A Clinical Approach to Alopecia in Cats
The workup of alopecia in cats involves a combination of thorough history, categorization, and use of targeted investigative techniques.
One of the more common dermatologic complaints for which clients seek veterinary attention for their cat is fur loss. Unfortunately, the lack of diagnostic specificity for this condition can prove challenging, especially if the client insists on a quick fix. It is beyond the scope of this article to describe in detail the clinical appearance and treatment of each of the various causes of alopecia in cats. Instead, the article lists common differentials and provides a logical algorithm for approaching these cases.
In the author’s opinion (and the opinions of others), the single most important diagnostic tool for any skin disease (including alopecia) is a thorough history.1 The following information is especially useful for pointing the practitioner toward certain categories of disease.
- Onset at a young age or exposure to other animals may suggest infectious or parasitic diseases such as dermatophytosis, Otodectes,
- Dermatitis in other animals and/or humans in contact with the patient is suggestive of some form of contagious disease (e.g., dermatophytosis, ectoparasitism).4,5
- Onset in older patients may suggest hyperthyroidism or paraneoplastic alopecia.6,7
- A very recent significant illness may suggest anagen defluxion, whereas history of significant physiologic stress 1 to 3 months before alopecia onset may suggest telogen effluvium.8-11
It is helpful to categorize alopecia in cats as spontaneous or self-inflicted and to further subdivide self-inflicted alopecia into pruritic or nonpruritic. These categories can help focus the initial diagnostic approach and decrease the number of potential differentials (FIGURE 1).
In the author’s experience, spontaneous alopecia is much less common than self-inflicted alopecia in cats, especially if the affected area is diffuse or widespread (FIGURE 2). In some cats, spontaneous alopecia can be readily demonstrated; large amounts of fur can be easily epilated by gentle tugging, especially at the edges of the alopecic area.12,13 In the absence of such evidence, the distinction from self-inflicted alopecia can be more challenging. Clients can be asked whether they have noticed the cat excessively licking, biting, or pulling at the fur or if they have seen the cat scratching. Although the client may be able to answer in the affirmative, a negative answer does not rule out self-trauma because clients may mistake these actions for normal behavior. Furthermore, some cats may prefer to groom when they are alone. You can ask clients if the cat vomits frequently (and if they have noticed fur in the vomitus), has appreciable amounts of fur in the feces, or has been constipated. Gentle brushing of the hand against the fur in the affected areas may facilitate the identification of short, broken “stubble” fur. Examination of this short fur under a microscope may demonstrate frayed or broken ends. For extreme cases, an Elizabethan collar can be placed on the cat for 2 to 3 weeks; the presence of fresh fur growth at the end of this period strongly indicates that the alopecia is indeed self-inflicted. If so, you then need to determine whether the self-inflicted condition is pruritic or nonpruritic.
The most common causes of self-inflicted alopecia are pruritic rather than nonpruritic, although both causes can overlap.14 Because true cases of nonpruritic self-inflicted alopecia are relatively scarce, it is not unreasonable to preliminarily assume pruritic disease until demonstrated otherwise. This assumption may be further supported by a good clinical response to a 3- to 4-week course of medium to high anti-inflammatory doses of glucocorticoids or other antipruritic agents.14
Pruritic Self-Inflicted Causes of Alopecia
After you have established self-inflicted alopecia caused by pruritus, the next question is whether the pruritus is caused by infection, infestation (e.g., ectoparasites), or hypersensitivity. Although most causes of pruritus in cats fall into 1 or more of these 3 categories, other causes are occasionally encountered (TABLE 1).10 At first glance, this categorization might seem to be useless because of the large number of potential differentials, especially in the first 2 categories. However, a relatively small number of inexpensive, rapid, and easily performed diagnostic tests can be used to simultaneously identify (or exclude) most of these conditions.
Identify and eliminate the easy causes first. Although many (or even most) cats with pruritic alopecia experience some form(s) of cutaneous hypersensitivity, leaping directly into a hypersensitivity disease workup is generally not the most efficient way to approach the pruritic cat for the following reasons:10,15
- Identification of infectious and parasitic causes of pruritus is relatively straightforward, whereas properly conducting a hypersensitivity workup can take months.
- The sensation of pruritus may be thought of as being additive. A hypersensitive cat with a secondary infection may be considerably more pruritic than a cat experiencing hypersensitivity alone. Fortunately, the reverse is also true, and the elimination of infection or parasitic disease may considerably improve the cat’s condition and allow a more accurate estimation of the baseline level of pruritus.
- Infectious and parasitic causes of pruritus are generally curable, whereas most hypersensitivity disorders are manageable at best.
