Herpetic Whitlow in Adults: Condition, Treatments, and Pictures – Overview

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Information for
Adults

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Images of Herpetic Whitlow

Overview

Herpetic whitlow—also called digital herpes simplex, finger herpes, or hand herpes—is a painful viral infection occurring on the fingers or around the fingernails. Herpetic whitlow is caused by infection with the herpes simplex virus (HSV).

Infections with HSV are very contagious and are easily spread by direct contact with infected skin lesions. HSV infection usually appears as small blisters or sores around the mouth, nose, genitals, and buttocks, though infections can develop almost anywhere on the skin. Furthermore, these tender sores may recur periodically in the same sites.

There are 2 types of HSV: herpes simplex virus type 1 (HSV-1) and herpes simplex virus type 2 (HSV-2). HSV-1 infections usually occur around the mouth, lips, nose, or face, while HSV-2 infections usually involve the genitals or buttocks. However, HSV-1 can sometimes cause infections in the genitals or buttocks, while HSV-2 can occasionally cause infections around the mouth, lips, nose, or face.

Both types of HSV produce 2 kinds of infections: primary and recurrent. Because it is so contagious, the herpes simplex virus causes a primary infection in most people who are exposed to the virus. However, only about 20% of people who have a primary infection with the herpes simplex virus actually develop visible blisters or sores. Appearing 2–20 days after a person’s first exposure to HSV, the sores of a primary infection last about 1–3 weeks. These sores heal completely, rarely leaving a scar. Nevertheless, the virus remains in the body, hibernating in nerve cells.

Certain triggers can cause the hibernating (latent) virus to wake up, become active, and travel back to the skin. These recurrent herpes simplex virus infections may develop frequently (every few weeks), or they may never develop. Recurrent infections tend to be milder than primary infections and generally occur in the same location as the primary infection.

People develop herpetic whitlow when they come into contact with areas already infected with HSV, either on their own bodies or on someone else’s body. Usually, there is a break in the skin, especially a torn cuticle at the base of the fingernail, which allows the virus to enter the finger tissue and establish an infection. HSV-1 causes approximately 60% of herpetic whitlow infections, while HSV-2 causes the remaining 40%.

Who’s at risk?

Herpetic whitlow can affect people of all ages, of all races, and of both sexes. However, it is more common in children and in dental and medical workers. Children often contract herpetic whitlow as a result of thumb- or finger-sucking when they have a herpes infection of the lips or mouth. Dental and medical workers may contract herpetic whitlow by touching the contagious lesions of a patient with herpes simplex virus infection. In these groups of people—children and health care workers—herpetic whitlow is most commonly caused by HSV-1. In everyone else, herpetic whitlow is usually caused by infection with HSV-2.

Signs and Symptoms

The most common locations for herpetic whitlow include:

• Thumb
• Index finger
• Other fingers

Approximately 2–20 days after initial exposure to the herpes simplex virus, the infected area develops burning, tingling, and pain. Over the next week or 2, the finger becomes red and swollen. Small (1–3 mm) fluid-filled blisters develop, often clustered together on a bright red base. The blisters usually rupture and scab over, leading to complete healing after an additional 2 weeks.

Other symptoms occasionally associated with the primary infection of herpetic whitlow include:

• Fever
• Red streaks radiating from the finger (lymphangitis)
• Swollen lymph nodes in the elbow or underarm area

If a person contracts herpetic whitlow from himself or herself (autoinoculation), then he or she is likely to have a primary herpes simplex virus infection of the mouth area or of the genital area.

Repeat (recurrent) herpes simplex virus infections are often milder than the primary infection, though they look alike. A recurrent infection typically lasts 7–10 days. Recurrent herpetic whitlow is rare.

However, people with recurrent HSV infections may report that the skin lesions are preceded by sensations of burning, itching, or tingling (prodrome). About 24 hours after the prodrome symptoms begin, the actual lesions appear as one or more small blisters, which eventually open up and become scabbed over.

Triggers of recurrent HSV infections include:

• Fever or illness
• Sun exposure
• Hormonal changes, such as those due to menstruation or pregnancy
• Stress
• Trauma
• Surgery

Self-Care Guidelines

Acetaminophen or ibuprofen may help reduce fever and pain caused by the herpes simplex virus sores. Applying cool compresses or ice packs may also relieve some of the swelling and discomfort.

Because herpes simplex virus infections are very contagious, it is important to take the following steps to prevent spread (transmission) of the virus during the prodrome phase (burning, tingling, or itching) and active phase (presence of blisters or sores) of herpetic whitlow:

• Avoid sharing towels and other personal care items
• Cover the affected finger with a bandage
• Wear gloves if you are a health care provider
• Don’t pop any blisters—it may make the condition worse

Unfortunately, the virus can still be transmitted even when someone does not have active lesions. However, this is very unusual for patients with herpetic whitlow.

When to Seek Medical Care

If you develop a tender, painful sore on the finger, see a physician, especially if it is not going away or if it seems to be getting worse. You should definitely seek medical attention if you have a finger sore as well as typical symptoms of oral or genital herpes.

Treatments Your Physician May Prescribe

Most herpes simplex virus infections are easy for physicians to diagnose. On occasion, however, a swab from the infected skin may be sent to the laboratory for viral culture, which takes a few days to grow. Blood tests may also be performed.

Untreated HSV infections will go away on their own, but medications can reduce the symptoms and shorten the duration of outbreaks. There is no cure for herpes simplex virus infection.

Although herpetic whitlow symptoms will eventually go away on their own, your physician may prescribe antiviral medications in order to help relieve symptoms and to prevent spread of the infection to other people:

• Acyclovir pills
• Valacyclovir pills
• Famciclovir pills
• Topical acyclovir ointment

These medications are usually taken for 7–14 days.

More severe herpetic whitlow may require oral antibiotic pills if the area(s) are also infected with bacteria.

Although it is rare, recurrent herpetic whitlow can be treated with the same oral antiviral medications:

• Acyclovir pills
• Valacyclovir pills
• Famciclovir pills
• Topical acyclovir ointment

People who experience early signs (prodromes) before recurrent infections may benefit from episodic treatment, by starting to take medication after the onset of tingling and burning but before the appearance of blisters and sores.

Very rarely, individuals may have recurrent herpetic whitlow outbreaks that are frequent enough or severe enough to justify suppressive therapy, in which medications are taken every day in order to decrease the frequency and severity of attacks.

Trusted Links

MedlinePlus: Finger Injuries and Disorders
MedlinePlus: Herpes Simplex
Clinical Information and Differential Diagnosis of Herpetic Whitlow

References

Bolognia, Jean L., ed. Dermatology, pp. 1237-1238. New York: Mosby, 2003.

Freedberg, Irwin M., ed. Fitzpatrick’s Dermatology in General Medicine. 6^th ed, pp.1317, 2063, 2068. New York: McGraw-Hill, 2003.

Herpetic whitlow (whitlow finger) | nidirect

Herpetic whitlow (whitlow finger) is a painful infection of the finger. It is caused by the herpes virus. It’s easily treated but can come back.

Symptoms of herpetic whitlow

The symptoms of herpetic whitlow include:

• a red, swollen and painful finger
• blisters or sores on your finger

When to see your GP

You should see your GP if you think you have herpetic whitlow.

Treatment is more effective if started early and will help stop the infection spreading.

You may be prescribed antiviral tablets if you see a GP within 48 hours of your symptoms showing.

Antiviral tablets can help your finger to heal more quickly.

If you can’t see a GP within 48 hours, the infection will go away without treatment. But there are things you can do yourself to help.

Things you can do yourself include:

Do

• keep your finger clean and covered with a dressing
• take painkillers such as ibuprofen or paracetamol to ease the pain

Don’t

• touch your finger – the infection can spread easily
• touch other parts of your body or other people with your infected finger
• try to drain the fluid – this can cause the infection to spread
• use contact lenses – you could spread the infection to your eye

Go back to your GP if your infection gets worse or if you have a very high temperature (you feel hot and shivery).

Causes of herpetic whitlow

Herpetic whitlow is caused by a virus called ‘herpes simplex’. You can get it if you touch a cold sore or blister of another infected person.

You’re more likely to get herpetic whitlow if you’ve had cold sores or genital herpes.

You may also get it if you have a weakened immune system – for example, if you have diabetes or you’re having chemotherapy.

The first time you have herpetic whitlow will usually be the most severe.

Once you have the virus, it stays in your body for the rest of your life.

The condition is rare, but if you get it once you can get it again. For example, it might come back if you have a cut or sore on your finger, or if you’re feeling stressed or unwell.

There’s not much you can do to prevent herpetic whitlow. But it can be treated in the same way if it comes back.

Pictures, Symptoms, Causes, and Treatments

Painful, pus-filled blisters that form on the face near the lips. Caused by the herpes simplex virus 1 (HSV-1). Usually spread by close contact with an infected person.

Prevalance: Very common Ages Affected: All

• Blisters on or around the lips
• Pain and tenderness to the touch
• Burning or itching sensations

• Topical creams (Abreva, acyclovir, penciclovir, zinc oxide)
• Antiviral drugs (oral acyclovir, valacyclovir, famciclovir)
• Home remedies (bee propolis, lemon balm, aloe vera, lysine)

Cold sores, or “fever blisters”, are painful blisters that form on the face, usually near the lips.  

They’re caused by one of the most common viral infections in the world. According to the CDC, nearly 50% of people have at least one cold sore outbreak every year.

You can’t cure cold sores permanently, but certain medications and home remedies may help shorten outbreaks and improve symptoms.

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What is a cold sore?

A cold sore is a red or dark pink fluid-filled blister around the mouth caused by the herpes simplex virus. Cold sores may appear on other parts of your face. Rarely, cold sores can spread to your nose, inside of your mouth, or even your fingers.

Cold sores are also known as fever blisters, herpes labialis, or oral herpes.

Generally, cold sores spread through close contact, like kissing or oral sex, with another person during an outbreak. Even before you can see the blisters, cold sores may be contagious if skin contact is made.

Cold sores may come back at any time, even after an active outbreak has ended. There is no known cure for cold sores, which are a recurring skin condition.

What does a cold sore look like? 

There are 5 cold sore stages that each look different:

• Stage 1/Tingling: For about 24 hours, your mouth may itch and/or tingle. Many people describe the feeling as a burning sensation. No visible signs may appear.
• Stage 2/Blistering: Blisters form and fill with fluid. You may develop several small blisters or one large blister. Sores appear white, greyish, or yellow while skin becomes inflamed and red.
• Stage 3/Weeping: Blisters break (burst) and may ooze. Painful sores form and are often varying shades of red.
• Stage 4/Crusting: After a few days, sores dry out and a scab forms. Itching and cracking are common.  
• Stage 5/Healing: The scab falls off and the skin heals.

Cold sores are contagious at every stage until they heal completely. They spread most easily during stage 3.

You cannot speed up cold sore healing by popping it or by ripping off the scab. Both of these actions may lead to a scar once the cold sore has healed completely.

Cold Sore Symptoms

Tingling, burning, and itchy facial skin are the first signs of a fever blister/cold sore. Catching a cold sore early is important to shorten its duration, so begin treatment immediately.

As the cold sore virus progresses, you’ll experience pain and tenderness. Multiple sores may appear.

Especially during your first cold sore outbreak, you may also experience symptoms like:

• Sore throat
• Painful gums
• Dehydration
• Swollen lips
• Fever
• Headache
• Nausea
• Swelling of the lymph nodes
• General muscle and joint aches

During your first cold sore, you may contract gingivostomatitis, an infection of the gums and mouth. This may be accompanied by swollen lymph nodes, bad breath, and a desire to avoid drinking water. 

Rarely, your eyes may become infected. If you experience any symptoms in or around your eyes during a cold sore infection, call a doctor immediately. HSV-1 infections in the eyes may lead to vision loss if not addressed right away.

What causes cold sores?

Cold sores are caused by the herpes simplex virus (HSV-1). 

“Herpes” can sound alarming, but it’s an incredibly common virus. 50-80% of adults in the United States carry HSV-1, according to Johns Hopkins Medicine. However, some individuals never develop a cold sore even though they carry the virus.

Most people, however, will experience at least one or two cold sores in their lifetime. 

