Overview
Genital Herpes (Herpes Simplex-II) attacks the area on and around sex organs, causing blisters and sores. It is highly contagious and very aggressive, causing frequent outbreaks.
Genital Herpes symptoms can vary in severity and may well be severe for 2 to 10 days. However for some patients, blisters or open, weeping lesions can last weeks or months. In addition, genital herpes patients can suffer from significant emotional distress because of the intimate nature of the infected area and its social consequences.
Transmission of Genital Herpes
Genital Herpes is spread easily. It is most commonly contracted by contact with an infected person during sexual intercourse. The virus enters the body through a crack or cut in the skin or through the skin around the mouth, penis or vagina, urinary tract opening, cervix or anus.
Genital Herpes is most contagious when blisters or sores can be seen on the infected person. However, it can be spread at any time, even when there aren't visible symptoms.
Genital Herpes can also be spread from the original site to other parts of the body, such as from the genital area to the hands or feet. The eyes can also be infected. Genital herpes can also be spread from a mother to her baby during birth.
Stages of Genital Herpes
Once infected, an individual will go through different stages of infection.
Primary stage The initial stage begins up to 8 days after infection, however the virus may remain dormant in the body for a longer period of time. The typical initial outbreak results in groups of small, painful blisters. The blister fluid can be clear or cloudy. The skin in the area will become red and inflamed. The blisters are easily ruptured and become open sores. The transition from blister to sore can occur so rapidly the blister stage may not even be noticed.
Besides having tender blisters or sores in the genital area, the patient may experience pain when urinating. A fever and other flu-like symptoms may also be experienced.
The majority of individuals infected experience a painful primary stage of infection. It is also possible not to experience any symptoms at all. These individuals are not aware they are even infected.
Latent stage After the initial outbreak, the genital herpes virus will go into a latent stage, where the individual will experience no blisters, sores or other symptoms. During the dormant or latent cycle, the genital herpes virus travels to the nerve ganglia in the spinal region.
Shedding stage The virus multiplies in number in the nerve ganglia. The virus can also migrate to body fluids, such as saliva, semen or vaginal fluids. The process is called shedding. Although no symptoms are evident during the shedding stage, the virus can still be transmitted to other areas of the body or another individual.
Recurrences Most people experience additional outbreaks although, in most cases, the symptoms are not as severe.
Stress, being sick or being tired may result in a recurrence. Exposure to the sun or the menstrual period may also cause a recurrence. Typically a recurrence gives advanced warning by the individual feeling an itching, tingling or pain in the area of the initial outbreak.
What should I do if I think I have herpes? The sooner treatment is administered, the less pain will be experienced.
Treatment
Prior to the advent of PHOTHERAPY, there was no medical option that could both stop an outbreak of genital herpes and prevent subsequent outbreaks.
There is no prescription medicine that will cure Genital Herpes. Some medicines can help. For example, acyclovir (brand name: Zovirax) can speed up healing and lessen the pain of Herpes for some people. It can treat primary or recurrent herpes and may lessen the number of recurrences.
Famciclovir (brand name: Famvir) and valacyclovir (brand name: Valtrex) are other medicines used to treat recurrent Genital Herpes.
Shedding Light on the Solution for Genital Herpes… PHOTOTHERAPY
PHOTOTHERAPY is not a prescription medicine; no pills to swallow, no side effects to endure. It is a remarkably effective treatment that utilized a unique combination of light energy and an activating solution.
With PHOTOTHERAPY you can physically see the treatment progress as it isolates and kills the Genital Herpes virus.
When the Genital Herpes blisters are opened, the PHOTOTHERAPY solution applied, and the areas exposed to the IMULUX light, the Genital Herpes virus will react within a few seconds to the light bombardment.
The infected area will actually begin to fluoresce (glow brightly). You may feel a tingling sensation and, at the same time, pain will begin to subside. The exposed area provides a passageway for the Genital Herpes virus itself to be attacked by PHOTOTHERAPY.
