Note: These materials are intended as supplements for students in Ant. 301. These pages are in development and will contain errors.

Sustainable development and sustainable agriculture


Ecology and Disease


Water Treatment


AIDS


Radiation

Paul and Anne Ehrlich (1990; pages 180-181) suggest three changes that if implemented, might leave some high quality of life for future human populations:

1. Halt human population growth as quickly and as humanely as possible, and embark on a slow population shrinkage toward a size that can be sustained over the long term while allowing every person the opportunity to lead a decent, productive life.

2. Convert the economic system from one of growthism to one of sustainability, lowering per-capita consumption so as to reduce pressures on both resources and the environment.

3. Wherever possible, convert to more environmentally benign technologies.

(return to outline)

A catastrophic feature of most modern "developed" societies is that the ecological features of their subsistence systems are not sustainable. They are fueled by nonrenewable resources or fed by an agricultural technology that eventually destroys or depletes productivity. In some third world countries that still have relict islands of forests, conservationists are able to discuss the possibility of sustainable development. They propose to limit development to those types of activities that are renewable and thus sustainable within the limits of the local carrying capacity.

Unless they are fortunate enough to have valuable petroleum or mineral deposits, many of the large ranches of the southwestern United States are "land poor." In some areas, the local property taxes (to support schools and local government) are greater than the potential income from livestock if the ranch is operated below its carrying capacity. Those lands that fall in the reach of urban areas are taxed on their development value as subdivisions rather than on their food producing value. As new subdivisions are planned, preference for development is often given to cropland, since it is cleared and relatively flat in topography, attributes that lower construction costs.

In the past, our culture encouraged an intensive and damaging type of "high input" agriculture. Rules governing taxation and governmental subsidies encouraged overstocking, clearing, and planting procedures that maximized soil erosion, irrigation, and use of fertilizers and pesticides. This system, which is the basis for most of the world's food exports, produced great surpluses of food largely as a result of better varieties of plants developed by plant geneticists. However, it has become clear that these are short-lived ways of producing food. Even with improved plant genotypes, eroded fields are not as fertile. The state of Iowa, for example reports a loss of more than one-half of its topsoil, and the United States as a whole has lost more than one-third of its topsoil to erosion. This relatively thin fertile resource requires hundreds of years to regenerate what can be lost in a single planting season. The estimated rate of topsoil loss for the United States is about 18 tons per hectare per year. Increasingly larger amounts of chemical fertilizers produced progressively lesser yields as soils lost their organic components. Accumulations of mineral salts from irrigation water lower soil quality and eventually make fields unusable. There are limits to the productivity of contemporary agribusiness, and the food demands of the United States population have reached the point where everything must go well, including the weather, for our annual production of grain to meet our annual consumption. These problems have been addressed by legislation, perhaps the most important being the Food Security Act of 1985, that promotes soil conservation.

A new kind of "low input" agriculture is being promoted in the United States. It emphasizes crop rotation instead of extra pesticides, and incorporates a minimum of plowing in order to minimize soil erosion. Any decrease in productivity is balanced by lower costs and longer sustainability. In many ways, the "new" agriculture is similar to farming practices prior to 1945. It is based upon three principles: (1) adapting the agricultural practice to the environment of the region, including the selection of crop species appropriate to that environment; (2) optimizing the use of biological resources such as biological pest control, organic fertilizers, cover crops, and crop rotation; and (3) instituting procedures that minimize the use of fossil fuels and minimize the changes in the natural local ecosystem. In brief, the idea is to conserve soil and water while discouraging pests.

Soil erosion is one of the farmer's worst problems, and one of the most serious threats to the local environment. Erosion reduces water-holding capacity, speeding run-off and reducing vegetation. Organic matter and finer soil particles are eroded faster than the least fertile soil components. Probably the most effective way of reducing erosion is to reduce the amount of plowing. The spread of contour planting and no-till technology from China seems to produce increased yield of both cotton and corn while reducing erosion by nearly one-half. Some of the common weeds in corn fields (Bidens pilosa in Mexico and Brassica kaber in the United States) actually secrete compounds that attack corn-destroying fungi and nematodes. By managing the weeds, increased corn yields were achieved without a significant loss of soil nutrients.

One of the greatest misconceptions about modern agriculture is that we successfully manage pests. United States farmers lose about 37% of their total crop production to pests in spite of the use of about 350,000 tons of pesticides annually. In fact, although there are yearly fluctuations, crop losses due to insects have increased from 7% in 1945 to 13% in the present, during which time insecticide use increased tenfold. This increased insect damage is largely due to acquired resistance to pesticides, lack of crop rotation, poor field sanitation, and increased farm monoculture. Insecticides also reduce natural enemies of pests and kill pollinating insects necessary for production of some crops. Surprisingly, the low-till techniques can assist in the control of some insect pests since diversity encourages insect predators. Combined with biological controls, judicious use of insecticides, substitution of green manures for fertilizers, and the use of cover crops, crop rotation, and long-term planning, farms of the future may look surprisingly like those farms of the 1940s.