The herpes virus “hides” in the ganglion of nerve cells under the skin of your face after an initial outbreak has ended. There, it is considered “dormant” or “latent.” When triggered again, HSV-1 replicates through the nerve and out to the skin to create a new cold sore. This is why recurring oral herpes outbreaks often happen around the same area of the face as prior outbreaks.

HSV-2 (herpes simplex virus 2) is a related viral strain that causes genital herpes. HSV-2 can rarely spread to the face, and HSV-1 can be transmitted to the genitals. 

A person may not develop their first cold sore for up to 20 days after exposure to HSV-1. During this time, they may still spread the virus. 

Risk Factors

As 90% of people carry the herpes virus that causes cold sores, most people are at risk of developing a cold sore at some point in their lifetime. A weak immune system is the most significant risk factor for cold sores.

If you have any of the following conditions, your immune system is weaker than average. This puts you at a higher risk of HSV-1 infections or complications:

• Eczema (atopic dermatitis)
• HIV/AIDS
• Autoimmune disease
• Third-degree burns over much of the body
• Cancer (especially during chemotherapy treatment)
• Organ transplants (because of anti-rejection drugs)

Certain genetic factors may also increase your risk of cold sores. The C21orf91 gene is associated with more frequent herpes labialis outbreaks.

What triggers a cold sore? New or recurring cold sore outbreaks may be triggered by:

• A weak immune system for any reason
• Any viral or bacterial infection (cold, flu, etc.)
• Sun exposure
• Chronic stress
• Fatigue
• Menstruation
• Dental work
• Injury to facial skin

Complications

In some cases, cold sore outbreaks may lead to serious medical complications such as:

• Eczema: Eczema combined with cold sore infections can cause eczema herpeticum, a potentially life-threatening medical emergency. People with eczema are more susceptible to cold sores because they have an inflammatory autoimmune condition across a large area of skin. No longer limited only to the face, cold sores can spread to any area of the body. This is most common in children.
• Herpetic whitlow: HSV-1 may be transferred to the fingertips, a condition known as herpetic whitlow (“whitlow finger”). This is why some babies and toddlers who suck their thumbs and fingers will get fever blisters on fingers. Dentists suffer from this type of cold sore complication more frequently than the general population.
• Eye infections: Herpes simplex can travel to the eyes and cause infections like herpetic keratoconjunctivitis or viral keratitis. This can result in inflammation and ulcers on the cornea. If left untreated, eye infections from cold sores can result in permanent vision loss. Call a doctor right away if you experience eye symptoms during a cold sore outbreak.
• Genital sores: Usually, HSV-1 causes cold sores on the face and HSV-2 causes genital herpes. However, it’s possible to spread HSV-1 sores to the genitals or HSV-2 sores to the face.
• Acute herpetic pharyngotonsillitis: In adults, cold sores may lead to this throat/tonsil infection. You may develop a fever, headache, tiredness, and a sore throat, but this infection is not usually serious.
• Gingivostomatitis: This gum/mouth infection usually happens only once, if ever, and heals in 7-10 days. However, it can spread to the central nervous system and may lead to meningoencephalitis and/or death.
• Meningitis or encephalitis: In immunocompromised individuals, HSV viruses may travel to and cause inflammation in the spinal cord (meningitis) and brain (encephalitis). This is a very rare and dangerous complication of the herpes virus. 

When to Call a Doctor

Most cold sores can be treated at home without problems. However, children and people at risk of complications should be monitored more closely and may need professional attention.

You should contact a doctor immediately if you or your child have a cold sore and:

• High or long-lasting fever
• Breathing or swallowing problems
• Irritation around the eyes which may or may not cause redness or discharge
• The spread of cold sores to an eczema breakout

You should also call your doctor if you develop a cold sore and have a compromised immune system, such as with cancer or AIDS.

Diagnosis

To diagnose a cold sore, your doctor can perform a physical exam. Cold sores are usually easy to identify, but he or she may order lab tests to confirm the diagnosis in some cases.

If you are at high risk of complications, your physician may sample the fluid from an oozing cold sore.

Cold Sore Treatment

How do you get rid of a cold sore fast? Over-the-counter topical ointments or creams like Abreva may shorten the length of a cold sore outbreak. 

In some cases, your doctor may recommend prescription antiviral medications to prevent recurring infections.

Several home remedies may also improve symptoms of cold sores. 

According to available scientific evidence, no treatment can get rid of a cold sore in 24 hours. 

Without treatment, most cold sore infections will clear up within 7-10 days.

Creams & Ointments

Prescription topical creams or ointments that your doctor may prescribe for a cold sore include:

• Viroxyn Professional (benzalkonium chloride and benzocaine)
• Xerese (acyclovir and hydrocortisone)
• Soothelip (acyclovir)
• Denavir (penciclovir)

Viroxyn may be able to reduce the time to cold sore healing by over 3 days more than Abreva. A 2010 study found Viroxyn healed a cold sore in just 4 days on average.

Over-the-counter topical creams or ointments that may help improve cold sore symptoms and/or shorten an outbreak include:

• Abreva (docosanol)
• Zinc oxide cream (typically sold for diaper rash)
• Aloe vera gel
• Zilactin (benzyl alcohol)

Abreva (docosanol) is the only over-the-counter antiviral treatment approved by the FDA to shorten the healing time of cold sores. Abreva may heal a cold sore in just 4-7 days.

Aloe vera gel and zinc oxide cream may also shorten outbreaks and reduce cold sore symptoms.

Zilactin is marketed for topical cold sore relief. No studies support its efficacy for improving symptoms, but it may dry out the area and reduce the pain caused by a cold sore.

All topical creams or gels for cold sores should be applied to the tingling or burning area 4-5 times each day for maximum effectiveness.

Touching a cold sore directly greatly increases your risk of spreading the infection to another part of your body or another person. When using creams and ointments for cold sores, always apply with a cotton swab.

Medications

Oral medications are available by prescription for prolonged or recurring cold sore infections:

• Zovirax (acyclovir)
• Valtrex (valacyclovir)
• Famvir (famciclovir)

These antiviral medicines may be prescribed for daily use if you have frequent cold sore outbreaks and/or you are at a high risk of complications. 

Home Remedies

Several cold sore remedies may improve your symptoms or even reduce your risk of future infections. These include:

• Bee propolis
• Apple cider vinegar
• Essential oils (eucalyptus, tea tree, peppermint, ginger, thyme, hyssop, and sandalwood)
• Lemon balm (salve or oral dietary supplement)
• Kanuka honey
• Aloe vera gel
• Lysine

Does toothpaste get rid of cold sores? No one knows for sure if toothpaste can get rid of cold sores. Anecdotal reports suggest that toothpaste containing SLS may help to dry out cold sores. However, no scientific evidence supports this claim.

Sodium lauryl sulfate (SLS) may actually cause canker sores, so avoid using this as a treatment for your cold sores.

Cold Sore Pain Relief

Even if your infection time is shortened by effective treatment, you’ll probably still experience pain during your outbreak.

To reduce pain from a cold sore:

• Use ice or a cold compress against the skin
• Take over-the-counter painkillers like ibuprofen (Advil) or acetaminophen (Tylenol)
• Use benzocaine or lidocaine gel to numb the area

Remember not to touch the sore with your hands and use a cotton ball or swab when applying a topical anesthetic.

Aspirin should not be used for cold sore pain — or any pain during a viral infection — especially in children.

Rarely, aspirin use during a viral infection may lead to Reye syndrome, a serious childhood condition that begins with persistent vomiting and may lead to neurological problems and other life-threatening complications.

How to Prevent Cold Sores

The virus is generally passed through skin contact or by touching personal items used by an infected person. To prevent spreading cold sores, do not:

• Share drinking glasses, water bottles, or eating utensils
• Use someone else’s lip balm
• Share toothbrushes or other hygiene products
• Kiss someone who has a cold sore or has been in close contact with another person who has a cold sore
• Perform or receive oral sex with someone who may have a cold sore or genital herpes

You should also wash your hands frequently and thoroughly during a cold sore outbreak.

To prevent or reduce your risk for recurring cold sore infections, you should avoid triggers for new outbreaks and keep your immune system healthy:

• Use a lip balm with sunscreen: Use an SPF 30 or higher lip balm.
• Avoid sun overexposure: Always use sunscreen and avoid spending several hours in the sun on a regular basis.
• Replace your toothbrush regularly: Your toothbrush or toothbrush head can hang onto viruses including HSV-1. Replace your toothbrush every 1-3 months and immediately after a cold sore outbreak.
• Practice stress-relief techniques: Journaling, meditation, time outdoors, exercise, and restful sleep can all help reduce stress and fatigue that can trigger cold sores.
• Support immune health during menstruation: Women may be more prone to cold sores during their periods. Don’t neglect immunity and healthy habits/eating during your cycle, as this could increase your risk of new cold sores.
• Boost your immune system: As with any virus, cold sores are less likely if your immune system is strong. Ensure you’re getting plenty of vitamin C, vitamin D, and nutrient-dense foods. You may also try a probiotic supplement and/or oral probiotics to support a healthy microbiome.
• Be cautious after dental work: Dental cleanings and other procedures can temporarily weaken your immune system by exposing your bloodstream to higher amounts of oral bacteria than normal. 

How long do cold sores last?

First cold sore outbreaks may last as long as 2 weeks. 

Recurrent outbreaks usually heal in 7-10 days.

The cold sore virus does not go away, even when a cold sore outbreak has healed. It remains dormant in nerve cells until the infection is triggered again.

Cold Sores vs. Canker Sores

A cold sore outbreak is the result of a viral infection, while canker sores are non-contagious ulcers caused by several different factors.

The easiest way to spot the difference between cold sores and canker sores is by their location and appearance.

Popping a Cold Sore

Does popping a cold sore help it heal faster? No, popping a cold sore does not help the blister heal faster. In fact, popping your cold sore will more than likely lead to:

• More cold sores as the blister fluid spreads
• Risk of new, different infections by exposing an open sore
• Scarring
• Increased pain

Popping a cold sore is especially dangerous if you are at risk of complications due to a compromised immune system. Skin conditions like eczema or psoriasis make it easier for the HSV-1 virus to spread all over the body, which may lead to life-threatening complications.

FAQs

Q: Are there clinical trials available for people with frequent cold sores?

Q: Do cold sores mean you have an STD?

A:
Most people contract the HSV-1 virus during childhood years, not related to any type of sexual contact. Cold sores are not considered an STD, unlike genital herpes caused by HSV-2. 

Keep in mind, though, that HSV-2 outbreaks in the genital area can pass to the mouth during oral sex and cause sores on the face. It’s also harder to prevent with condoms than other STDs since it can be transferred from the skin not covered by a condom.If you’re concerned you’ve contracted the HSV-2 virus, see your doctor for treatment options.

