More Than “Just an Ulcer”: What Alpaca Breeders Should Know About Corneal Ulcers

By Austin Swain, O.D.

As an optometric physician and an alpaca breeder, I probably look at an alpaca eye a little differently than most breeders do. When one of our animals begins squinting, tearing, or suddenly develops a cloudy eye, my attention immediately turns to the anterior segment, and particularly to the cornea.

I am not suggesting that human and veterinary ophthalmology are the same. They are not. But the basic principles of corneal anatomy, wound healing, inflammation, infection, and tissue breakdown are familiar enough that they help me think through what I am seeing when an alpaca has an abnormal eye.

Corneal disease is worth taking seriously in alpacas. In a recent retrospective review of 68 New World camelids presented for ophthalmic disease, the cornea was the most commonly affected ocular structure, accounting for 36.4% of recorded abnormalities. Diagnoses included keratitis, corneal ulceration, melting corneal ulcers, and corneal perforation.[1]

That spectrum is important. A watery or uncomfortable eye may be something relatively straightforward, but it can also be the first sign of a rapidly progressive, globe-threatening corneal problem.

Quick Plain-English Roadmap

In plain language, this article is about learning to tell the difference between a simple surface injury and a corneal ulcer that is becoming deeper, infected, inflamed, or structurally unsafe.

For breeders, the most important point is that “an ulcer” is not one single level of risk. Some ulcers are shallow and heal well with appropriate care. Others can involve deeper corneal tissue, infection, melting, inflammation inside the eye, or even impending perforation.

As you read, think of the cornea as a clear window with layers. A surface scratch is very different from damage that is moving deeper into that window. Changes in color, cloudiness, blood vessels, depth, discharge, pupil size, or comfort level can all provide clues about whether the eye is improving or becoming more serious.

My goal is not for breeders to diagnose and treat eye disease on their own. My goal is to help breeders recognize when an eye deserves prompt veterinary attention, understand why rechecks matter, and appreciate why a painful, cloudy, or changing cornea should never be dismissed as “just an ulcer.”

Important Medication Note

Do not assume that previously prescribed ophthalmic medication is appropriate for a new red, painful, or cloudy eye. Some commonly prescribed ophthalmic medications contain corticosteroids. While corticosteroids are valuable medications for appropriate inflammatory eye disease, they can be dangerous in the presence of active corneal ulceration.

A more detailed discussion appears later in this article under “A Word About Corticosteroids.”

I. Understanding Corneal Ulcers

Understanding the Anterior Segment

When I talk about the anterior segment of the eye, the front portion of the eye, I am referring to structures such as the conjunctiva, cornea, anterior chamber, iris, and lens. For this discussion, though, the cornea is the structure I keep coming back to.

The normal cornea is transparent and avascular, meaning it is clear and normally has no blood vessels running through it. Maintaining that transparency requires an intact epithelium, highly organized stromal collagen, controlled corneal hydration, and normal endothelial function.[2,3]

Clinically, the most important corneal layers are:

• the epithelium, the thin outer “skin” of the cornea,
• the stroma, the thick structural layer that gives the cornea most of its strength,
• Descemet’s membrane, a very thin inner support layer, and
• the endothelium, the innermost cell layer that helps keep the cornea from swelling with fluid.

The depth of an injury through these layers has enormous clinical significance. A superficial epithelial defect is very different from an ulcer extending deeply into the stroma. A corneal ulcer is not simply a scratch on the eye. It represents disruption of the epithelial barrier, and its seriousness depends on depth, cause, microbial involvement, and inflammatory response.

What Is a Corneal Ulcer?

A corneal ulcer occurs when an area of corneal epithelium has been lost. Once the epithelial barrier is disrupted, the underlying hydrophilic stroma, the deeper corneal layer that attracts and holds fluid, becomes exposed. Fluorescein dye adheres to this exposed stromal tissue, producing the bright green staining we associate with an epithelial defect.

An intact corneal epithelium generally does not retain fluorescein. A positive fluorescein test tells us that the surface layer has been compromised, but it does not tell the whole story.

