Lime Disease Essay, Research Paper Lime Disease Lyme disease is caused by Borrelia burgdorferi, which is a tick-borne spirochete. The dangers of this disease became more publicised in 1977, where a geographic
Lime Disease Essay, Research Paper
Lyme disease is caused by Borrelia burgdorferi, which is a tick-borne spirochete.
The dangers of this disease became more publicised in 1977, where a geographic
grouping of children in Lyme, Conneticut were thought to have juvenile rheumatoid
arthritis1. Soon after, it was discovered that lyme disease was an illness that mainly
affects the skin, nervous system, heart, and joints. The borrelia species is part of the
eubacterial phylum of spirochetes. Containted within a protoplasmic cylinder is a cell
membrane, followed by wavy flagella, and then an outer membrane. The genes
encoded within the outer membrane are located on plasmids which allows the organism
to make antigenic changes in these proteins. When a borrelia cell attaches to its host,
the whole outer membrane moves to one end of the cylinder, which is called capping to
patching1. B. burgdorferi do not live in water, soil, or plants. Borrelia grow slowly
compared to most bacteria. They elongate for 12 to 24 hours before dividing into two
cells. B. burgdorferi is approximately 20 to um long and 0.2 to 0.25 um wide, with 7 to
11 flagella. More than 30 proteins are contained within B. burgdorferi1. This bacteria
uses white-footed mice, mosquitoes, and deer as their hosts.
This disease does not discriminate between sex and age; male and female, as
well as old and young are affected. It is widely distributed around the world in the
temperate zones3. A person is infected when a black-legged tick imbeds itself into
them while out in the open in wodded and forested areas. This usually occurs between
the months of May and July. Tick abundance is associated with humidity, temperature,
landscape slope, forested areas with sandy soils, and the extremity of residential
Generally, lyme disease occurs in stages, which are not always clear-cut; they
may overlap. The first stage involves the injection of B. burgdorferi by the tick. Shortly
thereafter (3 days to 4 months), it spreads throughout the skin, causing erythema
migrans (EM), which is basically a skin lesion. This lesion can vary in size, body site,
color, duration, intensity, and recurrence. Erythema migrans is a marker of the
disease, yet may also be absent altogether. EM resolves spontaneously in a few
weeks or months4. Also like to occur during this stage are mild fever, chills, headache,
and stiff neck (flu-like symptoms)?.
Within days or weeks after infection, in stage 2, the specimen has been seen in
specimens of myocardium, retina, muscle, bone, spleen, liver and brain1. Secondary
skin lesions may occur but are smaller and migrate less. The main symptoms include
fatigue and excruciating headache, lasting only hours or days. Meningitis, poor
memory, mood change, cardiac problems, and facial palsy are also very common.
They may recur or become chronic1. Six months later (on average), many patients
have brief attacks of arthritis in the large joints, especially in the knee.
Stage 3 is classified as the late persistent infection, where arthritis lasts longer
(ie. months) and chronic arthritis (a year or more of joint inflammation) begins. More
than a year after infection, B. burgdorferI may affect the central and peripheral nervous
There has been a lot of work carried out in this field, particularly where children
are affected. For example, the transplacental transmission of B. burgdorferi has been
reported in 2 infants whose mothers were infected with Lyme borreliosis during the first
trimester of pregnancy. Both of these infants dies in their first week of life. One had
encephalitis and the other had congenital cardiac malformations1. Spirochetes were
seen in various fetal tissues.
Studies reviewing lyme disease in pregnant women before knowing the outcome
of their pregnancy, in order to assess the frequency and the type of adverse pregnancy
outcomes associated with lyme disease have also been carried out in the field5.
One study found adverse outcomes in 5 out of 19 children tested. These outcomes
included cortical blindness, intrauterine fetal death, prematurity and rash in the
newborn. It is of great importance to determine whether such outcomes are directly
related to B. burgdorferi5.
Another study performed by Szer et al tested the long-term course of lyme
arthritis in children, who had not received any antibiotic treatment for at least the first
four years of the illness.
Another study by Garcia-Monco et al looked at the experimental and clinical
evidence for early invasion of Borrelia burgdorferi in the central nervour system, by
intravenously inoculating rats with the bacteria and examining their cerebrospinal
Such work leads me to my specific research topic: studying cognitive skills in
children who have been treated for lyme disease using antibiotics. It seems likely that
the lyme disease spirochete can cause an adverse fetal outcome. However, the
question is, how likely and just what are the outcomes, which is what I would like to test
for. My proposed study will be an experimental study in which lyme disease treated
pediatric populations will be examined to identify possible cognitive or psychologic
abnormalities resulting from lyme disease. The focus will be on children
because they have a high incidence of lyme disease? and are less likely to have
cognitive deterioration due to confounding factors, such as aging.
Children between the ages of 5 and 15 who have been treated with lyme disease
will be studied. These children will be randomly chosen for endemic areas such as
Delaware. Serologic testing (ie. enzyme-linked immunosorbent assa; ELISA) will be
used to determine the presence of B. burgdorferi antibodies.
The following hypotheses will be tested:
Ho: No cognitive differences between lyme disease children and control group
HA: Cognitive differences between lyme disease children and control group are
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