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Carcinoma erysipelatodes, also known as inflammatory metastatic carcinoma, is a type of cutaneous metastatic disease. We describe a 64-year-old woman with metastatic breast carcinoma who presented with a blistering erythematous eruption resembling erysipelas with formation of vesicles and bullae. She was found to have carcinoma erysipelatodes with a formation of vesicles and bullae.
Swellings in the legs, caused by lymphedema, are encountered quite frequently in everyday orthopedic practice. The swellings are hard, pale in color and usually painful. Swellings of this kind occasionally atrain a completely disproportionate size and are the referred to as elephantiasis. Lymphedemas fall into two categories: 1. Congenital lymphedemas. These comprise lymphedemas occuring as a result of aplasias or dysplasias of lymph vessels. 2. Acquired lymphedemas: In such cases the edema may be due to mechanical causes, or it may be the result of a disturbance of lymph drainage, e.g., due to the destruction of lymph vessels by metastases, following extirpation of lymph nodes and radiation therapy; or it may be the result of inflammatory processes, e.g., following erysipelas, in filariasis or after a wound infection. Four stages of lymphedema are also distinguished: Stage I - latent lymphedema Stage II - reversible lymphedema Stage III - irreversible lymphedema Stage IV - Elephantiasis. Apart from clinical diagnosis the most comprehensive and reliable diagnostic procedure is lymphangiography. A simple and well-tried method of diagnosing lymphedema is to inject lymphotropic dye subcutaneously. The technique is outlined. The differential diagnosis of lymphedema is described. With regard to treatment, reference is made to surgical possibilities. However, these do not always augur success and the complication rate is high. Massive lymphedemas, therefore, are usually treated conservatively, by Van der Molen's tube method, with intermittent cuff pressure (pressure-curve therapy) and manual lymph drainage. The various treatment methods are described and some of the disadvantage and risks involved are pointed out.
Ophthalmic diseases reported in the age of Goethe are difficult to identify today because the nomenclature used at that time is now antiquated. However, it is not difficult to establish from available documents that Goethe's left eye was seriously affected by an erysipelas (tenonitis? orbital phlegmon?), though it was not permanently damaged. With regard to differential diagnosis, an ophthalmic zoster may also be considered, but this is most unlikely considering the documentary evidence and the absence of lasting ocular damage.
The butterfly rash and malar flush are common facial manifestations of several disorders. Systemic lupus erythematosus may produce a transient rash before any other signs. In pellagra, symmetric keratotic areas on the face are always accompanied by lesions elsewhere on the body. Erysipelas produces brawny, fiery red facial lesions, and scarlet fever causes facial eruptions as part of a generalized eruption. Lupus vulgaris and lupus pernio produce nodules that may spread in a butterfly pattern, and seborrheic dermatitis has a predilection for the malar prominences and other areas of the face. Carcinoid syndrome often causes flushing attacks that vary in duration, and facial flushing that lasts throughout treatment may accompany chemotherapy if the patient has a hypersensitivity reaction. Deep-red rashes and/or lichenoid lesions may be caused by graft-versus-host disease in a patient undergoing bone marrow transplantation.
The results of treating chronic lymphedema using microwave heating are described in 45 patients with postmastectomy lymphedema of the upper extremity. Forty-five patients showed a significant (p < 0.01) reduction in the amount of peripheral edema after two courses of treatment. The incidence and severity of secondary acute inflammation (erysipelas) were also sharply reduced (p < 0.01). The elasticity of the soft tissue was restored.
Chemotactic migration, production of superoxide anion (O2-), and the release of beta-glucuronidase from azurophilic granules were determined in polymorphonuclear leukocytes (PMN) from 135 patients with infectious (e.g., pyoderma, acne conglobata, erysipelas) as well as noninfectious (psoriasis) skin diseases. Purified C5a and the formylated tripeptide FMLP were used as stimuli. In addition, longitudinal profiles of PMN activities were performed at daily intervals in several patients. There was a complete absence of PMN responses (chemotaxis, O2--production, and enzyme release) specifically induced by C5a in 25 patients suffering from various inflammatory diseases of the skin. In these patients PMN responsiveness for the tripeptide FMLP was either normal or increased. The C5a-dependent defect of PMN was transient and correlated with disease activity. When normal PMN were incubated with sera from C5a-defective patients, no inherent stimulatory or inhibitory activities compared to control sera were seen. Pretreatment of normal PMN in vitro with various concentrations of C5a failed to completely deactivate PMN without affecting FMLP dependent functions. These observations demonstrate the presence of a functional defect in circulating PMN during acute cutaneous inflammation. The in vitro experiments suggest transient blocking of C5a-dependent PMN functions by a cell-bound factor which seems not to be C5a or C5adesarg.
