Membranoproliferative glomerulonephritis in dogs with a genetically determined deficiency of the third component of complement.

Renal disease is a common clinical manifestation of genetically determined deficiencies of the complement system in man. Like their human counterparts, dogs with a genetically determined complete deficiency of C3 also develop renal disease. Five of 20 C3-deficient dogs developed clinical evidence of renal failure. However, 14 of the 15 remaining dogs had histological evidence of type I membranoproliferative glomerulonephritis. The lesions were characterized by mesangial cell proliferation, an increase in the mesangial matrix, thickening of the glomerular capillary wall, electron-dense deposits in the mesangium and subendothelial space, and the presence of IgG and IgM. In order to determine the effect of treatment with C3 on the renal disease of C3-deficient dogs, two C3-deficient dogs were infused with normal canine plasma twice weekly for 3 weeks. Their urinary protein excretion rose progressively from less than 200 mg/24 hr to greater than 1000 mg/24 hr; renal function remained normal. Renal biopsies performed 1 week after the last infusion revealed more severe glomerulonephritis and the presence of C3. As controls, a C3-deficient dog was given C3-deficient canine plasma and a normal dog was given normal canine plasma; neither control animal developed proteinuria or changes in their renal biopsy. These observations suggest that renal disease may be more common in humans with complement deficiencies than would be suspected based on clinical assessment. Furthermore, these results suggest that treatment with complement-containing blood products may worsen preexisting renal disease in complement-deficient individuals.

Animals↗
PubMed1991

Transmission of Helicobacter spp. A challenge to the dogma of faecal-oral spread.

Faecal oral spread is claimed by many to be the mode of transmission of the gastric pathogen Helicobacter pylori. This idea is based not on experimental data but because the epidemiology of H. pylori infection resembles that of other pathogens known to be spread by the faecal-oral route. This is in spite of the observation that no-one has been successful in culturing H. pylori from human stool. In this study, a series of transmission experiments are reported on animals infected with the gastric spirilla, Helicobacter felis and 'Gastrospirillum hominis'. Germfree mice and rats infected with H. felis did not transmit their infection to uninoculated mice despite prolonged contact in the same cage nor could the bacterium be isolated from their intestinal contents. This was confirmed in specific pathogen free mice where infected dams did not pass the helicobacter to their progeny. Similarly, mice infected with a human isolate of 'Gastrospirillum hominis' did not transmit the infection while in close contact with uninoculated mice. In contrast, in a limited series of experiments, both H. pylori and H. felis were transmitted from infected gnotobiotic Beagle puppies to uninfected animals in the same enclosure. In addition, the gastric mucus from a cat with indigenous 'Gastrospirillum'-like organisms was infectious for mice, whereas faecal content from the same animal was not. It is suggested that the difference between the murine and canine experiments is that the dogs are more likely to have oral-oral contact than rodents. Unlike dogs, mice and rats do not vomit and are coprophagous. It is concluded that the case for faecal-oral spread of Helicobacter species is 'not proven' and that the inter-oral route is more likely.

Animals↗
PubMed1991

Intranasal infection of ferrets (Mustela putorius furo) with canine parainfluenza virus.

Immunocompetent and cyclophosphamide-immunosuppressed ferrets were intranasally infected with canine parainfluenza virus (CPIV) and observed for clinical signs, histopathologic lesions, the immunocytochemical demonstration of CPIV antigen in the respiratory tract and scanning electron microscopic alterations of the tracheal epithelium until 36 days post infection (p.i.). In both groups, clinical signs were minimal, restricted to the upper respiratory tract and consisted of cough elicited by tracheal compression between 3 and 7 days p.i. Microscopically, inflammatory and degenerative lesions were observed in the trachea and less frequently in the nasal cavity; bronchiolitis or interstitial pneumonia was not demonstrated. By immunocytochemistry, CPIV antigen was demonstrated in tracheal epithelial cells, whereas nasal cavity, bronchi, bronchioles and lung were devoid of viral antigen. Ferrets given CPIV alone developed a minimal lymphocytic tracheitis with minimal loss of cilia and CPIV antigen was observed only 4 days p.i. 17 days p.i., normal epithelial organization and ciliary reappearance was reestablished. Ferrets treated with cyclophosphamide and infected with CPIV exhibited mild to moderate histological lesions as above with similar scanning electron microscopic changes until 36 p.i. Tracheal lesions consisted of intraepithelial and submucosal infiltration of lymphocytes and macrophages, focal epithelial hyperplasia and multifocal loss of cilia. In addition, mild and transient neutrophilic infiltration was observed. In immunosuppressed ferrets, viral antigen expression was prominent and demonstrated 4 and 8 days p.i. These data suggest that ferrets are susceptible to aerosol CPIV infection.

Animals↗
PubMed1991

Essential role of urease in pathogenesis of gastritis induced by Helicobacter pylori in gnotobiotic piglets.

