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OverviewHerpes simplex, a common viral disease, is caused by two strains of the herpes simplex virus (HSV). The initial infection (primary stage) of oral herpes is generally asymptomatic and is acquired through person to person contact such as kissing.
The stages of genital herpes are very similar to oral herpes with an initial stage that manifests with few symptoms and is less contagious. For both genital and oral herpes, the dormancy period involves the virus "resting" within the nervous tissue around the initially infected area. Herpes is commonly diagnosed based upon the symptoms described above paired with frequent recurrence in the same area. Once diagnosed with herpes, managing the disease includes caring for sores during outbreaks as well as preventing their recurrence. Since genital and oral herpes are extremely common in the United States, with an estimate of 45 million people or one out of every five infected, there are many places to turn for support. Viral infections or exacerbations are still the most difficult problem in medicine to date. To date, the pathogenesis of VZV infection is not fully understood because VZW is an exclusively human pathogen and is difficult to replicate in animal models (Breuer & Whitley, 2007). Among immunocompromised populations, herpes zoster rashes typically are more severe and prolonged and may become disseminated, indicating VZV viremia. VZV rashes typically are presented by a well-defined dermatomal distribution in immunocompetent individuals, so the diagnosis can be established by characteristic clinical presentation. Acyclovir, famciclovir, and valacyclovir are nucleoside analogs that inhibit replication of human herpesviruses and are approved by the U.S. Since VZV prophylaxis has been shown to effectively decrease the incidence of VZV reactivation and reduce disseminated VZV infection in BMT recipients, VZV prophylaxis should be considered for hematologic patients without BMT with severe myelosuppression. Among high-risk patients without transplantation, reactivation and disseminated VZV infection also can occur. This is a viral infection of the lips and mouth which is caused by the herpes simplex virus a€“ termed HSV.
Herpes doesna€™t always develop symptoms a€“ it does not always cause any outward, visible signs. Kissing or touching and any sexual contact with the area that is infected spreads oral herpes.
Many individuals have symptoms of itching, burning, and tingling proceeding the outbreak of blisters or sores. The most concentrated pain from these sores occurs at the onset and can make drinking or eating hard.
If a child with cold sores is less than 6 weeks old, the babya€™s physician needs to be notified if oral blisters or sores appear. Individuals with weakened immunity systems should also notify their primary care physician if sores or blisters appear.
A physician will make a tentative diagnosis on data provided by the patient and on the physician exam.
Topical anesthetic such as lidocaine (xylocaine, Nervocaine, Dilocaine, Zilactin-L) can be approved for pain relieve of oral blisters and lesions. Oral or IV drugs exist for HSV but only for individuals with weakened immune systems, infants younger than 6 weeks or those with severe disease.
Topical Denavir (penciclovir) creams can shorten attacks of recurrent HSV-if it is applied early, normally before lesions develop. These medications may stop viral reproduction in the skin but do not eradicate HSV from the body or stop later outbreaks. This website is for informational purposes only and Is not a substitute for medical advice, diagnosis or treatment. Herpes infection or Herpes simplex is a disease which is viral caused by herpes simplex virus type 1 or HSV-1 and type 2 or HSV-2.
These are other types of herpes which are all caused by herpes simplex virus: Herpes gladiatorum, herpes whitlow, ocular herpes or keratitis, encephalitis cerebral herpes infection, neonatal herpes, Mollaret’s meningitis.
Herpes simplex virus type 1 causes face, eye, mouth, throat, and central nervous system infections.
Through clinical examinations, orofacial herpes are identified to persons who have no history with such lesions or contact with persons having HSV type-1 infection. Genital herpes in persons infected with HSV type-2 virus are more difficult to diagnose because there are other conditions that resemble genital herpes such as lichen planus, fungal infection, urethritis and atopic dermatitis.


Herpes simplex virus can’t be eradicated in the body and there is still no discovered method for it. Typical grouped vesicles and pustules with erythema and edema of three contiguous thoracic dermatomes on the posterior chest wall.