Polymorphonuclear leukocytes contain well-defined proteolytic enzymes in their azurophilic granules that can be released into tissues during inflammation, producing a localized excess of proteases that causes a protease-antiprotease imbalance with subsequent tissue destruction. The antiproteolytic compounds of the epidermis, such as the protease inhibitors elafin and antileukoprotease, are thought to counteract the proteolytic tissue damage. We investigated the urine of patients suffering from inflammatory skin conditions (e.g., erysipelas, psoriasis) for the presence of urinary antiprotease activities. Purification of elastase-inhibitory activities from pooled urine samples by cation exchange high-performance liquid chromatography and preparative and analytical reverse-phase high-performance liquid chromatography yielded two different types of inhibitors. One was a cationic, acid-stable, and elastase-specific inhibitor of M(r) 6,000 by size-exclusion high-performance liquid chromatography. N-terminal amino acid sequence analysis of the first 28 residues showed identity with elafin, an elastase-specific inhibitor recently isolated from psoriatic scales. The second anti-protease activity was due to two forms of urinary bikunin, the inhibitory subunit of inter-alpha-inhibitor. Both bikunin fragments, with M(r) 4,000 and 16,000, were identified by N-terminal amino acid sequence analysis of the first 10 residues and were characterized by an antiproteolytic profile against human leukocyte elastase, cathepsin G, and trypsin. Urinary protease inhibitors may serve as diagnostic markers of inflammatory diseases.
A diabetic patient is described presenting psoriasis, necrobiosis lipoidica diabeticorum, granuloma annulare, and vitiligo and with a history of recurrent erysipelas and mycotic infections. Scrupulous physical examination excluded further systemic or cutaneous involvement. The immunological workup revealed both phenotypic and functional defects in cellular immunity.
BACKGROUND: More than 80% of leg ulcers are caused by venous insufficiency. The actual causes of venous ulcers, beyond the presence of venous insufficiency, are rarely referred to in the literature. This study evaluates the direct triggers for ulceration in patients with venous insufficiency. METHODS: Sixty-four patients with 110 chronic venous ulcers, treated in the Chronic Wounds Clinic of Soroka University Medical Center from 1999 through 2002, were included in the study. In each patient, the actual trigger of ulceration was determined by history taking and reviewing of the medical chart. RESULTS: The actual triggers of ulceration, based on data for 64 patients with an overall total of 110 ulcers, were identified as follows: cellulitis (or erysipelas), 17 ulcers (15.4% of 110 ulcers); penetrating injury, 13 ulcers (11.8%); contact dermatitis, 12 ulcers (10.9%); rapidly aggravating leg edema, 12 ulcers (10.9%); burn wound, seven ulcers (6.3%); dry skin with subsequent scratching, six ulcers (5.4%); blunt trauma, five ulcers (4.5%); deliberately self-inflicted trauma, five ulcers (4.5%); insect bite, two ulcers (1.8%); bleeding from a supeficial varicose vein, two ulcers (1.8%). In 29 ulcers (26.3%) no specific trigger was identified. CONCLUSIONS: The development of a cutaneous ulcer is not necessarily "spontaneous" and should not be attributed solely to the presence of venous insufficiency. In many cases, it is possible to identify a specific trigger that causes the ulceration. Clinical implementation of the above findings in routine examination and treatment of patients with venous insufficiency may prevent the development of venous ulcers.
In sera from 4 of 25,000 individuals tested for antibodies against streptococci, extremely high antideoxyribonuclease B titers ( > 10(6) U/ml) were found. Two of the cases were diagnosed as monoclonal gammopathies. The M-components were shown to possess the anti-deoxyribonuclease B activity. The other two cases were diagnosed as relapsing erysipelas. The high serum titers of deoxyribonuclease B antibodies were accompanied by a very inflammatory reactivity in the patients' sera and by an oligopolyclonal pattern of immunoglobulin G. In routine diagnoses of streptococcal infections with the anti-deoxyribonuclease B test, patients with extremely high serum titers should be examined for the possible occurrence of gammopathies.
Between 1999 and 2002, 496 invasive group A streptococcal (GAS) isolates from clinical microbiological departments in Denmark and subsequently 487 (98%) questionnaires from the clinicians treating the patients were received as part of a national surveillance. emm types and streptococcal superantigen (SAg) genes were determined. The incidence of invasive GAS infections was on average 2.3 per 100,000 per year. Bacteremia with no focal symptoms (27%) was together with erysipelas (20%) the most prevalent clinical diagnoses. Streptococcal toxic shock syndrome occurred in 10% of patients, of which 56% died. The overall case fatality rate within 30 days was 23%. In total, 47 different emm types were identified, of which emm1, emm3, emm4, emm12, emm28, and emm89 were identified in 72% of the 493 available isolates. During the 4-year period the presence of emm1 increased from 16% in 1999 to 40% in 2002. Concurrently, the presence of emm3 decreased from 23% in 1999 to 2% in 2002. The emm1 isolates predominantly carried speA, although the frequency decreased from 94% in 1999 to 71% in 2002, whereas the emm1-specific prevalence of speC increased from 25 to 53%. In a historical perspective, this could be interpreted as a reemergence of emm1 and could indicate a possible introduction of a new emm1 subclone. However, this reemergence did not result in any significant changes in the clinical manifestations during the study period. Our results show the complexity of invasive GAS infections, with time-dependent variations in the incidence and distribution of emm and SAg genes, which emphasizes the need for continuous epidemiological and molecular investigations.
