Who Speaks for the Microbes?
Stanley Falkow, Emerging Infectious Diseases, Vol 4, No 3, July/September 1998
In discussing emerging infectious diseases, the focus is often on the clinical effects of the host-parasite relationship, i.e., the impact on the health and survival of humans and animals, rather than the examination of the biology of the pathogen. It seems fitting to take a moment to reflect on how pathogens "got that way in the first place." Thus, while we discuss emerging infections, it is worthwhile to consider that from the beginning of recorded history in books or the pictographs of ancient cultures infectious diseases have been the leading cause of illness and death. Even today, because of infectious diseases most of the world's population does not have the luxury of living long enough to succumb to the chronic diseases of aging.
What were and what remain the reasons that infectious diseases are still the leading cause of death? I believe there are four answers.
The Enemy Is Us
Legionella pneumophila, the Legionnaires' bacillus, is found in nature as an infectious agent of predatory protozoa. Introduction of this organism, often as part of an aerosol of potable water into the alveolus of the lung, results in the microorganism's finding a new niche in the macrophage instead of in its usual host Acanthamoeba or Hartmanella. More absorbent tampons helped select for a new disease, toxic shock syndrome.
While pathogenic traits of the disease-causing microbes are of consequence, humans and their technology and social behavior have played a major role in providing pathogenic microbes with new venues for their wares. Food poisoning by Escherichia coli O157, Campylobacter, and Salmonella emerged more from food technology and food distribution networks than from any fundamental change in the virulence properties of the bacteria. In a sense, we have provided these bacteria with a moveable feast.
What Is a Pathogen,
Most microbes are commensal; that is, they "eat from the same table." Others are either commensal or transient microbes that are opportunistic; they can cause disease if one (or more) usual defense mechanism, evolved to restrict microorganisms from normally sterile inner organs and tissue, is breached by accident, by intent (as in surgery and, increasingly, in gunshot wounds), or by an underlying metabolic or even infectious disorder. Nevertheless, a small group of microorganisms often causes infection and overt disease in seemingly healthy persons.
Many of the microorganisms, for example, the typhoid bacillus, gonococcus, tubercle bacillus, and treponema of syphilis, are adapted exclusively to humans; others, for example, Salmonella typhimurium, can regularly cause disease in humans, animals, birds, and reptiles. The distinct difference between commensal, opportunistic, and pathogenic microbes is that pathogenic microbes have evolved the genetic ability to breach cellular and anatomic barriers that ordinarily restrict other microorganisms. Thus, pathogens can inherently cause damage to cells to forcefully gain access to a new, unique niche that provides them with less competition from other microorganisms, as well as with a ready new source of nutrients.
For microorganisms that inhabit mammals as an essential component of their survival tactic, success can be measured by their capacity to multiply sufficiently to be maintained or be transmitted to a new susceptible host. This is true for commensal and pathogenic organisms alike. However, if the pathogen gains a new niche free of competition and rich in nutrients, it also faces a more hostile environment designed by evolution to restrict microbial entry and, indeed, to destroy any intruders that enter these protected regions. Thus, pathogens have not only acquired the capacity to breach cellular barriers but also, by necessity, have learned to circumvent, exploit, and subvert our normal cellular mechanisms for their own selfish need to multiply at our expense.
How Did Pathogens
Get That Way?
The success of these genetic changes also depended on subsequent selective pressures and genetic fine-tuning by mutation and other genetic mechanisms. Nevertheless, the molecular fossil record in the DNA of contemporary pathogens leads to the inevitable conclusion that microbial evolution is still dynamic and that these periodic genetic upheavals in microbes affecting their pathogenicity can occur at any time. To underestimate the evolutionary potential of microorganisms and their ability to survive, even in the face of enormous pressures to eradicate them and their effects on humankind, would be a mistake.
Infectious agents will emerge so long as there are microorganisms. Humans help the evolutionary process sometimes unwittingly and sometimes by arrogance or ignorance. Antibiotic resistance on a global scale in what seems such a short time comes as no surprise. Does feeding animals antibiotics to promote growth have any effect on human microbes and the health of the human population as a whole?
Rachel Carson's book Silent Spring, which documents the devastating effects of insecticides (e.g., DDT) on the health of a number of living creatures far removed from the insects that were the target, was easily understood. Yet, application of a selective pressure on the microbes of the planet with antibiotics, a pressure that dwarfs the use of DDT in its scope, as well in the number of species that are affected, still remains a subject of debate after 50 years. Is it because we could see the effects of DDT in the pictures of fragile eagle eggs but not in the unseen microscopic world? As Pasteur said, the microbe will endure. Perhaps the fate of the last human is to be consumed by its own microorganisms.
Bäumler AJ. The record of horizontal gene transfer in Salmonella. Trends Microbiol 1997;5:318-22.
Falkow S. The evolution of pathogenicity in Escherichia, Shigella, and Salmonella. In: Neidhardt F, editor. Escherichia coli and Salmonella: cellular and molecular biology. Washington: American Society for Microbiology; 1995. p. 2723-9.
Finlay BB, Cossart P. Exploitation of mammalian host cell functions by bacterial pathogens. Science 1997;276:718-25.
Galán JE, Bliska JB. Cross-talk between bacterial pathogens and their host cells. Ann Rev Cell Dev Biol 1996;12:221-55.
Groisman EA, Ochman H. How Salmonella became a pathogen. Trends Microbiol 1997;5:343-9.
Hacker J, Blum-Oehler G, Muhildorfer I, Tachape H. Pathogenicity islands of virulent bacteria: structure, function and impact on microbial evolution. Mol Microbiol 1997;23:1089-97.
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