Diseases of the feline nasal planum
Skin lesions on a cat’s nose can be challenging in terms of differential diagnosis and treatment; Christina Gentry shows how to approach them in a logical fashion.
Nasal planum lesions in the cat may present alone or with other skin lesions.
The presence or absence of other lesions can help narrow the differential list.
Superficial impression cytology and biopsy are the most frequently used diagnostics.
Immune-mediated, infectious and paraneoplastic disorders may also have systemic signs; these can include malaise and decreased appetite.
Diseases of the nose and the bridge of the nose are uncommon to rare in feline patients. Some conditions will affect both the non-haired area (nasal planum and nasal philtrum) and the haired bridge of the nose, while others will affect only the nasal planum. A variety of conditions may lead to lesions on the nose, including neoplastic, parasitic, immune-mediated, infectious, genetic, environmental and idiopathic causes. Diseases affecting the nasal planum may also involve both the surrounding skin and distant sites. The goal of this article is to briefly review the pathogenesis, diagnostics, treatment options and prognosis for conditions that the practitioner is likely to encounter, based on the underlying etiology.
Neoplastic and paraneoplastic
Squamous cell carcinoma
Squamous cell carcinomas (SCC) are a common occurrence in the cat, accounting for around 15% of all feline cutaneous neoplasms 1. Most cutaneous SCC are found on the face, especially the minimally haired tips of the ears, bridge of the nose, eyelids, and non-haired nasal planum (Figure 1). The pathogenesis involves chronic exposure to UV radiation, with white or light-colored cats being at an increased risk due to the higher amount of UVB light reaching the skin surface 2. The initial lesions that develop – which may at first resemble a non-healing scratch or other trauma 3 – are actinic keratosis (pre-cancerous lesions of chronic sun exposure), then squamous cell carcinoma in situ, followed by squamous cell carcinoma. A combination of lesions may be present at the same time, but typically they are inflamed with crusts overlying erythematous, alopecic, and eroded skin 3, varying in size from a few millimeters to a few centimeters in diameter. Affected areas may be depressed and the crusts can be hemorrhagic, with papillary or fungiform masses sometimes present in more advanced cases.
Diagnosis is typically made by biopsy or excision. A punch biopsy method (see Box 1) can be used for the nasal planum, while a margin/shave biopsy may be more useful on the ear tips. Since the lesions affect the epidermis, a fine-needle aspirate may not be as helpful for diagnosis for smaller lesions. The histopathology of a well-differentiated SCC will have trabeculae and islands of epidermal cells that dive into the dermis. These lesions have more basal-appearing keratinocytes on the periphery, with gradual differentiation to keratinized epidermal cells in the center of the lesions. These epidermal cells form keratin "pearls" that can found in the center of the neoplastic epidermal islands 3.
Squamous cell carcinomas of the face have a low metastatic rate 4 and most therapy is directed at individual lesions. Staging may be recommended prior to treatment, including blood work, local lymph node aspirates and chest radiographs. Treatment options for facial SCC include surgery, radiation therapy, and intralesional chemotherapy. Surgical excision is recommended for most SCC affecting the face 4, although surgical removal of larger tumors on the nasal planum may lead to disfigurement. In these cases radiation therapy is recommended; this includes the use of strontium-90 brachytherapy for tumors that are 3 mm deep or less, and teletherapy for deeper lesions 5. Smaller lesions that can be completely removed tend to have the best outcome, and radiation therapy on smaller lesions can significantly increase the disease-free interval by months to years 5. More invasive lesions have a faster recurrence rate.
Paraneoplastic alopecia is a rare syndrome reported primarily in the cat. The underlying pathogenesis is not fully understood, but almost all cases are secondary to malignant neoplasia of the pancreas, intestines, liver, or biliary tract 6. General clinical signs will include malaise, weight loss and decreased appetite in a previously healthy older feline. Cutaneous signs can be striking and include a rapid loss of easily epilating hair on the belly with progression to hair loss on limbs and face. The underlying skin is smooth, occasionally with a brown discharge from a secondary Malassezia dermatitis 7. The paw pads and nasal planum are shiny and smooth, whilst the bridge of the nose may be alopecic.
The outcome is generally poor, as metastases to lymph nodes, liver, and lungs have typically occurred before alopecia and loss of normal layering on the nasal planum is seen 6 7. Palliative care or euthanasia is recommended for most cases if surgical intervention is unlikely to be curative.
Squamous cell carcinomas are a common occurrence in the cat, accounting for 15% of all feline skin tumors, with most of them occurring on the face, especially the minimally haired tips of the ears, bridge of the nose, eyelids, and non-haired nasal planum.
