The History & Science of Vaccination
Previously, I talked
about the vaccination debate in the context of two opposite views: the good of
the public and the good for individuals. Immunization advocates typically argue
that the science supports the safety and effectiveness of immunization as an
absolute good. Immunization opponents argue that the science is incomplete, and
that this incompleteness is actually a deliberate act; they argue that drug
companies and doctors actually overlook science that doesn't support their view
that immunization should be universal and complete.
Vaccination is actually a very old
practice. There's evidence that in the 1100s, the Chinese, Turks, and Africans
used materials contaminated with smallpox to immunize against that disease. We
often think of smallpox as being very lethal. It's true that one series found a
case-fatality rate of 62%. On the other hand, smallpox epidemics existed during
times that were less technologically advanced. Moreover, some subtypes of
smallpox are more lethal than others, so overall the fatality rate is about
30%--still pretty scary! Mild cases exhibit a fatality rate of less than 1%
(CDC, 2007), and inducing "mild" cases was the basis of the crude
immunization techniques in the ancient world.
The story we are most familiar with is the
work of Edward Jenner, who in 1796 used material from the lesions of cowpox,
found on the hands of milk maids, to immunize against the similar virus,
smallpox. Later, Louis Pasteur and Emile Roux used the blood of a
rabies-infected mouse to immunize a boy who had been bitten by a rabid dog.
Allowing the blood to dry out for nearly 2 weeks "devitalized" the
virus, which must live in blood. This process preserved the viral proteins,
however, and the boy's immune system could recognize these proteins, and act on
them, reprogramming itself to fight the virus.
Rabies has a case-fatality rate of about
99%. Most victims die because their immune systems can't act fast enough to
fight the virus before it kills them. The cause of death is general neural
failure. Basically, nerve functions, including the drive to breathe, fail.
Introducing a germ--or parts (proteins) of a germ--allows the body to see and
begin to recognize it. There are two main branches of immunity, innate and
acquired. Innate immunity is prompt and readily attacks germs, but it does a
sloppy job and often misses a lot of them. Those germs that get past the innate
immune cells go on to cause disease.
Acquired immunity engages a series of very
specialized cells that go through a complex dance which results in the
generation of very specific, highly targeted antibodies and cells that are
highly lethal to those germs. Let's say you get a cut on your finger.
Immediately, special cells in the skin and blood go after whatever germs got
into that cut. But at the same time, a few cells "read" the proteins
on those germs and send signals to other cells that start to rearrange their
own DNA in order to develop a profile of those germs. They then grow and
divide, these new-reprogrammed cells, to create highly specific cells
("killer cells") and chemicals ("antibodies") to eliminate
those germs.
If there are any immunologists out there
reading this, I know I'm simplifying this quite a bit. The thing is this is a
well-understood mechanism for how we fight off disease, which we are exposed to
every day.
It's possible to take advantage of this
feature of our biology to prevent disease. Exposing people to germs or parts of
germs, whether viruses or bacteria, can engage this system of acquired
immunity. Once the acquired system has been activated, a lineage of these
specialized cells will persist in the body, one line for each unique germ.
These are called memory cells.
Because of these memory cells, whenever the body is re-exposed to a given germ,
instead of it taking 7-14 days to develop a targeted response, it takes only
hours to days.
One of the important features that we have
to know about is the stability of whatever germs we're trying to protect
ourselves against. Smallpox is very genetically stable. Cowpox is also very
stable, and presents a very similar protein "picture" to smallpox.
Again, I'm simplifying here to make a point, and that is that genetically unstable germs are more
difficult to vaccinate against. For example, the common cold still defies
attempts to develop a vaccine. That's because the viruses that cause the common
cold (mainly rhinoviruses or "nose viruses" literally! There are few
less common viruses that cause colds) are prone to mutate.
This is also why we get multiple colds.
Cold viruses mutate.
But if the infecting agent is genetically
stable in the wild, and you either had the infection before, or you got a
vaccine against it, your memory cells ramp right up to fight the infection if
you run into it again.
This is also the case with HIV, for
example. HIV mutates a lot! Those mutations often cause viruses to become
inactive, but it also often gives them a "stealth" characteristic
that makes it hard to the acquired immune lineage to recognize that this was
seen before, say in a vaccine shot. It's also why some people can have multiple
strains of HIV at one time.
Unfortunately, this system isn't perfect,
and we don't fully know why. Hepatitis B vaccine typically provides protection
to 96% of healthy adults (Merck & Co., 2014). Looked at another way, about
1 in 24 vaccinated adults will not develop immunity to hepatitis B when
vaccinated properly. I am one of those people. I was vaccinated four times when
I was ER nurse, and I never developed antibodies to give me immunity to an
infection that at the time had an incidence rate among ER personnel of 35%!
Infanrix, a product that immunizes against
diphtheria, tetanus provides, and whooping cough reportedly provides 100%
immunity for the first two conditions, and 84% of children achieve immunity for
whooping cough (GlaxoSmithKline, 2016).
Last year, the flu vaccine--which mutates
a lot--had a protection rate of 47% (CDC, 2016). Not all that great.
One study that looked at duration of
immunity over time found that this was disease-dependent, and that actually
having the disease tended to confer more durable immunity than having been
vaccinated for it (Amanna, Carlson, & Slifka, 2007).
In short, vaccination works most of the
time for its stated purpose. In cases like the flu, most years you could flip a
coin to predict who it will work in (until we figure out why, at least). And
while a lot of people get protected, that protection can wane over time,
necessitating booster shots.
The U.S. now immunizes for 18 diseases in
35 doses plus approximately another 15 doses if one includes annual flu
vaccines. Many of these are given in combinations (e.g., measles, mumps,
rubella), or several in one child health visit, and on several occasions, since
in many cases a single shot isn't enough.
References
Amanna, I.J. Carlson, E. & Slifka,
M.K. (2007). Duration of humoral immunity to common viral and vaccine
antigens. New England Journal of Medicine, 357: 1903-1915.