The examination still needs to answer several questions:

• How large is the epithelial defect?
• Where is it located?
• How deep is the lesion?
• Is the surrounding stroma clear or edematous, meaning swollen and cloudy from excess fluid?
• Is there a stromal infiltrate, which often looks like a white or yellow-white spot where inflammatory cells or infection may be present?
• Is corneal tissue being lost?
• Is neovascularization present, meaning new blood vessels are growing into tissue that should normally be clear?
• Is there evidence of anterior uveitis, meaning inflammation inside the front chamber of the eye?
• Does the lesion appear stable, improving, or progressive?

Those findings are what start to separate a relatively uncomplicated superficial ulcer from something much more serious.

Why Alpacas Develop Corneal Ulcers

Alpacas are naturally curious, ground-level browsers with large, prominent eyes and faces that spend a lot of time close to hay, pasture, brush, bedding, and fencing. That combination makes minor eye trauma fairly easy to understand. A stiff piece of hay, a seed head, dust, plant awn, or small bit of debris can irritate the ocular surface, become trapped beneath an eyelid, or create a scratch that allows a simple injury to become a corneal ulcer.

In alpacas, trauma stays high on my list when I am thinking about corneal disease. Trauma-related ocular disease has long been recognized as an important problem in South American camelids.[3]

That makes sense on the farm. Hay, plant material, seed heads, bedding, dust, fencing, and other environmental debris all create opportunities for mechanical injury, and alpacas spend a lot of time with their faces directly in forage.

A particularly useful example comes from a published outbreak involving 21 alpacas that developed ocular disease associated with weed-contaminated grass hay. Five of six animals evaluated ophthalmologically had superficial ulcerative keratitis, surface-level corneal ulceration and inflammation, with intense corneal neovascularization and edema. Plant material was identified within the conjunctival fornices, the pocket-like spaces under the eyelids, and the authors noted that fan-shaped temporal corneal ulceration may be an important clue to the presence of a retained conjunctival foreign body.[4]

That case series illustrates something I think is easy to overlook:

Sometimes the ulcer is not the primary problem. The ulcer is the footprint of the primary problem.

If plant material or another foreign body stays tucked beneath an eyelid or in the conjunctival fornix, treating only the corneal ulcer may allow the original source of trauma to keep rubbing the eye.

Trauma also compromises the epithelial barrier, creating an opportunity for microorganisms to gain access to the underlying corneal tissue.

At that point, a traumatic ulcer can become something significantly more complicated.

II. Reading What the Cornea Is Telling You

When I evaluate a corneal lesion, fluorescein staining is only the starting point. What I really want to know is what the cornea is telling me about depth, inflammation, infection, tissue loss, and whether the problem has moved beyond the cornea itself.

The Epithelial Defect

The first question is whether the epithelium is intact. Once an epithelial defect has been identified, the pattern of fluorescein staining can be informative.

A small focal lesion may suggest direct trauma. A linear defect raises different questions than a broad geographic lesion. A peripheral or unusually shaped ulcer makes me want to look closely beneath the eyelids and within the conjunctival fornices for retained foreign material.

The location of a lesion matters. Its shape can matter. And sometimes the appearance of the ulcer provides the clue needed to find its cause.[4]

Corneal Edema

A normal cornea should be optically clear. When normal hydration and organization are disrupted, fluid builds up in the corneal tissue and scatters light. Clinically, that is when the cornea takes on the familiar blue-gray or hazy appearance of edema.

The amount and distribution of that edema can tell us something about what is happening. Mild localized edema adjacent to an epithelial defect may simply accompany local inflammation. More extensive edema makes me more concerned about deeper stromal inflammation, significant keratitis, endothelial dysfunction, or intraocular inflammation.

One important point is that the size of the fluorescein-positive epithelial defect does not necessarily reflect the severity of the overall disease. A relatively small epithelial defect can sit over a much larger area of abnormal stroma. For that reason, simply watching whether the fluorescein-positive area becomes smaller can sometimes provide a false sense of security.