Mosquito bite hypersensitivity is especially common in outdoor, darker-coated cats during the warmer months in certain warmer climates such as the southern United States and the Mediterranean countries. Indoor-only cats are rarely affected. This is considered to be a Type 1 hypersensitivity , although it also has features of a Type 4 hypersensitivity. Some affected cats may start to show wheal formation within 20 minutes of being bitten 8. Miliary dermatitis and occasionally eosinophilic granulomas are seen on the bridge of the nose, ear tips, and foot pads (Figure 2). These lesions may progress to larger crusts, erosions, and excoriations from pruritus. The lesions may extend into the nasal planum from the bridge of the nose in more severely affected cats, and there may be regional lymphadenopathy 8 9.
This condition is often diagnosed based on history and physical examination. A biopsy can be considered in more severe cases where there is concern for pemphigus foliaceus or herpes virus dermatitis. Superficial cytology is recommended to check for secondary bacterial infection; in non-infected cases, this will often predominately demonstrate eosinophils, with other cell types being less common. Histopathology of mosquito bite hypersensitivity typically reveals a marked eosinophilic inflammation with overlying crusts and serum exudate. It may be difficult to differentiate from other eosinophilic skin disease in the cat or from herpes virus dermatitis if viral inclusion bodies are not seen 9.
Successful treatment requires therapy for the acute inflammation and secondary infection (if present), along with decreasing or eliminating the number of mosquito bites. Oral or injectable short-acting steroids at mid to high anti-inflammatory doses (1-2 mg/kg daily) are most likely to be effective at controlling the inflammation 8. Therapy may only be needed for 2-4 weeks if further bites can then be avoided, but treatment can be continued during the peak mosquito season if environmental changes cannot be made (e.g., in barn/farm cats).
Avoidance is the best strategy. This may include keeping the cat indoors during peak mosquito hours and seasons, eradicating stagnant water sources where mosquito larvae may be present, removing shrubs and tall grass near water sources, and using environmental repellents 8. Topical repellents can be applied if cats cannot be kept indoors, but they can have variable efficacy and should be applied daily whenever possible. Permethrin products (formulated for cats), citronella, neem oil, or essential oil of the catnip plant can also be used although the risk of toxicity should be considered 8. In the author’s anecdotal experience picaridin-containing preparations can be effective for several hours when applied on the cat’s dorsum and ear tips.
Prognosis is excellent for cats that can be housed indoors, but is still fair to good for patients where significant environmental management is not possible.
Pemphigus foliaceus (PF) is the most common cutaneous immune-mediated disease in the cat 10, although overall it is uncommon in the feline population. Pemphigus foliaceus affects the desmosomal junctions between the more superficial epidermal cells. This attack leads to separation of superficial epidermal cells prior to full maturation as anucleated keratinocytes. Most cases are idiopathic, with a smaller proportion being triggered by certain drugs 11. Typically affected cats are middle aged, but cats of any age, including kittens, can develop the condition.
PF lesions are more commonly seen on the concave surface of the pinna, face, bridge of nose and nasal planum (Figure 3); nasal planum lesions are seen in up to 50% of cats (Figure 4) 11 12 . Affected animals may also have lesions surrounding the mammary papilla, the footpads, nail beds and haired skin 11. Some cats have facially centered lesions, some will only have paw and nail bed involvement, while others have lesions in multiple body areas. The primary lesions consistent of yellow pustules that span multiple hair follicles which then progress into annular yellow crusts, possibly with underlying erosion. Loss of the normal cobblestone appearance can be seen in the affected nasal planum and footpads, and nail beds may have thick yellow, or occasionally green, purulent discharge exuding from the claw folds. Pruritus is variable with PF; significant self-trauma may alter the appearance of lesions, especially on the face and ears, and affected cats may develop fever, malaise and a decreased appetite.
Initial diagnostics should include impression cytology of lesions, either by rupturing a pustule or lifting of a crust. Cytology will show mainly non-degenerate neutrophils and variable number of acantholytic keratinocytes; these are rounded nucleated keratinocytes that have lost desmosome junctions and appear blue with routine staining. Dermatophyte test medium (DTM) cultures, Wood’s lamp examination and skin scraping may be recommended to rule out dermatophytosis and ectoparasites (i.e., Demodex spp. and Notoedres cati). Baseline blood work may demonstrate a leukocytosis and hyperglobulinemia 13.