Long-term prophylaxis of cold sores is indicated when you get cold sores frequently, at a rate of about 6 or more times per year.
However, the clinical presentation may be atypical or may have disseminated disease without rashes in immunocompromised patients; as a result, laboratory tests, including polymerase chain reaction, direct fluorescent antibody, and viral culture are needed to confirm the diagnosis.
Monitoring CD4 counts may be useful for clinicians in determining the need for VZV prophylaxis among high-risk populations, such as (a) hematologic patients with cancer following cytotoxic chemotherapy who fail to recover from myelosuppression over a prolonged period of time, (b) patients with myelodysplastic syndrome who have severe leukopenia refractory to granulocyte-colony-stimulating factor or granulocyte- macrophage-colony-stimulating factor, and (c) patients anticipating a prolonged course of immunosuppressive therapy who also are VZV seropositive (indicting a latent VZV state). Two patients with solid cancers in the first author's practice developed disseminated VZV infections -- one patient with breast cancer receiving standard adjuvant chemotherapy and one patient with metastatic colorectal cancer who received chemotherapy over four years.
Persons with weak and suppressed immune system like in newborns, AIDS, and transplant patients are more prone to acquiring this infection. The distribution and appearance of sores appear as round, multiple, superficial oral ulcers with acute gingivitis. Laboratory tests are done to diagnose genital herpes which include virus culture, virus detection through direct fluorescent antibody studies, polymerase chain reaction to identify DNA virus, and skin biopsy.
However, there are antiviral medications that can lessen the outbreak severity, duration and frequency of infection.
Acyclovir is the first discovered drug for herpes simplex virus and is now available in generic forms.
Also known as a cold sore, this lesion is caused by the contagious herpes simplex virus Type-1 (HSV-1), and should not be confused with a canker sore, which is not contagious. The potential side effects of daily oral medication must be considered with infrequent cold sores.
Primary infection with VZV results in varicella or chickenpox, which largely affects children with a mild, self-limiting course (Wharton, 1996). Women have a slightly higher risk than men, and African Americans have a lower incidence of herpes zoster (Opstelten, Van Essen, Schellevis, Verheij, & Moons, 2006). During initial viraemia, infected CD4 T cells cause down regulation of the histocompatibility complex class I expression and allow VZV to escape from the immune system (Ku, Padilla, Grose, Butcher, & Arvin, 2002).
The most common rash sites are the thoracic and lumbar dermatomal zones (Yawn et al., 2007).
Therefore, considering VZV prophylaxis is clinically reasonable to reduce the risk of deadly disseminated VZV infection among high-risk patients with cancer without BMT.
After a primary infection, the nerves are entered by the virus at the primary infection site, migrate to the neuron’s cell body and become hidden in the ganglion. Sometimes, orofacial herpes lesions are mistaken as impetigo, a bacterial infection, if lesions are not seen inside the mouth. These laboratory tests are specific when it comes to diagnosing but because of high cost, it constrains the infected persons from submitting themselves to test.
After clinical resolution of primary infection, viral latent infection is established when VZV retrogrades into the sensory dorsal roots of ganglia (Breuer & Whitley, 2007).
In addition, infected T cells transport VZV via T-cell trafficking from tonsillar tissue to the skin, where VZV replicates and produces cell-free VZV, resulting in highly infectious skin lesions. The rashes initially are erythematous and maculopapular, then progress to coalescing clusters of clear vesicles that contain high concentrations of VZV, which are contagious for VZV seronegative individuals. However, direct fluorescent antibody offers rapid diagnosis and is highly sensitive (Chan, Brandt, & Horsman, 2001).
Therapy should be initiated within 72 hours of rash onset or as soon as possible (Dworkin et al.) (see Table 1). A retrospective analysis of 192 allogeneic peripheral blood stem cell transplantation recipients indicated that a very low dose of acylovir (200 mg daily) protected against VZV reactivation (Kim et al., 2008).
