Six Reason to Question Vaccinations

I really don't believe kids who get Prevnar get more ear infections :rolleyes:
It was made to prevent ear infections by the pneumococcal bacteria (among other things).

What study are using to make that claim kelly??

There is no data saying they get MORE than anyone else.

They can get different types from different bugs, but they don't get MORE infections. Unless you can prove otherwise, of course.

In the news lately, there is a new staph superbug. Depending on what NEWS story you read, some blame Prevnar for making a niche, but most of the blame is on overuse of antibiotics. Whether or not Prevnar was ever on the scene, the staph strain would have shown up more, as it was already on the scene. There is no reliable source that can actually just blame Prevnar for the emergence of this staph strain. There also no accusation that only kids who got Prevnar also got this type of ear infection.
http://www.sciencedaily.com/releases/2007/10/071016160615.htm

Kids who get Prevnar at no more higher risk of getting the superbug staph than anyone else who might get exposed to it.

It's huge misinformed leap to go around saying kids who got Prevnar actually get more ear infections than anyone else.
 
Last edited:
Some studies find that the effectiveness of Prevnar for ear infections is 6%, some say 8%, some say zero.
Kids who get Prevnar do get more staph ear infections, though. (I'll go dig up the links again if you want.)
Staph and pneumococcus are natural competitors for space in people. Pneumo "poisons" staph with hydrogen peroxide.

Kids who get Prevnar at no more higher risk of getting the superbug staph than anyone else who might get exposed to it.

Well, Prevnar isn't going to cause someone's staph to become antibiotic resistant, but if you increase colonization with staph as a result of Prevnar, there's no reason to think the resistant staph species will be excluded. There's no reason to think the only increase to be found will be the antibiotic susceptible types.
ETA:
That article, Eos, isn't about a staph strain. That's a non-prevnar pneumo strain.
 
Last edited:
The effects seem to be all over the place with Prevnar.

http://jama.ama-assn.org/cgi/reprint/297/16/1784


RESULTS: In the first 3 years after introduction of routine vaccination with heptavalent pneumococcal conjugate vaccine, overall invasive pneumococcal disease decreased 67% in Alaska Native children younger than 2 years (from 403.2 per 100,000 in 1995-2000 to 134.3 per 100,000 per year in 2001-2003, P<.001). However, between 2001-2003 and 2004-2006, there was an 82% increase in invasive disease in Alaska Native children younger than 2 years to 244.6/100,000 (P = .02). Since 2004, the invasive pneumococcal disease rate caused by nonvaccine serotypes has increased 140% compared with the prevaccine period (from 95.1 per 100,000 in 1995-2000 to 228.6 in 2004-2006, P = .001). During the same period, there was a 96% decrease in heptavalent vaccine serotype disease. Serotype 19A accounted for 28.3% of invasive pneumococcal disease among Alaska children younger than 2 years during 2004-2006. There was no significant increase in nonvaccine disease in non-Native Alaska children younger than 2 years. CONCLUSIONS: Alaska Native children are experiencing replacement invasive pneumococcal disease with serotypes not covered by heptavalent pneumococcal conjugate vaccine.

IPD in Adults
Between the baseline and 2004-2006,
PCV7 serotype IPD decreased among
both Alaska Native and non–Native
Alaska adults 18 years or older (Table 1
and Table 2). Among adults 45 years
or older, non-PCV7 serotype IPD increased
in Alaska Native (P.001) and
in non–Native Alaska adults (P=.03).
Accordingly, among adults older than
45 years overall IPD rates increased 43%
for Alaska Natives
(P=.03) but declined
24% for non–Native Alaskans
(P=.02).

Overall, 57% of Alaska children
younger than 5 years old during 2004-
2006 presented with pneumonia. The
proportion of IPD cases with meningitis
in children younger than 5 years did
not change over the 3 time periods
;
however, there was an increase in the
proportion of cases with empyema
(from 2% to 13%
, P for trend .001),
an increase in the proportion of cases
with pneumonia and bacteremia
(from
40% to 57%, P=.007), and a decrease
in bacteremia with no other focus (from
54% to 40%, P=.02). During 2004-
2006, cases of empyema in Alaska
children younger than 5 years were
from several serotypes: 1 case each of
3, 7F, 9V, 12F, 15A, 22F, and 33F, and
4 cases of 19A. The proportion of IPD
cases in Alaskans younger than 5 years
who were hospitalized increased from
39% (109/279) in 1995-2000 to 62%
(51/82) in 2004-2006
(P for trend
.001).

