Lime disease

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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.