The mesquite tree of the American Southwest is an example of how our value systems sometimes make improvements difficult. A small hardwood, the mesquite produces a crop of edible beans and is an important source of nectar, gum, and pollen to the insect communities of its ecosystem. The beans are particularly important to agriculture since they mature in dry seasons, when other forage is minimal. Because its leaves are small and its canopy sparse, grass grows in its light shade. It has deep tap roots, finding its water far below the subsoil, and thus can bear a large crop of beans when surface grasses are devastated by drought. As a legume, it produces nitrogen-rich substances in its root nodules. Mesquite wood is valued for its hot, aromatic cooking fires, but its thorns are cursed by operators of pneumatic wheeled vehicles. In the 1950s, the practice of bulldozing and root-plowing large acreages of mesquite brush land began to convert the "useless" brush lands to cattle grasslands. Ranchers though they were "destroying" the brush, when in reality the process of root-plowing distributed the nitrogen-bearing substances from the root nodules, effectively fertilizing the plowed areas, and grass flourished. Mesquite regenerates quickly. Livestock eat the bean pods during the season of bean production, every pile of cow manure contains germinating mesquite seeds. Fields are root-plowed every 7 to 10 years to return them to grasslands. However, mesquite became labeled a "pest" and ranchers often went to great lengths to eliminate the trees. The increase in grass production after root-plowing was misinterpreted as evidence that the trees took water and nutrients away from the grass. Indeed, the trees do not take nutrients or water from surface grasses; rather they are sources of natural fertilizer when they are plowed. No such benefit accrues when a herbicide is used to kill mesquite trees. When understood and managed, the "pest" tree of the past decade becomes a useful component, a cover crop, of "low input" ranching. (return to outline)

Typhus

We tend to forget or have never been aware of the impact that microorganisms have exerted on geopolitical events. In a real sense, disease has played a major role in shaping world political history. For example, in June of 1812, Napoleon assembled an army of about 600,000 men and invaded Russia. Russia was already at war with the Turks and its army of 258,000 troops was in no position to resist Napoleon. But Napoleon's army fell victim to typhus (Rickettsia prowazekii), a disease transmitted by lice, and to dysentery, an acute infection of the bowel caused by the use of contaminated water supplies .

Bacteria	Intestinal Protozoa
Typhoid fever (Salmonella)	Amebiasis (Endamoeba)
Paratyphoid fever (Salmonella)	Balantidiasis (Balantidium)
Cholera (Vibrio)	Giardiasis (Giardia, Trichomonas)
Bacillary dysentery (Shigella)	Isosporiasis (Isospora)
Enteritis (Salmonella)
Food poisoning (Salmonella, Staphylococcus, Streptococcus. Clostridium)

Rickettsia are small parasites that live and multiply in arthropod tissues. They resemble bacteria in size and visibility, yet require living host cells for growth as do viruses. European typhus is caused by Rickettsia prowazekii, a microorganism transmitted by the human body louse, Pediculus humanus. The body fluid of the louse, louse feces, or a crushed louse are the sources of human infection. Rickettsia remain virulent in dried louse feces for months, contaminating clothing and skin. Abrasions, dusting of the eyes, or inhalation of Rickettsia introduces the microorganism into humans. Clothing passed from one victim to another also constitutes a vector for contagion. After an incubation period of one to two weeks, there is a rapid onset of fever, severe headache and extreme prostration. A rash appears about the fifth day of symptoms and in epidemics the mortality rate reaches 70%.

Though typhus was endemic in Poland and Western Russia, Napoleon's armies were not prepared for it. The first sickness occurred near the end of July, killing or disabling 80,000 troops (Robins, 1981). As health conditions deteriorated, dysentery added to Napoleon's problems. It was a dry autumn and clean water supplies were almost nonexistent. By the time Napoleon faced the first Russian troops in opposition, his army had been reduced by disease to 130,000 men. Napoleon's initial victory cost him another 28,000 battle casualties, but the toll from typhus and dysentery continued. Finally, with a shrinking army from disease losses, Napoleon had to abandon Moscow and flee back to France. He was harassed by Russian troops, but they too were handicapped by these diseases as they pursued Napoleon. Only 40,000 of Napoleons troops survived the campaign, and of these troops only 1000 were ever again fit for service. Napoleon had lost his most experienced troops and leaders. His defeat also encouraged his enemies to form alliances that later defeated him. His military genius and charisma were outdone by a couple of microorganisms.

Disease also played a major, perhaps dominant, role in the colonization of America. Amerindians had little natural immunity for chicken pox, the common cold, diphtheria, gonorrhea, influenza, measles, scarlet fever, smallpox, tuberculosis, typhoid, yellow fever, or whooping cough. These are only a few of the diseases that Europeans introduced to the New World. Shortly after contact, epidemics among the Amerindians were common. In many areas, at least half the population was lost and local political institutions badly shaken. Epidemics preceded the conquest of both Mexico and Peru in the 16th century. The new microorganisms caused continued annual population loss among Amerindians.

Whereas disease facilitated conquest of the Americas, it inhibited colonization of Africa. Table 6-9 lists a few African microorganisms and their vectors. These diseases are inhospitable to Africans as well as colonists, but most colonists were unprepared for the conditions and mortality rates they encountered. For centuries the tsetse fly, mosquitoes, and parasitic worms have protected much of Africa from development.

The Most Damaging Diseases Affecting Europeans in Africa

Disease	Vector
Malaria, yellow fever, dengue fever, elephantiasis	Mosquito
Bubonic plague, viral typhus	Flea
Kala azar	Sand fly
Cholera, typhoid, and dysentery	House fly
Relapsing fever	Tick
Viral typhus	Louse
Sleeping sickness	setse fly
Viral jungle typhus	Mite

Modified from Rothschild (1981), p. 165

Travelers moving into an area found themselves subject to diseases of that locality. They also transmitted microorganisms from their home areas to the colonies, and as they traveled these people served as vectors to move microorganisms to new locations. For example, Stanley's famous 1888 expedition to the Congo carried West African sleeping sickness to new areas.

Pandemics still effect most of the world's human population, influenza being the most familiar to modern Americans. Even this microorganism exerts a strong influence on human affairs. Although the mortality rate was low (about 4% of those infected compared to 75% or higher for bubonic plague victims in areas without modern hospitals), some 20 million people died in the 1918-1919 pandemic. There is always the danger as we become a world community that we will unleash a microorganism and its vectors from some local area upon the global community of humanity.

