Anaphylaxis

We present evidence that M proteins from three different serotypes of group A streptococci share epitopes with cardiac myosin. Rabbit antisera evoked by a purified fragment of type 5 M protein crossreacted with myosin, but not alpha-tropomyosin, actin, or myosin light chains. In enzyme-linked immunosorbent assays, the myosin-crossreactive antibodies were totally inhibited by type 5 M protein and partially inhibited by types 6 and 19 M proteins. The affinity-purified myosin antibodies opsonized type 5 streptococci, indicating that they were directed against protective M protein epitopes on the surface of the organisms. Immunoblot analyses demonstrated the binding of the crossreactive antibodies to myosin heavy chains. Sera from patients with acute rheumatic fever showed significantly stronger reactions with myosin than did sera from their siblings, hospitalized controls, or patients with poststreptococcal glomerulonephritis.

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Epitopes of streptococcal M proteins shared with cardiac myosin.

Post-cardiac injury syndromes. An emerging cause of pericardial diseases.

Modification of the cardiac rhythm by histamine has been appreciated almost since the compound's isolation from ergot by Barger and Dale in 1910. The major arrhythmogenic actions of histamine are an Hi-receptor-mediated slowing of atriovenrricular (AV) conduction and H2-receptor-mediated increases in sinus rate and ventricular automaticity. These actions were elucidated by observing the salutary effects of histamine antagonists on the arrhythmias of anaphylaxis, and by administering exogenous histamine to various cardiac preparations in the presence and absence of histamine antagonists. The ability to record transmembrane action potenrial(s) (TAP) from single cells has permitted the study of electrophysiological mechanisms underlying histamine-induced arrhythmias.

Histamine and cardiac arrhythmias.

Heart-reactive antibody (HRA) appears in the sera of experimental animals inoculated with group A streptococci as well as patients with acute rheumatic fever. Adsorption of either serum with group A streptococcal membranes will remove the HRA. Blocking experiments between these two types of HRAs have demonstrated that the antibodies are directed towards different antigenic determinants on either the same or different molecules. To isolate and purify the antigen from the group A streptococcus cross-reactive with sarcolemmal sheaths of cardiac myofibers, it became necessary to purify the HRA from rheumatic fever patients' sera. Isolated gamma globulin containing all of the HRA was adsorbed onto human sarcolemmal sheaths. The specific HRA was released by using potassium iodide. Over 99 percent of the purified HRA was shown to bind the sarcolemmal sheath whereas less than 1 percent of the antibody would bind nonspecifically to other material. Preparations of group A streptococcal membrane will bind HRA purified from the sera of acute rheumatic patients at levels of 97 percent or greater. The cross-reactive antigen solubilized by nonionic detergent was purified 120-fold by column chromatography. On sodium dodecyl sulfate polyacrylamide electrophoresis, the antigen was demonstrated to be composed of four polypeptides with mol wt of 32,000, 28,000, 26,000, and 22,000 daltons, respectively. Only proteolytic enzymes could destroy the antigenic determinant whereas glycosidases and lipases had no effect. The purified antigen blocked the binding of purified HRA to normal human heart sections.

https://rupress.org/jem/article-pdf/146/2/579/1393178/579.pdf

Group A streptococcal antigens cross-reactive with myocardium. Purification of heart-reactive antibody and isolation and characterization of the streptococcal antigen.

Histamine is released into the systemic circulation during anaphylaxis, by drugs and by surgical procedures. Studies in animal models have conclusively demonstrated that released cardiac histamine is a major mediator of arrhythmias that occur during anaphylaxis and following the administration of histamine-releasing drugs. Several lines of evidence suggest a similar arrhythmogenic role for cardiac histamine in humans: (1) The human heart is rich in histamine; (2) cardiac histamine can be readily released from human heartin vitro by therapeutic concentrations of drugs; (3) histamine has potent arrhythmogenic effects on the human heartin vitro.

Dysrhythmias caused by histamine release in guinea pig and human hearts.

Circulating heart-reactive antibodies in the postpericardiotomy syndrome

SUMMARY
While continuing a study of immunologic and virologic aspects of the postpericardiotomy syndrome (PPS) in infants and children, we undertook a companion study in adults. Whereas the incidence in 119 children was 27.8%, as is usual for our hospital, the incidence in 142 adults was 17.6%. Most of the operations (95 of 142) were performed on patients who were 50–69 years old. Incidence decreased as age increased: 28.5% for ages less than 40 years, 19.7% for ages 40–59 years, 14.2% for ages 60–69 years, and 10% for ages 70 years and older. Heart-reactive antibody in high titer was found in all patients with PPS; a rise in antiviral antibody to one or more of a battery of eight common viruses (adenovirus, cytomegalovirus, and coxsackievirus B 1 to 6) was identified in 68% of these with PPS but in only 5% of those without clinical manifestations. We conclude that in adults, as in children, PPS may be an autoimmune phenomenon triggered by viral illness.

Postpericardiotomy syndrome in adults: incidence, autoimmunity and virology.

Summary During the fifteen year period from 1955 through 1970, 169 patients with villous lesions of the colon and rectum were treated. Sixty-nine per cent of the lesions occurred in the rectum and rectosigmoid, and these patients most often presented with rectal bleeding (47 per cent). Forty-eight per cent of the lesions were malignant; however, only 10.3 per cent or twelve of these patients died of metastatic adenocarcinoma. The over-all five year survival was 77.7 per cent. Large villous tumors located above the rectum should be treated by bowel resection and small lesions by colotomy and polypectomy. Benign rectal lesions or those with carcinoma in situ can be adequately treated by local procedures; however, the entire lesion must be removed to eliminate the possibility of invasion. Invasive carcinoma arising in a villous tumor should be treated in a manner similar to that used for other lesions of the colon.

John C. McCabe

Papers

Dysrhythmias caused by histamine release in guinea pig and human hearts.

Circulating heart-reactive antibodies in the postpericardiotomy syndrome

Postpericardiotomy syndrome in adults: incidence, autoimmunity and virology.

Villous tumors of the large bowel

Chronic pericardial effusion requiring pericardiectomy in the postpericardiotomy syndrome.