Author Archives: Melanie Schaab

Is Circumcision Cosmetic?

A philosophical question sometimes raised is the following:

“Is circumcision cosmetic?”

The answer is YES and NO.

baby-boy

Definition of Cosmetic

The term “cosmetic” comes from the Greek kosmetikos, which comes from kosmein (“arrange” or “adorn”), which comes from kosmos (“order” or “adornment”). Thus, “cosmetic” would refer to anything that restores or improves the appearance of something. However, “cosmetic” is also very much subjective.

For example, a very decorative bridle has both the non-cosmetic function of controlling the horse and the cosmetic function of improving the horse’s appearance. However, to an animal rights activist who sees any form of animal bondage as ugly, the bridle would not serve a cosmetic purpose. Obviously, it also serves no cosmetic purpose to the horse himself, either. As in this situation, almost anything may be either cosmetic or non-cosmetic depending on the subjective feelings of the audience.

 

Cosmetic, Medical, or Both?

When something is referred to as “purely cosmetic” or “only cosmetic” or “solely cosmetic,” the implication is that it serves no purpose other than to improve the appearance.

For example, breast augmentation is purely cosmetic. However, breast reduction surgery may be cosmetic or it may be a combination of medical and cosmetic because reducing the size of the breasts reduces strain on the upper back, posing health benefits.

It is also possible for something to have medical purpose without being cosmetic, and this is, by far, the most common reason for a given surgery.

For example, a mastectomy for breast cancer serves medical purpose, but does not improve the woman’s appearance (in any culture) and thus is not cosmetic. If, however, the woman and her physician opted for a combination mastectomy and breast reconstruction surgery, it would be both medical and cosmetic since the mastectomy is purely medical and the breast reconstruction is purely cosmetic.

 

So What About Circumcision?

Even intactivists must admit that there are times when circumcision poses medical benefits. Anti-circumcision physicians around the globe admit that prophylactic (preventive; i.e., before there’s a problem) newborn circumcision poses medical benefits; the disagreement is whether the medical benefits outweigh the cultural, cosmetic drawbacks to circumcision in anti-circumcision cultures where the foreskin is highly valued. Nonetheless, it is undeniable that circumcision does have medical benefits, and so newborn circumcision cannot sincerely be labeled “purely” or “only” or “solely” cosmetic.

Furthermore, circumcision may not be cosmetic at all. If you consider a circumcised penis to be more attractive than an uncut penis, then circumcision would be cosmetic for you. If, however, you consider an uncut penis to be more attractive, then circumcision, like a mastectomy, would not be cosmetic. Thus, whether circumcision is cosmetic depends entirely on the subjective feelings of the people who would be affected by, and must make decisions regarding, that penis—e.g., the parents, the child, and his future partners. If the parents oppose circumcision for cultural reasons (e.g., most Western Europeans), then their choice is solely cosmetic. If the parents or the individual choose(s) circumcision for cultural reasons without regard for the proven health benefits (e.g., certain tribal circumcisions), then their choice is purely cosmetic, but the procedure itself is not purely cosmetic because the procedure still has health benefits.

Parents in developed nations rarely make the decision to circumcise based on a desire for their child’s penis to be “attractive.”* Rather, nearly all parents in developed nations choose circumcision at least in part due to a belief in the medical benefits. Thus, it cannot be argued that the choice is cosmetic in all, or even most, cases. In fact, because the medical benefits are cited even by those making a primarily religious choice, one would be hard-pressed to find a pro-circ parent (i.e., one who currently identifies as pro-circumcision, regardless of the choice they ended up making for financial or other reasons) whose reason was entirely cosmetic.

 

The Bottom Line

So in short, because it has health benefits, the circumcision procedure cannot be considered “purely” cosmetic. Furthermore, circumcision is almost never a cosmetic choice in the developed world because it is not made based on a belief in the greater attractiveness of the circumcised penis. However, the end-result may be cosmetic if the people involved generally consider it to be more attractive. Thus, circumcision is either: (1) purely medical and non-cosmetic, or (2) a combination of medical and cosmetic. However, circumcision cannot sincerely be labeled “purely cosmetic.”

 

Side Notes

*However, intactivists’ projection of this (the belief in the circumcised penis’s attractiveness) on pro-circ parents as their primary reason for choosing circumcision strongly implies that intactivists’ choice not to circumcise is largely based on a belief that the uncut penis is attractive—which, frankly, is quite disturbing—as demonstrated by their inability to conceive of people choosing circumcision for any other reason and projection of their own reasons onto others.

Why Most Scientific Research is False

13886392_10153793077472218_3373684752844201882_n
Sparks’ Notes Version (A Summary of This)
`
Most science is false. Why?
`
1. Statistics. Even if your test is 99% accurate, if there are only 100 possibilities to test, the chances that your test result will be correct is less than 50%. This is because there are so many possible wrong answers that several wrong answers are certain to incorrectly test positive, so your positive test result is more likely to be wrong (a false-positive) than to be right. For example, if testing 20,000 genes for a possible link to Alzheimer’s and only one is a true link, and your test is 99% accurate, you will likely get 200 false positives in addition to the 1 true positive. Unfortunately, a “good” level of accuracy on a test is lower than 99%, more like 95%, so statistically speaking, most scientific research results today are false. See John P Ioannidis’s paper Why Most Published Research is False.
`
2. Researcher Bias. Research has shown that when a scientist expects a certain result, he’s more likely to get the result he expects. Part of this is accident, such as mathematical errors that he’s less likely to discover because he got the expected result. Probably a bigger part of it is outright fraud. Research has shown the majority of researchers admit to committing various degrees of fraud. This makes it even less likely that a positive result is a true positive. It’s also extremely easy to manufacture a certain result without committing massive, blatant fraud by simply using a different data analysis method or selecting a small group out of a larger population for analysis, making it harder for honest scientists to detect the false-positive.
 `
3. Publisher Bias. Publishers are in competition with each other and so they want flashy results. Therefore, they are extremely unlikely to publish boring results such as “X is not the cause of Y.” Therefore, among 20 studies on the subject, the one that falsely says X *does* cause Y is highly likely to get published while the 19 that say X doesn’t cause Y are extremely unlikely to be published.
 `
4. Cultural Bias. Both the broader popular culture and the scientists’ own micro-culture affect the results. If a research result was considered exciting, scientists in that field are less likely to want to prove it wrong and research proving it wrong is more likely to get intentionally buried. Furthermore, if something is considered ridiculous or unacceptable in the scientific or popular culture, scientists are less likely to pursue or publish research in that area because it may mean the ends of their careers. (Example: Dr. Semmelweis suggested a very unpopular theory–that doctors can carry disease on their unwashed hands–and studied it and ultimately recommended hand washing to prevent the spread of disease. It was an unpopular idea, and so he was ostracized in the scientific community and ultimately lost everything.)
 `
5. Sucky Peer-Review. Research is peer-reviewed prior to publication. In theory, this means other highly educated researchers in the same field comb the article for flaws and make recommendations for changes to improve the article or correct errors. In reality, research has shown that peer review fails to do its job. In one study, even when told they were part of a study and that they might find something “off” about an article submitted for publication, peer reviewers on average only caught one of eight *major* errors intentionally added to the paper and only 30% recommended rejecting the paper for publication. Peer review also has the tendency to reject unpopular ideas, making peer review switch from useless to actively harmful in a shockingly high proportion of cases.
 `
6. Failure of Self-Correction. In theory, science is self-correcting, meaning that over time, enough evidence will accumulate to replace a wrong theory with a right one. But there are many cases in human history where the correct theory was replaced with a wrong theory, even for over 1,000 years, before being replaced again with the right theory–for example, vitamin C deficiency as the cause of scurvy and geocentric theory (the belief that the sun revolves around the earth). How many correct theories have been replaced with a wrong theory and we just don’t know it yet?
 `
7. When Theory Becomes “Fact.” Often, new theories are proposed and bad science published at such a great speed today that a false theory quickly outpaces the natural self-correction of science, and new theories, subspecialties, careers, and grants spring up based on this bad science before it has a chance to naturally self-correct. At that point, a powerful barrier to self-correction has arisen. The old theory is treated like fact, and research that is unpopular due to popular or scientific cultural bias is rejected in the peer review process, while biased research that aligns with cultural bias is accepted in the peer review process. Sadly, one study found that bad cancer research that could not be reproduced was cited hundreds of times more frequently than was good, reproducible research in part because it had spawned new branches of research, along with their associated careers, grants, and prestige.
 `
8. Peer Pressure. Publishing something critical to a theory that is the foundation of your colleagues’/mentors’ careers is not going to endear you to them. If your colleagues/mentors don’t like you, that can interfere with your ability to get a job. Thus, the micro-culture of your scientific field and, more specifically, peer pressure prevents criticism of widely accepted ideas.
 `
9. Careerism and Opportunism. The present culture is such that scientists are lauded as heroes and science is held up as the only legitimate basis for policy making. Once upon a time, scientists were generally poorly-reimbursed for their efforts and so the profession attracted those earnestly interested in genuine scientific advancement. When suddenly given incredible influence, as science has today, any discipline will become flooded with opportunists and charlatans.
 `
10. The Religion of Science. The popular culture treats science as though it is the greatest truth and its practitioners as though they are infallible. They treat science as the greatest aim and scientists as the best advisors in all areas of life. Some refer to this as “scientism” or “The Cult of Science.” At best, it encourages a love of science without teaching adherents to distinguish between good and bad science. At worst, it actively fights against unpopular theories, impeding the progress of science.
 `
A final note…
 `
Proof by Replication/Reproducibility. Theoretically, if a certain result can be replicated/reproduced (i.e., other scientists running the same experiment get the same result), it’s more likely to be true. Groups that repeat published experiments have found at least 65% were not reproducible and many of the remainder were less effective than the original results showed them to be in social sciences, and at least 75% of drug research was false. Another study of cancer research found 89% could not be reproduced.

Does Forced Retraction Cause Phimosis?

In short: No. Not only is there NO evidence that forced retraction DOES cause phimosis, there is actually POSITIVE evidence–cataloged on intactivists’ own websites–that forced retraction DOES NOT cause phimosis.

What are Adhesions?

The foreskin is naturally stuck to the glans by what we call “adhesions.” Virtually 100% of uncut boys have adhesions that prevent the foreskin from retracting. In fact, because circumcision often doesn’t remove the entire foreskin, adhesions occur in 45% [Van Howe, 2001] to 71% [Ponsky et al, 2000] of circumcised boys as well. Breaking the adhesions by retracting the foreskin before it’s ready—called “forced retraction”—is very painful and has no known medical benefits. In order to circumcise, these adhesions must be broken, but the boy receives highly effective numbing medicine beforehand [Shockley & Rickett, 2011]. However, there’s no numbing medicine in day-to-day life, and there’s no evidence that forced retraction is beneficial to the boy’s health. So… cut or uncut… don’t do it.

Why Do We Forcibly Retract?

Intactivists claim that Americans retract the foreskin because of cultural ignorance of proper care of the foreskin due to unfamiliarity with the foreskin thanks to the relatively low number of uncut males in our society—in other words, cultural ignorance. However, this argument is false. In reality, retraction of the foreskin even in infants is a hold-over from early 1900s medicine which has not yet been fully dropped, and this practice was common in Europe, as demonstrated by a landmark British Medical Journal article (archived in intactivists’ own websites in full text format) wherein the (anti-circumcision) author stated, “mothers and nurses are often instructed to draw the child’s foreskin back regularly” [Gairdner, 1949, p. 1435]. At that time, the American newborn circumcision rate was very low—lower, in fact, than the British newborn circumcision rate. Furthermore, in spite of the vast majority of American boys being circumcised, most physicians don’t know how to properly care for the circumcised penis, either, and thus retract the skin, breaking the adhesions, and causing pain [Ponsky et al, 2000]. It’s not cultural ignorance. It’s prehistoric medicine.