Crowd Diseases and Zoonoses

Disease has an important demographic component. Some diseases are persistent even in small human populations (chicken pox, hepatitis B, herpes simplex, herpes zoster, infectious mononucleosis, and cytomegalovirus) because of their modes of transmission. Other infections appear to be crowd-dependent, that is they are one-time epidemics that require high population densities to be sustained (influenza, measles, mumps, rubella, parainfluenza, and polio). If one counts the number of human zoonoses (diseases of animals that may be secondarily transmitted to humans) that are unique to one continent, Central and South America rank the highest with 37% of the world's total (Way, 1981; page 259). Why did the Americas have so many zoonoses that did not become "crowd infections?" Perhaps this is related to the Old World origins of humanity or to the particular history of agriculture and cities in the two areas, but it seems that the crowd diseases of humanity came from Europe and Africa.

Measles

Measles (rubeola) is a good example of a crowd disease. The microorganism is a virus that is transmitted by droplets expelled or taken in through the upper respiratory tract. It has an incubation period of about 10 days and the victim is contagious beginning about three days before the skin eruptions appear. Those individuals who survive its infection are permanently immune. The only susceptible people are those born after the epidemic has run its course. Only a community population greater than 200,000 people will have a birth rate large enough to provide susceptible children to keep the disease from become extinct. One of the most dramatic epidemic of measles occurred in the Fiji Islands in 1875. The disease was unknown to the Islanders and a combination of illness and social disorganization may have produced as many as 40,000 casualties. Measles appears to have declined in pathogenicity before prophylactic immunizations were available, similar to the decline described for Myxomatosis and the European rabbit. Rubeola should not be confused with the less virulent German measles (rubella) whose major importance is the danger of malformations to the fetus if the mother is infected in early pregnancy.

Plague

Plague is a natural disease of certain rodents that is produced by the bacillus Pasteurella pestis. Rodent hosts often exhibit only a mild or non-fatal infection. Pasteurella is quickly killed by drying in sunlight, but in moist conditions it can remain virulent for up to a month. In cold or freezing conditions, these bacilli remain viable for prolonged periods. Fleas spread the plague bacillus from animal to animal when they bite their rodent host for blood meals. When an infected flea bites a human, the bacilli enter the circulatory system where they accumulate and multiply in lymph glands, especially the armpit or groin. After an incubation period of two to four days there is an abrupt onset of fever, rapid pulse, and mental dullness. The bubo, an inflamed and painful enlargement of a lymph gland, forms in about 75% of cases, usually in the inguinal, axillary, or cervical lymphatic plexus. The plague bacillus can also produce pneumonia in the lungs which can be spread by droplet contagion. Freezing temperatures and high relative humidity favor transmission of the pneumonic form of plague, since sputum and cough droplets retain virulent bacilli that can infect other humans. The pneumonic plague is the most deadly form of the disease.

Crusaders unintentionally brought the black rat (Rattus rattus), a native of India, to Europe, where it displaced indigenous rats. The black rat especially invades human habitations and its fleas seek blood meals from humans. The plague bacillus is indigenous from southern Russia into China, and in the 14th century there was a plague outbreak in the Crimea. Some Italian traders were trapped in a small Crimean port that was besieged by Tartars. Plague broke out among the Tartars, forcing the siege to be lifted and allowing the Italian traders to escape by ship. Though none of the shipmates exhibited plague, the rats and fleas on board ship were probably infected when the ship returned to Genoa in 1347. There was a terrible epidemic of pneumonic plague in the winter of 1347-1348, and of the bubonic plague the following summer, ultimately devastating Europe and producing changes that hastened the end of the peasantry system and medievalism. It strengthened the Church holdings in property but it decimated the priesthood, leading to a decline in educational level among church leaders. Its overall effects are unknown, but the Black Death appears to have promoted the rise of modern governmental and religious institutions in Europe.

For three centuries, the Black Death was a periodic threat to Europe where the rodents were contaminated with plague. It may have ended when the black rat was replaced by the brown rat, Rattus norvegicus, from Asia. The brown rat, also known as the sewer rat, is not so attracted to human habitations and its fleas do not readily bite humans. The black rat became the wharf rat or the common ship rat, transporting plague to every port in the world and infecting local rodent populations. Today plague is endemic in rodents of the western USA, the steppes of Asia, the veldt of Africa, and South America. It is a threat anywhere humans live with rats, especially black rats from waterfront warehouses.

Malaria

The most harmful disease of the modern world (hundreds of millions of people affected each year) is malaria, a disease produced by a protozoan of the genus Plasmodium that spends part of its life cycle in humans and part in an Anopheles. When an infected mosquito bites a human to get a blood meal, some needle-shaped Plasmodium sporozoites travel from the mosquito's salivary glands into the human host. The human liver is invaded by these protozoans, where they multiply. About 12 days after the insect bite introduced the parasites, the protozoans begin to emerge in quantity from the liver into the blood stream in the form of merozoites, small protozoans that feed upon red blood cells, multiplying every 48 or 72 hours, depending upon the malarial species. The toxic byproducts of merozoites produces the shivering and fever of malaria. If the human host does not die, the body's immune system and phagocytes begin to destroy most of the parasites, but by this time a new phase of the organism has appeared in quantity. This new phase is sexually differentiated (male and female phenotypes) and when a mosquito takes a blood meal from a human at this time, the male and female malarial organisms mate in the mosquito's intestine. Over a period of about 7 to 20 days, depending on the malarial species, their progeny invade the mosquito intestine and form sporozoites that pass to the mosquito salivary glands.

