Varicella zoster virus (VZV), when transmitted to a previously uninfected individual, results into two different patterns of manifestations or syndromes. The initial infection, chickenpox, usually transmitted during the childhood years, is a communicable but usually harmless febrile disease. After this initial infection, the virus particles of chickenpox stay in the dorsal root of the spinal nerves or other sensory ganglion and lay inactive for several years, sometimes even decades.
Because of the effects of aging in the body, an individual tends to have a weakened immune system; becoming more at risk to the development of illnesses, emotional or psychological stress, and side effects of certain medical treatments. This vulnerability to certain factors results into a decreased response of the virus-specific, cell-mediated immune system. In these specific circumstances, the inactive VZV residing in the dorsal roots become reactivated and develops in the form of localized skin rashes coming out in a dermatome. This development is called herpes zoster (HZ) or shingles. In the event that the virus resided in the ophthalmic branches and trigeminal nerve and becomes reactivated, the disease is now termed as herpes zoster ophthalmicus (HZO).
History of Herpes Zoster Ophthalmicus
Several centuries ago, herpes zoster ophthalmicus (HZO) was already described by the famous Greek philosopher Hippocrates. But, it was not that long ago, during the actualization of modern medical tools when HZO was related to VZV; such as the utilization of immuno-histochemical assays.
When released from the trigeminal nerve, the reactivated Varicella zoster virus (VZV) moves down the ophthalmic division of the trigeminal nerve toward the naso-ciliary nerve. This system of nerve connection then divides to supply nerves to the surface of the eye orbit and the skin of the nose up to its tip. This movement of the viral particles usually takes three to four days to get to the nerve endings. As the viral particles make their movements, they influences the development of intra-neural (within the nerve) and perineural (near a nerve or nerves) leading to damaging effects of the eye and/or its surrounding structures.
Damage within the eye can lead to keratitis (corneal inflammation), uveitis, and/or conjunctivitis. This inflammation, when not treated promptly, will eventually lead to blindness. In any region of the body, one of the most common complications of shingles or herpes zoster is post-herpetic neuralgia, a nerve pain that occurs after the rashes of the shingles have healed. Post-herpetic neuralgia can continue adjacent to the affected dermatome (a region of the skin primarily supplied by one nerve) that persists for several weeks or even up to years after the rashes have healed. Certain complications of herpes zoster ophthalmicus (HZO) can produce devastating effects to the eye structures observed in the form of several eye diseases that have high potential to causes permanent eye sight loss.
Affected Parts of the Eyes
Usually, affected structures in the eye include the eyelids, conjunctiva and sclera. During the first week, peri-orbital and conjunctival swelling ensue. Because of the damaging changes in the eye, there is a significant risk for the development of Staphylococcal infection within one to two weeks. Late in the course of the disease, focal scleral atrophy develops leading to partial eyelid closure and can dry out the affected eye. In the cornea, significant changes become apparent through examination. Inflammation of the cornea or keratitis develops.
In deep stomal keratitis, lipids infiltrate and eventually the formation of working small vascular networks with red blood cell perfusion (corneal neovascularization) advances within a period of one month to several years. Erosions, continuing defects and corneal ulcerations occur in months to years (neurotrophic keratopathy). In the anterior portion of the affected eye, swelling and scarring of iris (uveitis) can lead towards development of glaucoma and cataract starting from two weeks to a couple of years after infection.
Development of eye symptoms of herpes zoster can have different onsets and patients can have damage in the affected eye without the appearance of the rashes. One good predictor as to how the disease is progressing is the appearance of the Hutchinson sign which are typical herpes zoster rashes found at the tip or side of the nose. The nerves around the area of the nose have connections around and within the ocular structures. When this sign is manifested there is a good chance that ocular structures can be involved.
In herpes zoster ophthalmicus, it is essential to seek medical intervention especially when manifestations of the Hutchinson sign begin to show up. Unnecessary complications can be prevented through early and prompt treatment.