Does Forced Retraction Cause Medical Problems?

Intactivists claim that forced retraction causes tiny, microscopic tears in the delicate inner skin of the foreskin, causing infection and scarring. The scarring then allegedly results in phimosis, for which the treatment is often circumcision. So it’s considered ironic that “most” medically-necessary circumcisions are necessary only because the foreskin was not properly cared for in the first place. Intactivists make this claim as a matter of fact, so I believed it was actually based in fact. However, what I found was that their own sources say the exact opposite.

I wanted to have a primary source for articles like this, rather than a heavily biased secondary or tertiary source, so I searched all of the intactivist websites for all their articles on forced retraction in order to farm their resources. For their theory that forced retraction causes infections and scarring, they almost exclusively cited tertiary sources—predominately, old pediatric textbooks. (For those who don’t know, textbooks often don’t differentiate between theory and proven fact, so a textbook should never be taken as an authoritative source.) However, one article in Psychology Today actually provided a tertiary resource that was published in a medical journal. So I used the anti-circumcision online Circumcision Resource Library to look it up.

A Psychology Today Blog post, which originated from another blog post by a Ms. Cannon, instructs parents not to retract the foreskin and states that forcibly retracting the foreskin “tears the foreskin and the tissue… that connects it to the head of the penis, leading to scarring and infection” [Nervaez, 2011]. It provided no reference for the claim that retraction causes scarring, but for the instruction not to retract, it provides as its reference a 2002 article, which states, “Parents should be educated to avoid forcible retraction of the prepuce; the tearing that may result could lead to fibrosis [scarring] and subsequent true phimosis…” [Camille, Ramsay, & Wiener, 2002] For this claim, it provided a 1998 reference, which I followed, and which states, “True pathologic phimosis occurs when fibrosis, induration and scarring occur in the tip of the foreskin usually secondary to inflammation or trauma” [Simpson & Baraclough, 1998]. For this claim, it provided a 1980 reference [Rickwood et al, 1980], which I followed, and which turned out to be the primary source I’d been looking for.

The primary source was a study of phimosis in boys aged 4-11 years undergoing a medically-necessary circumcision for scarring on the tips of their foreskins, resulting in pathological phimosis. Cross-sections of their foreskins were compared to cross-sections of the foreskins of non-phimotic boys circumcised for religious reasons. Their histories of infection, forced retraction, and other foreskin or penile issues (even their fathers’ histories of phimosis in search of a potential genetic basis) were also gathered and compared. The authors discussed three previous theories from the 1950s-1960s of the causes of phimosis, that it is caused by forced retraction [Twistington Higgins, Williams, & Ellison Nash, 1951], or by repeated bacterial infection [Campbell, 1951], or by irritation caused by ammonia (present in urine) [Robarts, 1962]. Ultimately, they could find no correlation between phimosis and any of these theoretical causes and concluded, “There was little to support the contention that the condition is caused by trauma, or by ammoniacal [urine-caused] or bacterial inflammation of the prepuce…” and “Our data do not support previous contentions that it is due to forcible retraction, ammonia dermatitis or recurrent balanoposthitis [infection of the glans and foreskin].”

Interestingly, what they did find was that balanitis xerotica obliterans (BXO) was present in almost every case (20 of 21 specimens) [Rickwood et al, 1980]. This was similar to another British study by the same author, which found that 84% of pathological phimosis specimens had BXO [Shankar & Rickwood, 1999]. As I’ll discuss further in a later post, we don’t know the cause of BXO and therefore don’t know how to prevent it, and the treatment is typically circumcision. Perhaps if certain intactivists could get off their high horses and stop fallaciously insisting that the only cause of circumcision is forced retraction (due to its falsely alleged causal relationship with phimosis), we could get some real research done to find out what causes BXO, realizing that BXO may be the primary—or even the only—cause of phimosis. Then, perhaps we could prevent phimosis from ever occurring, and thereby prevent the most common cause of medically-necessary circumcisions. Personally, I believe this theory has significant merit because it has even been demonstrated in women, where the cause of clitoral phimosis (where the clitoral hood is too tight) has been demonstrated to be caused primarily by BXO and secondarily by surgical trauma [Flynn et al, 2015].

At any rate, the very interesting, but not completely surprising, part is that these secondary sources I found cited this primary source as evidence that phimosis is caused by trauma, specifically forced retraction, yet the primary source they’re citing says the exact opposite. In other words, the authors either didn’t check the sources they were citing or were intentionally lying.

Conclusion

So to sum up, there’s actually no evidence that forced retraction causes any medical problems whatsoever.

However…. That being said… It’s still painful to forcefully retract a boy, cut or uncut, so it’s probably best to just leave it alone.

 

References

Camille, C.J., Ramsay, L.K., & Wiener, J.S. (2002). “Caring for the uncircumcised penis: What parents (and you) need to know.” Contemporary Pediatrics, 11:61. http://www.cirp.org/library/hygiene/camille1/

Campbell, M. (1951). Clinical Pediatric Urology. Philadelphia: Saunders. Cited in: Rickwood, A.M.K., Hemalatha, V., Batcup, G., & Spitz, L. (1980). “Phimosis in boys.” British Journal of Urology, 52L147-150. http://www.cirp.org/library/treatment/phimosis/rickwood/

Flynn, A.N., King, M., Rieff, M., Krapf, J., & Goldstein, A.T. (2015). “Patient satisfaction of surgical treatment of clitoral phimosis and labial adhesions caused by lichen sclerosus.” Sexual Medicine, 3(4):251-255. doi: 10.1002/sm2.90. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4721030/

Gairdner, D. (1949). “The fate of the foreskin: A study of circumcision.” British Medical Journal, 2(4642):1433-1437. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2051968/

Nervaez (2011). “More circumcision myths you may believe: Hygiene and STDs.” Psychology Today Blog. https://www.psychologytoday.com/blog/moral-landscapes/201109/more-circumcision-myths-you-may-believe-hygiene-and-stds

Ponsky, L.E., Ross, J.H., Knipper, N., & Kay, R. (2000). “Penile adhesions after neonatal circumcision [Abstract].” Journal of Urology, 164(2):495-496. doi: http://dx.doi.org/10.1016/S0022-5347(05)67410-1. http://www.ncbi.nlm.nih.gov/pubmed/10893633

Rickwood, A.M.K., Hemalatha, V., Batcup, G., & Spitz, L. (1980). “Phimosis in boys.” British Journal of Urology, 52L147-150. http://www.cirp.org/library/treatment/phimosis/rickwood/

Robarts, F.H. (1962). “Penis and prepuce.” In Surgery of Childhood, ed. Mason Brown, J.J. Chapter 39, pp. 1159-1181. London: Edward Arnold. Cited in: Rickwood, A.M.K., Hemalatha, V., Batcup, G., & Spitz, L. (1980). “Phimosis in boys.” British Journal of Urology, 52L147-150. http://www.cirp.org/library/treatment/phimosis/rickwood/

Shankar, K.R., & Rickwood, A.M. (1999). “The incidence of phimosis in boys [Abstract].” BJU International, 84(1):101-102. http://www.ncbi.nlm.nih.gov/pubmed/10444134

Shockley, R.A., & Rickett, K. (2011). “What’s the best way to control circumcision pain in newborns?” The Journal of Family Practice, 60(4):233-234. http://www.jfponline.com/specialty-focus/pain/article/whats-the-best-way-to-control-circumcision-pain-in-newborns/d9d56c4483f56e3d0f9b55d68dc49985.html

Simpson, E.T., & Baraclough, P. (1998). “The management of the paediatric foreskin.” The Australian Family Physician, 27(5):381-383. http://www.cirp.org/library/hygiene/simpson1/

Twistington Higgins, T., Williams, D.L., & Ellison Nash, D.F. (1951). The Urology of Childhood. London: Butterworths. Cited in: Rickwood, A.M.K., Hemalatha, V., Batcup, G., & Spitz, L. (1980). “Phimosis in boys.” British Journal of Urology, 52L147-150. http://www.cirp.org/library/treatment/phimosis/rickwood/

Van Howe, R.S. (2001). “Re: Penile adhesions after neonatal circumcision.” The Journal of Urology, 165(3):915. doi: http://dx.doi.org/10.1016/S0022-5347(05)66571-8. http://www.jurology.com/article/S0022-5347(05)66571-8/fulltext

Toward Understanding: Circumcision Terminology

There’s an issue in conversations about male circumcision today. Well, there are a lot of issues, such as the complete shutting down of opposing viewpoints and slinging of ad hominems and cyber bullying. But the one out of the dozens of issues that I want to address in this post is terminology.

The United Nations’ official term “Female Genital Mutilation” (FGM) refers to the cultural practice that involves removing part or all of a girl or woman’s clitoris, clitoral hood, and labia, and sometimes sewing her vagina closed [1] (see Footnote 1). It’s a horrific practice, and so “mutilation” seems fitting. However, they discovered that when discussing the practice with natives and trying to educate them about how harmful the practice really is, the term “mutilation” is so emotionally-charged that it tends to shut down conversation entirely and do more harm than good in advancing their anti-FGM cause (see Footnote 2). Thus, when conversing with natives and educating them about the harms of the practice, the WHO advocates the use of the emotionally neutral and anatomically accurate term “Female Genital Cutting” (FGC). [1]

A very similar thing is happening in online conversations about circumcision. I would like us to advance toward a better understanding of each other and an improved ability to communicate effectively, and this may be one small part of that.

I apologize if this makes your eyes glaze over.

Terms for the Penis

If a penis has been circumcised, there are a number of terms used to describe it. The most common are “circumcised” and “cut.” People who are very against circumcision often use the term “mutilated.” Obviously, that’s intentionally inflammatory and offensive to males who are circumcised. Circumcised men sometimes refer to their penis as “clean” or “clean-cut.” Obviously, that’s offensive to males who are not circumcised. Therefore, I recommend the terms “circumcised” and “cut.”

If a penis has not been circumcised, there are also a number of terms used to describe it. The most common is “uncircumcised.” I’m going to take a slight rabbit trail for a moment. My children are not vaccinated. Anti-vaxxers often take offense at the term “unvaccinated” because, they argue, “you can’t un-vaccinate a child.” To me, this has always demonstrated a profound misunderstanding of the English language. If I am “unlicensed,” that doesn’t necessarily mean I once was licensed but now am not (that would be “de-licensed”). It simply means I am not licensed. The English prefix “un-” simply means “not.” Ergo, “unlicensed” means “not licensed,” “unvaccinated” means “not vaccinated,” and “uncircumcised” means “not circumcised.” So this whole argument doesn’t make any sense to me, but in the same way that anti-vaxxers often take offense at the term “unvaccinated,” people who are opposed to circumcision often take offense at the term “uncircumcised.” My children are not vaccinated and I use the term unvaccinated. I don’t understand the offense at the terms “unvaccinated” or “uncircumcised.” In fact, I think it’s stupid in both situations. But I’m going to respect that opinion by not using the term “uncircumcised” in conversations where people opposed to circumcision might be involved.