In less than 30 minutes the treatment will be complete and your Genital Herpes virus killed. The PHOTOTHERAPY treatment will enhance most patients’ ability to fight future symptoms: another outbreak will never occur.
Note: If the infected area does not fluoresce, the condition is other than Genital Herpes, which may not be successfully treatable by PHOTOTHERAPY. If so, simply return the product for a prompt and full refund with in 30 days of purchase.
Background: Chemical-based medicine falls short
The need for a new approach to infectious and other life-threatening diseases arose from the failure of conventional medicine to provide effective solutions.
For the past 100 years or longer, conventional practitioners have depended on a chemical resolution for treatment of foreign pathogens of the body, such as the herpes virus.
From the earliest days of antibiotics -- when it was discovered that bread mold helped to heal infected lesions, leading to the discovery of penicillin -- we have embraced chemical treatment as the utilitarian goal of medicine.
We have added various tools for diagnosing various pathogens, and even found enhanced antibiotics through scientific research and development.
For the herpes virus, an array of expensive pharmaceuticals on today's market can perhaps shorten the duration of an outbreak. But these medications are unfortunately unable to conquer this particularly insidious pathogen.
Energy medicine offers solutions
The concept of energy medicine, once a dream of the medical community, became reality in the last 30 years. It is based on developing techniques that help the body's own natural defense mechanisms maintain good health.
Energy medicine has gained significant traction throughout the medical community; it has been utilized with great success for many years.
For example, ultra-sound instruments aid in the healing process of many diseases. In addition, devices using electrical stimulation can diagnose and alleviate pain from a range of discomforting and deforming conditions.
Finding a solution for herpes
It is only natural that energy medicine is now being deployed in empowering the body's cells to repel the invasion of pathogens, such as the herpes virus.
This has been accomplished by dedicated scientists, who have turned to energy medicine to pioneer the first truly breakthrough solution for the treatment of herpes.
The Process of Illumination
Just as harnessed energy of the sun can be productively used, so can the specially designed ultraviolet (UVA) rays emitted by IMULUX lamps.
This light energy source, in tandem with the PHOTOTHERAPY solution, can effectively suppress further outbreaks from the virus at hand.
Why PHOTOTHERAPY works
Ultraviolet light and herpes viruses do not get along. The herpes virus does not survive well in the presence of ultraviolet light. The PHOTOTHERAPY protocol discovered a way to deliver ultraviolet light beneath the skin, the home of the virus during an active outbreak. This photon lending substance removes the protection of the skin which absorbs and reflects the ultraviolet light in our environment. Once light enters the viral home there are several theories have been proposed to explain how PHOTOTHERAPY achieves its goal. Here at PHOTOTHERAPY we know that it works even if we don’t have the final explanation as to why it works. Most drugs on the market today have an unexplained mechanism of action.
The cells of every living organism - except viruses - have energy powerhouses called mitochondria.
The mitochondria in our cells accept nutrients and convert them to usable energy to maintain life.
Since viruses lack mitochondria, they have no way to process nutrients to sustain their own life. Without a power source to convert nutrients the virus will die.
True parasites, viruses must have a host to survive. So they turn our epithelial cells, hook up to the cells mitochondria and create an infection, essentially using the epithelial cells as a host. As the infection completes its cycle and the virus leaves this host, it then travels to nerve cells, converting them into their host and borrowing their mitochondria to process nutrients.
See the drawing below.
Figure 1. The herpes simplex virus life cycle. (a) Herpes simplex virus (HSV) is shown undergoing the lytic cycle (entry, uncoating, viral transcription and DNA replication in the nucleus, particle assembly, exit from the cell) in epithelial cells of the skin to cause a primary infection. (b) Some virus enters the sensory neuron terminals and travels retrogradely to the nucleus where it establishes latency. (c) Periodic reactivation results in anterograde transport of viral particles, shedding from the neuron, and re-infection of epithelial cells, which leads to asymptomatic shedding or recurrent lesions.
