Wednesday, May 4, 2016

When It Comes to YouTube, Google Is Only Half The Problem…The Other Half Is Major Labels And Publishers

It is common knowledge that the creative community has been discontent with YouTube for some time.  In recent weeks, a variety of articles have surfaced featuring various members of the music industry as they decry the paltry payouts issued by the streaming giant.1-5  This outrage is not without merit, for despite YouTube being the largest music streaming platform (in terms of both content and users), it is also the lowest paying.6-9  These substandard payouts stem from the price of YouTube ad space, along with the revenue splits employed by YouTube in distributing ad revenue.  Indeed, the latter is the bigger issue, as YouTube pays content providers a mere 55% of net earnings.10-12

It is unclear exactly how much YouTube takes off the top before splitting the remaining ad revenue, but it has been reported that this figure is 10%.13  Of course, without the ability to audit the company, it’s impossible to verify this with certainty, but if true, it means that YouTube is paying artists (and all content owners) 49.5% of the gross ad revenue.14  Importantly, when it comes to monetizing user-generated content, this percentage gets further reduced for the many artists who are dependent upon intermediary Content ID service provides that take commission on the content owner’s side of the earnings - for this group, payouts drop even further, typically between 37-42% of the total pie.15

Now, depending on the artist, there may or may not be labels, publishers, managers, etc with their hands in the pot on the artist side of earnings; but the literal amount that ends up in an artist's pocket is irrelevant from the standpoint of how big (or small) the artist pot is to begin with.  It’s one thing to assess a platform in terms of the revenue it generates, and another thing to assess the fairness of how that revenue gets divided.  Consider that iTunes, which has become the unofficial benchmark of revenue splits, pays 70% of gross earnings to the artist.16  Spotify does the same.17  Apple Music pays 71.5-73% of gross.18  And other services, such as Bandcamp, pay as much as 90% of gross to the artist.19  That is a substantial difference in comparison to YouTube, with important financial consequences.  

Google asserts that such comparisons are misguided,20 as download services and paid subscription streaming services are structurally different than a free ad-supported framework - instead, they argue YouTube is more akin to traditional radio.  Well, last time I checked you couldn’t turn on the radio and choose the songs you want to hear.  In contrast, YouTube is an interactive on-demand service…it may be different from other on-demand streaming platforms, but not in a way that justifies paying 55% of net revenues to creators.

So, how has YouTube managed to successfully implement an obviously unfair and exploitative system?  There are a few variables involved, three of which I will briefly summarize.

First, YouTube is able to facilitate the uploading of unauthorized user-generated content, while being legally protected under the “safe harbor” provision of copyright law.  In short, anyone can upload anything they want, and YouTube is not liable for their actions.

Second, the DMCA process, whereby a copyright owner can notify YouTube of an unauthorized video containing their work, with instructions for it to be taken down, is severely flawed in a variety of ways, ultimately making it useless as a method of keeping content off of the platform.21

Third, access to YouTube’s audio recognition Content ID System, which thoroughly addresses the above by identifying user-generated content on an automated and ongoing basis, is granted by YouTube only at their discretion.13,21  Accordingly, they have elected to grant access to just a subset of content owners, access which is conditioned upon consenting to the terms of Google’s label and/or publishing agreement.4,21,22  Essentially, Google leverages the value of Content ID to strong-arm parties into accepting what are widely held to be substandard deal terms.  For those denied access to Content ID (a substantial portion of applicants), and for those that refuse to consent to Google’s label / publishing deal, the only recourse is to engage one of a variety of independent services that will broker Content ID access in exchange for their ability to monetize your work.12,21

The upshot of these 3 variables is that it is impossible for copyright owners without direct access to Content ID to remove their content from YouTube.  And for those with direct access, they have begrudgingly accepted YouTube’s monetization terms in order to gain that access.  Consequently, the music industry has been stripped of negotiating power with respect to securing more equitable compensation from the platform.  It is a strategy part divide and conquer, and part blackmail - you can accept YouTube’s payout rates and make some money from user-generated content with Content ID access…or you can reject them and earn nothing, with no access to Content ID (in which case your content will often end up being monetized by others without your consent or participation).21

But there is a 4th variable, one which is just as important as the others, but which rarely (if ever) gets discussed.  While only a subset of content owners have direct access to Content ID, that subset is inclusive of the largest media companies - companies that include major record labels and publishers.  Even though YouTube succeeded in leveraging Content ID and the inefficiencies of DMCA to compel these companies into entering unfavorable licensing deals, those deals do not obligate said parties to monetize the content in question.  In fact, the “majors” are free to utilize Content ID in whatever manner they wish - monetize, track without monetization, or block all user-generated content.  Thus the majors, whose catalogs presumably account for the majority of music streaming on YouTube, possess the ability to effectively pull their catalogs from YouTube with the click of a mouse.  And make no mistake, a system wide Content ID block by the majors would create sizable ripples, changing the landscape of music streaming for all parties, major and non-major alike.  So why haven’t they?  Because they are pussies.  No seriously, they really are pussies.

Many of the music industry representatives complaining about YouTube’s low payouts in the press are the same people that are in a position to cut their ties - but instead of actually doing that, they choose to continue taking it up the ass from Google.  Now, don’t get me wrong, if someone wants to take it up the ass, that’s their prerogative.  But you can’t choose to take it up the ass and then start complaining about how your ass is all sore.

If you’re like me, you are perplexed by this behavior.  Surely the labels / publishers are comprised of intelligent individuals that see the absurdity of the current situation.  Even Google has publicly pointed out the obvious, stating in response to claims that YouTube unfairly devalues music: “Thanks to Content ID, record labels…can remove any or all user-uploads of their works from the platform on an automated and ongoing basis”.1  While this conveniently leaves out the fact that not all content owners have direct access to Content ID, their statement is 100% accurate as it pertains to major labels and publishers.  Moreover, the failure of labels / publishers to utilize Content ID to remove all of their material, or to at least cease all YouTube monetization of both direct uploads and user-generated content, renders them complicit in the exploitation that transpires, and it serves to reinforce and reward such behavior by Google.

So, why is the music industry continuing to monetize their content on YouTube when they object to what they’re being paid?  I can only speculate.  Maybe they are afraid of making Google angry.  Or maybe the people calling the shots at these labels / publishers have hidden loyalties to Google, while everyone else is unaware or powerless to stop the coup.  More than likely though, I suspect the real reason is that although they are unhappy with the revenue splits in principle, the amount of money being made is still substantial, despite being a fraction of what it should be…I think they simply can’t bring themselves to leave the money on the table and walk away.  But of course, that is precisely what’s required to get Google to the negotiating table.  You have to be prepared to endure financial sacrifice.  You have to have a spine.  You have to be willing to not be the bitch of a corporate behemoth.

Easier said than done, it would seem.  To be clear, I acknowledge that it can be difficult to walk away from sizable sums of money.  How much would you be willing to walk away from, for the sake of principle?  $10,000?  $100,000?  $1,000,000?  Many probably wouldn’t be willing to walk from any of these sums.  I get it.  After all, I am currently receiving YouTube monetization income, via indirect Content ID access.12  As much as I detest the conditions and circumstances that led to me receiving this supplemental income stream, I don’t detest having more money in and of itself.  Who can’t use extra money?

But at the end of the day, if you don’t want to be exploited and taken advantage of, you need to stop allowing yourself to be exploited and taken advantage of.  It’s pretty straightforward.  And the reality is that we’re not talking about a poverty stricken class facing a financial dilemma…we’re talking about major label artists and bands.  If Taylor Swift is making 5 million dollars in YouTube ad revenue, she’s making hundreds of millions elsewhere.  This is to say, it’s all relative and any potential ad income from YouTube is indicative of much greater revenue outside of YouTube.  They can afford to leave the money on the table.  And remember, for every dollar paid out to the music industry (reportedly $2-3 billion to date),1,23 YouTube retains an equal or greater sum; if there’s one thing that corporations deplore, it’s losing billions of dollars of revenue.

Now, I will grant you that it is convenient for me, one who does not have direct access to Content ID and therefore can’t lead by example, to argue that other people should cease YouTube monetization for the greater good.  But note that not one of the 34 million views to date on my personal YouTube channel is or has been monetized by me.  I assure you, if tomorrow I were granted direct access to Content ID, I would not hesitate to cease monetization of the now 209,000 user-generated videos that have been identified and their resulting 33 million average monthly Content ID views.  Why?  Not because I don’t want or can’t use the money, but because fuck you if you think I’m accepting 55% of net proceeds.

It’s worth considering too that in all likelihood, a system wide Content ID block by the majors would lead to increased traffic on other paid streaming platforms, all of which pay more than YouTube.  Of course, Google claims2,4 that YouTube is monetizing a substantial portion of music consumers who otherwise would not be willing to pay for music…but even if this is true, it just means that many of these consumers will find a different free streaming service, such as Spotify, whose free ad-supported tier payouts, while also controversial, are still higher than YouTube.  And sure, perhaps some of these consumers will end up resorting to piracy, or utilizing a non-paying streaming service, or simply consuming less music - so what?  What’s the alternative, to continue getting exploited indefinitely while lining the pockets of Google?  But let’s not forget the other possibility, that a system wide Content ID block ends up leading to a renegotiated and more equitable distribution of YouTube ad revenue…imagine that.

Of course, even if YouTube were to increase revenue splits comparable to its competitors, giving a minimum of 70% of gross earnings to artists, it may still remain the lowest paying music company with respect to the actual payments it disperses.  But that, in and of itself, is not the real issue at hand - after all, any comparison of this kind will always yield a hierarchy - someone has to be on the bottom.  Drawing conclusions based on total or individual payouts is highly misleading.  It’s about how revenue gets distributed, and the freedom (or lack thereof) on the part of creators to participate.  Thus, artists and music reps pointing to per stream rates, or earnings per X number of views, is a misguided approach.  Similarly, Google praising itself for having paid $3 billion to the music industry to date completely misses the point.  The exploitative nature of the exchange that led to that $3 billion is the issue at hand.  And while the overall amount that YouTube pays may be growing with every year,20 unless you fix the underlying inequity inherent in the formulation of those payments, you will only be compounding that exploitation.  So a more equitable revenue split will not only narrow the gap between YouTube and competing services, but it will also shift focus to the proper value of YouTube as a promotional and advertising space.

To that end, one could argue that user videos that contain music in the background (e.g. cat videos, sports videos, etc) constitute a partially new and unique revenue source.  At the same time, one could argue that music-specific YouTube videos cannibalize income from higher paying competing services.  Then there are the myriad variables that go into how ad payments are calculated per view, one of which is geography (e.g. a view in the United States is worth more than a view in Spain).  All of this complicates straightforward comparisons between YouTube and other platforms, but the bottom line is that if creators choose to participate in the service, they should reap a fair percentage of revenue from that participation.  I’m not, and I don’t think anyone is, anti-YouTube in principle…I’m simply against being forced to participate while being monetarily exploited.

I do concede that it’s within the realm of possibility that Google could react to a music industry revolt by revoking all direct Content ID access.  But such an action by Google would escalate the conflict, serving to greatly strengthen the legal argument and current lobbying efforts to rework the existing DMCA and safe harbor provisions.  The fact is that Content ID is the best defense that Google has in maintaining the status quo - to take that away from the majors would be to potentially shoot themselves in the foot, and it goes without saying that a successful DMCA “take down and stay down” revision would take considerable wind out of YouTube’s sails.

I will also concede that perhaps major labels and publishers began their partnership with YouTube in good faith that initial unfavorable terms would improve over time.  But even if that was the case, the ship has long since sailed.  What you have now is not going to change, for there is no incentive on Google’s part to do so…at the end of the day, despite stamping their feet in protest, the music industry is complying with what Google wants it to do.

And just to be clear, DMCA and safe harbor are most certainly in need of a serious overhaul - they can, and should, immediately be revised to properly apply within the current context of digital consumption.  This is particularly all the more pressing if YouTube is going to continue withholding direct Content ID access to so many content owners, therein stripping away their ability to abstain from the platform.  But this has no bearing on the fact that the largest sectors of the music industry already have the capacity to effectively and efficiently withdraw their catalogs via direct Content ID access - and there is no greater negotiating power than that.

So majors, you have a choice to make.  You can continue to do what daddy Google tells you to do, or you can grow a pair and have some dignity.  If you choose the former, so be it, but please shut the fuck up about your discontent moving forward…you have become the battered wife that refuses to leave her abusive husband, and it’s depressing to witness.  So right after you finish chastising Google for being evil, do us all a favor and stop being a bunch of pussies.

