Many vaccines are said to be highly effective, but what does that mean? When vaccine efficiency and effectiveness are discussed, they refer to the ability for a vaccine to prevent infection.

However, many vaccines are tested, not for efficacy (preventing infections in a controlled environment) or efficiency (preventing infections in the real world). Instead, vaccine studies look at variables like hospitalization rates and rates at which clinical symptoms emerge. In other words, many vaccines are tested not for their ability to prevent infections, but rather for their ability to prevent clinical infections. The difference may seem minor, especially to a person who is vaccinated, but in other discussions, I have already pointed out an issue with ignoring asymptomatic carriers.

The bigger issue is that at least in some cases, there is a conflation between ability to prevent colonization & transmission and ability to prevent disease. For instance, the CDC does not address what the B. pertussis vaccine is effective at doing. Instead it just says that it is 80% – 90% effective. People argue that people need to be vaccinated in order to generate herd immunity and because unvaccinated people are a risk to others, but this is only true if the vaccine is effective at preventing transmission.

But how common are these studies, and does the medical community really conflate the ability for a vaccine to prevent infection with its ability to prevent clinical infections? I have found numerous examples for B. pertussis vaccines, rotovirus vaccines, flu vaccines, and diptheria toxoid vaccines. In the final case, poor efficacy was ruled out as a cause for an outbreak because of the potentially incorrect conclusion that the vaccine was effective. I am not going to go into a full discussion on each of these items, but there are sources. As I have addressed before, it’s already known that the true efficacy at preventing the spread of infection, for pertussis, is next to nil for the acellular B. pertussis vaccine, even though it has been assessed to be very effective, when studying only the impact on clinical cases. How many other vaccines are far less effective than we think? And how much more prevalent are these infections than we think?

Even the CDC admits that its primary source of information on vaccine efficacy is through case reports:

Most infectious disease surveillance systems rely primarily on receipt of case reports from physicians and other health care providers. These data are usually incomplete and may not be representative for certain populations; completeness of reporting has been estimated to vary from 6% to 90% for many of the common notifiable diseases (16). However, if the level of completeness is consistent over time, these data usually are the best source of information regarding the temporal and geographic trends and the characteristics of the persons affected. Clinician-based surveillance has also been useful in identifying common-source outbreaks of diseases, eg, hepatitis A (17), hepatitis B (18,19), and hepatitis non-A, non-B (20).

But since case reports do not allow us to determine the ability of a vaccine to prevent the spread of an infectious agent, we need something else. The best course of action would be to conduct a meta analysis of vaccine studies, separated by vaccine class, and see how many actually check the effectiveness of the vaccine against infection, and how many just look for the impact on reported cases, and how many conflate efficiency of the vaccine in general, with the ability to reduce case reports. Finally, any future study, any reference to studies and any mention of vaccine efficiency, must use the proper wording. This includes discussions by organizations like the CDC. Claims like “in general, DTaP vaccines are 80-90% effective” is misleading. It is not 80 – 90% effective. It is 80 – 90% effective at reducing the number of clinical infections.

Why does it matter? It matters for a view reasons. Many of the reasons have been addressed in my article on estimating B. pertussis infections in the US. However, another issue is that a vaccine, which is only effective at reducing symptoms, means nothing to those who cannot be vaccinated. A failure to reduce the rate of infection means that those who cannot be vaccinated are at just as high a risk from people who are vaccinated as from those who are not.

A new study, “The Timing of Pertussis Cases in Unvaccinated Children in an Outbreak Year: Oregon 2012,” published in April 2017 also shows the issue with bad vaccine science. The study attributes a 2012 outbreak of Pertussis to unvaccinated individuals. The study looks at cases, not infections, in both the vaccinate and unvaccinated populations of Oregon. It notes that cases, again not infections, are identified in unvaccinated populations first. But this is not surprising. Even if both populations were just as susceptible to infection, the unvaccinated population, which is more prone to seeing actual symptoms, will be identified as being infected first because asymptomatic and sub-clinical infections will go unnoticed in the vaccinated population. The shear ignorance on the part of the authors, regarding asymptomatic infections and the conflation between cases and infections turns this study into nothing more than fuel for a witch hunt.

One final issue is that vaccine medicine is working backwards from how medical science normally works. In medical science, we do not assume that a drug is effective until we have found reasonable evidence to justify that it is. But for vaccines, even though there isn’t necessarily a lot of evidence that a vaccine does not prevent transmission, there really is little evidence that there is. It is just assumed that the vaccine is effective at preventing transmission.

Sources and Studies and Further Reading