Three major species of Plasmodium are known to be pathogenic to humans - Plasmodium vivax (attacks reticulocytes and does not usually damage mature erythrocytes), P. malariae (which invades only aging erythrocytes) and P. falciparum (which invades all red cells and is the most deadly in humans). Other malarial species are known, but they are relatively unimportant to humans. Since parasitized blood cells tend to agglutinate they disrupt circulation. Acute malaria disrupts body chemistry, including water balance and blood viscosity. Symptoms include a recurring fever, headache, vomiting, and jaundice. Victims of malaria become adept at diagnosing recurrent episodes. Immediate mortality rates are low for all forms except P. falciparum where it reaches 25% in some localities. Mortality rates reach 50% in blackwater fever, a complication in which the urine turns dark red or black as the kidneys try to cope with advancing hemolysis and a disturbed body chemistry.

If an area has conditions that facilitate the breeding of large numbers of Anopheles mosquitoes and a substantial human population with malaria, each person will be repeatedly reinfected throughout their lives. Infants acquire the disease early and those not resistant will die in early life. Indeed, the highest mortality rates from malaria occur between the ages of 1 and 4 years. Malaria also increases vulnerability to other infections. In many non-industrialized countries, malaria and malnutrition combine to weaken a child's resistance to additional infections.

Control of malaria rests primarily on reducing the number of Anopheles mosquito bites that humans receive that could be infectious. Eliminating breeding places for mosquitoes, spraying insecticides around human residences to kill adult mosquitoes, and using screens to protect humans greatly reduces the rate of malaria. Drugs can be taken regularly to suppress development of the infection. DDT is sprayed on the walls and ceilings of houses where it kills mosquitoes when they rest on these surfaces. This practice is effective but it has selected for strains of mosquitoes with different resting habits and DDT resistant phenotypes.

Yellow Fever

Yellow fever is an example of a zoonosis that belongs to a particular class of viruses called the arboviruses. Several hundred similar viruses have been recognized to date and their ecology makes them, to a certain extent, "protectors" of the rain forest. Each has its natural host (a nonhuman primate, a bird, or other animal), and an animal vector (usually an insect) that transmits the virus from host to host. Yellow fever, normally a disease of non-human primates, seems to play an important role in regulating population levels of some species, especially howler monkeys. When humans enter an environment harboring an arbovirus, they risk an infection that is sometimes lethal or disabling. The yellow fever virus is primarily transmitted by the mosquito Aedes. Incidentally, as in malaria transmission, only female mosquitoes spread yellow fever. Male mosquitoes do not bite or have blood meals. After the bite by an infected mosquito, the virus multiplies rapidly. Following an incubation period of 3 to 6 days there is a sudden onset of fever and chills. At this point and for the next three or four days, the virus is recoverable from the patient and mosquitoes that have blood meals will become infected. Infected mosquitoes are not capable of infecting mammalian hosts until a viral incubation period of more than a week has passed. Fever peaks about the second day of symptoms and a patient exhibits an unusual combination of a dropping pulse rate in the presence of a high temperature. After three or four days, the temperature returns to normal. Jaundice, hemorrhage, and nausea may occur. Gastrointestinal hemorrhage producing bloody vomitus or a secondary rise in fever are ominous signs. Death is usually due to renal failure. The usual mortality rate is about 7% but can be as high as 50% during epidemics. Survivors are permanently immune to repeated infection. There are immunizations available against yellow fever, but most arboviruses are not economically important enough to stimulate vaccine development.

Parasitic diseases are endemic (constantly present), and have different consequences than epidemic diseases that sweep through a population and disappear until the next outbreak. Endemic diseases too, often have animal vectors that transmit the organisms from host to host, and play an integral role in the life history of the disease. The more common parasites place all who live in their habitats at risk, and it is common for an individual to be infected by several infectious agents at the same time.

The protozoan family Trypanosomidae, which is of great ecological importance, contains two pathogenic genera, Leishmania and Trypanosoma. The various leishmaniases are usually transmitted by biting flies of the genus Phlebotomus. The American form of trypanosomiasis, Chaga's disease, is a lethal infection transmitted to humans by the bite of insects of the family Reduviidae, especially the genus Panstrongylus, the "assassin" bug. Old world trypanosomiasis, transmitted by tsetse flies (Glossina), produces African sleeping sickness, a chronic infection of the central nervous system, characterized by mental and physical apathy, coma, and death. Several species of Trypanosoma inhabit different regions of Africa, affecting humans and livestock as well as native ungulates. The tsetse fly is infected when it feeds on the blood of an infected human or animal. Between 18 to 34 days after the infecting meal, trypanosomes have multiplied and their infective metacyclic forms can pass into new hosts through the tsetse fly's salivary ducts. The first phase of infection in humans is characterized by fever and swelling of lymph nodes, especially the cervical nodes. The second stage of the disease is marked by progressive headaches, mental confusion, and hysteria. The course of the infection culminates in lethargy, slow speech, and a somnolent "sleeping" state. Secondarily the somnolent phase is accompanied by marasmus with increasing wasting and weakness. Death may result from malnutrition, another infection, or from the progress of the trypanosomiasis disease itself.

The distribution of tsetse flies that are potential vectors is much greater than the distribution of dangerous Trypanosoma. Human cultivation and pastoralism destroyed forest vegetation in some areas, promoting the savanna vegetation preferred by tsetse flies. Many breeds of cattle, horses, and other livestock suffer fatal infections if bitten by tsetse flies carrying trypanosomes that occur naturally in native ungulates. This meant that many of the savanna ecosystems were protected from encroachment by stock-rearing. After the explorations of the 19th century, mobility of the human populations dispersed trypanosomes dangerous to humans from infected areas to other regions where suitable tsetse fly vectors were already established. A major outbreak of sleeping sickness may mean that an agricultural area must be abandoned by humans, since trypanosomes persist as long as a host reservoir population is available. A dilemma of tsetse fly control measures is that overgrazing by livestock and a total loss of savanna wildlife often follow successful fly eradication. (return to outline)

