With only a few exceptions (mainly for “blood-borne diseases”, such as malaria and Lyme disease, which are spread by insect bites), almost every disease-causing microbe on this planet evolved in ways that caused them to become “mucosal pathogens”, which infect animals by penetrating into cells on mucosal membranes. Even if their main damage occurs in other types of tissues, they must establish an initial infection, to establish a “foothold” (or beachhead, or similar terms) where they can begin reproducing, so that their progeny can then try to spread into other parts of the body.

          Two major aspects of animal anatomy and physiology drove pathogens to mutate and evolve in that direction:

          1.    “Dry skin” is covered by “epidermal” cells, and those are not really “cells” at all; instead, they are empty-bag “pseudo-cells” which are dead from the moment they are created. Instead of being formed by cell division, they are formed by a “budding” process, in which precursor cells (located about 6-8 layers deep, in most areas of dry skin) rapidly enlarge to nearly twice their normal size, and then “pinch off” something which is basically an empty bag – with a normal outer membrane, having surface proteins which microbes can latch on to, but with almost nothing but slightly salty water inside that membrane. That makes epidermal cells ideal as “decoys” or “bait” for pathogens, which use their tricks and tools to break into those cells, only to discover that they have broken into an empty shell of a building, with none of the things they need, to reproduce, and none of the things they need, to escape.

          2. By contrast, mucous membranes are covered by an entirely different class of cells, called “epithelial” cells. Those are full and complete cells, with all of the biochemical machinery and supplies that pathogens need, to reproduce. And unlike cuts, nicks, or wounds, which disappear fairly rapidly as they heal, mucous membranes are always available, and accessible, at all times, in any animal. Therefore, they are very tempting targets, for any type of pathogen which has evolved with some type of mechanism for grabbing hold of one or more types of epithelial cells, and then invading those cells (and, different types of microbes use a wide variety of such mechanisms).
         3.  Although most people are startled when they hear this number, the total area of the mucous membranes, in an adult human, is estimated to be about 200 times larger than the total area of dry skin, which covers the body. While that ratio might seem exaggerated or even preposterous, two factors help explain it:
         (i) it includes all of the microscopically small sacs inside both lungs, when fully inflated to bursting pressure. That surface area, by itself, is (and must be) quite large, to provide enough gas transfer, across those membranes, to supply all of the muscles, organs, brain, and other tissues of the body with enough oxygen to keep them fully functioning, even under periods of strenuous exertion; and,
         (ii) most mucosal surfaces have very large numbers of folds, ripples, invaginations, and other irregularities. Some are visible, but many more are microscopic in size. Those folds, ripples, etc., provide mucous membranes with numerous advantages, including remarkable flexibility and stretchability, as well as greatly expanded surface areas, which allow very large numbers of surface-mounted cells (and even specific types of cell surfaces) to perform specialized functions.
         In addition, another huge advantage helped promote and enlarge the class of mucosal pathogens. If a pathogen can infect a surface mucosal cell and begin reproducing in that cell, it almost certainly will be able to begin forcing that host cell to either: (i) die and split open, thereby releasing dozens, hundreds, and in some cases thousands of new copies of that pathogen; or, (ii) become “leaky”, and begin secreting pathogens, in ways that keep the host cell alive, so that it will keep making even more copies of that pathogen. Since nearly all types of viruses and bacteria can reproduce very rapidly after they “set up shop” inside a host cell, the pathogens will be able to reproduce, and release multiple copies of themselves, long before all of the necessary steps can be completed to: (i) enable the infected cell to begin creating and moving distress-signaling cytokine molecules to its basal surface; (ii) enable a “killer T cell” to find that infected cell; and, (iii) wait for the killer T cell to engulf and destroy the infected cell. By the time all those steps can be completed, the infected cell is likely to be already dead, or actively spewing out copies of that pathogen. This is a major part of the reason why, even if someone has been vaccinated against COVID viruses, and has even been previously infected by COVID, if that person gets COVID again, s/he is likely to have very high numbers of active and infective COVID viruses, in his/her saliva.
         With those and other factors actively encouraging the development of mucosal pathogens, animal immune systems had to develop a “first line of defense” against mucosal pathogens; and, “MALT patches”, and a special type of secreted antibodies – with a completely different structure and function than classic Y-shaped internal antibodies – became two of the main components of that “first line of defense” against mucosal pathogens. Those topics are described on the next two pages.

​