Zinc Deficiency and Dog Skin Problems: Signs and Supplements

By Emiel Maddens  ·  Reviewed in consultation with licensed veterinary professionals  ·  Updated April 2026  ·  11 min read

Photo by Tima Miroshnichenko on Pexels

Zinc deficiency is one of the most underdiagnosed nutritional causes of skin disease in dogs, yet it produces some of the most distinctive and distressing dermatologic signs in veterinary medicine. The characteristic thick, tightly adherent crusts that form around the eyes, muzzle, ears, and paw pads of affected dogs are often misdiagnosed as autoimmune disease, severe allergies, or fungal infections, leading to months of inappropriate treatment before the true cause is identified. For breeds predisposed to zinc malabsorption, particularly Siberian Huskies and Alaskan Malamutes, zinc-responsive dermatosis is a lifelong condition that requires ongoing dietary management and supplementation.

Understanding the critical role zinc plays in skin health, recognizing the clinical signs of deficiency, knowing which breeds and dietary patterns put dogs at risk, and learning how to supplement effectively can prevent significant suffering and avoid the frustration of ineffective treatments. In this guide, we cover the two recognized syndromes of zinc-responsive dermatosis in dogs, examine the dietary and genetic factors that contribute to zinc deficiency, review the diagnostic approach including skin biopsy findings, and provide evidence-based supplementation protocols. Whether your dog is an Arctic breed with suspected zinc malabsorption or a large-breed puppy showing signs of nutritional deficiency, this guide provides the comprehensive information you need.

What Is Zinc-Responsive Dermatosis in Dogs?

Zinc-responsive dermatosis is a skin condition caused by inadequate zinc availability in the body, either from impaired absorption, insufficient dietary intake, or increased demand. Zinc is required for over 300 metalloenzymes involved in DNA synthesis, cell division, protein synthesis, and immune function. In the skin specifically, zinc is essential for normal keratinization (the process by which skin cells mature and form the protective outer layer), wound healing, and antimicrobial defense. When zinc is deficient, the skin's normal maturation process breaks down, producing the characteristic clinical signs of parakeratotic hyperkeratosis.

Syndrome I: Breed-Associated Zinc Malabsorption

Syndrome I primarily affects Arctic and Northern breeds, most commonly Siberian Huskies, Alaskan Malamutes, and Samoyeds. These breeds appear to have a genetically determined defect in intestinal zinc absorption that prevents them from maintaining adequate zinc levels even on nutritionally complete diets. The condition typically manifests in young adults (1 to 3 years of age) and requires lifelong supplementation. Clinical signs include symmetrical crusting and scaling around the eyes, muzzle, ears, chin, elbows, hocks, and footpads. Without treatment, the crusts become progressively thicker and may crack, creating painful fissures that invite secondary bacterial and yeast infections.

Syndrome II: Diet-Related Zinc Deficiency

Syndrome II occurs in rapidly growing puppies of large and giant breeds fed diets that are either genuinely zinc-deficient or that contain factors blocking zinc absorption. Diets high in phytates (found in grains, legumes, and soy), excessive calcium supplementation, and diets high in iron or copper can all interfere with zinc absorption. This syndrome is most commonly seen in puppies between 2 and 6 months of age and typically resolves completely when the dietary issue is corrected. Clinical signs are similar to Syndrome I but may be more generalized, affecting the trunk and limbs in addition to the face and extremities.

Generic Dog Food Disease

A related condition sometimes called generic dog food disease was historically seen in dogs fed low-quality, plant-heavy commercial diets with poor zinc bioavailability. These diets technically contained zinc but in forms poorly absorbed by dogs, or with high levels of phytates and fiber that bound zinc in the intestinal tract. While improved pet food regulations have reduced the incidence of this presentation, it still occurs in dogs fed bargain-brand foods with predominantly plant-based protein sources and excessive grain content.

Hepatocutaneous Syndrome (Superficial Necrolytic Dermatitis)

While not technically zinc-responsive dermatosis, hepatocutaneous syndrome (also called superficial necrolytic dermatitis or metabolic epidermal necrosis) produces similar skin lesions and involves zinc metabolism derangement secondary to severe liver disease. This condition affects older dogs with hepatic dysfunction and carries a much poorer prognosis than primary zinc-responsive dermatosis. Differentiation from zinc-responsive dermatosis requires liver ultrasound and blood work showing characteristic changes in amino acid and zinc metabolism. This is an important differential diagnosis that your veterinarian will consider.