One theory is called the polarity principle;
The Polarity Principle
For a virus to find its host, it has to be attracted to it.
We recall from high-school science class that positive and negative charges attract each other, while charges with the same polarity repel one another.
If we assume that the virus has a negative polarity and the host cell has a positive polarity, they would attract each other.
By training the IMULUX light on the accompanying treatment solution, pure photon energy bombards the infected cells, which changes the virus' polarity from negative to positive. With this polarity change, the herpes virus is repelled, loses its hosts, cannot find other hosts in which to reside, and dies.
This action effectively eliminates any herpes outbreak on the spot. Even better, the virus dies in one infected cell after another throughout the body. As this occurs, the dead viruses cause the body to form antibodies -- protecting you from future outbreaks. The effectiveness of this treatment process has been validated by scores of patients for whom PHOTOTHERAPY has proven to be the solution after years of herpes suffering.
Another theory involves Ace Pigments (alternative cellular energy) Ace pigments theory;
We all remember a process in plants called photosynthesis. The Ace pigment theory proposes that there is an alternative energy source for epithelial cells in the human body that collects light and converts it to energy; thus making the host cell more vital or giving the host cell enough renewed metabolic energy to allow it to eject the parasitic virus. It is a known fact that the virus seems to attack stressed cells and is less likely to be found in cells with a good metabolic activity. In effect the PHOTOTHERAPY protocol gives the host cell the ability to fight off its invaders.
With this renewed energy the lesion site is better able to heal itself and the outbreak is cancelled. The virus unable to find a new host simply dies.
A third theory has to do with physical destruction of the virus itself.
It has been observed in the laboratory that the virus actually absorbs the photon lending solution and when exposed to the ultraviolet light the solution expands its molecular structure several hundred times in a millisecond. This physical change in the molecule of the solution blows the virus up into pieces to which the body can make an army of antibodies. This kills the virus instantly stopping pain and spread of the lesion on the spot. The lesion dries up and begins healing immediately. Since the virus is dead it cannot escape and hide in the nerve ganglion.
PHOTOTHERAPY works effectively on any of the eight human herpes types provided there is a skin outbreak. This includes oral, genital and shingles (herpes zoster). PHOTOTHERAPY also works effectively on Condyloma (a general class of viruses known to be responsible for genital warts). It has even been found in clinical studies to be an effective treatment for common non-genital warts.
Success is achieved by applying the PHOTOTHERAPYsolution to the affected area in the first 24 to 96 hours of an outbreak. The solution is absorbed by the cell wall of the virus. When exposed to the IMULUX treatment light, the solution transfers pure photon energy to the infected cells, which effectively eliminates any herpes outbreak within 24 hours.
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PHOTOTHERAPY for Genital Herpes Treatment Directions
Read through all instructions carefully before beginning treatment
Your IMULUX for Genital Herpes Treatment Kit Includes:
Clean and Scrub lesion. This should be done for 30 minutes, by soaking in a hot bath just prior to administering the procedure.
Puncture and open the scabs or blisters in the area to be treated. This can be accomplished by one of the following methods:
Important: For successful treatment the PHOTOTHERAPY solution must be allowed to enter the open scabs or blisters. Take great care in making sure the scabs or blisters are properly opened.
Tap the Genital Powder container softly several times on a flat surface to knock the contents to the bottom then carefully unscrew the top.
Unscrew the top of the Activating Solution bottle and carefully pour into the Powder container approximately ½ of the solution.
Stir the mixture with the cotton swab until the solution turns bright red. The red solution is now ready to apply directly with the cotton swab to the cleaned and scrubbed lesion site. Note the solution only has an effective life of about two hours so do not mix the solution until you are ready to do the treatment.
Paint the open lesion site, using the cotton swab, with the red solution. There should be no pain or burning associated with applying the solution to the lesion site. There might be a mild tingling sensation, which is normal.