Stromal Infiltrate

A stromal infiltrate changes the conversation. It may look like a focal white, cream, or yellow-white spot in tissue that should normally be clear. When I see that, I start thinking harder about depth, stromal loss, increasing edema, pain, anterior chamber reaction, and whether the eye is responding the way we would expect.

Both bacterial and fungal organisms deserve consideration in complicated alpaca keratitis. In a study examining ulcerative keratitis in domestic animals, obligate anaerobic bacteria were isolated from 18.8% of the alpaca corneal samples submitted for anaerobic culture, demonstrating that bacterial infection in these lesions can involve organisms beyond the usual aerobic suspects.[5]

Fungal disease is particularly important. In a retrospective series of 11 alpacas with fungal keratitis, reported lesions included stromal ulcers, stromal abscesses, nonulcerative keratitis, and corneal perforation. Aspergillus fumigatus and Fusarium solani were among the organisms most frequently cultured. Ten of the eleven alpacas were evaluated during the summer or fall, and trauma or foreign-body exposure was documented in some animals.[6]

That is why a corneal lesion that continues to worsen despite treatment should not automatically be assumed to just need “more antibiotic.” Sometimes we need to reconsider what we are actually treating.

Corneal Neovascularization

The normal cornea is avascular. When inflammation persists, new blood vessels can migrate from the limbus into the corneal tissue and may appear as fine red vessels extending inward toward the lesion.

These vessels tell us that inflammation has persisted long enough for the cornea to recruit a vascular response, and their direction may help localize the active area of disease.

Neovascularization can help healing by bringing cells, nutrients, and medications into tissue that normally has no direct blood supply, but it can also contribute to scarring and permanent opacity. Intense corneal neovascularization was a prominent feature of the hay-associated ulcerative keratitis outbreak described in alpacas.[4]

Stromal Loss

Once the corneal stroma itself is being lost, I no longer think of the problem as simply a surface ulcer. At that point, we are dealing with the structural framework of the cornea. The stroma accounts for the majority of corneal thickness. Progressive collagen destruction therefore means progressive loss of the tissue responsible for maintaining the integrity of the globe.

Depth becomes extremely important. A shallow stromal ulcer and one extending through most of the corneal thickness may both be called “corneal ulcers,” but they represent very different levels of risk. This is why surface area alone should never determine how serious an ulcer appears. A small ulcer can be deep. A large ulcer can be superficial. Depth and stromal behavior often matter more than diameter.

The Melting Cornea

A melting ulcer, or corneal stromal malacia, represents one of the most concerning stages of corneal disease. In plain terms, the cornea is softening and breaking down instead of holding its normal clear, firm structure. Clinically, the affected cornea can develop a soft, gelatinous, irregular, or almost liquefied appearance.

The process occurs when proteolytic enzymes, including matrix metalloproteinases and other collagen-degrading enzymes, essentially chemical “scissors” that break down corneal tissue, begin destroying the stromal collagen matrix faster than the cornea can repair itself.

Inflammatory cells, microorganisms, and corneal cells can all contribute to this enzymatic environment. Once melting begins, stromal thickness can disappear rapidly.

A published case involving a young Suri alpaca documented bilateral progressive melting corneal ulcers with severe progression. The authors specifically emphasized the need for rapid, intensive treatment in young or debilitated alpacas presenting with corneal ulceration.[7]

This is why I am uncomfortable casually watching an abnormal, painful cornea for several days just to see what happens. There are superficial lesions that heal uneventfully. A melting ulcer is not one of them.

The Descemetocele

If stromal destruction continues until essentially the entire overlying stroma has disappeared, Descemet’s membrane may become exposed. This produces a descemetocele, a dangerously deep ulcer where only a very thin inner layer remains between the inside of the eye and the outside world.

At this stage, the eye is dangerously close to perforation. The fluorescein staining pattern can also be tricky. Descemet’s membrane itself does not retain fluorescein, so the surrounding exposed stroma may stain brightly while the deepest central portion remains dark.

To someone unfamiliar with that pattern, the nonstaining center could look less concerning than it really is. In reality, it may represent the thinnest and most dangerous portion of the cornea. That is why fluorescein needs to be interpreted, not just performed.