Zinc-responsive dermatosis classically affects the areas around the eyes, muzzle, ears, and paw pads, producing thick, adherent crusts that are difficult to remove.

Photo by Alexander Mass on Unsplash

What Causes Zinc Deficiency in Dogs?

Zinc deficiency in dogs results from one or more of three mechanisms: inadequate dietary intake, impaired intestinal absorption, or increased physiological demand. Understanding which mechanism is at play in your dog determines both the treatment approach and the long-term prognosis.

1. Genetic Zinc Malabsorption in Arctic Breeds

The most well-recognized cause of canine zinc deficiency is the inherited absorption defect in Arctic breeds. The exact genetic mechanism has not been fully characterized, but affected dogs demonstrate impaired uptake of zinc across the intestinal mucosa despite adequate dietary levels. This defect appears to be partially autosomal recessive, meaning carrier dogs may show mild subclinical signs. Siberian Huskies and Alaskan Malamutes are by far the most commonly affected, but cases have been reported in Samoyeds, Bull Terriers, and several other breeds.

2. Phytate-Rich Diets That Block Zinc Absorption

Phytic acid (inositol hexaphosphate), found abundantly in cereal grains, legumes, and soy, binds zinc in the intestinal lumen to form insoluble zinc-phytate complexes that cannot be absorbed. Dogs are particularly susceptible because they lack significant levels of phytase, the enzyme that breaks down phytic acid. Diets where grains or legumes constitute the primary ingredients can significantly reduce zinc bioavailability even when the total zinc content appears adequate on paper. This is one reason why dogs fed grain-heavy, budget-brand foods are at elevated risk.

3. Excessive Calcium Supplementation

Calcium competes with zinc for intestinal absorption, and excessive calcium intake can substantially reduce zinc uptake. This is particularly problematic in large and giant breed puppies whose owners add calcium supplements to an already calcium-adequate diet in an attempt to support bone growth. The resulting calcium excess not only blocks zinc absorption but can also interfere with other trace mineral uptake. Feeding an appropriately formulated large-breed puppy food without additional calcium supplementation is the simplest prevention strategy.

4. Gastrointestinal Disease and Malabsorption

Any condition that damages the intestinal mucosa or impairs nutrient absorption can lead to secondary zinc deficiency. Inflammatory bowel disease, exocrine pancreatic insufficiency, chronic enteritis, and intestinal parasitism can all reduce zinc absorption. Dogs with these conditions may present with skin signs of zinc deficiency as one of multiple manifestations of broader malabsorption. Treating the underlying gastrointestinal condition is essential for long-term zinc status normalization.

5. Rapid Growth and Increased Physiological Demand

Large and giant breed puppies during their most rapid growth phases (2 to 6 months) have dramatically increased zinc requirements for bone mineralization, organ development, and immune system maturation. If their diet does not provide zinc significantly above maintenance levels during this critical window, deficiency can develop quickly. Pregnant and lactating dogs also have elevated zinc requirements, and zinc deficiency during these periods can affect both the mother's skin and the developing puppies.

Which Breeds Are Most Affected?

Zinc-responsive dermatosis has strong breed predispositions, particularly for Syndrome I. While Syndrome II can theoretically affect any rapidly growing puppy on an inappropriate diet, certain breeds are diagnosed far more frequently than others.

