Streptococcal infections, and

Boyle et al. (2001) used the Ciphergen SELDI protein chip to analyze the secretion and autoactivation of a cysteine protease (SpeB) from Streptococcus pyogenes that has been implicated in the onset of group A streptococcal infections and may contribute to toxic shock symptoms. SpeB could be detected at 0.75 ng protein in a 30-min assay based upon SELDI-TOF... 

Group A Beta-Hemolytic Streptococcal Infections and Host Immune Response... 

Gibofsky, A., Khanna, A., Suh, E., and Zabriskie, J.B. (1991) The genetics of rheumatic fever relationship to streptococcal infection and autoimmune disease. / Rheumatol (Suppl 30) 18 1-5. 

Streptokinase is the oldest available fibrinolytic. By itself it lacks enzymatic activity only after binding to a plasminogen molecule is a complex formed that activates plasminogen. Streptokinase is produced by streptococcal bacteria. Streptokinase antibodies may be present as a result of previous streptococcal infections and may lead to incompatibility reactions. 

Watanabe-Ohnishi R, Low DE, McGeer A, Stevens DL, Schlievert PM, Newton D, Schwartz B, Kreiswirth B, Kotb M Selective depletion of V beta-bearing T cells in patients with severe invasive group A streptococcal infections and streptococcal toxic shock syndrome. Ontario Streptococcal Study Project. J Infect Dis 1995 171 74-84. 

A few isolated clinical trials of the drug took place in Germany during the period 1933-1935, and Domagk wrote a number of reports about his discoveries but the first serious clinical trial was carried out in 1936 at Queen Charlotte s Maternity Hospital in London. Here, Leonard Colebrook was trying to reduce still further the number of deaths from puerperal fever (which then stood at 2-3 per 1000 deliveries). Initially, he treated 38 women who were very seriously ill with streptococcal infections and saved the lives of all but three of them. Normally, at least 25% of these patients would have died. His Lancet paper generated considerable interest, as did a subsequent trial with a further 26 women, all of whom were saved. 

Patients with rheumatic fever have heart-reactive antibodies in their sera. In addition, these antibodies are at higher titre than in people with streptococcal infection and no rheumatic fever. In addition, they persist for up to three years following an acute attack — the period of time at which patients are at risk of recurrence. A rise in antibodies is seen at the time of second attacks when these are associated with endocarditis. 

The sulfonamides are as efficacious as oral penicillin in preventing streptococcal infections and recurrence of rheumatic fever in susceptible subjects and are used in patients who are hypersensitive to penicillin. Untoward responses usually occur during the first 8 weeks serious reactions after this time are rare. White blood cell counts should be checked weekly during the first 8 weeks. 

Because it is a foreign protein, streptokinase is associated with significant hypersensitivity reactions. Most people have, at some point in their lives, had a streptococcal infection and, therefore, have developed circulating antistreptococcal antibodies. These antibodies frequently are active against streptokinase as well. The response of the streptokinase to these antibodies can vary widely, from inactivation of the fibrinolytic properties of the protein to rash, fever, and rarely, anaphylaxis. Significant allergic reactions to streptokinase occur in approximately 3% of patients. 

Hoge, C.W., Schwartz B., Talkington D.F., Brieman, R.F., MacNeill, E.M., and Eglender, S.J. 1993. The changing epidemiology of invasive group A streptococcal infections and the emergence of streptococcal toxic shock-like syndrome. JAMA 269 384-389. 

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