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Focal infection in perspective
Focal infection in perspective
\‘olurllc? 44 xuIlll,er 4
Focctl kfectio)!
in perspectiu
627
matwin1 from these cells cx~ultl proride fresh stimulus for an existing inflammatory process. IIypersc~nsitivity to microbial products or components of the anaph~lactic typca, the drthus phenomenon, 0~’ the tnberculosis type may contribate to tissue injury in sonif eases. dnotlicr possibility is that tissue components arc altered antigenieally as a result of the inflammatory cnr-ironmcnt. In other C;ISCS,COW 177071 antigens from host ant1 microbe ha\-c IWW clescribccl. 111 cithcr case antigivcl rise to tissue damage. Ithcumatic* bodies against “Sdf” JM)&WlO~, alld Fever prodcs a useful clsamplc of a disease in which it is likely that many factors 0, interact to produce the clirlici~l pidnro. The streptococcal t,oxin, streptolyiin has a toxic effect on isolated mammalian hearts and myocarclial cells in CUltWe; antibody formed against, it is evidence of in viva production. Patients with rheumatic fever can be tlemonstratcd to be hgperscnsit,i\-c to strcptococcal products, itntl common antigens between the streptococcus and the heart havc been demonstrated. The sequcncc of events operatin, 07in clinical rheumatic fever renlains Llnknown, however. The association of rheumatic fever with streptococcal infection is dl documented. Other diseases may hare a, microbial origin which is at present olxwn~~ct. For example, rheumatoid arthritis seems to be closely connected to a self-perpctuating immunologic reaction in the joints.” This could bc a. result of alteration of tissue antigens, but the rcquircd initial antigenic stimulus remains to be identifietl. It is quite possible that a series of microbial insults to the joints initiates the proc*css. The extcndcd persistence of microbial antigens in the joints of CCpcrimental animals’ supports this hypothesis. In conclusion, an attempt has been made to cstcntl the con~cpt of focal illfection through an appreciation of the complex pathogenic mechanisms which may be operating under partienlar c~ondit,ions. REFERENCES
I. Ginsburg, I. : Mechanisms of Cell and Tissue Injury Induced by Group A Rtreptocowi : Rvktiou to Post-Streptococcnl Sequelac, J. Infect. Dis. 126: 294.340, 419-455, 1972. 2. Gillsllurg~ I., et al. : ( +roup A Atrcptococci: Localization in RalblGts and Guinea Pigs E’oIlowing Tlssuc Injury, Science 166: 1161-1163, 1969. X. Glynn, I,. E.: Pathologr, Pathogenesis ant1 Aetiology of Rheumatoid i2rthritis, Ann. Kheum. I)is. 31: 412, 19’72. 4. 1TcDPrmott, W. : Microl)inl Pcrsistenw, Tale J. Riol. Med. 30: 257-291, 1958. Eeprint requests to: I)r. N. Hunter Department of Oral Biology University of Adelaide Adelaide, South Australia
\‘olurllc? 44 xuIlll,er 4
Focctl kfectio)!
in perspectiu
627
matwin1 from these cells cx~ultl proride fresh stimulus for an existing inflammatory process. IIypersc~nsitivity to microbial products or components of the anaph~lactic typca, the drthus phenomenon, 0~’ the tnberculosis type may contribate to tissue injury in sonif eases. dnotlicr possibility is that tissue components arc altered antigenieally as a result of the inflammatory cnr-ironmcnt. In other C;ISCS,COW 177071 antigens from host ant1 microbe ha\-c IWW clescribccl. 111 cithcr case antigivcl rise to tissue damage. Ithcumatic* bodies against “Sdf” JM)&WlO~, alld Fever prodcs a useful clsamplc of a disease in which it is likely that many factors 0, interact to produce the clirlici~l pidnro. The streptococcal t,oxin, streptolyiin has a toxic effect on isolated mammalian hearts and myocarclial cells in CUltWe; antibody formed against, it is evidence of in viva production. Patients with rheumatic fever can be tlemonstratcd to be hgperscnsit,i\-c to strcptococcal products, itntl common antigens between the streptococcus and the heart havc been demonstrated. The sequcncc of events operatin, 07in clinical rheumatic fever renlains Llnknown, however. The association of rheumatic fever with streptococcal infection is dl documented. Other diseases may hare a, microbial origin which is at present olxwn~~ct. For example, rheumatoid arthritis seems to be closely connected to a self-perpctuating immunologic reaction in the joints.” This could bc a. result of alteration of tissue antigens, but the rcquircd initial antigenic stimulus remains to be identifietl. It is quite possible that a series of microbial insults to the joints initiates the proc*css. The extcndcd persistence of microbial antigens in the joints of CCpcrimental animals’ supports this hypothesis. In conclusion, an attempt has been made to cstcntl the con~cpt of focal illfection through an appreciation of the complex pathogenic mechanisms which may be operating under partienlar c~ondit,ions. REFERENCES
I. Ginsburg, I. : Mechanisms of Cell and Tissue Injury Induced by Group A Rtreptocowi : Rvktiou to Post-Streptococcnl Sequelac, J. Infect. Dis. 126: 294.340, 419-455, 1972. 2. Gillsllurg~ I., et al. : ( +roup A Atrcptococci: Localization in RalblGts and Guinea Pigs E’oIlowing Tlssuc Injury, Science 166: 1161-1163, 1969. X. Glynn, I,. E.: Pathologr, Pathogenesis ant1 Aetiology of Rheumatoid i2rthritis, Ann. Kheum. I)is. 31: 412, 19’72. 4. 1TcDPrmott, W. : Microl)inl Pcrsistenw, Tale J. Riol. Med. 30: 257-291, 1958. Eeprint requests to: I)r. N. Hunter Department of Oral Biology University of Adelaide Adelaide, South Australia