1 "Here's why the music labels are furious at YouTube. Again." Re/Code. April 11, 2016.
2 "Europe's divi-boss tells YouTube to cough up proper music royalties". The Register. April 19, 2016.
3 "Debbie Harry: "Music matters. YouTube should pay musicians fairly". The Guardian. April 26, 2016.
4 "Nikki Sixx launches campaign to get YouTube to 'do the right thing' over music royalties". The Guardian. April 24, 2016.
5 "Nelly Furtado: "YouTube pays more than nothing. That doesn't make it fair". The Guardian. May 2, 2016.
6 "What Major Music Streaming Services Pay Artists, Visualized". Co.Design. July 15, 2015.
7 "YouTube Music Is Growing 60% Faster Than All Other Streaming Music Services Combined". Digital Music News. September 14, 2015.
8 "How Much Do the Most Popular Streaming Services Pay Per Stream". Sonicbids Blog. July 20, 2015.
9 "YouTube - Not Spotify, Pandora Or Apple Music - Is The Number One Music Streaming Service Worldwide: Here's Why". Tech Times. July 8, 2015.
10 "YouTube to Tv Networks: No More 'Sweetheart' Ad Deals for You!" Ad Age. October 31, 2013.
11 "How YouTube Pays Artists by East Bay Ray". Janky Smooth. December 3, 2015.
12 "Shining Some Light On The Dark Side Of YouTube". Zack Hemsey Official Blog. January 28, 2016.
13 "YouTube Revenue Explainer". Music Tech Solutions. March 10, 2016.
14 10% off the top means content owners would be getting 55% of the remaining 90% of revenue, which equates as follows: .55 X .9 = .495 (49.5%).
15 Assuming a commission of between 15-25% on the artist portion of earnings (49.5% in this scenario), this would leave the artist with 75-85% of their original share: .85 X .495 = .42075 (42%) / .75 X .495 = .37125 (37%).
16 "Sell Your Music on iTunes". Tunecore Official Website.
17 "How we pay royalties: an overview". Spotify Official Website.
18 "Here's how much Apple Music is going to pay artists". Business Insider. June 22, 2015.
19 "Pricing". Bandcamp Official Website.
20 "No other platform gives as much money back to creators". The Guardian. April 28, 2016.
21 "The Dark Side Of YouTube". Zack Hemsey Official Blog. January 28, 2015.
22 "What should I do about YouTube?" Official Zoe Keating Blog. January 22, 2015.

Saturday, April 23, 2016

Prim’s Cat: The Real Mockingjay?

Last night I watched The Hunger Games: Mockingjay - Part 1.  Am I the only one who was scratching their head at the sheer ridiculousness that was exhibited?  Not with respect to the dystopian future portrayed.  Not with respect to blowing up planes with exploding arrows, while the archer remains unscathed despite standing directly in the path of the aircraft’s machine gun fire.  I’m fine with all of that.  What I cannot get on board with is the behavior exhibited by Prim’s cat.  Let’s walk through the events that unfolded.

Katniss visits what remains of District 12, where she discovers her sister’s cat within the family’s former residence.  She then picks up and places the cat inside her satchel bag, as she peruses the house for other items to salvage, at one point opening the bag and tossing a picture frame in alongside the cat.  All things (and cat) in bag, she returns to District 13 (presumably by air since that is how she got to District 12 in the first place), makes her way through the compound to find her mother and sister, opens up the bag, and out comes the cat…a cat who has been shockingly indifferent to hanging out in a bag during the tumultuous journey over land and air.

At this point I turned to my wife and said, “this movie has lost all credibility”.

Ok, well maybe this cat hangs out in satchel bags devoid of breathable mesh screens all the time.  Maybe he spent his adolescent years at a military base where he was a frequent flyer.  And maybe he’s got an extremely serene disposition to top it all off.

But alas, the plot thickened.  Later in the film, residents of District 13 are rushed into an underground bunker to take shelter from an impending airstrike from the Capitol.  However, the bombing commences before Prim makes it into the bunker - you see, she had gone to retrieve her cat and is now racing down the stairs with the animal in her arms, in the midst of explosions, falling debris, and cascading water spewing from what I assume was a sprinkler system set off by the bombing.  At the last moment, they make it into the bunker in one piece, as the cat continues to hang out in Prim’s arms without ever having squirmed an inch; wet and seemingly content with the entire ordeal.

Now, I ask you, what kind of mystical fucking cat is this?  Unless the cat’s actually a robot, this is either the most relaxed cat in the history of the feline species, or the movie decided to cut out the part where the cat gets injected with Valium.  Or the movie was produced by dog owners who have no experience with cats and are strangely under the assumption that they are meditative beings capable of achieving extraordinary levels of zen.  

Regardless of how the cat came to be portrayed in this manner, rest assured - I don’t care how awesome that cat is (and I’ve known some pretty awesome cats in my day), Prim’s arms, body, and/or face should have been cut up and bleeding from the clawing that would have transpired as that cat lost its fucking nerve.  Merely managing to hold onto the cat at all during that fiasco would have been miraculous.  To do so and remain unscathed…perhaps the single greatest feat of all time.  To have the cat stay as calm as a summer afternoon nap throughout it all…fucking impossible.  The movie should have just made Prim a sorceress, as a magic spell would have been more believable than what was depicted.

But in case you thought that was the last of the cat, fear not, for at the end of The Hunger Games: Mockingjay - Part 2, he makes one more appearance.  By now, days or weeks have elapsed since the bombing of District 13, a war has been waged, and many have perished.  Katniss is now back in District 12, trying to make sense of the chaos that has led her to this point, when lo and behold, the cat appears in the window.  He has traveled untold miles, through battlefields and ruins, persevered against bombings and starvation, and has finally made it back home.  In response to the cat’s truly heroic efforts, Katniss goes completely psychotic, unleashing all of her pent up anger onto the cat who has unknowingly become the symbol of everything she lost.  The screams escalate into attempted battery, as Katniss throws a glass across the kitchen with the intention of stoning the cat, all in a furiously loud and violent rage as she aggressively moves closer toward the cat…a cat who remains stoically silent and still in response.  He doesn’t run away; he doesn’t hiss; he doesn’t even flinch when the glass flies within inches of his face, smashing into shards upon contact with the countertop and backsplash…he just looks at Katniss, as if to say, “Katniss - I know - it’s not your fault”.


My wife turned to me and said, “that cat would never have sat there like that”.  To which I replied, “are you kidding me, if that cat did anything other than sit there, the movie would have been totally inconsistent”.

Thursday, January 28, 2016

Shining Some Light On The Dark Side Of YouTube

Not too long ago, I wrote about my frustrations with YouTube - a platform that enables unauthorized uploads of copyrighted content (commonly referred to as “user generated content”, or UGC) - uploads that are often illegally monetized, as facilitated by YouTube, and the revenue of which YouTube shares and participates in.

There is also the matter of YouTube’s Content ID System - a digital audio fingerprinting system that is a necessary tool for copyright owners to police UGC, but a system that YouTube selectively allows access to (access which I was denied for reasons unknown), thus creating the ability of those with access to fraudulently utilize Content ID to illegally claim and monetize the content of those without access (with no mechanism in place for the rightful copyright owner to notify YouTube of the fraudulence in question or properly dispute it).

And then of course there’s the matter of YouTube, along with uploaders of illegally monetized UGC and parties misusing Content ID, keeping all the money that was earned as a result of the illegal monetization of copyrighted content.

I was repeatedly falling victim to the above (as detailed here), so I had a decision to make.  I could do nothing and let the anarchy continue.  Or I could engage an intermediary service to gain indirect access to the Content ID System.  While YouTube is extremely selective in granting copyright owners direct access to Content ID, there are a variety of independent companies with direct access, which broker indirect access to the common man.  As far as YouTube is concerned, anyone is free to deal with such “Content ID brokers”.

It is important to note that intermediary Content ID brokers all require monetization of UGC, for which they take a commission on the resulting ad revenue.  In this way, YouTube basically forces the hand of a copyright owner - join us (indirectly) and monetize, or otherwise let us get back to monetizing your shit without your involvement.

After considerable internal debate, I decided that as much as I dislike the online ad culture, I hate people hijacking and illegally monetizing my content far more.  Plus, I reasoned I could keep my official YouTube channel ad free, while only monetizing UGC - this would maintain an ad free user experience for fans that come to my channel, while also allowing me to earn money from the use of my music in unauthorized non-official videos - this seemed like an acceptable balance and appropriate compromise.

Ok, so what are the deal terms?  YouTube takes a flat 45% of ad revenue across the board.1  Already, I hate the deal.  There is no justification for YouTube’s cut to be that large.  None.  Yes, YouTube has bandwidth and server costs,2 and yes they are the ones selling the ad space - but they are also monetizing millions of videos, the content of which they don’t own and the creation of which they had no involvement in (at least for the vast majority of cases) - if the sheer volume of videos that YouTube is monetizing doesn’t sufficiently offset their costs (as is reportedly the case),3 they should raise the price of the ad space instead of taking a higher % from content owners.  Let’s all keep in mind that nobody petitioned for the creation of the service - it shouldn’t be the burden of content owners to keep YouTube afloat financially (especially since it is the unauthorized appropriation of their content that forms the foundation of the service). 

But it gets worse, because YouTube’s 45% cut is apparently of net profits, not gross.4,5  If you have a YouTube channel, try searching for the phrase “55% of net revenues recognized by YouTube” in your agreement…you might be surprised to discover that’s your share.  In other words, YouTube recoups its costs (whatever they are deemed to be by YouTube) from the gross ad earnings, after which it keeps 45% of what’s left.  I think we can all agree that is definitively monstrous.  To be clear, these revenue splits are in connection with direct monetization of a YouTube channel’s content by the channel itself - and so in theory may not apply to Content ID revenue distribution, where content owners monetize other people’s unauthorized uploads of their content - however, I have been told by more than one source that Content ID splits are identical.

So out of the remaining 55% that goes to the content owner, the intermediary service would then take their commission, the amount of which varies depending on the company and the negotiating power of the content owner.  Suffice it to say, there is a lot of bullshit when it comes to intermediary services, with some taking large percentages because they can, or because their clients simply don’t know any better.  So unfortunately, this can be an area where a copyright owner gets an additional layer of exploitation.  That being said, not all intermediary services are villainous, and some will agree to reasonable commissions.  

I should also point out that a commission is warranted in virtue of the fact that someone has to manually monitor and respond to claim disputes that arise when uploaders contest the validity of various Content ID matches - occasionally Content ID does get it wrong, but most of the time uploaders of UGC either don’t understand what is happening and ignorantly dispute a legitimate copyright claim, or mistakenly invoke the “fair use” provision of copyright law, or intentionally try to game the system by disputing what they know is a legitimate claim in the hope that the content owner won’t respond in time (if a claimant fails to respond to a dispute within 30 days, YouTube automatically releases the claim).  So there is certainly some labor involved, which is in direct relationship to the volume of copyright claims a given content owner has (the more claims, the more time required).

What I do object to however, is the principle that a content owner should be forced to engage an intermediary company to provide this service, and therein be forced to give up an additional % of revenue (whatever that % may be), especially when YouTube is taking 45% of net earnings.  For that amount, YouTube should be assigning their own staff to monitor and resolve claim disputes, without forcing content owners to finance the process - after all, it is YouTube that created the platform in which such a process is necessary in the first place!  And if YouTube doesn’t want to deal with the headache, preferring instead to outsource the task to intermediary services, so be it - but those service commissions should come out of YouTube’s share, not the content owners.  This much should be obvious to anyone with any semblance of ethics, but to the extent corporations are people, they be bitches…

So here I was, caught between a rock and a hard place.  On the one hand, I do not want to participate in an exploitative system.  On the other, there is no alternative to stop my ongoing exploitation at the hands of 3rd parties.  In the end, I can protest YouTube’s outrageous deal terms with respect to the videos I personally upload to my own channel by boycotting monetization - YouTube gets nothing, and I get nothing - fair enough.  But boycotting Content ID affords me no benefits whatsoever - if I’m not monetizing UGC, someone else is (or will be), so I can either ensure those earnings come to me or I can let them go elsewhere (YouTube gets its cut either way).  

Some might be tempted to think that perhaps there is still a moral victory in boycotting Content ID, but I would disagree - it’s simply a choice between letting one party exploit me (YouTube), and letting multiple parties exploit me (YouTube + UGC uploaders and Content ID abusers).  Generally, I think it’s wise to minimize the number of people exploiting you to the greatest degree possible.  And so, I have now joined the trend of monetizing UGC by enlisting an intermediary service.

Onwards and upwards…

After uploading my assets, Content ID got to work scanning YouTube for matches, a process that doesn’t finish overnight.  After 4 months of searching, as of this writing Content ID has identified 191,735 videos that use my music (all without authorization).  Some of these videos have millions of views, and some have less than a hundred.  All together, the collective views during the 4 months that Content ID has been tracking them amount to 128,370,896…and accordingly, we can deduce that the total combined views since the respective upload date of each of these videos probably exceeds 1 billion.  I have no way of knowing how many of these videos were monetizing my music beforehand, nor any way of determining how much money has been illegally made from my content to date.  However, I am now making money from these videos, and no one can illegally claim and monetize my music ever again moving forward.

I can’t help but be perplexed at the fact that YouTube previously denied my Content ID application, when it turns out there are literally thousands of unauthorized uploads containing my music.  I had no way of knowing this in advance, of course, but neither did YouTube…so what exactly was their evaluation based on?  Whatever the criteria, it appears woefully insufficient, as 192 thousand copyright claims and millions of UGC views per month certainly warrants direct access to the service (access that should not be conditioned upon signing an unrelated Google Publishing Agreement6,7).  It seems to me that assessing a creator’s need for Content ID requires knowing how many of YouTube’s videos contain that creator’s content, something which can only be determined using Content ID itself, and therefore, that YouTube should not prejudicially withhold access to Content ID on account of mere guesswork and assumptions.

