Lyme disease is caused by bacterium within the Borrelia burgdorferi species
complex, including B. burgdorferi sensu lato, B. burgdorferi sensu stricto, and B. mayonii. In humans, the spirochetes
are transmitted by the bite of an infected blacklegged tick. Lyme disease has
an incidence of roughly 300,000 cases a year, and it is the most common vector
borne disease in the United States. Lyme disease is primarily a diagnosed clinically,
and  laboratory testing is often used for
confirmation supporting the diagnosis.

            The hallmark of Lyme disease is erythema migrans, also
referred to as a bulls eye rash. This rash is typically followed by flu like
symptoms, arthralgia, myalgia, headache, and fatigue, but not all cases will present
with a rash. The signs and symptoms mentioned are commonly associated with this
disease process. For Lyme disease, treatment with a short course of antibiotics
of 10-28 days, is current practice. However, after treatment some patients will
experience symptoms similar to those experienced during the active infection.  Is the standard treatment protocol enough to resolve
the infection of Lyme disease?  Are
symptoms of  post-treatment Lyme disease
syndrome (PTLDS) related to bacteria that were not eradicated? Does standard pharmacologic
therapy address all potential forms of the bacterium possibly present?

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Review of Literature:

            In
the scientific community there is not a widely accepted standard definition of
post -treatment Lyme disease syndrome, the lack of data on its pathogenesis has
caused confusion and controversy on the syndrome. The most widely accepted
definition of Post-treatment Lyme disease syndrome describes the pattern of persistent
symptoms that continue for six months or greater after the completion of
treatment for Lyme disease. It has been reported that as many as 40-50% of
people treated early for the disease experience recurrent symptoms such as:
chronic fatigue, cognitive dysfunction, myalgias, neuropathy, and joint pain.

           

            Lyme disease causing bacteria have been noted to utilize
multiple forms of evasion,  including
cyst formation, production of biofilms, spirochete form, and employing a tactic
of intracellular evasion. Adding further complexity to the situation, Borrelia
is known to have the ability to change and manipulate outer surface proteins
regularly, this allows for immune cell evasion 
from the host. One study demonstrated  that in monkeys there was persistence of  bacteria in the heart; however, PCR, skin
biopsy cultures, and in vivo cultures were negative on analysis. Further
findings demonstrated that intact spirochetes were found in three out of five
treated monkeys by xenodiagnosis at 12 months after the tick bite. Immune
responses to B. burgdorferi  were shown to vary significantly after
treatment for Lyme disease. Widespread variable microscopic disease, primarily
inflammation, was observed in all infected subjects, despite having received
antibiotic treatment. Another area that makes this syndrome problematic happens
to be that there is no definitive testing to verify  curative therapy. On the other hand,
diagnosing a reinfection  without the characteristic
erythema migrans is difficult, relying cautiously on acute serology for
insight. The question can be raised was the patient ever cured in the first
place, or was the infection only subdued to an asymptomatic level? The sequela
experienced from PTLDS could be hypothesized to be that the infection with the
Lyme causing bacterium was never eradicated in its entirety and is still causing  the symptomatic condition to persist.

           

 

Expected Outcomes:

            The goal of this literary study is to utilize
current  research to hypothesize the
pathogenesis of post treatment Lyme disease. Explore the possible mechanisms of
evasion by the Borrelia species and
address potential pitfalls in current therapeutic practices.