I'm only a layperson speaking about experiences I know of on a
firsthand basis.  I'm glad they're continuing studies, but the
research that others have done indicates it makes no difference
whether a two year old is exposed, or an adult is exposed.  If
the bacteria results in asthma, it can be cured with longer term
antibiotics.  If the asthma they already had when they were
exposed becomes worse, it can be improved with the use of longer
term antibiotics.

And I still stand by my earlier post that I'm more inclined to
believe people whose asthma is getting worse, isn't because
they're on antibiotics all the time, but they're on them all the
time because their asthma is getting worse due to bacteria.

So then you must wish to read it for yourself. And I only cut what I thought
my newsreader would handle. Dr. Cassell is a recent past president of the
American Society for
Microbiology, a member of the National Institutes of Health Director's
Advisory Committee, and a member of the Advisory Council of the National
Institute of Allergy and Infectious Diseases of NIH. She was named to the
original Board of Scientific Councilors of the National Center for
Infectious Diseases, CDC, and is the immediate past chair of the board.

Address for correspondence: Gail H. Cassell, Lilly Research Laboratories,
Lilly Corporate Center, Indianapolis, IN 46285, USA; fax: 317-276-1743;
e-mail:
Cassell_Gail_H@Lilly.com.http://ftp.cdc.gov/pub/EID/vol4no3/ascii/vol4no3.tx
tInfectious Causes of Chronic Inflammatory Diseases and Cancer

Gail H. Cassell
Lilly Research Laboratories, Indianapolis, Indiana, USA

---------------------------------------------------------------------------
     Powerful diagnostic technology, plus the realization that
     organisms of otherwise unimpressive virulence can produce
     slowly progressive chronic disease with a wide spectrum of
     clinical manifestations and disease outcomes, has resulted in
     the discovery of new infectious agents and new concepts of
     infectious diseases. The demonstration that final outcome of
     infection is as much determined by the genetic background of
     the patient as by the genetic makeup of the infecting agent is
     indicating that a number of chronic diseases of unknown
     etiology are caused by one or more infectious agents. One
     well-known example is the discovery that stomach ulcers are due
     to Helicobacter pylori. Mycoplasmas may cause chronic lung
     disease in newborns and chronic asthma in adults, and Chlamydia
     pneumoniae, a recently identified common cause of acute
     respiratory infection, has been associated with
     atherosclerosis. A number of infectious agents that cause or
     contribute to neoplastic diseases in humans have been
     documented in the past 6 years. The association and causal role
     of infectious agents in chronic inflammatory diseases and
     cancer have major implications for public health, treatment,
     and prevention.

The belief that infectious agents are a cause of chronic inflammatory
diseases of unknown etiology and of cancer is not new. Approximately 100
years ago, doctors noted a connection between cervical cancer and sexual
promiscuity that transcended mere coincidence (1). By 1911, a connection
between viruses and cancers in animals had become well established (2). As
early as the 1930s, mycoplasmas were proposed as a cause of rheumatoid
arthritis in humans, and shortly thereafter, they were proven to be the
most common cause of naturally occurring chronic arthritis in animals (3).
Proof of causality of cancer and arthritis in humans was more difficult.
When searches for infectious agents in cancer and arthritis found none,
research began to focus on mechanisms of inflammation, tumorogenesis, and
drug discovery. More recently, however, scientists have renewed searches
for infectious agents.

Advances in molecular biology and medical devices have revolutionized our
ability to detect very low numbers of infectious agents in specimens
collected directly from the affected site. HIV has demonstrated the ability
of infectious agents to produce slowly progressive, chronic disease with a
wide spectrum of clinical manifestations and disease outcomes. Increased
understanding of the body's defense mechanisms and the demonstration that
final outcome of infection is as much determined by the genetic background
of the host as by the genetic makeup of the infecting agent suggest that a
number of chronic diseases of unknown etiology may be caused by an
infectious agent.

Recent data suggest a role for one or more infectious agents in the
following chronic diseases: chronic lung diseases (including asthma),
cardiovascular disease, and cancer. Many of the agents implicated are
commonly transmissible and are either treatable with existing antibiotics
or are potentially treatable with antiviral drugs. Thus, proof of causality
in any one of these diseases would have enormous implications for public
health, treatment, and prevention. Few areas of research hold greater
promise of contributing to our understanding of infectious diseases and the
eventual relief of human suffering.

The intent of this paper is not to provide a comprehensive review of
chronic inflammatory diseases of unknown etiology and the agents implicated
but rather to utilize several models to discuss available data and to
illustrate the difficulty in proving causality in chronic inflammatory
diseases. The discussion is based upon the following assumptions. Most
chronic inflammatory diseases are likely multifactorial. Heredity,
environment, and nutrition are critical determinants of disease expression
with heredity being the most important.