Importantly, it turns out that the advertising revenue being generated is significant.  There are a variety of factors that determine how much money a given video earns, making it impossible to predict with any certainty what future earnings, or the earnings of others, will amount to; but the potential as a source of sustained income is clear.  Of course, not every content owner will have 192 thousand claims - many will have much less (and some will have much more), but with a more equitable distribution of ad revenue, it could make a measurable difference in the life of a struggling artist.  This is ultimately good news for an industry that is grappling with its transition into modernity, and for independent musicians hoping to make a living off of their craft.  YouTube has created a system that has the ability to positively contribute to the music ecosystem, and this should be embraced and encouraged - at the same time, YouTube is currently exploiting content owners by taking an unfair share of the pie, and strong-arming creators into take-it-or-leave-it deals while tacitly leveraging piracy as a consequence of not conforming.  

This should be decried at every turn, but too often, we’re instead exposed to claims of this or that creator making boat loads of money from YouTube revenue.  Yes, that’s true - you can make boat loads of money.  But what are the other players making as part of the deal?  That should matter to you.  You made 6 figures from YouTube, and I can potentially do the same?  Wow, that’s fantastic.  But think about it this way: if for every $1 you made, your “partner” was making $3, would you still feel good about that?  I’d hope not, at least not when it’s your content that is the bedrock of the earnings, and not when you were bullied and essentially blackmailed into being a partner.

So the question is, can anything be done to improve this state of affairs?  The short answer is, not really (at least not without changes to current copyright law).  Even if I remove all of my personal uploads from YouTube, it won’t have any impact on the 192 thousand unauthorized uploads containing my music.  It also won’t stop any of those users - and YouTube - from illegally monetizing my music.  For clarity, let’s review:

1.  Anyone can upload anything they want - if they upload copyrighted content without consent, YouTube is protected by safe harbor (i.e. “We said they needed to possess the necessary rights - we had no way of knowing the uploader didn’t own the copyright or have permission”).

2.  If the user monetizes their unauthorized upload, YouTube is (apparently) still protected by safe harbor, despite directly participating in and sharing the profits generated (a fact that continues to baffle me).

3.  Even if you’re willing to devote all of your time to finding unauthorized videos and sending YouTube DMCA notices to have them removed, not only is there not enough time in the day to complete this task, and not only will you have to indefinitely perform this task for the duration of YouTube’s lifespan, but in the best case scenario you will have only succeeded in taking down a small fraction of unauthorized videos, because the vast majority of UGC use copyrighted content anonymously (i.e. without crediting or listing the content in the video or video description).  So the exploitation and illegal monetization will continue in the shadows.

4.  The only way to locate all (or most) unauthorized content is by utilizing Content ID, presumably created expressly to solve the above problem.  However, YouTube won’t issue you a Content ID account - they will force you to go to an intermediary company.  And that intermediary company will require that you allow them to monetize the unauthorized uploads (otherwise there is no point in them being in business).  And either way, you have absolutely no control over the deal terms of that monetization.

The genius of YouTube’s methodology is that all paths lead to monetization.  In every scenario, YouTube earns money off of your content.  I can loudly proclaim from the hilltops that I want no part in their advertising monetization system, but I am absolutely powerless to prevent YouTube (through the actions of its users) from monetizing my content - it will either happen legitimately with my consent, or illegitimately without my consent.

There is only one solution that can address this, and it requires having your own Content ID account.  Armed with direct access, you could set the policy to “track only” - this would still place copyright claims on all unauthorized videos (preventing the uploader from being able to monetize the content), but it would also mean that no ads are placed on the videos…so you as a copyright owner wouldn’t make any money, but neither would YouTube.  Consequently, if every label / publisher / intermediary service / creator that has direct access changed their settings from monetize to track, then the lost revenue to YouTube just might be enough to get them to the negotiating table.  

Then again, Google earns unfathomable amounts of money overall, and might be content to simply wait out such a protest.  In response, all said parties would have to be prepared to switch from “track” to “block” (effectively pulling the content off of YouTube).  Consider that a very large percentage of YouTube traffic is music driven (it is apparently the largest music on-demand streaming service around),8-12 and the fact that music is used within an exorbitant amount of non-music-specific YouTube videos (e.g. home videos) - if you remove the music, you remove much of the incentive to go to YouTube, which undermines the YouTube culture, which lowers the value of the service to advertisers and weakens the brand overall … at that point, you stand a pretty good chance of motivating YouTube to resolve the issue, as they are likely too invested in the platform to let it wither away.

Of course, the above strategy requires coordination between multitudes of disparate companies and persons, in order to be effectively implemented en masse, and admittedly that is not likely to occur - but it remains possible nonetheless.  If it were to happen, there is also the risk that independent artists unaffiliated with a label / publisher might get left out in the cold, with YouTube negotiating non-standard deals for major players exclusively (and for all I know, maybe this is already secretly the case).  Regardless, the larger point remains - the entire YouTube edifice is built on a foundation of copyright owners’ creations, and to that end, is forever vulnerable to being dismantled at any moment - it just takes the will of creators to effect change.  While I enjoy making money as much as the next person, I would be more than willing to leave it all on the table.  What says you?

1 "YouTube to Tv Networks: No More 'Sweetheart' Ad Deals for You!" Ad Age. October 31, 2013.
2 "YouTube Standardizes Ad-Revenue Split for All Partners, But Offers Upside". Variety. November 1, 2013.
3 "YouTube still doesn't make Google any money". Business Insider. February 25, 2015.
4 "YouTube Revenue Explainer". Music Tech Solutions. March 10, 2016.
5 "How YouTube Pays Artists by East Bay Ray". Janky Smooth. December 3, 2015.
6 "The Dark Side Of YouTube". Zack Hemsey Official Blog. January 28, 2015.
7 "What should I do about YouTube?" Official Zoe Keating Blog. January 22, 2015.
8 "Forget CDS. Teens Are Tuning Into YouTube". The Wall Street Journal. August 14, 2012.
9 "YouTube as you know it is about to change dramatically". The Verge. August 28, 2015.
10 "YouTube boosted by music videos to pull behind Facebook". BBC. October 26, 2011.
12 "YouTube Music Is Growing 60% Faster Than All Other Streaming Music Services Combined". Digital Music News. September 14, 2015.

Tuesday, October 20, 2015

Fuck Singles

We’re all familiar with the standard industry practice of bands and recording artists releasing “singles” in advance of a new album’s release.  This is so commonplace, and has been going on for so long, that no one ever seems to question the philosophy or merits behind it.  Well, I think it’s time someone lay waste to what is in my estimation a misguided undertaking.

Let’s begin by examining the often-cited motivation for releasing singles - generating a “buzz” - that electric gossip over something so cool and interesting that no one can stop talking about it.  Without a buzz, your album will be released into anonymous oblivion amidst the endless sea of content that humanity swims in; the world won’t stop to take notice of your contribution, and no one will realize you even exist.  But fear not, for the single has the potential to avert this creative and existential disaster.  This is that one song that will change everything.  A song so special, it makes you believe in magic.  Yes, the single holds the power to generate that coveted buzz, but…and this is the important part…it must be released in advance of the album to which it belongs!  Failure to abide by this tenant will render the single powerless; for reasons unknown, people simply will not feel the same way about the song otherwise.

So this is the apparent mythology at work.  But while I am certainly not opposed to the principle of generating a buzz, I would rather do without the supposed benefits that result from this exercise.  After all, why would I want listeners to hear only one song from an album?  This doesn’t make sense to me, and even less so in situations where a single (or singles) are released months in advance of the album, such that by the time the album becomes available, listeners’ perception of the entire body of work is unavoidably distorted on account of having heard the single(s) out of context and disproportionately more frequently.  Fuck that.  When I finish an album, I release the album.

Now there are some that view the single as being representative of the album as a whole - that it functions as a sort of emissary, communicating the identity of the new album to listeners.  However, unless every song sounds the same, this is an aural impossibility.  And while I suppose a single could be representative of the spirit of the overall work, heterogeneity notwithstanding, and while I also concede that there are albums in which every song does in fact sound the same, there is nevertheless no compelling reason to release that single in advance of the album’s release.  Unless of course the album is subpar, in which case the utility of an advanced single lies in deceiving your audience in an attempt to manipulate listeners into pre-ordering an album they haven’t had the ability to vet, or buying it on faith upon release.  Fuck that.  I am not in the business of aural bait-and-switchery.

This brings us to the idea that singles constitute the “strongest” songs on an album, a notion that once again implies a subpar album, and to which I again refer you to my lack of interest in bait-and-switchery.  But I am also confused by the principle of an artist / label creating a work that is comprised of “strong” and (by implication) “weak” songs.  If a song is weak, why the fuck is it on the album?  Of course, it may very well end up that a listener gravitates to one particular song on an album while ignoring the rest of the work, in which case, so be it…but I’m not going to decide or predict on their behalf which song on that album they will / should perceive as being more worthy of their attention than others, nor will I assume that such an outcome is a forgone conclusion.  Fuck that.

Still, there remains the practical consideration of radio play (be it traditional or digital in nature).  Stations aren’t going to play an entire album, so you need to deliver a single in order to participate in the process.  Well, note there is nothing inherent in this concept that requires delivering a single in advance of an album’s release; not to mention, it makes more sense for people to fall in love with a song whose album they can immediately purchase or stream, rather than have to wait a few months, at which point they will hopefully a) remember there was an item they were previously interested in, b) realize this item has now become available, and c) still be interested in it.  And correct me if I’m wrong, but shouldn’t the stations / DJs / tastemakers decide which song(s) to play from a given album?  Otherwise, what purpose do they serve, apart from feeding the masses musical fodder as directed by their label overlords?  And while we’re at it, why should there be a moratorium on playing multiple songs or a full album from an artist?  Am I crazy to think that stations should simply play whatever music they think best satisfies the genre / style parameters they seek to service?  What’s with all the arbitrary and contrived rules about music consumption?

In light of the above, I have been and will continue to be a conscientious objector to this indefensible pastime.  The only singles you will find from me are self-contained songs that do not belong to a larger body of work.  After all, that’s what a single should be…one single fucking song!!!!

Friday, September 11, 2015

The Hemsey Hold

When my daughter turned 1 year old last month, the occasion sparked a look through the good old photo library.  Lo and behold, we uncovered pictures of a rather unique practice, one which we had forgotten all about - it was a method of holding Scarlet that has come to be known as the "Hemsey Hold” (trademark and patent pending).

On first glance, it may look like my daughter is being suffocated, or attacked by a face sucker out of the Alien franchise, but rest assured she is alive and well (and not carrying an alien pod inside her…as far as we know).  The baby is sucking on my wife’s pinky finger, with the remaining fingers covering her eyes and face, while all of the weight is distributed across two hands, two boobs, and one forearm, working in concert to form the perfect baby cocoon.  This was typically accompanied by a soft rocking up and down, while walking about.

It’s not something that we planned in advance or purposefully designed; it just sort of happened one day, as we navigated the task of soothing an infant without a pacifier.  And I can tell you that the Hemsey Hold is in fact the ultimate soothing and putting-to-sleep method of any we ever tried, and is quite comfortable for mom to boot.  Darkness + Rocking + Sucking + Close Proximity To Mom and Boobs + Lying Face Down = Content Baby.

I can also tell you that the hold is tailor made for moms, but less so for dads - while men certainly can perform the maneuver, their lack of breast tissue means the arms have to carry all the weight, and so it becomes a test of endurance, one which you will inevitably lose given enough time.  But women will be capable of going the distance, as much of the baby’s weight gets supported on their mammary shelf.

I encourage all those intrigued to give it a try…just be prepared for some puzzled stares if you do it in public.  We haven’t utilized the Hemsey Hold since Scarlet was about 5 months old, but we’re prepared to break it out again when she eventually goes through puberty, or turns 16.  And for anyone who may be worried that this technique will in some way impede their child’s development, fear not; as you can see below, Scarlet has ended up just fine.

Wednesday, August 12, 2015

I Swear, I Did It For Acoustic Reasons

When I finished renovating my studio in 2014 (see here), I knew there was still one element that needed addressing: my computer monitor.  Sure, it was a decently sized 30”, but at ten years old the resolution wasn’t the best, and additionally it felt obtrusive in the room…like when someone sticks their genitals in your face while you’re trying to make an origami.

Although the computer screen was positioned far enough back to avoid blocking the direct sound path from the speakers, it still hovered over the apex of the desk, so if you leaned too far forward it caused a “window” type of effect on the frequency spectrum, making it sound goofy.  And I wondered if a 30” surface hovering in mid air might be creating some unwanted acoustic reflections.

Of course, if you remove the computer screen, you have to replace it with something else.  And what better thing to replace it with than a giant flat screen TV flush against the wall?  This would give you everything: no reflective surface hovering above the desk, no “windowing” when leaning forward, and aesthetic awesomeness.

But not just any TV would do - it would need to be big enough and sharp enough to allow comfortable viewing, and most importantly comfortable reading, at a distance of 7-8 feet.  Upon testing in the field (i.e. hooking up a laptop to various TVs in-store) I confirmed the only suitable candidate was a 4k TV at 58”.  This would yield super crisp text from the computer at the required distance, and would optimally maximize the space in between the speakers.

So earlier this year I put my plan into action, and the result speaks for itself:

Thursday, April 23, 2015

Male Ring Card Girls

I’m not sure when the custom of ring card girls began in combat sports, but the history of how it came to be is less interesting than the question of why the custom persists.  I concede that it may be difficult for intoxicated onlookers to retain exactly which round is about to transpire, but I imagine it’s even harder to retain such information when it’s delivered via scantily clad women with bouncing appendages.  So it’s fair to say the utilization of ring card girls hasn’t lingered for practical reasons.