The 3 main infectious organisms associated with pruritus in the cat are dermatophytes (FIGURES 3,4), staphylococci, and yeast (particularly Malassezia).10,16 With the exception of dermatophytosis, infectious causes of pruritus in cats are often secondary. Nonetheless, bacteria and yeast can contribute to cutaneous inflammation and enhance pruritus by serving as sources of pathogen-associated molecular patterns, proteolytic enzymes, and exotoxins.17
Cats may be infested with a wide variety of ectoparasites, any of which can cause pruritus. Surface-dwelling parasites include fleas, lice (Felicola subrostratus) (FIGURES 5–7), Cheyletiella species, fur mites (Lynxacarus), and chiggers (Eutrombicula, Neotrombicula species)18-20 (FIGURES 3,4). Otodectes mites may leave the ear canals and transiently infest the skin surface.21 Superficial-dwelling parasites include Notoedres (i.e., feline scabies; FIGURES 8,9), Demodex gatoi, and occasionally the unnamed feline Demodex mite.21,22 The only common representative of the deep-dwelling parasite group is Demodex cati. Fleas may contribute to pruritus through nonspecific inflammatory responses (e.g., the unpleasant sensation associated with the fleas crawling on the skin) as well as true hypersensitivity responses.
Cats, like dogs, can experience a variety of pruritic cutaneous hypersensitivities. The 3 most common hypersensitivities typically associated with significant alopecia in cats are flea hypersensitivity, food hypersensitivity, and feline atopic skin syndrome (hereafter referred to as atopic dermatitis).15 With the exception of flea hypersensitivity (which may also be considered a parasitic cause of pruritus), diagnostic pursuit of these differentials is often deferred until after infectious or parasitic conditions are controlled or eliminated. Compared with most infectious and parasitic conditions, diagnosis of hypersensitivity-associated pruritus is typically a bit more involved. The diagnostic approaches for each of the 3 major cutaneous hypersensitivities in cats are discussed below.
Flea hypersensitivity: Generally, the first step in a hypersensitivity workup is elimination of fleas, assuming that aggressive flea control has not already been instituted as part of the workup for parasitic causes of pruritic alopecia. Although practitioners in areas where fleas are not commonly found may be tempted to skip this step, a good faith effort must be made to eliminate the possibility of flea infestation because few geographic areas can truly be considered flea free.23 Fortunately, modern flea control agents have made elimination of fleas possible in all but the most challenging circumstances. A detailed discussion of the available agents and their selection is beyond the scope of this article, but other resources are available.24 Regardless of the agent(s) chosen, treatment must be maintained for a minimum of 4 to 6 weeks to be certain that the local flea population has been eliminated. All in-contact animals should also be treated, regardless of whether they are demonstrating clinical signs. Free-roaming cats should be confined for the duration of the treatment trial. Environmental flea control measures may include frequent vacuuming of the area to which the cat has access and spraying the household with insect growth regulators (such as pyriproxyfen). If dogs share the household, measures should be taken to ensure that they do not come into contact with open sheds, crawl spaces, etc., which may be “reseeded” by wildlife that may also access these areas.25
Food hypersensitivity: Despite the plethora of alternate diagnostics (e.g., IgE serology, quantification of fecal or salivary IgE), the only valid way to diagnose food hypersensitivity and identify the culprit foods in cats is controlled dietary elimination trials.26 Elimination diets may contain novel proteins (whether home cooked or commercial) or hydrolyzed proteins (low molecular weight peptides that can be absorbed by the digestive tract with a reduced risk of triggering an immune reaction).
- If a novel protein diet is selected, the ingredients should be carefully selected from sources phylogenetically distant from the patient’s normal diet ingredients. For example, a rabbit-based diet may be an acceptable empirical choice for a cat normally fed a fish-based diet.
- If a hydrolyzed protein diet is selected, ultrahydrolyzed diets (fragments of 1 to 2 kilodaltons) are considered superior to semihydrolyzed diets (fragments of ~10 kilodaltons) for diagnostic purposes.27,28
There is no consensus on the required length of a diet trial. A recent review article recommends a minimum of 8 weeks, with 10 to 12 weeks required to identify 90% of cases.29 For at least the first few weeks of the trial, it may be prudent to provide the patient with anti-inflammatory/antipruritic support (such as prednisolone). Doing so may be advisable not only for patient welfare but also because some evidence suggests that early suppression of cutaneous inflammation may shorten the necessary duration of the diet trial.30
Even if the cat does not become asymptomatic, all elimination diets should ideally be followed by rechallenge with the cat’s previous diet. Exacerbation of clinical disease after challenge both confirms the diagnosis of food hypersensitivity in asymptomatic cats and demonstrates a food hypersensitivity component in cats that showed limited improvement during the trial.
