Sunburn (solar dermatitis or actinic dermatitis) and photosensitization are important integumentary conditions affecting camelids (llamas, alpacas, vicunas, guanacos) and cervids (deer, elk, moose, reindeer).
Overview and Clinical Importance
Sunburn (solar dermatitis or actinic dermatitis) and photosensitization are important integumentary conditions affecting camelids (llamas, alpacas, vicunas, guanacos) and cervids (deer, elk, moose, reindeer). These conditions result from ultraviolet (UV) radiation damage to the skin and are particularly significant in animals with non-pigmented or sparsely haired skin. Understanding the distinction between true sunburn (phototoxicity) and photosensitization is essential for accurate diagnosis and effective treatment.
In both camelids and cervids, these conditions can cause significant welfare concerns, economic losses due to skin damage, and may progress to squamous cell carcinoma with chronic exposure. The NAVLE frequently tests candidates on differentiating primary versus secondary photosensitization and understanding species-specific risk factors and management strategies.
| UV Type |
Wavelength |
Biological Effects |
| UVA |
320-400 nm |
Penetrates deep into dermis; causes skin aging; associated with photosensitivity reactions; penetrates glass |
| UVB |
290-320 nm |
Primary cause of sunburn (phototoxicity); damages keratinocytes; causes DNA mutations; blocked by glass |
| UVC |
Less than 280 nm |
Most damaging but absorbed by ozone layer; does not reach earth's surface |
Pathophysiology of UV-Induced Skin Damage
Understanding the UV Spectrum
The solar spectrum reaching the earth's surface consists of approximately 40% visible light (400-700 nm), 50% infrared radiation (700-20,000 nm), and 9% ultraviolet radiation (100-400 nm). For dermatological purposes, UV radiation is divided into three categories with different biological effects.
High-YieldUVB (290-320 nm) is the primary cause of sunburn in animals. UVA causes photosensitization reactions. Remember: B = Burn, A = Aging and Allergic-type (photosensitization) reactions.
Sunburn (Phototoxicity) vs. Photosensitization
A critical distinction for the NAVLE is understanding that sunburn and photosensitization are NOT the same condition, despite similar clinical appearances. This distinction affects both diagnosis and treatment.
Classification of Photosensitization
Photosensitization is classified into four types based on the source of the photodynamic agent. Type III (hepatogenous) is the most common form in production animals and should always be suspected when multiple animals in a herd are affected.
NAVLE TipWhen you see multiple animals affected with photosensitization, think hepatogenous (Type III) first! Always evaluate liver function (GGT, ALP, bile acids, bilirubin) in suspected photosensitization cases. The mnemonic 'PHIL' helps remember: Phylloerythrin is the photodynamic agent in Hepatogenous photosensitization causing Inflammation of Light-exposed skin.
| Feature |
Sunburn (Phototoxicity) |
Photosensitization |
| Mechanism |
Direct UV damage to keratinocytes; dose-dependent response |
Photodynamic agent in skin absorbs UV energy and transfers to tissues |
| Photodynamic Agent |
Not required |
Required (phylloerythrin, hypericin, or other chromophore) |
| Oxygen Requirement |
Can occur without molecular oxygen |
Requires molecular oxygen for reaction |
| Onset |
Delayed (hours after exposure) |
Can be rapid (minutes) or delayed (days) |
| Severity |
Generally mild to moderate |
Often severe; can cause deep tissue necrosis |
| Liver Involvement |
None |
May be present (hepatogenous Type III) |
Sunburn and Photosensitization in Camelidae
Species-Specific Anatomy and Risk Factors
Camelids (llamas, alpacas, vicunas, guanacos) have unique integumentary features that influence their susceptibility to solar damage. Unlike Old World camelids (camels, dromedaries), New World camelids display a wide variety of coat colors, which affects their vulnerability to UV radiation.
Key Anatomical Considerations:
- Hair coat variability: White-haired areas are most sensitive to solar damage; dark-fleeced areas are paradoxically more vulnerable to other skin diseases due to increased warmth attracting insects
- Skin thickness: Thickest on neck and dorsal thorax; thinner ventrally. Alpaca skin is thickest on neck, pasterns, and interdigital spaces
- Fleece protection: Dense fleece on trunk provides significant UV protection; face, ears, and ventral areas have sparse coverage
- Lack of lanolin: Unlike sheep, camelid fiber lacks lanolin, making skin more susceptible to clipper burn and solar damage post-shearing
Clinical Presentation in Camelids
Sunburn (Solar Dermatitis)
True sunburn in camelids occurs most commonly in animals with white or lightly pigmented skin that are exposed to intense UV radiation. Post-shearing animals are particularly vulnerable. Clinical signs progress through predictable stages.
Photosensitization in Camelids
Camelids are particularly susceptible to facial eczema (sporidesmin toxicosis from Pithomyces chartarum fungus), which is a form of hepatogenous photosensitization. This condition is especially significant in New Zealand and Australia. Camelids appear more sensitive to sporidesmin than cattle or sheep.