Corneal Perforation

If the remaining tissue fails, the anterior chamber, the fluid-filled space just behind the cornea, becomes continuous with the external environment. The cornea has perforated.

Aqueous humor, the clear fluid inside the front of the eye, may escape, and depending on the location and size of the defect, the iris can move anteriorly into or through the wound. Iris tissue can occasionally plug a small perforation, but that does not make the situation benign.

There is a published case of an adult alpaca with traumatic corneal perforation and iris prolapse that required surgical repair with a conjunctival pedicle graft. Structural integrity of the globe was restored, and approximately ten months later the affected eye appeared to retain good vision with only a small residual corneal scar.[8]

I like that case because it makes an equally important point: A severe-looking corneal lesion does not automatically mean the eye is lost.

Early recognition and appropriate intervention can dramatically affect the outcome.

Look Behind the Cornea

One of the biggest differences between simply finding a corneal ulcer and really evaluating the anterior segment is remembering to look behind the cornea. The anterior chamber should normally be optically clear.

Significant corneal inflammation can trigger secondary anterior uveitis, involving the iris and ciliary body.[2,3]

Clinical findings can include:

• miosis, meaning a smaller-than-normal pupil,
• increased ocular pain,
• aqueous flare, meaning protein and inflammatory material visible in the normally clear fluid inside the eye,
• fibrin, a sticky inflammatory protein that can form strands or clumps,
• hypopyon, a visible layer of white inflammatory cells or debris inside the front chamber of the eye,
• posterior synechiae, meaning abnormal adhesions where the iris sticks to the lens behind it, and
• alterations in intraocular pressure.

This is why I compare the pupils. If one eye contains a significant corneal lesion and that pupil is noticeably smaller than the fellow eye, the finding matters.

The cornea may be the most obvious abnormality, but the pupil may be telling us that the inflammatory response extends beyond the ocular surface.

Uveal disease is also well documented in New World camelids. In the 2026 retrospective study, uveal abnormalities accounted for 15.4% of recorded ophthalmic disorders.[1]

Fibrin and Hypopyon

With sufficiently severe inflammation, material may become visible within the anterior chamber. Fibrin may appear as strands, sheets, clumps, or more organized inflammatory material. A hypopyon represents accumulation of inflammatory cells and debris within the dependent portion of the anterior chamber.

Importantly, a hypopyon associated with severe keratitis does not necessarily prove that microorganisms have physically entered the anterior chamber. A severe corneal inflammatory response alone can produce substantial intraocular inflammation.

But either finding changes how I view the eye. This is no longer an uncomplicated superficial ulcer. The eye is mounting a significant inflammatory response.

III. Evaluating a Painful Alpaca Eye

When an alpaca presents with a painful eye, I try not to start with the assumption that it “just has an ulcer.” Blepharospasm, epiphora, conjunctival hyperemia, discharge, and corneal haze, or squinting, tearing, redness of the eye tissues, drainage, and cloudiness, tell me the eye is abnormal and uncomfortable. They do not, by themselves, tell me why.

My goal is to figure out where the primary problem is, how deep it goes, whether infection or tissue breakdown is present, and whether other anterior segment structures are involved. I approach the examination systematically.

Start Before Touching the Eye

Some useful information can be obtained before restraining the animal or placing anything into the eye. I look at how the alpaca is holding the affected eye compared with the opposite eye.

• Is there obvious blepharospasm?
• Is the eye completely closed or only intermittently squinting?
• Is there excessive tearing?
• Is the discharge clear, mucoid, or mucopurulent?
• Is the animal rubbing the face?
• Does the cornea appear clear from a distance, or is haze, edema, vascularization, or a focal opacity already visible?

I also compare the pupils whenever possible. Before focusing exclusively on the cornea, it is worth remembering that a painful eye is a clinical sign, not a diagnosis.

Gross Vision Still Matters

Even when the cornea is the obvious concern, I still want some sense of whether the eye appears visual. Severe edema or a dense infiltrate can make an eye look dramatic while useful visual potential remains.