Learn More: Cold Sores vs. Canker Sores: Why You Should Know the Difference

11 References

1. McQuillan, G. M., Kruszon-Moran, D., Flagg, E. W., & Paulose-Ram, R. (2018). Prevalence of herpes simplex virus type 1 and type 2 in persons aged 14-49: United States, 2015-2016 (pp. 1-8). US Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Health Statistics. Full text: https://www.cdc.gov/nchs/products/databriefs/db304.htm
2. Kolokotronis, A., & Doumas, S. (2006). Herpes simplex virus infection, with particular reference to the progression and complications of primary herpetic gingivostomatitis. Clinical microbiology and infection, 12(3), 202-211. Full text: https://www.researchgate.net/profile/Stergios_Doumas/publication/7323444_Herpes_simplex_virus_infection_with_particular_reference_to_the_progression_and_complications_of_primary_herpetic_gingivostomatitis/links/59dd40ba458515f6efef4cd7/Herpes-simplex-virus-infection-with-particular-reference-to-the-progression-and-complications-of-primary-herpetic-gingivostomatitis.pdf
3. Arduino, P. G., & Porter, S. R. (2008). Herpes Simplex Virus Type 1 infection: overview on relevant clinico‐pathological features. Journal of oral pathology & medicine, 37(2), 107-121. Abstract: https://www.ncbi.nlm.nih.gov/pubmed/18197856
4. Kriesel, J. D., Jones, B. B., Matsunami, N., Patel, M. K., St. Pierre, C. A., Kurt-Jones, E. A., … & Hobbs, M. R. (2011). C21orf91 genotypes correlate with herpes simplex labialis (cold sore) frequency: description of a cold sore susceptibility gene. Journal of Infectious Diseases, 204(11), 1654-1662. Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3203230/
5. Rowe, N. H., Heine, C. S., & Kowalski, C. J. (1982). Herpetic whitlow: an occupational disease of practicing dentists. Journal of the American Dental Association (1939), 105(3), 471-473. Abstract: https://www.ncbi.nlm.nih.gov/pubmed/6957456
6. Dawson, C. R., & Togni, B. (1976). Herpes simplex eye infections: clinical manifestations, pathogenesis and management. Survey of ophthalmology, 21(2), 121-135. Abstract: https://www.ncbi.nlm.nih.gov/pubmed/988644
7. Klastersky, J., Cappel, R., Snoeck, J. M., Flament, J., & Thiry, L. (1972). Ascending myelitis in association with herpes-simplex virus. New England Journal of Medicine, 287(4), 182-184. Abstract: https://www.nejm.org/doi/pdf/10.1056/NEJM197207272870411
8. Mccarthy, J. P., Browning, W. D., Teerlink, C., & Veit, G. (2012). Treatment of herpes labialis: comparison of two OTC drugs and untreated controls. Journal of Esthetic and Restorative Dentistry, 24(2), 103-109. Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3472024/
9. Sacks, S. L., Thisted, R. A., Jones, T. M., Barbarash, R. A., Mikolich, D. J., Ruoff, G. E., … & Morrow, P. R. (2001). Clinical efficacy of topical docosanol 10% cream for herpes simplex labialis: a multicenter, randomized, placebo-controlled trial. Journal of the American Academy of Dermatology, 45(2), 222-230. Abstract: https://pubmed.ncbi.nlm.nih.gov/11464183/ 
10. Godfrey, H. R., Godfrey, N. J., Godfrey, J. C., & Riley, D. (2001). A randomized clinical trial on the treatment of oral herpes with topical zinc oxide/glycine. Alternative therapies in health and medicine, 7(3), 49. Abstract: https://pubmed.ncbi.nlm.nih.gov/11347285/ 
11. Rezazadeh, F., Moshaverinia, M., Motamedifar, M., & Alyaseri, M. (2016). Assessment of anti HSV-1 activity of Aloe vera gel extract: an in vitro study. Journal of Dentistry, 17(1), 49. Abstract: https://pubmed.ncbi.nlm.nih.gov/26966709/
12. Chavan, M., Jain, H., Diwan, N., Khedkar, S., Shete, A., & Durkar, S. (2012). Recurrent aphthous stomatitis: a review. Journal of Oral Pathology & Medicine, 41(8), 577-583. Full text: https://www.researchgate.net/profile/Mahesh_Chavan5/publication/221891773_Recurrent_aphthous_stomatitis_A_review/links/5b69611392851ca650512153/Recurrent-aphthous-stomatitis-A-review.pdf

Herpes Simplex Type 1 – StatPearls

Continuing Education Activity

Herpes simplex virus type 1 (HSV-1) is a linear dsDNA virus that is a member of the Alphaherpesviridae subfamily. HSV-1 is responsible for establishing primary and recurrent vesicular eruptions, primarily in the orolabial and genital mucosa. HSV-1 infection has a wide variety of presentations, including orolabial herpes, herpetic sycosis (HSV folliculitis), herpes gladiatorum, herpetic whitlow, ocular HSV infection, herpes encephalitis, Kaposi varicelliform eruption (eczema herpeticum), and severe or chronic HSV infection. Antiviral therapy limits the course of HSV infection. This activity describes the evaluation, and treatment herpes simplex virus type 1 and reviews the role of the interprofessional team in evaluating and treating patients with this condition.

Objectives:

• Describe the pathophysiology of a herpes type 1 infection.

• Review the risk factors for herpes type 1 infection.

• Explain the presentation of a patient with herpes type 1 infection.

• Outline the importance of improving care coordination amongst interprofessional team members to improve outcomes for patients affected by the herpes type 1 virus infection.

Earn continuing education credits (CME/CE) on this topic.

Introduction

Herpes simplex virus type 1 (HSV-1) is a member of the Alphaherpesviridae subfamily. Its structure is composed of linear dsDNA, an icosahedral capsid that is 100 to 110 nm in diameter, with a spikey envelope. In general, the pathogenesis of HSV-1 infection follows a cycle of primary infection of epithelial cells, latency primarily in neurons, and reactivation. HSV-1 is responsible for establishing primary and recurrent vesicular eruptions, primarily in the orolabial and genital mucosa. HSV-1 infection has a wide variety of presentations, including orolabial herpes, herpetic sycosis (HSV folliculitis), herpes gladiatorum, herpetic whitlow, ocular HSV infection, herpes encephalitis, Kaposi varicelliform eruption (eczema herpeticum), and severe or chronic HSV infection. Antiviral therapy limits the course of HSV infection.[1][2][3]

Etiology

Risk factors for HSV-1 infection differ depending on the type of HSV-1 infection. In the case of orolabial herpes, risk factors include any activity that exposes one to an infected patient’s saliva, for example, shared drinkware or cosmetics, or mouth to mouth contact.

The major risk factor for herpetic sycosis is close shaving with a razor blade in the presence of an acute orolabial infection.

Risk factors for herpes gladiatorum include participation in high-contact sports such as rugby, wrestling, MMA, and boxing.

Risk factors for herpetic whitlow include thumb sucking and nail biting in the presence of orolabial HSV-1 infection in the child population, and medical/dental profession in the adult population (although HSV-2 most commonly causes herpetic whitlow in adults).

A major risk factor for herpes encephalitis is mutations in the toll-like receptor (TLR-3) or UNC-93B genes. It has been postulated that these mutations inhibit normal interferon-based responses.

The major risk factor for eczema herpeticum is skin barrier dysfunction. This can be seen in atopic dermatitis, Darier disease, Hailey-Hailey disease, mycosis fungoides, and all types of ichthyosis. The increased risk is also associated with mutations in the filaggrin gene, which is seen in atopic dermatitis and ichthyosis vulgaris. Pharmaceutical risk factors for eczema herpeticum include the use of topical calcineurin inhibitors such as pimecrolimus and tacrolimus.

Risk factors for severe or chronic HSV infection include immunocompromised states such as transplant recipients (solid organ or hematopoietic stem cells), HIV infection, or leukemia/lymphoma patients.[4][5]

Epidemiology

It has been hypothesized that approximately one-third of the world’s population has experienced symptomatic HSV-1 at some point throughout his or her lifetime. HSV-1 first establishes primary infection in patients with no existing antibodies to HSV-1 or HSV-2. Non-primary initial infection is defined as infection with one HSV subtype in patients who already have antibodies to the other HSV type (i.e., HSV-1 infection in a patient with HSV-2 antibodies, or vice versa). Reactivation results in recurrent infection and most commonly presents as asymptomatic viral shedding.

Approximately 1 in 1000 newborns in the United States experience a neonatal herpes simplex virus infection, resulting from HSV exposure during vaginal delivery. Women with recurrent genital herpes have a low risk of vertically transmitting HSV to their neonate. However, women who acquire a genital HSV infection during pregnancy have a higher risk.

Epidemiologically, it is important to note that herpes encephalitis is the leading cause of lethal encephalitis in the United States, and ocular HSV infection is a common cause of blindness in the United States.[6][7][8][9][10]

Pathophysiology

HSV-1 is typically spread through direct contact with contaminated saliva or other infected bodily secretions, as opposed to HSV-2, which is spread primarily by sexual contact. HSV-1 begins to replicate at the site of infection (mucocutaneous) and then proceeds to travel by retrograde flow down an axon to the dorsal root ganglia (DRG). It is in the DRG that latency is established. This latency period allows the virus to remain in a non-infectious state for a variable amount of time before reactivation.  HSV-1 is sly in its ability to evade the immune system via several mechanisms. One such mechanism is inducing an intercellular accumulation of CD1d molecules in antigen presenting cells. Normally, these CD1d molecules are transported to the cell surface, where the antigen is presented resulting in the stimulation of natural killer T-cells, thus promoting immune response. When CD1d molecules are sequestered intercellularly, the immune response is inhibited. HSV-1 has several other mechanisms by which it down-regulates various immunologic cells and cytokines.[11][12][13][14][15][16]

Histopathology

Classic, though not pathognomonic, histologic findings for HSV infection include ballooning degeneration of keratinocytes and multinucleated giant cells. Multinucleated keratinocytes may contain Cowdry A inclusions, which are eosinophilic nuclear inclusions that can also be seen in other herpesviruses such as varicella-zoster virus (VZV) and cytomegalovirus (CMV). There is no pathognomonic histologic finding for HSV-1 infection, and therefore, clinical correlation is crucial during histopathologic evaluation.[12]

History and Physical

It is important to note that HSV-1 infection is frequently asymptomatic. When symptoms do occur, there is a wide range of clinical presentations including orolabial herpes, herpetic sycosis (HSV folliculitis), herpes gladiatorum, herpetic whitlow, ocular HSV infection, herpes encephalitis, Kaposi varicelliform eruption (eczema herpeticum), and severe or chronic HSV-1 infection.

HSV-1 is the most common culprit of orolabial herpes (a small percent of cases are attributed to HSV-2). It is important to note that orolabial HSV-1 infection is most commonly asymptomatic. When there are symptoms, the most common manifestation is the “cold sore” or fever blister. In children, symptomatic orolabial HSV-1 infections often present as gingivostomatitis that leads to pain, halitosis, and dysphagia. In adults, it can present as pharyngitis and a mononucleosis-like syndrome.[17]

Symptoms of a primary orolabial infection occur between three days and one week after the exposure. Patients will often experience a viral prodrome consisting of malaise, anorexia, fevers, tender lymphadenopathy, localized pain, tenderness, burning, or tingling prior to the onset of mucocutaneous lesions. Primary HSV-1 lesions usually occur on the mouth and lips. Patients will then demonstrate painful grouped vesicles on an erythematous base. These vesicles exhibit a characteristic scalloped border. These vesicles may then progress to pustules, erosions, and ulcerations. Within 2 to 6 weeks, the lesions crust over and symptoms resolve.[18]

Symptoms of recurrent orolabial infection are typically milder than those of primary infection, with a 24-hour prodrome of tingling, burning, and itch. Recurrent orolabial HSV-1 infections classically affect the vermillion border of the lip (as opposed to the mouth and lips as seen in primary infection).[19]

Initial or recurrent HSV-1 infections may affect the hair follicle, and when this occurs, it is termed herpetic sycosis (HSV folliculitis). This will present on the beard area of a male with a history of close razor blade shaving. Lesions exist on a spectrum ranging from scattered follicular papules with erosion to large lesions involving the entire beard area. Herpetic sycosis is self-limited, with a resolution of eroded papules within 2 to 3 weeks.

Lesions of herpes gladiatorum will be seen on the lateral neck, side of the face, and forearms within 4 to 11 days after exposure. A high suspicion for this diagnosis is crucial in athletes, as this is commonly misdiagnosed as bacterial folliculitis.

HSV-1 infection can also occur on the digits or periungual, causing herpetic whitlow.  Herpetic whitlow presents as deep blisters that may secondarily erode. A common misdiagnosis is an acute paronychia or blistering dactylitis.  Herpetic whitlow can also lead to lymphadenopathy of the epitrochlear or axillary lymph nodes in association with lymphatic streaking, mimicking bacterial cellulitis.

HSV-1 infection of the eye leads to ocular HSV in children and adults. Primary ocular HSV presents with keratoconjunctivitis that can be unilateral or bilateral. There can be associated eyelid tearing, edema, photophobia, chemosis (swelling of the conjunctiva), and preauricular lymphadenopathy. It is common for patients to experience recurrence, and in these cases, it is usually unilateral. Ocular HSV is a common cause of blindness in the United States when it manifests as keratitis or a branching dendritic corneal ulcer (which is pathognomonic for ocular HSV).