Another term for a penis that is not circumcised is “intact.” This is the term those who oppose circumcision most often use. However, it’s insulting to circumcised males because the term was first used in animal husbandry to mean an animal that has not been neutered or castrated. Thus, using the term “intact” for a man who is not circumcised implies that a man who is circumcised has been castrated and/or emasculated. For this reason, some men take offense to the term. In fact, an acquaintance of mine calls himself “intact” even though he’s circumcised. So in conversations with people from both groups, I recommend against the use of the term “intact.” Other terms used include “natural” and “normal,” which are also obviously insulting to circumcised men and intentionally inflammatory; and “anteater,” which is obviously insulting to men who are not circumcised and intentionally inflammatory. The only completely neutral term* I can find that isn’t highly medico-lingal, and which people on both sides use, is “uncut.” So that’s the term I recommend.

Two completely neutral medico-lingal terms are “prepucal” and “aprepucal.” The “prepuce” is the foreskin, so a “prepucal” penis is one that has a prepuce and an “aprepucal” penis is one without a foreskin. However, I thought these terms were too difficult to catch on with non-medical persons.

Therefore, I recommend “circumcised” or “cut” versus “uncut.”

Terms for People

People who support circumcision typically use the terms “pro-circumcision,” “pro-circ,” or “PC.” People opposed to circumcision call them “pro-cutters.” Although the term is technically somewhat neutral, it is always used in a derogatory way, so it’s considered offensive by pro-circs. People opposed to circumcision also call them “pro-mutilators,” “pedophiles,” “child abusers,” “child molesters,” etc. For obvious reasons, I recommend avoiding those terms as well and sticking with “pro-circumcision,” “pro-circ,” or “PC.”

People who oppose circumcision call themselves “intactivists,” which is a combination of “intact” and “activist.” Pro-circs sometimes call them “intactonuts” or “intactic*nts,” which are obviously offensive, so I won’t use those terms. Because the term “intactivist” comes from the offensive use of the word “intact,” it could be argued that “intactivist” shouldn’t be used, either. However, “anti-circumcision activists” is too long and pro-circs most often use the term “intactivist” anyway, so I recommend “intactivist.”

A somewhat neutral term is “PPC” or “pro-parental-choice.” This refers to people who support a parent’s right to choose whether to circumcise, even if they disagree with their choice. Typically, intactivists believe that circumcision is evil and should be completely abolished, so it will be very rare for you to find an intactivist who is also PPC. Therefore, PPC typically only refers to people who are neutral on circumcision or are pro-circ. I have yet to meet a person who actually believes that circumcision should be mandated, but most intactivists believe that circumcision should be legally prohibited.

Conclusion

To help us move toward a better understanding and more fruitful conversations on the topic of circumcision, I recommend the use of emotionally neutral terminology, including “uncut” versus “cut”/”circumcised” and “intactivist” versus “pro-circ”/”PC.” You don’t advance your cause by insulting the other side, and anyone can see that you’re being a jerk. If you really care about helping boys to live healthier, fuller lives, you should consider reaching their parents in the most effective way possible.

 

*Well, I thought it was completely neutral. I’ve seen it used almost exclusively in a positive light. But just today, after writing this but before publishing it, I discovered that there are even people opposed to that term as well. At any rate, it’s still the least offensive term I can find.

 

Footnote 1

A brand new and exceedingly rare version of this involves removing only the clitoral hood, but this is not a traditional practice [1]. Because removing only the hood is similar to removing only the foreskin in the man, it is accurate to call it “female circumcision.” However, this is distinct from the practice of FGM, which has never traditionally involved only the hood but rather has always involved some degree of harm to the clitoris and almost always removal of some portion of the labia minora. Some may argue that female circumcision can also be performed for genuine medical reasons such as the treatment of clitoral phimosis [2].  However, in that case, if you read the entire study, you’ll find that the treatment involves cutting a slit in the hood, not removing the entire clitoral hood. Therefore, the only accurate use of the term “female circumcision” is in reference to a new, rare practice that is most common in Egypt and is only one small part of traditional FGM.

 

Footnote 2

From Reference [1]:

“The language used to describe these practices remains controversial and requires careful ethical consideration. The term ‘Female Genital Mutilation,’ formerly adopted by the United Nations (UN) calls attention to the gravity of the harm caused by FGC practices. ‘Female Genital Mutilation (FGM)’ is the terminology used within campaigns to end these practices by anti-FGC advocates from practicing countries of origin and the western world. FGM terminology positions the practice of FGC as an extreme human rights violation. This term is often perceived as inflammatory, judgemental and stigmatising, particularly for women previously exposed to the practice who do not view their bodies, or the bodies of their daughters, as mutilated [3]. The implication within this terminology is that FGC is practiced as an act of intentional violence against female children, adolescents and women. Those who do not understand FGC as such an act, but as a valued cultural tradition, may experience the language of “mutilation” as alienating [7,911]. The delicate challenge of reconciling respect for cultural values associated with these practices and addressing their perceived harmful effects on health is evident in this discrepancy between the intent and impact of language.

” ‘Traditional women’s practices,’ ‘Traditional health practices,’ and ‘Initiation,’ are some of the preferred terms identified by individuals who subscribe to the socio-cultural benefits from these practices. Chalmers & Omer Hashi [10] as well as Vissandjée et al. [7] conducted focus groups with overall 600 women from different practising countries living in Canada which revealed “circumcision” to often be the preferred terminology. Several other authors have also identified “circumcision” as an alternative term, yet this term has been argued to trivialise the procedure, falsely attributing to FGC the legitimacy afforded to male circumcision within the West [12,13]. “Female Genital Cutting (FGC)” and “excision and infibulation” have been identified as more neutral, ethically sensitive terminology [4,6]. For the purpose of this chapter, we will use FGC as a term comprising procedures which alter the female genital organs for cultural or non-therapeutic reasons.”

References

[1] http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4012131/

[2] http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4721030/

 

Pneumococcal Vaccine (Pneumonia, Meningitis)

This is the LONG version. See also the SHORT version here.

streptococcus_pneumoniae_2

S. pneumoniae

What are the “meningitis vaccines”?

There are two basic types of meningitis: viral and bacterial. There are no vaccines targeting viral meningitis. There are three vaccines targeting causes of bacterial meningitis: HiB, pneumococcal, and meningococcal. Meningococcal was Weekly Topic 03, HiB was Weekly Topic 05, and pneumococcal will be discussed here.

There are two types of pneumococcal vaccines: conjugated (PCV) and unconjugated (PPSV). PPSV were the first created and are thus the oldest, but were generally recommended only in adults until very recently. PCV are newer and recommended primarily in children. According to the CDC Vaccination Schedule (2015), pneumococcal vaccination (primarily with PCV, followed by one PPSV dose) occurs at 2, 4, 6, and 12-18 months; if the series begins at 12 months, only two doses are recommended, and if it begins at 24 months, only one dose is recommended [1, 2]. In Canada, depending on province/territory, pneumococcal vaccination occurs typically at 2, 4, and 12 months, with a few recommending an additional 6 month dose and/or moving the 12 month dose to 18 months [3].

 

What is pneumococcus?

Streptococcus pneumoniae, often referred to as pneumococcus, is a bacterium and “one of the most extensively studied microorganisms” [4, p. 591]. It was first isolated in 1881 by Louis Pasteur himself. Some strains have capsules while others do not, but when simultaneously infected with both a capsular strain and a noncapsular strain, the noncapsular bacteria steal the capsular bacteria’s DNA and thereby create a capsule and convert to the same strain as the capsular bacteria. It’s also possible for capsular bacteria to steal other capsular bacteria’s DNA and begin making a new capsule. Since the capsule is how the serotype (strain) is determined, this is termed “serotype switching” or “capsular switching.” Capsular bacteria are 105 times more virulent than noncapsular strains. Based on unique characteristics of their capsules, the bacteria can be divided into over 90 serotypes. The serotypes vary drastically by geographic area; for example, in the 1980s, researchers found that the same 20 serotypes that are responsible for ~90% of infections in the U.S. and Europe were responsible for less than 70% of infections in Asia. Antibiotic resistance or sensitivity also varies significantly by geographic region, though they are generally sensitive to penicillins. [4, 5]

S. pneumoniae is commonly carried asymptomatically by healthy people, though the rates vary by population. For example, carriers may make up 20-60% of school-aged children, 5-10% of adults without children, and 50-60% of military personnel [5]. A study that tested several hundred children for pneumococci approximately every four weeks for two years found that 54% became carriers at least once by age 6 months and 97% became carriers at least once by age 2 years [6]. Carriage seems to be more common after influenza infection [4] and is more likely when the patient has recently had sinusitis, has one or more older siblings, is enrolled in daycare, or lives in the city [7]. One study of penicillin-resistant pneumococcus found asymptomatic carriage ranged from 3 days to 267 days (median 19 days) [8] and one study in mice found that lower number of bacteria was associated with longer carriage while a higher number of bacteria was quickly cleared [9]. Different serotypes are carried for different lengths of time and one study found that the duration of carriage ranged from 5.9 weeks (serotype 15C) to 19.9 weeks (serotype 6B), and that longer duration of asymptomatic carriage correlated to a lower incidence of disease [6]. Pneumococcal disease mostly occurs after new infection with a new serotype rather than after a long period of asymptomatic carriage [4]. Because carriage is so common, disease is relatively very rare.

The incubation period for pneumococcal infections is only 1-3 days and the symptoms include a sudden onset of fever and chills or rigors, as well as pleuritic chest pain; cough with rusty, mucousy sputum; shortness of breath; rapid breathing; low oxygen levels; rapid heart rate; malaise (general feeling of sickness); and weakness. Less commonly, patients also experience nausea, vomiting, and headaches [5]. It is the most common cause of pneumonia in adults; and is one of the most common causes of bacterial meningitis in children and adults, alongside the HiB and meningococcal bacteria discussed previously [4]. S. pneumoniae is also a common cause of otitis media (middle ear infections) [5].

Vaccines targeting S. pneumoniae were first developed in the early 1900s but were not effective and had many adverse effects. A more effective vaccine was developed in the 1930s, but the interest in antibiotics led to the vaccine being largely ignored, rarely used, and ultimately removed from the market. New pneumococcal vaccines were developed in the 1970s and 1980s. [4]

 

How can I prevent or treat pneumococcal infection in my child?

Conditions that make an individual more susceptible to pneumococcal disease include recent viral infection, immune suppression, and a generally unhealthy lifestyle [4]. Infection and carriage cannot be prevented (discussed later), so the best prevention of disease is to boost the immune system, avoid people who are sick, and engage in a generally healthy lifestyle.

The destruction of S. pneumoniae releases the toxin pneumolysin, which causes inflammation, and this toxin-mediated inflammation is thought to be responsible for the symptoms of pneumococcal disease. Furthermore, the bacteria also produce hydrogen peroxide, an oxidant which causes further damage and is thus also responsible for some of the symptoms of pneumococcal disease. This peumolysin- and hydrogen peroxide-mediated damage is thought to be responsible for enabling the bacteria to migrate into the lungs or bloodstream, causing pneumonia or invasive disease; the bacteria may migrate to the meninges and cause meningitis either through the bloodstream or directly through the nasopharynx (nose and throat). Furthermore, the pneumolysin damages the cilia in the host’s throat, making it more difficult to move mucus up and out, similarly to pertussis. Also similarly to pertussis, antibiotics attack the bacteria but do not repair the damage and thus may shorten the contagious period or prevent disease if given before symptoms develop but do not improve the progression of the disease or the outcome if given after symptoms have already developed. In fact, by killing the bacteria and thus releasing more of the bacteria’s pneumolysin toxin, antibiotics may actually worsen the disease. [4] Furthermore, unfortunately, the most common strains are also the strains most commonly antibiotic-resistant [7]. Addressing this inflammation and oxidation directly by the use of a safe anti-inflammatory and anti-oxidant that is also effective in the treatment of pertussis—such as vitamin C [10]—may help alleviate some of the symptoms and prevent progression to pneumonia and invasive disease.

