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In determination (in the precipitation reaction in agar gel) of antibodies to the polysaccharide (streptococcus, group A) in the sera of patients suffering from erysipelas there were revealed antibodies against the specific determinant of polysaccharide A. An increase in antibodies in the patients with primary and repeated erysipelas was observed from the second week of the disease; in patients suffering from relapsing erysipelas their titre was increased from the first days of the disease and persisted at this level during the whole observation period (4 weeks). The majority of the patients suffering from relapsing erysipelas 4 weeks and 6 to 12 months after the relapse displayed no changes in the serum antibody level, or its slight fall was seen. The duration of persistence of antibodies to polysaccharide A in testing at the remote periods after the relapse apparently depended on slow reduction of their level and was not associated with any new infection with streptococcus, since the great percentage of the patients studied at this period were subjected to bicillin-5 therapy. The data obtained served as an additional confirmation of participation of hemolytic streptococcus of group A in the development of erysipelas.
Several immuno-pathological aspects of polyarthritis following experimental infection with erysipelas in pigs were studied for two years. Aseptic and specifically pathogenfree animals were infected subcutaneously and intravenously-intraarticularly with living erysipeals bacteria (erysipelothrix rhusiopathiae) of serotype B. After an initial febrile phase a progressive polyarthritis and disco-spondylitis developed. Some animals also developed thrombo-endocarditis. Hypergammaglobulinemia and high titers of specific antibodies were observed during the whole experimental period. Antiglobulin factors, however, were not detected in the serum or the synovium. In some animals collagen antibodies were demonstrated in synovial tissue. Bacterial examination of the synovium showed that erysipelas bacteria were present in arthritic joints for months. Living erysipelas bacteria were isolated 24 months after the experimental infection from synovial tissue of two pigs. The polyarthritis was characterised by exudates rich in fibrin, villous proliferation, pannus formation, cartilage erosions, and peri-articular fibrosis. IgG and specific erysipelas antibodies were demonstrated in plasma cells from synovial tissue by immuno-histological methods. The findings emphasize the morphological resemblance of the erysipelas induced chronic polyarthritis in pigs to human rheumatoid arthritis.
The passive hemagglutination test was used to determine antibodies to type antigens of the cell wall of streptococcus group A in 167 patients suffering from erysipelas, from whom 488 sera were obtained. Antibodies were revealed in 97.2% of the sera. There was a definite relationship between the clinical form of the disease and the level of antibodies: their lowest level and the absence of elevation in the course of the disease was noted in continuous-relapsing form of erysipelas; the appearance of antibodies to the new types of streptococcus was usually noted in late relapses of the disease, which permitted to attribute their occurrence to infection by the new types of the microbes. In individual cases the appearance of antibodies to the new types of streptococcus was observed at the early relapses of erysipelas; this could be explained by the exacerbation of a focus of chronic (endogenous) infection in the skin in the absence of reinfection. Continuous prophylactic administration of bicillin-5 produced no depressive effect on the antibody level in patients with relapsing erysipelas.
INTRODUCTION: In part I of this paper (Schulz et al., 1975) it was shown that in the initial phase of experimental erysipelas a transition from the vascular processes to a systemic connective tissue reaction can be demonstrated in different species. It is the purpose of this paper to describe the chronic phase of the disease with special emphasis on polyarthritis. MATERIALS AND METHODS: 12 spontaneously diseased and 22 experimentally infected pigs were used in experiments to study the pathogenesis of the disease. In addition, 74 Wistar rats and 148 Sprague-Dawley rats were used in the experiments. All experimental animals were specific-pathogen-free and were parenterally infected with the standardized E. insidiosa serotype B strain T 28. The observation period for the pigs was up to 2 years, for the rats up to 11 months. The methods used for pathohistological and electron microscopical studies are described in part I. Immunihistological studies were carried out on synovial tissue with peroxidase-conjugates of goat-anti-pig-IgG, goat-anti-pig-IgM, pig-collagen, E. insidiosa-homogenate and heat-aggregated-pig-IgG. Furthermore, goat-anti-pig-IgG and rabbit-anti-pig-C3 conjugated with FITC were used. Passive hemagglutination tests and Latex agglutination test (Singer and Plotz) were performed to demonstrate rheumatoid factors and collagen antibodies. RESULTS: Polyarthritis occurred in pigs between the 4th and 10th day p.i. and between the 4th and 8th day p.i. in nearly 100% of the infected rats. Fibrinous exudation, proliferation and destruction with pannus formation are marked in most of the joints examined during the first three months. Fibrosis begins 30 days p.i. in the rats' joints and is most severe in both species between the 5th and 8th month. 3 types of lining cells may be differentiated electron microscopically: A (M) cells, B (F) cells and an intermediate form which is found in both species most frequently. Swelling of the endothelial cells together with constriction of the lumen and thickening of the basal membrane occurs in the capillaries. DISCUSSION: A comparison of chronic erysipelas polyarthritis in pigs and rats with rheumatoid arthritis of men reveals many morphological and immunological similarities between the two diseases. Systemic connective tissue activation manifests itself in organs predilected for rheumatic changes, such as heart valves, endocardium and joints. The possible prepetuation of the processes by specific or nonspecific immunomechanisms or by deposits of fibrin is discussed. In addition, experimental erysipelas is reproducible in nearly 100% of the animals given one single subcutaneous application of one defined bacteria strain. Therefore too, erysipelas is suited as an animal model for human rheumatic diseases.