Atopic dermatitis: Hypersensitivity testing is often mistakenly used to diagnose atopic dermatitis. However, there is currently no in vivo or in vitro test that can clinically distinguish between atopic and nonatopic cats.31,32 As is already known in dogs with atopic dermatitis, cats may also have clinically irrelevant positive reactions or may have false-negative reactions for a variety of reasons (e.g., stress during testing, drug interference). Atopic dermatitis is thus considered to be a clinical diagnosis of exclusion and should be made only after all other factors have been eliminated or identified. The true purpose of hypersensitivity testing is to identify potential allergenic triggers so that they can be avoided or desensitization can be attempted. Both intradermal testing and IgE serology are valid tools for these purposes. The methods used in serologic assays vary greatly between laboratories and can significantly affect study results.33 The practitioner is advised to seek the advice of a veterinary dermatologist before selecting a laboratory.
Other Causes of Pruritus
Hyperthyroidism: Although hyperthyroidism may not be the first differential that comes to mind for an alopecic cat, it can nonetheless be associated with pruritus and alopecia secondary to overgrooming.6 Affected cats are typically older and also demonstrate other clinical signs of hyperthyroidism. However, the author has seen one cat in which the first sign noted was fur pulling.
Cutaneous lymphoma: Epitheliotrophic cutaneous lymphoma may occasionally be associated with pruritic (or occasionally nonpruritic) alopecia, often accompanied by scaling and erythema.34 Affected cats are typically mature to older. Depending upon the extent of the disease, cats may or may not be clinically ill at the time of presentation.
Nonpruritic Self-Inflicted Causes of Alopecia
The most well-known cause of nonpruritic self-inflicted alopecia is psychogenic disease. Affected cats methodically or episodically lick or bite at their fur in reaction to a psychologic stressor. Evidence suggests that psychogenic alopecia is widely overdiagnosed, and it may be the least common of the potential differentials for alopecia. In a recent study, only 2 of 21 cats presented for evaluation of “psychogenic alopecia” were found to have a behavioral disorder as their only problem. In contrast, 16 of those cats were found to have medical abnormalities (e.g., food hypersensitivity or atopy) and the other 3 cats were found to have both psychogenic and medical causes for their overgrooming.14 Indeed, cats may first have a medical abnormality and then a later, secondary obsessive or behavioral component to their disease (possibly secondary to endorphin release), similar to what is believed to occur in some dogs with acral lick dermatitis.
For this reason, in the absence of chronologic association with the appearance of an obvious stressor (e.g., new house, addition or loss of a family member, stressors associated with poor social status), psychogenic alopecia is usually considered only when pruritic self-inflicted alopecia is ruled out. However, failure to respond to an antipruritic agent trial may lend support to the possibility of psychogenic disease and may lead practitioners to consider investigating this differential sooner than they otherwise might. Recently, Titeux et al. developed a welfare score to aid assessment of cats with idiopathic ulcerative dermatitis.35 In their study, identification and elimination of stressors and environmental enrichment resulted in the near-immediate cessation of this previously chronic, treatment-refractory disorder. Indeed, adaptation of this score for the evaluation of cats with suspected psychogenic alopecia may be of considerable diagnostic and therapeutic value. For an in-depth workup, the practitioner is encouraged to seek the advice of a qualified veterinary behaviorist.
Compared with self-inflicted alopecia, significant spontaneous fur loss in the cat is fairly uncommon and the potential causes are relatively few (TABLE 2). Fur loss may result from fungal, bacterial, or parasitic folliculitis, in which irritation of the hair follicle causes damage to and/or premature shedding of the hairs. Affected cats may experience significant fur loss without demonstrating evidence of pruritus (e.g., scratching, overgrooming, broken hair). Significant physiologic stress may result in acute (anagen defluxion) or delayed (telogen effluvium) fur loss.8
Less commonly, spontaneous alopecia may represent a cutaneous manifestation of systemic neoplastic disease (FIGURES 10,11). Some cats with thymomas will develop marked exfoliative scaling associated with progressive fur loss and easily epilated fur.36 Another variant of alopecic dermatitis has been associated with other forms of neoplasia (most frequently pancreatic, hepatocellular, or bile duct carcinomas).37,38 Cats affected by any of those 3 tumors may rapidly shed clumps of fur, particularly on the ventrum. Histologically, severe follicular atrophy and hair bulb miniaturization can be seen.38,39 Secondary infection with Malassezia is not uncommon and may be associated with significant pruritus.40 Infected cats may obsessively groom their bellies, resulting in the development of shiny skin. These cats are frequently systemically ill at the time of presentation.
