An infection of the lips or mouth which results in a blistery sore
that is caused by Herpes simplex type 1. Most Americans think of it as
a cold sore that comes and goes. But the Herpes Virus is a highly
contagious microbe that never really leaves.
Eight out of every 10 American adults are infected with the herpes
simplex virus, or HSV. The virus is either dormant within a variety of
tissues or is activated and highly contagious. As a contagious virus,
HSV is either the direct cause or a cofactor associated with a number
of different diseases and disorders. Its best-known manifestation: the
common cold sore. The cold sore, or herpetic lesion, typically shows
redness, swelling, pain and heat over an eight-to-10 day period. After
that, its clinical signs and symptoms appear resolved, leaving no
apparent scar. But the virus leaves with a promise to return.
The virus, infecting the lips, oral mucosa or tongue, can be
transmitted to the hand or eyes--and it can be transmitted to another
person, expanding the sphere of influence of this highly contagious
microbe.
HSV also can be associated with other diseases or disorders that
compromise the immune system such as protein-calorie malnutrition and
AIDS. The virus provides oral health professionals an excellent
opportunity to reassess their appreciation of infection and immunity.
We can learn from HSV.
For thousands of years, redness and swelling, with pain and heat,
have been recognized as the four cardinal signs of inflammation. Aulus
Cornelius Celsus in the first century described the typical reaction of
flesh to microbes. Since then, astute health care professionals have
appreciated that inflammation is the host's response to traumatic
injuries as well as to microbe infections.
Inflammation is our protective response to dilute, destroy or
compartmentalize both the infectious agent (infectious microbes such as
viral, bacterial, fungal or parasitic invasion) and the injured tissue.
Redness, swelling, pain, heat and loss of function are clinical
characteristics of HSV.
The inflammatory process activates the inflammatory reaction with
increased blood flow (redness), increased vascular permeability
(swelling), increased leukocyte migration and infiltration with
attendant production of cytokines and eventual destruction of the
infectious agents (pain, heat and possibly loss of function).
From a Darwinian perspective, infection-meets-immunity is high
drama. It is a drama that presents a sophisticated confrontation of the
opportunistic microbe (virus, bacteria, fungi, parasite) vs. the highly
evolved human immune system, with its enormous capacity to confront
diversity and provide an advantage for the host against a changing
microbial environment.
The "simple" cold sore has many lessons to teach. Humanity's
recognition of cold sores is so long-standing that it has led to
complacent acceptance. Descriptions of the infection have been
documented in early Greek manuscripts, particularly in the writings of
Hippocrates (460-377 B.C.). Scholars of Greek civilization define the
word herpes to mean "creep or crawl," describing the spreading nature
of the visual skin lesion. The early, imprecise visual descriptions of
the sore ended in the 20th century when, in 1919, Lowenstein described
the infectious nature of the causative virus (herpes simplex) and
demonstrated that the virus retrieved from the lesions of the sore
produced a similar lesion on the cornea of a rabbit.
Like many viruses, the herpes viruses take up permanent residence in
the body once they are introduced. After an initial infection, the
virus goes into hiding, escaping the host's immune system by remaining
latent in a specific group of cells, causing no apparent harm to the
host. The exact cell in which they remain latent varies from one virus
type to the next. In cells harboring the latent virus, the viral
genomes take the form of closed molecules and only a small subset of
virus genes are expressed. Production of infectious progeny virus is
invariably accompanied by the irreversible destruction of the infected
cell. All of the human herpes viruses have been detected in the saliva
sometime during infection.
Primary infection with HSV can produce great variability in clinical
symptoms--from being totally asymptomatic to suffering with
combinations of sore throat, ulcerative and vesicular lesions,
gingivostomatitis, edema of the mucosal membranes, localized
lymphadenopathy, anorexia and malaise.
The incubation period for HSV ranges from two to 12 days. In
children, the infection characteristically involves a swelling of the
gingival and buccal mucosa, making it difficult or impossible to
swallow liquids. The clinical illness, accompanied by fever and pain
from the lesion, generally lasts two to three weeks. After infection,
the virus goes into hiding, entering nerve endings and traveling to
ganglia (clusters of nerve cells).
For most people, a herpes outbreak is confined to recognizable
variations of the classical symptoms. While outbreaks can be physically
and emotionally uncomfortable, and sometimes painful, the infection is
usually self-limiting and results in complete healing of the infected
site.
The virus in the inflamed site, however, is infectious and can be
transmitted to a new site on the host's body (autoinoculation) or to
another person through contact with any part of the body where the
virus finds a way to penetrate the skin.
Transmission in most cases requires direct skin-to-skin contact
between the infected site and a receptive site. Risk of transmission is
highest when the virus is active. But first outbreaks or primary
lesions are the most infectious because they include more virus
particles on the skin, and the lesions persist for a longer period.
Treatment includes the use of antiviral creams (acyclovir) and oral
medications (acyclovir). Pre-treatment with oral acyclovir, in those
prone to cold sores (prior to sun exposure, etc.) has been shown to
decrease exacerbations.
Research on drug therapies for HSV has focused mainly on treating
genital herpes to prevent sexual transmission and the effects on
newborns. Since its introduction in 1985, oral acyclovir has been the
preferred treatment for genital herpes. It also has been found
effective in treating oral herpes. The U.S. Food and Drug
Administration is reviewing an application that would extend oral
acyclovir's use in treating oral herpes.
People who suffer from frequent bouts of HSV can take acyclovir
daily for up to one year. Unfortunately, though, it is not a cure for
the virus that remains in the body. The drug interferes with virus
expression; it doesn't kill it.
Oral herpes is usually treated by the time-tried methods of keeping
the blisters clean and dry, being careful not to touch the sores and
spread the virus to new sites, and avoiding contacts with people in
ways that could transmit the virus.
The following Combinations are those recommended for the treatment of Cold Sores.
| Vitamins :- | B Complex, C (Large doses) |
| Minerals :- | Calcium, Zinc |
| Amino Acids :- | L-Lysine |
| Food Supplements :- | Acidophilus |
The
nutrients mentioned above reflect the major nutritional supplements
that may help the condition. Please do remember however that
nutritional supplementation is an adjunct to medical treatment and in
no way replaces medical treatment.