The
illnesses due to IPD replacement disease
among Alaska Native children were
similar to IPD cases before PCV7 introduction
except for increases in the
proportion of hospitalized IPD, pneumonia,
and empyema cases. An increasing
proportion of IPD cases associated
with empyema have been reported in
other populations
 
.... To put that figure into perspective, you are 7 times more likely to be killed walking down the street in the same time period.
Let's try putting that figure into a little different perspective. Why should someone not prevent a child's preventable death? Is health care rationed in the UK?

Are premature infants for instance, allowed to die because salvaging an infant born at 24 weeks costs on average, ~$17,000,000?

Outcome of infants born at 24-26 weeks' gestation: I. Survival and cost
The likelihood of having a surviving infant without chronic lung disease or severe retinopathy of prematurity was 35% at 24 weeks and 78% at 26 weeks. Hospital costs for the 29 nonsurvivors were $1.46 million and for the 94 surviving infants were $16.9 million.
 
If I were you I'd delete that post (oh darn, you can't; I've just quoted it). I think you'll find wishing someone dead is against the forum rules. I think wishing my children dead is still ok, though;)
But, Ivor, you have been telling all of us to risk letting our kids die of a vaccine preventable disease because you personally judge the cost per life saved to be too high.
 
Why should someone not prevent a child's preventable death?

It is a matter of choices, isn't it? In preventing a child's preventable death what are we then unable to do that might be as important or more important?

Is health care rationed in the UK?

Yes, and every where else, too.
 
Where are you getting these 50/50 odds from?
That's not what's been happening. We have a pattern at this point.
The emerging serotypes become pathogens. Not in 100% of people, just like the vaccine serotypes aren't pathogens in 100% of people.
My goodness, this is the second time on this subject your brain was running on concrete. It was a hypothetical example to illustrate a concept for criminy's sake. The actual risk of a pathogen replacing a pathogen is vastly lower than 50%. You need to read some references on the percentage of human pathogens in the entire body of microorganisms. It would be considerably less than 1%!!!


The new emergers ARE bad, too. They are causing a variety of infections and invasive diseases. And yes, my argument is that there's an unknown probability that eventually we'll open up space for something to take off that's MUCH MUCH worse.
This reflects pure ignorance about microorganisms and infectious disease.


How do you know the chances are "incredibly small"? Meningococcal serotype W135 that emerged as a result of vaccination against A,B,C, and Y managed to do all by itself in the middle east what it took 4 serotypes to do before.
The concept you are missing here is "selective attention". Rather than looking at the effects vaccines had on colonization and normal flora, you are simply taking the one organism that because it is a pathogen, comes to the researcher's attention. You would need to compare the disease caused by the emerging pathogen with the disease from the entire group of organisms the vaccine eliminated in order to make your comparison relevant.

And what nonsense, that eliminating a killer isn't a good idea because another killer might emerge. I can't even comprehend such bizarre thinking. That's along the lines of the thought process of an antivaxer claiming, "the 'natural' infection is better because it offers better future immunity". Well yeah, if you survive.


So?
Prevnar'ed kids get more staphylococcal ear infections. The emerging staph is pathogenic.
I don't really want to trade in pneumococcal infections for staph infections + god knows what else.
That seems like a really bad idea to me.
Well you'd be wrong. How many cases of staph meningitis did you find in that group? Eliminating pneumococcal otitis is not the goal of the pneumococcal vaccine in young children. The goal is to eliminate pneumococcal meningitis.
 
Last edited:
It is a matter of choices, isn't it? In preventing a child's preventable death what are we then unable to do that might be as important or more important?



Yes, and every where else, too.
If Ivor weren't focusing on the cost return ratio of vaccines, I would be more moved by his argument. It is just absurd to focus on such a simple means of preventing morbidity and mortality in lieu of the trillions of dollars wasted elsewhere. Why not exclude the elderly from expensive intensive hospital care and spend that money? Why not trade the single 17 million dollar 24 week premie's care and spend that money saving 10 kids from varicella fatalities?

It is simply a haphazard way of analyzing health care dollar priorities.

The real issue Ivor has here is underestimating the risk of these vaccine preventable infectious diseases.
 