The chronic Erysipelas-polyarthritis in pigs has been considered an animal model resembling human rheumatoid arthritis. Fifteen specifically pathogenfree (SPF) pigs 45 days old were experimentally infectec with strain T 28 of Erysipelothrix rhusiopathiae-bacteria. During the subsequent 32 weeks several enzymatic, immunohistological and microbiological parameters were monitored. Compared to 5 age and sex matched healthy controls the infected pigs showed increased activity of plasma acid phosphatase starting 4 weeks after the infection. Acid phosphatase activity was usually enhanced in synovial fluid of chronically ill animals. Histochemically increased activity of acid phosphatase, beta-glucuronidase and beta-acetylglucosaminidase was found in lining cells and fibroblasts of the synovial membrane of chronically diseased joints. Immunohistochemically Erysipelas-antigen was demonstrated in the synovial membrane even of those inflamed joints from which no living bacteria had been isolated. The microbiological and immunohistochemical results correlated positively with the enzymehistochemical data. The release of lysosomal enzymes from cells of the synovial membrane in chronically diseased joints due to the influence of Erysipelas-bacteria and the possible implications of persistent bacteria on the perpetuation of chronic Erysipelas-polyarthritis are discussed.
In an outbreak of idiopathic erysipelas ten women patients, aged 42-74, in a long-stay unit of a psychiatric hospital were simultaneously affected. Group A streptococci M-type 1 were isolated from two isolated from two patients with erysipelas and 18 carriers, but subsequent serological tests for type-specific antibody, antistreptolysin O, and anti-deoxyribonuclease B showed that the infection had been widespread in the unit. Treatment with ampicillin proved ineffective and to prevent relapse it was substituted by a standard course of intramuscular penicillin. This seems to be the first epidemic of this type to be reported and certainly the first outbreak of idiopathic erysipelas to be investigated by modern serological techniques.
INTRODUCTION: The similarities between erysipelas in animals and rheumatic diseases in man have been discussed since the work of Nieberle (1931). The present work sets out to investigate the course of organ manifestations in pigs, rats, and mice using germ-free or specific pathogen-free experimental animals. Particular consideration will be given to the initial systemic vascular processes as well as to the significance of the erysipelas antigen. MATERIAL AND METHODS: In several experiments, a total of 166 pigs--partly gnotobiotic or specific pathogen-free animals--37 specific pathogen free Wistar rats and 57 albino mice were orally and/or parenterally infected with standardized erysipelas strains of serotype B. Clinical examination post infection were carried out with the EKG and by x-raying the joints of the extremities. All large parenchymatous organs, as well as heart valves, aorta and synovia were examined histologically in paraffin sections. In mice and rats, joints of the extremities were embedded in toto in metracrylate. Besides various histological staining methods, histochemical reactions were used to demonstrate mucopolysaccharides and fibrin. The myocardium, central nervous system and synovia of several joints were examined with the electron microscope. In the pig, immunohistological methods demonstrating the presence of fibrin, complement and IgG, as described by Seidler et al. (1971) and Trautwein et al. (1972), were used. RESULTS: The most important changes in joints, heart valves heart musculature and blood vessels occur during the early bacteriemic phase. A distinct sticking effect develops in the mouse 3.5 hours p.i., in the rat 24 hours p.i., and in the pig 36 hours p.i. Simultaneously, hyaline thrombi occur in capillaries and venules; these are seen as parallel, loosely-packed fibrin fibers in the electron microscope. With the aid of immunofluorescence fibrin, IgG and complement C3 can also be demonstrated here. Exudates rich in fibrin develop parallel to the microthrombosis. In pigs and rats vascular and myocardial necroses develop to 3 days p.i. The mice do not survive the 3rd p.i. 39% of the pigs showed edema and mesenchymal activation of varying intensity in the heart valves between the 3rd and 8th day p.i. Besides the insudation of the valves, endocardial thromboses developed in 80% of the mice. Endocarditis, aand in addition large aortic thromboses were recognized in more than 50% of the rats. As early as the 4th day p.i., coagulopathy, angionecrosis and exudation led to acute arthritic symptoms..
Two cases of facial lymphangitis have been described, and the pathophysiology of erysipelas has been discussed. Now rarely observed by hospital residents, this potentially serious infection can create considerable diagnostic confusion in medical as well as dental services. Rapid response of erysipelas to penicillin therapy is the modern expectation.