Herpes encephalitis is a severe, typically fatal (mortality is greater than 70% if untreated) infection caused by HSV-1. It primarily affects the temporal lobe of the brain leading to bizarre behavior and focal neurological deficits localized to the temporal lobe. Patients may have a fever and altered mental status as well.

Kaposi varicelliform eruption, or eczema herpeticum, presents as an extensive spreading of HSV infection in the setting of a compromised skin barrier (e.g., atopic dermatitis, Darier disease, pemphigus foliaceous, pemphigus vulgaris, Hailey-Hailey disease, mycosis fungoides, ichthyosis). Patients will display 2 to 3 mm punched-out erosions with hemorrhagic crusts in widespread distribution. There may be secondary impetigo with Staphylococcus or Streptococcus species.

Neonatal herpes virus presents at day 5 to 14 of life and favors the scalp and the trunk. It may present with disseminated cutaneous lesions and involvement of oral and ocular mucosa. Central nervous system (CNS) involvement may occur and manifest as encephalitis with lethargy, poor feeding, bulging fontanelle, irritability, and seizures. 

In the immunocompromised patient population, HSV infection can result in severe and chronic infection. The most common presentation of severe and chronic HSV infection is quickly enlarging ulcerations or verrucous/pustular lesions. It is not uncommon for patients to have respiratory or gastrointestinal tract involvement and present with dyspnea or dysphagia.[20][21][22][23][24]

Evaluation

The gold standard for diagnosing HSV-1 infection is HSV-1 serology (antibody detection via western blot). The most sensitive and specific mechanism is viral polymerase chain reaction (PCR). However, serology remains the gold standard. Viral culture, direct fluorescent antibody  (DFA) assay, and Tzanck smear are alternative methods of diagnosing. It is important to note that the Tzanck smear identifies multinucleated giant cells, so it cannot distinguish between HSV and VZV. The DFA assay, however, can distinguish between the 2 entities.[14]

Treatment / Management

For the treatment of orolabial herpes, the current recommendation is oral valacyclovir (2 grams twice daily for one day). If the patient has frequent outbreaks, chronic suppression is warranted. For chronic suppression of immunocompetent patients, oral valacyclovir 500 mg daily (for patients with less than ten outbreaks per year) or oral valacyclovir 1 gram by mouth daily (for patients with greater than 10 outbreaks a year) is recommended.

For the treatment of eczema herpeticum, it is recommended to use 10 to 14 days of either acyclovir (15 mg/kg with a 400 mg maximum) 3 to 5 times daily or Valacyclovir 1 gram by mouth twice a day.

For immunocompromised patients with severe and chronic HSV, treatment is aimed at chronic suppression. For chronic suppression of immunocompromised patients, oral acyclovir 400 to 800 2 to 3 times daily, or oral valacyclovir 500 mg twice daily is recommended.[25][26][27][28]

Differential Diagnosis

The differential diagnosis of orolabial HSV-1 infection includes aphthous stomatitis, Stevens-Johnson syndrome, erythema multiforme (EM) major, and herpangina. These entities can be distinguished from orolabial herpes by history and physical exam findings. The differential diagnosis of herpetic whitlow includes blistering dactylitis and acute or chronic paronychia.

Prognosis

Overall, the vast majority of HSV-1 infections are asymptomatic, and if symptomatic present with mild recurrent mucocutaneous lesions. The prognosis of HSV-1 infection varies depending on the manifestation and location of the HSV-1 infection. The majority of the time, HSV-1 infection follows a chronic course of latency and reactivation. HSV encephalitis is associated with high mortality; approximately 70% of untreated cases are ultimately fatal. The prognosis of ocular HSV can also be grim if the patient develops globe rupture or corneal scarring, as these processes can ultimately lead to blindness.[29]

Enhancing Healthcare Team Outcomes

Herpes type 1 infections are best managed by an interprofessional team that includes the primary provider, pediatrician, nurse practitioner, infectious disease specialist and the internist. The key to treatment is starting the antiviral within 24 hours of symptoms. It is important to understand that most infections spontaneously subside on their own and delayed treatment has no impact on duration or severity of symptoms. During the infection, the patient should be educated on washing hands and avoiding close contact with others.

Continuing Education / Review Questions

Figure

Herpes Simplex. Contributed by DermNetNZ

Figure

A. Herpetic keratitis with neovascularization of the cornea
B. Herpes Simplex I of the lips and skin of the chin
C. Stage 1 Neurotrophic Keratitis: fluorescein epithelial staining together with Gaule spots. Gaule spots are scattered areas of dried epithelium, (more…)

Figure

This image depicts a close view of a patient’s penile shaft, highlighting the presence of a crop of erythematous vesiculopapular lesions, which were determined to have been caused by a herpes genitalis outbreak. Genital herpes is a sexually transmitted (more…)

Figure

Herpes Simplex on genitals. Contributed by Dr. Shyam Verma, MBBS, DVD, FRCP, FAAD, Vadodara, India

Figure

Herpes Simplex mouth. Contributed by Dr. Shyam Verma, MBBS, DVD, FRCP, FAAD, Vadodara, India

References

1.

Rechenchoski DZ, Faccin-Galhardi LC, Linhares REC, Nozawa C. Herpesvirus: an underestimated virus. Folia Microbiol (Praha). 2017 Mar;62(2):151-156. [PubMed: 27858281]

2.

Soriano V, Romero JD. Rebound in Sexually Transmitted Infections Following the Success of Antiretrovirals for HIV/AIDS. AIDS Rev. 2018;20(4):187-204. [PubMed: 30548023]

3.

Mostafa HH, Thompson TW, Konen AJ, Haenchen SD, Hilliard JG, Macdonald SJ, Morrison LA, Davido DJ. Herpes Simplex Virus 1 Mutant with Point Mutations in UL39 Is Impaired for Acute Viral Replication in Mice, Establishment of Latency, and Explant-Induced Reactivation. J Virol. 2018 Apr 01;92(7) [PMC free article: PMC5972887] [PubMed: 29321311]

4.

Pfaff F, Groth M, Sauerbrei A, Zell R. Genotyping of herpes simplex virus type 1 by whole-genome sequencing. J Gen Virol. 2016 Oct;97(10):2732-2741. [PubMed: 27558891]

5.

van Oeffelen L, Biekram M, Poeran J, Hukkelhoven C, Galjaard S, van der Meijden W, Op de Coul E. Update on Neonatal Herpes Simplex Epidemiology in the Netherlands: A Health Problem of Increasing Concern? Pediatr Infect Dis J. 2018 Aug;37(8):806-813. [PubMed: 29356762]

6.

Chaabane S, Harfouche M, Chemaitelly H, Schwarzer G, Abu-Raddad LJ. Herpes simplex virus type 1 epidemiology in the Middle East and North Africa: systematic review, meta-analyses, and meta-regressions. Sci Rep. 2019 Feb 04;9(1):1136. [PMC free article: PMC6362060] [PubMed: 30718696]

7.

Fedoreyev SA, Krylova NV, Mishchenko NP, Vasileva EA, Pislyagin EA, Iunikhina OV, Lavrov VF, Svitich OA, Ebralidze LK, Leonova GN. Antiviral and Antioxidant Properties of Echinochrome A. Mar Drugs. 2018 Dec 15;16(12) [PMC free article: PMC6315383] [PubMed: 30558297]

8.

Jiang Y, Leib D. Preventing neonatal herpes infections through maternal immunization. Future Virol. 2017 Dec;12(12):709-711. [PMC free article: PMC5751513] [PubMed: 29339967]

9.

Marchi S, Trombetta CM, Gasparini R, Temperton N, Montomoli E. Epidemiology of herpes simplex virus type 1 and 2 in Italy: a seroprevalence study from 2000 to 2014. J Prev Med Hyg. 2017 Mar;58(1):E27-E33. [PMC free article: PMC5432775] [PubMed: 28515628]

10.

Finger-Jardim F, Avila EC, da Hora VP, Gonçalves CV, de Martinez AMB, Soares MA. Prevalence of herpes simplex virus types 1 and 2 at maternal and fetal sides of the placenta in asymptomatic pregnant women. Am J Reprod Immunol. 2017 Jul;78(1) [PubMed: 28440579]

11.

Rosenberg J, Galen BT. Recurrent Meningitis. Curr Pain Headache Rep. 2017 Jul;21(7):33. [PubMed: 28551737]

12.

Cruz AT, Freedman SB, Kulik DM, Okada PJ, Fleming AH, Mistry RD, Thomson JE, Schnadower D, Arms JL, Mahajan P, Garro AC, Pruitt CM, Balamuth F, Uspal NG, Aronson PL, Lyons TW, Thompson AD, Curtis SJ, Ishimine PT, Schmidt SM, Bradin SA, Grether-Jones KL, Miller AS, Louie J, Shah SS, Nigrovic LE., HSV Study Group of the Pediatric Emergency Medicine Collaborative Research Committee. Herpes Simplex Virus Infection in Infants Undergoing Meningitis Evaluation. Pediatrics. 2018 Feb;141(2) [PMC free article: PMC5810597] [PubMed: 29298827]

13.

Zhang J, Liu H, Wei B. Immune response of T cells during herpes simplex virus type 1 (HSV-1) infection. 2017 Apr.J Zhejiang Univ Sci B. 18(4):277-288. [PMC free article: PMC5394093] [PubMed: 28378566]

14.

Giraldo D, Wilcox DR, Longnecker R. The Type I Interferon Response and Age-Dependent Susceptibility to Herpes Simplex Virus Infection. DNA Cell Biol. 2017 May;36(5):329-334. [PMC free article: PMC5421632] [PubMed: 28278385]

15.

Rajasagi NK, Rouse BT. Application of our understanding of pathogenesis of herpetic stromal keratitis for novel therapy. Microbes Infect. 2018 Oct – Nov;20(9-10):526-530. [PMC free article: PMC6037561] [PubMed: 29329934]

16.

Bin L, Li X, Richers B, Streib JE, Hu JW, Taylor P, Leung DYM. Ankyrin repeat domain 1 regulates innate immune responses against herpes simplex virus 1: A potential role in eczema herpeticum. J Allergy Clin Immunol. 2018 Jun;141(6):2085-2093.e1. [PMC free article: PMC5994174] [PubMed: 29371118]

17.

Darji K, Frisch S, Adjei Boakye E, Siegfried E. Characterization of children with recurrent eczema herpeticum and response to treatment with interferon-gamma. Pediatr Dermatol. 2017 Nov;34(6):686-689. [PubMed: 29144049]

18.

Wei EY, Coghlin DT. Beyond Folliculitis: Recognizing Herpes Gladiatorum in Adolescent Athletes. J Pediatr. 2017 Nov;190:283. [PubMed: 28728810]

19.

Williams C, Wells J, Klein R, Sylvester T, Sunenshine R., Centers for Disease Control and Prevention (CDC). Notes from the field: outbreak of skin lesions among high school wrestlers–Arizona, 2014. MMWR Morb Mortal Wkly Rep. 2015 May 29;64(20):559-60. [PMC free article: PMC4584520] [PubMed: 26020140]

20.

Kolawole OM, Amuda OO, Nzurumike C, Suleiman MM, Ikhevha Ogah J. Seroprevalence and Co-Infection of Human Immunodeficiency Virus (HIV) and Herpes Simplex Virus (HSV) Among Pregnant Women in Lokoja, North-Central Nigeria. Iran Red Crescent Med J. 2016 Oct;18(10):e25284. [PMC free article: PMC5286443] [PubMed: 28180012]

21.

El Hayderi L, Rübben A, Nikkels AF. The alpha-herpesviridae in dermatology : Herpes simplex virus types I and II. Hautarzt. 2017 Dec;68(Suppl 1):1-5. [PubMed: 28197698]

22.

Shenoy R, Mostow E, Cain G. Eczema herpeticum in a wrestler. Clin J Sport Med. 2015 Jan;25(1):e18-9. [PubMed: 24714395]

23.

Li Z, Breitwieser FP, Lu J, Jun AS, Asnaghi L, Salzberg SL, Eberhart CG. Identifying Corneal Infections in Formalin-Fixed Specimens Using Next Generation Sequencing. Invest Ophthalmol Vis Sci. 2018 Jan 01;59(1):280-288. [PMC free article: PMC5770184] [PubMed: 29340642]

24.