Of course, men (and some women) enjoy any excuse to fix their eyes upon the female anatomy.  But I’m not convinced that’s all there is to the story.  After all, there are other sports (even male-dominated ones) which lack any equivalent.  Sure, there are some similarities between ring card girls and the cheerleaders that perform at football and basketball games, but these are distinctly different phenomena.  And ask yourself, why don’t we have ring card girls at the DMV?  Or at the grocery store?  Or at funerals?   Why aren’t they holding up signs listing the current wait time, or a ticket #, or the parting words of the deceased?  If it were truly as simple as “it’s fun to look at hot chicks”, wouldn’t we have found a way to expand their contributions to society?  Indeed, the exclusivity among combat sports is intriguing.

Ultimately, I don’t think the custom is much thought about one way or the other, neither by spectators, combatants, promoters, event planners, nor the participants themselves.  It’s just something that is done, and seemingly always has been.  At best, the practice is an archaic pastime that endures out of a sense of nostalgia, serving as a celebration of the human form, while providing a helpful reminder of the upcoming round as an added bonus.  At worst, it is a demeaning exercise without any utility whatsoever, fostering a strange mix of sex and violence while engaging some latent archetype of the male psyche unconsciously rooted in fighting over the female sex.

All of that is fine.  I have no problem gazing upon attractive women as they walk around in circles.  But what strikes me as totally unacceptable in 2015, a time when females comprise a sizable and growing portion of MMA athletes, a time when the 135 lb champion Ronda Rousey is widely regarded as one of the best pound for pound fighters in the world (and one of the biggest stars in sports overall), is that there are no male ring card girls.  This, quite frankly, is an outrage.  It undermines the ideals of equality that we tirelessly strive toward as a society, it’s disrespectful to female fighters, and it should be highly offensive to you.  But most of all, it’s damaging to all the young boys out there who aspire to be the greatest ring card girls the world has ever seen.  Maybe you can sleep at night knowing we’ve trampled the dreams of our youth in blindly clinging to this custom, but I cannot.

I want to see scantily clad men in speedos and loin cloths parading around the octagon, doing their part to ensure everyone is aware of the upcoming round.  Rather than 3 designated ring card chairs filled with lady parts, I want to see 6 chairs next to the UFC cage occupied by male and female kibbles and bits.  And I want to applaud both sexes as they demonstrate how nimbly they walk while simultaneously holding up cards that show information more effectively communicated via the giant screens already present at each venue, and then deftly sit down ringside.  And I want to know that every MMA fan, whether male, female, straight, or gay, can behold a ring card girl within their attractive domain.

If we come together, we can turn this dream into a reality.  The world, and MMA, can be better.  We just have to choose to make it better.  Write to your representatives.  Write to your favorite fighters.  Write to the UFC.  And proudly spread the message that everyone should have the right to become a ring card girl, even if they have testicles.

Thursday, March 5, 2015

The Puzzling Case of GBS

1. What is GBS?
2. GBS in the United States
3. GBS and IAP Studies
4. The Source of GBS Rates
5. Examining the GBS Narrative
6. Fluctuating Variables
7. GBS Hospital Surveys
8. GBS by Gestation
9. GBS by Race
10. Late-Onset GBS
11. GBS and the Cesarean Complication
12. GBS False Negatives / Positives
13. GBS and Mortality
14. GBS at the State Level
15. GBS Around the World
16. Risks of IAP
17. Alternatives to IAP
18. GBS Conclusions

Your body is literally teeming with microbes - tiny organisms invisible to the naked eye.  In fact, you actually have more microbes than you do human cells.  Countless species of bacteria live in every nook and cranny you have to offer, from your skin, to your hair, fingernails, mouth, intestines, and colon.  For some, the thought of being covered in bacteria may be disturbing, but the reality is that we need them as much as they need us.  All of the bacteria in our bodies have coevolved with us, such that they perform essential tasks within our physiology and play a vital role in our immunity.1,2  They are quite literally indispensable to our health.

Of course, bacteria also have the propensity to cause illness, but it’s important to understand that there is a difference between being colonized with a bacterium and being infected by it.  Colonization involves a mutually beneficial (or neutral) arrangement, whereby bacteria live inside you without causing sickness.  Your body is a source of food and shelter for your microbes, and it is generally not in their interests to destroy their own habitat - in fact, the native bacteria within you actually protect and defend against invading pathogenic microbes.  Having said that, the microbiome is a dynamic system, in which the right set of conditions can lead to changes in the makeup, distribution, and behavior of our microbes…and thus, within certain contexts, normally harmless microbes can become harmful.1  So we are walking ecosystems, the balance of which directly relates to our well being.

There is a specific bacterium called group beta streptococcus (GBS) that is carried by 10-30% of the female population.3  This bacterium lives in the intestines, rectum, and/or vagina, and its colonization can be transient - that is, a woman may carry it this month, and not the next.4  Most of the time its presence is asymptomatic, but occasionally group-b strep can cause health complications such as urinary tract infection, or in the extreme, serious life-threatening infection in the form of sepsis, pneumonia, or meningitis.3,4  Infection in adults occurs primarily among elderly and those with medical conditions,5 but surprisingly, GBS infection is most common among newborn babies.  The consequences of neonatal infection can be quite grim: from long term neurological damage, to hearing or vision loss, to fatality.6,7  Fortunately such horrific outcomes are only a subset of overall infection cases, but even when no permanent damage is sustained, GBS neonatal infection remains a highly traumatic and disruptive ordeal for families.  

If this all sounds pretty scary, it should.  But don’t climb into your panic room yet - just as the majority of women colonized with GBS do not exhibit any adverse side effects, so too the majority of babies born to GBS colonizers do not develop infection.  In fact, the percentage of babies that develop a GBS infection is remarkably minuscule - between 0.5 and 2% of newborns born to GBS colonized mothers3,8 - in practice, this amounts to less than 2 cases of infection for every 1,000 babies that are born.  While such incidence is rare, given the devastating effects when GBS infection does strike, it certainly makes sense to attempt to reduce or eliminate its occurrence to the greatest degree possible.

There are two categories of infection that occur in newborns, early-onset and late-onset.  Early infection occurs within the first week of life, and late-onset between 7 and 90 days after birth.  Although both involve the GBS bacterium, they are evaluated separately.  Prevention efforts to date have been focused on early-onset infection.  

We know that early-onset infection takes hold in the vicinity of birth, because symptoms typically manifest within the first 24 hours of life.  There are a variety of maternal and labor risk factors that have been associated with it, the presence of which are believed to increase the likelihood of infection occurring, but a sizable portion of infections do not exhibit any clinical risk factors.9-11  GBS infection can manifest in both vaginal and Cesarean delivery, with or without prolonged rupture of membranes, and in both full term and preterm births, all of which leads to the deduction that the bacterium must be capable of traveling vertically up the vaginal canal to the uterus, wherein the baby is presumably swallowing amniotic fluid containing the bacterium.3,4,12

At the end of the day, we simply can’t predict when GBS infection will occur, but it seems self-evident that you cannot have GBS infection without the GBS bacterium being present in the first place.  To that end, GBS colonization is considered to be the most predictive and reliable risk factor, and accordingly the medical community in the United States has adopted a strategy of screening all women for GBS at 35-37 weeks of pregnancy, and then treating those with positive cultures using intravenous antibiotics during labor, commonly referred to as IAP (intrapartum antimicrobial prophylaxis).3

Testing is done at 35-37 weeks because it takes a few days for cultures to be analyzed, and results are required before the onset of labor (the timing of which obviously varies from woman to woman).  Given the transient nature of the GBS bacterium, this methodology allows for the possibility that GBS colonization status will change between the time of the test and the time of delivery.  So utilization of a “rapid test” in which a culture could be quickly analyzed on the spot during labor would be ideal, but such has not yet become available to clinicians.  Nevertheless, it is said that culture results obtained at 35-37 weeks match GBS status during delivery with 87-96% accuracy.3,13   

Now, if the prospect of administering antibiotics to every GBS colonized mother, when only .5-2% of their babies are at risk of developing GBS infection, strikes you as inelegant … that’s because it is inelegant.  However, IAP was not intended to be a perfect or permanent solution; it was intended to provide a temporary fix until a better solution was devised (such as a GBS vaccine)14 - and at the end of the day, it doesn’t need to be elegant, it just needs to work.  To that end, since adopting IAP protocols, the U.S. has observed its lowest incidence of GBS early-onset infection to date.  Success!  Case closed then, right?  Well, this is where things get interesting.

Below is a graph from the CDC3 showing GBS infection rates in the U.S. between 1990 and 2008.

Early-onset rates began to decline in correlation with statements from the gynecological and pediatric community, which outlined practices believed to be effective in reducing GBS infection, followed by definitive prevention recommendations by the CDC in 1996 and 2002.  The initial 1996 recommendations entailed a choice by the healthcare provider to utilize either a risk-based strategy (i.e. presence of risk-factors determine who receives antibiotics) or a universal screening strategy (treating anyone colonized with GBS, regardless of risk factors).  Then in 2002, based on a study comparing the effectiveness of both strategies, the CDC revised their recommendations to adopt universal screening only, which was found to be over 50% more effective.11

The above correlation is consistent with the claim that IAP reduces the incidence of GBS early-onset infection, but in and of itself, it does not constitute actual evidence.  It’s only an observation, and it’s important to understand that correlation is not synonymous with causation.  That is to say, two things can appear to be related to each other without a causal component being involved.  So the question is whether infection rates declined coincidentally with the implementation of IAP, or if they declined specifically because of IAP.  The latter is the belief, and it is certainly a sensible one.  However alternative scenarios could also explain the observation (for example, natural changes in GBS colonization or virulence).  So in order to determine if a correlation entails actual causation, you need to conduct clinical research, the gold standard of which is double blind randomized controlled trials - in the case of GBS, this would entail comparing the effectiveness of IAP to a placebo, such that neither patient nor provider knew what was being administered.

There are only a few randomized controlled trials that have tested the effectiveness of IAP.15-17  The CDC’s recommendations are fundamentally based on a handful of studies from around the late 1980’s, which demonstrated IAP was 80% effective in reducing GBS early-onset infection.18  The problem, however, is that those studies suffer from a wealth of flaws.  A review by the Cochrane Collaboration (a well respected research group) found a high risk of bias in a variety of areas “sufficient to affect the interpretation of the results” and which “seriously weakens confidence in the results.”  Ultimately the findings were held to be too flawed to inform clinical procedure, and the review concluded that “there is a lack of evidence from well designed and conducted trials to recommend IAP.”19  Nonetheless, the studies in question are the only randomized controlled trials that have been published to date on this issue (and of course, they did end up influencing clinical procedure).

Non-randomized and observational studies have been done to assess the impact of IAP.  To that end, many have shown IAP has a statistically significant effect in reducing GBS early-onset.20-24  However, other studies show effects that are not statistically significant,25,26 and some show IAP is of little value in treating low birth weight infants.27,28  There is also a 1993 meta-analysis of IAP research which concluded IAP is effective,29 but this was followed by a 1994 meta-analysis which concluded IAP’s effectiveness is not sufficiently supported by the available evidence.30  Then another study from 1999 concluded that the available IAP research was not suitable for formal meta-analysis, due to a wide variety of factors, limitations, and flaws, but that despite such shortcomings the data was not “compromised beyond utility,” and ultimately concluded that IAP is effective.18  

At the end of the day, double blind randomized controlled trials are the gold standard of research for a reason - namely, because anything short of these rigors has the potential to mislead.  This is why the paucity of clinical trials and the Cochrane analysis is troubling.  That being said, as one professional mentioned to me in conversation, there are practical and financial limitations to conducting randomized controlled trials for every single aspect of healthcare, and if such was a requirement for making policy decisions, nothing would ever get done.  This person illustrated the point with a colorful example, “would you advent a randomized controlled trial to evaluate the merits of a parachute?”  I would not.  However, the comparison is faulty, and regardless, GBS prevention was obviously an area in which such clinical research was deemed to be necessary, since a few trials were conducted.  So given the discrepancies in the research mentioned above, I’m left unsettled.

Now, if the quality of existing IAP research does not meet our highest standards, then why not simply conduct new clinical trials in the modern era to sort this out?  Well, from what I’ve gathered, it would be considered unethical to conduct such a study, because we can’t deny pregnant women with GBS access to effective treatment.  Of course, this is comical given the effectiveness of treatment is exactly what we’re looking to establish.  And moreover, is it not unethical to administer antibiotics to laboring women in the absence of reliable clinical evidence?

So we find ourselves back at square one.  The problem posed by this information gap is more than simply academic, in light of the fact that IAP is not without associated risks.  In weighing the costs of these risks against the benefits of preventing infections, naturally it’s important to know that IAP really is reducing GBS early-onset rates.  So before we explore the risks involved with treatment, we must utilize other means of analysis to further investigate the merits of IAP.

In the United States, GBS infections are tracked through the Active Bacterial Core surveillance network (ABCs), which monitors the presence of six different invasive pathogens in the general public.  It is a coordinated effort between the CDC, state health departments, and universities.  The network was officially established in four states in 1995, after which a series of expansions ensued and by 2004 it grew to comprise 10 states, where it remains today.31,32

Prior to ABCs, the CDC had established precursor sites that conducted population-based surveillance of GBS between 1988 and 1994 - these were subsets of what eventually became the ABCs.33,34  Before 1988, there is no population-based surveillance data for GBS.