A biopsy is recommended for definitive diagnosis, but because the diagnostic lesions (i.e., neutrophilic pustules with acantholytic keratinocytes) are superficial in nature, biopsy sites should not be clipped, shaved or scrubbed, as the diagnostic sample may be lost. Histopathology will reveal neutrophilic crusting; epidermal and superficial dermal infiltrate will be predominately neutrophilic, or mixed neutrophilic and eosinophilic 14. The pustules may have predominately neutrophilic or eosinophilic infiltrate with acantholytic keratinocytes, either alone or in rafts, and the hair follicles may also be affected (Figure 5) 14.
Corticosteroids are the primary treatment option, with monotherapy being successful in many cats. Induction doses of prednisolone at 2-6 mg/kg PO per day have been used, with 2-3 mg/kg per day being sufficient in most patients 12. Oral therapy is preferred and likely more effective compared with injectable long-acting steroids, although exceptions can be made for patients that are difficult to medicate. Remission is typically achieved in 2-8 weeks, although the majority of patients will require lifelong therapy. Once remission occurs, steroid dosage is tapered by approximately 25% every 2-3 weeks until the patient is either fully off steroids or begins to flare again.
Adjunctive immune modulators should be considered due to the long-term nature of feline PF and the potential for steroid-adverse events, such as weight gain, risk of diabetes development, and increased risk of viral upper respiratory infections. Modified cyclosporine, either in liquid or capsule form, at 5-7 mg/kg per day can be used to reduce (and in certain cases eliminate) corticosteroid requirements. The dosage can be tapered to 2-3 days per week in some cases 15. Chlorambucil can be considered for cases that are refractory to modified cyclosporine, if the patient has significant gastrointestinal side effects from the drug, or there is a concern for long-term steroid-adverse events 15. Azathioprine is not recommended in cats due to the potential for bone marrow suppression 15. The outcome for most cats is good if they tolerate oral medications well and do not develop steroid-related adverse events 11.
Pemphigus foliaceus lesions are more commonly seen on the concave surface of the pinna, face, bridge of nose and – in up to 50% of cats – the nasal planum; affected animals may also have lesions surrounding the mammary papilla, the footpads, nail beds and haired skin.
Feline herpesvirus dermatitis is an uncommon manifestation of feline herpesvirus-1 (FHV-1) infection. This virus is a common pathogen that affects the upper respiratory tract, frequently causing self-limiting rhinotracheitis and conjunctivitis. In the majority of cats respiratory signs resolve but the virus remains latent within the trigeminal ganglia 16. Cats that develop skin lesions may have a history of upper respiratory infection, corticosteroid use, or stressors prior to the development of lesions, with adult cats being affected more often than kittens. The cutaneous lesions are vesicles, erosions and ulceration of the face with overlying crusts. The bridge of the nose, nasal planum, muzzle, and periocular region may be affected, but body-wide ulcerations can develop 17.
Suspicion of this condition may be raised based on history and physical examination, especially if concurrent upper respiratory signs are present. Biopsy is strongly recommended for definitive diagnosis. FHV-1 can appear similar to mosquito bite dermatitis, pemphigus foliaceus, eosinophilic granulomas, and erythema multiforme depending on the level of crusting and self-trauma. Histopathology reveals necrosis of the epidermis which can extend into the dermis. There is considerable exudate and crusting, with a significant eosinophilic infiltrate being found more commonly than a neutrophilic infiltrate 9. The presence of intranuclear inclusion bodies in keratinocytes or giant cells is diagnostic, but will not be detected in all cases. PCR of the affected tissue or immunohistochemistry may be needed if inclusion bodies are not found in the sample. A recent study has demonstrated reliability in using RNA scope® in situ hybridization to diagnose FHV-1 on formalin-fixed paraffin-embedded tissues 18. Note that viral PCR of respiratory or ocular lesions cannot confirm or exclude cutaneous herpes virus, although it may help in diagnosing the cause of a concurrent upper respiratory disease.
Treatment depends on the severity of the condition; oral and topical antivirals, interferon omega, and imiquimod have all been recommended 16 19. If an affected cat is being treated with corticosteroids these should be discontinued wherever possible.
This is the clinical disease caused by infection with the dimorphic fungus Sporotrix schenckii. This environmental organism is found in organic matter and soil and the fungal conidia are traumatically inoculated via plant matter or by animal (mainly cat) scratches or bites. This condition is endemic in central and South America – with an epidemic in Brazil over the last 20 years 20 – and is occasionally seen in North America 20 21. Importantly, this disease is zoonotic, with the most common route of transmission being cat bites or scratches to their human caretakers 20.
