Did Mycotoxins Play a Role in Bubonic Plague Epidemics?

DID MYCOTOXINS PLAY A ROLE IN BUBONIC PLAGUE EPIDEMICS? MARY KILBOURNE MATOSSIAN* The staff of life was perversely the scepter of death during plague epidemics.—Michael Dols, 1977 Of all the epidemics in Europe prior to the sixteenth century, the bubonic plague pandemic of 1348—1350 was the one most fully described by contemporaries and therefore the one which may be diagnosed ex post facto with greatest confidence. There can be little doubt that plague caused a severe demographic setback. In the second half of the seventeenth century it grew less common in Western Europe and, after 1722, ceased to be a serious threat. In southeastern Europe, Russia, and the Near East, plague remained a serious health problem until the mid-nineteenth century. A great deal is known about the etiology of the bubonic plague, but there are many questions about its epidemiology which have never been answered. The purpose of this article is to seek answers to those questions by asking what role, if any, mycotoxins may have played in causing plagues, in causing high mortality generally at the time of plague epidemics , and/or both. Mycotoxins are poisons produced by microfungi. Some of these poisons, such as T-2 toxin, are potent immunosuppressants. When such a toxin damages the immune system it may not produce immediately any easily identifiable symptoms. The role of such damage in causing a disease may be obscure. In the USSR immunocompromised persons in the second stage of alimentary toxic aleukia seemed perfectly healthy, they functioned normally and reported no acute discomfort. Only a laboratory test could detect abnormality. When acute symptoms finally appeared, many phy- *Department of History, University of Maryland, College Park, Maryland 20742.© 1986 by The University of Chicago. AU rights reserved. 0031-5982/86/2902-0476$01.00 244 I Mary Kilbourne Matossian ¦ Mycotoxins and Bubonic Plague sicians thought that "the cause" was an observable, virulent pathogen and misdiagnosed the disease as diphtheria or scarlatina. They mistook a precipitating cause of an infection for a prime mover. It is logical that any condition of the human body involving the action of the immune system can be influenced by damage to the immune system. How can one understand the etiology of a disease without taking this into consideration? A "primary pathogen" may be the first pathogen known to be involved in a pathological condition: this does not necessarily give it the status of "primary cause" of a disease. The concept of a "primary pathogen" developed because it was useful in the prevention and treatment of infectious diseases. A theoretical question was left unresolved. How can the concept of a "primary pathogen " explain why some patients do not get sick and die even when exposed to such an organism? For example, the primary pathogen for tuberculosis was identified over a century ago, yet many patients exposed to it never got sick. Many of those who do get sick are now known to be immunocompromised—to have a T helper cell deficiency. The same may be said of leprosy. In the case of AIDS, the primary pathogen may be a virus that attacks the immune system, creating vulnerability to secondary infections. However , it has been suggested that AIDS itself is an opportunistic infection, able to express itself only in patients immunocompromised by mycotoxins [1, 2]. There is no experimental evidence linking the occurrence of plague with immunosuppression in humans. However, it is well known that mortality from plague may vary widely in neighboring communities. Moreover, the case mortality rate from plague, even before the introduction of antibiotics, varied, being 96.2 percent in Astrakhan gubernia (1909-1910) and only 26.7 percent in Odessa in 1910. Could it be that variance in the amount of immunosuppressant mycotoxins in grain could account for these differences [3, 4]? But even if no such link exists between human diet and the occurrence of plague, mycotoxins in rat diet may play an important role. For an increase in rat deaths, even ifnot from plague, may increase the number of plague-infected fleas seeking human hosts. The physician ordinarily starts with a clinical picture, so a brief review of the characteristics of plague seems in order. Its many...