Allergy-Associates

I’ve been privileged to be in the medical field since the discovery of Lyme disease and witness the ongoing research to understand it and to treat it.  I happened to be an intern at Yale when a mother returned her child to the medical center insisting that the original diagnosis of juvenile rheumatoid arthritis, they had received on their initial visit might not be correct.  After her first visit, she returned home to Old Lyme, Connecticut and by talking to neighbors found out that several other children in her neighborhood had gone to Yale and received the same “rare diagnosis”.  A team of epidemiologists was dispatched to Old Lyme and indeed found a number of additional cases. 

Thus, the research ball started rolling.  I’ve often thought the illness should have been named after that intrepid mother rather than the town. 

Lyme disease is caused by the bacteria Borrelia burgdorferi.  Initially, the bacteria and the disease were limited to New England but have spread throughout the eastern states including Florida.

A vaccine for humans was developed and became available in 1998.  But since consumer demand was low it went out of production in 2002.  But because of increasing cases in the US a new vaccine is undergoing clinical trials by Pfizer pharmaceuticals. 

Meanwhile, a different strategy is being implemented, a vaccine for mice.  Mice are one of the most important reservoir hosts for Lyme disease.  Living in the wild they transfer the bacteria via the ticks they carry and the ticks’ progeny.

The mouse vaccine is in edible pellets.  It’s interesting that both the human vaccine and the mouse pellet vaccine contain a protein called OspA which is found on the surface of B.burgdorferi.  The OspA spurs antibody production in the vaccine which in turn prevents infection. 

A recent five-year study done in New York state using the mouse pellets found a 23% reduction in infected ticks after two years of distributing the pellets and a 76% reduction after five years. 

Some compelling research on Lyme disease was recently published in the Proceedings of the National Academy of Science.  The focus for the research was to try and elucidate the reason that in some patients with Lyme disease they continue to have symptoms despite prompt and appropriate treatment with antibiotics.  It turns out to be caused by post-infection inflammation caused by ongoing immune response against part of the bacteria.

 

Lyme disease is caused by the tick born bacteria Borrelia burgdorferi.  This bacterium contains a peptidoglycan (PG) molecule in its cell wall that is released but not degraded when the bacteria die.  Since the bacteria invades the skin, brain, joints, and heart, the PG molecules remain in these areas.  The immune system “sees” these foreign proteins and tries to eliminate them, but in so doing creates inflammation.  The immune inflammation is caused by cytokines especially one called tumor necrosis factor (TNF).  The presence of TNF especially in the joints can cause a chronic arthritis, which is the most common post–Lyme complication.  But, other less common complications include chronic skin rash, cardiac problems and chronic fatigue.  The latter is felt to be due to chronic meningeal inflammation.

 

Research is ongoing on two fronts.  One focus is to try and find a way to degrade the residual PG “debris” and remove it from the body.  The other is to try and find a way to stop the post–infection inflammation by schooling the immune system to stop targeting the PG protein.