Plug IMULUX treatment lamp contained in your treatment kit into a 120V outlet. If your outlet current is different then 120V you must use a voltage adaptor set to change your electric output to match the fixture’s 120V requirement. The fixture would be destroyed if the adaptor set is not used for voltage other then 120V.
Darken room for light treatment.
Position yourself so you are comfortable and support the lamp so it is approximately 1 inch above area to be treated. Turn on lamp by pressing the white switch located on the power cord to the “ON” position.
Expose the lesion site to the IMULUX light for a period of not less than 10 minutes and a maximum exposure of 30 minutes. (Note: The IMULUX light is an ultraviolet light source, which has been designed with a precise level of intensity and light frequency which delivers specific photons of light necessary for the IMULUX treatment. When used per these instructions; exposure to the light is harmless to surrounding tissues. Treatment with a light source other than the IMULUX light will be in effective and void the PHOTOTHERAPY guarantee.)
*In the first minute of treatment the lesion site will start to fluoresce. You may experience a mild tingling sensation after one or two minutes and the lesion site may begin to ooze a small discharge of fluid. Under the illumination of the IMULUX light, this discharge will appear yellow to orange at first and then turn a darker yellow or orange. As the virus is destroyed, the color change takes place.
*The tingling sensation may subside after as little as 10 minutes or continue for up to 30 minutes. If the tingling sensation ends in less then 10 minutes continue the treatment for the minimum exposure time of 10 minutes.
*When the discharge has changed to darker yellow or orange, or when the tingling sensation subsides, the procedure is complete.
*Pain and irritation should be gone immediately after the procedure.
Bathe and clean the treatment area with soap and water immediately following completion of treatment.
Attempt to keep the area dry for the next 24 hours.
STEP #10 Two additional treatment “med paks” are enclosed should you need additional treatments as a result of treating too soon or too late. Sometimes individuals will treat a skin rash that is not herpes but rather a “jock itch” or fungal infection. Should you make this mistake additional “med paks” are provided.
The human herpesviruses, including Herpes simplex virus (HSV), Varicella zoster virus (VZV), cytomegalovirus (CMV), Epstein-Barr virus (EBV), human herpesvirus 6 (HHV-6), human herpesvirus 7 (HHV-7), and human herpesvirus 8 (HHV-8) may produce a variety of clinically significant manifestations either as self-limited infections or non-resolving opportunistic infections.
Many herpesviruses commonly infect man, but clinically apparent or life-threatening illness are most often seen in persons who are immunocompromised, including persons with primary or secondary immunodeficiencies (including AIDS), persons undergoing cancer chemotherapy, transplant recipients, persons with lymphoreticular malignancies involving the hematologic and/or mononuclear phagocyte system, persons receiving chronic corticosteroid therapy or having increased endogenous corticosteroid production (Cushing's syndrome), and persons who are severely debilitated and/or malnourished.
HERPESVIRUSES, TYPES 1 AND 2 VARICELLA ZOSTER VIRUS
Both HSV types 1 (HSV-1) and 2 (HSV-2) primarily infect skin and mucus membranes (mucocutaneous infections) to produce inflammation, often vesicular, progressing to sharply demarcated ulcerations. Herpes simplex type 1 mainly involves the oral cavity, often as the so-called "cold sores" that many people have experienced. HSV-2 more often involves the genital region as a sexually transmitted disease. However, either body region may be infected by either subtype to produce clinically and histologically indistinguishable disease, which is not surprising, given the 50% homology between the genomes of HSV-1 and -2. The lesions, though small, can be quite painful.
Two distinct clinical manifestations are seen with the Varicella zoster virus (VZV):
All herpesviruses exhibit latency following initial infection. Either HSV or VZV infection initially occurs through mucosal surfaces or through abraded skin via contact with a person who is excreting virus through active, usually ulcerative, lesions. Excretion of HSV-1 can be detected in 2 to 9% of asymptomatic adults, while HSV-2 can be isolated from the genital tract in up to 5% of males and up to 8% of females in sexually transmitted disease clinics.