A mutant strain of Helicobacter pylori with weak urease activity was created by using N-methyl-N'-nitro-N-nitrosoguanidine. The urease activity of the mutant (0.036 +/- 0.009 nmol of urea per micrograms of bacterial protein per min) was 0.4% of that of the parental strain (8.20 +/- 2.30 nmol of urea per micrograms of bacterial protein per min). The mutant was otherwise indistinguishable from the parental strain. Both demonstrated prominent catalase and oxidase activities, and both produced vacuolating cytotoxin. Restriction endonuclease and sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) patterns and ultrastructure were identical for the two strains. The mutant was fully motile, as evaluated by spreading in soft agar and by direct microscopic examination. Growth rate and colony size and morphology were identical for the mutant and parental strains. Seventeen gnotobiotic piglets were challenged with either the mutant or the parental strain and sacrificed 3 or 21 days after challenge. Gastric tissue was examined histologically and cultured for H. pylori. Of seven piglets challenged with the parental strain, all became infected. H. pylori was not recovered from any of 10 piglets challenged with the urease-negative strain. Lymphofollicular gastritis was present in all seven piglets challenged with the parental strain but in none of the piglets challenged with the urease-negative strain. These results suggest that prominent urease activity is essential for colonization by H. pylori.

Animals↗
PubMed1991

In vitro cytopathogenicity and in vivo virulence of two strains of canine parainfluenza virus.

In vivo and in vitro properties of two strains of canine parainfluenza virus (CPIV) were investigated. One strain, designated CPIV(+), induced syncytial giant cell formation and cytolysis in vitro, whereas the second strain, CPIV(-), caused only a mild strand-forming cytopathic effect with few, small syncytial giant cells. Vero cells infected with CPIV(+) or CPIV(-) were 100% positive for CPIV antigen as determined by immunofluorescent staining; however, 100% of CPIV(+) and less than 10% of CPIV(-) infected cells were hemadsorption positive. Sodium dodecyl sulphate-polyacrylamide gel electrophoresis analysis revealed no differences in electrophoretic mobility of viral polypeptides between both strains; however, in CPIV(-), reduced or absent synthesis of the putative HN and F1 proteins was observed. Isopycnic separation of CPIV(+) progeny virions showed a high proportion of viral particles with a buoyant density of 1.18 g/cm3. In contrast, CPIV(-) progeny virions had a heterogeneous density profile ranging from 1.08 to 1.18 g/cm3. Intracerebral infection of six ferrets with CPIV(+) resulted in moderate lymphocytic and histiocytic choroiditis, meningitis, and ependymitis, whereas CPIV(-) infection caused only mild to moderate inflammation. Immunohistologically, CPIV antigen was prominent in ependymal lining cells of the ventricles in CPIV(+)-infected ferrets and was reduced or lacking in CPIV(-)-infected ferrets (n = 6). Sham-injected ferrets (n = 6) did not have histologic lesions and no viral antigen was identified. The present findings suggest that certain changes in the activities of CPIV glycoproteins may lead to alterations of CPIV virulence in vivo.

Animals↗
PubMed1991

Gastric spiral bacilli in captive cheetahs.

Two kinds of gastric spiral bacilli were identified in the stomachs of captive cheetahs with naturally occurring gastritis. One type was morphologically similar to 'Gastrospirillum hominis'. This organism could not be cultured in vitro. Some of these bacteria had superficial helical filaments, and others did not. The other type was morphologically, biochemically, and bacteriologically similar to Helicobacter pylori. This organism is most likely a new species of Helicobacter. One or both of these bacteria may have been responsible for the gastritis seen in these cheetahs.

Acinonyx↗
PubMed1990

Experimental Haemonchus contortus infection in three breeds of sheep.

Nine- to 10-month-old Florida Native, St. Croix and Dorset/Rambouillet sheep were infected with Haemonchus contortus. The primary infection was terminated by anthelmintic treatment 9 weeks later and animals were then reinfected with H. contortus. Dorset/Rambouillet sheep showed higher fecal egg counts and decreased packed cell volumes and plasma protein levels compared with the other two breeds during the primary infection. However, no breed differences were found in total worm burdens in either primary or secondary infection. Differences between breeds were also not detected in lymphocyte responsiveness to parasite antigen, H. contortus specific mucosal antibody levels, numbers of abomasal mast cells and globule leukocytes or abomasal histamine levels.

Animals↗
PubMed1990

Persistence of Helicobacter pylori in conventionalized piglets.

Gnotobiotic piglets were challenged at 3 days of age with Helicobacter (Campylobacter) pylori and then transferred to conventional housing at 24 days of age. Piglets were sacrificed 43-45, 57-60, and 87-90 days after challenge. H. pylori was recovered from the stomachs of all piglets challenged except for two piglets sacrificed 45 days after challenge. H. pylori was not recovered from uninfected control piglets. In addition to H. pylori, Lactobacillus and Bacillus species were recovered from conventionalized piglets. Serum from infected piglets contained H. pylori-specific IgG, IgM, and IgA. IgM titers peaked at 14 days after challenge and then declined. IgG and IgA titers continued to rise over the course of the experiment. Piglets in both uninfected control and challenged groups demonstrated lymphofollicular gastritis, but the gastritis was more severe in challenged piglets.

