Tag Archives: infection

Deadly incurable viruses abound: The plagues to come.

As we discuss the effectiveness of the various COIVD vaccines, and ask if we will need another booster in a year, this time for the delta variant, or epsilon, it’s worth noticing that none of these is that deadly, especially if you’ve had a previous version. There are far worse viruses out there, like Ebola-Zaire, for example. This virus kills 60-90% of the people infected, typically by causing the body’s connective tissue to dissolve. Now that’s a deadly virus; imagine an ebola pandemic.

We live surrounded by many really deadly viruses, most of them incurable. In general our protection from them is that they usually show a slow infection rate or a slow progress to death. Drug resistant leprosy is one of these. Here’s the beginnings of a list of deadly viruses we could worry about: Lassa, Rift Vally, Oropouche, Rocio Q Guanarito, VEE, Marburg, Herpes B, Monkey Pox, Dengue, Chikunguanya, Hantavirus, Machupo, Junin, Rabies-like Mokola, drug-resistant leprosy, Duvenhage, LeDantec, Kyasanur, Forest Brain virus, HIV-AIDs, Simliki, Crimean-Congo virus, Sindbis, O’nyongnyong, Sao Paulo, SARS, Ebola Sudan, Ebola Zaire, Ebola Reston, Mid-East Respiratory (MERS), Zika, Delta-COVID. (I got 2/3 of this list from a 1993 book called “The Hot Zone” about the first US outbreak of Ebola — Washington DC in 1989 — a good book, worth a read).

Ebola is a string-like virus with loops. It causes your body to dissolve and bleed out from every pore. The strings form crystals that are virtually immortal.

As an ilk, these viruses are far older than we are, older than the first cellular creatures, and far tougher. They are neither dead nor alive, and can last for years generally without air, water or food if the temperature is right. Though they do not move on their own, nor eat in any normal sense, they do reproduce, and they do so with a vengeance. They also manage to evolve by an ingenious sexual mechanism. In a sense, they are the immune system of the earth, protecting the earth from man or any other invasive life form. We humans have only survived the virus for 100,000 years or so. Long term, the viruses are likely to win.

Zika is a ball-shaped virus. Incurable, it causes encephala. Ball-viruses are not as immortal as string viruses. COVID is a ball virus with spikes, a crown virus.

Some viruses are string shaped; Marburg and Ebola are examples. Such viruses can crystalize and live virtually forever on dry surfaces. Other viruses are ball-shaped, COVID and Zika, for example. These are more easily attacked on surfaces, e.g. by iodine. They become inactive after just a few minutes in air– and are killed instantly by iodine, alcohol, bleach, or peroxide.

Most viruses enter by cuts and body fluids. This is the case with AIDS and herpes. Others, like measles, shingles, and Zika, enter by way of surfaces and the hands. Virus-laden droplets collect on surfaces and are brought to a new host when the surface is touched and hand-transported to the nose or eyes. A few viruses, like SARS, Ebola, and COVID-19 can enter the body by breathing too. I’ve collected some evidence in favor of Iodine as a surface wipe, a hand wipe and as mouthwash in this previous essay.

Dr. Robert E. Buxbaum, November 3, 2021. The US has three facilities where they deal with the most deadly, contagious viruses. One is in Washington DC; they had leak in 1989, a part of the ebola outbreak. China has only one such facility, in Wuhan, China. It’s one block from where the COVID-19 outbreak supposedly originated. Have a nice day.

Zombie invasion model for surviving plagues

Imagine a highly infectious, people-borne plague for which there is no immunization or ready cure, e.g. leprosy or small pox in the 1800s, or bubonic plague in the 1500s assuming that the carrier was fleas on people (there is a good argument that people-fleas were the carrier, not rat-fleas). We’ll call these plagues zombie invasions to highlight understanding that there is no way to cure these diseases or protect from them aside from quarantining the infected or killing them. Classical leprosy was treated by quarantine.

I propose to model the progress of these plagues to know how to survive one, if it should arise. I will follow a recent paper out of Cornell that highlighted a fact, perhaps forgotten in the 21 century, that population density makes a tremendous difference in the rate of plague-spread. In medieval Europe plagues spread fastest in the cities because a city dweller interacted with far more people per day. I’ll attempt to simplify the mathematics of that paper without losing any of the key insights. As often happens when I try this, I’ve found a new insight.

Assume that the density of zombies per square mile is Z, and the density of susceptible people is S in the same units, susceptible population per square mile. We define a bite transmission likelihood, ß so that dS/dt = -ßSZ. The total rate of susceptibles becoming zombies is proportional to the product of the density of zombies and of susceptibles. Assume, for now, that the plague moves fast enough that we can ignore natural death, immunity, or the birth rate of new susceptibles. I’ll relax this assumption at the end of the essay.

The rate of zombie increase will be less than the rate of susceptible population decrease because some zombies will be killed or rounded up. Classically, zombies are killed by shot-gun fire to the head, by flame-throwers, or removed to leper colonies. However zombies are removed, the process requires people. We can say that, dR/dt = kSZ where R is the density per square mile of removed zombies, and k is the rate factor for killing or quarantining them. From the above, dZ/dt = (ß-k) SZ.

We now have three, non-linear, indefinite differential equations. As a first step to solving them, we set the derivates to zero and calculate the end result of the plague: what happens at t –> ∞. Using just equation 1 and setting dS/dt= 0 we see that, since ß≠0, the end result is SZ =0. Thus, there are only two possible end-outcomes: either S=0 and we’ve all become zombies or Z=0, and all the zombies are all dead or rounded up. Zombie plagues can never end in mixed live-and-let-live situations. Worse yet, rounded up zombies are dangerous.