Viral replication begins within epithelium and underlying dermis or within submucosa. From these initial sites, HSV or VZV spreads to nerve endings and is transported intra-axonally to neurons in ganglia, from which spread is then via peripheral sensory nerves back to other, usually adjacent, skin and mucosal sites.
Thus, vesicular HSV or VZV lesions may later appear or recur away from the initial site of involvement.
After an initial host response in which both cell-mediated and humoral mechanisms take part, the infection usually becomes latent, with HSV or VZV present but not actively replicating within ganglia. It is unclear just how reactivation of HSV, or VZV as HZV, occurs but lack of cell-mediated immunity in immunocompromised patients may be implicated.
Clinical Diagnosis:
Diagnosis of HSV or HZV infections is suggested by the appearance of crops of clear vesicles in groups on mucocutaneous surfaces. Vesicles may resolve completely, but in some cases infection becomes persistent and ulcerations occur, most commonly with HSV infections about the oral cavity or perianal region. The typical patient with HSV or HZV has a grouped vesicular skin eruption that ruptures, crusts, and heals in seven to ten days. Infection may be associated with a history of severe pain, often persisting for months after the skin lesions resolve. Scarring also occurs, and secondary bacterial infection may complicate herpetic lesions.
Ulceration may obscure the features and make diagnosis difficult unless a Tzanck preparation, biopsy, or viral culture is done to establish the diagnosis. Multiple herpetic lesions tend to ulcerate due to persistence for prolonged periods (with or without therapy), excoriation, or secondary infection.
Microbiologic Diagnosis:
Viral culture remains the most sensitive clinical method for HSV or HZV diagnosis; methods for antigen detection are less sensitive. Culture sensitivity is higher when the herpetic vesicular lesions first appear and before they ulcerate. Later ulcerative lesions may have no detectable virus. Serologic testing is mainly of value for detection of past infection, but not acute infection, for immunocompromised patients are unlikely to mount a significant (fourfold or greater) rise in anti-HSV titer between acute and convalescent samples.
Tissue Diagnosis:
Microscopically, lesions of HSV and HZV both in tissue biopsies or from cytologic preparations (Tzanck or Pap smears) demonstrate characteristic acantholytic epithelial or discohesive parenchymal cells, often multinucleated or in clusters, with mauve to pink to steel-gray ground glass intranuclear (Cowdry type A) inclusions. The cytoplasm of infected cells is not prominent and, unlike CMV, does not contain inclusion bodies of any kind. With ulceration, such cells may be infrequent or autolyzed. Surrounding sqaumous epithelium may show ballooning degeneration.
For HZV, typical cytologic features most often occur in cells between papillae and dermal adnexae. On average, cells infected with HSV or HZV do not reach the size of those with CMV, and the intranuclear inclusions of CMV tend to be darker and larger, and intracytoplasmic inclusions may accompany CMV. Immunoperoxidase staining with primary antibody against HSV-1, HSV-2, and HZV will help to exclude other viral etiologies such as CMV, EBV, and human papillomavirus (HPV).
Organ Involvement:
Encephalitis from HSV is the most common viral infection of the CNS in the U.S., with an estimated incidence of 2.3 cases per million per year. The clinical course and radiologic findings of HSV encephalitis may closely mimic those of progressive multifocal leukoencephalopathy (PML), though computed tomograpahic or magnetic resonance imaging scans showing evidence of hemorrhage, a mass effect, or gray matter involvement more strongly suggest herpes.
Grossly, HSV produces areas of necrosis most commonly in temporal lobe, inferior frontal lobe, insula, or cingulate gyrus. Microscopically, herpetic lesions can have petechiae with fibrinoid necrosis, perivascular mononuclear inflammatory cell infiltrates, and Cowdry type A inclusions in either neurons or glial cells.
Ocular herpes is the most frequent etiology for corneal blindness in the U.S. However, with AIDS deeper infection is more frequent, with the complication of chorioretinitis reported.
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