 

How effective are the vaccines at preventing asymptomatic carriage?

“These three factors—increased carriage of vaccine-targeted strains, increased carriage of dangerous strains, and increased carriage of other bacteria—suggest ironically that vaccinated (not unvaccinated) children pose significant risk to the vulnerable members of the population and that vaccination therefore should not be relied upon for herd immunity.”

Pneumococcal carriage occurs among vaccinated individuals in proportions similar to unvaccinated individuals. For example, the CDC states, “Studies comparing patterns of pneumococcal carriage before and after PPSV23 vaccination have not shown clinically significant decreases in carrier rates among vaccinees” [5] and a study on PCV7 found that the overall rate of carriage did not change because the decrease in vaccine-targeted serotype carriage occurred alongside an increase in non-vaccine serotypes [11]. The same study found that there was no change in the distribution of asymptomatically carried PPSV23-targeted serotypes, in agreement with the CDC [11]. The CDC goes on to say that carriage of the vaccine-targeted strains may be reduced in recipients of the PCV [5], though it says nothing of serotype replacement (i.e., whether those serotypes are simply replaced by different serotypes, having no net effect on carriage rates). However, studies have demonstrated that extensive serotype replacement occurs with the PCV, with increased carriage occurring in the vaccinated. One study found carriage of nonvaccine serotypes to be 79% in vaccinated children vs. 42.5% in unvaccinated children; another found 39% in vaccinated vs. 21% in unvaccinated; and similar findings have been recorded in other studies [12]. Another study found the overall carriage rate did not change due to simultaneous increases in non-vaccine serotypes and decreases in vaccine-targeted serotypes [13].

The rate of carriage of vaccine-targeted strains is higher among those more recently vaccinated. For example, one study of asymptomatic carriage in children found that 73.1% of the isolates in children <2 years old, 68.9% of the isolates in children 2-5 years old, and 51.2% of the isolates in children >5 years old were vaccine-targeted strains. [7] This indicates that the vaccine increases the risk of asymptomatic carriage of the vaccine-targeted strains. This same study found that all of the invasive strains found in these asymptomatic carrier children were vaccine-targeted strains [7], indicating that vaccinated children may be more likely to be infected with a dangerous strain (because they are less likely to develop disease from it). Another study that compared carriage rates in the same communities before and after widespread use of the PCV7 found that the rate of carriage increased in those younger than 6 months (those most recently vaccinated) and decreased in those older than 36 months (those least recently vaccinated) [11]. Interestingly, this study also found that carriage of H. influenzae B (HiB) slightly and Moraxella catarrhalis significantly increased in the same timespan [11]. Another study duplicated those results, finding no change in S. pneumoniae carriage and increase in M. catarrhalis carriage. It also found that the vaccinated children were more likely to be carriers of pathogenic (disease-causing) bacteria [14]. Yet another study found that decreased pneumococcal carriage is associated with increased Staphylococcus aureus carriage, suggesting that pneumococcal vaccination may result in increased Staph infections [15].

These three factors—increased carriage of vaccine-targeted strains, increased carriage of dangerous strains, and increased carriage of other bacteria—suggest ironically that vaccinated (not unvaccinated) children pose significant risk to the vulnerable members of the population and that vaccination therefore should not be relied upon for herd immunity.

As discussed previously, pneumococcal asymptomatic carriage is more common after influenza infection. [4] I’m unaware of any studies on the effect of the live virus intranasal FluMist influenza vaccination on pneumococcal carriage in humans, but it’s reasonable to believe that FluMist recipients may be more susceptible to pneumococcal carriage than those who received an injected influenza vaccination or no influenza vaccination. This theory holds up to a study in mice, which found that live influenza vaccination increases carriage of S. pneumoniae and Staphylococcus aureus [16].

 

How effective is the pneumococcal vaccine?

The pneumococcal vaccines are said to protect against otitis media (ear infections), pneumonia, meningitis, and sepsis. If the infection moves past the ears and/or lungs to infect the normally sterile linings of the lungs (empyema), meninges of the brain (meningitis), or the blood (sepsis), it’s referred to as invasive pneumococcal disease (IPD). To explain the effectiveness of the pneumococcal vaccines, we’ll consider:

  1. Special Populations (in whom the vaccines may have varying efficacy),
  2. Serotype Replacement and Capsular Switching (which helps the bacteria avoid the pressures of the vaccine),
  3. Otitis Media, and
  4. Invasive Pneumococcal Disease, which will encompass
    • Pneumonia,
    • Meningitis, and
    • Sepsis

1. Special Populations

Unfortunately, the vaccine is not very effective at producing an antibody response in the populations that might benefit from it most: immune-suppressed patients (those lacking a spleen, infected with HIV, etc.), patients with frequent respiratory infections, the elderly, and young children [4]. Furthermore, after the introduction of the vaccine, there was an increase in drug-resistant IPD in the most susceptible populations (those aged <5 and 65+), and a decrease in drug-resistant IPD in the least susceptible populations (those aged 5-64) [17]. Another study in Alaska confirmed these findings, with an increase in the IPD rate in children under 2 and adults over 45, particularly in Alaska Natives, following PCV7 vaccination of infants and toddlers [13]. This poses particular danger to “the herd,” since the vaccine is associated with an increased incidence of disease in the populations most vulnerable to disease complications.

2. Serotype Replacement and Capsular Switching

It was thought that vaccination would be very effective because the majority of cases were caused by only a few serotypes [4], but some researchers warned that other serotypes may quickly move in to replace them (called “strain replacement” or “serotype replacement”) and that the new serotypes may be more dangerous [12]—in colloquial terms, it was a discussion of whether to fight “the devil you know or the devil you don’t.” They also warned that the pneumococci’s ability to switch its capsule in order to change serotype (“serotype switching” or “capsular-switching”) would mean that after infecting a host that had been vaccinated, the bacteria would simply change its serotype in order to avoid the host’s vaccine-induced defenses, a phenomenon called “vaccine escape” [12, 18] (as is the case with meningococcal bacteria [19]). Unfortunately, these researchers’ predictions were correct.

The CDC states that no change in serotypes was noted following the use of PPSV23 in adults [5]. However, serotype-replacement has been observed with the PCV, the first of which (PCV7) was licensed in 2000. For example, one 2004 CDC study examined only serotype 19A, a serotype not included in the PCV7, and found that it almost tripled in incidence between 1999 and 2004 (another study using the same data found that it more than quadrupled [17]), and that it had become more genetically diverse and more drug resistant. Furthermore, their results indicated that many clones (genetic bases) targeted by the vaccine took up the genetic code for the capsule of serotype 19A—in other words, the vaccine-targeted strains changed into serotype 19A, a strain not targeted by the vaccine, an example of capsular-switching as vaccine escape [18]; unfortunately, other studies have shown serotype 19A to be more dangerous, so the decrease in vaccine-targeted serotypes has nonetheless occurred alongside an increase in at least one more dangerous non-vaccine serotype [20]. Other studies have provided further evidence to support capsular-switching and oppose antibiotic-directed evolution as the causes of increases in non-vaccine serotypes [20, 21], though some studies have found that while drug-resistant bacterial samples decreased, drug-resistant infections caused by non-vaccine serotypes increased [13]. In most populations, serotype replacement occurs within 3-4 years after introduction of the vaccine [13].

[22] Note that this occurred in Salt Lake City, Utah, and may not be representative of the general population.

[22] Note that this occurred in Salt Lake City, Utah, and may not be representative of the general population.

The pre-licensure vaccine trials showed no changes in serotypes in response to vaccination. However, this was likely due to the fact that relatively few children were vaccinated in the trials, whereas post-licensure, the vast majority of children have received the vaccine. When the vaccine is used on a large scale, it pushes the serotypes to switch. [11, 12, 20] Populations where PCV7 use was widespread (such as Alaska Natives) experienced significant serotype replacement while populations where pneumococcal vaccination was low or moderate (such as Navajo and Australian aboriginal children) did not experience serotype replacement. In fact, the proportion of Alaska children receiving the pneumococcal vaccine was significantly higher than either the national average or any other individual state [13]. Ironically, this means the pneumococcal vaccine would be most effective in recipients if fewer children received it—the opposite of what is usually asserted.

Another potential issue is that some studies had incomplete data and so chose to extrapolate from the data they did have, essentially guessing about the data they didn’t have and using those guesses in their final results. For example, the 2004 CDC study mentioned above did not have the serotype data for all of the samples and so estimated the actual number and proportions of serotypes by extrapolating from the data they did have [17, 18]. It’s unclear how this affected the results.

Finally, and most likely to have the greatest effect on the results, many studies are of low methodological quality. A meta-analysis of studies on the effect of pneumococcal vaccination against pneumonia in older adults found that when only high-quality studies were included, the results were very homogenous: they all agreed that the vaccine is ineffective. However, when studies of all quality were included, the results were very heterogeneous: the effectiveness of the vaccine was uncertain. [23] In this regard, pneumococcal vaccine effectiveness studies mirror influenza vaccine effectiveness studies [24].

3. Otitis Media

“the vaccine slightly reduces the incidence of [ear infections] in some children, but increases the incidence of [ear infection] that is difficult to treat or comes back again and again”

At least 60% of acute otitis media (AOM) is viral, pneumococcus makes up about 25% of all AOM causes, and over 80% of children with AOM recover without antibiotics. The vaccine was not licensed for prevention of otitis media, though it was nevertheless widely advertised for that use since its introduction. It has been suggested that the vaccine was advertised for this purpose because ear infections are very common among vaccinated children while the more serious concerns of pneumonia and meningitis are very rare [25]. Although the drug manufacturer and others found the vaccine to result in a 6-7% reduction in AOM (there was approximately a 34% reduction in S. pneumoniae ear infections, but S. pneumoniae only caused 25% of ear infections pre-vaccine, so the total effect on ear infections was minimal) with simultaneous decreases in vaccine-targeted serotype AOM and increases in non-vaccine serotype AOM [14, 26, 27], it is not effective at reducing the incidence of recurrent ear infections [28]. Another study found that while pneumococcal ear infections decreased from 48% of ear infections to 31% of ear infections in pneumococcal-vaccinated children, other bacterial causes of ear infection doubled, more than replacing the drop in pneumococcal ear infections. Interestingly, one of the bacteria that increased was nontypeable H. influenzae [29] (for more information on HiB, please refer to our previous publication on that topic here). Other studies found increases in carriage of M. catarrhalis (which is more difficult to treat) and HiB, and that vaccinated children were more likely to be infected with pathogenic (disease-causing) bacteria, increasing the risk of antibiotic treatment failure and recurrent AOM [11, 14]. Another study found not only that there was no reduction in AOM among pneumococcal-vaccinated children, but also that pneumococcal-vaccinated children were more likely to have ear infections caused by Staphylococcus aureus, which poses serious concerns about antibiotic resistant ear infections caused by methicillin-resistant Staphylococcus aureus (MRSA) [15, 30]. Another study found no decrease in AOM in children who received pneumococcal vaccines compared to children who received hepatitis A or B vaccines [31], which may be an odd choice for comparison, given that the hepatitis A vaccine may cause AOM [32]; this means they compared the AOM rate after pneumococcal vaccines to the AOM rate after another vaccine which can cause AOM; as there was no difference in AOM rate between the PCV-vaccinated and Hep A-vaccinated children, this seems to indicate that PCV increases AOM rates. At any rate, that last odd study aside, the vaccine slightly reduces the incidence of AOM in some children, but increases the incidence of AOM that is difficult to treat or comes back again and again.

