Erysipelothrix rhusiopathiae endocarditis: report of a case and review of the literature.
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The chelating agents oxine, acetylacetone, tropolone, and 2-mercaptopyridine 1-oxide were analysed for their suitability in labeling the bacterium Erysipelothrix rhusiopathiae (E.r.), strain B10, with 111In and 67Ga. The labeling conditions were improved. The bactericidal activity of the labeling process was investigated. The different chelates did not result in a significant difference in labeling yield. The addition of 0.01% detergent to the labeling buffer doubled the labeling yield up to 45%. Labeled bacteria were injected intravenously into rats. The percentage organ distribution was determined and compared with a control group.
Tested was the simultaneous vaccination of pigs against swine fever, swine erysipelas, and Aujeszky's disease. Parallel to this experiment a second group of test pigs were treated with each of the three vaccines at twenty-day intervals. The effect of vaccination was assessed through clinical observations with the test groups and by challenging part of the animals with virulent strains of the swine fever and erysipelas agents. It was found that the successive application of the three vaccines at 20-day intervals (at the age of 50, 70, and 90 days) could induce immunity that lasted for a longer period than the immunity resulting from the simultaneous treatment at the age of 90 days. In order to protect the pigs for sure up to the end of the fattening period a revaccination against swine fever with the simultaneous use of the vaccine against swine erysipelas in both cases was necessary.
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The carriage of Erysipelothrix rhusiopathiae by pigs reared under free range and intensive systems of management was compared. Large white (exotic) breeds kept under an intensive system and local (native) breeds kept under a free range system were studied. Of the 29 pigs kept under the intensive system, 44.8% carried E. rhusiopathiae in their tonsils while 51.7% of pigs kept under free range system also carried the organism in their tonsils. In each of the systems 6.9% of the pigs carried E. rhusiopathiae in their bile and muscles. Blood samples from all the animals surveyed were negative for the organism. There was no significant difference in the carriage of E. rhusiopathiae in pigs reared under the two systems of management. The ubiquity of E. rhusiopathiae in the environment, its resistance to environmental influences, poor standards of hygiene and the problem of detecting apparently healthy animals, are possible epidemiological factors which may have increased the carrier rate in the intensive system where E. rhusiopathiae was supposed to be less. The total number of carrier-pigs in the intensive system was 44.8% while in the free range system it was 51.7%.
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Mice and swine vaccinated (subcutaneous inoculation) with live acriflavine-fast attenuated Erysipelothrix rhusiopathiae, strain Koganei 65-0.15 (serovar 2), were challenge exposed with 10 strains of E rhusiopathiae pathogenic for swine; the latter strains comprised serovars 9 and 10 and other previously undetermined. Vaccinated mice did not die after they were challenge exposed (subcutaneous inoculation) with serovars 4, 6, 7, 8, 9, 10, 15, 16, or N, but vaccinated mice challenge exposed with strain 2553 (serovar 20) had 30% mortality. Nonvaccinated control mice died after they were challenge exposed with all serovars tested. One of 2 vaccinated swine challenge exposed (intradermal inoculation) with each of strains 911 (serovar 8), 2179 (serovar 10), or 2553 developed localized urticarial lesion at the site of intradermal inoculation. Vaccinated swine challenge exposed with serovars 4, 6, 7, 9, 15, 16, or N did not have clinical signs of acute swine erysipelas. Nonvaccinated control swine developed localized lesions at the site of intradermal challenge inoculation.
Mice and swine inoculated subcutaneously with culture filtrate vaccine prepared from acriflavine-fast attenuated Erysipelothrix rhusiopathiae strain Koganei 65-0.15 (serovar 2), were challenge exposed to 20 pathogenic strains of E rhusiopathiae of 18 serovars and type N. Vaccinated mice survived after challenge exposure to serovars 1b, 2, 8 (strain Goda), and type N, but mortality occurred in vaccinated mice challenge exposed to other strains: 20% to 30% mortality in mice challenge exposed to serovars 1a, 11, 12, 15, 16, or 21; 40% to 50% mortality in mice challenge exposed to serovars 4, 5, 6, 7, or 8 (strain 911); and 60% to 80% mortality in mice challenge exposed to serovars 9, 10, 18, or 19. All vaccinated mice died after challenge exposure with strain 2553 (serovar 20). Non-vaccinated control mice died after challenge exposure to all strains. Of 2 vaccinated swine challenge exposed to strain 2553, 1 developed a local urticarial lesion at the site of intradermal exposure. Vaccinated swine challenge exposed to serovars 1a, 1b, 2, 4, 5, 6, 7, 8, 9, 10, 11, 12, 15, 16, 18, 19, 21, or type N did not have clinical signs of acute erysipelas. Nonvaccinated control swine developed acute generalized erysipelas or localized urticarial lesions at the site of intradermal exposure.
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The acute phase of the arteritis of the common iliac artery induced in young rats by the inoculation of viable Erysipelothrix rhusiopathiae was examined. Arteritis of the common iliac artery was observed within 4 days after inoculation in every rat that was inoculated with the live bacteria. Within 2 days after the inoculation, infiltration by mononuclear and polymorphonuclear cells was first detected in the periarterial tissue extending centripetally to the outer two-thirds of the media. Invasion by the bacteria always preceded cell infiltration. Immunofluorescence test by FITC-labeled peanut lectin demonstrated the desialated sites by the effect of neuraminidase produced by the bacteria in the arterial wall concomitantly with the invasion of the bacteria. Linear presentation of C3 along the external elastic lamina of that artery was also detected. The results showed that viable E. rhusiopathiae could induce arteritis of muscular arteries and that the neuraminidase produced by the bacteria might play a role in the progress of arterial inflammation. We consider that this model will contribute to clarifying the progression of the arteritis process, and to assessing the efficacy of antiinflammatory drugs to inhibit the arterial inflammation.
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The changes in the percentage of serum proteins and erythrocyte sedimentation rates in 14 swine given weekly injections of Erysipelothrix insidiosa or other antigens were studied. A sharp rise in the erythrocyte sedimentation rate and in the percentage of alpha globulin occurred at the seventh day after the first injection in seven of the eight pigs which received the viable cultures. The erythrocyte sedimentation rate and percentage of alpha globulin then returned to normal. Later, as arthritis developed, the erythrocyte sedimentation rate again increased, but this time the increased rate was accompanied by an increase in the percentage of gamma globulin. The erythrocyte sedimentation rate and percentage of serum proteins remained virtually unchanged in the three animals which were given dead erysipelas organisms and in the three animals which were given culture medium alone.