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Supplement

Chronic Nutritional Diseases of Infectious Origin: An Assessment of a Nascent Field¹

The Department of Nutrition and Food Science and the Center for Molecular Medicine and Genetics, Wayne State University, Detroit, MI 48202

²To whom correspondence should be addressed. E-mail: ndhurand{at}sun.science.wayne.edu.

	INTRODUCTION

TOP INTRODUCTION LITERATURE CITED

 
The main objective of this symposium was to bring to the forefront the emerging role of pathogens in chronic diseases. Although several pathogens are increasingly being linked to various chronic diseases, ranging from gastric ulcer to schizophrenia, in order to maintain the focus, this symposium was restricted to chronic conditions such as gastric ulcer, obesity, atherosclerosis and diabetes, which have a nutritional component in their etiology and/or management. Science often progresses from noticing an association of a pathogen with a condition to eventually establishing a causal role. While animal experiments have clearly shown infectious etiologies for many of the conditions described in this symposium, only the associations of these pathogens have been described in humans (with the exception of helicobactor pylori and gastric ulcer). However, unlike animal experiments, humans cannot be experimentally infected with infectious agents and, therefore, direct evidence of a causative role for these pathogens may never be obtained. Nonetheless, the emerging relationships of pathogens with chronic diseases of humans bring up some important issues.

The main question being, why were these pathogen-disease interactions not discovered earlier? Have the pathogens recently changed their pathophysiology? Or has this age-old phenomenon been discerned lately? Both are potential possibilities. For instance, two different viruses are known to "merge" into each other to form a new strain of virus by reassortment, as in the case of James Town Canyon virus and La Crosse virus (1) , and to thereby acquire new characteristics. Such adaptations and changes in pathogens may reflect in symptom manifestations in a host, and newer disease expressions may be detected. Similarly, mutations may enable viruses to change host species and/or resulting pathology. A well-known example of this phenomenon is the sudden outbreak of Canine Distemper Virus (CDV)³<-foot;1781f3;10;ZPICKFOOT;Fn3>, a member of the morbillivirus family, in the lions of Serengeti, Tanzania (2) , who were thought to have received the virus from domestic dogs, the established host of CDV (3) . Historically, CDV is known to infect members of the canine but not the cat family. The Serengeti epidemic was due to the mutation of CDV, which probably enabled the virus to jump the host species as well as the expression of the disease.

New relationships with pathogens emerge because of changes in pathogens as well as because of the discovery of new pathogens. Pathogens such as Scrapie agent and hepatitis C virus are relative newcomers in the area, and it is possible that much remains to be discovered in regard to their pathogenic potential. The roles of Scrapie agent in obesity and hepatitis C virus in type 2 diabetes are described in the symposium.

On the other hand, perhaps, the emerging link of pathogens with various chronic diseases is not a recent development but a result of the modern sophisticated investigational abilities. A case in point is the recent research on Borna Disease Virus (BDV), the agent responsible for Borna Disease (BD). For more than a century, BD was known to be an affliction of horses and sheep, in which it caused nonpurulent encephalomyelitis. Traditionally, BDV was not thought to infect humans, but this belief has been overturned by several publications in the last decade, such as the reverse transcriptase–polymerase chain reaction–aided demonstration of BDV RNA in the peripheral blood of humans (4) . It is not surprising that, when armed with new technology, we find pathogens in new places and we discover new roles for pathogens.

It is unknown if any of the above-stated theories are applicable to the chronic diseases–pathogens links discussed in this symposium. By definition, chronic diseases have an insidious onset, which makes it difficult to recognize the link between a causative organism and the expression of the disease. To make matters worse, establishing a causal link is more difficult if the pathogen is of the "hit-and-run" type (i.e., the presence of the organism is undetectable by the time the disease is diagnosed). In addition, there remains the task of determining the relative contribution, if any, of an infectious agent to the etiology of the suspected chronic disease.

This symposium was planned to critically examine the claims concerning the role of various infectious agents in the chronic diseases presented. In an accompanying article, Dr. Lawrence Cheskin has nicely summarized the symposium. A relative lack of information about the "modus operandi" of various pathogens thwarts this nascent field. Clearly, more research is needed to firmly establish pathogens as one of the causes in human obesity, diabetes, autoimmune liver disorders and atherosclerosis. Nevertheless, the current data in the area are provocative. The concept of infectious agents as one of the causative factors may lead to appropriately directed management efforts for these diseases as well as to a search for additional pathogens that may be causally involved in various other chronic diseases.

	FOOTNOTES

 
¹ Presented as part of the symposium entitled "Emerging Role of Pathogens in Chronic Diseases Requiring Nutritional Intervention" given at the Experimental Biology 2001 Meeting held March 31–April 4, 2001 in Orlando, FL. This symposium was sponsored by the American Society for Nutritional Sciences and was supported in part by educational grants from Novartis Nutrition and Ortho McNeil. The proceedings of this symposium are published as a supplement to The Journal of Nutrition. Guest editors for the symposium publication were Nikhil V. Dhurandhar, Wayne State University, Detroit, MI, and Lawrence J. Cheskin, Johns Hopkins School of Medicine, Baltimore, MD.

³ Abbreviations used: CDV, Canine Distemper Virus; BDV, Borna Disease Virus; BD, Borna Disease.

	LITERATURE CITED

TOP INTRODUCTION LITERATURE CITED

 

1. Cheng L. L., Rodas J. D., Schultz K. T., Christensen B. M., Yuill T. M. & Israel B. A. (1999) Potential for evaluation of California serogroup bunyaviruses by genome reassortment in Aeded albopictus. Am. J. Trop. Med. Hyg. 60:430-438.[Abstract]

2. Roelke-Parker M. E., Munsonn L., Packer C., Kock R., Cleaveland S., Carpenter M., O’Brien S. J., Pospischil A., Hofmann-Lehmann R. & Lutz H. (1996) A canine distemper virus epidemic in Serengeti lions (Panthera leo). Nature 379:441-445.[Medline]

3. Cleaveland S., Appel M. G., Chalmers W. S., Chillingworth C., Kaare M. & Dye C. (2000) Serological and demographic evidence for domestic dogs as a source of canine distemper virus infection for Serengeti wildlife. Vet Microbiol 72:217-227.[Medline]

4. Chen C. H., Chiu Y. L., Shaw C. K., Tsai M.T., Hwang A. L. & Hsiao K. J. (1999) Detection of Borna disease virus RNA from peripheral blood cells in schizophrenic patients and mental health workers. Mol. Psychiatry 4:566-571.[Medline]

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