Similar to workups for cats with pruritic skin disease, it is prudent to begin the workup of the cat with spontaneous alopecia by first focusing on more common causes and leaving the more esoteric entities until after the common conditions have been identified or eliminated. Of note, some cats may have more than one problem (e.g., secondary overgrowth with D cati may develop in a cat with paraneoplastic alopecia).
The workup of alopecia in cats involves a combination of thorough history, categorization, and use of targeted investigative techniques. Although there are a large number of differential diagnoses for feline alopecia, a very large proportion of these differentials can be identified or excluded by using a relatively small number of inexpensive, rapid, and easy diagnostic techniques.
1. Miller WH Jr, Griffin CE, Campbell K. Chapter 2. Diagnostic methods. In: Miller WH Jr, Griffin CE, Campbell K, eds. Muller and Kirk’s Small Animal Dermatology. 7th ed. St. Louis, MO: Elsevier Mosby;
2. Beugnet F, Bourdeau P, Chalvet-Monfray K, et al. Parasites of domestic owned cats in Europe: co-infestations and risk factors. Parasit Vectors 2014;7:291.
3. Hnilica KA. Chapter 5. Parasitic skin disorders. In: Hnilica KA, ed. Small Animal Dermatology, A Color Atlas and Therapeutic Guide. St. Louis, MO: Elsevier Saunders; 2011:120–158.
4. Moriello KA, Coyner K, Paterson S, Mignon B. Diagnosis and treatment of dermatophytosis in dogs and cats. Vet Dermatol 2017;28(3):266-e68.
5. Miller WH Jr, Griffin CE, Campbell K. Chapter 6. Parasitic skin disease. In: Miller WH Jr, Griffin CE, Campbell K, eds. Muller and Kirk’s Small Animal Dermatology. 7th ed. St. Louis, MO: Elsevier Mosby;
6. Peterson ME, Kintzer PP, Cavanagh PG, et al. Feline hyperthyroidism: pretreatment clinical and laboratory evaluation of 131 cases. JAVMA 1983;183(1):103–110.
7. Turek MM. Cutaneous paraneoplastic syndromes in dogs and cats: a review of the literature. Vet Dermatol 2003;14(6):279–296.
8. Miller WH Jr, Griffin CE, Campbell K. Chapter 11. Miscellaneous alopecias. In: Miller WH Jr, Griffin CE, Campbell K, eds. Muller and Kirk’s Small Animal Dermatology. 7th ed. St. Louis, MO: Elsevier Mosby; 2003:554–572.
9. Gross TL, Ihrke PJ, Walder E, Affolter VK. Chapter 19. Atrophic diseases of the adnexa. In: Gross TL, Ihrke PJ, Walder E, Affolter VK, eds. Skin Diseases of the Dog and Cat, Clinical and Histopathologic Diagnosis. Oxford, UK: Blackwell Science; 2005:480–570.
10. Scott DW, Miller WH, Erb HN. Feline dermatology at Cornell University: 1407 cases (1988-2003). J Feline Med Surg 2013;15(4):307–316.
11. O’Dair HA, Foster AP. Focal and generalized alopecia. Vet Clin North Am: Small Anim Pract 1995;25(4):851–870.
12. Grandt LM, Roethig A, Schroeder S, et al. Feline paraneoplastic alopecia associated with metastasising intestinal carcinoma. JFMS Open Rep 2015;1(2):2055116915621582.
13. Tasker S, Griffon DJ, Nuttall TJ, Hill PB. Resolution of paraneoplastic alopecia following surgical removal of a pancreatic carcinoma in a cat. J Small Anim Pract 1999;40(1):16–19.
14. Waisglass SE, Landsberg GM, Yager JA, Hall JA. Underlying medical conditions in cats with presumptive psychogenic alopecia. JAVMA 2006;228(11):1705–1709.
15. Hobi S, Linek M, Marignac G, et al. Clinical characteristics and causes of pruritus in cats: a multicentre study on feline hypersensitivity-associated dermatoses. Vet Dermatol 2011;22(5):406–413.
16. Bond R, Morris DO, Guillot J, et al. Biology, diagnosis and treatment of Malassezia dermatitis in dogs and cats: Clinical Consensus Guidelines of the World Association for Veterinary Dermatology. Vet Dermatol 2020;31(1):28–74.
17. Santoro D, Marsella R, Pucheu-Haston CM, et al. Review: pathogenesis of canine atopic dermatitis: skin barrier and host-micro-organism interaction. Vet Dermatol 2015;26(2):84-e25.