An ugly eye is not necessarily a blind eye.

Examine the Eyelids and Conjunctival Fornices

Before blaming the cornea alone, I want to know what is contacting it. The eyelid margins should be examined for abnormal position or mechanical irritation. The conjunctiva and fornices deserve deliberate evaluation for plant material and other foreign bodies.

The hay-associated alpaca outbreak is an excellent example of why this matters. Removing the plant foreign material was fundamental to resolving the disease.[4] Treating an epithelial defect while leaving the source of repeated mechanical trauma in place addresses the consequence rather than the cause.

Magnification Matters

This is probably where my own background influences the examination most. I want magnification and good illumination.

A gross examination may tell me the cornea is abnormal. Magnification allows me to better separate epithelial disease from stromal disease and to evaluate:

• ulcer margins,
• approximate depth,
• stromal edema,
• stromal infiltrate,
• vascularization,
• thinning,
• malacia, and
• the relationship between the lesion and the limbus.

Slit-lamp biomicroscopy is particularly useful when available because optical sectioning, using a narrow beam of light to view the cornea in layers, provides a much better appreciation of lesion depth and anterior chamber involvement.[2,3]

For me, depth is one of the most important pieces of information in the examination. Two eyes can both stain with fluorescein and still have completely different prognoses.

Fluorescein: More Than Positive or Negative

Fluorescein is one of the simplest and most useful tools available in evaluating corneal epithelial integrity. I think it is frequently oversimplified into: Green equals ulcer.

That is true, but there is more information available. I want to look at the pattern.

• How large is the defect?
• Where is it?
• Are the margins smooth or irregular?
• Is it linear?
• Is it geographic?
• Is there evidence that the lesion extends deeply?
• Does the staining pattern suggest a foreign body?
• Is there a nonstaining center within a very deep defect?

The test becomes much more valuable when the staining pattern is interpreted in the context of the rest of the anterior segment.

Examine the Anterior Chamber

After evaluating the corneal surface, I deliberately shift my attention deeper.

• Is the anterior chamber optically clear?
• Is there flare?
• Is there fibrin?
• Is there hypopyon, or white blood cells in the anterior chamber?
• Is the iris architecture normal?
• Is the affected pupil smaller than the fellow pupil?
• Is the pupil distorted?

These findings help determine whether an apparently corneal problem has produced a significant intraocular inflammatory response.[2,3]

A corneal ulcer accompanied by marked miosis and anterior chamber inflammation represents a very different clinical picture from an isolated superficial epithelial defect.

Intraocular Pressure Has Context

Tonometry, which measures the pressure inside the eye, can provide useful information when evaluating intraocular inflammation. An eye with significant anterior uveitis may have reduced intraocular pressure as inflammation alters aqueous humor dynamics.

However, no diagnostic test should be performed simply because it is available. If there is severe corneal thinning, a descemetocele, or concern for impending or actual perforation, unnecessary manipulation or pressure on a structurally compromised globe should be avoided. The examination has to fit the eye in front of us.

When Cytology and Culture Become Important

Not every superficial traumatic epithelial defect requires an extensive microbiologic workup. My threshold changes when the lesion stops looking simple.

Findings that increase concern include:

• stromal infiltrate,
• progressive stromal loss,
• malacia,
• rapid deterioration,
• failure to respond as expected,
• an unusual clinical appearance,
• deep ulceration, or
• concern for fungal infection.

Cytology, looking at cells and organisms under a microscope, and microbial culture, growing organisms to identify them, can become particularly valuable in these cases.[2,6]

Culture identifies what grows.

Cytology can potentially provide clinically useful information much sooner. The presence of inflammatory cells, bacterial organisms, fungal elements, and degenerating stromal material can help characterize a lesion while culture results are pending.

Neither test is perfect, and sample quality matters, but a rapidly deteriorating cornea is not a situation where I want to assume that every infection is behaving the same way. The alpaca fungal keratitis series demonstrates exactly why.[6]

Simple Versus Complicated

One of the most useful ways to organize corneal ulcers mentally is to ask whether the lesion appears simple or complicated. A relatively simple ulcer is primarily an epithelial defect without substantial stromal infiltrate, stromal loss, malacia, or other complicating features. A complicated ulcer has crossed that line.