Last edited:
If Ivor weren't focusing on the cost return ratio of vaccines, I would be more moved by his argument. It is just absurd to focus on such a simple means of preventing morbidity and mortality in lieu of the trillions of dollars wasted elsewhere. Why not exclude the elderly from expensive intensive hospital care and spend that money? Why not trade the single 17 million dollar 24 week premie's care and spend that money saving 10 kids from varicella fatalities?

It is simply a haphazard way of analyzing health care dollar priorities.

The real issue Ivor has here is underestimating the risk of these vaccine preventable infectious diseases.


I don't understand your response. I question your use of single consequence examples, and instead of responding to my remarks, you again attack Ivor's position and repeat the single consequence examples.

Why not direct your comments to Ivor?
 
The effects seem to be all over the place with Prevnar.

http://jama.ama-assn.org/cgi/reprint/297/16/1784
From your source:
overall invasive pneumococcal disease decreased 67% in Alaska Native children younger than 2 years (from 403.2 per 100 000 in 1995-2000 to 134.3 per 100 000 per year in 2001-2003 ... the invasive pneumococcal
disease rate caused by nonvaccine serotypes has increased 140% compared with the
prevaccine period (from 95.1 per 100 000 in 1995-2000 to 228.6 in 2004-2006...

...eroded the overall decline to 41%.
So the overall decrease went from 403/100,000 to 229/100,000 plus the 134 you didn't eliminate you still get 363/100,000 incidence and that is still a net decrease in incidence.

Using our knowledge of emerging pathogens one can expect a finite number of competing pneumococcal organisms with the ability to cause invasive disease.The trend in replacement pathogens should eventually exhaust the current members with simple expansion of the current vaccine to include more serotypes. There are no clear selection factors here forcing the emergence of invasive serotypes.


Accordingly, among adults older than 45 years overall IPD rates increased 43% for Alaska Natives
Which means there is more here than simply the introduction of the vaccine.

there was an increase in the proportion of cases with empyema (from 2% to 13%, P for trend .001), an increase in the proportion of cases with pneumonia and bacteremia
Look at "Table 1. Rates of Invasive Streptococcus Pneumoniae by Time Period, Age Group, and Vaccine Serotype in Alaska Natives, 1995-2006*" in the article. The paragraph you quote compares a change in a small subset of the whole. Are you suggesting the increase applies to the entire population?

In addition, look at the figures in the chart. First, you have to look at what the time period is the change refers to. There was an initial decrease in cases, then an increase but not to pre-vaccine levels. If you just compare the increase during the use of the vaccine, you miss the fact the overall result is a decrease.

And, more importantly, where increases are noted, the p values are high meaning the statistical difference is nil.
 
I don't understand your response. I question your use of single consequence examples, and instead of responding to my remarks, you again attack Ivor's position and repeat the single consequence examples.

Why not direct your comments to Ivor?
I was agreeing with you but explaining why it didn't apply to Ivor's arguments.

What "single consequence" are you referring to?

Originally Posted by skeptigirl
Why should someone not prevent a child's preventable death?


It is a matter of choices, isn't it? In preventing a child's preventable death what are we then unable to do that might be as important or more important?
 
Last edited:
....
Staph and pneumococcus are natural competitors for space in people. Pneumo "poisons" staph with hydrogen peroxide....
For the record, not all pneumococcal bacteria produce this substance. And if pneumococcal bacteria were a perfect colonizer, you would expect all pneumococcal and no staphylococcal bacteria in everyone's nasopharynx.

Interference between Streptococcus pneumoniae and Staphylococcus aureus: In Vitro Hydrogen Peroxide-Mediated Killing by Streptococcus pneumoniae
Bacterial strains used in this study are described in detail in Table 1. S. pneumoniae strains used were TIGR4 (21), Rx1 (16), and Pn-20. In addition, SpxB-negative variants of TIGR4 and Pn-20 and LytA-negative variants of Rx1 and Pn-20 were created using the Janus cassette (20). Strains of three other Streptococcus spp.—S. gordonii, group A streptococcus, and group C streptococcus—were also tested. Staphylococcal species used in the study were the following: S. aureus strains Newman (NCTC 8178) and ALR and coagulase-negative staphylococci (CNS) (Staphylococcus epidermidis, Staphylococcus xylosus, and Staphylococcus sciuri).

