Fourth, vaccines are only active while pathogens are inside hosts, but drugs can remain active in environmental reservoirs [89], suggesting that the strength of selection for resistance may differ for drug and vaccine resistance. However, drug resistance readily evolves even in pathogens that lack environmental life stages such as HIV [8].
Well that’s just some hand wavy pseudoscience right there.
Regarding the OPV Polio Vaccine, from the Global Polio Eradication Project site - “For several weeks after vaccination the vaccine virus replicates in the intestine, is excreted and can be spread to others in close contact”
Source: http://polioeradication.org/polio-today/polio-prevention/the...
To give you an idea of the weight difference, an average human IgG[1] antibody is about 500 more massive than a pretty average small molecule antibiotic like levofloxacin[2]
Their fate mostly lies in catabolism, i.e. they are broken down and the components reused. Biliary excretion accounts for a very small amount of the elimination of IgG antibodies.
[0] "Pharmacokinetics of Monoclonal Antibodies" http://onlinelibrary.wiley.com/doi/10.1002/psp4.12224/pdf
I missed it when I wrote my reply, concentrating on the immediate question (interesting psychological problem) - and then I could not edit it. It bothered me quite a bit but I did not want to write a third reply. Interesting to see how easy it is to get sidetracked on an irrelevant (albeit interesting) question, and how hard it is to get the discussion back on track.
I tried adding this quote from the linked paper:
> Thus, IgG elimination occurs mostly through intracellular catabolism by lysosomal degradation to amino acids after uptake by either pinocytosis, an unspecific fluid phase endocytosis, or by a receptor-mediated endocytosis process.
Explanation of two words in there that maybe not everybody knows:
pinocytosis: The ingestion of liquid into a cell by the budding of small vesicles from the cell membrane.
endocytosis: The taking in of matter by a living cell by invagination of its membrane to form a vacuole.
EDIT: I can still edit this comment more than five minutes later, as expected. Hmm... why could I not do that with my first comment...?
I'll add one more reason not explored by the authors: antibodies don't "leak" in the environment, in contrast to the antibiotics which are everywhere.
For example, if I'm vaccinated against S. pneumoniae (one of the bacteria that can cause pneumonia), the bacteria have to get inside my body to gain exposure to my vaccine-induced antibodies. This makes the emergence of resistance very unlikely because :
(1) the number of bacteria that are exposed to the antibody is relatively small, because the antibody response is pretty fast and happens before the bacteria had a chance to multiply to significant numbers; (2) any bacteria clones who evolve resistance to the antibody remain susceptible to the myriad of other immunes peptides, to macrophages, and so on. In other words, as long as I survive my pneumonia, no resistance can ever emerge, because I will kill all the resistant clones through other means.
Contrast this to antibiotics. I have pneumonia, I take antibiotics, I'm cured. However, I excrete those antibiotics in urine and stool. Outside of my body, enormous numbers of bacteria are exposed to minute doses of antibiotics. The number of surviving clones is likely to be very high, and those survivors do not face any supplemental threat. Thus, resistance to that antibiotic can be transmitted to later generations.