[Reactivity of rats inoculated intravenously with the L-phase variants of erysipelothrix rhusiopathiae].
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Natural disease outbreaks of erysipelas and fowl cholera occurred in several lines of turkeys maintained for genetic studies. There were line differences in mortality during both outbreaks, suggesting that there is genetic variation in resistance to these diseases. A line developed by selection for increased egg production had a higher mortality rate from fowl cholera than did the randombred control line from which it was developed. Both the egg line and its control line had a lower mortality rate in the erysipelas outbreak than did a line selected for increased growth rate. Both diseases induced high mortality in a line selected for increased growth.
Mice and swine immunized subcutaneously with live vaccine prepared from acriflavine-fast attenuated Erysipelothrix rhusiopathiae, strain Koganei (serotype 2), were challenge exposed to virulent strains of E rhusiopathiae of various serotypes. Vaccinated mice did not die after challenge exposure to serotypes 1a, 1b, 2, 3, 5, 6, 7, 8, 9, 11, 12, 15, 16, 18, 19, 21, or N, but 20% to 30% mortality occurred in vaccinated mice challenge exposed to serotypes 10, 14, 20, or 22. Nonvaccinated control mice died after challenge exposure to all serotypes tested. Vaccinated swine challenge exposed to strain 14B (serotype 9) or strain 2179 (serotype 10) developed localized urticarial lesions at the site of intradermal exposure. Vaccinated swine challenge exposed to serotypes 1a, 1b, 2, 5, 8, 11, 12, 18, 19, or 21 did not have clinical signs of acute erysipelas. Nonvaccinated control swine developed acute generalized erysipelas or localized lesions at the site of intradermal exposure.
Hydrolysate was obtained through enzyme hydrolysis from waste residual fibrin in the production of hyperimmune swine blood. Fibrin hydrolysate and gelatose in 2.5 : 1.5 ratio were tested as protective medium for the freeze-drying of VR2 vaccine against swine erysipelas. It was found that the freeze-drying of the vaccine with the addition of the hydrolysate-gelatose medium at the rate of 4-5 per cent of the vaccine volume met the requirements of the standard for sterility, innocuity, vaccinal titer, and residual moisture.
Out of a litter of 7 two-week old Landrace piglets, 6 developed cutaneous haemorrhages especially on the limbs and ears. Two of these piglets died within 24 hours of the haemorrhages appearing whilst the other 4 recovered following penicillin therapy. The histopathological lesions were centred around the smaller vessels of the dermis and hypodermis. These included hyperaemia, leukostasis and intravascular fibrin coagulation or thrombosis. Bacterial emboli were present within the vessels of the skin, spleen, liver and kidney and loose in the areolar tissue of the dermis and hypodermis. Other lesions included scattered but extensive dermal and hypodermal haemorrhages and a mild cellular infiltration of the dermis and hypodermis.
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Serotypes of 46 previously unclassified isolates of Erysipelothrix rhusiopathiae from porcine tissues in the United States and serotypes of 31 isolates of the organism from porcine tissues received from Puerto Rico were determined. The 46 isolates from the United States were classified in serotype 21. Four isolates (from Georgia, Minnesota, Ohio, and Oklahoma) were tested and found to be pathogenic for swine. Serotypes 1 (subtypes 1a and 1b), 2, 5, 6, and 21 were found in porcine tissues from Puerto Rico. The relative frequency of the various serotypes was similar to that previously reported in the United States.
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Gross and histopathologic lesions were studied in 10 Broad-Breasted White turkeys with acute erysipelas induced experimentally. The gross pathologic features of the disease conformed very closely with descriptions in the literature (7). Histopathologic evaluation was concentrated on the inoculation site (skin), proventriculus, ileocecal area of the intestine, liver, spleen, kidney, lung, and heart. In all organs examined the dominant histopathologic alteration was vascular damage as evidenced by: generalized congestion, edema, focal hemorrhage, disseminated fibrin thrombi, and numerous bacterial aggregates either within fibrin thrombi or engulfed by cells of the reticuloendothelial system. Degenerative changes or overt necrosis of parenchymal cells were evident in liver, spleen, and kidney. The cellular inflammatory component of acute lesions was minimal. Heterophil and mononuclear leukocytic infiltrates were observed in scarified skin and, in turkeys surviving several days, in livers and hearts.
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The incidence, economic implications, aetiology and possible public health significance or porcine arthritis in South African slaughter pigs is discussed. An investigation into the aetiology and pathology of porcine arthritis as found at a South African abbattoir revealed that Erysipelothrix rhusiopathiae was present in 48% of the affected joints and Streptococcus spp., Corynebacterium spp. and Staphylococcus spp. in 20%, 4% and 2% respectively. The joints showed various degress of subacute to chronic proliferative sero-fibrinous to fibrinopurulent arthritis regardless of whether bacteria were isolated. It is essential that the Lnn. axillares primae costae which drain the forelimb joints also be examined routinely during meat inspection.
The stable L-form of Erysipelothrix rhusiopathiae is a typical protoplast type L-form. Cells are surrounded by a trilamellar cytoplasmic membrane only. They grow in form of aggregations in liquid media and their diameters vary between 0.1 and 2 micrometer. Always a large portion of cells undergoes lysis. It seems to be characteristic for L-form cultures of E. rhusiopathiae that always many artifact structures are formed. The artifacts are spherical particles with diameters of 0.1 micrometer to more than 3 micrometer. They can be differentiated from L-form cells only by electron microscopy. The artifacts consist of electron dense amorphous material and their surface is irregular without a clear boundary line. Obviously, these artifacts are produced from protein components of the medium and from cytoplasmatic components of the lysing L-form cells.