Re: HIB vaccination

Here are some things you might like to consider.

Firstly, the obvious. Most doctors, particularly young doctors **have** to advocate vaccines. If they don't, and their numbers build up, they really get it in the neck from their peers, what was NIP, and what is CDC, FDA.

Therefore, while lip service is given to informed choice, in reality, every meeting with a doctor is now a vaccination opportunity they are told to push. So if you arrive at ER with a bee sting, don't be surprised to be offered a tetanus shot, and then find you got bulldozed into the new adult tetanus diphtheria and pertussis, becuase in practice, you can't get tetanus alone now, and haven't been able to for several years.

Now, about Hib, and prevnar.

The first thing to consider in terms of prevnar is what the real risks are.

You might like to read this medical article and see if you fall into the catagory of those really at risk:

I hope these URLs work:

http://pediatrics.aappublications.org/cgi/reprint/103/3/e28

Risk Factors for Invasive Pneumococcal Disease in Children: A Population-based Case-Control Study in North America


Then consider this article here:

http://www.newsrx.com/library/topics/Pneumococcal-Vaccine/26799.html

Pneumococcal parapneumonic empyema is more common since pneumococcal conjugate vaccine introduction

Which is confirmed by this BMJ letter here:

http://bmj.bmjjournals.com/cgi/eletters/330/7489/456

The same trend was note in this journal here:

Clinical Microbiology and Infection, Volume 12 Number 9, September 2006
Invasive pneumococcal disease among children in a health district of
Barcelona: early impact of pneumococcal conjugate vaccine
E. Calbo1, et al.

Furthermore, the same article talks about serotype replacement, in that the vaccinated children still carried pneumococcus, but types NOT in the vaccine.

There is considerable discussion about the fact that both Hib and prevnar force a bacterial type shift, which is what you'd expect. Nature abhors a vacuum, and if you make a hole, something else will fill it. This is proven in this article here:

http://www.cbc.ca/story/science/national/2006/06/13/vaccines-north.html?ref=rss

June 2006.

Medical officials have relied on the vaccine Prevnar for several years to protect infants against the bacteria, responsible for 80 per cent of pneumococcal disease. Now, they say, it's beginning to fail to protect infants against new strains on the rise.

"The vaccine is covering those serotypes that were most prevalent in Alaska and has reduced them dramatically," said Dr. Michael Bruce of the Centre for Disease Control, based at the Arctic Investigations Program in Anchorage.

"And now we're seeing other serotypes moving in to fill the niche and so that is worrisome."

....Larke also points to worrisome developments with the Haemophilus Influenza type B vaccine, which he says has been almost miraculous in the fight against meningitis. The disease can lead to brain damage and deafness in infants.

Medical officers are now seeing another serious strain, called Type A, and there's no vaccine for it.



Many of us told them about this for years right from the start. When Hib was used, it was then that the Pneumococcus started to radically increase, and when it started, new types shifted in, and now new Hib are coming forward.

I've raised this issue with Dr Marc Lipsitch, who has written stuff on bacterial serotype replacement, but so far he has had nothing to say on the matter.

But its a serious evolving issue, and the fact is that the ACTUAL amount of all bacterial meningitis hasn't reduced one iota. All the vaccines appear to do is to make a hole, into which something else steps, because the key factor isn't the bacteria. The key factor is individual host susceptibilities. That's why 4,999 out of 5,000 people who meet any meningitis bacteria get nothing other than natural immunity.

That's why you have a family tree.

The reason for the huge upswing in meningitis problems in my opinion is multifactorial. First, the use of Antibiotics , while they have saved many lives, went on to become Antibiotic abuse, given for every sniffle and sneeze, and disturbed drastically, the biotic flora in humans. Given that the "gut" is 70% of the immune system, if you mess it up, you increase susceptibilities to a lot of things, not just gram negative bacteria. And what doctors, apart from Melchinek (spelling) and other probiotic officionados, ever bothered to tell parents gut flora needs to be re-established after being trashed by Antibiotics ?!

Second the use of vaccines has further created problems and imbalances, which if I go into here, will result in a tome tome and tome...

Third, there is evidence that we have broad spectrum immunity to all bacterial meningitis's, but when you vaccinate against one, you reduce that radically. The work on this has never been done officially. It was started in the forties, raised worrying issues, and has never been followed up since. That can be found in

‘THE YOUNGEST SCIENCE; notes of a medicine-watcher” by Lewis Thomas, OUP, 1984, pp 75-78

Here is the relevant passage.

“So we packed again, and flew to Halifax, where I went to work on the treatment of meningococcal meningitis with a new sulphonamide called sulfadiazine, of which I had never heard, and Beryl was recruited as a laboratory assistant to keep the records and carry cultures from one place to another.