In cats the cutaneous and cutaneous-lymphatic form are more common. The face and head are commonly involved, with lesions on the bridge of the nose extending into the nasal planum 21. Cutaneous lymphatic progression to the disseminated form is less common. A retrospective evaluation of 23 cases noted that almost all infected cats had outdoor access, and most cats were previously systemically healthy, although a small proportion were found to have co-morbidities, including retroviral infection at the time of diagnosis 21.
Infection may be diagnosed by fine-needle aspirate and cytology, fungal culture and histopathology 22. Treatment with the azole antifungals (most commonly itraconazole) is typically successful, although sodium or potassium iodide have also been used 22. Therapy is typically continued for several months, and for at least 1-2 months after resolution of clinical signs. The prognosis is good for the cutaneous and cutaneous lymphatic forms, but may be less favorable for systemic cases.
Idiopathic nasal dermatitis is an uncommon disorder of unknown etiology and pathogenesis that has been reported to occur on the nasal planum of Bengal cats. Affected animals are typically less than one year of age, and only the nasal planum is affected by crusting, fissures, and ulceration. One study reviewed 48 cases and reported that the affected cats had no other cutaneous lesions and were otherwise unaffected 23. The condition is typically diagnosed by history and physical examination.
Several treatments, including oral prednisolone, topical salicylic acid and tacrolimus have been employed. Prednisolone tablets and salicylic acid cream were reported to be variably successful, while topical tacrolimus was most likely to lead to a clinical remission 23, although some cats will improve spontaneously. Prognosis is good to excellent, since most affected cats will respond to therapy.
This is an uncommon condition that occurs mainly in adult orange-colored cats. It appears as black lesions (asymptomatic macular melanosis) most commonly on the lips, although the nose, gingiva and eyelids can also be affected 24. The lesions are typically flat, annular to ovoid and are less than 1 cm in diameter (Figure 6). The skin is deeply pigmented but not irregular, and whilst the pigmented areas may slowly enlarge over time (Figure 7) they do not progress to plaques or masses 24. Diagnosis is typically made on physical examination, but a biopsy can be performed if there is concern for melanoma; histopathology will show marked melanosis, especially in the deepest layers of epithelium. As this is a cosmetic condition no treatment is indicated.
Vitiligo occurs when the majority of melanocytes (pigment-producing cells) are destroyed within an area of skin, and is rarely seen in the cat. The cause is multifactorial and may involve genetic susceptibility, immune-mediated destruction, and oxidative damage. Signs include symmetric depigmentation of both non-haired areas of skin (leukoderma) and haired skin (leukotrichia). In cats the pigment loss can be seen around the eyes, on the nose, lip margins, foot pads, and extremities. Other body regions are affected less commonly. There will be no inflammation, erosion or crusting in affected areas 25. The literature references are limited to Siamese cats, most of which were female and young adult to middle age at diagnosis 25. The diagnosis may be made on physical examination in a young adult Siamese cat presented for pigment loss without inflammation or crusting. Biopsy is recommended in cats that do not fit this profile or to rule out diseases such as cutaneous epitheliotropic lymphoma, a nutritional deficiency, or early discoid lupus erythematosus.
Vitiligo is considered a cosmetic disease in the cat, but the loss of pigment around eyelids and nose may predispose an otherwise pigmented cat to actinic keratosis and potentially squamous cell carcinoma. Treatment is not recommended.
ConclusionExternal nasal lesions in the cat are relatively rare but the clinician should approach these with the same care and logic as when investigating other dermatological conditions, remembering that the external nasal signs may be part of a more widespread problem. The lesions may be differentiated by a thorough history and physical examination, cytology, and potentially biopsy, but discussion with a veterinary dermatologist can be helpful for assistance with the more difficult or complicated cases.
Murphy S. Cutaneous squamous cell carcinoma in the cat: current understanding and treatment approaches. J Feline Med Surg 2013;15(5):401-407.
Dorn CR, Taylor DO, Schneider R. Sunlight exposure and risk of developing cutaneous and oral squamous cell carcinomas in white cats. J Natl Cancer Inst 1971;46:1073-1078.
Gross TL, Ihrke PJ, Walder EJ, et al. Epidermal tumors. In: Skin diseases of the dog and cat, clinical and histopathologic diagnosis. 2nd ed. Oxford, Blackwell Science Ltd 2005;562-600.
Hauck ML. Tumors of the skin and subcutaneous tissues. In: Vail DM, Withrow SJ (eds.) Withrow and MacEwen’s Small Animal Clinical Oncology. St Louis, Elsevier Saunders 2013;305-320.
