Is Lymphogranuloma Inguinale A Systemic Disease?

Abstract

Discussion and Summary Comparison of experimentally induced lymphogranuloma inguinale in animals with the disease in the human leads us to assume properly, we believe, that generalized infections in man are possible, such infections probably depending principally upon the route of entry of the virus. However, since clinical experience shows the mucous membrane of the genitalia to be the most frequent portal of infection in the human, it is justifiable to theorize, as is actually the case, that the localized type of infection should be more frequently observed in man than the generalized type. The severe constitutional symptoms so frequently encountered, even though evanescent, certainly suggest widespread invasion. Such symptoms often overshadow the local manifestations of the disease and are of the same character as those seen in generalized invasions by infectious agents. Extragenital lesions, widespread in distribution and protean in character, undoubtedly occur during the course of lymphogranuloma inguinale infections and are possibly due to the action of the virus. Unfortunately definite proof of this is lacking. Such occurrences have led many authors to postulate the existence of various types of lymphogranuloma inguinale viruses or to designate the virus as “lymphotropic,” “dermotropic,” etc. We are most emphatic in disagreeing with such views. A virus which may be responsible for the production of adenitis, dermatitis, pelvic peritonitis, arthritis, stomatitis, meningoencephalitis, etc., can hardly be spoken of as having “certain affinities.” We believe that dissemination, when and if such occurs, and localization of the virus is dependent essentially upon the same well-known factors responsible for such with any infectious agent—the portal of entry, the invasive character of the agent, the host resistance. Variations in these account for the varying clinical pictures encountered. We do agree, however, with Remlinger and Bailley that there can exist differences in the “agressiveness” of viruses. These views naturally place us in disagreement with Coutts who postulates the existence of two viruses, A and B, responsible for localized and generalized manifestations of lymphogranuloma inguinale respectively. While some of the cases in our series showed the classical symptoms described by this Chilean investigator as ascribable to the A virus and some of those ascribable to the B virus, we encountered many cases showing features of both groups, such as primary lesions with bilateral adenitis and severe constitutional symptoms, or unilateral suppurating buboes without demonstrable primary lesions and no constitutional symptoms. The viruses recovered from cases presenting these various syndromes produced no histological differences when injected into experimental animals. Investigation of the antigenic properties, as regards the diagnostic cutaneous test, of virus material secured from such different types of cases showed some differences in degree of reactivity in infected patients. This observation, however, certainly does not allow us logically to postulate biological differences in the infectious agent. As a result of our studies of the experimental production, symptomatology and pathology of lymphogranuloma inguinale we believe it logical to conclude that there are many indications pointing to frequent general dissemination of the virus during the early stages of the infection. In most instances, however, the virus is soon destroyed or neutralized and only the local lesions develop. Certainly the possibility of a severe generalized infection should always suggest itself when considering this disease.