• Siberian Husky: The Siberian Husky is the breed most commonly diagnosed with Syndrome I zinc-responsive dermatosis. Some estimates suggest that a significant minority of Huskies will develop clinically apparent zinc deficiency at some point in their lives. The characteristic periocular (around the eyes) crusting in a young adult Husky is considered almost pathognomonic for this condition. Many Husky breeders are familiar with the condition and may proactively supplement zinc in their breeding lines.
• Alaskan Malamute: Alaskan Malamutes share the same genetic predisposition to zinc malabsorption as Huskies and are the second most commonly affected breed. Malamutes tend to present with more severe, widespread lesions than Huskies, potentially reflecting their larger body size and correspondingly higher absolute zinc requirements. The muzzle, periocular regions, and paw pads are typically the first areas affected, with lesions spreading to the ears, elbows, and hocks as the deficiency progresses.
• Great Dane: Great Danes are one of the breeds most commonly affected by Syndrome II zinc deficiency due to their extraordinarily rapid growth rate. Puppies that double or triple their weight in a matter of weeks have extreme nutritional demands, and zinc deficiency can develop quickly if the diet is suboptimal. Over-supplementation with calcium, a common mistake with giant breeds, exacerbates the problem by blocking zinc absorption.
• German Shepherd: German Shepherds appear on both sides of the zinc deficiency spectrum. As a large breed with rapid growth, puppies can develop Syndrome II on inadequate diets. Additionally, some lines appear to have a breed-related predisposition to zinc malabsorption that produces milder versions of Syndrome I. The breed's predisposition to exocrine pancreatic insufficiency and inflammatory bowel disease further increases the risk of secondary zinc deficiency through malabsorption.
• Bull Terrier: Bull Terriers have a documented breed-specific zinc-related dermatosis that is sometimes classified separately from the classic Syndrome I. Affected Bull Terriers develop acrodermatitis, a lethal inherited disorder of zinc metabolism that causes severe growth retardation, immunodeficiency, and progressive skin disease. This condition is more severe than typical zinc-responsive dermatosis and carries a guarded prognosis. Genetic testing may be available for some breeding lines.

Signs and Symptoms

The clinical signs of zinc-responsive dermatosis are among the most recognizable in veterinary dermatology once you know what to look for. The distribution pattern and the quality of the skin lesions are highly characteristic and help differentiate this condition from other skin diseases.

Periocular Crusting and Scaling

One of the earliest and most distinctive signs is the development of thick, tightly adherent, silvery-white to yellowish crusts around the eyes. The crusts follow the margins of the eyelids and may extend onto the bridge of the nose. Unlike the loose flakes of dandruff, these crusts are firmly attached and resist removal. When forcibly removed, the underlying skin is red, moist, and may ooze. This periocular distribution is so characteristic of zinc deficiency in Huskies and Malamutes that it should prompt immediate consideration of this diagnosis.

Crusty Muzzle and Chin

The muzzle and chin develop similar thick, hyperkeratotic (thickened) crusts, particularly along the lip margins and the nasal planum (nose leather). The nose may lose its normal smooth texture and become rough, cracked, and covered with a thick, grayish scale. Dogs may rub their faces on furniture or carpet, and the crusts may crack and bleed, especially in cold, dry weather. The mucocutaneous junctions (where skin meets mucous membrane) around the lips are commonly and prominently affected.

Paw Pad Hyperkeratosis

The footpads develop excessive keratin buildup, becoming thickened, cracked, and rough. In severe cases, the pads may develop painful fissures that cause lameness and reluctance to walk on hard surfaces. The interdigital skin (between the toes) may also become crusty and inflamed. Paw pad changes can be subtle initially but progress to obvious thickening that is visible even to owners unfamiliar with dermatologic conditions.

Ear Margin and Elbow Crusting

The margins of the ear pinnae (ear flaps) and the pressure points of the elbows and hocks develop crusty, scaly lesions similar to those on the face. Ear margin crusting may be mistaken for sarcoptic mange or vasculitis, but the concurrent facial lesions and breed predisposition point toward zinc deficiency. The elbows may develop thick, cracked calluses with superimposed hyperkeratotic crusts that extend beyond the normal callus margins.

Secondary Bacterial and Yeast Infections

The disrupted skin barrier created by zinc deficiency is highly susceptible to secondary infections. Bacterial pyoderma and Malassezia yeast overgrowth commonly complicate zinc-responsive dermatosis, adding itching, odor, and exudation to the primary crusting. These secondary infections can obscure the underlying zinc deficiency and lead to misdiagnosis if the treating veterinarian focuses only on the infectious component.

Dull Coat and Generalized Poor Skin Quality

Beyond the localized crusting, dogs with zinc deficiency often have an overall dull, dry, brittle coat and generalized skin that appears dull and unhealthy. Hair may be slow to regrow after clipping or shedding. Some dogs develop patchy alopecia (hair loss) in the most severely affected areas. The overall impression is of a dog whose skin and coat are simply not thriving despite otherwise adequate nutrition and care.

Diagnosis

Definitive diagnosis of zinc-responsive dermatosis requires a combination of clinical presentation, breed and dietary history, response to zinc supplementation, and ideally skin biopsy. While the clinical picture in an Arctic breed with periocular crusting is highly suggestive, histopathology provides the most reliable confirmation.

