Free Why We Get Sick by Randolph M. Nesse

of worm,
Angiostrongylus cantonensis
, which burrow through the brain. Both of these defend themselves with secretions that inhibit inflammation. Still others, such as the trypanosomes, a group of protozoans that cause diseases such as African sleeping sickness, live in the bloodstream and absorb nutrients directly from the plasma. Whatever the means, parasites secure their resources from the host and then use them for their own maintenance, growth, and reproduction.
    These activities of pathogens incidentally damage the host, but this damage is not a pathogen adaptation. It does not do a tapeworm any good to have its host malnourished. It does not do the malarial parasite any good to destroy its host’s blood cells (unless, perhaps, this frees up iron for use by the parasite). Most often, the opposite must be true. The survival and well-being of the parasite depend on the host’s continued survival and ability to provide it with nourishment and shelter. Such incidental damage must therefore be considered a cost to both host and pathogen.
    The cost may be a general reduction in host resources or an obviously localized destruction. Bacteria that attack bone where a tooth is rooted cause structural damage and perhaps the loss of the tooth. The bacteria that cause gonorrhea may erode the connective tissue and cartilage of joints, causing functional impairment. Hepatitis viruses may destroy substantial portions of the liver, so that all liver functions, such as the clearing of toxins from the blood, become less effective. Such functional impairments are simply incidental consequences of pathogen adaptations. It does not do bacteria any good to make the host’s chewing less effective or its running less rapid.
    It’s important to keep damage conceptually separate from any resulting functional impairment. The damage causes the impairment, which can then itself be a cause for another host adaptation, which we call
compensatory adjustment
. There are many examples, somemuch more subtle than chewing on the left side of your mouth if it hurts to chew on the right. For instance, when disease-damaged lungs become less effective at oxygenating the blood, this may be partly compensated for by an increase in blood hemoglobin concentration. The body has a mechanism that monitors the oxygen level in the blood. If there is too little, whether from living at a high altitude or from lung damage, the body makes more erythropoietin, a hormone that stimulates the production of more red blood cells.
    Another obvious host adaptation is repair of damage. Natural selection has adjusted the ability to regenerate various tissues according to how useful it would normally be to do so. The skin, which is often damaged, is a first line of defense against pathogens and injuries. As might be expected, it quickly regenerates and rapidly recovers its protective capabilities. Other structures that regenerate quickly are the lining of the gut and organs such as the liver, which are in open communication with the gut and therefore with the outside world and its infectious agents. By contrast, the heart and especially the brain are less accessible to most pathogens. If pathogens do gain access and cause serious damage, it is ordinarily fatal, so regenerative capabilities would rarely be of benefit.
P ATHOGEN E VASION OF H OST D EFENSES
    S o far we have mentioned only one kind of pathogen adaptation, the ability to nourish itself in the body of the host. We can also expect it to have evolved ways of shielding itself from the host’s efforts to destroy, expel, or sequester it. We will now turn to one such mechanism,
evasion of host defenses
.
    The first trick for many parasites, once inside the body, is to gain entrance to cells. Invaders may accomplish this just as door-to-door peddlers do, by appearing to offer something else. The rabies virus binds to acetylcholine receptors as if
it
were a useful neurotransmitter; the cowpox virus to epidermal growth-factor