The expansion of ABCs coincides with the observed decline in early-onset rates.  So we have to ask whether this expansion could be skewing our perceptions of GBS incidence over time.  To that end, because the rate of late-onset infection has been stable throughout the expansion, it is believed that the decline in early-onset is a genuine decline and not a surveillance artifact.35  In addition, disease trends within consistent surveillance areas have been reported to closely match trends when all 10 surveillance areas are combined.36

One other thing to note is that the current GBS surveillance network covers about 10% of the U.S. population.9  So there is a general question as to how reliable national projections based on 10% of the population are, and the CDC is aware that ABCs data may not be generalizable to the entire U.S.38  Nevertheless, by tracking the rate of infection within ABCs over time, we can observe disease trends within the surveillance population and glean useful information.  Having said that, it’s important to remember that ABCs can’t tell us why disease trends change or explain their behavior - it can only report the trend in and of itself.39  

Let’s take another look at the graph from earlier, showing GBS infection rates between 1990 and 2008.  

From 1993 onwards, the amount of hospitals implementing IAP began increasing, as well as the degree of compliance with national guidelines among hospitals (e.g. using appropriate media when culturing for GBS, taking both vaginal and rectal specimens when screening, etc).40-42  All of this correlates with the decline in GBS early-onset, although it is not clear how much credit can be given to IAP between the years 1990 and 1996 - while IAP had begun to be implemented in limited fashion during this period, the degree of compliance therein was far from optimal, yet rates were declining substantially nonetheless.10

The above graph begins at 1990, however a previous graph published by the CDC included data for the year 1989.43  Early-onset was listed somewhere between 1.4 and 1.5, with late-onset at 0.4.  I’m not sure why the 1989 figure was subsequently omitted.  

Also, the early-onset rate for 1990 is listed at around 1.8.  However, a population-based study published in 1992 reports an early-onset rate of 1.4 in 1990.44  There is a similar discrepancy between the rates of late-onset infection as well, cited at 0.3 in the study but listed higher by the CDC.  It seems that the CDC’s graph is adapted from a 2008 study36 in which GBS rates for 1990 were calculated from a surveillance population that did not include a region from the 1992 study’s surveillance population - the entire state of Oklahoma - and this could explain the discrepancy between the reported rates for 1990.  While small differences of this kind may seem trivial at face value, they can be crucial when assessing the effectiveness of a protocol that treats an inherently rare phenomenon.  Tiny alterations matter.

As to why researchers in the 2008 study would exclude Oklahoma from their 1990 calculation, this was not explicitly addressed, so one can only speculate.  Perhaps they felt its exclusion yielded a more consistent surveillance population (since Oklahoma did not end up becoming part of the ABCs network), and thus a more reliable comparison of GBS incidence over time.  However, the more data available, the more accurate the portrayal of disease burden will be, and since ABCs network expanded over the years anyway, I fail to see why the inclusion of Oklahoma in the 1990 calculation would be any more subversive than the addition of new states after 1995.  So I am uncomfortable excluding relevant data in this way.

Now, obviously GBS infections didn’t appear out of nowhere in 1989.  GBS as an infectious agent is said to have “emerged” in the 1970’s, for reasons unknown.4,37,45,46  There are isolated reports, prior to the establishment of surveillance networks, that cite early-onset infection rates of 2-3 per 1,000.4,9  However, these are based on single hospital studies and/or small geographic areas, which may or may not be accurately representative of overall disease incidence.14,34,44  Nevertheless, that’s all we have to go by.  

So let’s take a look at a new graph that I have assembled (click to enlarge), inclusive of all of the above information, along with additional surveillance data for 2009-2012.

An alternative narrative has now become visible.  If GBS infection rates were as high as reported in the 70’s and 80’s, then the obvious question is why did they decline of their own accord by 1990?  Going from 2-3 cases to 1.5 cases per 1,000 births is a rather significant change to have transpired without any IAP contribution.  If early-onset rates were already declining prior to the implementation of IAP, this would cast doubt on IAP’s causal role in their continued decline.  Of course, it’s possible that the estimated incidence of 2-3 per 1,000 in the 70’s and 80’s is not accurate - maybe it was actually lower or higher.  If lower (and there are reported estimates of 1.3 and 1.09 per 1,000),47,48 with rates stable or increasing leading into 1990, then this would be consistent with IAP’s efficacy.  But if higher (and there are reports of 5.1, 5.4, and even 10 per 1,000),11,48,49 then this would cast even greater doubt on IAP’s efficacy.

GBS wasn’t always a major cause of neonatal infection, and whatever factors led to the emergence of GBS, presumably changes in those factors would lead to changes in GBS incidence.  But since we don’t know the conditions that led to the emergence of GBS disease in the first place, we’re not in a position to identify if / when those conditions change.  Moreover, since we don’t have sustained reliable surveillance prior to IAP efforts (e.g. population-based surveillance for a 10 year period with no intervention efforts), we can’t presume to know what degree of fluctuation naturally occurs (if any), in order to compare against trends during the intervention era - by the time reliable surveillance began in the ABCs precursor sites, GBS was already on the radar of the medical community and it was not long before IAP began to be implemented in limited fashion.

In examining GBS disease trends, an important variable is colonization rates.  GBS colonization is not continuously tracked, so we extrapolate general colonization rates from various studies that have been done over the years.  The trouble is that there are a wide range of reported rates,22,49-57 so it’s no surprise that the CDC estimates between 10 and 30 percent of women are colonized…apparently colonization fluctuates.4   However, 10-30% is a rather large window, and it’s important to note that changes in overall colonization can have consequences to the overall incidence of GBS infection.

For the sake of discussion, let’s assume that 1% of colonized mothers have babies that develop infection.  At 4 million births in a year, an overall colonization rate of 10% would result in 4,000 infections, whereas a colonization rate of 30% would result in 12,000 infections.  That’s quite a difference!  So if colonization rates change from one period to the next, so too would the amount of infections automatically.  But of course, the percentage of babies that develop infection isn’t precisely 1%…it’s reportedly between .5 and 2%.3,8  Now we have another fluctuating variable.  Assuming a colonization rate of 20% among 4 million births, an infection rate of .5% would yield 4,000 infections - but an infection rate of 2% would yield 16,000 infections!  So the interaction of both of these variables can lead to increases or decreases, having nothing to do with intervention efforts.

Ideally, culture screening results should be part of the data regularly collected and tracked by ABCs, as this is the only way to factor colonization rates into an analysis of infection rates.  But alas, this is not the case.88  Nevertheless, it is important to realize that an incidence of 1.5 per 1,000 births within the context of a 30% colonization and 2% infection rate, means something very different than 1.5 per 1,000 births within the context of 10% colonization and .5% infection rate.  Without being able to track these variables, we cannot accurately interpret observed disease trends.  As one editorial stated: “We should keep in mind that colonization and infection rates due to GBS change over time, and the results we have seen following…guidelines may be only temporary associations without causal relationships.”58

Perhaps in an effort to get around these limitations, various hospital surveys have been conducted over the years, in order to calculate the proportion of hospitals implementing IAP and compare the infection rates between hospitals with and without IAP protocols.  

A survey of births from 1994 found that hospitals with a screening policy of any kind had fewer early-onset infections than hospitals without a screening policy.40  Another survey of births from 1996-1997 found hospitals that established or revised their IAP policies in 1996 had a significantly lower average amount of early-onset infections in 1997.59  Interestingly, there was also a lower average of early-onset infections among hospitals that did not have prevention policies from 1996-1997, however researchers assessed this decrease as not being statistically significant.  

Take a look at this graph from the CDC,41 illustrating the number of hospitals that established GBS prevention policies each year between 1989 and 1997.

The number of hospitals implementing prevention policies began slowly rising, and then skyrocketed in 1996.  The curious thing to me is that we don’t see a corresponding skyrocketing decline in GBS rates during this time.  Now, after a policy was established, it was presumably carried forward, adding to the total amount of policies overall.  So I have assembled a new graph, reformulating the same data to show the total additive amount of hospitals with prevention policies created since 1989 (i.e. every year includes previous years’ values) in conjunction with GBS early-onset rates.

Look at the rate of change between 1993 and 1999.  There is a steady decrease in early-onset infection (the blue line) during this period.  However, note that the rate of increase in hospitals with GBS disease prevention policies (the green bar) is not linear - it’s exponential.  After the 1996 consensus guidelines were issued, there were substantially more hospitals with prevention policies, and yet this exponential growth was not mirrored by exponential decline in infection rates.  Put differently, the rate of decline in GBS early-onset infection is not proportional to the rate of increase in IAP measures, even though the latter is said to have caused the former.

This discrepancy is all the more curious, given that there was also substantially greater compliance with prevention guidelines in hospitals after 1996.40-42,59  So not only were a significant amount of IAP protocols newly established in 1996, but all of the hospital protocols that were already previously in place had supposedly become more effective.  

To illustrate the importance of this, consider that the use of selective broth media when culturing for GBS is 50% more effective than alternative media in identifying GBS41,60,61 - the proportion of hospitals using this recommended media increased from 6% in 1994 to 47% in 1997.41  Similarly, universal screening is said to be over 50% more effective than a risk-based strategy11 - the proportion of hospitals that screened all women rose from 26% in 1994 to 52% in 1997.41  Screening at 35-37 weeks of pregnancy yields a colonization status more likely to match that at the time of delivery, compared with screening earlier in pregnancy - the proportion of hospitals that were screening at the recommended time increased from 22% to 65% between 1994 and 1997.41  And finally, a combined vaginal and rectal culture is 40% more accurate in identifying GBS than vaginal culture alone60,62 - the proportion of hospitals complying with this recommendation rose from 31% in 1994 to 75% in 1997.41

So I am left confused.  On the one hand, we have survey data showing hospitals with IAP policies have lower incidence of GBS.  On the other hand, there is a mismatch between the linear decline of GBS rates, and the exponential uptake of IAP policies and improved methodology.

This brings us to a 3rd possible narrative.  Namely, that IAP reduces early-onset infections and that early-onset rates are naturally declining on their own - in other words, that IAP is not 100% responsible for the observed decline of early-onset rates, but rather, is enhancing a pre-existing decline.   This scenario would mean that current assessments of IAP’s impact are an overestimation, and notably, it could account for the discrepancy between hospital survey data and GBS rates outlined above.  Of course, the only way to precisely ascertain the degree of IAP's effectiveness is through randomized controlled trials.

Preterm infants have a considerably higher rate of early-onset infection, compared with full term infants.9  Although IAP is said to be 78% effective in preventing early-onset infection in preterm infants,3 a substantial portion of preterm deliveries among GBS colonized mothers occur without IAP, because colonization status is often unknown at the time of delivery (as a result of not having had the standard 35-37 week culture), and despite CDC recommendations, not all practitioners administer IAP in preterm labors where colonization status is unknown.3  So it can be helpful to analyze GBS trends among full term and preterm infants, separately.  

To that end, early-onset incidence among full term infants has declined, in correlation with IAP.  I do not have gestational data prior to 1996, so an assessment of pre-prevention disease trends among full term infants is not possible.  There is an interesting spike in the incidence of preterm infants between 2003 and 2007, however no real conclusions can be drawn from this, due to the above referenced challenges of preterm screening.

There is a disparity in the rates of early-onset infection among whites and blacks, the latter being significantly higher.9,48  The degree of this disparity has diminished since the advent of IAP,64 however it continues to persist nonetheless.  

A similar disparity exists with respect to late-onset infection rates as well.36,63  There are multiple reasons believed to possibly account, or partly account, for this.  One is that in the areas under surveillance, blacks have a higher proportion of preterm births than whites.39,64  Since preterm birth carries a higher risk of GBS infection,3,36 a higher rate of preterm birth would naturally result in a higher rate of overall infection.  However, even when we factor preterm births into the analysis, infection rates for full term black infants remain higher than whites.9,36

Another factor is that black women are believed to have higher general rates of colonization.39,55,64-66  If so, higher colonization rates would be expected to naturally yield more overall infections.  In addition, some speculate that disparities in access to prenatal care could account for the racial discrepancy in GBS incidence.36  However, one study found that even when controlling for these variables, black race remained an independent risk factor for disease.48 

Now, it is interesting to note that incidence among black infants actually increased 70% between 2003 and 2005,39 during a time when universal screening was in full force, despite comparable screening rates and IAP administration for both black and white mothers.63  This increase persists even when we factor gestational age into the analysis.  To that end, both early and late-onset infection among black full term infants rose between 2003 and 2006.9,36  This increase should give us pause, as it flies in the face of IAP’s presumed efficacy - and even though the increase was only temporary, it speaks to the notion that there are other factors at work influencing GBS incidence.

While there have also been significant increases in the rates among black and white preterm infants at various points, as mentioned in the previous section, there are too many variables involved with preterm incidence to draw reliable conclusions.

While the incidence of GBS early-onset infection has decreased dramatically since 1990, rates of late-onset infection (those occurring 7-90 days of life) have remained stable.9  This is to say, IAP (giving antibiotics to laboring women colonized with GBS) has had no appreciable effect on the incidence of late-onset infections as reported from ABCs,3,36 and there are currently no prevention strategies in place to address it.3,4,32  This is partly because the GBS bacterium can be acquired post-delivery (e.g. from caregivers), but half of late-onset infections are believed to have a maternal origin at birth,36,37,53 which begs the question, why would IAP not have had some impact on late-onset rates?

