And the newly designated species
C. pneumoniae
Chlamydia pneumoniae is not what you would expect. It is less famous than its cousins
which cause sexually transmitted disease (C. trachomatis) or conjunctivitis (C. psittaci),
but it is far more widespread and may be far more dangerous.7-8
We will all encounter this bacterium sooner or later, most of us more than once. It is
commonly spread through coughs and sneezes, causing a flulike respiratory condition that
sometimes progresses to pneumonia.9,10
A high proportion of adults from different countries are positive for antibodies to C.
pneumoniae, implying a high prevalence of these infections.
Several lines of evidence suggest that Chlamydia pneumoniae can make its way into the
walls of various blood vessels, linger for years inducing the inflammation and immune
reaction that causes heart attacks and strokes.
This does not imply that C. pneumoniae infection is the sole cause of atherosclerosis,
or that diet and exercise do not matter. But mounting evidence suggests that the leading
cause of death in the western world is to some degree contagious and that common
antibiotics might help bring it under control.
This is how scientists made the connection between a germ and America's leading
cause of death.
The bug first came under suspicion in 1988, when Dr. Saikku and his colleagues11
published an article in Lancet about the serological evidence of an association of a novel
Chlamydia, with coronary heart disease and acute myocardial infarction. In this study they
showed that people with coronary artery disease were more likely than healthy control
subjects to have circulating IgG and IgM antibodies to C. pneumoniae in their blood.
The second study by the same group12 published in Annals of Internal Medicine was
entitled "Chronic Chlamydia pneumoniae infection as a risk factor for coronary heart
disease in the Helsinki Heart Study." In this study unusually high antibody levels
turned up in the blood of heart attack victims. While most experts dismissed the Finnish
findings, Dr. Grayston at the University of Washington, who during 198113 described the
association between childhood myocarditis and Chlamydia Trachomatis infection, was
intrigued enough to launch his own study and in three different publications documented
the same pattern in Seattle that other researchers had seen in Helsinki. Since then eight
different research teams from five countries have confirmed these findings.15-22
Does the Association Between Antibody and Heart Disease Mean Anything?
The antibody presence tells you only that sometime during his lifetime a person has
encountered this pathogen and mounted an immune response. It does not reveal whether
Chlamydia is still present or, if so, how it is affecting the body.
With those questions in mind, researchers in the early 90's by using
immunocytochemistry, electron microscopy, and especially electron microscopy to look for
direct evidence of C. pneumoniae in the blood and clogged blood vessels.
The first piece of evidence came in 1993 when researchers spotted a tiny, pear-shaped
bacteria after histopathological examination of diseased arteries.
These results were confirmed by another group after examinations and detection of C.
pneumoniae's genetic material in 20 out of 36 tissue samples.24
Other labs followed, and most of them found bacterial fingerprints or genetic material
by one method or another.24-26
But similar to Helicobacter pylori and its association with ulcers, only a few paid
attention to the relationship between this Chlamydia and diseased arteries until 1994. It
was Dr. Summersgill's (of the University of Louisville) efforts which resulted in direct
detection of alive and kicking bacteria from a patient's blood vessels. This patient, who
was undergoing a heart transplant, without a recent history of respiratory illness, when
his coronary artery tissue was placed in a culture dish colonies of C. pneumoniae were
detected.27
Based on this pioneering work today , no one familiar with the scientific literature
denies that Chlamydia pneumoniae is associated with vascular disease. Regardless of their
age, sex or nationality, people with sclerotic arteries tend to show signs of infection.
Unlike the other infectious agents sometimes shown in both healthy and unhealthy patients,
this organism never shows up in truly healthy tissue.
Finding The C.pneumoniae at the Crime Scene Does Not Prove That it is a Criminal.
Scientists have long known that atherosclerosis is an inflammatory disease which
affects vessels throughout the body in particular those supporting the heart and the
brain. So far no one has shown conclusively that C. pneumoniae causes the damage that
leads to heart attack but there are good reasons to believe that it plays an important
role in the inflammatory response.
One of the functions of the immune system is to remove fat, cholesterol and other
irritants from the vessel walls.
As it is shown by its designation, Chlamydia pneumoniae has been established as an
important human respiratory pathogen causing both endemic and epidemic disease, including
pneumonia, bronchitis, pharyngitis and sinusitis.9,10 Up to 10% of community-acquired
pneumonia cases in adults and up to 50% of pneumonia cases during epidemics are caused by
this organism emphasizing the role of the respiratory system in this cross-infection.
Although association of this organism with coronary heart disease, erythema nodosum and
asthma has been demonstrated it is not clear how this organism is transferred from
respiratory system to the circulation.9,10
It seems that macrophages which have helped to clear C. pneumoniae from the respiratory
system under certain conditions become active carriers of the microbe. And when an
infected macrophage travels down on a vessel wall, it may infect the cells lining the
arterial surface. Under these conditions, the artery would attract more immune cells,
which will deliver more bacteria to the site and cause more serious inflammation. This
hypothesis with preliminary evidence supporting it nicely is depicted in Figure 1.
Researchers at Johns Hopkins and Louisiana State University have shown in test-tube
experiments (in-vitro) that C. pneumoniae can indeed survive within macrophages and
arterial cells.28-31
In these studies the ability of C. pneumoniae to infect cells that make up
atherosclerotic lesions, including endothelial cells, smooth muscle cells, and
cholesterol-loaded smooth muscle cells was examined. It was shown that C. pneumoniae can
infect rabbit, bovine, and human smooth muscle cells, and cholesterol-loaded smooth muscle
cells were more susceptible to C. pneumoniae infection.28-31
At the same time C. trachomatis inefficiently infected smooth muscle cells,
demonstrating that this is not a characteristic of all members of the genus Chlamydia.31
It was concluded that C. pneumoniae has the capacity to infect one of the most
important types of cells (smooth muscle) found within atherosclerotic lesions.
Recent animal studies reinforce evidence found in test-tubes during 1997 where
different groups from Canada, USA and Finland have shown that C. pneumoniae invades
arterial tissues.28-31
In these studies researchers infected a dozen rabbits through the nose and within seven
weeks of contracting the organism, the majority of them developed arterial plaques. This
plaque formation occurred despite the fact that rabbits do not normally get
atherosclerosis, even when they are fed high-fat diets.
Even with this extensive information about the role of C. pneumoniae in heart disease,
there will still be plenty of questions.
- What is the mechanism of action?
- Why are some people more susceptible than others?
- Do fat and cholesterol make us sick by themselves, or only in combination with C.
pneumoniae?
- Could antibodies quickly rid the body of infection?
- Would clearing the infection stop the disease process?
A. Laboratory Gold Standards For Detection Of Chlamydia Pneumoniae
