Herpes Simplex keratitis

Herpes Simplex Keratitis

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Herpes Simplex Keratitis

HSV keratitis is caused by the herpes simplex virus, a double- stranded DNA virus made up of an icosahedral shaped capsid surrounding a core of DNA and phosphoproteins of viral chromatin. HSV- I and HSV- II are differentiated by virus specific antigens. HSV- I typically affects the orofacial region whereas HSV- II usually causes genital infections, though studies have shown that both viruses may affect either location.

Risk Factors

Risk factors for development of primary HSV involve direct contact with infected secretions or lesions.

Risk factors for reactivation of disease have been postulated to include:

  • Sunlight
  • Trauma
  • Heat
  • Menstruation
  • Stress
  • Trigeminal nerve manipulation
  • Infectious disease and immunocompromised states.
Herpes Simplex keratitis
Image from Coreem.net

Physical examination

In addition to a standard biomicroscopy, special attention should be paid to the presence of a preauricular lymph node, vesicular lesions on the lids or adnexa, bulbar follicles, decreased corneal sensation, and most notably the presence of epithelial dendrites on the cornea.

For primary HSV keratitis, it is more common for patients to present with a blepharoconjunctivitis than with cornea involvement. However, diffuse punctate keratopathy or corneal microcysts may be visible.

Recurrent HSV keratitis can present as epithelial keratitis. The earliest sign of epithelial disease include raised clear vesicles that later coalesce to form the classic dendritic lesion. The dendritic ulcer, the dichotomous branching cornea lesion, can be stained with fluorescein and is the hallmark of HSV epithelial keratitis. These epithelial lesions represent active replicating virus. As the dendritic ulcer may evolve into a geographic ulceration of the cornea, especially in patients with compromised immunity or on topical steroids.

Clinical diagnosis

The clinical diagnosis of HSV may be suggested by the presence of the multiple arborizing dendritic epithelial ulcers with terminal bulbs. The bed of the ulcer stains with fluorescein, while the swollen corneal epithelium at the edge of the ulcer typically stains with rose bengal. Several dendrites may also coalesce to form a geographic epithelial ulcer.

In addition, there may be mild conjunctival injection, ciliary flush, mild stromal edema and subepithelial white blood cell infiltration. Following resolution of the primary infection, a “ghost dendrite” may be visible just beneath the prior area of epithelial ulceration.

Diagnostic procedures

The diagnosis of HSV is often made clinically, however, laboratory tests are available to confirm the diagnosis in difficult cases (and in all cases of neonatal herpetic infection). Serologic testing may be performed but is usually not helpful in recurrent disease as most adults are laterally infected with HSV.

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However, conjunctival scrapings, impression cytology specimens, and scrapings from vesicular lesions on the skin may be tested by cytology, culture, or polymerase chain reaction (PCR) for the presence of HSV.

Fluorescent antibody (FAB) testing involving impression cytology using nitrocellulose membrane or a cornea smear. A Tzanck smear can reveal multinucleated giant cells and intranuclear eosinophilic inclusion bodies. Serum antibody testing is typically of limited use.

Management

Primary ocular herpes simplex virus infection may manifest as lid, conjunctival, or corneal ulceration. The ability of the virus to colonize the trigeminal ganglion leads to recurrences that may be precipitated by fever, excessive exposure to sunlight, or immunodeficiency. The dendritic (branching) corneal ulcer is the most characteristic manifestation of recurrent ocular disease. More extensive (“geographic”) ulcers also occur, particularly if topical corticosteroids have been used.

The corneal ulcers are most easily seen after instillation of fluorescein and examination with a blue light. Such corneal epithelial disease in itself generally does not lead to corneal scarring. It responds well to simple debridement and patching.

More rapid healing can be achieved by the addition of topical antivirals, such as trifluridine drops, ganciclovir gel, or acyclovir ointment, or oral antivirals, such as acyclovir, 400–800 mg five times daily.

Long-term oral acyclovir, 400 mg twice daily; famciclovir, 250 mg once daily; or valacyclovir, 500 mg once daily, reduces the rate of recurrent epithelial disease, particularly in atopic individuals.

Stromal herpes simplex keratitis produces increasingly severe corneal opacity with each recurrence.

Topical antivirals alone are insufficient to control stromal disease, so topical corticosteroids are used as well but they may enhance viral replication, exacerbating epithelial disease, and steroid dependence is common.

Oral acyclovir, 200–400 mg five times a day, is often helpful in the treatment of severe herpetic keratitis. Severe stromal scarring may require corneal grafting, but the overall outcome is relatively poor.

Caution: For patients with known or possible herpetic disease, topical corticosteroids should be prescribed only with ophthalmologic supervision

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