4. Invasive Pneumococcal Disease (IPD)

It’s difficult to say what impact the vaccine has on IPD because studies examining all serotypes have observed both a decrease [22] and an increase [21] in IPD. A study in Spain found the proportion of IPD cases caused by non-vaccine serotypes increased from 38% in the prevaccine period to 72% in the

[21]

[21]

postvaccine period with an increase in the total number of IPD cases [21]. Although about half of the children in the Spain study had received the PCV7, and this is suggested as a possible reason for the increase, the same phenomenon of sharply increased IPD (specifically due to non-vaccine serotype increases significantly outweighing the vaccine-targeted serotype decreases) was observed in Alaska as well, where the vast majority of the children had received the PCV7 (the proportion who had received at least 3 doses of PCV7 ranged from 88% in 2003 to 96% in 2006). Particularly interesting is that the proportion of IPD cases designated serious and requiring hospitalization also increased (i.e., IPD cases increased in number and became proportionately more dangerous) [13]. However, another 2004 study that looked at all serotypes found a simultaneous decrease in vaccine-targeted serogroups and increase in non-vaccine serogroups such that the total number of IPD cases did not change, though the proportion of cases caused by drug-resistant bacteria and the proportion of cases identified as serious or life-threatening increased. Especially important to note was that the cases caused by non-vaccine serotypes were the most severe [22], suggesting that the vaccine-targeted serotypes were replaced with more dangerous serotypes, which, as discussed above, researchers had previously warned might occur. It is interesting to note that the increase in drug resistance was noted in PCV7-targeted serotypes in one study [22] but in non-vaccine serotypes in another study [11], while another study found a decrease in drug resistance [21]. Another study found a decrease in drug-resistant bacteria overall but a total increase in drug-resistant IPD in young children and the elderly; and an increase in drug-resistant IPD caused by vaccine-targeted serotypes with the greatest increase in drug resistance in serotype 19A (the nonvaccine serotype which increased the most in overall number and proportion of cases) [17]. Other more recent studies have found further increases in both 19A and other non-vaccine serotypes as well as a further increase in drug-resistant pneumococcal infections among the vaccinated but not among the unvaccinated, with the risk highest among those who’d received the most doses of vaccine [20].

Why are the results so variable between studies? It’s probably mostly an issue of which populations are included in the study. For example, the CDC study mentioned above, which found a drop in total IPD cases and apparently no change in the seriousness of IPD cases [17, 18], did not include the population reported by another study, where there was no change in total IPD cases and an increase in serious and life-threatening cases [22]. As discussed previously, the proportions of each serotype vary significantly from population to population, so the vaccine may be very effective in one population and very ineffective in another. If a study of the entire nation, which necessarily must sample various populations rather than including every single case across the country, selectively studies the populations where the vaccine is most effective, as the CDC apparently did (probably unintentionally, since they examined data from the designated CDC surveillance sites), this will skew the results. For this reason, I’m afraid all that can really be said is some studies found the vaccine to be productive and others found the vaccine to be counter-productive, and unfortunately we can’t really know which is true for the general population, nor can we accurately predict which populations will be most benefitted by the vaccine or most harmed by it. (And I know that statement will be unpopular with both pro-vaxxers and anti-vaxxers. Sorry, not sorry.)

A. Pneumonia

“…in children, the vaccine may increase or slightly reduce the incidence of pneumonia but increases the incidence of severe pneumonia that is more dangerous and more difficult to treat. [….] …pneumococcal vaccination does not prevent pneumonia in older adults… but was associated with an increase in severe pneumonia requiring hospitalization.”

In 2004, just four years after the PCV7 was licensed, researchers noted an increase in parapneumonic empyema (a very severe form of pneumonia where the lining of the lungs becomes infected, with mortality as high as 30% in non-immunocompromised patients) caused by pneumococci in spite of decreases in pneumococcal disease and pneumococcal pneumonia, data which confirmed previous studies [22]. A Cochrane Review from 2004 found no effect of PCV7 on clinical pneumonia rate [33] while the Cochrane Review from 2009 found that PCV7 slightly decreases the clinical pneumonia rate [34]. However, a more recent study from 2010 found that PCV7 vaccination was associated with an increase in drug-resistant pneumonia among the PCV7-vaccinated but not among the PCV7-unvaccinated [20]. As discussed above, serotype prevalence differs significantly from population to population and so the vaccine may be very effective in one population and very counter-productive in another. This was exemplified in Britain, where the PCV7 was introduced in 2006, and by 2008, health authorities noted that the incidence of empyema (very severe pneumonia) had risen significantly, due in part to the 10-fold rise in serotype 1 (not included in the vaccine). Though the rise in serotype 1 began before introduction of the vaccine and thus cannot be blamed solely on the vaccine, serotype-replacement surely contributed [35]. Spain also saw an overall increase in IPD in children under 2 after introduction of the PCV7, including a more than fourfold increase in pneumonia [21]. Alaska saw the same pattern, with an overall increase in pneumonia cases and an increase in the proportion of pneumonia cases that involved empyema [13]. In other words, in children, the vaccine may increase or slightly reduce the incidence of pneumonia but increases the incidence of severe pneumonia that is more dangerous and more difficult to treat.

A rigorous meta-analysis published in 2009 found that pneumococcal vaccination does not prevent pneumonia in older adults [23]. As in studies of children discussed above, the use of the PPSV in elderly adults was not associated with a decrease in pneumonia, but was associated with an increase in severe pneumonia requiring hospitalization [36].

B. Meningitis

A study in Spain found that though the rates of sepsis and pneumonia increased after introduction of the PCV7, the rate of meningitis decreased. Nevertheless, the decrease in meningitis cases was not great enough to offset the large increases in pneumonia and sepsis [21].

C. Sepsis

Also called septicemia or bacteremia and “blood poisoning,” this refers to a bacterial infection of the blood. A study in elderly adults found a decrease in pneumococcal sepsis following pneumococcal vaccination, but did not examine other potential causes of sepsis [36]. However, as early as 2004, researchers noted that the number of invasive pneumococcal disease cases did not change due to simultaneous decreases in vaccine-targeted serogroups and increases in non-vaccine serogroups, and there was an increase in cases of severe disease (those classified as “serious” or “life-threatening”) [22]. In 2005, researchers noted that though the overall pneumococcal IPD rate decreased, the proportion of IPD cases caused by non-vaccine serogroups increased (a form of serotype replacement), and the proportion of cases caused by drug-resistant bacteria increased [18]. Studies in other countries, such as Spain, confirmed some of these results. Oddly, the Spain study found that sepsis rates overall increased (from a per 100,000 population rate of 14.5 to 21.4 in children <2 and 1.5 to 5.8 in children 2-4) and the specific causes of sepsis that increased in incidence were S. pneumoniae, the species targeted by the vaccine, and E. coli [21]. A study in Alaska also found an increase in bacteremia [13].

 

So if it’s not effective, why did it get licensed and put on the CDC vaccine schedule?

Of the 12 committee members at the FDA responsible for determining whether to approve Prevnar for licensing, four had financial ties to the drug company making Prevnar. Of those four, three were granted waivers so that they could still vote. [37] For this reason, some believe the committee’s approval of the pneumococcal vaccine was largely a matter of bias. For a long time, Prevnar was the most expensive vaccine on the market. At one time, Prevnar alone accounted for 40% of the cost of vaccination according to the CDC schedule. Financially speaking, Prevnar performed exceptionally well compared to other vaccines.

 

Are there other infectious diseases related to pneumococcal vaccination?

The use of other bacterial vaccines, particularly pertussis, seems to have contributed to the sudden increase in HiB infections in the 1970s and 1980s. [38] This led to the creation of the HiB vaccine. However, the introduction of the HiB vaccine also seems to have caused the sudden increase in pneumococcal infections, which are more dangerous and less treatable than HiB. This led to the introduction of the pneumococcal vaccine. However, the introduction of the pneumococcal vaccine seems to have caused the sudden increase in meningococcal infections, which are more dangerous and less treatable than pneumococcal infections. This led to the introduction of the meningococcal vaccine. There is concern that meningococcal vaccination will also be followed by the sudden increase of another more dangerous and less treatable bacterial disease. [39, 40]

 

What are the risks of the vaccine?

Prevnar has a troubled history. As mentioned above, there were significant financial conflicts of interest in the licensing process. Furthermore, a whistleblower came forward in 2004 with allegations that the company was violating certain FDA rules regarding quality control [41]. Many in developing nations such as Argentina were apparently coerced into participating in the Prevnar vaccine trials under threat of having their children taken from them if they refused [42]. It was also halted or outright banned in many countries shortly after introduction due to severe adverse reactions, particularly death, including, but not limited to, the Netherlands [43], Portugal [44, 45], Japan [46], and India [47].

The drug company making Prevnar performed short-term safety studies in which Prevnar was compared to an experimental vaccine. Prevnar was found to cause more seizures and rashes, and higher fevers than the experimental vaccine. Prevnar was not compared to a placebo. [25, 37]

Please note that having had the vaccine once without any serious reactions does not mean serious reactions will not happen with future vaccination. For example, this article reported a case where a patient with previous pneumococcal vaccination nevertheless had a serious local reaction (severe pain and swelling that extended beyond the area of the injection) upon repeat vaccination [48] and, in fact, reactions are more common in those who have had the vaccine before than in those receiving the vaccine for the first time [49].

Seizures. One study conducted by the vaccine manufacturer found seizures to occur four times as often in children receiving the pneumococcal vaccine than in children receiving another experimental vaccine (it was not compared to a saline placebo) [25].

Asthma. One study found the incidence of asthma in pneumococcal-vaccinated children (2.96/1000) was nearly double the incidence in pneumococcal-unvaccinated children (1.66/1000). The authors postulated that this was related to “the hygiene hypothesis of decreased childhood infections” [50]. The hygiene hypothesis notes that children who have fewer childhood infections (including measles and hepatitis A) have a higher incidence of allergies and asthma, and hypothesizes that induction of a Th1 response early in life prevents or even reverses the imbalanced Th1/Th2 ratio in people who are prone to asthma [51].

Thrombocytopenia. The vaccine has been noted to cause relapses of immune thrombocytopenia [52].

