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Reservoirs and carriers of disease

A disease reservoir is a source of infection outside the human species. Reservoirs are usually animals in whom the infection is mild or even causes no disease. For example, bats are a reservoir for rabies and probably also for Ebolavirus.

A carrier is a human who is infected but does not become ill. Although carriers show no symptoms, they may transmit the disease to others. Even if all the susceptible human victims are dead or incapacitated due to a virulent infection, a few carriers may keep the infectious agent in circulation. Carriers may travel from one town to another, or they may stay where they are and keep the disease alive to emerge at some future time. Clearly, a disease that can rely on symptomless carriers or an animal reservoir is under less pressure to become milder.

Many diarrheal diseases cause symptoms in only a fraction of their human hosts. The proportion of symptomless carriers varies immensely. It may be more than half, as in Cryptosporidium or amebic dysentery, or very rare (about 2%–3%), as in typhoid. In most cases, the germs simply live in the intestines without causing disease. Intestinal diseases in which a large fraction of the population shows no symptoms are, by their nature, relatively mild, at least in most adults. The casualties from such diseases are mostly infants in poor countries. Malnutrition and lack of medical care make infantile diarrhea a major killer under such conditions.

A few special cases are known of germs that have adapted specifically to inhabit some tissue other than the intestines. In such cases, the disease may remain much more virulent. In typhoid carriers, the bacteria inhabit the gall bladder, emerging now and then into the intestine. From there, they can reemerge into human society. Salmonella typhi, the agent of typhoid fever, is one of the most virulent infections spread by the contamination of food or water with human waste. It is also a specifically human disease, unlike many other varieties of Salmonella, which are shared with assorted animals. These less dangerous relatives have no special hiding place and must therefore refrain from killing their multiple hosts to stay in circulation.

Some viruses also lay low in specific tissues, biding their time. The best known are chickenpox and herpes. In fact, chickenpox (Varicella) is a member of the Herpesvirus family and is unrelated to the true Poxviruses (smallpox, cowpox, and so on). Several related variants of herpesvirus cause cold sores and genital herpes. Although the symptoms may be suppressed by treatment or vanish spontaneously, herpes never disappears completely. A few viruses remain hidden in a quiescent state. Symptoms may re-emerge under certain circumstances—if, say, the victim undergoes a period of stress. Chickenpox may also lie latent in nerve cells, re-emerging later in life as shingles, a painful skin rash. After reemerging, the virus may be passed on to others.

Milder germs or mutant people?

When a disease gets milder, what has really happened? Did the disease change, or did the humans? Germs may mutate to avoid killing their victims too quickly, in order to spread themselves around. Humans may become resistant because sensitive individuals die off. Both processes occur in real life. Syphilis became milder. Humans became resistant to measles. In many cases, such as with malaria or leprosy, both processes have occurred. Because we are embarrassed talking about death and dislike thinking of the millions of humans weeded out by influenza, measles, and smallpox, we tend to talk of a disease getting milder even when humans became resistant.

Consider two alternative approaches for a disease to avoid killing its victims too fast. One is for the disease to become genuinely milder and nonlethal. Alternatively, the disease may remain lethal but kill only slowly. This is probably what happened to leprosy. Historical accounts suggest that leprosy was once highly contagious and far more virulent. Today leprosy is difficult to catch and will still kill if untreated, but this takes many years. Both victims and disease have changed genetically over time. Many Europeans carry genes for resistance to infection by leprosy.

Today we have direct genetic evidence for human resistance to schistosome worms, malaria, tuberculosis, leprosy, typhoid/cholera, HIV (AIDS), hepatitis B, and hepatitis C. The great sensitivity of indigenous Americans, both North and South, to influenza, measles, smallpox, and other Old World diseases implies that, here, too, genetic resistance has evolved in the Old World populations.

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