Chronic polyarthritis was induced in pigs by injection of Erysipelothrix rhusiopathiae and the in vivo activation of chondrocytes by cytokines was then investigated in the affected joints by immunocytochemistry. A polyclonal antiserum which recognises surface markers on in vitro interleukin 1 activated porcine chondrocytes was used to detect activated chondrocytes in all zones of the cartilage from diseased joints. In contrast, cartilage removed from an unaffected joint in the same animal showed no chondrocyte activation. Inflammatory synovial tissue removed from diseased joints and cocultured with cartilage from the unaffected joint induced activation of adjacent chondrocytes. The presence of interleukin 1 in the inflammatory cells of the synovium was confirmed and major histocompatibility complex (MHC) class II antigens were detected as a marker of synovial activation. Chondrocytes were found not to express class II antigens in cartilage from either the diseased or the unaffected joint. These observations show that the porcine erysipelas model of arthritis will be useful in facilitating a novel approach to monitoring the behaviour of individual chondrocytes under pathophysiological conditions.
Teicoplanin is a new glycopeptide antibiotic chemically related to vancomycin with a similar bactericidal activity against aerobic and anaerobic Gram-positive bacteria but with a longer plasma elimination half-life of 40-100 h allowing a once daily parenteral administration. In an open prospective study, we treated 20 patients with skin and soft tissue infections such as erysipelas, cellulitis, folliculitis and furunculosis with a a success rate of 84%. The peak and trough serum levels of teicoplanin were above the minimal inhibitory concentrations of the bacteria isolated and the therapeutic index measured at the plateau level was between 24 and 146. We observed a moderate increase of the transaminases in 3 patients which returned to normal at the end of treatment. We conclude that this new antibiotic, teicoplanin, is safe and effective in the treatment of skin and soft tissue infections. It can be administered once daily and is well tolerated even in long-term therapy.
This paper examines changing strategies of isolation in the New York Hospital between 1771 and 1930 by correlating the facilities available for isolation with changing reactions to internal disease incidence, changing medical rules and regulations, and shifting ward categories. To prevent internal "epidemics" of telltale diseases such as erysipelas, pyemia, and "hospital gangrene," what (or who) was isolated from what, and how that isolation was achieved, altered drastically. Traditional strategies of increasing the air space and flow around each patient gave way to Florence Nightingale's sanitary nursing, Joseph Lister's antisepsis, Joseph Grancher's barrier system of nursing, D. L. Richardson's aseptic nursing, and Charles Chapin's advocacy of individual cubicles. The larger social and medical transformations of the hospital colored all of these shifts. But the changing isolation strategies also reveal a transformation of the underlying understanding of the role that hospital architecture played in disease incidence.
8 male patients (age 65-82 years) suffering from bacterial pneumonia or erysipelas were subjected to skeletal muscle biopsies. Significantly lower activities of lactate dehydrogenase (LDH) and glyceraldehyde-3-phosphate dehydrogenase (TPD) of skeletal muscle were recorded in the acute phase of the illness as compared to after the end of the convalescent phase. For citrate synthetase (CS) a similar although non-significant tendency was observed, while cytochrome c oxidase (CYTOX) was not altered by infection. Similar results have been reported in young patients with viral and mycoplasma infections. In the old patients the activity of LDH was approximately half of that found in the young patients (and in young controls confined to bed) on all occasions of measurement.
It was found that donor's serum and serum of patients with rheumatic fever, erysipelas and myasthenia gravis contained autoantibodies to the cytoplasmic antigens and to the antigen of perinuclear zone of differentiated layers cells of human epidermis. Using the serum with different level of autoantibodies to these epidermal antigens it's localization in the human thymus epithelium was determined. It was shown that perinuclear antigen of differentiated epidermis cells is localized in the cytoplasm of cortical and medullar thymus epithelial cells and in the perinuclear zone of some cells in Hassall's corpuscles. The cytoplasmic antigen of differentiated epidermal cells is detected only in the cytoplasm of the Hassall's corpuscle cells. The ability of many tissues (possibly all of them) and in the first turn of epidermis to produce lymphokine along with immunomodulating properties of thymus hetero-organic antigens enables to consider these thymus antigens as a complex of immunomodulating factor proper for other tissues. These factors may provide the competence of certain T-cell subpopulations to different organ's tissues necessary for proceedings them the immunological survey both in normal and pathological conditions.
Painful sensation of heavy or swollen legs are non-specific symptoms frequently associated with chronic venous insufficiency. Clinical evaluation is the first step in defining the cause of the complaint and offering adequate treatment. When a heavy or swollen leg is associated with oedema, venous insufficiency, lymphatic or systemic disease must be considered. If symptoms occur during walking a vascular or nervous disease must be suspected. Associated erythema suggests infection (erysipelas). If clinical data are the cornerstone of diagnosis, difficulty may arise from the high frequency of superficial venous insufficiency and the readiness of linking too quickly any non specific complaint to this particular venous disease.
Cytomegalovirus (CMV) is widespread. In most cases CMV infection is asymptomatic. The most significant clinical syndrome is mononucleosis and hepatitis. We report a case of 38 old woman with CMV hepatitis associated with erysipelas.