Autoimmune Diseases. Pneumococcal vaccination has been shown to cause onset or rebound of the following autoimmune conditions: idiopathic thrombycytopenic purpura, peripheral and central demyelinating disease, Henoch-Schönlein Purpura (a form of leukocytoclastic vasculitis), Guillain-Barre Syndrome, minimal-change nephritic syndrome, neuromyelitis optica (a.k.a., optic neuritis), Sweet’s syndrome, autoimmune hemolytic anemia, systemic lupus erythematosus, migrating arthralgia, angioimmunoblastic lymphadenopathy with dysproteinemia (a type of lymphoma), and chronic fatigue syndrome. It has been involved in at least two cases of bullous phemigoid, myositis, but other vaccines were given simultaneously, so causation with pneumococcal vaccination cannot be demonstrated. These conditions have largely occurred following PPV rather than PCV, as the PCV is too new for most autoimmune conditions to have presented themselves and is given primarily in children, in whom many autoimmune reactions are missed due to age-related difficulty expressing or recognizing symptoms [53]

Local Reactions. Local reactions, such as severe pain and swelling that extends far beyond the area of the injection, have been reported to occur even in those who have previously received pneumococcal vaccination or had extensive laboratory contact with pneumococci with no previous reaction [48]. These local reactions may mimic cellulitis and have high white blood cell counts, leading to unnecessary hospitalization and antibiotic treatment if the treating physician is unaware that this is a typical, noninfectious reaction to the vaccine. A local reaction occurs in as many as 50% of vaccine recipients, with the highest rate in those who have previously had pneumococcal vaccination [49].

Apnea in Preemies. Apnea (temporary suspension of breathing) has been observed in premature infants who receive Prevnar. [54]

Bronchiolitis, Gastroenteritis, Pneumonia. Ironically, one of the most common serious adverse events following this pneumonia vaccine is pneumonia. [54]

Hypotonic-Hyporesponsive Episodes. This is similar to fainting; the child may be awake but have altered consciousness. This is one of the most common serious adverse reactions reported. [54]

 

What vaccines are offered against pneumococcal?

In the U.S., there are two pneumococcal vaccines, the PCV13 (the replacement for PCV7), which targets 13 strains and is recommended for children under 5 and adults over 64 (and those aged 6+ who are at high risk), and the PPSV23, which targets 23 strains and is recommended for adults over 64 (and those aged 2-64 who are at high risk). (NOTE: These ingredients lists are not complete; they only list the most alarming ingredients.)

  • Prevnar 13: diphtheria-pneumococcal (diphtheria CRM197 protein, pneumococcal 13 serotypes, soy, yeast, ammonium sulfate, polysorbate 80, aluminum) [54]
  • Pneumovax 23: pneumococcal (pneumococcal 23 serotypes, phenol) [55]

 

So what’s the bottom line?

The bottom line is that S. pneumoniae is so common that almost 100% of the population carries it at some point and develops some degree of immunity by age 2. There are over 90 serotypes, and the bacteria easily change their serotype (serotype switching) to avoid the host’s vaccine-induced defenses. The vaccine does not prevent asymptomatic carriage—in fact, it may increase asymptomatic carriage not only of S. pneumoniae but also of other bacteria—and so cannot contribute to herd immunity and may, in fact, pose greater risk to the herd. The vaccine is said to protect against ear infections, pneumonia, meningitis, and sepsis, but may actually be ineffective for all of these purposes due partly to serotype switching and serotype replacement, and partly to increases in other bacteria. The serotypes not covered by the vaccines are more dangerous, and so the proportion of serious infections is higher in vaccinated children than in unvaccinated children. Because it is mostly ineffective, the risks, no matter how mild, outweigh the benefit.

 

References

[1] http://www.cdc.gov/vaccines/schedules/downloads/child/0-18yrs-child-combined-schedule.pdf

[2] http://www.cdc.gov/vaccines/vpd-vac/pneumo/default.htm

[3] http://healthycanadians.gc.ca/healthy-living-vie-saine/immunization-immunisation/children-enfants/schedule-calendrier-table-1-eng.php

[4] http://www.ncbi.nlm.nih.gov/pmc/articles/PMC239389/pdf/590591.pdf

[5] http://www.cdc.gov/vaccines/pubs/pinkbook/downloads/pneumo.pdf

[6] http://jid.oxfordjournals.org/content/194/5/682.full

[7] http://wwwnc.cdc.gov/eid/article/8/5/01-0235_article

[8] http://www.ncbi.nlm.nih.gov/pubmed/9402367

[9] http://www.ncbi.nlm.nih.gov/pubmed/24749506

[10] http://www.vaccinationcouncil.org/2012/09/07/vitamin-c-for-whooping-cough-updated-edition-suzanne-humphries-md/

[11] http://pediatrics.aappublications.org/content/116/3/e408.full-text.pdf

[12] http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2640786/pdf/10341170.pdf

[13] http://jama.jamanetwork.com/article.aspx?articleid=206757

[14] http://www.ncbi.nlm.nih.gov/pubmed/16651345

[15] http://jama.jamanetwork.com/article.aspx?articleid=199212

[16] http://mbio.asm.org/content/5/1/e01040-13.full

[17] http://www.nejm.org/doi/full/10.1056/NEJMoa051642

[18] http://jid.oxfordjournals.org/content/192/11/1988.long

[19] See the previous Meningococcal Weekly Topic located here: https://schaabling.wordpress.com/2016/01/01/meningococcal-vaccine-meningitis/

[20] http://jama.jamanetwork.com/article.aspx?articleid=186547

[21] http://cid.oxfordjournals.org/content/46/2/174.long

[22] http://cid.oxfordjournals.org/content/41/1/21.full.pdf+html

[23] http://www.cmaj.ca/content/180/1/48.full

[24] Per Cochrane Collaboration: “An earlier review of 274 influenza vaccine studies in all age groups (including most of the studies in this review) showed an inverse relationship between risk of bias and the direction of study conclusions. Conclusions favourable to the use of influenza vaccines were associated with a higher risk of bias. In these studies, the authors made claims and drew conclusions that were unsupported by the data they presented. In addition, industry-funded studies are more likely to have favourable conclusions, to be published in significantly higher-impact factor journals and to have higher citation rates than non-industry-funded studies. This difference is not explained by either their size or methodological quality (Jefferson 2009a). Any interpretation of the body of evidence in this review should be made with these findings in mind.” http://onlinelibrary.wiley.com/doi/10.1002/14651858.CD001269.pub5/full

[25] https://web.archive.org/web/20010605115354/http://www.wfaa.com/wfaa/articledisplay/0,1002,20489,00.html

[26] http://www.nejm.org/doi/full/10.1056/NEJM200102083440602#t=article

[27] http://cid.oxfordjournals.org/content/40/12/1738.long

[28] http://www.ncbi.nlm.nih.gov/pubmed/16510637

[29] http://www.ncbi.nlm.nih.gov/pubmed/15361721

[30] http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(03)13772-5/fulltext

[31] http://www.thelancet.com/journals/lancet/article/PIIS0140673603137725/abstract

[32] http://www.fda.gov/downloads/BiologicsBloodVaccines/Vaccines/ApprovedProducts/UCM110049.pdf

[33] http://onlinelibrary.wiley.com/doi/10.1002/14651858.CD004977/abstract NOTE: The link provided goes to the abstract; however, the information about clinical pneumonia is in the full text of the article, not in the abstract.

[34] http://onlinelibrary.wiley.com/doi/10.1002/14651858.CD004977.pub2/abstract

[35] http://www.independent.co.uk/life-style/health-and-families/health-news/increase-in-severe-pneumonia-in-children-may-be-caused-by-vaccine-808633.html

[36] http://columbiamedicine.org/education/r/ID/Outpatient%20and%20Prevention/Pneumonia%20Vaccine.pdf

[37] https://web.archive.org/web/20010825174745/http://www.wfaa.com/wfaa/articledisplay/0,1002,20550,00.html

[38] http://www.wellwithin1.com/HibPneuButler1993to2006letters.pdf

[39] “Several factors indicate that mass immunisation with pertussis and other non-Hib vaccines may have been responsible for the unprecedented epidemics of invasive bacterial infections such as Hib, during the 1970’s and 1980’s.” (p. 315) Miller, N.Z. (2008). Vaccine Safety Manual.

[40] https://www.youtube.com/watch?v=QVE2l2RJ8lY

[41] https://www.lawyersandsettlements.com/articles/whistleblower/wyeth-00187.html

[42] http://abcnews.go.com/Health/story?id=5735276&page=1

[43] http://www.dutchnews.nl/news/archives/2009/11/vaccine_use_halted_after_baby

[44] https://web.archive.org/web/20120531095007/http://www.oserledire.com/article-portugal-suspension-des-vaccins-prevenar-et-rotateq-apres-effets-secondaires-graves-102046008.html

[45] http://www.rtp.pt/noticias/mundo/infarmed-suspendeu-vacinas-rotateq-e-prevenar-13-por-suspeita-de-reacao-adversa_n537610

[46] http://blogs.wsj.com/health/2011/03/07/scrutinized-in-japan-pfizers-prevnar-vaccine-is-used-widely-in-u-s/

[47] http://www.livemint.com/Home-Page/j4W7C2aW2imlLjKZPUSfNM/Wyeth-drug-tests-fall-foul-of-watchdog.html

[48] http://www.ncbi.nlm.nih.gov/pubmed/7355337

[49] http://www.tandfonline.com/doi/full/10.4161/hv.28559

[50] http://www.nejm.org/doi/full/10.1056/NEJMoa035060#t=article

[51] http://www.tandfonline.com/doi/abs/10.3109/07853890008995946

[52] http://jama.jamanetwork.com/article.aspx?articleid=377409

[53] Shoenfeld, Y., Agmon-Levin, N., & Tomljenovic, L. (2015). Vaccines and Autoimmunity (pp. 193-195, 227, 323, 340, 346, 354). Hoboke, NJ: Wiley Blackwell.

[54] http://www.fda.gov/downloads/BiologicsBloodVaccines/Vaccines/ApprovedProducts/UCM201669.pdf

[55] http://www.fda.gov/downloads/BiologicsBloodVaccines/Vaccines/ApprovedProducts/UCM257088.pdf

Pneumococcal Vaccine (Pneumonia, Meningitis) SHORT

This is the short version. See the long version with references here.

streptococcus_pneumoniae_2

What are the “meningitis vaccines”?

There are two basic types of meningitis: viral and bacterial. There are no vaccines targeting viral meningitis. There are three vaccines targeting causes of bacterial meningitis: HiB (Weekly Topic 05), pneumococcal, and meningococcal (Weekly Topic 03).

There are two types of pneumococcal vaccines: conjugated (PCV) and unconjugated (PPSV).

What is pneumococcus?

Streptococcus pneumoniae, often referred to as pneumococcus, is a bacterium. It may have a capsule or not have a capsule. The structures on the capsule determine its serotype. It can adopt or change its capsule, thus changing its serotype. This is called “serotype switching.” There are over 90 serotypes. Which serotypes are most common and how many are resistant to drugs varies significantly by geographic location.

S. pneumoniae is normally carried by healthy people with no symptoms (asymptomatic carriers). Depending on the population, 5-60% may be carriers. About half of babies become carriers by age 6 months and almost 100% become carriers by age 2 years. Carriage is more common after viral infection (especially influenza). Asymptomatic carriage typically lasts months. Because carriage is so common, disease is relatively rare.

S. pneumoniae is a common cause of otitis media (middle ear infection). If disease develops, complications are uncommon but include pneumonia, meningitis, and sepsis.

How can I prevent or treat pneumococcal infection in my child?

Conditions that make an individual more susceptible to pneumococcal disease include recent viral infection, immune suppression, and a generally unhealthy lifestyle. The best prevention is to boost the immune system, avoid people who are sick, and engage in a generally healthy lifestyle. The vitamin C protocol for pertussis may help treat pneumococcal infection.

