rifing, burst bacteria, & inflammation

[Guest guest]

I 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 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. 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