Theoretically, chronic inflammatory diseases currently of unknown etiology
could result from three different types of pathogens: 1) those that are
fastidious and previously recognized but because of their fastidiousness or
lack of appreciation of their disease-producing potential are not included
in the differential diagnosis, and 2) infectious agents previously not
recognized that therefore go undetected. Infection with either group can
result in misdiagnosis and lack of treatment. Depending upon the biology of
the organism and intrinsic and extrinsic factors of the host the organism
can persist, resulting in chronic inflammation. The third group of
pathogens would be those that elicit an autoimmune response resulting in
persistent inflammation without the persistence of the inciting agent.
Examples of the first two groups of pathogens will be discussed here using
mycoplasmas to typify the first group and Chlamydia pneumoniae the second.
Finally, recent advances in our understanding of the role of infectious
agents in cancer will also be summarized.

Chronic Lung Diseases

Murine Chronic Respiratory Disease as a Model System

The difficulty in establishing the infectious etiology of a chronic
obstructive lung disease is well illustrated by Mycoplasma pulmonis and
murine chronic respiratory disease. Proof that M. pulmonis can cause this
disease took nearly 50 years and required inoculation of germ-free animals
(4). Chronic bronchopneumonia in rats was first described in 1915 when this
species came into general use for experimental purposes (5). In
approximately 1940, a Mycoplasma, later identified as M. pulmonis, was
recognized as a possible cause (6), but the ubiquity of the organism and
its frequent isolation from healthy as well as diseased rats and mice (even
from trachea and lungs) soon gave it the reputation of being a commensal
with little pathogenic potential. The failure of pure cultures of this
organism to consistently produce disease of the lower respiratory tract
also precluded its acceptance as the etiologic agent. Only in the early
1970s was M. pulmonis alone shown to consistently reproduce all of the
characteristic clinical and pathologic features of the natural respiratory
disease when inoculated into animals maintained under germ-free conditions
(7). Subsequent studies provided explanations for previous difficulties in
reproducing the disease.

The respiratory disease caused by M. pulmonis is slow to begin and
long-lasting. Consequently, the disease has various stages of pathologic
lesions and a lack of uniform lesions, even among animals in the same cages
(due partly to variables that can affect development of the disease in the
lower respiratory tract, such as intracage ammonia produced by bacterial
action on soiled bedding, synergy with murine respiratory viruses and other
bacterial pathogens, and nutritional factors) (7). However, comparison of
animals matched for age, sex, and microbial and environmental factors
indicates that heredity is the most critical determinant of susceptibility,
lesion character, and disease severity. Susceptibility among animal species
and among strains of the same species differ dramatically (8-11).

Intranasal inoculation of M. pulmonis produces markedly different lesions
in F344 rats and in CD-1 mice, even when the dose is comparable on the
basis of lung and body weight. In rats the lesions progress slowly from the
upper respiratory tract distally, with alveolar involvement occurring days
to months following inoculation, whereas in mice, alveolar lesions develop
within hours after infection and are responsible for acute alveolar disease
and death within 3 to 5 days. Depending on their genetic background, mice
that survive the acute disease develop chronic lung disease characterized
by bronchiectasis that persists for up to 18 to 24 months or the lifetime
of the animal.

Studies of naturally occurring and experimentally induced disease indicate
that M. pulmonis also causes a slowly progressing upper genital tract
disease in LEW and F344 rats (18). Pups can become infected in utero, at
the time of birth due to cervical and vaginal infection of the dams, or via
aerosol from dams shortly after birth. Even though the organisms can be
shown to colonize the ciliated epithelium of the upper and lower
respiratory tracts of pups, microscopic lesions are not detectable for 2 to
6 months depending on the strain of rat. Development of obstructive lung
disease can require as long as 12 to 18 months.

Differences in severity and progression of the lung lesions due to M.
pulmonis in LEW and F344 rats are related to differences in the degree of
nonspecific lymphocyte activation in the two strains or an imbalance in
regulation of lymphocyte proliferation in LEW rats (12). M. pulmonis
possesses a potent B cell mitogen, and, in addition, the organism is
chemotactic for B cells (13). Interestingly, LEW rats are also more
susceptible to other chronic inflammatory diseases, including streptococcal
cell-wall induced arthritis, adjuvant-induced arthritis, and allergic
encephalomyelitis (12).

Ureaplasma urealyticum as a Cause of Pneumonia in Newborns and Its
Association with Chronic Lung Disease (CLD) in Premature Infants

mcs too long? Right the states with most people with  asthma usually have
most pollution concentrations. Only you doc can correlate that withk anti
biotics, Keep trying. long long wait .

The one at JHU is one that I have been aware of recently. I see no
reason to disregard it. And as you say there is another in Wisconsin.
I'm not sure why a trial could not be valid withotu Dr. Hahn running
it. He is impressive but not the only competant researcher out there.

Here is one in Australia:
http://www.newcastle.edu.au/news/media-releases/2005/hmriasthmatrial.htm

So that makes three without going past the first 10 hits on Google.

I'm not sure it is really reasonable to aks for links to "every post".
Is there anyone else that doubts that you frequently jump to a
recommendation for antibiotics even before information sugesting
infection is given? It seems to me that you have asked this in the past
and specific posts have been discussed. You talk aboutt he subject so
much that I can't imagine a search term that would not lead to tons of
posts to sift through. If others really are having their doubts I'll
consider making the effort.