Ocular Herpes

Caused by the type 1 herpes simplex infection, eye herpes (ocular herpes) is a typical, recurrent viral infection impacting the eyes. This type of herpes infection can cause inflammation and scarring of the cornea that sometimes is described as a cold sore on the eye. Herpes of the eye can be transmitted through close contact with an infected person whose virus is active.

Herpetic simplex keratitis, also known as herpetic keratoconjunctivitis and herpesviral keratitis, is a form of keratitis caused by recurrent herpes simplex virus (HSV) infection in the cornea.

The National Eye Institute (NEI) states an estimated 400,000 Americans have experienced some type of ocular herpes, with close to 50,000 brand-new and recurring cases happening each year.

Types of Ocular Herpes

Ranging from a basic infection to a condition that can possibly cause loss of sight, there are a number of types of ocular herpes:

• Herpes keratitis is the most common form of ocular herpes and is a viral corneal infection. Ocular herpes in this kind generally impacts only the leading layer, or the epithelium, of the cornea, and usually heals without scarring.
• Stromal keratitis takes place when the infection goes deeper into the layers of the cornea. This can lead to scarring, loss of vision and, periodically, blindness. Stromal keratitis is thought to be caused by a late immune reaction to the initial infection. Although the condition is rare, the NEI reports that stromal keratitis is the leading reason for corneal scarring that subsequently causes blindness in the United States.
• Iridocyclitis is a serious type of ocular herpes where the iris and surrounding tissues inside the eye ended up being swollen, triggering severe level of sensitivity to light, blurred vision, pain and red eyes. Iridocyclitis is a kind of uveitis that impacts the more frontal portions of the within the eye.

When this infection occurs in the retina or the inside lining of the back of the eye, it is referred to as herpes retinitis.

The source of infection is generally a relative or friend who is quietly shedding virus in the saliva or nasal secretions, or who has an active fever blister. When the infection first gets in the body, typically through the nose or mouth, it travels through the nerves approximately the exact same center, which also sends nerves to the eye. There it goes to sleep in a non-active infection state and may never ever reawaken. Sometimes, the infection does reactivate (stress!) and, instead of taking a trip pull back the nerves to the mouth or nose, it goes to the eye triggering the illness there.

Ocular Herpes Symptoms and Signs

Different symptoms and signs are connected with an ocular herpes outbreak. You may experience swelling of the cornea, which can cause an inflammation or sudden and severe ocular pain. Likewise, the cornea can end up being cloudy, resulting in blurred vision.

Other qualities of ocular herpes include:

• Swelling around the eyes
• Tearing
• Frequent eye infections
• Irritation
• Foreign body experience
• Eye redness
• Eye sores
• Watery eye discharge
• Sensitivity to light

Due to these numerous symptoms, your eye doctor may ignore a preliminary diagnosis of ocular herpes in its really early stages.

What Causes Ocular Herpes?

Ocular herpes is sent through contact with another person who is having a break out, or through self contact and contamination during an active herpes infection (such as a cold sore of the lip).

The herpes simplex infection enters the body through the nose or mouth and takes a trip into the nerves, where it may be non-active. The virus can stay dormant for many years and may never awaken.

The exact cause of an outbreak is unidentified, however stress-related aspects such as fever, sunburn, major dental or surgical procedures and trauma are often connected with occurrences.

Once the preliminary break out occurs, the NEI states without treatment ocular herpes has about a 40-50 percent chance of returning. There is no particular amount of time for ocular herpes to reappear; it might be a number of weeks or even numerous years following the initial incident. Although symptoms typically provide themselves in only one eye, the virus possibly might affect the other eye too.

Treatment for Ocular Herpes

Treatment for ocular herpes depends on where the infection is located in the eye — in the corneal epithelium, corneal stroma, iris, retina, and so on. Some ocular herpes treatments might intensify the outbreak and for that reason must be considered on a case-by-case basis.

If the corneal infection is only shallow, it can generally be relieved using antiviral eye drops or ointments, or oral antiviral tablets.