Water Treatment

Napoleon's unsuccessful invasion of Russia underscores the importance of public health measures such as immunizations, hygiene, and water treatment in the modern world. An immediate risk to any individual in an unindustrialized country is a contaminated water supply. Fecal contamination of drinking water or food produces exposure to diarrheal diseases, bacteria, protozoa, and certain helminthic parasites that produce inflammatory infections of the intestinal tract. The most devastating organisms affecting humans are Escherichia coli (colon bacillus), Endamoeba (amebic dysentery), Salmonella (typhoid fever), Shigella (bacillary dysentery), and Vibrio (cholera). If neonates are given infant formulas prepared with contaminated water, diarrheal diseases are established early and result in high mortality. These diseases often interfere with nutrient absorption and retention as they dehydrate and drain an infant of critical electrolytes. Hence mothers in less than optimal environments are especially encouraged to breast feed their children. Cholera and hepatitis are scourges that follow natural or man-made disasters, floods, wars, earthquakes,... The classic problem of humanity since the rise of agriculture is that affluence breeds effluence, and contaminated water and soil produce health risks. Urban effluents are often contaminated as well with heavy metals and other toxic materials that make them dangerous even when processed by modern waste systems. Runoff waters from our yards and gardens are contaminated with petroleum, pesticides, fertilizers, and fecal waste from pets. The United States has the technology to recycle most of our water and nutrients in the ecosystem but our value systems do not yet put enough pressure on individuals to handle resources wisely.

AIDS

The history of AIDS (acquired immune deficiency syndrome) research is still being made, and only the future will determine which steps constitute breakthrough discoveries and which were false possibilities. The first identified human retrovirus, human T-cell leukemia virus type I or HTLV-I, was isolated in 1980. Prior to this, some animal retroviruses, such as feline leukemia virus were known to produce AIDS-like immune suppression in cats. AIDS as a new human disease was first recognized in 1981. The following year, the Centers for Disease Control reported evidence that AIDS was a new infectious disease. The first likely hypothesis was that AIDS was probably caused by a retrovirus similar to HTLV-I. HTLV-I is the only type of leukemia known to be transmitted through sexual contact or blood transfusions. HTLV-I seemed to disrupt the function of T4 cells, a major feature of AIDS. Intensive research attention turned to the HTLV type retroviruses and a number of different new viruses were quickly identified. In May 1983, another virus, the lymphadenopathy-associated virus or LAV, was isolated by Luc Montagnier at the Institut Pasteur in Paris. Other researchers reported that a HTLV-III virus could be isolated from AIDS patients. Evidence began to accumulate that LAV and HTLV-III were the microorganism responsible for AIDS. By 1986 researchers began to identify related viruses in nonhuman primates. The discovery of an AIDS-like virus in African green monkeys that did not appear to be pathogenic to its hosts but which produced immunodeficiency and lymphomas when transmitted to macaque monkeys stimulated a broader survey for simian AIDS viruses. As the number of known variants of AIDS viruses expanded, the International Committee on the Taxonomy of Viruses simplified the nomenclature by designating the human AIDS viruses as human immunodeficiency viruses (HIVs) and the monkey viruses as simian immunodeficiency viruses (SIVs). Different varieties are simply numbered. Thus, LAV and HTLV-III became HIV-I. As additional varieties are found, the are numbered HIV-II, HIV-III, etc.

Acquired immune deficiency syndrome is an example of a disease caused by a microorganism that has the potential to affect world populations and world history as much as did the plague during medieval times. The breakdown of the immune system is due to proliferation of human immunodeficiency viruses (HIV), members of a special class of virus called retroviruses. These retroviruses that have the ability to make a DNA transcription of part of their RNA and integrate it into a eukaryotic chromosome. Though retrovirus infections can alter the functioning genotype of infected cells, most endogenous retroviruses are not pathogenic. However, HIV infections appears to impair the immune system by attacking T-cells in the bloodstream. Once the immune system is dysfunctional, the infected host falls victim to other diseases. Once the host exhibits symptoms of AIDS-related complex (ARC), the disease is always lethal.

HIV is transmitted through certain body fluids, and is usually referred to as a sexually transmitted disease. The viruses are quickly destroyed by exposure to air or dehydration. The usual medium is semen. It is five times more likely to transmit HIV from male to female than from female to male during intercourse. Of course any activity involving exchange of body fluids from one person to another could constitute exposure (sexual activities, blood transfusions, intravenous drug use with a shared needle). The time interval between exposure to the virus and onset of AIDS symptoms varies greatly. Production of anti-bodies to the microorganism, the earliest detectable indication, may be delayed as long as 15 years. However most individuals become serum positive within months. Unfortunately AIDS in the U.S. has been mistakenly labeled a disease of homosexuals and minorities. In fact it is an infection of the general public, sustained by unsafe sexual practices and contaminated intravenous needles.

There are similar retroviruses in other animals, but most relevant to AIDS research are those reported from our primate relatives. There is a simian immunodeficiency syndrome (SIDS) that occurs when viruses which are not pathogenic to their normal hosts are transmitted to new host species. Since humans in many tropical areas butcher and eat nonhuman primates, this may be a source of pathogenic viruses in humans.

It is also possible that the virus could have been released into the world human population from a smaller, relatively isolated human deme, one in which the AIDS symptoms were not recognized as a constellation of related traits.

Viruses also mutate, and sometimes a small genetic change produces a lethal transmutation of phenotype. For example, a mutation occurred in a mild avian influenza virus among poultry in 1983. The pathogenic new virus killed more than 17 million chickens in the next six months. Because viruses lack the "proofreading" and error correcting mechanisms seen in eukaryotic cells, the rate of viral mutants is much higher.

The positive outlook of the AIDS epidemic is that it can be curtailed by modifications in human sexual practices such as reduction in promiscuity and use of condoms.

