Lime Disease Essay Research Paper Lime DiseaseLyme

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

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

development?.

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

systems.

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

fluid2.

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

present.