Clinical Features of Photosensitization in Camelids:
- Photophobia: Animals frantically seek shade; agitation and discomfort when exposed to sunlight
- Affected areas: Ears (drooping, curling), nose, periocular region, lips, ventral abdomen, perineum, teats
- Lesion progression: Rapid erythema and edema progressing to severe necrosis, exudation, and skin sloughing
- Systemic signs: With hepatogenous photosensitization - icterus, anorexia, depression, elevated liver enzymes
Differential Diagnosis: Zinc-Responsive Dermatosis
An important differential diagnosis for solar-related skin disease in camelids is zinc-responsive dermatosis (idiopathic hyperkeratosis). This condition can predispose animals to secondary sunburn and may present similarly to solar dermatitis.
High-YieldThe term 'zinc-responsive' is used rather than 'zinc-deficient' because affected camelids may not have demonstrable zinc deficiency. High-calcium diets (alfalfa, lucerne) can interfere with zinc absorption. Improvement is typically seen within 30-90 days of zinc supplementation.
| Type |
Pathophysiology |
Examples |
| Type I (Primary) |
Photodynamic agent ingested, injected, or absorbed through skin; reaches skin in native form |
St. John's Wort (hypericin), Buckwheat (fagopyrin), Tetracyclines, Phenothiazines, Lush alfalfa (chlorophyll overload) |
| Type II (Endogenous) |
Inherited defects in heme synthesis pathway cause porphyrin accumulation |
Bovine congenital erythropoietic porphyria (pink teeth), Bovine erythropoietic protoporphyria |
| Type III (Hepatogenous) |
Liver damage impairs phylloerythrin excretion; accumulates in skin. MOST COMMON type in livestock |
Facial eczema (sporidesmin), Pyrrolizidine alkaloid toxicity (Senecio, ragwort), Lantana, Blue-green algae, Brassica-associated liver disease |
| Type IV (Idiopathic) |
Unknown mechanism; photodynamic agent not identified |
Spring eczema in calves, Moldy hay associated cases, Some alfalfa-related cases |
Sunburn and Photosensitization in Cervidae
Species-Specific Considerations
Cervids (deer, elk, moose, reindeer) are susceptible to both sunburn and photosensitization, though these conditions are more commonly documented in farmed cervids than wild populations. Farmed deer (particularly red deer, fallow deer, elk, and reindeer) are increasingly important in agricultural systems worldwide.
Key Risk Factors in Cervids:
- White or piebald animals: Albino and piebald deer lack protective melanin in non-pigmented areas
- Velvet antler stage: Antlers in velvet are highly vascularized and sensitive to UV damage
- Facial and tongue exposure: Deer that lick affected areas (especially with hepatogenous photosensitization) can develop glossitis with severe ulceration and necrosis
- Facial eczema susceptibility: Farmed deer are highly susceptible to facial eczema (sporidesmin toxicosis) in endemic regions
Clinical Presentation in Cervids
According to the Merck Veterinary Manual, in cattle and especially in deer, exposure of the tongue while licking affected areas can result in glossitis characterized by ulceration and deep necrosis. This is a unique clinical feature in cervids that should prompt evaluation for photosensitization.
NAVLE TipWhen you see a deer with severe glossitis (tongue ulceration/necrosis) along with skin lesions, always think photosensitization! This is a species-specific presentation that distinguishes deer from other ruminants. The tongue lesions result from the deer licking its photosensitized skin.
| Stage |
Clinical Signs |
| Early (Acute) |
Erythema (redness), warmth, mild edema of exposed areas. Animal may seek shade. Often affects ears, bridge of nose, periocular areas |
| Intermediate |
Vesicle or blister formation, serous exudation, crusting, skin thickening. Pain and pruritus evident |
| Severe/Chronic |
Skin necrosis and sloughing, secondary bacterial infection, scarring, alopecia. Risk of squamous cell carcinoma with chronic exposure |
Diagnostic Approach
Clinical Evaluation
Diagnosis of sunburn and photosensitization relies on a combination of history, clinical examination, and laboratory evaluation. The pattern of skin lesions (restricted to non-pigmented, sun-exposed areas) is often pathognomonic.
Key Historical Questions:
- Duration and intensity of sun exposure? Recent shearing?
- Recent pasture changes? Access to lush green forage, alfalfa, or brassicas?
- Presence of potentially toxic plants (St. John's Wort, buckwheat, Senecio)?
- Recent medication administration (tetracyclines, phenothiazines, sulfonamides)?
- Number of animals affected (herd vs. individual problem)?
- Access to standing water or ponds (blue-green algae)?
Laboratory Diagnostics
| Feature |
Description |
| Lesion Character |
Nonpruritic papules with tightly adherent crust progressing to plaques and thickened, crusted areas |
| Distribution |
Less densely haired areas: perineum, ventral abdomen, inguinal region, medial thighs, axilla, medial forearms, face |
| Diagnosis |
Skin biopsy (histopathology). Note: serum zinc levels may be normal as camelids naturally have lower zinc levels |
| Treatment |
Zinc sulfate 1 g/day OR zinc methionine 2-4 g/day PO. Minimize calcium supplementation. Discontinue alfalfa hay |
Treatment and Management
Immediate Management
The cornerstone of treatment for both sunburn and photosensitization is immediate removal from sun exposure. Additional treatment depends on the underlying cause and severity of lesions.