Inhibitory and bactericidal effects of hydrogen peroxide production by Streptococcus pneumoniae on other inhabitants of the upper respiratory tract.
Hydrogen peroxide is produced by the pneumococcus through the action of pyruvate oxidase (SpxB) under conditions of aerobic growth. Both an spxB mutant and a naturally occurring variant of S. pneumoniae, which is downregulated in SpxB expression, were unable to kill H. influenzae.


In fact, the ability to produce H2O2 is also the downfall of pneumococcal bacteria.

SpxB is a suicide gene of Streptococcus pneumoniae and confers a selective advantage in an in vivo competitive colonization model.
 
Last edited:
.....

But when I investigated the committee membership for the CDC vaccine policy (this would have been approximately 10 years ago), every single member of the committee had requested and been granted an exception to the regulations regarding potential conflict of interest. There was a good deal of rhetoric I waded through about how it was necessary and not an impedence to an impartial judgement of the available scientific evidence. My conclusion: committee recommendations are likely to show a bias towards recommending vaccinations. The actions I've taken as a result: I use more caution when accepting vaccinations for myself and my children. I don't get a vaccination done just because it's on the schedule of recommended vaccines. I only get vaccination if I do some research and decide it's right for me/my family.


No, I'm not making any sort of charge about anyone being in bed with the drug companies. When I looked into the matter about a decade ago, I was shocked to discover that so many of the members of the policy making committee on vaccination had sufficient financial ties with vaccine manufactures that, as required by federal law, they had filed conflict of interest forms reporting the details of their association. That fact has colored my perception of the committee recommendations.
If you start with the premise the health care community is full of greedy corrupt people then no amount of discussion about this matter is going to correct that misconception. If you start with the premise that the vast majority of health care researchers and professionals are just that, researchers and professionals dedicated to their work, then the following addresses your concerns:

TESTIMONY ON VACCINE ADVISORY COMMITTEES
DIXIE E. SNIDER, M.D., M.P.H.
ASSOCIATE DIRECTOR FOR SCIENCE
CENTERS FOR DISEASE CONTROL AND PREVENTION
U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES

BEFORE THE COMMITTEE ON GOVERNMENT REFORM
U.S. HOUSE OF REPRESENTATIVES

JUNE 15, 2000
Federal advisory committees inherently have members who may have potential financial conflicts of interest because, as I�ve mentioned, the members are chosen for service based on their expertise in the areas in which advice is sought by the government. Experts in the vaccine field frequently have affiliations with, or may be engaged in research conducted by, academic institutions or other institutions which may receive funding from vaccine manufacturers. Physicians in private practice who are considered experts often do consultancies, work for managed care organizations involved in clinical trials, and/or accept honoraria for lectures given at scientific meetings sponsored by manufacturers. This professional experience which contributes toward the development of their immunization expertise also may result in potential conflicts of interest. Congress has recognized the need for service on federal advisory committees by these experts and has provided for waivers of the conflict of interest prohibitions under 18 U.S.C. � 208 when the need for the individual�s services outweighs the potential for a conflict of interest created by the financial interest involved. CDC is sensitive to any perception regarding potential conflicts of interest of members serving on the ACIP and is committed to taking steps to ensure not only that there is technical compliance with the provisions of 18 U.S.C. � 208, but that the spirit of those provisions is also fulfilled.

I can understand your underlying premise because I have a similar one when I look at corporate America and especially the Bush crony tradition. However, my experience in the health care profession leads me well away from lumping these professionals into the greedy corrupt corporate group. There are some corporate actors who are not greedy and corrupt. But in the scientific and health care professions it is the rule not the exception.
 
Last edited:
skeptigirl said:
The actual risk of a pathogen replacing a pathogen is vastly lower than 50%.
I'm going to have to say that the degree and speed of replacement disease with s.pneumo is rather solid evidence that you're just making things up here.
So far, it's been closer to 100%.

This reflects pure ignorance about microorganisms and infectious disease.
I love it when you do that!
"I have no idea, so I'm just going to say you don't know anything."
It's almost charming in a weird way.

Eliminating pneumococcal otitis is not the goal of the pneumococcal vaccine in young children. The goal is to eliminate pneumococcal meningitis.

