Lyme disease is probably the most common vectored disease in the world. Its causative agent is a spirochete: Borrelia burgdorferi. Borrelia normally requires both a tick host of the Ixodes genus and a warm-blooded host to complete its infectious cycle, but insects may occasionally also be vectors, transmitting Borrelia from one host to another.
Spirochetes undergo multiple changes as the ticks are biting their warm-blooded host. But these pale in comparison with the changes that occur inside a human.
Inside the Human
If left alone once inside a warm-blooded host, spirochetes move through the blood stream, reproduce slowly, produce blebs, change shape, and move into the host's organs and tissues where they give off toxins that often reduce host mobility. Reduced host mobility increases the probability that new ticks will find and bite the infected host and transfer the spirochetes to more vertebrates.
Spirochetes Release “Cluster Bombs”
Each active bacterium releases into the body thousands of infectious packages, called blebs. Although the bacteria reproduce only about once every two weeks, these blebs are produced almost continuously, are hyper infective and appear to cause most of the symptoms of LD. Blebs are a sort of smoke screen against the immune system. As immune cells and antibodies are attacking the blebs, the bacteria (hidden inside other cells) can continue to release more blebs without injury. Since blebs are not true cells, they may be destroyed without eliminating the actual bacteria.
Borrelia Attacks our Immune System
Our immune response is slowed down and even rendered ineffective by bacteria that can rapidly change their surface characteristics. Borrelia's ability to swiftly generate new combinations of surface proteins while the tick is feeding makes it important to remove I. scapularis ticks early in the feeding bout. But it is even more important to be treated as soon after infection begins as possible. If Borrelia are given time to change their surface proteins and develop other defenses against our immune systems and antibiotics, Borrelia may become able to escape our most concerted efforts to eradicate them.
Spirochetes are Shape Shifters
As if the arsenal of attack by ticks and spirochetes does not perplex the host's immune system enough, the bacteria will change their characteristics when the host marshalls defenses against the spirochetes. They seem to have programs that instruct them to:
- Produce new forms of both surface protein groups (vlsE and Osp).
- Change shape and discard surface proteins.
- Move from the blood stream into body fluids.
- Enter cells and become invisible to antibodies and killer T-cells.
- Destroy immune system cells.
- Hide behind the blood-brain barrier where many antibiotics cannot penetrate.
There are no fewer than three shapes of Borrelia, two of which are highly infective:
- the spirochetal form,
- an L-form that discards its cell wall and integrated surface proteins, and
- a cystic form that enters cells and becomes inactive.
The infective shapes of Borrelia disrupt cell function, destroy connections between them, and eventually kill the cells. Being inactive, the cystic form is resistant to antibiotics, does not present antigens to the immune system, and escapes destruction from most medications. The few medications that are active against the cystic forms are dangerous.
Neurological Damage
Most neurological damage in the body is caused by the L-form of Borrelia. This form easily enters cells, can break into small round cells (cocci), and in the nervous system, disrupts connections (synapses), destroys neurons and their supporting tissues, and produce holes (lesions) in the brain that cannot be repaired. These changes become manifest as:
- altered sensory perception,
- forgetfulness,
- muscle weakness,
- slow or rapid heartbeat,
- low or high blood pressure,
- personality changes,
- dementia – sometimes extreme,
- “Lyme rage,”
- and many others.
A full blown disease with these characteristics needs a multi-pronged attack to be eliminated.