Once I see infection, infiltration, progressive stromal loss, melting, a retained foreign body, significant anterior uveitis, or failure to heal as expected, my level of concern changes. The distinction is more meaningful than describing an ulcer merely as “big” or “small.”

Again: Surface area does not equal severity.

Document the Eye

One thing I strongly encourage breeders to do is photograph the eye. A cell-phone photograph does not replace a proper examination, but corneal disease is dynamic, and serial photographs can be remarkably useful. When possible, photographs should be taken under similar lighting and from similar angles.

I want to compare:

• Is the opacity expanding?
• Is the edema increasing or decreasing?
• Are vessels progressing toward the lesion?
• Is the infiltrate becoming more dense?
• Does the defect appear deeper?
• Is the pupil changing?

When we look at the same eye several times every day, gradual progression can be difficult to appreciate. A photograph gives us yesterday’s eye to compare with today’s.

Rechecking Is Part of Treatment

With corneal disease, I consider the recheck part of the treatment plan. It is not simply something that happens after treatment.

I want to know whether:

• the epithelial defect is getting smaller,
• stromal depth is stable or worsening,
• infiltrate is resolving,
• melting has stopped,
• corneal edema is improving,
• vascularization is developing appropriately,
• the anterior chamber is becoming quieter, and
• the animal is becoming more comfortable.

A cornea can change quickly, particularly when infection and enzymatic stromal degradation are involved.[2,7]

Improved comfort is encouraging, but it should not be the only measure of improvement. The structural behavior of the cornea matters.

IV. Critical Considerations for Breeders

A Word About Corticosteroids

There is one practical point I want to emphasize strongly.

Topical corticosteroids should not be placed into an eye with an active corneal ulcer unless specifically directed as part of appropriate veterinary ophthalmic management after the corneal disease has been fully assessed.

Corticosteroids are extremely useful medications for appropriate inflammatory ocular disease. They can also interfere with epithelial healing, suppress local immune responses, and worsen infectious or collagenolytic corneal disease.[2,3]

This matters because combination antibiotic/corticosteroid ophthalmic medications are common and may already be sitting in a medicine cabinet. Reaching for one simply because an eye appears red can create a serious problem. A red eye is a sign. It is not a diagnosis.

What the Color of the Cornea Can Tell Us

For breeders, one practical way of recognizing change is simply to pay attention to the appearance of the cornea.

• A clear cornea with a small fluorescein-positive epithelial defect represents one clinical picture.
• A blue-gray cornea suggests edema.
• A white or yellow-white focal opacity raises concern for stromal infiltration.
• A cornea developing red vessels indicates an active vascular response to ongoing inflammation.
• A soft, irregular, gelatinous cornea raises concern for stromal melting.
• A deep crater with a nonstaining central area can indicate a descemetocele.
• A severely abnormal cornea accompanied by miosis, fibrin, hypopyon, or other anterior chamber changes tells us the disease is no longer limited to the ocular surface.

These findings should not all be grouped under the same description of “an eye ulcer.” They represent very different levels of disease.

V. Cases From Our Farm

Case Documentation, Not a Treatment Protocol

Before sharing these cases, I want to be very clear that I am not a veterinarian and do not present these examples as treatment recommendations.

These are real cases from our own farm and describe how these individual animals were managed in consultation with veterinary professionals. Medication names, concentrations, frequencies, and other details are included to accurately document what occurred in these specific cases. They should not be interpreted as instructions for treating another animal.

Every painful, cloudy, deep, melting, or perforated eye deserves prompt veterinary evaluation, and treatment decisions should be made with the veterinarian responsible for that animal’s care.

Case 1: A Small Ulcer That Was Nearly Full Thickness

Presentation

This case involved a two-year-old female alpaca that first caught my attention because of a central cloudy area on the cornea. With fluorescein, there was a positive epithelial defect measuring approximately 3 mm.