Zirgan (Sirion Therapeutics, Tampa, Fla.) was approved by the FDA in late 2009 as a topical antiviral treatment for ocular herpes. The treatment (ganciclovir ophthalmic gel, 0.15 percent), which became commercially available in the United States in late April 2010, involves instilling eye drops 5 times daily till the associated corneal ulcer heals.

You ought to not wear contact lenses while undergoing treatment with Zirgan, which is marketed in Europe as Virgan.

An optometrist might treat ocular herpes by scraping away the infected corneal epithelial cells with a cotton swab or corneal “spatula” instrument. This is called debridement. Following debridement, a patch or soft contact lens might be had to help the cornea to recover.

Steroid drops can help decrease swelling and avoid corneal scarring when the infection appears deeper in the corneal layers. Steroid drops are usually used in combination with and simultaneously with antiviral drops.

Steroid drops reduce the efficiency of the eye’s body immune system. Therefore, individuals with a history of ocular herpes should use only a steroid drop specifically prescribed by their eye doctor.

Steroid drops have actually been known to cause a frequent ocular herpes infection in susceptible patients. Also, an antibiotic eye drop along with a therapeutic contact lens might be used to avoid a secondary bacterial infection while the herpes eye infection is being dealt with.

Surgery is required if scarring takes place in the cornea and the treatments consisting of the steroids do not help clear the center of the cornea. In cases where corneal scarring is irreversible, a corneal transplant may restore vision.

Although ocular herpes has no cure, treatment can assist control outbreaks. Studies are underway to figure out better approaches for handling the disease.

As an example, a study reported in the September 2010 issue of Archives of Ophthalmology discovered that treating individuals with oral antiviral medication as a preventive step considerably decreases the possibility that ocular herpes symptoms will repeat.

Which medications in the drug class Antiviral representatives are used in the treatment of Herpes Simplex Virus (HSV) Keratitis?

Antiviral agents

These agents hinder herpes simplex virus (HSV) replication. Treatment of viral infections begins with mechanical debridement of the included rim together with a rim of normal epithelium. This is followed by the topical instillation of antiviral medications (eg, trifluridine, ganciclovir).

Trifluridine ophthalmic option 1% (Viroptic).

A structural analogue of thymidine, this agent prevents viral DNA polymerase. Viroptic has much better penetration through the cornea and greater effectiveness (95% heal rate) than other topical representatives. If no response occurs in 7-14 days, consider other treatments.

Valacyclovir (Valtrex).

Valacyclovir is a prodrug that is rapidly converted to the active drug acyclovir. It produces a higher serum concentration of acyclovir with smaller sized oral dosing. Valacyclovir is more pricey than acyclovir however can be as reliable with an easier dosing routine. The optimum dose for ocular disease has actually not been identified.

Famciclovir (Famvir).

This agent is a prodrug that, when biotransformed into its active metabolite, penciclovir, might hinder viral DNA synthesis/replication. It has actually been used successfully in the suppression of genital herpes. Its effectiveness in HSV keratitis presently is under research study.

Acyclovir (Zovirax).

Acyclovir is a synthetic guanosine analogue that requires activation by viral thymidine kinase. The activated acyclovir triphosphate, focused 50-100 times in HSV-infected cells, reduces viral duplication by preferentially hindering viral DNA polymerase, serving as a DNA chain terminator and inducing irreversible binding in between polymerase enzyme and the interrupted DNA chain.

Acyclovir is a potent inhibitor of viral growth with very little toxicity to uninfected epithelial cells. Oral acyclovir at a dose of 2 g/day for 10 days has actually been reported to be as efficient as topical representatives for epithelial keratitis, with the advantage of no ocular toxicity.

Ganciclovir ophthalmic gel 0.15% (Zirgan, Vitrasert).

This agent is an acyclic nucleoside analogue of 2′ deoxyguanasine. It phosphorylates first to monophosphate form by a viral-encoded protein kinase homologue, and then to diphosphate and triphosphate types by cellular kinases. This permits higher concentration of ganciclovir in virus-infected cells, possibly since of preferential phosphorylation of this agent in infected cells.

Ganciclovir is believed to prevent HSV duplication by competitive inhibition of viral DNA polymerases and by including itself into viral DNA, causing termination of viral DNA elongation. Like acyclovir, ganciclovir is virostatic and applies its result only on duplicating virus.