Ebola

As humans become a single global community, we increase our contact with local or regional zoonoses, and we also become at risk as a global deme if a zoonosis erupts in epidemic form. We have experienced some "close calls" in recent years. For example, in 1976 there was an outbreak of Ebola virus in Zaire and Sudan. This infection with a mortality rate greater than 90% quickly killed many of the doctors and nurses treating infected patients. At the time, the route of infection was unknown. Though the epidemic produced hundreds of fatalities, it fortunately did not become regional. In 1989 and 1990, some monkeys imported into the U.S. from Asia were found to have Ebola-like viruses, raising the specter of a virulent lethal microorganism released into human populations. The later variety of ebola was particularly frightening because, unlike the other ebola strains that required blood or fluid contamination, it could be transmitted by aerosol.

The special properties of some "Ebola-like" viruses sound like an invention in a science fiction horror film. They share properties of aerosol transmission (like measles), transmissibility to rodents, short incubation periods, and high fatality rates among humans. One can readily imagine a tourist bringing the virus by jet plane to an urban area, producing a modern day replay of the black death of the 14th century. (return to outline)

Wilhelm C. Roentgen (1845-1923) discovered and described the physical properties of x-rays in 1895. It was common in following years for scientists and engineers to x-ray their hands as a method for checking the output of x-ray tubes. The phenomenon of radioactivity was discovered by A. H. Becquerel (1852-1908) the following year, when he placed uranium potassium sulfate on a photographic plate covered in black paper. Soon afterward Becquerel noted a burn on his skin beneath the vest pocket in which he carried his uranium sample. Thereafter many of the scientists who worked with x-rays noticed skin lesions on their hands. Ernest Rutherford (1871-1937) demonstrated the ionization effects of radiation in 1899. At the same time Marie Curie (1867-1934) and her husband Pierre Curie (1859-1906) tested numerous chemical compounds for radioactivity. She discovered, isolated, and named several radioisotopes, including polonium and radium. Rutherford and the Curies independently described most of the properties of radiation, including induced radioactivity. Rutherford and F. Soddy (1887-1956) measured and recognized the concept of half life. X-rays (or roentgen rays) quickly found their way into medical practice, and in the first few years, this life-saving device took a toll on physicians, nurses, and engineers. Before the danger was recognized, there were 336 fatalities thought (in retrospect) to be from radiation exposure, 251 from cancer, and 56 from leukemia. Marie Curie died of radiation-induced leukemia in 1934, seven years after the biological effects of radiation were first demonstrated by Hermann J. Müller (1890-1967). Müller demonstrated that X rays produced artificial transmutations of genes, changes that are now called mutations.

This Table summarizes a vocabulary for the measurement of radiation.

Vocabulary for Radiation Energy Measurement

Curie = 37 billion atomic disintegrations per second - the number of atoms disintegrating per second in one gram of radium

Erg = the work done by a force of one dyne acting over a distance of one centimeter

Dyne = the force needed to accelerate 1 gram of mass one cm per second

Roentgen unit = the quantity of radiation that induces 1 cc of air to acquire 1 electrostatic unit of charge - roughly equivalent to absorption of 87 ergs per gram (r)

RAD = the absorption of 100 ergs of energy per gram (radiation absorbed dose)

REM = RAD x RBE

RBE = relative biological effectiveness

Note: Since different types of radiation have various biological consequences, the REM, which stands for "roentgen equivalent man", is adjusted to express the magnitude of expected biological consequences. One REM is a dose of radiation from any source that produces the biological effects equivalent to one RAD of x-rays.

There are two types of radiation; electromagnetic waves and high-energy particles. Electromagnetic waves are emitted by radio and radar transmitters (radio waves), hot bodies and excited gases (infrared, visible, and ultraviolet light), atoms struck by high-energy particles (x-rays and gamma rays), radio-active substances (x-rays and gamma rays), and cosmic sources (x-rays and gamma rays). Atoms are composed of a nucleus surrounded by a cloud of electrons. When any of these components (electron, proton, alpha particle, neutron,...) are separated from their atom, they become high energy particulate radiation that is capable of transferring energy to substances through which they pass by collisions with atoms. Wave radiation transfers energy to planetary electrons, bringing their atoms into levels of excitation that make them more chemically reactive. If enough energy is present, the electrons may escape from the atom, producing ionization.

The biological effects of radiation are observable in both germ and somatic cells. Genetic effects are measurable in the form of mutations in germ cells, a process first demonstrated by H.J. Müller in 1927. Exposure of germ cells to 30 r of high intensity x-ray exposure or 100 r of low-intensity exposure doubles the mutation rate above the background level. The second form of radiation effect is seen in somatic cells, where mutation produces clones or cell deaths. Somatic mutations can result in mosaic tissues, those derived from cells with varying genotypes and that usually have contrasting properties. Radiation is known to be carcinogenic, even at low levels.

In the natural world, there are numerous sources of radiation exposure. Direct solar and cosmic radiation is somewhat dependent upon altitude since the intervening atmospheric gases shield the surface:

Altitude / Cosmic Radiation
sea level/ 28 millirads
1,600 meters (Denver, CO)/ 50 millirads
3,200 meters (Leadville, CO)/ 125 millirads

Cosmic radiation produces radioactive isotopes of tritium (₁H³) and carbon (₆C¹⁴) from nitrogen (₇N¹⁴) in the upper atmosphere:

₇N¹⁴ + neutron -> ₆C¹² + ₁H³

₇N¹⁴ + neutron -> ₆C¹⁴ + proton

Note that the atomic number, the number of protons in an atom, is written as a subscript preceding the symbol N (nitrogen). A superscript following the symbol denotes atomic weight, the average mass of atoms of that isotope. The human exposure from ₁H³, usually found in water, is about .001 millirem per year. Unstable ₆C¹⁴ moves from the atmosphere to the food chain during photosynthesis that produces carbohydrates from carbon dioxide. The average human exposure from ₆C¹⁴ is about 1.3 millirem per year. Other potentially dangerous isotopes, notably radon (₈₆Rn²²²), occur in air.