Let's look at prevnar's track record so far. Remember, it was approved, in 2000, recommended in 2001, but there was a shortage through most of that year, and in 2002 uptake was still at 40%, but it's pretty darn high now. (80%?)

http://www.cdc.gov/ncidod/dbmd/abcs/survreports.htm

~~~~~~~~~~~~~~~~~~~~
http://www.cdc.gov/ncidod/dbmd/abcs/survreports/spneu99.pdf
1999: -deaths-
Kids under one: .77
Age1 : 1.18
Age 2-4: .52


Meningitis: 5.2
~~~~~~~~~~~~~~~~


http://www.cdc.gov/ncidod/dbmd/abcs/survreports/spneu01.pdf
2001- deaths-

Kids under one: .6
Age1 : 1.2
Age 2-4: .5


Meningitis: 5.3


~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
http://www.cdc.gov/ncidod/dbmd/abcs/survreports/spneu05.pdf
2005: -deaths-

Kids under one: .97
Age1 : 2.4
Age 2-4: .33


Meningitis: 5.8


~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
http://www.cdc.gov/ncidod/dbmd/abcs/survreports/spneu06.pdf
2006: -deaths-

Kids under one: .7
Age1 : .24
Age 2-4: .4


Meningitis: 6.1
~~~~~~~~~~~~~~~~~~~~~~`

The numbers kind of speak for themselves.

Skeptigirl said:
Using our knowledge of emerging pathogens one can expect a finite number of competing pneumococcal organisms with the ability to cause invasive disease.The trend in replacement pathogens should eventually exhaust the current members with simple expansion of the current vaccine to include more serotypes. There are no clear selection factors here forcing the emergence of invasive serotypes.

Right...you just never know what's coming next or how nasty it'll end up being.

Here's a little of what is known:

http://www.medscape.com/viewarticle/557492_4

A given serotype of SP may be a frequent cause of IPD either as a result of widespread colonization with a low invasive potential, or modest colonization with a high invasive potential.

And then there's capsule switching:

http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1479257

Streptococcus pneumoniae frequently colonizes the upper respiratory tract of young children and is an important cause of otitis media and invasive disease. Carriage is more common than disease, yet the genetic factors that predispose a given clone for disease are not known. The relationship between capsule type, genetic background, and virulence is complex, and important questions remain regarding how pneumococcal clones differ in their ability to cause disease

Knowledge of clonal types and the extent of capsule switching is important in understanding or predicting the impact of pneumococcal vaccine programs, since these programs may provide selection pressure for virulent genotypes to switch capsules and escape coverage by the Pnc vaccines

Therefore, should a clone not previously identified as invasive acquire the capsule of a more invasive isolate, we might expect the new clone to become more invasive. If such a capsular switch results in the expression of a capsule not covered by the present vaccine, there may be potential for increased rates of IPD

Capsular switching among successful disease-associated clones may be driven by selective pressure from the immune response.

Here's another little thing...sort of a basic synopsis.


http://www.brown.edu/Courses/Bio_160/Projects2005/meningitis/vaccines.htm
First, Pneumovax23, that totally craptastic Merck vaccine we argued about a while back:
Some studies have shown that PPV23 could actually increase one’s susceptibility to pneumococcal meningitis. Several studies have shown that successively smaller antibody responses have been shown after repeated administration of doses of certain polysaccharide antigens. The mechanism of hyporesponsiveness is yet unknown, but some have hypothesized that repeated antigenic stimulation depletes B memory cell pools while failing to sufficiently restore them1. Therefore, PPV administration can lead to transient protection, then may cause subsequent immunological paralysis. Further study about this concern is in progress.

And now Prevnar (PCV-7)
Highly, highly effective, but quite possibly too effective for it's own good:
Experiments have shown that children who received PCV CRM197 in infancy, and a second dose of PPV23 at 18 months, have successfully shown a reduction of vaccine serotypes. However, those who received three doses of PCV showed a significant increase in non-vaccine-type pneumococci than unvaccinated children8. In most studies of this nature, there were 50% reductions of vaccine serotype carriage, but a rise in non-conjugate vaccine serotypes. This serotype replacement effect could be a result of “unmasking” antigens that were formerly competitively inhibited by the more predominant serotypes. Once the vaccines caused a decreased in these serotypes, these non-vaccine types were able to take effect9. Therefore, the administration of conjugate vaccines could pose a serious danger by leading to greater disease rather than protection against it.
 
Last edited:
I'm going to have to say that the degree and speed of replacement disease with s.pneumo is rather solid evidence that you're just making things up here.
So far, it's been closer to 100%.


I love it when you do that!
"I have no idea, so I'm just going to say you don't know anything."
It's almost charming in a weird way.
Let's review one more time the specific aspects of micro you are missing. Maybe you'll not understand but perhaps other people reading will.