Prevention Strategies
High-YieldRemember 'SHADE' for photosensitization management: Sun avoidance, Hepatic support if needed, Antibiotics for secondary infection, Dietary changes (remove inciting feed), Emollients and wound care.
| Clinical Finding |
Description in Cervids |
| Skin Lesions |
Erythema, edema, vesicles, necrosis of ears, muzzle, eyelids, vulva, teats, and non-pigmented skin |
| Glossitis (Tongue) |
UNIQUE TO DEER: Severe ulceration and deep necrosis of tongue from licking photosensitized skin |
| Ocular Signs |
Epiphora (excessive tearing), corneal edema, potential blindness regardless of coat color |
| Behavioral Changes |
Photophobia, agitation, shade-seeking behavior, reluctance to graze during daylight |
| Hepatogenous Signs |
Icterus, anorexia, depression, elevated GGT, ALP, AST, bilirubin. Liver may be enlarged (acute) or atrophied (chronic) |
Prognosis
| Test |
Purpose |
Expected Findings |
| Serum Biochemistry |
Evaluate liver function; differentiate primary from hepatogenous |
Type III: Elevated GGT, ALP, AST, SDH; increased direct bilirubin, bile acids, cholesterol |
| Skin Biopsy |
Histopathology of affected skin |
Epidermal necrosis, dermal edema, vascular damage, solar elastosis (chronic) |
| Liver Biopsy |
Confirm hepatogenous photosensitization |
Bile duct proliferation, periportal fibrosis, megalocytosis (PA toxicity), hepatocellular degeneration |
| Pasture Spore Count |
Confirm facial eczema risk |
Pithomyces chartarum: Greater than 100,000 spores/g grass = dangerous |
| Serum Zinc |
Rule out zinc deficiency (camelids) |
Camelid reference: 3.5-10 micromol/L (lower than cattle). May be normal in zinc-responsive dermatosis |
| Treatment |
Details and Dosages |
| Sun Avoidance |
House indoors or provide deep shade. Allow grazing ONLY at night until lesions resolve. This is the MOST IMPORTANT intervention |
| Remove Inciting Cause |
Remove from suspect pasture, discontinue photosensitizing drugs, change feed source |
| Anti-Inflammatory Therapy |
Flunixin meglumine: 1.1-2.2 mg/kg IV/IM q12-24h (caution in dehydrated animals). Topical corticosteroids for mild cases. Note: systemic steroids may cause abortion in camelids |
| Wound Care |
Gentle debridement of necrotic tissue. Topical emollients (aloe vera, petrolatum). Silver sulfadiazine for severely damaged skin. Fly control essential |
| Antibiotics |
For secondary bacterial infection: Penicillin (procaine penicillin G 22,000 IU/kg IM q24h) or broad-spectrum based on culture |
| Hepatic Support (Type III) |
IV fluids with 5% dextrose for hypoglycemia. Low-protein, high-energy diet (beet pulp). B-vitamins. Avoid stress |
| Zinc Supplementation (Camelids) |
Zinc sulfate 1 g/day PO OR Zinc methionine 2-4 g/day PO. Response seen in 30-90 days. Discontinue alfalfa; minimize calcium |
| Strategy |
Implementation |
| Shade Provision |
Natural (trees) or constructed shelters. Essential during peak UV hours (10 AM - 4 PM) |
| Topical Sun Protection |
Zinc oxide or titanium dioxide-based sunblock on vulnerable areas (ears, nose). SPF 30 or higher. Reapply frequently |
| Pasture Management |
Remove toxic plants (St. John's Wort, Senecio). Avoid young brassicas (less than 90 days for rape, less than 150 days for kale). Monitor spore counts in endemic facial eczema areas |
| Dietary Management |
Gradual introduction to lush pastures. Avoid sudden changes from dry to green forage. Zinc supplementation during high-risk periods |
| Post-Shearing Care (Camelids) |
Limit sun exposure immediately after shearing. Camelids lack lanolin and are highly susceptible to clipper burn and sunburn |
| Breeding Selection |
Select for pigmented skin in high-risk environments. Avoid breeding albino or extensively white animals in sunny climates |
| Condition |
Prognosis |
| Simple Sunburn |
GOOD - Full recovery with sun protection. New skin regenerates within weeks |
| Primary Photosensitization (Type I) |
FAVORABLE - Skin lesions resolve within 48 hours to 6 months once agent removed and sun avoided |
| Hepatogenous Photosensitization (Type III) |
GUARDED to POOR - Depends on extent of liver damage. Severe hepatic failure carries grave prognosis. Even recovered animals may have chronic liver disease |
| Zinc-Responsive Dermatosis |
GOOD - Most animals respond to zinc supplementation within 30-90 days. May require lifelong supplementation |
| Chronic/Neoplastic |
VARIABLE - Squamous cell carcinoma from chronic UV exposure requires aggressive surgery; prognosis depends on location and metastasis |