Interestingly, a recent study of 322 NICUs between 1997 and 2010 found that rates of GBS late-onset actually increased.67  This increase correlated with the implementation of universal screening, which taken at face value, appears to suggest that IAP is “shifting” some of the burden of neonatal infections into later periods.  However, the researchers noted that a portion of the observed increase in late-onset infections may be attributable to the study having included more very low birth weight (VLBW) infants over time.  Such infants are more susceptible to infection (having less developed immune systems), and since NICUs in general treat more preterm and VLBW infants compared with other facilities, this could be introducing a bias that is not present within the ABCs dataset.  

That being said, a separate controlled study of full term infants found an association between IAP and late-onset infections.68  And an analysis of late-onset incidence within ABCs found about half of case-infants between 2003 and 2005 were exposed to antibiotics during labor.36  These associations may or may not be indicative of anything, but we have to consider whether it’s possible that ostensibly stable rates of GBS late-onset within ABCs would have been different in the absence of IAP (i.e. that late-onset rates would have declined, but now appear stable as a result of being offset by an increase from IAP, thus masking IAP’s effect).

Another thing worth noting is that the study of 322 NICUs included urine cultures in their analysis, an important source of neonatal infection in their estimation.67  In contrast, the study of late-onset within ABCs excluded GBS urine cultures from their analysis.36  So this may also play a role in the discrepancy between the datasets.

Regardless, reported increases in late-onset infection are outweighed by the decreases in GBS early-onset infection.  But if IAP is causing an increase in late-onset infections, then obviously this would change the cost-benefit ratio of IAP overall.

Cesarean birth does not reduce the risk of GBS infection in newborns.3  However, if a Cesarean is performed before the onset of labor, with intact amniotic membranes, then the risk of neonatal GBS infection becomes negligible and IAP is not recommended.3,4  This would likely apply to virtually all of the following situations:  1) Cesareans scheduled in advance by maternal request  2) Cesareans scheduled in advance because of maternal or fetal health concerns  3) Cesareans scheduled in advance by doctor request, in the absence of health concerns  4) repeat Cesareans scheduled in advance because no VBAC (vaginal birth after Cesarean) will be attempted.  It’s worth noting that the medical community does not advise electing Cesarean as a means of GBS prevention, because Cesarean birth introduces new health risks that outweigh the initial risk of GBS infection.69

Now, GBS rates from ABCs are calculated using the total number of live births that occur in the surveillance area.  “Live birth” refers to birth of a living newborn via vaginal or Cesarean delivery.  But if scheduled Cesareans entail practically no risk of GBS infection, and are not treated within IAP protocols, then we should exclude such births from our calculations of GBS incidence.  If we fail to do this, we will end up padding the numbers by including births outside the scope of GBS among the total births from which GBS rates are derived, and this will decrease the resulting rate of infection that gets calculated.  So we need to examine how many Cesareans are performed before the onset of labor with intact membranes, how that statistic has changed over time, and whether the resulting figures could potentially distort our evaluation of IAP.

This is easier said than done, because no one actually knows the percentage of Cesareans that fall into this category.  Only information included on birth certificates can be tracked at large by health institutions, and birth certificates do not include whether a Cesarean was scheduled or emergency,70 and ABCs does not collect such information either.  So any conclusions to this end are going to be educated estimates, rather than precise figures.  Nevertheless, it is worth attempting to sort this out.  

The Cesarean birth rate overall has dramatically increased since the early 1990’s, rising about 60% between 1996 and 2009.71  There is much debate as to why this rate has risen so drastically, but the relevancy to this discussion is that if the subset of Cesareans that are scheduled was the same or larger over time, then this would result in more padding each successive year during this period (all the more so given the number of total births within the surveillance population also increased each year until 200872).

There are varying estimates on the percentage of Cesareans by maternal request and the percentage of primary Cesareans (women undergoing Cesarean for the first time) without any indicated medical risk.73-76  Some of these estimates conflict, and some are from differing years.  But a study of California births in 1995 found that 4.25% of deliveries were attributable to primary Cesareans in the absence of labor.77  With respect to repeat Cesareans, it is not unreasonable to assume a substantial portion are scheduled, given the prevailing “once a Cesarean, always a Cesarean” mentality in the U.S.

When you factor everything together, I believe it is fair to estimate the percentage of Cesareans without labor or ruptured membranes as accounting for 5% of total births (or 25% of Cesarean births) in the mid 1990s, as some have done.10  It is believed that the proportion of scheduled primary Cesareans has been increasing since 199675 - and the proportion of scheduled repeat Cesareans undoubtedly increased between 1996 and 2004 (as the rate of VBACs declined significantly).75,78  So, it’s plausible that by 2009 (the year in which the U.S Cesarean rate peaked) 50% of Cesareans may have been scheduled in advance, which would be 16.5% of all births.  Of course, we’re not factoring in those women that go into labor prior to their scheduled Cesarean date, but these scenarios are probably rare enough as to be negligible for our purposes.

If we proceed using these estimates, we can re-calculate GBS infection rates for 1997-2009 while excluding scheduled Cesarean births from the analysis, and therein get a sense for how this variable might potentially alter our perceptions of GBS incidence over time.

While these graphs begin at 1997, obviously somewhere between the 1970’s and 1990’s the percentage of scheduled Cesareans was zero, at which point the two lines would overlap.  So the effect of including scheduled Cesareans within an analysis of GBS incidence is that the degree of decline in early-onset rates becomes exaggerated.  Of course, if the assumptions incorporated into these calculations are underestimations, then the discrepancy observed above would be greater, and vice versa.  In addition, a proper analysis would take into account state-specific Cesarean rates and live birth data for each area within ABCs network independently; but my use of national data is sufficient to illustrate the point.

Although the exaggeration depicted here is not significant enough to fundamentally alter overall trends, it’s certainly a variable that should be taken into account, and one that could become more subversive in combination with other potential fluctuating variables and/or in the event that the proportion of scheduled Cesareans continued to increase.

Even with perfect implementation, IAP is not expected to be 100% effective, due to some amount of antibiotic failures and changes in colonization status between the time of screening and delivery.4,10,14,79  However, there are reports of unexpectedly large portions of GBS infection occurring in infants whose mothers tested negative for GBS (i.e. false negatives).  In a study of early-onset infections from 1997-2003 at a Boston hospital, 82% of the mothers of term infants that acquired infection had negative screening test results.80  Another study of a Tennessee birth cohort found 52.5% of early-onset infections resulted from mothers who screened negative.81  Then in a study analyzing GBS incidence in ABCs 10-state network during 2003-2004, 61.4% of the GBS infections that occurred in full term infants were among mothers who screened negative for GBS.49

Now, universal screening at 35-37 weeks of pregnancy is said to have a negative predictive value of 96%3,13 - that is, 96% of the time if you’re not colonized with GBS at the time of screening, you won’t be during delivery.  So the question is if the 4% of negative screening results that we know will be inaccurate accounts for the amount of false negative infections seen in the studies mentioned above.   

To that end, the researchers of the ABCs study calculated the number of infections that would be expected to occur from false negatives - they took 4% of the women who tested negative for GBS, and then applied a rate of infection assumed to transpire in the absence of antibiotic treatment (remember, false negatives do not receive IAP).  Accordingly, they expected to see between 44 and 86 cases of infection.  The number of such infections that actually occurred was 116 cases.  It’s important to note, however, that the researchers assumed a GBS incidence of between 5.1 and 10 cases per 1,000 births in their calculations.  As previously discussed, such incidence was the highest among the ranges reported from the 70’s and 80’s.  If we instead use lower reports for the calculation, or if we use the 1990 overall incidence of 1.8 per 1,000 (since that rate was before IAP guidelines), then the discrepancy between the expected number of infections resulting from false negative cultures and those that actually occurred would be significantly greater than what was concluded in the study.

As to why this discrepancy exists, the researchers speculate it may be the result of a combination of factors such as screening more than 5 weeks before delivery (which decreases the accuracy of screening results), or inferior specimen collection, culture processing, and/or errors in the recording of screening results.  Regardless, if the assumed negative predictive value of screening is underperforming in practice, it stands to reason that the assumed positive predictive value of screening might also be underperforming in practice.  We can’t deduce false positives in the way that we can with false negatives, because false positives only result in unnecessary antibiotics - not infection.  

The positive predictive value (PPV) of universal screening is said to be 87%, which is the figure cited by the CDC and based on a study from 1996.3,13  However, a study from 2002 concluded that the positive predictive value of GBS screening is lower than that previously suspected - their results showed a PPV of 67%.82  This finding was supported by another study from 2010 also showing a PPV of 67%,83 while a study from 2006 showed a PPV of 52%.84  A systematic review of nine separate studies found an average PPV of 69%.85  These lower PPV’s are perhaps in keeping with a study that showed significant changes in GBS colonization occurred in just a 24 hour period, thus casting doubt on the predictive reliability of 35-37 week screening tests in general.86

Of course, rapid testing for GBS administered during actual labor would eliminate all of this ambiguity.  But the current confusion is relevant because IAP’s perceived success is built around the assumption that the mothers receiving antibiotics are the ones actually colonized with GBS - so if the accuracy of our determinations to that end are in doubt, with evidence showing prior assumptions of positive / negative predictive values to be inflated, then it means there are more colonized women not receiving antibiotics than we thought, and more non-colonized women who are receiving antibiotics than we thought - and this would necessarily change our evaluation of IAP’s performance to date.

In full term infants, GBS infection is said to be fatal in 2-3% of cases.3  To be clear, that refers to 2-3% of the 0.5-2% of infants that develop infection from the 10-30% of mothers that are colonized with GBS.  Suffice it to say this is a very tiny amount of overall births.  In preterm infants, the percentage of fatalities from GBS infection is higher, at 20-30%.3

Reports from the 1970’s cited fatality ratios as high as 50%,9,44,48,61 however by 1990 (prior to the IAP era) this amount had drastically declined to 5.8%44 - this reduction is credited to advancements in the quality of neonatal care.14,44,61  From 1990 to 2013, there are many gaps in the mortality data that has been published.  I could not find year-specific rates for early-onset mortality between 1991 and 1996.  ABCs surveillance reports from 1997 onwards list the number of deaths that occur per year in children less than 1 year of age, but they do not differentiate between early and late-onset, nor between full term and preterm.  This makes it difficult to perform a thorough analysis of GBS mortality over time, but the available information is worth examining.

Given the decline in the amount of early-onset infections in the U.S., logically there should be reductions in the number of deaths resulting from GBS each year (since less overall infections means less potential fatalities).  However, since ABCs network expanded between 1990 and 2004 (along with the population in general), this will mean a larger number of births get factored into mortality calculations over time (and more births means more potential infections), which could end up counterbalancing expected declines in the amount of deaths that occur each year.  So if we want to properly assess GBS mortality, we’ll need to look at the percentage of GBS infections that result in fatality (i.e. the case-fatality ratio), rather than the absolute number of deaths.

Here is a graph showing GBS case-fatality ratios, derived from ABCs surveillance reports between 1997 and 2013:

As you can see, case-fatality has increased since 1997, and has remained mostly stable since the advent of universal screening in 2002.  The question is, should this be the case?

If advances in neonatal care were single-handedly responsible for reducing mortality from 50% to 5.8% by 1990, then presumably any additional improvements to the neonatal care system after 1990 would also result in further declines.  Of course, while it seems reasonable to assume that some amount of neonatal care improvement took place during the 23 years between 1990 and 2013, there is no way to objectively confirm this or precisely measure the degree.

The next thing to consider is, how would we expect mortality rates to behave in the absence of IAP?  I would expect that the percentage of babies that die from GBS infection would remain the same without any IAP intervention (assuming equivalent neonatal care)…colonization rates and GBS incidence might fluctuate from year to year, but any acquired infection would presumably entail the same level of severity.

However, if early-onset rates declined because of IAP, then it seems reasonable to expect that case-fatality would also decline (with or without advances in neonatal care).  After all, IAP is eliminating or reducing the population of GBS microbes in the mother, thus preventing the baby from becoming colonized with GBS or otherwise colonized with a lower proportion of the bacterium.  So of the babies that still end up developing infection, the level of GBS in their system is less than it would have been in the absence of IAP, and as a result, this would presumably decrease the likelihood that infection would end in fatality.  It’s impossible to say how much decline we would expect, but we could reasonably expect some decline to occur.

Nonetheless, the case-fatality ratio in 2013 was the same as it was in 1990, and this doesn’t seem to comport with expectations from IAP or improvements in neonatal care.  This raises an interesting question - is it possible that IAP is increasing the severity of infection?  This could potentially occur if the GBS bacteria that survive the onslaught of IAP go on to create a more antibiotic resistant colony in the newborn.  Such would account for the discrepancy between expected declines resulting from neonatal care advancements and IAP, and observed case-fatality rates.  It could also account for why GBS case-fatality appears to have declined between 1990 and 1997 (reaching a low of 2.6%),35,44,72 before steadily climbing back up between 1997 and 2002 (the period of transition to widespread adoption and implementation of IAP36,).