Hammond GM, Gordon IK, Theon AP, et al. Evaluation of strontium Sr90 for the treatment of superficial squamous cell carcinoma of the nasal planum in cats: 49 cases (1990-2006). J Am Vet Med Assoc 2007;231(5):736-741.
Miller WH, Griffin CE, Campbell, KL. Miscellaneous Alopecias. In: Small Animal Dermatology 7th Ed. St. Louis, Elsevier Mosby 2013;554-572.
Caporali C, Albanese F, Binanti D, et al. Two cases of feline paraneoplastic alopecia associated with a neuroendocrine pancreatic neoplasia and a hepatosplenic plasma cell tumour. Vet Dermatol 2016;27(6):508-e137.
Nagata M. Mosquito Bites. In: Noli C, Foster A, and Rosenkrantz W (eds.) Veterinary Allergy. 1st ed. Oxford, John Wiley and Sons Ltd 2014;265-270.
Gross TL, Ihrke PJ, Walder EJ, et al. Ulcerative and crusting diseases of the epidermis. In: Skin diseases of the dog and cat, clinical and histopathologic diagnosis. 2nd ed. Oxford, Blackwell Science Ltd, 2005;116-135.
Scott DW, Miller WH, Erb HN. Feline dermatology at Cornell University: 1407 cases (1988-2003). J Feline Med Surg 2013;15(4):307-316.
Bizikova P, Burrows A. Feline pemphigus foliaceus: original case series and a comprehensive literature review. BMC Vet Res 2019;15(1):22.
Simpson DL, Burton GG. Use of prednisolone as monotherapy in the treatment of feline pemphigus foliaceus: a retrospective study of 37 cats. Vet Dermatol 2013;24(6):598-e144.
Jordan TJM, Affolter VK, Outerbridge CA, et al. Clinicopathological findings and clinical outcomes in 49 cases of feline pemphigus foliaceus examined in Northern California, USA (1987-2017). Vet Dermatol 2019;30(3):209-e65.
Gross TL, Ihrke PJ, Walder EJ, et al. Pustular diseases of the epidermis. In: Skin diseases of the dog and cat, clinical and histopathologic diagnosis. 2nd ed. Oxford, Blackwell Science Ltd 2005;4-26.
Irwin KE, Beale KM, Fadok VA. Use of modified ciclosporin in the management of feline pemphigus foliaceus: a retrospective analysis. Vet Dermatol 2012;23(5):403-e76.
Miller WH, Griffin CE, Campbell, KL. Viral, Rickettsial, and Protozoal Skin Diseases. In: Small Animal Dermatology 7th Ed. St. Louis, Elsevier Mosby 2013;343-362.
Hargis AM, Ginn PE. Feline herpesvirus 1-associated facial and nasal dermatitis and stomatitis in domestic cats. Vet Clin North Am Small Anim Pract 1999;29(6):1281-1290.
Mazzei M, Vascellari M, Zanardello C, et al. Quantitative real time polymerase chain reaction (qRT-PCR) and RNAscope in-situ hybridization (RNA-ISH) as effective tools to diagnose feline herpesvirus-1-associated dermatitis. Vet Dermatol 2019;30(6):491-e147.
Gutzwiller ME, Brachelente C, Taglinger K, et al. Feline herpes dermatitis treated with interferon omega. Vet Dermatol 2007;18(1):50-54.
Gremião ID, Miranda LH, Reis EG, et al. Zoonotic epidemic of Sporotrichosis: cat to human transmission. PLOS Pathog 2017;13(1):e1006077.
Crothers SL, White SD, Ihrke PJ, et al. Sporotrichosis: a retrospective evaluation of 23 cases seen in northern California (1987-2007). Vet Dermatol 2009;20(4):249-259.
Lloret A, Hartmann K, Pennisi MG, et al. Sporotrichosis in cats: ABCD guidelines on prevention and management. J Feline Med Surg 2013;15(7):619-623.
Bergvall K. A novel ulcerative nasal dermatitis of Bengal cats. Vet Dermatol 2004;15:28.
Miller WH, Griffin CE, Campbell, KL. Pigmentary Abnormalities. In: Small Animal Dermatology 7th Ed. St. Louis, Elsevier Mosby, 2013;618-629.
Tham HL, Linder KE, Olivry T. Autoimmune diseases affecting skin melanocytes in dogs, cats and horses: vitiligo and the uveodermatological syndrome: a comprehensive review. BMC Vet Res 2019;15(1):251.