Skin Biopsy and Histopathology

Skin biopsy is the gold standard for diagnosing zinc-responsive dermatosis. Histopathologic examination reveals a characteristic pattern of marked diffuse parakeratotic hyperkeratosis, meaning the stratum corneum is dramatically thickened with retained nuclei in the keratinocytes (a sign of abnormal keratinization). The epidermis may show pallor and vacuolization of the upper layers, and the dermal-epidermal junction may show a distinctive pattern that pathologists familiar with the condition can recognize. These findings, combined with the clinical picture, provide a confident diagnosis.

Serum Zinc Level Testing

Blood zinc levels can be measured, but interpreting results requires caution. Normal canine serum zinc ranges from approximately 0.7 to 2.0 micrograms per milliliter, but levels can fluctuate based on recent meals, time of day, stress, and sample handling. Some dogs with clinical zinc deficiency have serum zinc levels within the low-normal range, making a single measurement unreliable as a standalone diagnostic test. A fasted morning sample submitted to a laboratory experienced in trace mineral analysis provides the most useful results.

Dietary History and Analysis

A thorough dietary history is essential and may reveal contributing factors. Your veterinarian or a veterinary nutritionist will evaluate the primary diet for zinc content and bioavailability, assess for phytate-heavy ingredients, check for calcium over-supplementation, review any treats or supplements, and calculate the overall zinc-to-phytate ratio. For dogs on home-prepared diets, submitting the recipe for formal nutritional analysis can identify zinc shortfalls that are not obvious from ingredient lists alone.

Response to Zinc Supplementation (Therapeutic Trial)

In many cases, the most practical diagnostic confirmation is a therapeutic trial of zinc supplementation. Dogs with true zinc-responsive dermatosis typically show visible improvement in skin lesions within 2 to 6 weeks of starting appropriate zinc supplementation. If the dog has Syndrome II (dietary deficiency), dietary correction alone may produce improvement. For Syndrome I (malabsorption), supplementation above dietary levels is required. A positive response to zinc, when combined with compatible clinical signs and breed predisposition, confirms the diagnosis.

Treatment

Treatment of zinc-responsive dermatosis centers on restoring adequate zinc levels through oral supplementation, dietary optimization, and management of secondary complications. The specific approach depends on whether your dog has Syndrome I or Syndrome II.

Oral Zinc Supplementation for Syndrome I

Dogs with breed-associated zinc malabsorption (Syndrome I) typically require lifelong oral zinc supplementation. Zinc methionine and zinc gluconate are generally preferred over zinc sulfate because they are better tolerated and have higher bioavailability. Starting doses are typically zinc methionine at 1.7 to 2.0 mg per kilogram of body weight daily or zinc gluconate at 3 to 5 mg per kilogram daily, given with food to reduce gastrointestinal side effects. Your veterinarian will adjust the dose based on clinical response and monitoring. Some dogs require doses at the higher end of the range, and a few may need intravenous zinc during severe flares before transitioning to oral maintenance.

Dietary Correction for Syndrome II

For puppies with diet-related zinc deficiency, the primary intervention is correcting the underlying dietary issue. Switching to a high-quality, AAFCO-compliant puppy food appropriate for the dog's breed size (large-breed puppy formula for large breeds) usually resolves the deficiency within 2 to 4 weeks. Discontinuing any calcium supplements, reducing excess phytate exposure by avoiding grain-heavy or soy-heavy foods, and ensuring the diet provides zinc from bioavailable sources (animal-based zinc) are the key dietary changes. Short-term zinc supplementation may be added to accelerate recovery.

Topical Management of Crusting

The thick, adherent crusts characteristic of zinc deficiency can be gently softened and removed to improve comfort and allow topical medications to reach the skin surface. Soaking crusted areas with warm, wet compresses for 10 to 15 minutes helps loosen the scale. Apply a thin layer of petroleum jelly or a veterinary emollient to softened crusts before gentle removal. Do not forcibly remove crusts, as this causes pain and bleeding. Medicated shampoos containing salicylic acid can help manage ongoing scale production. Between baths, our topical products can help manage the secondary infections that commonly complicate these lesions.

Treatment of Secondary Infections

Secondary bacterial pyoderma and Malassezia yeast infections are common in zinc-deficient skin and require concurrent treatment. Topical antimicrobial therapy using chlorhexidine spray for bacterial infections or antifungal spray for yeast dermatitis can be applied directly to affected areas between baths. Systemic antibiotics or antifungals may be necessary for severe or widespread secondary infections. As zinc levels normalize and the skin barrier improves, the susceptibility to secondary infections typically decreases.