Questions & Answers

What is the role of keratoplasty in the treatment of herpes simplex virus (HSV) keratitis?

Irregular astigmatism resulting from chronic stromal keratitis may be correctable with stiff, gas-permeable contact lenses. Patients with aesthetically considerable corneal opacities or corneal perforations might require keratoplasty for visual rehab.

Although an unusual event, progressive necrotizing stromal keratitis and impending corneal perforation might be much better handled with tissue glue and plaster contact lens before considering keratoplasty.

If possible, a little descemetocele or perforation in an inflamed eye may at first be managed with tissue adhesive, a plaster contact lens, and/or amniotic membrane hair transplant. Corneal hair transplant need to preferably be deferred up until the eye is less irritated.

The prognosis for an effective graft approaches 80% in eyes without inflammation prior to surgery. Prophylactic oral antiviral treatment following permeating keratoplasty decreases reoccurring ocular HSV disease and graft rejection episodes and enhances graft survival. Many cosmetic surgeons use a systemic antiviral agent (eg, acyclovir 400 mg bid) for a minimum of 6-12 months after penetrating keratoplasty. Interestingly, since recurrent HSV disease is the outcome of reactivation of hidden virus in the nerve ganglion, the rate of disease reoccurrence is not modified after penetrating keratoplasty. Anterior lamellar keratoplasty might be thought about in lieu of penetrating keratoplasty in patients with healthy corneal endothelium.

How is recurrent herpes simplex virus (HSV) keratitis avoided?

The major difficulties in treating herpetic keratitis associate with the propensity for reoccurrences and to the management of stromal disease. In its latent form, HSV can be present in the cells of the cornea and in the central connections of the trigeminal nerve, especially in the trigeminal ganglion. Disruption of host defense leads to reactivation of the virus, its subsequent passage centrifugally along the nerve, and resultant shedding from the nerve endings. Corneal lesions occur when the balance between latency and reactivation is disturbed, such as during febrile health problems, during menses, or on exposure to sunlight. As soon as trigger factors are identified, they need to be prevented.

Using 400 mg of acyclovir one or two times daily as prophylaxis can decrease the occurrence of reoccurrence. This is advised for patients with frequent stromal disease or more than 2 episodes of epithelial disease per year.

Active HSV keratitis is an outright contraindication to laser corneal refractive surgery (ie, LASIK, PRK) or other corneal treatments (collagen cross-linking). Non-active keratitis or a history of previous HSV disease is likewise thought about a relative contraindication. Reoccurrence of HSV keratitis after refractive surgery is a well-known problem. However, case reports have recorded good refractive surgery results in chosen patients whose keratitis has actually been non-active for a minimum of 1 year and in whom perioperative systemic antiviral prophylaxis is used.

What is the function of medications in the treatment of herpes simplex virus (HSV) keratitis?

Topical corticosteroids work in suppressing the inflammatory action of herpetic keratitis. Nevertheless, their inappropriate usage might result in serious epithelial disease or stromal necrosis, corneal perforation, increased propensity toward recurrence, secondary microbial infections, elevation of the intraocular pressure, and lenticular changes.

Patients needing topical corticosteroids for suppression of the inflammatory response generally require the drug for a period of months, and withdrawal typically is made complex by a recurrence of inflammation. The immunosuppressive complications of steroid administration (eg, recurrent epithelial disease) mostly can be avoided by the concurrent administration of antiviral treatment.

Patient cooperation is a requirement for the safe administration of corticosteroids in herpetic keratitis. A very sluggish corticosteroid taper generally is needed.

Antiviral agents, topical or oral, are recommended to hinder viral replication in infected cells. All topical antiviral medications readily available for scientific use in the United States are toxic, with signs of toxicity being similar for all such drugs. Punctate epithelial keratopathy, limbal follicles, a follicular conjunctival reaction, ptosis, punctal stenosis, and contact dermatitis can take place at any time after 10-14 days of treatment.

In moderate cases of antiviral toxicity, epithelial changes may be the only symptom. The poisonous capacity of antiviral representatives constantly must be thought about in patients who recover poorly, because these representatives are inhibitors of cell division.