Natural terrestrial sources of radiation exposure in the form of radioactive isotopes emit radiation as they decay. Potassium (₁₉K⁴⁰), rubidium (₃₇Rb⁸⁷), and other naturally occurring terrestrial isotopes produce an average exposure of about 50.4 millirads per year. About 42,000 deaths (cancer and leukemia) are thought to occur from natural radiation in the United States each year.

Radiation from human activities only adds to the dangers from natural sources. Krypton (36Kr85) gas is very soluble in body fat. Iodine (53I129 and 53I131) accumulates in the developing thyroid. Strontium (₃₈Sr⁸⁹ and ₃₈Sr⁹⁰) behaves somewhat like calcium in the body and is deposited in bone. Plutonium (₉₄Pu²³⁸, ₉₄Pu²³⁹, ₉₄Pu²⁴⁰, and ₉₄Pu²⁴¹)) and radium (₈₈Ra²²⁶) also accumulate in bone. The above-ground atomic bomb testing in 1958 alone produced isotopes that could ultimately cause about half a million deaths, many of them embryonic or neonatal. Some midwestern newspapers of the late 1950s periodically contained notices to the public, "Don't drink the milk today. Fallout contamination is too high."

It is not possible to distinguish a case of leukemia stimulated by natural radiation and one of industrial origin. Benefactors of, radioisotopes in industry or those who use nuclear-generated electricity are usually not the persons who are at increased risk. In fact, the use of radioactive isotopes in industry is quite safe from a probability point of view. If a small increased exposure to a population of 250 million people produces only 4,000 fatalities, the chances of any one person being affected is only 1 in 62,500. Those are favorable odds and usually would not concern anyone. Of course the rationale does not sound as attractive to any of the 4,000 victims (or their families) after they have been diagnosed. How safe are low doses of radiation? The lowest exposure that demonstrably increases the risk of cancer is between 20 and 49 REM. In theory a modern chest x-ray requires about 0.3 REM exposure. Three chest X-rays of 10,000 people (1 REM exposure each), should produce between one and three extra cases of cancer. Of the 10,000 people, about 2,000 would acquire cancer without the x-rays. Thus it is statistically impossible to validate the presence of one extra case among the 2,000 from other sources. Consequently we do not have reliable measures of the effects of low-level exposure.

No product or activity that increases human radiation exposure is safe. Someone will become ill or die. The only question is which activities are worth the cost. The next generation has been given a legacy of additional illness and death because their parents and grandparents put them at increased risk for short-term benefits. The nuclear industry developed a vocabulary for describing malfunctions without using inflammatory words.

Transient - a malfunction
Event - malfunction
Scram - unscheduled shutdown
Abnormal evolution - failure to function properly
Normal aberration - malfunction
Unauthorized diversion - theft
Rapid oxidation - fire
Power excursions - out of control
Unplanned hypercriticality - out of control
Spontaneous energetic disassembly - explosion
Nuclear bonus material - waste

In an age of nuclear weapons and possibilities of nuclear accidents, we should understand the immediate consequences of high levels of exposure .

Biological Effects of Radiation (Modified from Hiroshima and Nagasaki, page 128)

r /Effect

0.001 2.5 days normal background dose

0.01/ not detectable

1.0/ not detectable

10.0 /loss of lymphocytes

100.0 /radiation sickness (loss of blood cells, nausea & vomiting)

200.0 to 600.0 /lethal dose (LD50; half will die; severe diarrhea, depression of blood-cell and platelet function, damage to intestinal mucosa)

1,000.0 /all die from radiation sickness within 30 days

10,000.0 /immediate disorientation; death in hours

100,000.0 /death to some microorganisms, death to fruit flies

1,000,000.0 /death to some bacteria

10,000,000.0 /death to all living organisms; some proteins denatured

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Tissues most at risk are those that are rapidly growing, that is, undergoing meiosis or mitosis.


RADIOSENSITIVITY OF SPECIALIZED TISSUES
(Taken from S.L. Robbins, Pathologic Basis of Disease, 1974)

HIGH SENSITIVITY
lymphoid tissue
hematopoietic cells (marrow - source of blood cells)
germ cells (cells capable of developing into organs)
intestinal epithelium
ovarian follicular cells
growing tumors
lymphoma tissue
carcinoma tissue

FAIRLY HIGH SENSITIVITY
epidermal epithelium
adenexal structures (hair follicles, subaceous glands)
oropharyngeal stratified epithelium
urinary bladder epithelium
esophageal epithelium
gastric gland epithelium
uteral epithelium

MEDIUM RADIO-SENSITIVITY
connective tissue
glia (supporting structure of nerves)
endothelium
growing cartilage or bone

FAIRLY LOW SENSITIVITY
mature cartilage or bone cells
mucous or serous gland epithelium
pulmonary epithelium
renal epithelium
hepatic epithelium
pancreatic epithelium
pituitary epithelium
thyroid epithelium
adrenal epithelium
nasopharyngeal nonstratified epithelium

LOW SENSITIVITY
muscle cells
ganglion cells

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This is why children are more vulnerable than adults, and why a rapidly growing tumor is sometimes more vulnerable than the surrounding tissues. The reason that pregnant women should minimize their radiation exposure is because the rapidly dividing cells of the fetus are at risk. The characteristic pattern of radiation sickness is due to the differential susceptibility of body tissues. Young blood cells such as lymphocytes and hemoblasts or bone marrow cells, mucosal epithelial cells of the intestines, spermatogonia of testicles, and follicle cells of the ovaries are the most radiation-sensitive tissues in the bodies of adults. Next are the mucosal epithelial cells of the bladder, esophagus, eye lens, oropharynx, and stomach. Also sensitive are the epidermis, the bulb of the hair follicle, and sebaceous glands.

