Cancel the Subscription

Let’s stop supporting the belief that a dendrite means herpes simplex virus

Young, budding clinicians in optometry school are taught that there’s both an art and science to the practice of optometry: Diagnosing a patient is about a compilation of specific signs and symptoms and what can be learned about a condition via textbooks. That said, there are characteristics about certain ocular conditions that we, as a profession, have subscribed to, even though they are not always true. Examples include “itch means allergy,” “dry mouth means Sjögren’s syndrome” (see ) and “a dendrite means herpes simplex virus (HSK).”


Primary HSK infections can mimic both the signs and symptoms of DED or adenovirus without the presence of a dendrite. Think of the old saying, “all thumbs are fingers, but not all fingers are thumbs.” A dendrite can indicate a herpetic infection, but a lack of one does not mean its absence either.

The fact is, patients who have HSK infections may present with blepharoconjunctivitis and associated epithelial defects that heal without scarring. Follicles may or may not be identified, and if they are, they may be attributed to viral “pink eye.”

Patients who present with unilateral, non-epidemic keratoconjunctivitis, however, should be considered suspects for primary HSK. Additionally, instilling sodium fluorescein can highlight epithelial defects associated with HSK, and dyes, such as lissamine green and Rose bengal, can stain the leading edges of a dendrite, or terminal bulbs.

It also should be noted that the primary HSK infection often does not affect the cornea. That said, the HSK patient may move into a recurrent phase of HSK infection, in which the cornea is adversely affected, by causing epithelial defects, potential scarring and compromised vision, and a dendritic ulcer manifests as a result of the replicating virus. A geographic ulcer can also occur as a result of the replicating virus, although it loses the classic dendritic shape.


As the origin of an HSK infection is different from that of DED, its treatment must be different. Specifically, both topical and oral anti-virals may be necessary to manage the condition appropriately. A caveat: Topical trifluridine may result in epithelial defects, due to high toxicity, so patients should not use it past 21 days.

Additional therapies, such as a reduction in toxic medications, the use of non-preserved artificial tears, the application of an amniotic membrane and punctal occlusion, may be warranted, depending on the severity of the HSK infection and risk to the patient’s vision.

Once the infection has been eliminated, systemic prophylaxis can be prescribed by way of oral antivirals to protect against the reactivation of the infection.


It’s often said, “Call a spade, a spade.” However, if O.D.s are waiting for a dendrite before diagnosing an HSK infection, they might be waiting a long time. Let’s stop believing only the presence of a dendrite is indicative of an HSV infection. Also, let’s be careful to look at signs and symptoms and consider that a misdiagnosis of inflammatory DED may result in the prescription of a steroid drop, which will prove provocative at best and disastrous at worst. OM