100% of what? Where is your study of upper respiratory flora? Where is your comparison of pre-vaccine and post-vaccine samples of the bacteria which inhabit the throats and noses of HEALTHY people?

That is what one would look at to evaluate the impact of pneumococcal vaccine on the resident population of bacteria which inhabit the human mouth and upper airway.

You don't seem to understand the concept that you are only discussing a select replacement population which is not representative of the whole picture.

First some definitions:

Normal flora - non pathogens which live in an area of the body such as the nose and throat.
Pathogen - a disease causing organism.
Colonization - the presence of pathogens in a location of the body which is not sterile, however in this case the pathogens are not causing an infection.
Infection - the presence of microorganisms which are actively causing disease symptoms.

Do you have to be colonized to get an infection? No, you can get an infection as soon as the pathogens take up residence in your body. When the infection is over, the pathogens do not need to remain.

What role does colonization play in infection? It varies. Sometimes the bacteria which colonize one person cause infection in another when transmitted. Sometimes the colonization provides a source of infection in the same individual when an opportunity arises such as after major surgery.

What makes a pathogen cause infection and what makes it only result in colonization? That can vary from the individual's genetics, resolution of an infection by the immune response but not complete clearance of the organism, and in many cases, the genetics of the organism. We know that a lot of people are colonized with meningococcal bacteria, however, when this organism does result in meningitis or sepsis, we also know the strain itself may be more pathogenic. If it wasn't, then outbreaks of meningitis would appear strictly random or perhaps run in families. That is not the case. This bacteria can infect close contacts. That implies there is a bacterial variant involved. The same is true for H-flu bacteria.

Pneumococcal invasive disease on the other hand, is not spread from person to person. This implies there are much stronger host factors involved than microorganism factors.

Pathogenic strains of pneumococcal bacteria have been identified because they are found in infections, mainly as far as the vaccine is concerned, as invasive organisms causing pneumococcal meningitis in young children and as meningitis and pneumonia in the elderly. So those strains were the targets of vaccine development.

If I develop pneumococcal pneumonia, I don't do so solely because an invasive strain infects me, I develop that infection because something about me gave the organisms the opportunity to invade a location in my body where microorganisms don't normally reside.

It isn't that more pathogenic pneumococcal organisms are emerging since the vaccine was used, it is the fact the strains which were actually less likely to cause disease are unhindered by competing strains which the vaccine addresses.

What are the options in that case? We can forget the whole idea of preventing invasive pneumococcal infections with a vaccine. Or, we can continue surveillance for strains not covered in the vaccine and add them to it. The vaccine may be allowing strains to grow which the vaccine eliminated strains had been suppressing, but those strains are weaker, not stronger. If they were stronger then they should have been more invasive regardless of the competition.

In your citation above, remember, there were additional serotypes of pneumococcal bacteria, not some alternative organism so your concern about the pneumococcal bacteria competing with staph bacteria is moot in that case.

As far as which is worse, strep (pneumococcal bacteria are in the strep family) or staph, I don't think either as a species is worse. Both families of bacteria have many harmless members and some very pathogenic strains.

The numbers kind of speak for themselves.
What do they supposedly say? Because the rate of invasive disease in persons < 5 years went from 76.4/100,000 in 1997 to 21.2/100,000 in 2005; and for adults >65 years went from 61.5 to 39.6 respectively. The vaccine has exceeded the 2010 goals in both groups.

You mistakenly compared the percent of invasive disease which occurred as meningitis, not the rate of meningitis in each year. I think if you did a more careful analysis of those percentages you'd probably find they were not statistically significant but that is a guess on my part. In any case, you really goofed on this one. Not that I expect you to acknowledge your error.
 
Last edited:
Let's try putting that figure into a little different perspective. Why should someone not prevent a child's preventable death? Is health care rationed in the UK?

Yes. All health care is, even in the US. It's just that the NHS makes it explicit. I was reading this over the weekend. If you haven't got time to read all 5 sections, sections 2, 3 and 4 are the most thought prevoking.

Are premature infants for instance, allowed to die because salvaging an infant born at 24 weeks costs on average, ~$17,000,000?

Outcome of infants born at 24-26 weeks' gestation: I. Survival and cost

Actually, there's been a call to do just that. The prospects for an infant born that early are not very good, even if it does survive.
 

Back
Top Bottom