Severity of symptoms and long term effects from radiation are dosage-dependent. Although radiation sickness symptoms will be present, most people recover from exposures below 150 REM. Above that dosage, death rates increase, and at exposures between 200 to 600 REM, 50% will die. Radiation sickness is progressive. Victims display loss of appetite, nausea, vomiting, prostration, fever, and bloody diarrhea. White blood cell counts drop rapidly, weakening the body's defense against microorganisms. Mucosal tissues and intestinal epithelium are inflamed and bleed. As number of blood platelets decrease, blood clotting ability is lost, resulting in both internal and external bleeding. Nasal bleeding and uterine hemorrhage are frequent. Purpura, purplish spots caused by intradermal or submucosal hemorrhaging, appear on the skin. Hair follicles are damaged, and complete hair loss in 10 days is an indication of possible lethal exposure. If radiation has killed the bone marrow cells, a transplant of live cells from a compatible donor can seed replacement marrow. The patient can recover if protected from infections and nourished.

Much of our knowledge of the effects of large doses of thermonuclear radiation comes from studies of survivors of nuclear attacks on the cities of Hiroshima and Nagasaki in August 1945 by the United States. The Hiroshima bomb, a uranium (92U238) device with an explosive power of about 12.5 kilotons (12,500 tons of TNT, trinitrotoluene), killed about 118,661 civilians, injured 9,130, and 3,677 were missing. Casualty figures are incomplete since they do not include military personnel. The larger 22 kiloton plutonium (94P239) bomb dropped on Nagasaki caused fewer immediate casualties, 73,884 dead and 74,909 injured. However, energy figures obscure some important differences between nuclear and TNT explosions. Much of the energy released from these devices is in the form of radiation, including alpha particles, beta particles, gamma rays, and neutrons. People shielded within buildings received less radiation exposure. The initial blast irradiated both soil and building materials in the target area. Though induced radiation is relatively short-lived, a person working for 8 hours near the hypocenter at Hiroshima on the day following the blast received about 10 RADs of radiation from induced sources. Thermal effects of radiation were also devastating. Ground surfaces near the center of the explosions reached temperatures of several thousand degrees centigrade. Since infrared rays heat the surfaces they strike, and much more heat is absorbed by dark colors than by light ones, varied skin burn patterns resulted. The massive shock wave produced by high temperatures of the explosion caused extensive physical damage to the landscape.

The nuclear-fission products of uranium and plutonium and those isotopes that escaped fission were carried high into the atmosphere. Some were dispersed far from the blast site by winds, but many were returned to the ground in the form of contaminated rainfall. Only those long-lived radioactive isotopes are measurable and are of long term importance.

Survivors suffered immediate aftereffects from direct detonation injuries and explosive destruction of dwellings and buildings. Flying fragments and glass splinters produced many wounds. Many individuals within 3 km of the blast sites suffered thermal burns. Indeed, at Hiroshima, 50.2% of those hospitalized were burn victims. Many others who were exposed to nonlethal dosages, exhibited depressed blood cell counts and blood pathologies. Bone marrow cells of survivors from within 1 km of the hypocenter had high frequencies of abnormal chromosomes.

Thousands of fetuses were exposed in utero. After trauma and radiation exposure, pregnant women miscarried due to death in utero, malformation, and intracranial hemorrhages. Among the surviving children irradiated in utero whose mothers exhibited no radiation signs, the rate of mental retardation was 1.6%. For children of mothers with major radiation symptoms, retardation rates increased to 25%. About 8% of children exposed in utero exhibited microcephaly, a head circumference of more than two standard deviations below the expected size. Even in the decade following radiation exposure of this population, incidence of stillbirths was still higher than normal.

The first long term radiation aftereffect among both Hiroshima and Nagasaki adults was development of cataracts, opacity of the normally clear ocular lens. Because about 17% of the energy produced by the Hiroshima device was expended as radiation, the higher neutron exposures at that locality resulted in a greater leukemia-mortality-per-radiation dose. Radiation exposure is thought to contribute to numerous other disorders, particularly diseases of the heart, digestive tract, bile tract, and pancreas, as well as anemia, hypertension, arthritis, diabetes, and cirrhosis. Death rates among survivors were increased by postwar shortages of food and medicine and poor environmental conditions.

Long-term genetic damage to germ cells at Hiroshima and Nagasaki is more difficult to document. Children of survivors do not seem to have more impairments those of other Japanese populations. This may reflect several circumstances. First, small genetic changes may not be easily detectable. Industrialized Japan has a high background level of industrial pollutants whose effects may mimic or mask the deleterious genetic attributes of bomb survivors and make it more difficult to demonstrate causal relationships. Second, the mechanisms that detect and delete defects in nucleotides may offer some protection at low dosage levels. Since it is not possible to completely avoid radiation exposure, conservative standards are set for the maximum acceptable exposure.

We must hope that atomic weapons will never again be used in warfare. Everyone empathizes with the casualties and survivors of Hiroshima and Nagasaki, but few people realize that those numbers are dwarfed by the magnitude of casualties, many still to occur, as a result of introducing increased amounts of radioactive isotopes into our ecosystem.

Since low levels of radiation are part of a normal environmental background affecting living tissues, our body cells appear to have elaborate defensive and correcting mechanisms to perform damage control and to prevent serious threats from developing from minor, radiation damaged sites. Damaged segments of RNA and DNA in somatic cells are detected and corrected. Abnormal clones of somatic tissues are recognized and attacked by our immune system. However these defensive systems can be overwhelmed and damaged by a large exposure. It is easy to forget that sunshine is radiation, and that sunburn can also represent a serious radiation injury.

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