from: http://health.groups.yahoo.com/group/Rife/message/24286

 am posting this rather interesting release from St. Jude about influenza,
pneumonia and inflammation, because there may be a related rifing concept worth
considering here.

It may be counter-productive (and sometimes even dangerous) in a bacterial
infection, to "burst" the bacteria (akin to the common rife idea of "blowing up
bugs" as proven under a microscope) - as opposed to debilitating the bacteria in
some other way. As the article indicates, burst bacteria can release components
into the tissues and bloodstream, which then can sometimes trigger very strong
(and sometimes deadly) inflammatory reactions.

This is akin to what we see with lyme disease herxing problems in some people.
The herx sometimes gets so bad that the person cannot use the technology in what
might be an effective way.

Maybe future research needs to consider frequencies or power levels that
debilitate rather than burst bacteria in all circumstances. The situation may
vary from one bacteria to another, or whether the situation is chronic or acute
disease. Trying to do everything "fast" or "strong" may not always be in the
person's best interest. Perhaps slowing down the bacteria, or hampering its
usual life cycle or responses in some way could be other approaches to consider.

We see a lot of comments here and there, indicating that people think nothing is
happening if they are not getting a herx reaction. This is particularly true in
people with lyme complex. Might we want to be asking, does lack of herx
necessarily indicate lack of effectiveness? I realize that sometimes people
really do *want* to know - or need to know - *something* is happening. But
should we equate that as evidence of efficacy?

Likewise, would evidence of a "bug blow" under the microscope, indicate best
course of action for all in-vivo situations?

Food for thought...

Best wishes,
Char
____________________________________________________________________________

Study Finds More Effective Treatment for Pneumonia Following Influenza

Results of St. Jude study could shape new treatments for secondary pneumonia

MEMPHIS, Tenn., Jan. 8 /PRNewswire-USNewswire/ -- Scientists at St. Jude
Children's Research Hospital have demonstrated a more effective treatment for
bacterial pneumonia following influenza. They found that the antibiotics
clindamycin and azithromycin, which kill bacteria by inhibiting their protein
synthesis, are more effective than a standard first-line treatment with the
"beta-lactam" antibiotic ampicillin, which causes the bacteria to lyse, or
burst.

The finding is important because pneumonia, rather than the influenza itself, is
a principal cause of death from influenza in children and the elderly. During
pandemics -- such as the one that may arise from avian influenza -- up to 95
percent of influenza deaths are due to pneumonia. A bioterrorism attack using
the influenza virus would likely result in the same high percentage of pneumonia
deaths, according to the researchers.

The group, led by Jonathan McCullers, M.D., associate member of the St. Jude
Infectious Diseases department, expect the new findings, currently demonstrated
in mice, to be incorporated into standard clinical practice guidelines during
the next few years.

McCullers and his colleagues published their findings in the advanced, online
issue of the Journal of Infectious Diseases. The researchers based the new
treatment on growing evidence that beta-lactams are relatively ineffective
against secondary pneumonia because the drugs exacerbate inflammation caused by
influenza.

"With severe secondary pneumonia, it has seemed that physicians do almost
everything they can, and it doesn't work," McCullers said. "People still die
despite treatment with antibiotics that can kill the bacteria. Our research is
showing that the intense inflammatory response that is already there from the
virus is amplified by the bacterial infection. And, treatment with beta-lactams
releases bacterial components into the bloodstream that the immune system
recognizes, triggering an inflammatory burst that can be deadly.

"Traditional first-line therapy has been based on the belief that the bacteria
are bad, so we have to get rid of them as quickly as possible," McCullers said.
"But what we are finding is that maybe it is the inflammation we need to worry
about first, and the bacteria second. Protein synthesis inhibitors shut down the
bacterial protein-making factory, and they can avoid the inflammatory burst by
killing them over days instead of quickly lysing them."

In their experiments, the St. Jude researchers infected mice with a mild form of
influenza that restricted itself to the lungs. After a week, the scientists
infected the mice with pneumonia bacteria. This sequence mimics how humans with
influenza would contract secondary pneumonia.

The researchers treated groups of the doubly infected mice with ampicillin,
clindamycin, combined clindamycin and ampicillin, or azithromycin. They found
that 56 percent of the mice survived with ampicillin treatment, 82 percent
survived with clindamycin, 80 percent with clindamycin and ampicillin, and 92
percent with azithromycin. Significantly, while clindamycin and azithromycin
both inhibit protein synthesis, azithromycin also has anti-inflammatory
properties.

Ampicillin aggravated inflammation compared to clindamycin, the researchers
confirmed in test tube studies. The investigators also found evidence of
increased inflammation in lung cells of ampicillin-treated animals.

According to McCullers, lung tissue studies of ampicillin-treated animals also
revealed the antibiotic's deleterious effects.

"We saw in those animals that, even though we were clearing their lungs of
bacteria, the lungs looked just like those of animals in which the bacteria were
continuing to multiply," McCullers said. "The damage process was continuing."

McCullers said he would like the new findings to influence treatment guidelines
immediately for pneumonia secondary to influenza.

"The current guidelines still adhere to the theory that beta-lactams are the
only drugs of choice, because it is necessary to kill the bacteria as fast as
possible," he said. "However, our findings represent the first data showing that
inflammation is important, and that alternative therapies such as protein
synthesis inhibitors should be considered and incorporated into revised
guidelines."

More broadly, McCullers said, the new findings support a growing body of
evidence that treating severe pneumonia in general should take into account the
inflammatory response and not just the rapid demise of bacteria.

Other authors of this paper include Asa Karlstrom and Kelli Boyd (St. Jude); and
B. Keith English (Le Bonheur Children's Medical Center). This research was
supported in part by the U.S. Public Health Service and ALSAC.

St.Jude's