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PubMed1992

Immunological characterization of protective antigens prepared by alkaline treatment of whole cells and from the culture filtrate of Erysipelothrix rhusiopathiae.

Culture filtrate and alkaline-extracted antigens from whole cells of an attenuated strain of Erysipelothrix rhusiopathiae (strain Koganei: serovar 1a) were fractionated with ammonium sulfate; both induced protective immunity in mice. Sephadex G-200 gel filtration revealed three protein fractions in the alkaline-extracted antigen and four protein fractions in the culture filtrate antigen. A fraction in the alkaline extract (NaOH P-2) and in the culture filtrate (CF P-2) induced protection in mice against challenge with a different serovar strain (strain Agata: serovar 5). Anti-NaOH P-2 and anti-CF P-2 mouse sera were protective against different serovars. Glycoprotein fraction derived from CF P-2 antigen by affinity chromatography with Con A-Sepharose 4B did not show protective activity. Western blotting between the antisera (anti-NaOH P-2, Anti-CF P-2 and anti-Koganei strain) and the antigens (NaOH P-2, and sonicated antigens of Agata, Fujisawa and Koganei strains) showed strong recognition of the same bands at 62, 42 and 41 kDa.

Ammonium Sulfate↗
PubMed1993

Properties of a protective protein antigen of Erysipelothrix rhusiopathiae.

Erysipelothrix rhusiopathiae is a widely distributed mucosal commensal of the alimentary tracts of vertebrates. Antibodies to a 66-64 kDa protein released from the cell surface have been shown to be involved in protective immunity. Mice immunized with the purified 66-64 kDa protein from strain T28, serotype 2b were protected against challenge by the United States challenge strain E1-6P (serotype 1a) and by the official German challenge strain Frankfurt 1 (serotype N). Thus, protection is not serotype specific, a result consistent with previous observations that polysaccharide, non-proteinaceous antigens are the type specific antigens useful in serotyping. The 66-64 kDa protein appears to be most immunogenic when complexed to glycolipid. This may be due to an adjuvant effect of polysaccharide antigens. Further studies on the correlation between antibody titers to the 66-64 kDa protein and protection in pigs, turkeys and mice in vivo should be helpful in developing a basis for an in vitro assay to replace the mouse protection test in vaccine testing.

Animals↗
PubMed1995

Protective activity and antigenic analysis of fractions of culture filtrates of Erysipelothrix rhusiopathiae.

The protective activity in mice and antigenic composition of the culture filtrate of 11 strains of Erysipelothrix rhusiopathiae were compared. Protective activity was found in the first (P-1) fraction obtained by Sephadex G-200 gel filtration of the culture filtrate of each strain. Comparing the 50% protective dose (PD50) of the P-1 fraction of the 11 strains by active immunization, highly protective activity was shown by 5 strains, such as Agata, Fujisawa, Shizuoka-63, Koganei 65-0.15 and SE-9. For the 50% effective dose (ED50) determined by passive protective studies, the four strains, Agata, Fujisawa, Koganei 65-0.15 and SE-9 were shown to be highly protective. However, strains 2179 and 2553 showed low activities in both PD50 and ED50. The highly and weakly protective strains were compared by western blot analysis for the protein components. In most strains tested, there were two protein bands of molecular weight of 64 kDa and 43 kDa. Therefore, these two structural proteins were common to the strains and were associated with stimulation of a protective effect in mice.

Animals↗
PubMed1997

Disseminated intravascular coagulation in chickens inoculated with Erysipelothrix rhusiopathiae.

In a first experiment, 28 specific pathogen-free chickens aged 3 weeks showed clinical signs 1 to 5 days after intramuscular inoculation with Erysipelothrix rhusiopathiae. Twelve of 28 birds died 2 to 4 days after inoculation. Macroscopically, the liver, spleen and kidneys were seen to be enlarged and congested. Histologically, fibrinous thrombus formation, seen in the hepatic sinusoids, renal glomerular capillaries and small pulmonary blood vessels, was a characteristic feature. In addition, the liver showed marked congestion, increase of mononuclear cells and heterophils in the sinusoids, hyperplasia of sinusoidal lining cells, and vacuolar changes in hepatic cells. The spleen showed fibrinous exudation of the lymphoid follicles and ellipsoids with lymphocytic depletion, and hyperplasia of ellipsoidal reticular cells. There was oedema, congestion and cellular infiltration in the interstitium of the kidney. The bursa of Fabricius and thymus showed marked lymphocytic depletion. In a second experiment, the blood chemical values (uric acid, glutamic-oxalacetic transaminase, lactate dehydrogenase and gamma-glutamyl transpeptidase) of birds inoculated intramuscularly with E. rhusiopathiae were significantly higher than those of uninfected controls. The blood prothrombin times and activated partial thromboplastin times of the inoculated group were significantly greater than those of the control group. The pathological and haematological findings demonstrated that E. rhusiopathiae induced disseminated intravascular coagulation in the chickens.

Animals↗
PubMed1985

Experimental arteritis in young rats induced by Erysipelothrix rhusiopathiae.

