In this next installment of the revival of anticontagion theory, we'll zoom out to see how broad the class of diseases is that are described by the model. We want as general of a picture as we can manage, so that aspects of one sub-group can clue us in to what's going on in another group that's less well understood.
We've already covered a classic non-contagious disease like cholera, which is transmitted via a contaminated shared medium (i.e. water), into which the sick shed pathogens, and from which the healthy consume them, not through a sick and a healthy individual having an encounter. And we've shown that coronaviruses infecting humans and bats -- including the one causing SARS-2 -- are another textbook case, where they are spread through the medium of indoor air, not encounters between sick and healthy.
Now we return to the other major diseases that motivated the 19th-century debate over how diseases were spread -- plague and yellow fever. These are borne by insects (fleas and mosquitoes), which bite a sick person and thereby become carriers of the pathogens in the sick person's blood, then travel to a healthy person, bite them, and transfer these pathogens, making this person sick. We can add malaria and others to the list.
But first, there is one insect-borne disease that was classified as contagious -- i.e., spread through encounters -- even by the anticontagionists way back in the 19th C., which means we ought to consider treating it as such today as well. That is typhus (not to be confused with typhoid fever), which is spread by the human body louse. It was known to spread from one person to the next who were in close contact with each other in crowded settings like jails, hence the nickname "gaol fever".
What distinguishes typhus from all the others is that its insect carrier is not very mobile between human hosts -- unlike fleas that jump long distances, and which are riding on the backs of rats from one place to another, and unlike mosquitoes and flies that can fly long distances. The body louse only walks or crawls around a single host (their body and their clothing), so that the next host must be very close in order to crawl from one to the next.
This requires an encounter between a sick and a healthy person, so it behaves like other contagious diseases. For example, it does spread more as a function of higher population density, like in jails.
So technically, the diseases described by the shared-medium model are "mobile" insect-borne diseases, but I will drop that qualifier as too cumbersome, now that it's understood.
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Recall what the shared-medium model is tracking -- not only susceptible, infected, and recovered individuals, but also the concentration of the pathogen within the medium. I'll put up the formal mathematical model, and analyze it, later. First we're just getting all the conceptual stuff covered, so that the model will be motivated and make sense the first time around. Presenting the equations etc. first, and then explaining the details of it all, is putting the cart before the horse.
What, then, is the "medium" for an insect-borne disease? Why, the entire local population of the relevant insect. It may sound strange to describe it as a medium, since unlike water and air, people do not rely on mosquitoes, flies, and fleas to go about their daily business. However, those insects do rely on us for their survival -- so we very much come into inevitable contact with those species, even if it's them seeking out us rather than the other way around.
And by adding up a bunch of individual insects into an entire local population, they are like drops of water that add up to the entire local public water supply, or molecules of air that add up to the entire local volume of indoor air. The number of insects carrying the pathogen, as a share of their entire local population, is the same as the concentration of cholera particles in the water supply, or coronavirus particles in the indoor air of some locale.
A sick person "sheds" their pathogens into the medium by getting bitten by the insect, like someone with cholera excreting into the water supply, or someone with a coronavirus breathing into the air of an indoor building. Then a susceptible person comes into contact with this medium by being bitten by an insect. If it is a carrier, it's as though the person were drinking contaminated water or breathing contaminated air. If it's not a carrier, it's as though they were drinking a virus-free cup of water or breathing from a virus-free pocket of air.
Not every insect is a carrier, just as not every drop of water in the system contains cholera, and not every pocket of indoor air contains coronavirus. But as the concentration of the pathogen in the medium increases, it becomes more likely that a susceptible person will become infected by "consuming" or coming into contact with the medium.
There are differences among these shared-medium diseases, such as those whose medium is mobile -- running water in a public supply, jumping and flying insects -- vs. fairly fixed in place -- stagnant indoor air, slow crawling insects. But this is only a difference of degree, not kind, so we don't need multiple models to cover them. There will be a parameter for how frequently a sick person, or a susceptible person, comes into contact with the medium -- which will be higher for the mobile-medium diseases, and lower for the fixed-medium diseases.
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What lessons can we learn from insect-borne diseases, when looking at the prospect of dealing with SARS-2 or other respiratory diseases? Crucially, a vaccine is unlikely to solve the problem, and solutions will have to affect other parts of the environment to purify the medium -- or eradicate the medium altogether, if it's not beneficial for us anyway (like fleas and mosquitoes, and unlike air and water).
Even the non-mobile insect-borne disease, typhus, lacks a vaccine. And so do the other big ones spread by mobile insects, like malaria and plague.
The sole exception is yellow fever, but that vaccine is neither necessary nor sufficient to prevent outbreaks. The US and places under its control -- like the Panama Canal and Cuba -- eradicated the disease during the early 1900s through changing the environmental conditions. Namely, improved sanitation, spraying residences with pesticide, preventing stagnant water from forming (where the mosquitoes lay their eggs), and disrupting stagnant water by spraying it with oil. Control or eradication of the insect species remained the primary method of combating the disease during the Midcentury, when DDT was widely used.
A vaccine was developed by the 1940s, but was secondary at best even then, and did not play any role during the eradication of the early 20th C. It was beaten back in tropical regions as well, primarily through changing the parts of the ecosystem affecting the mosquitoes, not through mass vaccination of the human population.
Yellow fever has in fact reemerged as of the 1980s, despite availability of the vaccine, which does well in clinical studies but whose effects are evidently overwhelmed in the changing real-world ecologies of the past several decades. Since the most parsimonious explanation of the rise and fall of the disease up through the early 20th C. does not include the vaccine in the picture, we don't need to invoke it during the recent resurgence either.
Over the past 30 or so years, urbanization has skyrocketed in tropical regions, and since humans are the food source for mosquitoes, this has led to a surge in the mosquito population in those areas. With more mosquitoes swarming around, people come into contact with the medium far more often than before. Overcrowding strains the public water supply, so more people store their own water in large tubs near their house, which makes them stagnant and perfect breeding grounds for mosquitoes. Overcrowding strains sanitation services as well. These regions are a lot filthier than they used to be.
And perhaps just as importantly, pesticide use has fallen off a cliff, especially DDT. Pesticides are like a vaccine in that their widespread use will trigger a co-evolutionary arms race, where the target adapts by becoming resistant to the obstacle. Pesticides and vaccines also have side-effects on people, which must be weighed against their benefits.
Why shared-medium diseases are so hard to control via vaccines is a separate matter, which I'll speculate on sometime later. The point for now is simply that they are, and therefore we should not expect vaccines to do much work in controlling respiratory diseases, which spread through shared indoor air volumes, whether SARS-2 or anything else.
Improving sanitation and disrupting other parts of the transmission cycle -- before a susceptible person comes into contact with the already contaminated medium -- is the only reliable way to solve these problems. Draining stagnant water areas so mosquitoes can't breed, poisoning the rat population so plague-carrying fleas have no vehicles to get close to people, separating outgoing and ingoing water supplies to prevent cholera from passing from sewage to drinking water, and ventilating indoor spaces as much as possible to prevent respiratory pathogens from filling up the air.