If you start with a small fraction of infected people Z0/S0 <<1, the equations above suggest that the outcome depends entirely on k/ß. If zombies are killed/ rounded up faster than they infect/bite, all is well. Otherwise, all is zombies. A situation like this is shown in the diagram below for a population of 200 and k/ß = .6

FIG. 1. Example dynamics for progress of a normal disease and a zombie apocalypse for an initial population of 199 unin- fected and 1 infected. The S, Z, and R populations are shown in (blue, red, black respectively, with solid lines for the zombie apocalypse, and lighter lines for the normal plague. t= tNß where N is the total popula- tion. For both models the k/ß = 0.6 to show similar evolutions. In the SZR case, the S population disap- pears, while the SIR is self limiting, and only a fraction of the population becomes infected.

Fig. 1, Dynamics of a normal plague (light lines) and a zombie apocalypse (dark) for 199 uninfected and 1 infected. The S and R populations are shown in blue and black respectively. Zombie and infected populations, Z and I , are shown in red; k/ß = 0.6 and τ = tNß. With zombies, the S population disappears. With normal infection, the infected die and some S survive.

Sorry to say, things get worse for higher initial ratios,  Z0/S0 >> 0. For these cases, you can kill zombies faster than they infect you, and the last susceptible person will still be infected before the last zombie is killed. To analyze this, we create a new parameter P = Z + (1 – k/ß)S and note that dP/dt = 0 for all S and Z; the path of possible outcomes will always be along a path of constant P. We already know that, for any zombies to survive, S = 0. We now use algebra to show that the final concentration of zombies will be Z = Z0 + (1-k/ß)S0. Free zombies survive so long as the following ratio is non zero: Z0/S0 + 1- k/ß. If Z0/S0 = 1, a situation that could arise if a small army of zombies breaks out of quarantine, you’ll need a high kill ratio, k/ß > 2 or the zombies take over. It’s seen to be harder to stop a zombie outbreak than to stop the original plague. This is a strong motivation to kill any infected people you’ve rounded up, a moral dilemma that appears some plague literature.

Figure 1, from the Cornell paper, gives a sense of the time necessary to reach the final state of S=0 or Z=0. For k/ß of .6, we see that it takes is a dimensionless time τ of 25 or to reach this final, steady state of all zombies. Here, τ= t Nß and N is the total population; it takes more real time to reach τ= 25 if N is high than if N is low. We find that the best course in a zombie invasion is to head for the country hoping to find a place where N is vanishingly low, or (better yet) where Z0 is zero. This was the main conclusion of the Cornell paper.

Figure 1 also shows the progress of a more normal disease, one where a significant fraction of the infected die on their own or develop a natural immunity and recover. As before, S is the density of the susceptible, R is the density of the removed + recovered, but here I is the density of those Infected by non-zombie disease. The time-scales are the same, but the outcome is different. As before, τ = 25 but now the infected are entirely killed off or isolated, I =0 though ß > k. Some non-infected, susceptible individuals survive as well.

From this observation, I now add a new conclusion, not from the Cornell paper. It seems clear that more immune people will be in the cities. I’ve also noted that τ = 25 will be reached faster in the cities, where N is large, than in the country where N is small. I conclude that, while you will be worse off in the city at the beginning of a plague, you’re likely better off there at the end. You may need to get through an intermediate zombie zone, and you will want to get the infected to bury their own, but my new insight is that you’ll want to return to the city at the end of the plague and look for the immune remnant. This is a typical zombie story-line; it should be the winning strategy if a plague strikes too. Good luck.

Robert Buxbaum, April 21, 2015. While everything I presented above was done with differential calculus, the original paper showed a more-complete, stochastic solution. I’ve noted before that difference calculus is better. Stochastic calculus shows that, if you start with only one or two zombies, there is still a chance to survive even if ß/k is high and there is no immunity. You’ve just got to kill all the zombies early on (gun ownership can help). Here’s my statistical way to look at this. James Sethna, lead author of the Cornell paper, was one of the brightest of my Princeton PhD chums.

How Theodore Roosevelt survived being shot

Two more pictures of Theodore Roosevelt. The first is an x-ray showing the bullet he received as he entered a hall to give a 90 minute speech in 1912. How he survived the shooting: he did nothing. He left the bullet stay where it was for the rest of his life. It seems that both McKinley and Garfield had died from infection of their shooting wounds after doctors poked around trying to extract the bullet. It’s quite possible that Lincoln died the same way (Lincoln’s doctor was the one who killed Garfield by poking around this way).X-ray of Teddy Roosevelt showing the bullet where he let it lie.

X-ray of Teddy Roosevelt showing the bullet where he let it lie. The stripes look like lead paint, used to mark the spot. 

Roosevelt knew from hunting that a shot animal could last for years with the bullet still inside him. Roosevelt (and his doctors) knew, or suspected, that his bullet had stopped in a place where it would be harmless unless someone tried to extract it.

T. Roosevelt with Rhino, 1909.

T. Roosevelt with Rhino, 1909. Teddy would be shot 3 years later, in 1912.

In the speech, Roosevelt said, “it takes more than that to stop a Bull Moose.” He ought to know. For more T. Roosevelt pictures, click here.