El Hayderi L, Rübben A, Nikkels AF. [The alpha-herpesviridae in dermatology : Herpes simplex virus types I and II. German version]. Hautarzt. 2017 Mar;68(3):181-186. [PubMed: 28197699]

25.

Sanders JE, Garcia SE. Pediatric herpes simplex virus infections: an evidence-based approach to treatment. Pediatr Emerg Med Pract. 2014 Jan;11(1):1-19; quiz 19. [PubMed: 24649621]

26.

Kalogeropoulos D, Geka A, Malamos K, Kanari M, Kalogeropoulos C. New Therapeutic Perceptions in a Patient with Complicated Herpes Simplex Virus 1 Keratitis: A Case Report and Review of the Literature. Am J Case Rep. 2017 Dec 27;18:1382-1389. [PMC free article: PMC5753617] [PubMed: 29279602]

27.

Anderson BJ, McGuire DP, Reed M, Foster M, Ortiz D. Prophylactic Valacyclovir to Prevent Outbreaks of Primary Herpes Gladiatorum at a 28-Day Wrestling Camp: A 10-Year Review. Clin J Sport Med. 2016 Jul;26(4):272-8. [PubMed: 26540599]

28.

Mir-Bonafé JM, Román-Curto C, Santos-Briz A, Palacios-Álvarez I, Santos-Durán JC, Fernández-López E. Eczema herpeticum with herpetic folliculitis after bone marrow transplant under prophylactic acyclovir: are patients with underlying dermatologic disorders at higher risk? Transpl Infect Dis. 2013 Apr;15(2):E75-80. [PubMed: 23387866]

29.

Gottlieb SL, Giersing BK, Hickling J, Jones R, Deal C, Kaslow DC., HSV Vaccine Expert Consultation Group. Meeting report: Initial World Health Organization consultation on herpes simplex virus (HSV) vaccine preferred product characteristics, March 2017. Vaccine. 2019 Nov 28;37(50):7408-7418. [PubMed: 29224963]

Encephalitis, Herpes Simplex – NORD (National Organization for Rare Disorders)

ARTICLES

McJunkin JE, et al. La crosse encephalitis in children. N Engl J Med. 2001;11:801-807.

Maertzdorf J, et al. Herpes simplex virus type 1 (HSV-1) induced retinitis following herpes simplex encephalitis: indications for brain-to-eye transmission of HSV-1. Ann Neurol. 2000;48:936-39.

Sauerbrei A, et al. Virological diagnosis of herpes simplex encephalitis. J Clin Virol. 2000;17:31-36.

Garcia de Tena J, et al. The value of polymerase chain reaction in cerebrospinal fluid for the diagnosis of herpetic encephalitis: a report of 2 cases and a review of the literature. An Med Interna. 2000;17:81-83.

Chan PK, et al. Use of oral valaciclovir in a 12-year-old boy with herpes simplex encephalitis. Hong Kong Med J. 2000;6:119-21.

Garcia-Barragan N, et al. An unusual presentation of herpetic encephalitis. Rev Neurol. 2000;30:441-44.

Pavone P, et al. Early relapse of herpes simplex encephalitis. Clinical and therapeutic implications. Minerva Pediatr. 1999;51:395-98.

Ito Y, et al. Exacerbation of herpes simplex encephalitis after successful treatment with acyclovir. Clin Infect Dis. 1999;30:185-87.

Kaplan CP, et al. Cognitive outcome after emergent treatment of acute herpes simplex encephalitis with acyclovir. Brain Inj. 1999;13:935-41.

Levitz RE. Herpes simplex encephalitis: a review. Heart Lung. 1998;27:209-12.

McGrath N, et al. Herpes simplex encephalitis treated with acyclovir: diagnosis and long term outcome. J Neurol Neurosug Psychiatry. 1997;63:321-26.

Hokkanen L, et al. Cognitive recovery instead of decline after acute encephalitis: a prospective follow up study. J Neurol Neurosurg Psychiatry. 1997;63:222-27.

Paillard C, et al. Recurrence of herpes simplex encephalitis. Arch Pediatr. 1999;6:1081-85.

Foucher A, et al. Herpetic encephalitis: prognostic elements in adults and children (49 cases). Rev Electroencephalogr Neurophysiol Clin. 1985;15:185-93.

Taylor WB, et al. Ocular infection with herpes simplex virus type 1: prevention of acute herpetic encephalitis by systemic administration of virus-specific antibody. J Infect Dis. 1979;140:534-40.

What are the Clinical Differences Between Acute Paronychia and Herpetic Whitlow?

Patient Presentation
A 3-year-old female came to clinic with a rash around her mouth and on her finger. She had 3 days of fever and some drooling with decreased appetite and had complained of a sore throat. Her mother noticed red, blister-like lesions in clusters near the right upper lip, that began the evening before. That morning the mother noticed her right index finger was red and generally swollen. This was the same finger she sucked. The mother denied upper respiratory illnesses or ear pain and the child had been drinking and urinating well. The past medical history showed her to be previously well.

The pertinent physical exam revealed a tired but interactive child with a temperature of 38.6°C and normal vital signs. Her growth parameters were 50-75%. By her upper lip she had 5 clustered vesicular lesions (2-4 mm in size) with an erythematous base and clear fluid. It appeared that she was also developing another area on the left corner of the mouth. There was generalized erythema of the pharynx and one ulceration of the inner lower lip. The HEENT examination showed shoddy anterior cervical adenopathy but the rest of the examination was normal including her eyes. The proximal interphalyngeal joint to the tip of the index finger was generally red and slightly edematous. There were 2 clustered, flat lesions with clearish-yellow fluid in them with a surrounding erythema next to the base of the fingernail. The rest of her examination was normal.

The diagnosis of herpes labialis and herpetic whitlow was made. The child was begun on acyclovir. The patient’s clinical course showed when she returned for followup the next day that the right-sided lip lesions appeared to be stable, and there was no left sided lesion. The lesions on her finger were decreasing slightly in size and the finger was slightly less edematous. It was still erythematous but the erythema had not spread. Her mother said she was complaining of pain in her mouth and hand but it was controlled with ibuprofen. She had no other lesions include a negative eye examination. On telephone followup the next day, her mother said that the right lip lesion was decreasing and her finger was now only pink in color with the lesions appearing “improved.” Her fever had also resolved and she was eating soft food without problems.

Discussion
Primary herpes simplex virus (HSV) infection usually shows symptoms 2-20 days after contact. The virus enters the skin or mucous membranes and may then enter the dorsal root gangilons and become latent only to reactivate months to years in the future. Humans are the only known host. Recurrent infections may be caused by various stresses, including mental stress, fever, temperature extremes, sun or ultraviolet light exposure, trauma and immunosupression. HSV-1 usually causes gingivosomatitis and usually enters the trigeminal neuron. HSV-2 usually causes herpes genitalis and enters the sacral nerves. Primary oral HSV-1 usually has fever, with mouth lesions occurring and cervical and submandibular lymphadenopathy

In primary oral HSV-1, symptoms may include a prodrome of fever, followed by mouth lesions with submandibular and cervical lymphadenopathy. Other recognized forms of herpes include herpes gladiatorum where lesions occur on the skin in wrestlers, and herpetic sycosis, where lesions occur in the beard area due to autoinnoculation from shaving, or direct spread.

Learning Point
Herpetic whitlow has vesicular, clear to yellow lesions with an erythematous base on the fingers or hands that occurs in children who suck their hands. It can also occur in healthcare workers exposed when not wearing gloves. In children whitlow is caused almost exclusively by HSV-1 but in adults may be caused by HSV-1 or HSV-2. Direct transmission from saliva to the hand causes whitlow, although patients may be unaware that they are shedding virus and only present with whitlow. Vesicles are clear or pale yellow and have an erythematous base. The lesions may spread around and under the nail. Satellite lesions may occur in the first two weeks. Whitlow is treated with acyclovir and not incision and drainage. If not treated, herpetic whitlow resolves in about 3 weeks.

Acute paronychia and periungual felon may look like herpetic whitlow. They are caused by bacteria and usually appear with opaque, purulent fluid along the nail bed, and often will have surrounding erythema. The pressure may increase because of the paronychia and therefore incision and drainage is necessary, along with antibiotics.

Viral culture is the most sensitive test for herpetic whitlow but Tzank smear with multinucleated giant cells can be positive in 50-60% of cases. Tzank is not specific for herpes but can also be positive in varicella.

Questions for Further Discussion
1. What are the potential complications of herpetic whitlow?
2. What are the possible problems with a neonate or immunocompromized person who contracts HSV?
3. What is the treatment for herpes ocularis?
4. what is the treatment for herpes genitalis?

Related Cases

To Learn More
To view pediatric review articles on this topic from the past year check PubMed.

Evidence-based medicine information on this topic can be found at SearchingPediatrics.com, the National Guideline Clearinghouse and the Cochrane Database of Systematic Reviews.

Information prescriptions for patients can be found at MedlinePlus for these topics: Hand Injuries and Disorders and Herpes Simplex.

To view current news articles on this topic check Google News.

To view images related to this topic check Google Images.

Usatine RP, Tinitigan R. Nongenital herpes simplex virus. Am Fam Physician. 2010 Nov 1;82(9):1075-82.

Rubright JH, Shafritz AB. The herpetic whitlow. J Hand Surg Am. 2011 Feb;36(2):340-2.

Richert B, Andre´ J. Nail disorders in children: diagnosis and management. Am J Clin Dermatol. 2011 Apr 1;12(2):101-12.

ACGME Competencies Highlighted by Case

▷ Herpetic Whitlow – Pictures, Treatment, Contagious, Symptoms – (2021

Herpetic Whitlow is a fingertip infection that is intensely painful and involves one or even more fingers and normally involves the terminal phalanx. Herpetic whitlow causes blister and pain that is intense. Symptoms normally resolve in two weeks. With children as well as approximately 60% of all cases develop because of herpes simplex virus 1 or HSV-1. In adults as well as 40% of all cases develop due to herpes simplex virus type 2 which also is the cause of genital herpes.

This infection was first described in the year 1909 and fifty years later was designated to be an occupational hazard among workers in the healthcare field.

Herpetic Whitlow Symptoms

Signs and symptoms of this disorder include:

Inflammation

This is the first symptom that occurs with this disease. The condition begins with swelling on the finger that causes mild to severe pain.

Redness

Area that is affected normally is red and swollen.

Lesions

The area of the thumb or fingers will usually develop lesions.

Tenderness

Skin of affected area becomes tender and causes severe pain. Some individuals can also experience a tingling and burning sensation. Those suffering with this disease will find it extremely hard to perform normal daily activities.

Swelling of lymph nodes

Some individuals may suffer as well from painful and swollen lymph nodes located under their arms.

Fever

Cases of this disease that are severe can result in high grade fever. But these cases are extremely rare.

Herpetic Whitlow Causes

This infection is mainly caused by an infection with HSV 1 or HSV 2. These are viruses that mainly are found in genital or oral secretions. Workers in healthcare as well as dental workers are exposed constantly to this virus and can suffer from this disease or infection. Individuals with immunity that is low are at risk from this disorder. In those who are HIV patients are susceptible in high percentages.

In those cases of this infection in a child, the signs and symptoms usually develop in children who have mouth herpes symptoms. These children get this infection from sucking the thumb or other fingers. This is when virus from the lips or mouth may then be able to enter through cuts or breaks in the skin of the fingers. This is called “auto inoculation” which also may occur in healthcare workers and dentists who are quite prone to come in contact with individuals who have the virus. Others are mainly thought to be infected by contact with individuals having genital herpes.

In other words, this infection may be contracted by skin to skin contact with a person who is affected or from an infected part of the body of that same individual. When an individual is exposed, symptoms usually develop in two to twenty days. The individual will have a tingling or burning sensation in the finger together with pain. After about 10 to 12 days, the finger will become inflamed, red and tender. Tiny blisters will develop on the finger. The blisters normally are found to develop in clusters forming a red base. These blisters do heal by themselves usually within 2 weeks. Some individuals might also develop some added symptoms such as fever or swollen lymph nodes under the arm.