In addition, the prophylaxis regimen may decrease patients' physical suffering and associated hospitalizations. As a result, antibodies are produced by the body for the particular herpes simplex virus type to prevent further infection to a different site.
Vaccination in children to prevent primary VZV has reduced chickenpox cases in the United States (Marin, Guris, Chaves, Schmid, & Seward, 2007). Uninfected T cells also arrive at the infection sites, become primed with cell-free VZV, and mount a systemic immune response to control the initial infection (Ku et al., 2005). In immunocompetent people, the rashes crust in 7-10 days and are no longer infectious (Harpaz et al., 2008).
The specimen is obtained by scraping the bases of uncrusted vesicular skin lesions and placing the scrapings on a plain glass slide.


Similarly, 137 BMT recipients who were given long-term acylovir of 200 mg daily until the end of immune suppression and at least one year following BMT had significantly decreased incidence of VZV reactivation, and visceral dissemination and serious complications were completely eliminated (Asano-Mori et al., 2008).
In HSV type-1 infected persons, additional infection is infected through seroconversion or development of specific antibodies in the blood serum. In some instances, samples of representative lesions are taken and tested for the presence of the HSV1 or HSV2 virus.
Herpes zoster, the second clinical condition of VZV infection, results from the reactivation of this latent neurotropic virus and commonly presents with painful, unilateral vesicular skin eruption distributing within the dermatomal zones (Gnann & Whitley, 2002).
Following initial infection, the VZV-specific cell-mediated immunity keeps VZV in latency and prevents its reactivation (Breuer & Whitley). Although VZV cutaneous dissemination may start with a dermatomal rash, it presents without any primary dermatomal involvement in some cases.
If a person is infected with HSV type-2, the symptoms are minimal because of the help of seroconversion. When an individual's immune system is compromised, such as in older adults or people with cancer undergoing chemotherapy or transplantation, his or her VZV-specific cell mediated immunity also is likely to be impaired, leading to VZV reactivation.
The most common complication following herpes zoster infection is postherpetic neuralgia, a persistent pain that can last months to years and occasionally becomes permanent.
Type 1 virus is the usual cause of cold sores around the mouth, and herpes simplex infection in the eye. Adjunct therapy for pain and postherpetic neuralgia often is required for patients with herpes zoster. It is commonly passed on by close contact such as kisses from a family member who has a cold sore.) In many people the primary infection does not cause any symptoms, although in some cases symptoms do occur. A minor and temporary inflammation of the conjunctiva (conjunctivitis) or eyelids (blepharitis) may occur with active infection, often at the same time as the cornea is infected. Often people who get active eye infection will have had previous cold sores during their lifetime. They may also put some stain on the front of your eye to show up any irregular areas on the cornea.
If your doctor suspects a herpes eye infection you will usually be referred urgently to an eye specialist.
This is to confirm the diagnosis and to determine whether the infection is in the top layer of the cornea (epithelial keratitis), or if the deeper layers are involved (stromal keratitis). These do not kill the virus but stop it from multiplying further until the infection clears.
You are likely to be kept under review, until the infection clears, to check that the cornea does not become infected.
Note: if you have herpes simplex eye infection, you should stop wearing any contact lens until 24 hours after your symptoms and the infection have completely gone away. As mentioned above, these occur if the virus reactivates from time to time - similar to cold sores.
A recurrent infection may occur any time between a few weeks and many years after the first active infection.
At least half of people who have one episode of active infection will have a recurrence within 10 years of the first. If recurrences are frequent or severe, then your eye specialist may advise that you take antiviral tablets each day to prevent episodes of active infection. Studies have shown that, on average, the number of recurrences is roughly halved in people who take regular antiviral tablets. Some people say that episodes of active herpes infection may be triggered by strong sunlight. It is also possible that active infection may be triggered if you are run down or unwell for another reason.
Some women find that they get recurrences around the time of their period but again there is limited evidence to support this. However, severe and recurrent herpes simplex eye infections may lead to serious scarring, impaired vision and even blindness in some cases.



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