The effect of aflatoxin consumption on the development of acquired immunity to swine erysipelas was studied. Twenty-four pigs were divided into 4 groups (6 pigs/group). Two groups were fed a normal diet and 2 groups were fed the same diet but containing aflatoxin. One group from each diet treatment was given a single injection of an erysipelas bacterin, and 21 days later all pigs were given a challenge inoculum of virulent Erysipelothrix rhusiopathiae organisms. On the basis of the response to the challenge inoculation, pigs were classified as immune, partially immune (PI), or susceptible. Three of the vaccinated pigs fed the normal diet were immune, 2 were PI, and 1 was susceptible, whereas none of the vaccinated pigs given the aflatoxin diet were immune, only 1 was PI, and the remainder were susceptible. Two of the nonvaccinated pigs fed the normal diet were PI and 4 were susceptible; all of the nonvaccinated pigs fed the aflatoxin diet were susceptible. It was concluded that aflatoxin consumption interfered with the development of acquired immunity and apparently increased the severity of the E rhusiopathiae infection in unvaccinated pigs.
From 1960-1975 528 patients suffering from erysipelas were treated at the department of dermatology in Mannheim. The relative as well as the absolute incidence of erysipelas increased markedly during this period. There was also a considerable rise in the number of more seriously diseased, therapy-resistent cases. Microbiological studies must be conducted to find an explication for these phenomena.
A live freeze-dried bivaccine against swine erysipelas and Aujeszky's disease in pigs was produced, its antigen titers reaching 10(8) and 10(4.67) for the two components, respectively. The immunity conferred to the vaccinated pigs (so far as Aujeszky's disease is concerned) had an antibody titer of 1:4, and in sheep the titer was up to 1:16, these animals showing resistance at a control infection with 5000 LD50 per head. The vaccinated pigs likewise withstood a control infection with a mixed 24-48-hour broth culture of virulent strains causing swine erysipelas.
Severe granulomatous lesions in cervical muscles and lymph nodes, associated with the use of an oil-based erysipelas vaccine, caused considerable economic loss at slaughter in 1400 pigs from the one herd. The condition was reproduced experimentally using the same vaccine, and in a less severe form with another commercially available oil-based erysipelas vaccine.
The clinical features of a patient with macroglobulinemia and pneumococcal erysipelas are presented. The cellular and humoral factors generated by the host to contain acute pneumococcal tissue invasion are described, and their activities in patients with plasma cell dyscrasias are discussed.
Streptococcus pneumoniae produced an erysipelas-like eruption in a patient with the nephrotic syndrome. The eruption and accompanying fever resolved upon treatment with aqueous penicillin.
The clinical course of necrotizing fasciitis in 8 patients is compared with observations on 22 other patients with erysipelas. In necrotizing fasciitis the early erythematous areas turn into a dusky blue colour with later vesiculation and formation of bullae. An important finding is a non-pitting oedema extending outside the erythematous patches. The disease often progresses and involves further skin areas proximal to the initial ones. Gangrene tends to follow in multiple sites after the 1st week of illness. Group A streptococci in conjunction with widespread thrombosis and vascular necrosis of the involved skin are two major factors in the pathogenesis of the gangrene. Early debridement and excision of necrotic tissue in combination with large doses of penicillin and cloxacillin are confirmed as mandatory to remove toxaemia and inhibit further necrosis of the skin. In 3 of the 8 patients with necrotizing fasciitis the syndrome of disseminated intravascular coagulation complicated the course of the disease. A promising therapeutic result was seen in 2 further patients exhibiting alarming signs and symptoms of early necrotizing fasciitis; the combination of heparin, given intravenously in therapeutic doses guided by activated partial thromboplastin time studies, and of systemic antibiotics alleviated the symptoms, which vanished within 10 days of the start of treatment.
The PGE2 and PGF2 alpha content of bullae developing spontaneously on the skin was investigated by radioimmunoassay in 12 patients with different skin diseases. The PGF2 alpha level was also established in the plasma and urine. In herpes gestationis, dermatitis herpetiformis and bullous erysipelas the PGE2 and PGF2 alpha content of the bullae considerably exceeded the plasma and urinary PG levels. The findings were thought to be in relation with the acute inflammation of the skin, the mechanism of bulla formation as well as with pruritus.
A 72-year-old, healthy white woman presented with rapidly advancing necrotizing erysipelas of the upper and lower eyelids. There was no previous history of trauma or skin abrasions. The patient was treated with intravenous methicillin (Staphcillin) for 2 weeks and oral cloxacillin (Tegopen), for 1 week with intensive wound cleaning and debridement. After 3 months of continuous wound care, the patient has healed her wounds by second intention, with a moderate amount of lid contracture. Further surgical correction of the lower lid defect may be necessary.