FURTHER OBSERVATIONS ON PATHOLOGIC SIMILARITIES BETWEEN EXPERIMENTAL SCURVY COMBINED WITH INFECTION, AND RHEUMATIC FEVER.
In the guinea pig, chronic scurvy with superimposed infection (beta streptococcus) and to a lesser extent chronic scurvy alone, produces an arthropathy with striking pathologic similarities to that of rheumatic fever and the closely allied condition of rheumatoid arthritis. Considerable significance is attached to the widespread occurrence in the experimental animal subjected to scurvy and infection, and to a lesser extent in scurvy alone, of lesions similar to if not identical with the fibrinoid degeneration which has been considered the fundamental lesion of rheumatic fever. A subcutaneous nodule essentially similar to the subcutaneous nodules of rheumatic fever was observed in one experimental animal. Attention is called to a group of general pathologic changes frequently observed in rheumatic fever which were also found in the experimental animals subjected to scurvy and infection. These include degenerative changes in skeletal muscle, focal necrosis in the liver, fibrosis of the Malpighian bodies in the spleen, erythrophagocytosis in the lymph nodes, and focal lymphocytic accumulations in the kidneys. The problem of hemorrhage is considered. It is suggested that a scorbutic state may be the basis of the hemorrhagic manifestations common to the acute phases of rheumatic fever. The unsatisfactory nature of previous experimental attempts to reproduce the pathology of rheumatic fever is noted. The lesions produced by subjecting the guinea pig to the combined influence of scurvy and infection are considered to be fundamentally similar in character and distribution to those of rheumatic fever. The pathologic observations recorded in this and a previous publication (2) are believed to offer evidence that the disease known as rheumatic fever may be the result of the combined influence of scurvy and infection. It is suggested that a subclinical degree of scurvy may constitute the rheumatic tendency in which the added factor of infection causes the development of rheumatic fever or possibly the closely allied condition of rheumatoid arthritis. Epidemiological and clinical considerations appear to afford supportive evidence to this concept.
Departments of Pathology and Medicine, University of California Medical School, San Francisco.
J F
JF
Rinehart
C L
CL
Connor
S R
SR
Mettier