At first glance, the diameter was not that dramatic. What bothered me was the depth. The lesion extended almost through the posterior stroma and was approaching perforation. This case is a good example of why surface area alone can be misleading: a small ulcer can still be structurally dangerous.

Progression and Management

Initial treatment was started with polymyxin-bacitracin ophthalmic ointment four times daily. By the following morning, the fluorescein-positive area appeared smaller, measuring approximately 2 mm. That could have been interpreted as improvement if the eye were judged only by the size of the epithelial defect.

The depth told a different story. The lesion had progressed to the level of perforation, and a small amount of iris tissue had begun to protrude into the defect. In other words, the epithelial opening looked smaller, but the risk to the globe had become greater.

After consultation with a veterinary ophthalmologist, we continued the topical antibiotic ointment and added atropine 1% and timolol 0.5%.

In this case, timolol was used with the goal of lowering intraocular pressure, while atropine was used for its mydriatic effect, with the hope of helping draw the iris away from the wound and allowing the cornea to heal with some internal support.

At that point, the priority was not optical perfection. A central scar was likely. The priority was preserving the globe and avoiding enucleation. The antibiotic ointment was continued four times daily, while the additional drops were used twice daily as directed through the consultation.

Outcome

Within a week, the cornea had begun to heal. Ultimately, a small central scar remained. That scar may have impaired vision to some degree, but the eye was saved. More importantly, the alpaca avoided complete loss of the eye secondary to enucleation and went on to live a healthy life.

What This Case Illustrates

This case still stands out to me because it illustrates one of the most important points in the entire discussion: A shrinking fluorescein stain does not always mean the cornea is safer.

The epithelial defect may be closing while the remaining stromal tissue is dangerously thin. In this alpaca, depth, not diameter, was the finding that mattered most.

Case 2: A Perforated Ulcer in a Cria

Presentation

This case involved a cria that developed a perforated corneal ulcer while we were away from the farm. I do not know whether the original event was direct trauma or a rapidly progressive melting ulcer, but the important point is that the eye changed quickly.

I do not present this case to assign blame. Eye disease can be subtle in the beginning, and unless someone is deliberately looking for squinting, tearing, cloudiness, or a change in the way an alpaca is holding the eye, early findings can be missed. That is especially true when farm sitters are caring for animals whose normal behavior they may not know as well as the owner does.

By the time the lesion was recognized, the cornea had perforated. At that stage, this was no longer a situation where we could simply watch the eye and hope it improved. The practical options were limited: enucleation, meaning surgical removal of the eye, or an attempt to protect the globe and allow the tissue to stabilize.

Management

In consultation with our veterinarian, we elected to attempt a temporary tarsorrhaphy. With veterinary assistance, the upper and lower eyelids were partially sewn together, leaving a small opening so medication could still be placed into the eye.

The goal was simple: protect the compromised cornea, reduce exposure and mechanical irritation, and give the eye a chance to scar and seal rather than proceeding immediately to enucleation.

Polymyxin-bacitracin ophthalmic ointment was placed through the remaining opening twice daily. This was continued for approximately one month while the eye was monitored closely. The tarsorrhaphy was not meant to make the cornea look normal. It was meant to protect a structurally compromised eye long enough for healing and scarring to occur.

Outcome

After the stitches were removed, the lesion continued to scar over. The final result was not an optically perfect cornea, but the eye stabilized and enucleation was avoided.

What This Case Illustrates

The lesson from this case is that there are times when an eye cannot simply be watched. When a cornea has perforated, is melting, or appears structurally unstable, decisions may need to be made quickly. At the same time, a severe-looking eye is not always automatically lost.

In consultation with a veterinarian, there may be reasonable techniques worth attempting when the goal is to preserve the globe and keep the animal comfortable.

For breeders, this case reinforces two practical points: first, painful or cloudy eyes should be identified as early as possible, especially when someone else is providing farm care; and second, once an ulcer becomes deep, melting, or perforated, timely veterinary involvement can determine whether the outcome is loss of the eye or preservation of a comfortable, stable globe.

