Lime Disease Essay, Research Paper
Lyme disease is caused by Borrelia burgdorferi, which is a tick-borne spirochaete.
The dangers of this disease became more publicised in 1977, where a geographic
grouping of kids in Lyme, Conneticut were thought to hold juvenile rheumatoid
arthritis1. Soon after, it was discovered that lyme disease was an unwellness that chiefly
affects the tegument, nervous system, bosom, and articulations. The borrelia species is portion of the
eubacterial phylum of spirochaetes. Containted within a protoplasmic cylinder is a cell
membrane, followed by wavy scourge, and so an outer membrane. The cistrons
encoded within the outer membrane are located on plasmids which allows the being
to do antigenic alterations in these proteins. When a borrelia cell attaches to its host,
the whole outer membrane moves to one terminal of the cylinder, which is called cresting to
patching1. B. burgdorferi do non populate in H2O, dirt, or workss. Borrelia grow easy
compared to most bacteriums. They elongate for 12 to 24 hours before spliting into two
cells. B. burgdorferi is about 20 to um long and 0.2 to 0.25 um broad, with 7 to
11 scourge. More than 30 proteins are contained within B. burgdorferi1. This bacterium
utilizations white-footed mice, mosquitoes, and cervid as their hosts.
This disease does non know apart between sex and age ; male and female, as
good as old and immature are affected. It is widely distributed around the universe in the
temperate zones3. A individual is infected when a black-legged tick imbeds itself into
them while out in the unfastened in wodded and forested countries. This normally occurs between
the months of May and July. Tick copiousness is associated with humidness, temperature,
landscape incline, forested countries with sandy dirts, and the appendage of residential
By and large, lyme disease occurs in phases, which are non ever clear-cut ; they
may overlap. The first phase involves the injection of B. burgdorferi by the tick. Shortly
thenceforth ( 3 yearss to 4 months ) , it spreads throughout the tegument, doing erythema
migrans ( EM ) , which is fundamentally a skin lesion. This lesion can change in size, organic structure site,
colour, continuance, strength, and return. Erythema migrans is a marker of the
disease, yet may besides be absent wholly. EM resolves spontaneously in a few
hebdomads or months4. Besides like to happen during this phase are mild febrility, icinesss, concern,
and stiff cervix ( flu-like symptoms ) ? .
Within yearss or hebdomads after infection, in phase 2, the specimen has been seen in
specimens of myocardium, retina, musculus, bone, lien, liver and brain1. Secondary
skin lesions may happen but are smaller and migrate less. The chief symptoms include
weariness and tormenting concern, enduring lone hours or yearss. Meningitis, hapless
memory, temper alteration, cardiac jobs, and facial paralysis are besides really common.
They may repeat or go chronic1. Six months subsequently ( on norm ) , many patients
have brief onslaughts of arthritis in the big articulations, particularly one
n the articulatio genus.
Phase 3 is classified as the late persistent infection, where arthritis lasts longer
( Internet Explorer. months ) and chronic arthritis ( a twelvemonth or more of joint redness ) begins. More
than a twelvemonth after infection, B. burgdorferI may impact the cardinal and peripheral nervous
There has been a batch of work carried out in this field, peculiarly where kids
are affected. For illustration, the transplacental transmittal of B. burgdorferi has been
reported in 2 babies whose female parents were infected with Lyme borreliosis during the first
trimester of gestation. Both of these babies dies in their first hebdomad of life. One had
phrenitis and the other had inborn cardiac malformations1. Spirochetes were
seen in assorted foetal tissues.
Surveies reexamining lyme disease in pregnant adult females before cognizing the result
of their gestation, in order to measure the frequence and the type of inauspicious gestation
outcomes associated with lyme disease have besides been carried out in the field5.
One survey found inauspicious results in 5 out of 19 kids tested. These results
included cortical sightlessness, intrauterine foetal decease, prematureness and roseola in the
newborn. It is of great importance to find whether such results are straight
related to B. burgdorferi5.
Another survey performed by Szer et al tested the long-run class of lyme
arthritis in kids, who had non received any antibiotic intervention for at least the first
four old ages of the unwellness.
Another survey by Garcia-Monco et Al looked at the experimental and clinical
grounds for early invasion of Borrelia burgdorferi in the cardinal nervour system, by
intravenously inoculating rats with the bacteriums and analyzing their cerebrospinal
Such work leads me to my specific research subject: analyzing cognitive accomplishments in
kids who have been treated for lyme disease utilizing antibiotics. It seems likely that
the lyme disease spirochaete can do an inauspicious foetal result. However, the
inquiry is, how likely and merely what are the results, which is what I would wish to prove
for. My proposed survey will be an experimental survey in which lyme disease treated
paediatric populations will be examined to place possible cognitive or psychologic
abnormalcies ensuing from lyme disease. The focal point will be on kids
because they have a high incidence of lyme disease? and are less likely to hold
cognitive impairment due to confusing factors, such as aging.
Children between the ages of 5 and 15 who have been treated with lyme disease
will be studied. These kids will be indiscriminately chosen for endemic countries such as
Delaware. Serologic proving ( ie. enzyme-linked immunosorbent assa ; ELISA ) will be
used to find the presence of B. burgdorferi antibodies.
The undermentioned hypotheses will be tested:
Holmium: No cognitive differences between lyme disease kids and control group
Hour angle: Cognitive differences between lyme disease kids and control group are