It must be noted that this analysis is limited by a variety of information gaps.  The case-fatality trends in the above graph combine early and late-onset, and they do not assess the proportion of preterm births for each year - if there were increases in the proportion of preterm births within the surveillance population over time, this could inflate overall mortality figures (since preterm births are more prone to GBS fatality4,36).  In addition, there could be cases of infection / fatality between 90 days and 1 year embedded in the ABCs data used to calculate the above figures (although any amounts therein would very likely be negligible).  At the same time, we don’t know if 100% of the cases reported by ABCs for the years above had complete data (sometimes outcomes, gestational age, etc are not known for all reported cases of infection), so these calculations constitute a minimum estimation.

However, there is a population-based study of the ABCs network between 1990 and 2005, which found that late-onset mortality was lower in the era of universal screening (after 2002) than before the advent of IAP (prior to 1996).36  But note from the graph above that overall case-fatality temporarily decreased between 2002 and 2005, before significantly increasing in the years afterward - so it’s possible the findings of this study reflect a temporary association that was about to change.  Regardless, if the case-fatality ratio of late-onset within ABCs decreased after 2002, while the overall case-fatality remained stable on average, then by deduction case-fatality for early-onset would had to have increased.  This is in fact apparent in data from population surveillance for the specific years 1990 and 2004,32,44 data which is robust enough to offer a thorough comparison between the pre-prevention era and the IAP era.  Take a look at the following chart:

The overall case-fatality was higher in 2004 (when universal screening was in full effect) compared to 1990.  Early-onset case-fatality was higher in 2004 than 1990.  When we look at preterm births, case-fatality in 2004 was almost 3 times higher than in 1990.  Late-onset mortality was lower in 2004 than 1990 (outweighed by the aforementioned increases).  We still need to consider the possibility that 2004 had a higher proportion of preterm infections, which could have inflated it’s overall mortality - to that end, the percentage of deaths that were preterm was 80% in both years, and of the total GBS infections in each year (with complete data), 1990 had a higher proportion occur in infants less than 37 weeks gestation…and yet, 1990 still has a lower overall case-fatality compared with 2004.  I find this remarkable.

All together, it appears to suggest that while IAP may be decreasing the amount of GBS early-onset infections, it may be increasing the severity of the remaining infections that occur.

Interestingly, the study of 322 NICUs between 1997 and 2010 mentioned earlier in this article found increases in the mortality rate associated with both GBS and E. coli late-onset infection after universal screening was implemented in 2002 (increases of close to 50%), with stable mortality rates for early-onset.67  The researches speculate that improved survival of VLBW (very low birth weight) and preterm infants over time may be making them more susceptible to infection in the late-onset period.  However, while this may explain increased incidence of infection among VLBW and preterm infants, it’s unclear whether it would explain the increased percentage of fatalities resulting from those infections.  As I see it, if better neonatal care is allowing more VLBW and preterm infants to survive, then we should expect those same improvements in neonatal care to contribute to saving more of those babies that acquire infection (which would reduce the case-fatality ratio).  The fact that we don’t see this confuses me, and again speaks to the possibility of some kind of biologic or selective pressure at work, which is perhaps increasing the virulence of surviving microbes.  

Lastly, it’s also worth mentioning a study which found that when antibiotics were universally administered to neonates at birth (as an alternative strategy to IAP), overall neonatal mortality increased by 40% despite a 68% reduction in the rate of infection.79  Newborns are obviously exposed to IAP through placental transfer, so perhaps the mortality increases discussed in this section are in keeping with this study’s findings.  

In the end, everything we’ve examined here seems to point toward a net increase in case-fatality rates of one kind or another, and so I am left with the impression that IAP reduces the quantity of infections at the expense of increasing infection severity.

The GBS infection rates we have examined so far are representative of the entire ABCs network.  However, in combining data from multiple sources, there is the risk that averaging overall incidence can mask anomalous findings within isolated sites.  So it seems wise that we also examine state-specific GBS infection rates.  Of course, incidence within an isolated area is not a reliable predictor of national trends, but that is not the goal - we’re interested in assessing the effectiveness of IAP in the absence of reliable clinical research.  To that end, if antibiotics effectively reduce early-onset GBS infection, they should do so regardless of the location in which they are administered.  So the ABCs network can be viewed as a collection of separate regions testing the protocol independently, and we should see early-onset rates declining within each respective region in correlation with IAP.

There are two obstacles to this plan.  1)  Only a few of the 10 states that comprise ABCs network were tracking GBS prior to 1995.  However, seven states were tracking GBS from 1996 onwards, which may be of use in assessing the impact of universal screening guidelines.  2) There is no published study that comprehensively examines GBS incidence within each ABCs area for the entire respective history of surveillance - there are only a handful of studies that list state-specific rates, from which such an analysis can be conducted solely with respect to early-onset incidence between 1998 and 2005.32,35,39,64,87

Some states have published GBS data online, however much of the information is limited.  I inquired with the CDC as to how to obtain comprehensive state-specific rates, and they said I would need to contact each state’s health department or Emerging Infections branch.88  Accordingly, I have been in communication with 7 of the states with limited information, but my efforts have been met with very little success - this is mostly due to the fact that these offices are immersed in important workloads and busy schedules, and simply can’t spare the time to facilitate my request…of course, conducting this inquiry as a regular citizen unaffiliated with any institution doesn’t exactly help matters.

In my conversations with a few ABCs coordinators, I was surprised to learn that not all states are in possession of their own data.  I took it for granted that each ABCs state already had comprehensive GBS data specific to their region, and that it was just a matter of getting them to supply me with this information.  However, as it turns out, this is not the case - such information would need to be manually calculated for the first time, requiring the devotion of staff and resources.  It is baffling to me that any agency involved in tracking a disease would not by default have comprehensive internal records of that which they are tracking, but it seems that such information is simply sent to the CDC for integration.  Even still, one would think the CDC would possess compartmentalized records of each surveillance area’s findings, but apparently they either don’t, or otherwise did not wish to share such information with me.

I also got the sense that state-specific trends are generally viewed as unimportant, because the sites are collectively held to be representative of the country, and since assessing national incidence is the main goal of the CDC, isolated trends are essentially irrelevant.  However, this is extremely shortsighted in my opinion, because if you don’t look at state-specific trends, then you can’t ascertain whether a single site (or subset of sites) is disproportionately influencing the overall trend, nor can you ascertain whether all sites are conforming to national expectations.  Of course, even if a site did depart from national trends, there could be a variety of reasons accounting for why that is - but it seems obvious that we should be in a position to know if / when such departures occur, in order to be able to investigate them further.

So with all of that being said, let’s examine some limited state data I have been able to assemble.  Minnesota and Colorado both seem to comport with national trends.

On the other hand, in Connecticut it appears that universal screening has had no impact on early-onset infections.  There was a temporary dip in 2004, but by 2007 rates had increased higher than they were in 2001.

The impact of universal screening in Oregon is ambiguous, with no sustained effect apparent: 

With respect to the remaining states, the available information regarding early and late-onset infection is too limited to be useful, in my opinion.  

Now, it’s possible that the speed and degree of compliance with national guidelines might have varied in each state, and that this might explain the apparent lack of impact of universal screening on early-onset rates within Connecticut and Oregon.  However, based on a CDC analysis of per-state compliance before and after their 2002 guidelines, it is evident that this cannot account for the discrepancy observed, because adoption and implementation of universal screening within CT and OR was optimal.3

There is some additional per-state hospital data that is intriguing.  Take a look at this graph published by the CDC,41 comparing the relationship between the proportion of hospitals with GBS prevention policies and corresponding infection rates, per state.

What is immediately apparent is that the state with the most prevention polices (CT) has the lowest rate, and the state with the least prevention policies (TN) has the highest rate.  But now take a closer look at the middle section of the graph, and notice that Georgia and Minnesota have equivalent prevention polices, yet drastically different infection rates.  Also note that Oregon has a higher amount of prevention polices than Minnesota, yet also has a higher rate of infection.  And finally, note that Minnesota and Maryland have fewer prevention polices than California and Connecticut, yet comparable incidence.

So within the limited data we have examined, not everything is adding up.

There is one more item which I should mention, as it’s quite peculiar.  Georgia’s health department has published data on GBS in which early-onset rates are listed between 1994 and 2007.89  What’s curious, however, is that none of the rates match the figures separately listed by the CDC in connection with Georgia, despite the fact that the source for both is supposedly ABCs.  What makes this all the more curious is that Georgia’s self-published graph shows early-onset rates were increasing from 1995 to 1999, as well as between 2003 and 2007.

This increase is not mirrored in the limited data published by the CDC.32,35,39,64,87  I do not know what to make of this, as I find it hard to believe that either party could be in error.  

Nonetheless, Georgia’s publication explicitly states that the reduced incidence of early-onset observed in U.S. national data is not apparent within their state.  The publication speculates that the state’s increase could be a result of improved case-ascertainment stemming from expanded state-wide surveillance (which began in 2004) and audited surveillance (which also began in 2004 according to this document).  

However, if the expansion of Georgia’s surveillance network resulted in better detection and thus, higher reported incidence, then we would expect to see the same phenomenon occur within ABC’s network overall…which of course, we don’t.  Plus, the rising rates within Georgia’s publication occur within consistent surveillance periods (as opposed to rates jumping up only when the surveillance area expands).   In addition, while Georgia states that audited surveillance (which is said to improve the accuracy and yield of infection cases) began in 2004, it has been reported elsewhere that audited surveillance in Georgia was occurring as early as 1990,44 and ABCs claims to regularly audit surveillance in all of their territories.64,72

So I am quite confused.  I planned on getting to the bottom of this by contacting Georgia’s Emerging Infections branch to submit a data request for GBS rates and/or speak with the ABCs or GBS coordinator.  However, it turned out this was easier said than done.  After days of getting bounced around from place to place, I was unsuccessful in finding the appropriate office, and bizarrely, no one in the health department knew who oversaw this issue.  Eventually, a data coordinator at the health department contacted the State Epidemiologist for guidance on my inquiry, and many weeks later I am still standing by.  So for now, make of this what you will.

Exposure to GBS is said to be similar throughout the world among pregnant women, in developed and developing countries.12  Colonization runs the gamut, with reported rates between 1.6% and 36% depending on the region and year.4,19,90  In general, GBS incidence is said to be lower in countries and hospitals that implement some form of IAP protocols, compared to those that do not.91,92  Early-onset infection rates have declined, in correlation with IAP, in Canada,93,94 Spain,95 France,96 and Australia,97-99 which have adopted prevention strategies similar to the U.S.9  Needless to say, when the same exact correlation pops up independently in separate countries, a causal relationship becomes more compelling.

But as with the United States, things are not so straightforward.  There is limited GBS data available in Europe,100 and it appears many countries were not actively tracking GBS until around the time IAP began to be administered or guidelines were issued,101,102 thus preventing a comprehensive analysis of disease trends starting before IAP.  Furthermore, many international studies of GBS incidence stem from single hospital reports,103-106 and may not be adequately representative.  Amusingly, researchers concluded in one Australian study that IAP was the likely cause of GBS declines because early-onset infections from non-GBS pathogens also declined97 - by this logic, IAP would not be responsible for GBS declines in other countries (such as the U.S.3) where no such decline in non-GBS incidence occurred.  

With respect to Spain, an interesting curiosity was brought to light in a study of hospitals, which analyzed GBS incidence after prevention guidelines were established.101  Hospitals were grouped according to the year in which prevention guidelines were adopted: on or before 1998, and 1999.  Rates decreased in both groups after prevention guidelines were implemented, consistent with IAP’s effectiveness.  However, each group had differing degrees of decrease - rates declined 65% in the 1998 group, and 36% in the 1999 group.  Also interesting is that incidence of E. coli decreased in the first group (the group with greater GBS decline), but increased in the second group.  Lastly, sepsis mortality rates significantly decreased in the first group, but not for the second group.  This suggests to me that other important and relevant factors are at work, potentially skewing our evaluation of IAP.

In the U.K. and Republic of Ireland, where systematic screening is not practiced and IAP rarely administered,107 GBS early-onset infection rates have been .5 per 1,000 live births.19,107,108  This is markedly lower than what we would expect based on U.S. assumptions, and is comparable to the incidence among countries that implement universal screening.94  Some suspect the U.K. rate is a result of underreporting and/or differences in colonization rates,107 but there is no sufficient data to support or refute such assertions.  Interestingly though, the incidence of late-onset infections in the U.K. and Ireland between 1996 and 200412 was basically equivalent to the rate of incidence reported in the U.S. during the same period36…if differences in colonization between the U.S. and U.K. were responsible for the differences in early-onset rates, then presumably one would expect to see differences in the rates of late-onset as well.  

Some assert that incidence in England, Wales, and Northern Ireland has been rising since 2003 and that therefore universal screening should be adopted in the U.K.,109 however such claims are based on the total number of case reports per year, and thus misrepresent the true disease burden by not accounting for fluctuations in the birth population.  When analyzing rates per 1,000 live births, incidence of early-onset infection in these regions was identical in 2003 and 2013 (.37 and .38 respectively).110,111  On the other hand, rates of late-onset did increase during this period (from .18 to .23),112 but since no IAP protocol has ever been associated with decreased late-onset infection, it is reasonable to ask whether IAP is having unintended consequences in the late-onset period.

In Finland, overall neonatal GBS incidence (early and late-onset combined) declined from 3 per 1,000 to .76 per 1,000 live births between 1976 and 1994, in the absence of a universal screening policy or national guidelines.113-115  From 1995-2000, during which IAP was not routinely administered, early-onset was .6 per 1,000 live births,103 comparable to the U.K.