Animals↗
PubMed1990

Interaction of canine distemper virus nucleocapsid variants with 70K heat-shock proteins.

Cytoplasmic nucleocapsid (NC) isolated from Vero (V) cells infected in the logarithmic phase of growth with Onderstepoort canine distemper virus consists of light-NC (L-NC) and dense-NC (D-NC), encapsidating full-length genomic RNA, and defective-NC (Df-NC), encapsidating variably truncated RNAs. The 70K host cell protein constituent of L-NC and Df-NC was shown to be a member of the 70K heat-shock protein (70K hsp) family. Specifically, 72K hsp is associated with L-NC, and 72K and 73K hsp are associated with Df-NC. Variable L-NC production by three different Vero cell sublines was compared to cellular 70K hsp levels. V141 supported the highest level of L-NC production and expressed high basal levels of 70K hsp in uninfected cells. These high basal levels correspond to a large distribution of log phase V141s in the S phase of the cell cycle. V138-L and V138-H cells produced lower amounts of L-NC and exhibited similar low basal levels of 70K hsp expression, corresponding to low percentages of log phase cells in the S phase cell cycle compartment. Heat shock was effective in inducing L-NC expression in V138-H, which otherwise produced D-NC. Similar cell subline differences in L-NC production were obtained for eight different virus pools derived from the same plaque-purified parental stock. Enhanced biological activity was associated with L-NC based on correlation between L-NC production, viral titre, and plaque areas measured over infected cells.

Animals↗
PubMed1990

Helicobacter pylori gastric infection in gnotobiotic beagle dogs.

Establishment of infection with Helicobacter pylori and gastritis in nonhuman species is currently only successful in gnotobiotic piglets. This study was designed to determine whether H. pylori will colonize the gastrointestinal tract of gnotobiotic dogs. Gnotobiotic beagle pups were derived by standard methods. Group A (five dogs) was orally challenged with 3 x 10(8) H. pylori at 7 days of age. Group B (two dogs) received only peptone water but was contact-exposed beginning on day 23 postinfection (p.i.). Necropsy was performed on dogs on day 30 p.i. H. pylori colonized the stomach of all dogs (groups A and B). Urease map analysis correlated with the microbiologic findings and indicated that the density of colonization was less than that observed in human tissue. Organisms were also recovered from the pharynx, esophagus, duodenum, and rectum of 1, 2, 2, and 1 dog, respectively. All group A and one group B dog developed serum immunoglobulin G specific for H. pylori by day 30 p.i. Gross lesions were restricted to the stomach and consisted of small (less than 1 mm) lymphoid follicles. Microscopically, there were focal to diffuse lymphoplasmacytic infiltrates with follicle formation and mild to moderate infiltration of neutrophils and eosinophils in the gastric lamina propria. With the Warthin-Starry silver stain, organisms were seen on the surface of the gastric epithelial cells, beneath the mucus layer. We conclude that H. pylori colonizes the stomachs of gnotobiotic dogs for at least 1 month and the lesions resemble those seen in humans. H. pylori is transmissible by contact from infected to noninfected dogs.

Animals↗
PubMed1989

In vitro immunologic features of Weimaraner dogs with neutrophil abnormalities and recurrent infections.

In vitro evaluation of cellular and humoral immunity in Weimaraner dogs with recurrent infections and abnormal neutrophil function revealed significantly lower serum immunoglobulin (Ig) G and M concentrations than control dogs. Lymphocyte blastogenesis in response to three different mitogens, interleukin-1 and -2 production, natural killer (NK) cell activity, and in vitro IgG and IgM production were similar to those of control dogs.

Animals↗
PubMed1989

Lymphocyte function in obstructive jaundice.

Sepsis is a major factor in the high mortality and morbidity after surgery for obstructive jaundice. Several studies have suggested that reticuloendothelial function is depressed, but changes in lymphocyte function are poorly understood. A model of obstructive jaundice has been produced by chronic common bile duct ligation in eight dogs. In vitro lymphocyte studies were performed both at 2 and 3 weeks duration of jaundice and compared with simultaneous healthy control subjects. Icteric animals showed no abnormality of natural killer cell function. Relative numbers of T and B lymphocytes and their subsets were unchanged. T lymphocyte responses to three mitogens were not significantly reduced in jaundiced animals. Serum immunoglobulin levels were unchanged compared to those before surgery apart from a significant rise in immunoglobulin A. No evidence of circulating immunosuppressive factors was found by mitogen testing on normal lymphocytes in the presence of pooled serum from jaundiced animals, normal serum, or normal serum with added bilirubin. Our study does not suggest that impairment of lymphocyte function contributes significantly to the dangers of sepsis in obstructive jaundice.

Animals↗