What I Want Breeders to Take Away

One advantage of understanding the anterior segment is that the eye often gives visible evidence of how the disease is behaving.

Breeders do not need to diagnose the condition themselves, but they can recognize meaningful change: increasing cloudiness, a denser white opacity, advancing blood vessels, worsening pain, pupil changes, or a lesion that appears deeper than before.

Finding the fluorescein-positive defect is only the beginning. The more important task is determining what kind of ulcer is present, what the surrounding cornea and anterior chamber are doing, and whether the disease is moving toward healing or toward structural failure.

The cases described above are also reminders that a dramatic-looking eye is not automatically a lost eye, while a small-looking ulcer is not automatically a safe one. Ultimately, the goal is not simply to make fluorescein staining disappear. The goal is to preserve a comfortable, structurally intact, and, whenever possible, visual eye.

Key Points to Remember

• A corneal ulcer is not always “just a scratch.” Depth, infection, inflammation, tissue loss, and progression determine how serious it is.
• A small ulcer can be dangerous if it is deep, melting, infected, or associated with inflammation inside the eye.
• The appearance of the cornea matters. Cloudiness, white or yellow-white opacity, red vessels, soft or gelatinous tissue, or a deep crater can all signal a more complicated process.
• A fluorescein-positive area confirms loss of the surface layer, but the staining pattern must be interpreted in context. It does not tell the whole story by itself.
• Always think about what caused the ulcer. Plant material, hay, seed heads, bedding, or another foreign body may continue damaging the eye if it is not found and removed.
• Compare both eyes, watch the pupil, photograph changes, and pay attention to whether the opacity, redness, vessels, pain, or discharge is improving or worsening.
• Improved comfort is encouraging, but it is not enough by itself. The cornea also needs to be structurally improving.
• Topical corticosteroids should not be used in an eye with an active corneal ulcer unless specifically directed after appropriate veterinary ophthalmic assessment.
• Prompt veterinary attention and appropriate rechecks are essential when an alpaca has a painful, cloudy, worsening, deep, infected, or melting corneal lesion.

References

1. Giselbrecht J, Nell B. Ocular diseases in New World camelids presented to the Veterinary University in Vienna: 68 cases (2009–2025). Vet J. 2026;317:106663. doi:10.1016/j.tvjl.2026.106663.

2. Czerwinski SL. Ocular surface disease in New World camelids. Vet Clin North Am Exot Anim Pract. 2019;22(1):69–79. doi:10.1016/j.cvex.2018.09.001.

3. Gionfriddo JR. Ophthalmology of South American camelids. Vet Clin North Am Food Anim Pract. 2010;26(3):531–555. doi:10.1016/j.cvfa.2010.08.004.

4. Fischer K, Hendrix DVH. Conjunctivitis and ulcerative keratitis secondary to conjunctival plant foreign bodies in a herd of alpacas (Lama pacos). Vet Ophthalmol. 2012;15(2):110–114. doi:10.1111/j.1463-5224.2011.00939.x.

5. Ledbetter EC, Scarlett JM. Isolation of obligate anaerobic bacteria from ulcerative keratitis in domestic animals. Vet Ophthalmol. 2008;11(2):114–122. doi:10.1111/j.1463-5224.2008.00610.x.

6. Ledbetter EC, Montgomery KW, Landry MP, Kice NC. Characterization of fungal keratitis in alpacas: 11 cases (2003–2012). J Am Vet Med Assoc. 2013;243(11):1616–1622. doi:10.2460/javma.243.11.1616.

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Author’s Note

This article is intended for educational purposes and documents observations and individual cases from our own farm. It is not a substitute for examination, diagnosis, or treatment by a veterinarian. Austin Swain, O.D., is an optometric physician whose professional clinical practice is in human eye care and is also an alpaca breeder. Veterinary diagnosis and treatment fall outside his professional scope.

Ocular disease, particularly deep, progressive, infected, melting, or perforated corneal ulceration, can represent an ophthalmic emergency. Treatment decisions for an individual alpaca should be made in consultation with the veterinarian responsible for that animal’s care.