Most of all, the individuals will have intense pain caused by the lesions. Once the symptoms are gone, the virus remains but is inactive. The infection developing again is not that common but there are some cases where the virus is triggered by other factors and causes a renewed infection.

Herpetic Whitlow Treatment

Most infections by herpes simplex are quite easy for your physician to diagnose. But there are occasions, where a swab from the skin that is infected might need to be tested in the lab by viral culture that takes several days to grow. Tests of the blood might also be taken.

These infections when left untreated normally go away on their own, but drugs can lessen the symptoms as well as shorten the duration of any outbreaks. There is no cure for infections from herpes simplex virus.

Even though herpetic whitlow symptoms eventually leave on their own, your primary care physician usually advises prescription medications known as antivirals to help with symptom relief and to stop any infection from spreading to other individuals. These include: valacyclovir pills, acyclovir pills, famciclovir pills and topical acyclovir ointment. These drugs normally take seven to fourteen days.

When this infection is more severe it may need oral antibiotic pills especially of the area is also infected by a bacterium.

Though rare, this infection can return and may be treated with the same oral antiviral drugs.

Individuals who have early signs or prodromes prior to infections recurring might benefit from treatment episodically by starting medication after the onset of burning and tingling before the appearance of any sores or blisters. Other rare complications can be recurrent outbreaks which are so very frequent or severe enough to call for suppression therapy, where medications are given every day so as to decrease the severity or frequency of attacks.

Is Herpetic Whitlow Contagious?

Any infection with HSV is quite contagious and is spread easily by making contact with skin lesions that are infected. HSV infections normally appear as tiny sores or blisters around the nose, mouth, buttocks as well as genitals, though these infections may develop almost any place on skin. These tender sores also can recur from time to time in the exact same areas.

Herpetic Whitlow Pictures

Pictures, Images and Photos of Herpetic Whitlow…

   Herpetic Whitlow

Herpetic Whitlow Pictures

source: medicaltrash.com

Herpetic Whitlow on thumb

source: drhull.com

Herpetic Whitlow Photos

source: uiowa.edu

Herpetic Whitlow Images

Source: your-doctor.net

“Acute herpetic stomatitis (cold)”, by dentist O. Korobeynikova

Cases of a patient with a cold on the lips in the dental chair are quite common. As a rule, the doctor in such cases postpones dental treatment if there is no acute pain, since the herpes simplex virus without treatment can further spread in the oral cavity, penetrate into the lymph nodes, then into the blood and internal organs, the brain. This can cause herpetic bronchitis, pneumonia, and other infectious diseases.

What is herpes?

Herpes simplex, synonym – blister lichen. Herpes simplex often affects the skin. After the incubation period (3-4 days), bubbles with a diameter of 0.1-0.3 cm appear on the skin against the background of a limited, slightly edematous pink spot. Before the rash, patients feel a burning sensation and itching of the skin at the site of the future rash. In the future, the vesicles are opened, forming erosive surfaces covered with a white bloom in the form of aft, which heal without scars after 6-8 days.

The usual localization is the skin of the face: the circumference of the mouth, the red border of the lips, nose, less often the skin of the cheeks, eyelids, auricles. Often, skin rashes are accompanied by an increase in body temperature up to 38-39 ° C and symptoms of general intoxication.

Diseases caused by the herpes simplex virus are divided into primary and secondary (recurrent) herpes infection.

Primary herpes infection usually occurs when a person first comes into contact with the herpes simplex virus.This most often occurs in early childhood under 5 years of age. Usually, in 80-90% of the initially infected, the disease proceeds in a latent form, in 10-20% of those infected there are clinical manifestations in the form of a general infectious syndrome with fever and other signs of intoxication. Primary herpes can be manifested by lesions of the skin and mucous membranes, including the conjunctiva or cornea of ​​the eye.

Secondary (recurrent) herpes infection occurs at any age after primary herpes.It proceeds with a mild general infectious syndrome and, as a rule, against a background of diseases that reduce immunity: somatic diseases and other infectious diseases, as well as under the influence of a number of adverse factors: hypothermia, overheating, UV radiation, endocrine changes, emotional stress.

Herpes simplex relapses can occur with varying frequency. If they appear once every few years, the rash is moderate and fixed in the same place, then this is a good prognostic sign.If relapses occur more often, then this indicates a defect in the immune system and the need for its correction.

There are three degrees of severity of the disease with acute herpetic stomatitis – mild, moderate and severe.

At mild severity there are no symptoms of intoxication of the body. Formed aphthae quickly epithelialize, there are usually no new lesions.

Average severity proceeds with symptoms of severe intoxication – an increase in body temperature to 38-39 ° C, malaise, weakness, lack of appetite, nausea.On the edematous, hyperemic mucous membrane of the mouth, there are single or grouped aphthae. Intense salivation, soreness and enlargement of regional lymph nodes appear. Recovery occurs in 2-3 weeks.

Severe form of the disease is characterized by all signs of intoxication, adynamia, headache, nausea, vomiting. The body temperature rises to 38-39 ° C. The mucous membrane of the mouth is hyperemic, edematous, covered with a large number of aphthous elements, which can merge, forming large erosions.Lips, mucous membrane of the cheeks, hard and soft palate, tongue, gingival margin are affected. With insufficient care of the oral cavity, catarrhal gingivitis turns into ulcerative, and with the addition of fusospirochetous microflora, a transition to necrotizing gingivostomatitis is possible.

Herpes treatment

Treatment of viral (herpes) infection should be comprehensive.

General treatment. From the moment the first clinical signs of the disease appear, antiviral therapy is carried out: lubrication of the red border of the lips and skin around the mouth with antiviral ointments (0.25-0.5% bonafton, 0.5% florenal, 5% acyclovir, 1% alpisarin , 1% helepinic and others) 3-4 times a day for 5-7 days.

immunomodulatory drugs are prescribed: viferon, kipferon 1500 IU in rectal suppositories every 12 hours for 10 days, reaferon, imudon.

Reaferon is a recombinant interferon. The effectiveness of the drug increases in combination with antioxidants: vitamin A – retinol acetate, E – tocopherol and C – ascorbic acid.

The therapeutic effect of Imudon is directed against the main symptoms of inflammation: pain, erythema, edema, ulceration, bleeding.Imudon regulates local immunity, enhances salivation, reduces the viscosity of saliva – creates optimal conditions for the regeneration of the oral mucosa. Imudon tablets must be kept in the oral cavity until they are completely absorbed. Imudon is used in 6-8 sublingual tablets per day for 14-21 days.

The general treatment plan should include desensitizing therapy: suprastin, pipolfen, tavegil, fenkarol and others, 1 tablet 2 times a day for 5-10 days.30% sodium thiosulfate solution, 10 ml intravenously, slowly, every other day, for a course of treatment – 5-10 injections (the drug has a powerful anti-inflammatory, hyposensitizing and anti-toxic effect).

Complex vitamin preparations containing vitamins A, E, C, P and microelements (triovit, duovit, komplivit and others) should be taken in therapeutic doses 1-2 times a day for 2-3 weeks.

Local treatment should be aimed at relieving pain and regenerating lesions.In order to anesthetize the mucous membrane of the mouth and lips, 1% pyromecaine ointment is used; 0.5-1% solutions of anesthetics (novocaine, lidocaine, pyromecaine) in the form of applications or oral baths for 5 minutes; 10% aerosol lidocaine; 5-10% solution of anesthesin in peach oil. From modern drugs that have analgesic and at the same time inhibiting inflammation, you can use the Tantum Verde aerosol. Tantum Verde liquid is also used – a 0.15% solution for rinsing the mouth (15 ml).

To improve metabolic processes in the affected tissues and to accelerate the epithelialization of erosion, during the period of extinction of rashes, keratoplastic preparations are prescribed: rosehip and sea buckthorn oil, carotolin, vitamin A oil solution, ointment and solcoseryl gel.

From the first day of treatment of a patient with herpetic eruptions on the oral mucosa and red border of the lips and until the complete epithelialization of erosion is completed, physiotherapeutic treatment is used – laser therapy (has an anti-inflammatory, anti-edema effect, normalizes microcirculation, has an analgesic and bactericidal, bacteriostatic effect , stimulates metabolism and accelerates regeneration).

Due to the fact that herpetic eruptions are accompanied by symptoms of severe intoxication of the body, attention is paid to the introduction of a large amount of liquid, rational nutrition (crushed, high-calorie, fortified, non-irritating diet).

To prevent secondary infection, prescribe antiseptic rinses or oral baths for 15 minutes (1% hydrogen peroxide solution, 0.05% chlorhexidine, 0.01% miramistin) 4-5 times a day for 5 days.

Herpes viruses and how they are treated

Moreover, the same cytomegalovirus can threaten you with an autoimmune disease without additional stimulation. A publication in one of the most cited medical journals, The Lancet, indicates that cytomegalovirus is associated with type 1 diabetes. There are also reports that herpes viruses can contribute to the development of Guillain-Barré syndrome, in which muscle weakness occurs in patients due to autoimmune inflammatory processes.And this is not a complete list.

It is extremely rare for the Epstein-Barr virus to become chronically active, that is, to cause “lifelong” infectious mononucleosis. But even in such cases, according to research by immunologists, the amount of immunoglobulins in the body may soon increase, since the virus forces the cells to multiply, in which its lysogenic cycle passes. But it is B-lymphocytes that produce these same immunoglobulins. Why add them additionally is not entirely clear.

Interferons are not so diverse (although still enough) and cannot be personal guards for each type of viruses and bacteria, like antibodies. Rather, their function is to activate the immune system, calling on cells to defend themselves when an enemy is detected in the body. Thanks to them, various cells of the immune system come to full alert, and “civilians” begin to more actively show the pieces of proteins found inside, so that the presence of the enemy is easier to detect. But the body of a person who does not suffer from immunodeficiency produces all these substances in abundance on its own.Treating everything with them will not work, since the immune system is complex and delicate. Keeping your inner army in a state of incessant aggression is not the wisest decision to maintain peace and tranquility in the body.

In addition, according to a review in the Annual Review of Microbiology, many human herpes viruses successfully suppress the work of our interferons against themselves, so you can hardly influence them in any way.

On the other hand, immunotherapy can be effective against cancer and other complications caused by herpes viruses.However, it is important here which antibodies we use, because each antibody is aimed at a specific pathogen. With interferons, everything is also not easy, and although immune therapy promises a great future (especially in oncology), scientists have not yet fully figured out how to use such a powerful weapon. Therefore, in the fight against herpes viruses, it is easier to hope for the emergence of new vaccines than for an early complete cure and for packs of various “-ferons” that have become so popular in the CIS countries.

Our advice cannot be equated with a doctor’s prescription.Before you start taking this or that drug, be sure to consult with a specialist.

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DEVIRS®

INN:

ribavirin
Today ribavirin has the broadest spectrum of direct antiviral activity against most RNA and DNA viruses. DNA viruses, especially herpes simplex virus, are most sensitive to ribavirin.

Release form:

cream 7.5% for external use 15g.
VERTEX launched a new form of ribavirin on the market, which has no analogue in Russia – in the form of a cream for external use DEVIRS ^® .

Indications for use:

• Infections of the skin and mucous membranes caused by herpes simplex viruses type 1 and 2, including genital herpes;
• herpes zoster (as part of complex therapy).

Application of DEVIRS ^® for genital herpes reduces clinical manifestations in the lesion focus, accelerates epithelization and shortens the duration of virus isolation from the focus.Devirs inhibits the replication of new viruses, which reduces the viral load, selectively inhibits the synthesis of the viral genome, without suppressing DNA synthesis in normally functioning cells. It is important that DEVIRS ^® , providing a powerful antiviral effect in the lesion focus, does not have a resorptive effect.

Adding DEVIRS

^® to the treatment of a genital herpes episode provides the following benefits:

• Synergistic effect against the pathogen;
• overcoming resistance to systemic therapy;
• rapid relief of relapse;
• reduction of treatment time.

Pharmacy dispensing form:

on prescription.

CONTRAINDICATIONS ARE AVAILABLE, BEFORE USING
CONSULT A SPECIALIST

Trade name:

Devirs ^®

International non-proprietary name:

ribavirin

Dosage form:

cream for external use.

