Over the past months, I have been studying chronic rickettsial infection and trying to determine if it plays any role in causing CFS symptoms. Rickettsia is halfway between a virus and a bacterium and occurs commonly in the animal kingdom. It lives mainly in the cells making up the walls of blood vessels and can infect most organs of the body including the brain. It can produce a toxin that can cause symptoms in itself. Humans can become infected by prolonged contact with animals that have the infection. The infection is passed on by ticks, mites, lice or fleas. Some of the animals suspected of carrying this infection include rodents such as rabbits, guinea-pigs, mice, dogs, cats and livestock such as sheep and cattle.

Most doctors would be aware of the well known diseases caused by rickettsia including Rocky Mountain Spotted Fever, Queensland Tick Typhus, Q-fever etc. The strains causing these diseases usually lead to acute illnesses that cause severe symptoms which usually clear with quick administration of antibiotics. Q-fever can cause subclinical infections (causing few of no symptoms).

The strains I am looking into were extensively studied in the early 80s by a team of French researchers. Their work is not widely known, probably because it was all published in French medical journals in French. The strains they studied are believed to be able to exist in the human body for a long time without causing any symptoms. They often require another stress on the immune system, such as another infection, to enable to rickettsia to begin causing symptoms.

The French researchers carried out most of their studies in relation to Multiple Sclerosis (MS). One study they did looked at 56 MS patients and 42 healthy people (called controls). They found that 75% of MS patients and 19% of controls tested positive for at least one of the 4 strains of rickettsia tested for. They also claimed that long term treatment with antibiotics cleared the symptoms in those who tested positive. I did a similar study using the same testing procedure to try to determine if this infection had any part to play in CFS. Of the 14 CFS patients I had tested, 13 came back with at least one positive, but some of the healthy people I included in the study also came back with positive results. Nearly all the people used in the study had had long-term contact with animals suspected of carrying the infection.

How we interpret these results is important. Firstly, the study was far too small to come to any conclusions other than suggesting that a larger study would be worthwhile. But, the fact that both my study and the MS study found that some healthy controls tested positive, suggests that these strains are fairly common in the community, and can obviously exist without causing symptoms. Two other very recent papers also found this with Q-fever. This finding still fits in with the researchers original hypothesis, as I stated earlier. This fact will make it very hard to determine if this infection causes CFS, as testing positive cannot be interpreted as meaning that the person has CFS.

As the test used only detects antibodies and not the infection itself, it can only be said with certainty that a positive result means that the person has been in contact with the infection at some time. However, I found some very strong positive reactions in my study which would suggest that a current infection is likely. It may be that only certain susceptible people go on to develop symptoms once infected. These people may require some sort of immune system fault to be present. We donít know at this stage.

There are many pieces of information that makes me feel compelled to further investigate the possible link between CFS and chronic rickettsial infection. One of which is that a number of unpublished reports from doctors found that some patients had improved on long-term antibiotic therapy. These antibiotics are the type used to treat rickettsial infection.

I am now trying to attract the interest of CFS researchers to conduct a much larger, properly controlled study involving testing for rickettsia and long term treatment with antibiotics, as it will only be after such a study is done that we can be more confident if this infection has a part to play in CFS. It would be interesting re-testing people if improvement is gained to check the level of antibodies again. At this stage the test is only available in a research laboratory in Belgium. The common rickettsial tests will not detect the specific strains mentioned in the article.

Reprinted from Emerge, June 1993.