How effective are the vaccines at preventing asymptomatic carriage?

Neither PPSV nor PCV decrease asymptomatic carriage. Some studies find that asymptomatic carriage increases with PCV. After PCV, vaccine-targeted pneumococcal serotypes decrease but non-vaccine serotypes increase (called “serotype replacement”), and carriage of other species of bacteria (including HiB, M. catarrhalis, and Staphylococcus aureus) increase. FluMist vaccination also increases carriage of S. pneumoniae and Staph.

How effective is the pneumococcal vaccine?

The pneumococcal vaccines are said to protect against otitis media (ear infections), pneumonia, meningitis, and sepsis. If the infection moves past the ears and/or lungs to infect the normally sterile linings of the lungs (empyema), meninges of the brain (meningitis), or the blood (sepsis), it’s referred to as invasive pneumococcal disease.

1. Special Populations. The vaccine is less effective in the populations who are most susceptible to complications from pneumococcus: immunosuppressed patients, patients with frequent respiratory infections, the elderly, and young children. Some studies found that vaccination of children with PCV was followed by an increase in drug-resistant pneumococcal infections in young children and/or the elderly.

2. Serotype Replacement. S. pneumoniae can change its serotype after infecting someone. When one serotype is targeted by a vaccine, the bacteria can simply infect the vaccinated child and then switch its serotype in order to bypass the child’s defenses. This is called “vaccine escape.” The newest PCV targets 13 serotypes, but there are over 90 pneumococcal serotypes. After vaccination, researchers noted significant serotype replacement, which has often resulted in no change or an increase in the total number of IPD cases. Some studies have also shown an increase in antibiotic resistance.

3. Otitis Media (Ear Infection). At least 60% of acute otitis media (AOM) is viral, pneumococcus makes up about 25% of all AOM causes, and over 80% of children with AOM recover without antibiotics. Studies have found either a 6-7% decrease or no change in AOM; no change in recurrent AOM; and an increase in other serotypes (serotype replacement) and other species of bacteria which are more likely to be antibiotic resistant and harder to treat. In other words, the vaccine may or may not affect the rate of AOM but increases the likelihood that AOM will be difficult to treat.

4. Invasive Pneumococcal Disease (IPD). Studies vary significantly, with results ranging from a decrease to no change to an increase in IPD; however, serotype replacement is common. Disease caused by non-vaccine serotypes is more severe and some studies report it is also more likely to be antibiotic-resistant and more difficult to treat. The worst effects occur in the very young, the very old, and those who’ve received the most doses of the vaccine.

a. Pneumonia. In children, studies find slight decrease, no change, or significant increase in overall pneumonia cases; extensive serotype replacement; and an increase in empyema (severe pneumonia). In other words, the vaccine may or may not affect the rate of pneumonia in children, but it increases the rate of severe pneumonia that is difficult to treat. In older adults, pneumococcal vaccination is ineffective.

b. Meningitis. Studies seem to agree that meningitis rates decrease, but this drop in meningitis occurs alongside an increase in pneumonia and sepsis.

c. Sepsis. Studies have found decrease, increase, or no change in sepsis rate; extensive serotype replacement; and increases in severe disease, drug-resistant cases, and cases caused by other bacteria (notably E. coli). In other words, the vaccine may or may not affect the sepsis rate, but makes it more difficult to treat.

What are the risks of the vaccine?

A short list of the most concerning risks includes:
• seizures
• asthma
• thrombocytopenia
• autoimmune diseases
• local reactions that will be mistaken for infection and result in unnecessary hospitalization and antibiotic use

So what’s the bottom line?

S. pneumoniae is so common that almost 100% of the population carries it and develops some degree of immunity by age 2. There are over 90 serotypes, and the bacteria easily change their serotype to avoid the host’s vaccine-induced defenses. The vaccine may increase asymptomatic carriage not only of S. pneumoniae but also of other bacteria and so cannot contribute to herd immunity and may actually pose greater risk to the herd. The vaccine is said to protect against ear infections, pneumonia, meningitis, and sepsis, but may actually be ineffective for all of these purposes due partly to serotype switching and serotype replacement, and partly to increases in other bacteria. The serotypes not covered by the vaccines are more dangerous, and so the proportion of serious infections is higher in vaccinated children than in unvaccinated children. Because it is mostly ineffective, the risks, no matter how mild, outweigh the benefit.

HiB Vaccine (Meningitis)

This is a continuation of a weekly series I’ve been helping to write for an education forum. This is the long version. For the short version, click here.

H. influenzae type B, (c) NHS

H. influenzae type B, (c) NHS

What are the “meningitis vaccines”?

There are two basic types of meningitis: viral and bacterial. There are no vaccines targeting viral meningitis. There are three vaccines targeting causes of bacterial meningitis: HiB, pneumococcal, and meningococcal. Meningococcal was Weekly Topic 03, HiB will be discussed here, and pneumococcal will be discussed in a future Weekly Topic.

According to the CDC Vaccination Schedule (2015), HiB vaccination occurs at 2 mo, 4 mo, 6 mo, and 12/15 mo. No further doses are recommended after the 15 mo dose, even if it was the only dose ever received. It is not recommended after age 5 years in healthy children. It is only available as a combination vaccine, not alone [1, 2]. In Canada, depending on province/territory, a HiB combination vaccine is typically recommended at 2 mo, 4 mo, 6 mo, and 18 mo [3].

 

What is HiB?

Haemohpilus influenzae type B is a bacterium that normally lives in the respiratory tracts of healthy people without causing disease. Up to 5% of the population is infected at a given time, and most children become infected by H. influenzae bacteria by the age of 5, whereby they develop immunity. Infection is more common in crowded housing and settings such as daycare; in fact, in daycare, the infection rate is approximately 15%, 3-15 times the proportion of the general population. Asymptomatic carriers remain infected and contagious for months at a time and the bacteria may easily pass from one person with disease through a long line of asymptomatic carriers before causing disease in another. It is present in the nose and throat and thus is passed by coughing or contact with mucus. However, cribs and toys of daycare children known to be asymptomatic carriers test negative for the bacteria, so contact with contagious children’s belongings is not believed to be a route of transmission. [4]

Because H. influenzae bacteria are a normal part of our respiratory tracts, probably 100% of the population becomes infected at some point, and most infections are asymptomatic, HiB disease is relatively very rare. However, when it does occur, HiB disease may result in sepsis, meningitis, and even death. Among those with HiB disease, approximately 3-6% die and 15-35% suffer permanent neurological sequelae (the most common being partial hearing loss). The most common symptoms of HiB disease include fever, decreased mental status, and stiff neck. [4, 5, 6]

 

How can I prevent or treat HiB in my child?

Conditions that make an individual more susceptible to HiB disease include recent viral infection, smoking or other respiratory irritants, immune suppression (e.g., sickle-cell anemia, absence of a spleen, antibody deficiency disorders, cancer, chemotherapy, etc.), and crowded housing or environment. [4] Avoid exposing your child to these triggers as much as possible by smoking cessation, avoiding crowded living spaces if possible, boosting the immune system, etc., and engaging in a generally healthy lifestyle. If your child has a known exposure to HiB, prompt evaluation by a physician for prophylactic antibiotics may be prudent.

Breastfeeding offers significant protection against HiB, lasting years after weaning [4, 7]. If breastfeeding is not possible due to adoption or other issues, look into relactation, pumping, or donor milk.

Note as discussed later in this post that there is an increased risk of HiB disease in the first week following vaccination. Therefore, if you choose to vaccinate and your child develops symptoms of HiB following vaccination, take it seriously.

 

How effective are the vaccines at preventing asymptomatic carriage?

Several studies have found HiB carriage to be reduced (but not eliminated) by vaccination. [4] Other studies have shown that when HiB vaccination was introduced to a population, HiB disease rates in both vaccinated and unvaccinated infants decreased, but were not eliminated in spite of very high vaccination rates [4]. Because it does not eliminate asymptomatic carriage, and the bacteria can jump from asymptomatic carrier to asymptomatic carrier regardless of the carrier’s vaccine status before causing disease in a susceptible individual, the vaccine cannot be relied upon for herd immunity, as evidenced by continued HiB disease in highly vaccinated populations.

 

How effective is the HiB vaccine?

Prior to the introduction of the vaccine, HiB caused over 80% of all invasive H. influenzae disease among children [8]. The incidence of HiB began to drop before the introduction of the vaccine [9, 10] and continued to drop after vaccination.

The HiB vaccine is of questionable efficacy, with some studies finding it not to be protective in children younger than 18 months, others finding variable efficacy in children over the age of 2, and others finding an increased risk of meningitis immediately following vaccination, with efficacy ranging from 88% to -69%. [6, 11] Newer conjugate vaccines have widely ranging efficacy depending on the population in which it they are tested. For example, the diphtheria-HiB (PRP-D) vaccine ranged from 35% efficacy (in producing an antibody response) in Alaskan Natives and <40% in Finnish children to 87% in another group of Finnish children [12]. Even across a single country, the same vaccine may be associated with vastly varying efficacy, as in one study that found a HiB vaccine that was effective in other areas of the U.S. was not associated with increased antibody response or decreased disease rate in Minnesota [13]. Another study found that HiB-vaccinated children with HiB disease had significantly lower HiB antibody levels than unvaccinated children with HiB disease. This was in spite of appropriate antibody response to other vaccines they had received. It’s thought to be partly due to a genetic defect that affects their ability to produce antibodies specifically to HiB [14].

All of the above estimates of efficacy depend on assumptions regarding what antibody level will be effective at preventing HiB disease, though the CDC states, “the precise level of antibody required for protection against invasive disease is not clearly established.” [15] However, the change in HiB incidence following vaccination can give us an idea of the vaccine’s efficacy.

The introduction of the HiB vaccine was followed by a shift in the dominant strains of H. influenzae from type B (HiB) to predominately nontypeable and type F (HiF)—that is to say, the incidence of infections and invasive disease caused by type B dropped while the incidence of infections and invasive disease caused by other strains increased. The overall incidence of H. influenzae invasive disease and death increased after the introduction of the vaccine. In other words, the introduction of the vaccine was followed by a net increase in H. influenzae-related morbidity and mortality in spite of the decrease in type B disease and death. [8]

This suggests that the HiB vaccine increases the overall risk of H. influenzae morbidity and mortality by increasing one’s risk particularly to non-B H. influenzae. This goes back to the theory of original antigenic sin. In short, people who are vaccinated against one strain are able to produce antibodies only to the antigens included in the vaccine, which handicaps them in fighting other viruses or bacteria that are similar enough to trigger their body’s antibody response but different enough that they don’t have antibodies against the primary antigens. In the case of pertussis, we see how vaccination against PRN-positive B. pertussis increases the risk of PRN-negative B. pertussis, B. parapertussis, and sometimes B. holmesii [16]. In the case of N. meningitidis, we see how the meningococcal vaccine increases the risk of infection with serogroups not included in the vaccine [17]. And here we see that the HiB vaccine increases the risk of H. influenzae strains not included in the vaccine, as discussed above.

The majority of H. influenzae invasive disease occurs in those aged 65 years or older. Furthermore, the introduction of the vaccine in children was followed by a rise in H. influenzae invasive disease and death in adults, especially the vulnerable elderly, demonstrating a negative herd effect. The introduction of the vaccine in children was followed by a net increase in H. influenzae-related morbidity and mortality in those too old to be vaccinated and in the vulnerable. In other words, the vaccine seems to have the opposite effect on the herd—a harmful rather than a helpful effect. [8]

 

Are there other infectious diseases related to HiB vaccination?