The acute phase of arteritis of the common iliac artery induced in young rats by the inoculation of viable Erysipelothrix rhusiopathiae (E. rhusiopathiae) was examined. Within three days post inoculation, cell infiltration was first detected in the periarterial tissue, extending centripetally to the outer two-thirds of the media. However, the inner third of the media and the intima were free from cell infiltration, and the media showed no degeneration. E. rhusiopathiae first invaded the periarterial tissue and the adventitia, thereafter, invaded the outer two-thirds of the media, but not the inner third of the media or the intima. Invasion by the bacteria preceded cell infiltration. Arteritis was not induced by heat killed bacteria or the supernate from the culture medium. The arteritis was produced preferentially in large or medium-sized muscular arteries. Immunofluorescence test by FITC-conjugated peanut lectin demonstrated the desialated sites by the effect of the neuraminidase produced by E. rhusiopathiae in the arterial region that were concomitant with the invasion of the bacteria. C3 was also detected along the adventitia of the artery. The results demonstrated that viable E. rhusiopathiae can induce arteritis of muscular arteries and that the neuraminidase produced by the bacteria may play a role in the pathogenesis.

Animals↗
PubMed1986

Possible role of neuraminidase in the pathogenesis of arteritis and thrombocytopenia induced in rats by Erysipelothrix rhusiopathiae.

The role of the neuraminidase produced by Erysipelothrix rhusiopathiae (E. rhusiopathiae) in the pathogenesis of arteritis and induced thrombocytopenia was examined using young and adult rats. There was a close correlation between bacterial invasion, desialation and cell infiltration in the common iliac artery. E. rhusiopathiae induced arteritis from the second and third day after inoculation with 3 X 10(8) viable bacteria in the young and adult rats, respectively. This delay with age was closely related to the increase of free sialic acid in the plasma. The sites invaded by E. rhusiopathiae coincided with the desialated lesions, and the bacteria invaded the periarterial region which was always accompanied by desialation when examined with FITC-conjugated peanut lectin. The free sialic acid in the plasma was, at least partly, considered to originate from the desialation of the arterial wall caused by E. rhusiopathiae. The platelet number decreased significantly after inoculation. The sialic acid content of the platelets prepared from circulating blood at 12 and 18 hours after inoculation showed a slight decrease and decreased further when the platelets were incubated with the bacteria. Platelets obtained from circulating blood within 24 hours after inoculation or incubated with the bacteria had demonstrated desialated sites as detected by immunofluorescent staining with FITC-conjugated peanut lectin. In conclusion, free sialic acid in the plasma was considered to be a good marker of the desialation of the arteries caused by E. rhusiopathiae, and the neuraminidase produced by the bacteria would be a key to solve the pathogenesis of the arteritis and thrombocytopenia.

Age Factors↗
PubMed1987

Adhesion of Erysipelothrix rhusiopathiae to cultured rat aortic endothelial cells. Role of bacterial neuraminidase in the induction of arteritis.

The adhesion of Erysipelothrix rhusiopathiae (E. rhusiopathiae) to the cultured confluent monolayer of rat aortic endothelial cells (EC) and the role of neuraminidase in the interaction between EC and E. rhusiopathiae were examined. One EC line was obtained by collagenase treatment of rat aorta. The EC showed a typical cobblestone appearance and possessed the factor VIII related antigen. When cultured more than two weeks after reaching confluence, the EC formed a vascular plexus-like appearance. E. rhusiopathiae began to adhere to EC within 2 minutes after the beginning of culture and adhered at a constant rate for 20 minutes. The adhesion of bacteria to EC was closely related to the release of sialic acid from the EC. Significantly more bacteria adhered to neuraminidase treated EC, and bacterial adhesion was inhibited dose-dependently by N-acetylneuraminic-lactose, which is the substrate of bacterial neuraminidase. It is concluded that bacterial neuraminidase plays an essential role in initiating the interaction between EC and E. rhusiopathiae, which would contribute to the genesis of arteritis.

Animals↗
PubMed2001

Induction of cross-protection in mice against dolphin Erysipelothrix rhusiopathiae isolates with a swine commercial vaccine.

Erysipelothrix rhusiopathiae is well known to cause disease in dolphins. This disease occurs either in an peracute way, leading to mortality even before clinical signs are observed or in a sub-acute way, characterized by rhomboidal skin lesions, that can be treated with penicillin or its derivatives. Commercial swine vaccines, containing inactivated serotype 2 strains, are currently used for vaccination but it is not known whether these vaccines induce protection against E. rhusiopathiae isolates from dolphins. In the present study, it was demonstrated in a mouse model that vaccination with a commercial swine vaccine (Eurovac Ery, Eurovet, Belgium) containing inactivated serotype 2 E. rhusiopathiae strains induced protection against challenge with three E. rhusiopathiae isolates from dolphins. The duration of the protection varied, depending on the challenging isolate, between 8 and >23 weeks. There was however no positive correlation between the amount of antibodies at the moment of challenge and the observed protection. In conclusion, vaccination trials in mice indicate that commercial serotype 2 swine Erysipelothrix vaccines induce protection against erysipelas caused by dolphin pathogenic isolates.

Animals↗
PubMed2003

Molecular identification of Erysipelothrix isolates from the tonsils of healthy cattle by PCR.

For 79 isolates from the tonsils of healthy cattle identified as Erysipelothrix by cultivation, biochemical and serological tests, genotypic identification was performed by polymerase chain reaction (PCR) using four species-specific sets of oligonucleotide primers (ER1F-ER1R, ER2F-ER2R, ER3F-ER3R and ER4F-ER4R). The results of PCR for 79 bovine isolates were compared with those of serological typing. For 19 isolates, serotyping and genotyping results were the same. PCR allowed for the identification of 36 untypable isolates as Erysipelothrix species, strain 1. Serotyping and genotyping results of the remaining 24 isolates were different. Supplemental tests are frequently needed for Erysipelothrix identification.

Animals↗