Initially, medicine treated the disease just like any other bacterial infection-with antibiotics. These appeared to work, and doctors patted themselves on the back for having put paid so easily to this novel disease. But the story hasn't turned out to be that simple.
Although this medical field is still relatively small, there is already a schism appearing among LD clinicians; indeed, some would call it a war. One army of experts believe that Lyme disease can be easily cured by a short course of antibiotics, whereas the opposing side says no, LD is a complex, potentially long-term illness.
The problems begin with the diagnosis. If LD is spotted early on, then antibiotics can prove helpful. But, in practice, LD turns out to be very difficult to diagnose, and the later stages of the disease are much harder to treat with the usual drugs.
What's more, these antibiotics can sometimes make things even worse. Any Borrelia bacteria that are not totally killed off by the drugs don't just develop resistance-which is bad enough-but also become what is referred to as 'cell-wall deficient'. This makes them very elusive as, without walls, they can hide inside of healthy cells, thereby avoiding direct attack by the drugs (Infection, 1996; 24: 218-26).
Lyme patients also find that the types of antibiotics used to treat them may actually exacerbate their symptoms. This is thought to be the result of changes due to the drugs in the genetic sequencing of Borrelia, causing them to release toxins into the body. These toxins often get into the brain and nervous system, precipitating what is called the Jarisch-Herxheimer reaction (named after Karl Herx-heimer, the German dermatologist who first observed it). J-H reactions can be life-threatening, and are seen
in one in seven Lyme borreliosis patients treated.
The leaky brain
In fact, it has also been suggested that LD in itself-whether treated by antibiotics or not-may be neurotoxic. The idea is that Lyme disease creates ammonia in the brain, causing a 'leaky-brain syndrome'. Among the first to propose the idea was LD specialist Dr David Jernigan. As ammonia can alter permeability of the blood-brain barrier, he says, it would allow large molecules to reach the brain, causing 'cerebral allergies'. Jernigan believes that this may be a major cause of a variety of LD symptoms (Townsend Lett Docs, 2007; April: 141-8; online only).
Confirmation of this hypothesis has come from animal studies. Using radioactive tracers, researchers have shown that laboratory animals, when infected by Borrelia, lose the pro-tection of the blood-brain barrier
after just two weeks (Schutzer SE, ed. Lyme Disease: Molecular and Immunologic Approaches, Series 6. Current Communications in Molecular and Cell Biology. Plainview, NY: Cold Spring Harbor Press, 1992)
How does Borrelia do this? It's thought that the bacteria burrow their way between the cells of the brain's outermost membrane, causing a localized inflammation that, in turn, releases proteins to fight against the bacterial invasion; this then results in holes in the cerebral membrane. It's much the same mechanism as seen in the leaky-gut syndrome but, in this case, it's potentially more serious as it involves the brain.
In addition, there is now laboratory evidence that Borrelia can "attach to or invade human cortical neuronal cells", say researchers at the National Center for Infectious Diseases in Colorado, part of the US Centers for Disease Control and Prevention (CDC). This makes the bacteria difficult to kill by the immune system (Microbes Infect, 2006; 8: 2832-40). It also helps to explain why Lyme disease can be both relapsing and resistant to treatment.