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THE CORRELATION OF EXPERIMENTAL STREPTOCOCCIC ARTHRITIS IN RABBITS WITH CHRONIC RHEUMATOID ARTHRITIS.

HADJOPOULOS, L. G.; BURBANK, REGINALD
The Journal of Bone & Joint Surgery: July 1932
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It has been possible by injecting certain mannite-fermenting arthrotropic streptococci, isolated from the blood stream of afebrile arthritic patients, to produce in rabbits pathological lesions exactly comparable to those found in chronic arthritis in the human being.

This fact has also been substantiated by the almost complete similarity of the morbid anatomy of our streptococcic arthritic joints in rabbits to those naturally acquired in the human subject, and so carefully investigated and described by Nichols and Richardson, Llewellyn and Jones, Strangeway, Knaggs, and others.

Most of this morbid anatomy and the concomitant symptoms we were able to trace directly or indirectly to changes in capillary circulation, a finding which Pemberton upholds and ascribes to some toxic degeneration, either associated with or merely followed by disturbed metabolism.

Since toxic degeneration in capillaries is a common finding in the course of chronic disease, and because of the recent revival of the hypothesis that the changes of atrophic rheumatoid arthritis are toxic anaphylactic manifestations (Swift, Boots), we felt that the direct effect of infection on joints should first be definitely excluded before theorizing on the basis of indirect factors. In acute inflammatory conditions of a pyogenic nature, the demonstration of the causative micro-organism in diseased tissues is usually taken as a sufficient evidence of the direct [SEE THE FIGURE 22-A AND 22-B IN SOURCE PDF.] activity of the invading germ (the demonstration of gonococcus in gonorrhoeal arthritis or of staphylococcus in carbuncles). Changes in remote tissues or organs from which the presence of bacteria is excluded may be considered indirect degenerative alteration of a toxic or allergic nature.

We felt it necessary to exhaust all possible means of demonstrating the dissemination of streptococci in diseased tissues of our experimental animals before we ascribed such changes as were present to indirect causes such as toxaemia or allergy.

By incubating the whole joint we were able to demonstrate these infecting organisms in practically all lesions associated with chronic atrophic arthropathies. Streptococci were found in every part of the synovial tissues where pathological changes could be detected. No streptococci could be demonstrated in compact bone, yet the spread of infection in bone tissue could be traced step by step through its medullary and haversian vascular supply. In the avascular cartilage the spread of streptococci was through infected bone tissue and synovial infiltration. Normal joints were subjected to the same procedure with uniformly negative findings.

To complete the picture of infection, we have recently studied the tendons and muscles in the immediate neighborhood of arthritic joints. We had no difficulty in demonstrating streptococci in tendons at the zone of nuclear proliferation (Fig. 27). Muscles were extensively infiltrated with streptococci at their sheaths, but in spite of great care the possibility of outside contamination in surface areas must be considered.

Throughout this study the progress of the disease could always be traced directly to the terminal blood vessels, as is true in all infections of hematogenous origin. Despite the specific selectivity of the arthrotropic streptococci used in these experiments, internal organs, especially the liver and kidneys, were not exempt from pathological changes of toxic nature involving their parenchyma. Nevertheless, streptococci could be demonstrated in the interlobular connective tissue of the liver (Fig. 28), and occasionally even in the hepatic vessels (Figs. 29-A and 29-B). This finding is highly significant in that it forcibly brings home the fact that chronic rheumatoid arthritis is fundamentally a systemic disease, and it explains the transient septicaemias that occur intermittently in the course of the infection.

(C) 1932 All Rights Reserved.The Journal of Bone and Joint Surgery, Inc.

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