I. INTRODUCTION
This article is an introduction to communicable diseases. It is based on the Jared Diamond sources cited at the end of the article.
Diseases can be viewed in many ways, such as what causes them, their clinical symptoms, how they are spread, and the triumph of biomedicine in conquering a few of them.
In anthropology, we look at human strategies for survival. Examples come to mind quickly: best known is the 'subsistence strategy' which is how we get food. Here, we look at survival from the perspective of disease organisms-often called pathogens in biomedicine literature.
This article is written to give you a different perspective on disease and the pathogens that cause them. Our clinical symptoms are part of the pathogen's strategy for survival. Some of them are quite elegant. Of course, you'll say, they don't plot strategy. I know that. So do you. But it is more illustrative for our understanding of them to look at their mechanism of action, not as clinical symptoms, but as strategy used by an opponent in a chess game. .....
We think of pathogens--the bacteria, fungi, viruses and so on as villains who have contaminated our otherwise perfect world. This is a 'Garden of Eden' perception. In the broad historical and evolutionary perspective of biology, life is driven along by competition and what we perceive of as a will to live. Some think that an important reason for sexual reproduction is resistance to parasites.
A related topic to this one is Darwinian Medicine which specifically focuses on understanding disease in an evolutionary perspective. That will be a separate unit later on in this course.
In the first part of this article, we will draw liberally from Jared Diamond. In the second part of this article we will look at parasitism and elegant strategy of Leucochloridium paradoxum and its host, the snail of the genus Succinea. In the article following this one, we'll look at one parasite whose strategy is to make its human host itch, scratch, and seek water for relief. This one is a famous disease of history, appearing even in the Bible. It is commemorated in the caduces, the symbol of the medical professions today. That, however, is getting ahead of our story.
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II. MANIPULATIVE MICROORGANISMS
The common cold is a viral infection. We don't have a cure, yet we seek symptomatic relief with over-the-counter medicaments that earn billions of dollars for the drug manufacturers. The virus for the common cold is indeed a master strategist. At the cellular level, it 'takes command' of cells it invades for its replication. At the genetic level, its mode of action much like reprogramming a computer.
We consider the coughing and sneezing that accompanies a common cold to be an unfortunate nuisance. For the cold virus, however, it is a masterpiece of strategy: the air droplets we expel when coughs contain the virus in large numbers which find their way to a new (unsuspecting) host. Actually, the cold virus lets us off easily. The symptoms are mild. Recovery is rapid and complete.
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Herpes simplex virus is even more elegant. It has devised a way to hide in our central nervous system for life, making its way to the skin surface from time to time in order to spread to another host. The so-called 'cold sore' or 'fever blister' is the clinical expression of Herpes simplex type I. Let us look at its clever strategy for transmission and survival.
To get to another host, it needs moist skin-to-skin contact. The virus 'needs' a moist site that will be touched by another person. So, it produces a surface lesion teeming with the virus. When someone has a fever blister, a kiss or sexual contact provides moist contact to another person. Mucous membranes are an ideal portal of entry into a new host.
Upon entering the body, the characteristic fever blister is produced at the site of entry. The virus then makes its way up the sensory nerves to their cell bodies (called ganglia) near the central nervous system. There the virus takes up residence to lie in wait for years, even decades, waiting for a time of stress and reduced resistance. The virus then makes its way back to the skin surface, produces a lesion, and if the host cooperates (a kiss or sex), it can infect a new host.
Herpes type I is generally in the orofacial area, typically the lips. The Herpes type II infects genital areas and is spread by intimate sexual contact. The virus also 'lays in waiting' in the sensory nerve ganglia and reasserts itself from time to time.
Years ago before gloves became mandatory in dentistry, dental hygienists, dental assistants, and dentists could get an infection in their fingers. It was called herpetic whitlow. It was both disabling and a source of infection for unsuspecting patients. It was also a transmission coup for the virus: from one finger lesion, it could spread to many persons. Gloves have broken the path of transmission: herpetic whitlow has ceased to be a hazard in dentistry.
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As we leave this section, do remember to think of many disease symptoms as strategies by the disease for its own benefit. Lesions such as in chicken pox or syphilis are methods of transmission: they are teeming with organisms. The madness in dogs (a behavior modification) caused by rabies facilitate transmission of the virus that causes rabies. Running noses and coughing spread influenza, whooping cough, and the common cold via the nice wet medium (air droplets) that they require. Diarrheal diseases encourage big time discharges of human waste--all to their advantage.
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III. PARASITES
(My note: technically, a parasite is an organism lives at the expense of another without killing it. If you like terms, a parasoid kills its host. Bees and wasps are examples.)
Our bodies are an inviting environment for other organisms. They are moist, constant in temperature, abundant in food, and above all--mobile. We are a free ride, biologically and physically. Here is a superficial list
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Why a unit on parasites in this course? We live together with other life forms. Our cultural life has been transformed by sedentism and domesticated animals. Along the way we were exposed to epidemic "crowd" diseases. In this article it is argued that our biological evolution has been shaped greatly by disease. If you have any doubt about that statement, consider the impact of AIDS on human society today.