Ingredients:

100 g cream contain:

Active substance: ribavirin 7.5 g.

Excipients: glyceryl monostearate (glycerol monostearate 40-45) – 2.0 g, macrogol 6 cetostearyl alcohol ether (macrogol 6 cetostearyl ether) – 1.5 g, macrogol 25 cetostearyl alcohol ether (macrogol 25 cetostearyl ether) – 1.5 g, cetostearyl alcohol – 5.0 g, liquid paraffin (liquid paraffin) – 5.0 g, methyl parahydroxybenzoate (methylhydroxybenzoate, methylparaben, nipagin) – 0.1 g, propyl parahydroxybenzoate (propylhydroxybenzoate, propylparaben) – 0.02 gipazol purified water – up to 100.0 g.

Description:

Homogeneous cream of white or off-white color.

Pharmacotherapeutic group:

antiviral agent.

ATX code:

D06BB

Pharmacological properties:

Ribavirin triphosphate (RTP) is a potent inhibitor of inosine monophosphate dehydrogenase (IMP dehydrogenase), viral RNA polymerase and viral mRNA guanylyltransferase. Inhibition of the latter stops mRNA capping, which leads to a significant depletion of intracellular reserves of guanosine triphosphate and inhibition of viral RNA and protein synthesis.Ribavirin is also incorporated into the viral genome, causing lethal mutations, with a subsequent decrease in the pathogenicity of the virus. Ribavirin inhibits the replication of new virions, which reduces the viral load, selectively inhibits the synthesis of viral RNA, without suppressing the synthesis of RNA in normally functioning cells. DNA viruses most sensitive to ribavirin are herpes simplex virus, adenoviruses, CMV, smallpox viruses, Marek’s disease; RNA viruses – influenza A, B viruses, paramyxoviruses (parainfluenza, mumps, Newcastle disease), reoviruses, arenaviruses (Lassa fever virus, Bolivian hemorrhagic fever), Bunyaviruses (Rift Valley fever virus, Crimean-Congo haemorrhagic fever virus) (hemorrhagic fever virus with renal or pulmonary syndrome), oncogenic RNA viruses.DNA viruses insensitive to ribavirin: Varicella zoster, pseudo-rabies virus, natural vaccinia; RNA viruses: enteroviruses, rhinoviruses, Semliki forest encephalitis virus.

Pharmacokinetics

When applied to the skin and topically, systemic absorption is minimal and practically insignificant.

Indications for use:

The cream can be used both as monotherapy and in combination with other medicinal forms of ribavirin intended for parenteral and oral administration in the following diseases:

one.Infections of the skin and mucous membranes caused by Herpes simplex viruses of types 1 and 2, of various localization, including in the genital area.

2. Herpes zoster (as part of complex therapy).

Contraindications:

Hypersensitivity to ribavirin or other components of the drug, pregnancy, lactation, children and adolescents (up to 18 years).

With care:

Renal failure.Use with caution in women and men of reproductive age.

Application during pregnancy and lactation:

The use of the cream during pregnancy and lactation is contraindicated.

Method of administration and dosage:

Externally, apply to the affected areas of the skin and mucous membrane (previously washed and dried) in an even thin layer, rubbing gently.

Apply 5 times a day until the symptoms of the disease disappear completely.If there is no improvement within 8 days of using the drug, stop taking it and consult a doctor.

For best results, treatment should be started as early as possible when symptoms first appear.

In the event that Devirs cream is prescribed in combination with one of the dosage forms of ribavirin for oral or intravenous administration, the dose of the cream should be reduced.

Side effects:

Allergic reactions are possible (skin rash, urticaria, exanthema).Others: hair loss, changes in the content of thyroid-stimulating hormone (TSH), symptoms of autoimmune diseases (extremely rare).

The observed effects, as a rule, are reversible, do not affect the effectiveness of treatment, and stop after the end of treatment.

Interaction with other medicinal products:

Not found.

Special instructions:

Do not use to treat ophthalmic herpes, do not apply to eye area.The drug should be used with extreme caution in patients with renal insufficiency.

Men and women of childbearing age during treatment and within 7 months after the end of therapy should use effective contraceptives.

Release form:

Cream for external use 7.5%.

5 g, 15 g or 30 g in aluminum tubes. Each tube, together with instructions for use, is placed in a cardboard box.

Storage conditions:

Store in a dry place, out of the reach of children, at a temperature not exceeding 25 ° C.

Expiry date:

2 years. Do not use after the expiration date.

Vacation conditions:

Available on prescription.

Manufacturer / entity accepting claims:

ZAO Vertex, Russia

Legal address: 196135, St. Petersburg, st. Tipanova, 8-100.Manufacturing / address for filing consumer claims:

199026, St. Petersburg, V.O., 24 line, 27-a.

Tel./fax: (812) 322-76-38.

CONTRAINDICATIONS ARE AVAILABLE, BEFORE USING
CONSULT A SPECIALIST

Genital herpes – symptoms, diagnosis, treatment methods.

Primary infection is when the virus first enters the body, and a person has not yet developed antibodies to it.This can manifest itself both with new-onset rashes on the body, and asymptomatic, which happens most often. External manifestations of primary infection with the virus continue up to 14-22 days with an increase in symptoms in the first week. The disease can last for quite a long time, it can affect not only the genitals, and be accompanied by general and local / local symptoms. Common symptoms include fever, headache, malaise, and myalgia. Localized symptoms include pain, painful urination, itching, and discharge (from the vagina or urethra).Symptoms may gradually disappear up to 2–3 weeks. Sometimes a more complex course of HSV may occur, which requires hospitalization (severe aseptic meningitis, disseminated infection, etc.). In such cases, the course of the disease can be delayed up to 1.5 months.

Non-primary infection is observed in people who have already encountered the virus and who have antibodies to it. In these patients, the disease, as a rule, proceeds with less pronounced symptoms: the duration of which is about 15 days.Sometimes, the virus can be shed asymptomatically, and the course of the disease lasts 7-8 days.

Recurrent infection is detected in those patients who have both symptoms of genital herpes and antibodies to the reactivated type of the virus. The course of relapse can also be asymptomatic, and therefore, HSV can be diagnosed by performing specific research methods. The severity and duration of the course of the disease with relapse is even less than with the above forms of genital infection, and is only 2-3 days.Recurrence with HSV type 2 occurs more often than with HSV type 1. The frequency and nature of the appearance in patients can be quite different and affect the state of health.

Causes of activation and / or recurrence of HSV:

• decreased immunity;
• hypothermia, or vice versa, overheating of the body.
• stress and some physiological conditions of the body .;
• medical manipulations / surgical interventions.
• intercurrent diseases (an acute disease that has joined already existing chronic ones, for example: a secondary infection).

The first manifestation of herpesvirus infection, as a rule, manifests itself more violently than subsequent relapses. In some patients, they are short-lived. Most of those infected have no symptoms of genital herpes.

HSV affects the skin and mucous membranes (most often on the face and genitals), the central nervous system, causing meningitis, encephalitis, eyes (conjunctivitis, keratitis).Also, HSV can provoke a pathological course during pregnancy and childbirth, and cause a frozen pregnancy, spontaneous miscarriage, developmental anomalies and / or death of the fetus, generalized damage by the causative agent of the virus in all organs and systems of the newborn. There has been a link between cervical cancer in women and prostate cancer in men. HSV, like some other herpes viruses, is capable of a latent process, which is subsequently reactivated and can cause permanent exacerbations of the disease and asymptomatic virus shedding.

Routes of transmission of HSV

Airborne. Contact and household. Through non-sterile instruments, personal hygiene products (razors, etc.). Sexually. The vertical route of transmission of the virus (from mother to fetus). The disease is transmitted mainly sexually, regardless of the form of intimacy (genital, oral, anal) from a patient with genital herpes or a carrier of the virus. Infection can occur when the partner who is the source of the infection has a relapse of the disease or, which is especially important, when he sheds the virus without having clinical symptoms.Sometimes, HSV can infect individuals who do not have active manifestations of the virus at the time of intercourse or even episodes of virus activation, and therefore do not even know that they are infected. The likelihood of infection by household means through personal hygiene products is not excluded. HSV is introduced into the body through the skin mucous membranes, after which it is captured with the help of viral receptors by sensory nerve endings. Herpes destructively affects the patient’s immune system and, therefore, becomes the cause of secondary immunodeficiency.Recurrences of HSV disrupt the patient’s full sex life, and are often the cause of neuropsychic and psychological disorders. Manifestations on the mucous membrane and skin are the most frequent manifestations of the disease, and infection with genital herpes is one of the most common sexually transmitted diseases.

The risk of infection of a baby during pregnancy and childbirth depends on many factors, and can reach 75% of the probability. Intrauterine infection with HSV-2 is less common.In the overwhelming majority of cases, infection of a newborn occurs during childbirth when the baby passes through the mother’s birth canal. Moreover, the transmission of infection is possible both in the presence of lesions in the cervix and vulva, and in the case of asymptomatic virus isolation. When the virus is released during pregnancy, it can cause fetal death, causing frozen / undeveloped pregnancies and provoke miscarriages, both in the early and late periods of gestation. HSV ranks second after rubella virus in fetal anomalies.Possible infection of the newborn after childbirth, with an active manifestation in the woman in labor and honey. staff, but this is extremely rare.

Symptoms

Typical localization in women: on the labia majora and small labia, on the vulva, clitoris, in the vagina, and on the cervix, and also often on the perianal region, and the buttocks. In men, these are the glans penis, foreskin and urethra.

There are several forms of recurrent genital herpes:

1. The manifest form of recurrent herpes is characterized by the presence of herpetic elements in the lesion.Typical manifestations of the disease are vesicles, erosion, ulcers, exudation, recurrent nature of the disease. Some patients with genital herpes complain of general malaise throughout the body, headaches, fever up to subfebrile values, some have disturbed sleep, as well as anxiety and irritability. As a rule, at the stage of development of the disease, patients note a burning sensation, itching, “irritation and” tickling “, pain in the genital area. The affected area becomes somewhat edematous, turns red, and then, there are single or multiple small vesicles up to 2-3 mm.The contents of these vesicles are initially transparent, then cloudy and become purulent. Within a few days, the bubbles empty, dry out, crusts form, which gradually disappear, and spots remain in the place of these rashes for several days, and subsequently disappear altogether.
2. Atypical form occurs in the form of swelling and itching. The affected area is represented by deep recurrent cracks in the skin, mucous membrane of the genitals and underlying soft tissues, which heal in 4-5 days.
3. The abortive form of herpes most often occurs in patients who have already received antiviral drugs and vaccine therapy. Herpetic lesions in this form of herpes bypass the stages associated with the manifest form, and can manifest itself in the form of itchy spots or papules, which resolve on their own within 1-3 days. Abortive forms of herpes include: erythematous, papular, and prurigoneurotic, in which there are no vesicular elements. Diagnosis of varieties of genital herpes, flowing in an erased abortive form, sometimes causes great difficulties.The disease is usually recognized when typical recurrences of herpes alternate with rashes or occur simultaneously with them.
4. The subclinical form of genital herpes is mainly detected during examination of persons with STDs (sexually transmitted diseases), or in married couples with impaired reproductive functions. This form is characterized by “microsymptomatics” (short-term appearance of mild, superficial cracks, accompanied by slight itching), or the complete absence of any external manifestations.

Depending on the location and severity in patients with genital herpes, three stages are conditionally divided:

• Stage 1 – damage to the external genital organs.
• Stage 2 – herpetic colpitis, cervicitis, urethritis.
• Stage 3 – herpetic endometritis (infection with the virus of the uterine mucosa), salpingitis (damage to the fallopian tubes) or cystitis (inflammation of the bladder).

Herpetic vesicles form characteristic polycyclic scalloped shapes.Subsequently, superficial ulcers covered with a grayish bloom are formed, according to the number of former bubbles, or continuous erosion with a smooth bottom and not undermined edges, surrounded by a bright red rim. The sores are neither deep nor bleeding. Herpetic ulceration is sometimes very painful. Ulcers and erosions heal without scarring. Herpetic eruptions on the labia minora and vulva in women, in some cases, cause significant swelling of the labia. With herpetic cervicitis, the cervix is ​​swollen, often with erosion.Relapses occur either spontaneously, or after sexual intercourse, or before and after menstruation. Often the appearance of herpes of the genitals is provoked by other infections. Recurrent herpetic infection can be localized not only in the area of ​​the external genital organs, but also, affect the mucous membrane of the vagina, cervix and ascending through the mucous membrane of the uterus, fallopian tubes, mucous membrane of the urethra and bladder, and cause a specific lesion in them.