The use of other bacterial vaccines, particularly pertussis, seems to have contributed to the sudden increase in HiB infections in the 1970s and 1980s. [18] This led to the creation of the HiB vaccine. However, the introduction of the HiB vaccine also seems to have caused the sudden increase in pneumococcal infections, which are more dangerous and less treatable than HiB. This led to the introduction of the pneumococcal vaccine. However, the introduction of the pneumococcal vaccine seems to have caused the sudden increase in meningococcal infections, which are more dangerous and less treatable than pneumococcal infections. This led to the introduction of the meningococcal vaccine. There is concern that meningococcal vaccination will also be followed by the sudden increase of another more dangerous and less treatable bacterial disease. [5, 19]

 

What are the risks of the vaccine?

Type 1 Diabetes. The HiB vaccine is associated with a 25% increased incidence of type 1 diabetes as compared to vaccinated children who did not receive the HiB vaccine [5, 20, 21, 22; 23, p. 872; 24]. The risk increases with just one dose of HiB vaccine, but is highest in children who received all four doses [25]. In fact, the long-term complications from HiB-vaccine-induced type 1 diabetes alone outweigh the long-term complications from HiB disease if no children were vaccinated against HiB [26].

H. influenzae non-B Invasive Disease. As discussed above, the vaccine is associated with an overall increased incidence in H. influenzae infections and deaths. This is because the increase in non-B infections is more than the decrease in type B infections. The increase in non-B H. influenzae disease and death alone outweighs the drop in type B disease and death.

HiB Invasive Disease. Many studies have found an increased incidence of HiB invasive disease in the first week following vaccination with some types of HiB vaccine. “The evidence favors acceptance of a causal relation between unconjugated PRP vaccine and early-onset Hib disease.” [11] It’s said that this risk is only present with unconjugated vaccines (which we no longer use in the U.S.) [11], but it’s actually more common with conjugated vaccines (which we currently use in the U.S.) [27]. At times, this has occurred as early as 3 hours after HiB vaccination [28] and after a second HiB vaccine when there was no reaction to the first [29]. It’s important to note that this is not due to injection with live bacteria—that is, the contents of the vaccine do not directly cause the infection. Rather, it may be due to two related issues. One is that a dramatic decrease in antibody levels occurs in the first few days after vaccination due to the antibodies already present in the child pre-vaccination being quickly used up in fighting the antigens found in the vaccine, leaving the child susceptible to HiB in the environment due to inadequate antibody levels [28]. Another is the vaccine causing a briefly suppressed immune system, which makes the recipient more susceptible to disease. This is called “provocation disease” and was first recorded in medical literature in the 1960s in relation to polio, tuberculosis, and a few other diseases occurring secondary to vaccination [30, pp. 179-188].

Transverse Myelitis. There may be an association between the vaccine and transverse myelitis. This association is based on VAERS reports, not on medical literature. “The evidence is inadequate to accept or reject a causal relation between Hib vaccines and transverse myelitis.” [11]

Guillain-Barré Syndrome (GBS). There may be an association between the vaccine and transverse myelitis. This association is based on a published case series and VAERS reports. “The evidence is inadequate to accept or reject a causal relation between Hib vaccines and GBS.” [11]

Thrombocytopenia. This possible association is based on data from a HiB vaccine trial conducted in adults, as well as VAERS reports. “The evidence is inadequate to accept or reject a causal relation between Hib vaccines and thrombocytopenia.” [11]

SIDS. There are VAERS reports of SIDS cases occurring in close temporal association to HiB vaccination. [31] The association does not seem to have been studied in depth.

Asthma and Allergies. A Swiss study found HiB-vaccinated children to have a higher incidence of asthma and allergies as compared to HiB-unvaccinated children [32]. Studies in guinea pigs found asthmatic reactions to begin as early as four days following HiB vaccination [33].

Epiglottitis. The same Swiss study referenced above [32] found that an increase in epiglottitis was associated with the HiB-vaccine-associated increase in asthma and allergies.

Autism. The autism rate did not change significantly after the introduction of the MMR and DTP vaccines. However, it began to rise significantly after the introduction of the HiB and Hep B vaccines. Many parents have noted autistic regression following the MMR, which used to be given at the same time as the HiB vaccine. [34] Correlation does not equal causation, but a study comparing the autism rates in children who did and children who did not receive the HiB vaccine would be interesting. To my knowledge, such a study has not been conducted.

Encephalitis. There is at least one report of encephalitis occurring after HiB vaccination, but the child was simultaneously vaccinated against DPT (known to be associated with encephalitis) and OPV, so it’s uncertain whether the HiB vaccine can be blamed in this case. [35]

Others. Convulsions (seizures) and allergic reactions to the vaccine (including anaphylaxis) have also been reported. [36]

 

What vaccines are offered against HiB?

In the U.S. and Canada, there are no HiB-only vaccines. All HiB vaccines are combo shots. (NOTE: These ingredients lists are not complete; they only list the most alarming ingredients.)

  • ActHIB: tetanus-HiB (tetanus and HiB antigens, ammonium sulfate, formaldehyde, casein [milk protein]) [37]
  • Pentacel: DTaP-IPV-HiB (contains ActHIB; diphtheria, tetanus, acellular pertussis, 3 strains of inactivated poliovirus, and HiB antigens, aluminum, polysorbate 80, formaldehyde, cow serum, 2-phenoxyethanol, neomycin, polymyxin B, ammonium sulfate, casein [milk protein], and MRC-5 [aborted fetus cells]) [38]
  • MenHibrix: Men C/Y-tetanus-HiB (meningococcal C/Y, HiB, and tetanus antigens, formaldehyde) [39]
  • PedvaxHiB: Men B-HiB (meningococcal B and HiB antigens, aluminum) [40]
  • Hiberix: tetanus-HiB (tetanus toxoid and HiB antigens, formaldehyde, lactose) [41]
  • Comvax: Hep B-Men B-HiB (contains PedvaxHiB; hepatitis B, meningococcal B, and HiB antigens, yeast cells, soy, aluminum, and formaldehyde) [42]

 

So what’s the bottom line?

The bottom line is that HiB is so common that 100% of the population carries it at some point and virtually 100% of the population is immune to it by age 5. The vaccine does not prevent asymptomatic carriage and so cannot be relied upon for herd immunity. The vaccine simultaneously decreases the risk of H. influenzae type B, which makes up a minority of strains today, and increases the risk of all other H. influenzae strains. Vaccination of children is associated with an overall increased risk of H. influenzae invasive disease and death in both children and adults, especially the elderly. HiB vaccination is also associated with increased incidence of other more dangerous and less treatable bacterial infections. The vaccine is associated with type 1 diabetes, and the complications of vaccine-induced type 1 diabetes when vaccinated alone outweighs the risk of HiB disease when not vaccinated. The vaccine is also associated with other adverse events such as asthma, allergies, epiglottitis, an increased incidence of HiB disease in the first week after vaccination, and more. The bottom line is the risk of death is higher with the vaccine than without.

 

References

[1] http://www.cdc.gov/vaccines/schedules/downloads/child/0-18yrs-child-combined-schedule.pdf

[2] http://www.cdc.gov/vaccines/vpd-vac/hib/vac-faqs-hcp.htm

[3] http://healthycanadians.gc.ca/healthy-living-vie-saine/immunization-immunisation/children-enfants/schedule-calendrier-table-1-eng.php

[4] Evans, A.S. & Brachman, P.S. (2013). Bacterial Infections of Humans: Epidemiology and Control (Fifth Ed.). (pp. 315-316) New York: Springer-Verlag New York Inc.

[5] https://www.youtube.com/watch?v=QVE2l2RJ8lY

[6] http://www.cdc.gov/vaccines/pubs/pinkbook/downloads/hib.pdf

[7] http://www.ncbi.nlm.nih.gov/pubmed/10569222

[8] http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3322072/

[9] http://www.ncbi.nlm.nih.gov/pubmed/8417239

[10] http://www.unboundmedicine.com/medline/citation/8143010/Eradication_of_Haemophilus_influenzae_type_b_disease_in_southern_California__Kaiser_UCLA_Vaccine_Study_Group_

[11] http://www.ncbi.nlm.nih.gov/books/NBK236299/

[12] http://www.cdc.gov/mmwr/preview/mmwrhtml/00041736.htm

[13] http://www.ncbi.nlm.nih.gov/pubmed/2785147

[14] http://www.ncbi.nlm.nih.gov/pubmed/3491315

[15] http://www.cdc.gov/mmwr/preview/mmwrhtml/00023705.htm

[16] https://schaabling.wordpress.com/2015/12/18/pertussis-whooping-cough/

[17] Weekly Topic 03: Meningococcal Vaccine (Meningitis)

[18] “Several factors indicate that mass immunisation with pertussis and other non-Hib vaccines may have been responsible for the unprecedented epidemics of invasive bacterial infections such as Hib, during the 1970’s and 1980’s.” (p. 315) Miller, N.Z. (2008). Vaccine Safety Manual.

[19] http://www.wellwithin1.com/HibPneuButler1993to2006letters.pdf

[20] http://www.ncbi.nlm.nih.gov/pubmed/14679101

[21] http://www.ncbi.nlm.nih.gov/pubmed/12482192

[22] http://www.ncbi.nlm.nih.gov/pubmed/12793601

[23] http://care.diabetesjournals.org/content/23/6/872.long

[24] Shoenfeld, Y., Agmon-Levin, N., & Tomljenovic, L. (2015). Vaccines and Autoimmunity (pp. 185-190). Hoboke, NJ: Wiley Blackwell.

[25] http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1116914/

[26] http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1114674/

[27] http://www.ncbi.nlm.nih.gov/pubmed/1669664

[28] http://www.ncbi.nlm.nih.gov/pubmed/8762955

[29] http://www.ncbi.nlm.nih.gov/pubmed/9133234

[30] http://soilandhealth.org/wp-content/uploads/02/0201hyglibcat/020152.vac.haz/vac.haz.pdf

[31] http://www.ncbi.nlm.nih.gov/books/NBK236284/

[32] http://www.ncbi.nlm.nih.gov/pubmed/9027536

[33] http://www.ncbi.nlm.nih.gov/pubmed/6335351

[34] https://web.archive.org/web/20041029232155/http://mothering.com/articles/growing_child/vaccines/biochemistry.html

[35] http://www.ncbi.nlm.nih.gov/pubmed/8103131

[36] http://www.ncbi.nlm.nih.gov/pubmed/3497381

[37] http://www.fda.gov/downloads/BiologicsBloodVaccines/Vaccines/ApprovedProducts/UCM109841.pdf

[38] http://www.fda.gov/downloads/BiologicsBloodVaccines/Vaccines/ApprovedProducts/UCM109810.pdf

[39] http://www.fda.gov/downloads/BiologicsBloodVaccines/Vaccines/ApprovedProducts/UCM308577.pdf

[40] http://www.fda.gov/downloads/BiologicsBloodVaccines/Vaccines/ApprovedProducts/UCM253652.pdf

[41] http://www.fda.gov/downloads/BiologicsBloodVaccines/Vaccines/ApprovedProducts/UCM179530.pdf

[42] http://www.fda.gov/downloads/BiologicsBloodVaccines/Vaccines/ApprovedProducts/UCM109869.pdf