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Our relationship with disease producing parasites, whether they are a virus or a tapeworm, is a sort of arms race. They have the advantage of shorter generations (and faster evolution). In our defense is the immune system that has cells with a short generational life. Our immune cells busily reconfigure themselves in their immunological counterattack on invaders.
Sleeping sickness (African trypanosomiasis) randomly changes its surface proteins, a sort of biochemical chameleon, and thus cleverly eludes the immune response. Given enough time, some parasites and their hosts become mutualists, living together for their common good. A particularly good example are lichens which are a partnership of fungi and photosynthetic algae of great antiquity.
At the cellular level, the mitchondria contained in our body cells seem to be symbiotic unions that possibly began as parasitism long ago. The evidence is this: the DNA contained in mitochondria is more similar to some bacteria than it is to nuclear DNA.
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Malaria, transmitted by mosquitoes, illustrates a "coevolutionary arms race' between the plasmodium and people. In the 1950s, it was discovered that the genetic sickle cell trait confers resistance against malaria. In environments with malaria, it was advantageous to carry the sickle cell trait. This topic is developed in a future unit. But for now, let us know that for millions of people, a disease shaped biologic destiny.
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Why do some parasites seem to intensify their competitive struggle with their host, while some become more benign? One possibility is the mode of transmission. An insect vector, such as in sleeping sickness or malaria seems to contribute to greater parasite virulence. Accidental infection, as in zoonotic* disease, seem to be more virulent. Perhaps the most spectacular of these in our time is the dreaded Ebola hemorrhagic virus.
Many biologists believe that diseases encourage biodiversity and sexual reproduction. In domesticated plants, monocultures of plants such as modern day strains of wheat are more susceptible to plant disease--which, incidentally, are also evolving. In fish, inbred populations are less resistant to parasites than diverse wild populations. The biodiversity fostered by sex enhances disease resistance. The person with greater heterozygosity is more resistant to parasitism.
*(My note: What is a zoonotic disease? Take a moment and clearly learn these concepts now:
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IV. COME HERE, EAT ME!
We need a really good example to clinch our case for disease strategy. Here, we present the most remarkable life cycle of Leucochloridium paradoxum. Its life cycle is illustrated here and is beautifully shown in David Attenborough's TimeLife
video Living Together. For reading, see the cited Scientific American article with its splendid pictures.
Leucochloridium is a parasitic worm that lives in the gut of birds. There it lays eggs which are excreted in bird feces. Its problem is to find a host to complete its life cycle, and then make its way back to other birds.
Its technique is enough to draw the envy of any advertising executive. The eggs are eaten by the Succinea snail (found in Europe and North America). The parasite then turns the tables on the snail and proceeds to eat it from the inside. The snail becomes an incubator, shelter, and nursery in the Leucochloridium's life cycle. It isn't a shy guest, either: It often takes up one half of the volume inside the shell.
The larvae of the worm enter the snail's eyestalks in huge numbers. Strangely, if possible, they will select the left eye talk. There, the larvae assume vivid hues, turning their childhood home into bird food to solve their 'back to the bird' transportation problem.
The snail might as well be advertising with flashing neon signs on its head that read, "eat here!" Its slender eye stalks have been transformed into throbbing, brightly colored 'sausages' that bear more than a passing resemblance to caterpillars. The parasite even changes the snail's behavior, altering its normally reclusive ways and making the snail more accessible to hungry birds.
The birds certainly respond: they can easily spot such snails from the air and make a quick meal of them. The leucochloridium succeeds and completes its life cycle, a masterpiece of strategy. Another bird is infected.
What about the life of the snail before they get eaten? They continue to feed, crawl, and copulate apparently without disability.
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What is the message in all of this? The study of parasitism from an evolutionary perspective offers another dimension in the understanding of disease in general. The heroic solution we all want in dealing with HIV, herpes, and malaria (to name a few) is yet another 'magic bullet' like penicillin or smallpox vaccine. Some in medical research think that we have won all of the eas
Understanding disease as an evolutionary process should help us realize that parasites are flexible, adaptable, and even cunning in their strategies. A new dimension of understanding disease can help provide us with new strategies.
(My note: The 'weak link' in pathogen survival is transmission. This is an important clue to epidemiological management of infectious disease
..... CJ '99
Resources:
Diamond, J. "The Arrow of Disease" in Annual Editions Anthropology 97/98 Angeloni, E. ed. Guilford: Dushkin Publishing Group, 1997.
Diamond, J. Guns, Germs, and Steel. New York: W. W. Norton, 1997.
Ewalt, P. Evolution of Infectious Disease, New York: Oxford University Press, 1994.
Rennie, J. "Trends in Parasitology: Living Together" Scientific American January, 1992 pp 123-133.
Wills, C. Yellow Fever Black Goddess Reading: Helix Press Addison-Wesley, 1996.