Norway adopted a risk-based prevention strategy in 1998, after rates had been climbing from 1985 throughout the 1990’s.117,118  The impact of their prevention guidelines is somewhat unclear, but it seems that early-onset rates were stable overall before and after their implementation (with late-onset increasing in 2005 and 2006).116,119  Curiously, the country experienced an unexpected and quite significant spike in GBS mortality in 2006, for reasons unknown.116,220  

The Netherlands also established risk-based guidelines in 1999, but although rates initially decreased after it’s implementation,121 a subsequent national surveillance study conducted to assess the impact of prevention protocols found that they did not lead to decreased incidence among newborns.  Rates were analyzed over a 25 year period between 1987 and 2011, and incidence was higher in the period after protocols were implemented.122

Then there’s Israel, India, and Greece, three countries in which incidence is remarkably low in the absence of prevention guidelines, with reported rates between .1 and .3 per 1,000 births.123-126  Overall incidence in the region of Southeast Asia has been reported as low as .02 per 1,000 births.91  A study of women in Zimbabwe actually found that colonization was not even associated with adverse outcomes (i.e. infection).125  And incidence within developing countries is generally lower than developed countries,12,92 though there are some exceptions.91  

Reasons speculated for the aforementioned discrepancies include differences in maternal colonization rates, differences in the virulence of GBS strains and serotype distribution, and differences in clinical diagnosis, however all of these speculations can be refuted by the available evidence.128  Other potential reasons include differences in the quality of surveillance, genetic differences among populations, and differences in the levels of maternal protective antibodies acquired by newborns.12  A compelling case has been made that factors relating to inherent immunity among mother and fetus play a crucial role in explaining why such a small percentage of newborns are susceptible to GBS infection in the first place, why it’s higher in preterm infants, and why some regions have lower incidence despite relatively high rates of colonization.129

All of the confusion outlined in this article makes it impossible to definitively ascertain IAP’s effectiveness and overall worth.  IAP might work as claimed…or it might not.  Of course, most practitioners in the U.S. undoubtedly believe that IAP is effective, but such assurance appears to be based on habit alone.  The dilemma becomes all the more pressing in light of the fact that the use of antibiotics is not completely risk free.

The most extreme risk of IAP is that of maternal anaphylactic shock, which has been documented in response to penicillin (the primary antibiotic used during IAP)4,130-132 and cefazolin (a secondary alternative).133  Women with an allergy to penicillin are obviously given alternative antibiotics, however, one documented case of maternal anaphylaxis (which led to fetal demise) occurred despite the absence of such an allergy.134  However, it must be stressed that anaphylaxis is extremely rare.1,4  According to the CDC, about 1 in 10,000 mothers will experience severe allergic reaction.135  Fatal anaphylaxis has been estimated at 1-4 per 100,0004,136,137 (although some feel this estimate is grossly inflated107).  Regardless, the incidence of maternal anaphylaxis is significantly more rare compared to the incidence of GBS infection, and thus IAP’s reduction of the latter is considered to outweigh the occurrence of the former.3 

IAP also has been associated with increased incidence of maternal and neonatal yeast infection.128  Yeast infection of the breast can dissuade some mothers from breastfeeding their infants.139  Other milder reactions to antibiotics include rash, which occurs in 0.7-4% of penicillin treatments.3

Increasing resistance of bacteria to antibiotics is a major concern in the health community, and this concern extends to IAP protocols.  GBS resistance to erythromycin, clindamycin, and ampicillin following the implementation of IAP have been documented,36,68,90,140,141 as well as E. coli resistance to ampicillin,142-146 however no resistance has yet been observed in penicillin.4,14,36,68,90  That being said, there has been increased penicillin resistance among non-GBS pathogens throughout the world,1 so perhaps it is simply a matter of time before we see the same with GBS, and to that end there are limited initial reports of reduced GBS susceptibility to penicillin in Hong Kong and Japan.147,148  

There is also concern that while IAP may be decreasing the rate of GBS infection, it may be increasing the rate of infection from non-GBS pathogens.  Some studies have demonstrated this with respect to E-coli (particularly among very low birth weight infants)67,140,146,149-152 and late-onset infection from gram-negative pathogens other than E. coli,145 however other research disputes this.9,14,98,153

In general, IAP reflects a philosophy of care that has become standard, in which antibiotics are overprescribed and widely administered as a preventative measure.  Such practices are a primary factor in increasing antibiotic resistance among microbes.154  When an antibiotic is administered, it doesn’t target one specific bacterium, nor does it affect one isolated location.  Rather, there are a variety of bacteria that are susceptible, over and above the “bad” bacteria for which the antibiotic has been prescribed, and after an antibiotic enters the bloodstream it gets circulated throughout the entire body, eliminating susceptible bacteria everywhere (both “good” and “bad”).1  So antibiotics aren’t snipers; they’re bombers.  

This must be appreciated because the more we use antibiotics, the more we select for resistance in the overall bacterial population; i.e. those bacteria with resistant genes that survive an antibiotic onslaught go on to reproduce, which leads to more bacteria with such resistance.1,154  As this compounds, antibiotic resistance increases, which makes them less and less effective.  The more bacteria susceptible to a given antibiotic, the greater the selection for resistance will be.1  Thus, we want to be diligent about our use of antibiotics (particularly broad spectrum antibiotics) and guard against their excessive use so that we don’t facilitate, expedite, and/or exacerbate the creation of “superbugs”, which puts everyone at greater risk of acquiring life-threatening antibiotic-resistant infections.  Additionally, we want to limit the likelihood that small and rare colonies of bacteria (what Dr Martin Blaser refers to as “contingency species” in his book Missing Microbes) will become permanently wiped out from any given antibiotic exposure, as the absence of such species decreases our microbial diversity, which ultimately makes us more vulnerable to future potential pathogens.1

Given the low incidence of GBS infection and the uncertainty regarding when infection will occur, the current IAP strategy necessitates treating a great many so as to save a tiny few, which results in multitudes of women receiving antibiotics who don’t actually need them.  And while penicillin G (the preferred choice for IAP) is narrower in scope compared to alternative options,3 it nevertheless kills a variety of bacteria over and above GBS.156  So about a million mothers will receive antibiotics each year, in our attempts to prevent roughly 6 thousand babies from acquiring infection.37  But of course, antibiotics administered to laboring women also engage their babies via placental transfer, which means about a million newborns are exposed to antibiotics each year through IAP as well.  Of course, 6 thousand neonatal infections is something to take seriously, but so is 2 million exposures to antibiotics.

This becomes particularly relevant in the context of a newborn baby’s microbiome, which begins forming during birth.  Prior to labor, the baby is essentially a blank slate, bacteriologically speaking.2  As the baby moves through the vagina during birth, fundamental microbes are picked up.  Additional microbes are then picked up from the mother’s skin, rectum, and the surrounding birth environment.  Then more through the breast milk, the initial feeding of which typically takes place within the first hour after delivery.  All of this colonization is essential to a healthy infant,1,155 and importantly, the species of bacteria picked up by newborns are not random, but the result of coordinated changes in the microbiomes of mothers that occur throughout pregnancy.1

There is thus concern that IAP may undermine the acquisition of this founding wave of microbes.  The antibiotic, which is administered at regular intervals every four hours, kills both GBS and non-GBS bacteria in the mother.1,156  So the question is what are the consequences of this?  Unfortunately the data is scant.  There have been some studies showing IAP altered the gut microbes of infants when penicillin, ampicillin, and gentamicin were utilized,157,158 and the same has been found with respect to general antibiotic exposure in the first days of life,159 but no studies have investigated the longterm implications of this159 (if indeed there are any).  There has, however, been some such research with respect to Cesarean births, and since Cesarean delivery bypasses the biologically designed processes of newborn colonization (through both surgical delivery and antibiotic administration), it very well may be a useful guide with respect to IAP.  

To that end, it has been shown that the gut microbes of babies born via Cesarean section lack species normally acquired during vaginal birth,1,160 and have differing distributions of colonized bacteria,155,159,161 and this alteration has been associated with an increased risk of certain health conditions such as asthma, obesity, celiac disease, and allergies.1,2,162,163  To be clear, Cesarean delivery in no way guarantees that infants will acquire such maladies, but the point is that this increased risk is a direct result of alterations to the microbiome.  Although the microbiomes of Cesarean and vaginally born babies do begin to converge over time,1 these initial alterations can impact the future health of individuals by modulating the distribution of microbes moving forward, as one study found a significant difference in the gut microbes of 7 year old children born vaginally and via Cesarean.164

It’s reasonable to question whether IAP may have similar effects.  In general, research shows that antibiotic exposure at young ages increases the propensity to become obese and develop asthma,1 and antibiotic exposure in utero has been linked to asthma, eczema, and hay fever.165  The use of penicillin in labor has also been associated with a 2.6-fold increase in respiratory distress among GBS colonized newborns.166  While the microbiome in some babies may end up compensating or making up the gap eventually, this may not be the case for other babies, and even if IAP alterations are only temporary, they nevertheless are occurring during a critical window in newborn development,155 the consequences of which need to be thoroughly evaluated.

What we can say for certain is that the microbiome matters, that birth is the genesis of it, and that IAP has some effect on its formation.  This is an area where research is ongoing, but one that must be factored into any cost-benefit analysis of current GBS protocols.

Ultimately, if we’re going to expose families and society to the risks of antibiotics, whatever they may be, then we better make sure the treatment actually does what we think it does.  Only then can one make the value judgement that the rare amount of newborn GBS infections avoided through treatment outweigh the rarer amount of maternal anaphylaxis resulting from treatment, that the benefits of reducing GBS incidence are worth the risks of fostering antibiotic resistance, and that altering the microbiome of a million babies is acceptable in order to prevent GBS infection in a few thousand babies.  Of course, for those prepared to make the aforementioned value judgements, the limitations of IAP research would appear to make it difficult to do so with confidence.

The most discussed alternative to IAP would be a GBS vaccine, the need and usefulness of which has been cited many times throughout GBS literature.  Research and development has been underway for many years and clinical trials are ongoing.9,12  In comparison to IAP, there are many benefits to a GBS vaccine, along with some drawbacks.9  Regardless, it is not yet available as an option.

Another alternative strategy implemented by some practitioners is the use of probiotics.  The intent here is to effect a microbiome in which GBS is decreased and/or replaced by alternative bacteria, thus circumventing the entire GBS dilemma.  Scientific research on probiotics is generally limited,1,159 but there is a clinical trial currently underway researching its application to GBS,167 so the jury is out.   Still, given the general lack of harm involved with probiotics,1 some find it prudent to take them despite the lack of clinical data.  If they are effective, it would make sense to take them early in pregnancy regardless of GBS status, so as to allow maximum time for the probiotic to build up in the system by 37 weeks.

From my perspective, looking in from outside the medical community, there appears to be a double standard in the way that GBS research gets interpreted and discussed.  Declining incidence among countries with prevention strategies is assumed to be attributable to IAP, while increasing incidence among such countries is assumed to be attributable to compliance failures.  Low incidence in countries with universal screening is assumed to reflect the efficacy of IAP, while low incidence in countries without universal screening or without routine IAP is assumed to reflect underreporting and/or differences in colonization or virulence.  Fundamental assumptions are rarely (if ever) questioned, and contradictory findings typically go without mention.  In bizarre fashion, the clinical trials that spearheaded the IAP era, the quality and reliability of which were harshly criticized by the Cochrane Collaboration, routinely get cited as if beyond reproach.

I am troubled by the general lack of concern that I have encountered over the issues discussed in this article.  Many are dismissive of the Cochrane analysis, and many feel the observed correlation between IAP and GBS rates in the U.S. is sufficient evidence by itself.  But we cannot rely on correlation alone just because it tells us what we want to hear, and the discrepancies outlined above warrant careful consideration.

Although the likelihood of modern trials appears to be nonexistent, it might be within the realm of possibility among countries without IAP protocols, or those without universal screening guidelines.  There could also potentially be useful information gleaned from a study of GBS among homebirths or birthing centers - such families may be more likely to decline antibiotics than families planning to birth in a hospital, which might yield sizable treatment vs no-treatment comparison groups.  To that end, the Midwives Alliance of North America (MANA) compiles and maintains a statistics registry of health data in which a retrospective analysis of this nature would be possible.168-171

In the meantime, families contending with GBS find themselves in a difficult position.  Assessing the risk of developing GBS infection against the pros / cons of IAP is not a straightforward evaluation, and comes down to one’s personal perspective.  Some are uncomfortable with the idea of receiving antibiotics during labor, but the pressure to acquiesce to prevention protocols can be extreme.  Of course, when doctors strongly recommend treatment with unwavering conviction for the safety of the child, it is not surprising that most women agree to receive them.  This is unfortunate, as health recommendations and decisions should be informed by science, and not based in assumptions, intimidation, and/or exaggerated fear.  Equally unfortunate is the vitriol encountered by families that choose to decline antibiotics - it is quite remarkable how such families can be vilified, despite the uncertainties in the research.

In the end, if the medical community is going to continue recommending that laboring women receive antibiotics as a routine preventative measure, then I would argue they have a moral obligation to acquire reliable clinical evidence of its efficacy.  And if / when we subsequently confirm IAP is as effective as currently believed, such will not end the conversation or debate as to whether IAP strategies are ultimately in the best interests of society…but at least we would have a valid discourse to that end, based on known effectiveness and not presumed effectiveness.

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