Omega-3 and Vitamin E Co-Supplementation

Adding omega-3 fatty acids (EPA and DHA from fish oil) and vitamin E alongside zinc supplementation provides synergistic support for skin barrier repair. Omega-3s reduce inflammation and support the lipid matrix of the stratum corneum, while vitamin E provides antioxidant protection for the recovering skin cells. This combination approach often produces faster clinical improvement than zinc supplementation alone and supports long-term skin maintenance in dogs with chronic zinc-responsive dermatosis.

Prevention

While genetic zinc malabsorption (Syndrome I) cannot be prevented, dietary zinc deficiency (Syndrome II) is entirely preventable. Even for breeds predisposed to Syndrome I, proactive management can minimize flare severity and frequency.

Feed a High-Quality, Zinc-Adequate Diet

Choose a dog food where animal-based proteins are the primary ingredients, as zinc from animal sources (meat, organ, bone) has significantly higher bioavailability than zinc from plant sources. Look for foods that list specific zinc sources (zinc methionine, zinc proteinate, or zinc amino acid chelate) rather than zinc oxide, which has lower bioavailability. Use our Dog Food Ingredient Scanner to evaluate your dog's food for potentially problematic ingredients like excessive phytates or plant-heavy protein sources.

Avoid Excessive Calcium Supplementation

Do not add calcium supplements to a nutritionally complete commercial dog food. The calcium-to-zinc ratio in the diet affects zinc absorption, and excessive calcium is one of the most common dietary causes of secondary zinc deficiency in puppies. Large and giant breed puppy foods are formulated with appropriate calcium-to-phosphorus and calcium-to-zinc ratios. Adding supplemental calcium disrupts these carefully balanced ratios.

Proactive Supplementation for At-Risk Breeds

Owners of Siberian Huskies, Alaskan Malamutes, and other Arctic breeds should discuss proactive zinc supplementation with their veterinarian, particularly during periods of stress, rapid growth, or dietary transition. Starting low-dose zinc supplementation before clinical signs develop can prevent the painful, unsightly crusting that characterizes zinc-responsive dermatosis. Regular monitoring of skin condition, particularly the periocular area and paw pads, allows early detection and intervention.

Monitor During High-Demand Periods

Periods of increased physiological demand, including rapid growth, pregnancy, lactation, illness, and post-surgical recovery, increase zinc requirements. During these times, monitor your dog's skin closely for early signs of deficiency and consider temporary zinc supplementation if your veterinarian agrees. Stress also increases zinc utilization, so dogs undergoing significant life changes (new home, boarding, travel) may benefit from short-term supplementation.

Regular Veterinary Skin Checks

For dogs in predisposed breeds or those with a history of zinc-responsive dermatosis, schedule dermatologic rechecks every 6 months. These visits allow your veterinarian to catch early signs of relapse, adjust supplementation doses based on skin condition, and address any secondary infections before they become severe. Early intervention during a zinc flare produces faster resolution and less discomfort than waiting until lesions are widespread.

Related Symptoms

Dogs with this condition often show these symptoms. Our guides explain each one:

• Why Does My Dog Have Dandruff?, Explore how zinc deficiency causes flaking and scaling that is often mistaken for simple dandruff.
• Why Is My Dog's Skin Turning Black?, Learn how chronic inflammation from zinc deficiency can lead to hyperpigmentation.
• Why Does My Dog Smell Yeasty?, Discover how zinc-deficient skin creates an ideal environment for Malassezia yeast overgrowth.
• Why Is My Dog Licking Their Paws?, Understand how paw pad changes from zinc deficiency cause discomfort and licking behavior.

Frequently Asked Questions About Zinc Deficiency and Dog Skin Problems

Q: How do I know if my dog has zinc deficiency?

The most characteristic signs are thick, crusty, tightly adherent scales around the eyes, on the muzzle, around the ears, and on the paw pads. In Arctic breeds (Huskies, Malamutes), this pattern is highly suggestive. However, definitive diagnosis requires veterinary evaluation including skin biopsy showing parakeratotic hyperkeratosis. Serum zinc levels can support the diagnosis but should not be used alone, as some affected dogs have low-normal blood levels. A positive response to zinc supplementation provides practical confirmation.