18. Han HS, Chua HL, Nellinathan G. Self-induced, noninflammatory alopecia associated with infestation with Lynxacarus radovskyi: a series of 11 cats. Vet Dermatol 2019;30(4):356–e103.
19. Leone F, Di Bella A, Vercelli A, Cornegliani L. Feline trombiculosis: a retrospective study in 72 cats. Vet Dermatol 2013;24(5):535–e126.
20. Scarampella F, Pollmeier M, Visser M, et al. Efficacy of fipronil in the treatment of feline cheyletiellosis. Vet Parasitol
21. Milley C, Dryden M, Rosenkrantz W, et al., Comparison of parasitic mite retrieval methods in a population of community cats. J Feline Med Surg 2017;19(6):657–664.
22. Moriello KA, Newbury S, Steinberg H. Five observations of a third morphologically distinct feline Demodex mite. Vet Dermatol 2013;24(4):460–462, e106.
23. Crkvencic N, Šlapeta J. Climate change models predict southerly shift of the cat flea (Ctenocephalides felis) distribution in Australia. Parasit Vectors 2019;12(1):137.
24. Pucheu-Haston C. The flea-infested pet: how to manage the pet and its environment. Today’s Veterinary Practice 2017;4:1–5.
25. Rust W, Dryden M. The biology, ecology and management of the cat flea. Ann Rev Entomol 997;42:451–473.
26. Mueller RS, Olivry T. Critically appraised topic on adverse food reactions of companion animals (4): can we diagnose adverse food reactions in dogs and cats with in vivo or in vitro tests? BMC Vet Res 2017;13(1):275.
27. Olivry T, Bexley J, Mougeot I. Extensive protein hydrolyzation is indispensable to prevent IgE-mediated poultry allergen recognition in dogs and cats. BMC Vet Res 2017;13(1):251.
28. Bizikova P, Olivry T. A randomized, double-blinded crossover trial testing the benefit of two hydrolysed poultry-based commercial diets for dogs with spontaneous pruritic chicken allergy. Vet Dermatol
29. Olivry T, Mueller RS, Prelaud P. Critically appraised topic on adverse food reactions of companion animals (1): duration of elimination diets. BMC Vet Res 2015;11:225.
30. Favrot C, Bizikova P, Fischer N, et al. The usefulness of short-course prednisolone during the initial phase of an elimination diet trial in dogs with food-induced atopic dermatitis. Vet Dermatol
31. Taglinger K, Helps CR, Day MJ, Foster AP. Measurement of serum immunoglobulin E (IgE) specific for house dust mite antigens in normal cats and cats with allergic skin disease. Vet Immunol Immunopathol 2005;105(1–2):85–93.
32. Diesel A, DeBoer DJ. Serum allergen-specific immunoglobulin E in atopic and healthy cats: comparison of a rapid screening immunoassay and complete-panel analysis. Vet Dermatol 2011;22(1):39–45.
33. Plant JD, Neradelik MB, Polissar NL, et al. Agreement between allergen-specific IgE assays and ensuing immunotherapy recommendations from four commercial laboratories in the USA.
Vet Dermatol 2014;25(1):15–e6.
34. Fontaine J, Heimann M, Day MJ. Cutaneous epitheliotropic T-cell lymphoma in the cat: a review of the literature and five new cases.
Vet Dermatol 2011;22(5):454–461.
35. Titeux E, Gilbert C, Briand A, Cochet-Faivre N. From feline idiopathic ulcerative dermatitis to feline behavioral ulcerative dermatitis: grooming repetitive behaviors indicators of poor welfare in cats. Front Vet Sci 2018;5:81.
36. Scott DW, Yager JA, Johnston KM. Exfoliative dermatitis in association with thymoma in three cats. Feline Practice 1995;23:8–13.
37. Marconato L, Albanese F, Viacava P, et al. Paraneoplastic alopecia associated with hepatocellular carcinoma in a cat. Vet Dermatol 2007;18(4):267–271.
38. Barrs VR, Martin P, France M, Mason K. What is your diagnosis? Feline paraneoplastic alopecia associated with pancreatic and bile duct carcinomas. J Small Anim Pract 1999;40(12):559, 595–596.
39. Pascal-Tenorio A, Olivry T, Gross TL, et al. Paraneoplastic alopecia associated with internal malignancies in the cat. Vet Dermatol 1997;8:47–52.
40. Godfrey DR. A case of feline paraneoplastic alopecia with secondary Malassezia-associated dermatitis. J Small Anim Pract 1998;39(8):394–396.