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Herpetic keratitis
Last reviewed: 05.07.2025
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The incidence of herpetic keratitis is steadily increasing.
Herpes is the cause of keratitis in 50% of adult patients and 70-80% in children. The spread of herpes in recent years is associated with the widespread use of steroid drugs, as well as with an increase in the number of flu epidemics, which provoke outbreaks of viral eye lesions.
[ What causes herpetic keratitis?
Herpes simplex virus is a DNA virus that is pathogenic only for humans. The infection is widespread: almost 90% of the population has antibodies to herpes simplex virus type I (HSV-1), but most patients have no or weak clinical signs of the disease. With herpes simplex virus type I infection, the upper body (face, including lips, eyes) is mainly affected. With herpes simplex virus type II (HSV-2), which is a typical cause of acquired venereal disease, the lower body is usually affected (genital herpes). Infection of the eye with HSV-2 can occur as a result of contact with infected discharge from the genital tract during sexual intercourse or childbirth.
- Primary infection with herpes simplex virus
Primary infection occurs in early childhood by airborne droplets, less often by direct contact. During the first 6 months of life, the child is not susceptible to infection due to a high titer of maternal antibodies in the blood. During primary infection, the clinical picture of the disease may be absent or manifested by subfebrile temperature, malaise and symptoms of damage to the upper respiratory tract. In people with immunodeficiency, generalization of the process and the occurrence of life-threatening conditions are possible.
- Recurrent herpesvirus infection
After the primary infection, the virus enters the ganglion (trigeminal for HSV-1 and spinal for HSV-2) via the axons of sensory fibers, where it remains in a latent form.
Under certain conditions, the virus is reactivated, replicates, and moves along the same axons in the opposite direction to the target tissue, causing a relapse of the disease.
Without prophylactic treatment, recurrent attacks of herpetic keratitis occur within a year in approximately 33% of individuals and within 2 years in 66%.
Primary herpetic keratitis is keratitis that develops when the body first encounters the virus, when there are no specific antibodies in the blood yet. In the first six months of life, the child is protected from infection by antibodies received from the mother, so infection occurs between 6 months and 5 years.
Primary herpetic keratitis begins acutely, is severe and long-lasting, often against the background of influenza or other colds. The parotid lymph glands enlarge; conjunctivitis develops, and then whitish foci of infiltration or vesicles prone to ulceration appear in the cornea. Corneal syndrome (photophobia, lacrimation, blepharospasm) is sharply expressed, abundant neovascularization of the cornea develops, the iris and ciliary body can be involved in the pathological process. The inflammatory process ends with the formation of a coarse corneal leukoma. Primary herpes is characterized by recurrent inflammations along the edge of the formed corneal scar.
Post-primary herpetic keratitis is an inflammation of the cornea in a previously infected person who has a weak titer of antigens when the balance between the viruses that have settled in the body and the level of antibodies is disturbed.
Cooling, stress, ultraviolet radiation, inflammatory processes lead to a decrease in the body's resistance. Septic foci can be found in other organs. Post-primary herpetic keratitis has a subacute course, in pathogenetic terms it is a manifestation of a chronic infectious disease. Usually, herpetic keratitis is not accompanied by conjunctivitis. With a decrease in corneal sensitivity, photophobia and lacrimation are weakly expressed, neovascularization is insignificant. A tendency to relapse is noted.
Symptoms of herpetic keratitis
Based on the nature of clinical manifestations, superficial and deep forms of herpetic keratitis are distinguished.
Superficial forms of herpetic keratitis include vesicular (vesicular) corneal herpes, dendritic, landscaping and marginal keratitis. In clinical practice, we most often have to deal with vesicular and dendritic keratitis.
Vesicular herpes of the cornea begins with the appearance of pronounced photophobia, lacrimation, blepharospasm, a sensation of a foreign body in the eye, which are caused by the formation of small bubbles in the form of raised epithelium on the surface of the cornea. The bubbles quickly burst, leaving behind an eroded surface. Healing of defects is slow, they are often infected with coccal flora, which significantly complicates the course of the disease. Infiltrates occur at the site of erosions, they can acquire a purulent character. In an uncomplicated course, after the defects close, delicate scars in the form of a cloud remain in the cornea, the effect of which on the function of the eye depends on the place of their localization.
Herpetic keratitis is manifested by the following symptoms:
- Vesicular eruptions on the skin of the eyelids and periorbital area.
- Acute, unilateral, follicular conjunctivitis with enlargement of the preauricular lymph nodes,
- In some cases, secondary obstruction of the lacrimal canaliculi may occur.
What do need to examine?
What tests are needed?
Treatment of herpetic keratitis
Treatment of herpetic keratitis is aimed at preventing the occurrence of keratitis. Acyclovir ointment is used 5 times a day for 3 weeks. However, with primary herpes of the eye, keratitis occurs very rarely.
Antiviral treatment includes chemotherapy, non-specific and specific immunotherapy. At different stages of the disease, appropriate combinations of drugs are used. At the onset of the disease, frequent daily instillation of kerecide, deoxyribonuclease, ointments with tebrofen, florenal, bonafton, oxolin, zovirax are applied 3-4 times a day. Every 5-10 days, the drugs are changed. Acyclovir is taken orally for 10 days. If the eye disease is combined with herpetic inflammation of another localization, the duration of the course of treatment is increased to 1-2 months. In case of severe complications, intravenous infusions of acyclovir are administered every 8 hours for 3-5 days. This is a highly active drug, but has a narrow spectrum of action, so it is used against the herpes simplex and herpes zoster viruses.