We were in Halifax for about a month, culturing the spinal fluid of several hundred patients with meningitis, collecting samples of serum from these patients and other people who did not develop meningitis but were in close contact, in order to study the possible role of antibodies in protection against the disease, and recording with care the clinical course of the illness under treatment with sulfadiazine, which was administered to all patients with an established diagnosis. Sulfadiazine was wonderfully effective. The only patients who filed to recover were those with a rapidly developing and overwhelming infection – some of them became comatose within a few hours and were brought to the hospital in deep shock, their skin surfaces covered everywhere by areas of hemorrhagic necrosis (looking very much like the Shwartzman phenomenon which I was to study several years later), and these patients were dead before we could start treatment. All the rest, the majority, recovered promptly when given sulfadiazine, and we saw none of the late complications – blindness, deafness, mental confusion – which had occurred in earlier epidemics of untreated meningococcal meningitis.

We came back to Boston with crates of cultures and sera, and my laboratory was committed to the problem of the meningococcus and the mechanism of its peculiar affinity for the surfaces of the brain and spinal cord in human beings. None of the conventional laboratory animals were particularly vulnerable to this organism: rabbits, guinea pigs, rats and mice could tolerate the intravenous injection of huge numbers of live meningococci without turning a hair, and the bacteria disappeared from their bloodstreams within ten minutes or so. It was evident that the animals possessed a highly effective mechanism for their protection, and I settled down to find out more about this. The first and simplest possibility, that they were able to kill off the injected meningococci by means of an already existing “natural” antibody, was easiest to test in rabbits, so rabbits became the laboratory’s routine animal. We quickly learned that the serum of a normal adult rabbit was capable of destroying almost any number of meningococci; when up to a million organisms were added to a single millilitre of freshly obtained rabbit serum, and the mixture then incubated for a few hours at 17 degrees Centigrade, the specimens became sterile. If the serum samples were heated at 56 degrees Centigrade for an hour before adding the bacteria, the bactericidal action was complete lost, indicating that the killing power depended on the presence of complement (a sequence of proteins, still incompletely understood, which makes possible the action of antibodies against antigens on the surface of bacteria).

We though it useful, given so powerful an example of natural immunity already in existence in animals, to see whether we could obtain even stronger antibacterial sera by immunizing the rabbits. We injected animals with suspensions of heat-killed meningococci, and collected sera at weekly intervals. These samples were set up as in the initial experiments adding various numbers of live bacteria to the serum specimens and determining how many were killed and how quickly. Within the next few days we encountered our paradox: the sera from the immunized rabbits, which had been capable of killing a million meningococci in a few hours, had now lost this property. There were potent and specific antibodies in these sera, as we could show in other kinds of tests – agglutination, precipitation, and complement fixation tests. But with the appearance of a specific antibody, the bactericidal activity vanished.

Moreover, something of the same sort could be show in the whole rabbit in vivo. When we injected live bacteria into the bloodstream of our immunized animals, and then measured the survival of bacteria by serial blood cultures, we were surprised to learn that the blood cultures were still positive twenty-four hours later in the more intensively immunised rabbits, in contrast to the unimmunised animals, in which all of the meningococci had disappeared within ten to fifteen minutes.

By this time, it was late April of 1941 and I was in a hurry. The problem had turned into something fascinating, involving both paradox and surprise. I knew I was expected back in New York the next January to become a neurologist, so I worked as fast as I could. What I had run into was an antique immunologic phenomenon called the “prozone”, in which an excess of antibody turns off the immune reaction unless the serum is sufficiently diluted. However, the difference in my laboratory – what was new – was that it worked in vivo: an immunized animal could lose, as the result of being immunized, its own natural defense. This might I thought, have useful implications for susceptibility in certain human infections beyond meningitis – typhoid fever and brucellosis, for example – and I wanted to get on with it.

However, as it turned out, I never got to finish the problem or even answer the principal questions. Nor did I ever get back to the Neurological Institute. The Rockefeller Institute was put on notice in late 1941, then mobilized as a naval medical research unit; I was assigned to it as lieutenant, and received orders to turn up in New York, in uniform, by the end of March 1942. John Dingle and I reluctantly agreed to bring the still inconclusive problem of the in vivo prozone to a premature end and write the work up; to this day, I’ve never been able to return, full-time, to the problem. It still hangs there in my kind, and I don’t believe any other laboratory has ever settled it.”

Note about the author: Lewis Thomas was chancellor of the Memorial Sloan-Kettering Cancer Center in New York city, and a member of the National Academy of Sciences. He served as Professor of Pediatric Research at the University of Minnesota, as Chairman of the Departments of Pathology and Medicine, and also Dean at the New York University-Bellevue Medical Center, and as Chairman of Pathology and Dean at Yale Medical School.

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I have forwarded this to all the relevant meningo research people and so far, the answer is silence.

Hope this is of some use.


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