Q: What type of zinc supplement is best for dogs?

Zinc methionine and zinc gluconate are the preferred forms for canine supplementation because they have higher bioavailability and are better tolerated than zinc sulfate, which commonly causes nausea and vomiting. Zinc picolinate is another well-absorbed form used in some veterinary protocols. Zinc oxide, commonly found in over-the-counter supplements, has the lowest bioavailability and is generally not recommended for treating zinc-responsive dermatosis. Always give zinc supplements with food to minimize gastrointestinal irritation.

Q: Can too much zinc be harmful to dogs?

Yes, zinc toxicity is possible and can cause gastrointestinal upset (vomiting, diarrhea, loss of appetite) at moderately elevated doses and hemolytic anemia (destruction of red blood cells) at very high doses. Zinc toxicity is most commonly seen in dogs that ingest zinc-containing objects (pennies minted after 1982, zinc nuts and bolts, zinc-based skin creams). Oral zinc supplementation at veterinarian-recommended doses is safe, but do not exceed the prescribed amount. Regular monitoring through blood work helps ensure levels remain in the therapeutic range.

Q: Do Huskies always need zinc supplements?

Not all Huskies develop clinical zinc-responsive dermatosis, but the breed as a whole has a genetic predisposition to impaired zinc absorption. Huskies that show no clinical signs on a high-quality diet do not necessarily need zinc supplementation. However, Huskies that develop any periocular crusting, paw pad thickening, or nasal planum scaling should be evaluated for zinc deficiency, and those diagnosed with Syndrome I typically require lifelong supplementation. Some breeders and veterinarians recommend prophylactic low-dose supplementation for all Huskies, but this is not universally accepted.

Q: Can I treat zinc deficiency with diet changes alone?

For Syndrome II (diet-related) zinc deficiency, dietary correction is often sufficient. Switching to a high-quality, animal-protein-based food and eliminating calcium over-supplementation typically resolves the condition within 2 to 4 weeks. For Syndrome I (breed-associated malabsorption), dietary optimization helps but is usually insufficient on its own because the underlying absorption defect prevents adequate zinc uptake even from the best diet. These dogs require supplementation above and beyond dietary levels.

Q: How long does it take for zinc supplements to improve my dog's skin?

Most dogs with zinc-responsive dermatosis show initial improvement in skin crusting within 2 to 4 weeks of starting appropriate supplementation. Significant clinical improvement is typically evident by 4 to 6 weeks, with near-complete resolution of lesions by 8 to 12 weeks in responding dogs. Paw pad hyperkeratosis may take the longest to resolve because the thickened keratin must gradually wear away and be replaced by normally keratinized tissue. If no improvement is seen by 6 weeks at adequate doses, the diagnosis should be reconsidered and alternative conditions evaluated.

Sources

White SD, Bourdeau P, Rosychuk RA, et al. Zinc-responsive dermatosis in dogs: 41 cases and literature review. Veterinary Dermatology. 2001;12(2):101-109.

Colombini S, Dunstan RW. Zinc-responsive dermatosis in northern-breed dogs: 17 cases (1990-1996). Journal of the American Veterinary Medical Association. 1997;211(4):451-453.

Miller WH, Griffin CE, Campbell KL. Muller and Kirk's Small Animal Dermatology. 7th ed. Elsevier; 2013.

National Research Council. Nutrient Requirements of Dogs and Cats. National Academies Press; 2006.

Marsh KA, Ruedisueli FL, Coe SL, Watson TD. Effects of zinc and linoleic acid supplementation on the skin and coat quality of dogs receiving a complete and balanced diet. Veterinary Dermatology. 2000;11(4):277-284.

Related Reading

• Vitamin E for Dogs: Can It Improve Skin and Coat Health?, Learn about another essential nutrient that works synergistically with zinc to support skin health.
• Raw Diet for Dogs with Skin Allergies, Understand how home-prepared diets can affect zinc status and why balance is critical.
• Seborrhea in Dogs, Explore another keratinization disorder that shares some clinical features with zinc-responsive dermatosis.
• Hydrolyzed Protein Dog Food for Skin Allergies, Learn about dietary management when skin disease has a food allergy component alongside nutritional factors.

Emiel Maddens

Founder of Vetified. Develops topical antifungal and antimicrobial formulations for companion animals. Vetified products are listed on DailyMed and manufactured through FDA-registered facilities in the United States.