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14.3: Pathogen Mobility

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    While microscopic pathogens are not independently mobile, their hosts are, and pathogens have evolved ingenious ways of modifying the behavior of a host to enable their transferal to another host.

    Tiny Predators.JPG
    Figure \(\PageIndex{1}\). Tiny predators getting from one host to another.

    Sneezing and coughing reflexes, for instance, are ancient responses for clearing obstructions from the nose and throat, and some pathogens deceptively induce those responses for a pathway out (Figure \(\PageIndex{1}\)). What we call “symptoms of disease” are not, then, random effects of a disease, but can often be a pathogen’s way of getting out of one pond, so to speak, and into another. Any of the pathways listed in Chapter 14.1 can be exploited by a pathogen, which in doing so may upset these pathways and cause the host great distress.

    Pink eye and cold sores.JPG

    Figure \(\PageIndex{2}\). Pink Eye and Cold Sores.

    Some pathogens, for example, get into your eyes and tears and deceptively cause itching and soreness (Figure \(\PageIndex{2}\), left), inducing you to rub your eyes and transfer the pathogens to your fingers. This in turn can successfully move them to other locations like food, from which they can enter another host by the oral pathway.

    Other pathogens are able to break the skin and get out of the body on their own. Cold sores (Figure \(\PageIndex{2}\), right), a form of oral herpes, form around the mouth and nose, transmitting to what touches the sore. A related genital herpes is transmitted sexually, though evolution has been proceeding and the genital form is now able to infect orally and the oral form genitally. This and other sexually transmitted diseases have been increasing since about the middle of the twentieth century.

    One of the most successful pathogens to use the lungs and skin as pathways out of the body is smallpox (Figure \(\PageIndex{3}\)). It leaves its host with permanent scars, often over the entire body. Smallpox is an ancient disease, dating from the time before the pyramids, that can kill a majority of those it infects and at times can infect a majority of the population.


    Figure \(\PageIndex{3}\). Smallpox, the first disease consciously driven extinct from the natural world.

    The very success and horror of smallpox was part of its ultimate destruction—its eradication was the first complete victory in the conquest of disease. Thanks to prolonged diligent attention throughout the world, and of course to the invention of vaccine, smallpox has been made extinct in the natural world. (We say “natural world” because laboratory samples are being retained.)

    William Foege, a key player in orchestrating the extinction of smallpox, said that we can conquer disease because we evolve so much more rapidly than the disease. This may be startling to hear, given that our physiological evolution is much slower than that of viruses or bacteria. But, he explained, because we evolve socially much more rapidly than a disease can evolve biologically, we are able to “outsmart” the disease.

    Rinderpest, a viral disease causing high rates of mortality in cattle and wild mammals, was the second disease declared extinct in the natural world. Others—such as polio and Guinea-worm disease— may soon follow, though the latter may simply be eradicated from human populations by our continual isolation from sources of infection.

    Diseases can exploit blood-sucking parasites to move directly from the blood stream of one host to that of another. Lyme disease (Figure \(\PageIndex{4}\), left), for example, is spread by ticks, which puncture the skin to obtain a blood meal for themselves but in the process can transfer pathogens. And Ebola (Figure \(\PageIndex{4}\), right) leaves by almost every exit portal listed, destroying those portals by carrying not just the pathogen but chunks of lung, intestine, or skin in the process.

    lyme and ebola.JPG

    Figure \(\PageIndex{4}\). Lyme disease (left) and one form of Ebola (right).

    Human populations are so large and dense that even relatively inefficient pathogens can be successful. And diseases, of course, also affect wild and domestic animals as well as crops and other plants.

    As the next chapter illustrates, many diseases can evolve to be relatively harmless to their hosts, promoting transmission and allowing the disease to become widespread. Rust fungus infections, for example, are common in many plant species, but seldom lead to the death of the host. Powder mildew on the prairie plant Monarda fistulosa is so widespread that it is used in plant identification books as a way to identify the species (Figure \(\PageIndex{5}\), right).

    Pathogens can dramatically alter animal behavior. Rabies first gets through the salivary glands and into the saliva of an infected host. Physiological changes then make the host animal salivate profusely—foaming at the mouth—while psychological changes make it appear crazy and angry. The animal then bites through the skin of another animals, transferring the pathogen to that animal’s bloodstream, and the cycle continues. Both the physiological and psychological changes are caused by the pathogen and allow it to spread, even after the death of the initial host.

    prarie bush clover.JPG

    Figure \(\PageIndex{5}\). Prarie Bush Clover and Monarda fistulosa.

    “Mad dog behavior” is thus not an accidental consequence of the disease, but precisely the means the pathogen has developed for getting, so to speak, from pond to pond.

    It is useful to try to think of all the ways a pathogen might alter the behavior of its host to force the host to transfer the pathogen. This is not just an intellectual exercise, but could help identify potential for new emerging diseases. For example, what should a sexually transmitted disease do to its host in order to spread faster? It should render its host more active sexually! And indeed this happens. Female chimpanzees would normally mate only every two years or so, after having given birth and nursed their young to the point of weaning. But female chimps infected with SIV (simian immunodeficiency virus) reach estrus every month or so, and do not conceive. The pathogen changes their mating behavior to spread itself more than an order of magnitude faster than it would otherwise spread.

    Inspired to think in this way, one student came up with a novel idea: Imagine a disease that can escape through the sweat glands without harming its host. As behavioral modification, it makes infected hosts want to undergo strenuous exercise in groups, such as in gymnasiums—thus explaining the entire modern exercise phenomenon as a disease! (Gerbils may also harbor this disease.)

    This page titled 14.3: Pathogen Mobility is shared under a CC BY-NC 4.0 license and was authored, remixed, and/or curated by Clarence Lehman, Shelby Loberg, & Adam Clark (University of Minnesota Libraries Publishing) via source content that was edited to the style and standards of the LibreTexts platform; a detailed edit history is available upon request.

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