The clinical picture of lesions by the herpes virus in men appears most often in the form of small bubbles, and the formation of superficial ulcers on the head of the penis, foreskin, and groove area.The course of the disease is characterized by recurrent episodes. Complaints with herpetic urethritis in men begin with the appearance of pain, with irradiation to the scrotum, penis, urethra, legs, buttocks, perineum, burning sensation in the urethra. Patients also note these complaints during urination, the appearance of light or yellowish discharge from the urethra, redness and swelling in the area of ​​the urethral opening. At the stage of erosion healing, erythematous or pigmented spots are visualized at this site. The chronic course of recurrent balanoposthitis is detected in most patients with herpes.

Infection with a genital infection caused by HSV, in some patients provokes psychological and even psychosexual disorders, in the form of embarrassment, fear of sexual intercourse, depression, loss of self-confidence, mental trauma, anger, decreased self-esteem, loss of self-esteem, increased anxiety, negative emotions, hostility and even aggressiveness towards the source of infection. Many, for fear of rejection, hide information about the presence of genital herpes.Women perceive and transfer this news more emotionally, due to the psychological characteristics of the weaker sex. Moreover, those patients who first encountered genital herpes have deeper psychological problems than with other sexually transmitted diseases. Frequent exacerbations, and pronounced manifestations of the disease can affect his behavior and even change the character of the patient.

Insidious complications of herpes simplex (PHOTOS)

BAKU / Trend / – Herpes simplex is one of the most common diseases of herpes infection, the causative agent of which is the herpes simplex virus (HSV).The causative agent of herpes is one of those viruses that once invaded the body, remain in it forever. The source of HSV is a sick person or a virus carrier (there are no external manifestations of the disease, but the virus is excreted in saliva, urine, and secretions of the genitourinary system). The virus is transmitted by contact, airborne droplets, blood transfusions and organ transplants. During pregnancy, infection of the fetus can occur through the transplacental route (through the placenta) and during childbirth.

The classic symptom of in herpes is one: a rash of vesicles on the skin and mucous membranes.Bubbles appear in small, concentrated clusters. The disease also has warning signs: itching, burning sensation, slight tingling sensation around the mouth or genitals. But practically no one pays attention to them, although at this stage treatment can give the maximum effect. Further, the disease begins to manifest itself by the development of the inflammatory process. A slight swelling appears, which grows quite rapidly. The swelling turns into blisters with a clear liquid content.They burst and the liquid, in which millions of viral particles, flows out. Ulcers form at the site of the blisters. The sores dry up and turn into scabs, which can bleed and hurt a lot.

Complications of HSV . In people with weakened immune systems, HSV infections can lead to the growth and development of sores that take weeks to heal. The infection can progress inside the body to the esophagus, lungs, brain, tissues covering the brain and spinal cord (meninges), or the colon.Ulcers in the esophagus can be painful when swallowing, and an infection in the lungs can lead to pneumonia with cough and shortness of breath. HSV can also affect the cornea of ​​the eyes, causing significant vision loss. Children and adults with a skin condition called atopic eczema can develop a deadly infection of the skin area affected by the eczema (herpetic eczema) from the HSV virus. Rarely, during pregnancy, the HSV virus is transmitted from mother to child (called neonatal herpes).HSV infection is difficult for children. Newborns may have a general infection, brain damage, or skin damage. If untreated, about 85% die with generalized disease and about half with a brain infection.

Measures to combat HSV . There are currently no drugs that can kill HSV. However, antiviral drugs such as acyclovir, valacyclovir, or famciclovir can reduce discomfort and help manage symptoms. Treatment is most effective when started early, usually within the first few hours after symptoms start – best when tingling or discomfort occurs, before blistering occurs.Due to the fact that most people on the planet are carriers of the herpes virus, the main task of preventing the disease is not to prevent infection, but to prevent the development of the disease. A strong immune system copes with this task. To maintain it in this state, you need to adhere to a few simple rules: give up bad habits, eat well, alternate loads and rest in reasonable proportions, avoid stress, overheating and hypothermia.

The presented material was compiled by summarizing, translating and systematizing information from various sources, including popular science articles, materials from the Internet, official reports, etc.etc. When using the material, reference to the website www.aptekonline.az is required.

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Herpesvirus eye disease in cats

One of the most common ophthalmic problems in cats is eye damage from herpesvirus infection (viral rhinotracheitis).

Herpesvirus infects cells of the epithelium of the conjunctiva and upper respiratory tract, causes cell necrosis and inflammation of the mucous membranes, accompanied by discharge from the eyes, nose, blepharospasm, sneezing, coughing.

Infection occurs through contact with secretions from the eyes and nose of sick cats.

In addition to epithelial cells, the virus multiplies and persists for life in the trigeminal ganglion, which determines the long-term carrier of viruses.

Thus, once having met the herpes virus, the cat continues to be a carrier for almost life, while the cat does not get sick clinically, except for periods of decreased immunity (pregnancy, lactation, crowded animals, concomitant systemic diseases, stress).

Clinical manifestations of herpesvirus infection

Acute form herpesvirus infection occurs mainly in kittens at the age of 8-12 weeks, faced with the virus for the first time.Most often these are kittens that were in poor conditions: shelters, catteries with an abundance of cats, outdoor conditions.

Typical symptoms of eye damage: blepharospasm, hyperemia and edema of the conjunctiva, serous discharge from the conjunctival sac, gradually replaced by mucous and mucopurulent (due to complications of secondary microflora). With damage to the conjunctiva, rapid and extensive necrosis of the epithelium occurs, with the formation of diphtheria films and conjunctival adhesions (Figure 1).

Corneal lesions – dendritic (treelike) ulcers are pathognomonic (specific) signs of herpesvirus infection; fluorescein staining of the cornea is used to detect them (Figure 2).

In most cases, herpesvirus infection is complicated by secondary microflora, which can lead to melting of the cornea, deep, sometimes perforated ulcers with iris prolapse occur, and panophthalmitis, secondary glaucoma or subatrophy of the eyeball may develop later.The aggressive course of herpesvirus infection is the main reason for the loss of the eyeball in kittens.

In addition to ophthalmological signs, sneezing, nasal discharge, coughing, and fever are observed.

The immune system of cats can fight the herpes virus with subsequent self-healing, and clinical signs gradually disappear after 2-3 weeks. It is possible to reduce the risk of complications of the acute form of diseases (adhesions of the conjunctiva, melting and perforation of the cornea) with adequate and timely therapy.

Exacerbations in chronic course

In cats that have previously had a herpesvirus infection, repeated eye lesions occur as a result of the reactivation of a latent virus. Any stress factors can cause recurrence: animal transport, vaccination, pregnancy, lactation, corticosteroid treatment. Unlike the initial infection, the signs of upper respiratory tract involvement are insignificant; in many cases, slight conjunctival hyperemia and periodic discharge from the conjunctival sac are the only clinical signs.

Lesions associated with recurrent infection manifest themselves in different ways: conjunctivitis, dendritic corneal ulcers, chronic corneal erosion, stromal keratitis (Figure 3. Vascular keratitis and bullae in the central cornea in a cat). There is evidence that diseases such as corneal sequestration and eosinophilic keratitis may also be associated with herpesvirus.

Diagnostics

The basis for the diagnosis is clinical and pathognomonic signs.Laboratory diagnostics carried out using PCR is not 100% reliable, false-positive and false-negative data are not uncommon.

Treatment

Treatment consists of specific antiherpetic treatment and supportive therapy.

For specific local treatment, there are several types of eye drops (trifluridine, idoxuridine, cidofovir), their availability on the market for veterinary drugs is low, moreover, topical agents must be used up to 8 times a day, they can also irritate the conjunctiva and cornea, all this does these drugs are rarely used in veterinary medicine.

For specific systemic antiherpetic treatment, famciclovir tablets are used, since this substance is effective and safe for cats, the drug is given orally for 1-3 weeks.

Supportive therapy includes broad-spectrum antibiotics locally (in the conjunctival sac) and systemically to combat secondary microflora. There is conflicting information about the effectiveness of dietary supplements (L-lysine) in herpesvirus.

The intensity and duration of treatment for herpesvirus depends on the severity of the disease and can vary from 7 to 21 days.

Prevention

Vaccination of cats against the herpes virus allows you to maintain the level of active antibodies in the blood of cats and reduce the intensity of clinical signs of the disease upon contact with a sick animal or with a decrease in the body’s own resistance. After the first contact with the herpes virus, the animal remains in most cases a lifelong carrier of the virus.Viral shedding episodes of clinical signs are less common in vaccinated cats.

Consequences of herpesvirus infection

Simblefaron – fusion of the conjunctiva of the eyelids with the conjunctiva of the eyeball or cornea – the most frequent complication of herpesvirus infection, it does not progress, most often does not bother the animal and does not require treatment. Simblefaron can vary in size and location, with a small size it can be an accidental finding during a routine examination, or, in the case of extensive stratification of the conjunctiva on the cornea, it can be a cosmetic defect and an obstruction to the animal’s vision.In the case of severe visual impairment with simblefaron, a veterinarian ophthalmologist considers surgical options for treatment. However, it is not enough just to cut off the conjunctiva attached to the cornea; it will grow back due to the deficiency of corneal stem cells destroyed by the herpesvirus. An effective method of treatment being developed is considered to be the transplantation of donor limbus sections (the place of transition of the sclera into the cornea), which produce normal corneal epithelium, which prevents the re-growth of the conjunctiva.

Anterior synechiae – adhesions of the iris and cornea that occur after perforated corneal ulcers in animals that have not received treatment during the acute period of the disease, and if the eye has survived a through defect without subsequent panophthalmitis or glaucoma, then most often the anterior synechiae do not bother the animal and do not require treatment ( Figure 4).

Obstruction of the nasolacrimal canal due to adhesions of the mucous membrane of the nasolacrimal canal or closure of the lacrimal openings with sections of simblepharon, accompanied by lacrimation.The solution to this problem is to create an additional pathway for the outflow of tears; there are several surgical methods with varying degrees of effectiveness.

It is important to remember that herpesvirus infection is a serious disease that brings significant discomfort to the animal and entails many complications up to the loss of the eyeball, therefore it is necessary to take a responsible attitude to blepharospasm, redness of the eyes, discharge from the eyes, especially in small kittens, and avoid crowding cats.

Human herpes virus type 6 in children and adults

Human herpes virus type 6 (VG6) is an infection that is no less common than herpes viruses of types 1 and 2 known to many. At first, this virus remained a “disease-free virus” for a long time, but recently its possible role as a cause of many human diseases has been increasingly discussed.

How the herpes virus type 6 is transmitted:

1. The source of infection are patients with obvious clinical signs of the disease and carriers of VH6.
2. The leading transmission route is airborne, contact-household (less often).
3. Sexual transmission of the virus is also possible, through transfusion of infected blood and transplantation of organs and tissues from infected donors.
4. Possible vertical transmission of the virus from an infected mother to her fetus, both during pregnancy and after childbirth.
5. The virus can even be transmitted through saliva.

Symptoms and conditions that should alert you and force you to see a doctor:

• increased body temperature and the appearance of a pink maculopapular rash on the skin;
• blistering skin rashes;
• enlarged lymph nodes;
• immunodeficiency states.

Symptoms of HB6 in children

In young children (0.5-3 years old), HB6 infection may be evidenced by the development of sudden erythema, which makes itself felt by an increase in body temperature up to 40 ° C. In this case, any other symptoms are most often absent.

After the temperature drops, a pink rash appears on the child’s body, which first covers the face, chest and abdomen, and then spreads throughout the body. After the rash appears, the body temperature no longer rises.There may be an increase in lymph nodes.

Baby roseola should not be confused with chickenpox or SARS. The sick child must be isolated until the clinical signs disappear and immediately consult a doctor.