DVM, PhD, DACVD
Dr. Pucheu-Haston is an associate professor of veterinary dermatology and immunology at Louisiana State University. She received her veterinary degree from Louisiana State University and completed residency training at North Carolina State University. After a brief hiatus in private practice dermatology, she returned to NCSU to pursue a PhD in immunology, followed by 3 years of postdoctoral study at the U.S. Environmental Protection Agency’s Immunotoxicology Branch. Her clinical and research interests are cutaneous and respiratory allergic diseases in cats, dogs, and horses and the immunologic response to cutaneous fungal infections.Read Articles Written by Cherie Pucheu-Haston
Pruritus is one of the most common reasons why clients bring their dog to the veterinarian. Sometimes the cause of the pruritus is obvious (e.g., the dog is covered with fleas), and sometimes it is not so simple. The patient’s primary condition may be exacerbated by secondary infections or development of (new) allergic skin diseases. If necessary, the veterinarian must be ready to “peel back” diagnostic layers to get to the underlying cause—or causes. This article provides a logical approach to the workup of the pruritic dog.
Major Categories of Conditions Responsible for Pruritus
Although there are definitely exceptions, most conditions responsible for pruritus in the dog fall into 3 broad categories: infection, infestation/ectoparasitism, and allergy (TABLES 1-3).1-9 Frequently, conditions in more than 1 category are present simultaneously (e.g., the patient with atopic dermatitis may also have fleas and a secondary yeast infection). Furthermore, the sensation of pruritus can be considered to be an additive phenomenon in which each condition builds on the discomfort generated by the other(s).
The most common infectious conditions that can be associated with pruritus in the dog are staphylococcal pyoderma and yeast dermatitis (typically Malassezia, although Candida may also be seen, albeit rarely).9 Dermatophytosis may also be associated with pruritus, although less commonly than bacterial and yeast disorders.9 With the exception of dermatophytosis, infection is generally a secondary cause of pruritus.10 However, any microbial overgrowth or invasion can trigger production of a nonspecific inflammatory response in the skin by activating and recruiting inflammatory cells, which subsequently release inflammatory and pruritogenic substances. Together, these events induce or enhance the sensation of pruritus.11 TABLE 1 describes the most common infectious causes of pruritus and their distributions.
Parasites typically associated with the development or perpetuation of pruritus in the dog can be classified into those infesting the skin surface, the superficial aspect of the skin (e.g., the stratum corneum and epidermis), or the deep portions of the skin (especially the follicles).6
- Surface-dwelling parasites include fleas, lice, Otodectes and Cheyletiella mites, and chiggers (Eutrombicula, Walchia).
- Superficial parasites include Sarcoptes mites.
- Deep-dwelling parasites include Demodex canis and Demodex injai mites.
Other insects and mites may also contribute to pruritus through means other than direct parasitism, including mosquitoes, stable flies (Stomoxys), and black flies (Simulium). TABLE 2 describes the typical clinical appearance and distribution of dermatitis associated with parasites as well as relevant diagnostic techniques.
The 3 most common allergies associated with pruritus in the dog are flea allergy, food allergy (sometimes called adverse food reactions), and atopy (or atopic dermatitis) (TABLE 3).1,9,10 Dogs may be affected with 1 or more of these conditions or even all 3 concurrently. Dogs can also experience contact allergy, although less commonly than the other 3 allergy conditions. With the exception of flea allergy, workup of the other hypersensitivity disorders is more complex and involved than that of infectious and parasitic conditions. For this reason, an in-depth workup for allergy is often deferred until nonallergy causes of pruritus are identified and controlled or eliminated.
- Cytology: The initial workup of the pruritic dog should include at least skin and/or ear cytology.
- Skin scrapings: The initial workup of the pruritic dog should also include skin scrapings of affected areas. Superficial skin scrapings may demonstrate many surface and superficial mites; deep skin scrapings may demonstrate Demodex mites.
- Flea combing and/or surface tape impressions: Examination of debris obtained by flea combing or with surface tape impressions may be helpful for demonstrating surface-dwelling mites, fleas, “flea dirt,” and lice.
- Flea control: Aggressive flea control is an essential part of the workup and management of the pruritic dog. It is the author’s opinion that a good-faith effort to institute a flea control trial program is worthwhile even in areas where fleas are considered uncommon.1 This is particularly true given the potential effects of climate change and energy-efficient housing, which minimizes the effects of seasonal variations in temperature, humidity, etc., creating micro-environments that may be more conducive to flea survival.12
Flea control should be included in the workup of the pruritic dog even when flea allergy is not considered to be a likely differential because fleas and their bites can produce irritation even in nonallergic patients. It is beyond the scope of this article to provide a detailed discussion of the available agents, but other resources are available.13 The author particularly favors drugs in the isoxazoline class; however, in certain circumstances (e.g., patients with pre-existing neurologic disease or seizure history), these drugs should be used with caution, if at all. For these patients, other drugs (e.g., monthly indoxacarb or dinotefuran or weekly imidacloprid) may be sufficient.
To ensure that flea control products are being used appropriately, question clients carefully about their current flea control measures. Ask specifically about the presence and treatment of other animals that may have contact with the patient. Also ask whether the dog has been exposed to situations in which fleas can be transmitted (e.g., dog parks, doggie day care). Free-roaming animals should be confined to a controlled space for the duration of the flea control trial. Measures should be taken to ensure that the dog and in-contact animals do not have access to open sheds, crawl spaces, etc., which may be reseeded with fleas by wildlife that might also access these areas.14 In cases of heavy infestation (or if the clinical signs are particularly suggestive of flea allergy), treating the environment may be warranted. Indeed, many practitioners believe that environmental flea control is essential in geographic areas prone to heavy flea infestations (e.g., the southeastern U.S.). Environmental flea control measures may include frequent vacuuming of the area to which the dog has access and spraying the household with insect growth regulators (e.g., pyriproxyfen).
Other Diagnostics That May Be Useful
- Wood’s lamp examination, dermatophyte culture, dermatophyte polymerase chain reaction test, or careful examination of plucked hairs (trichogram): Any of these procedures may be helpful if dermatophytosis is suspected.
- Culture and sensitivity testing: For patients with a history of repeated antibiotic administration, deep pyoderma, or failure to respond to empirical antibiotic therapy, consider bacterial culture and sensitivity testing.
- Biopsy: For patients demonstrating little to no improvement despite appropriate antimicrobial and antiparasitic therapy, skin biopsy may be considered. A skin biopsy should not be performed in lieu of a good-faith effort to evaluate the patient for infectious, ectoparasitic, and (later) allergic disease. Although histology can demonstrate some infectious conditions (e.g., dermatophytosis, demodicosis), it is usually not the most efficient way to do so. Histology alone is unable to distinguish between many of the conditions described in this article.15 Nonetheless, with these limitations in mind, a biopsy may be considered to provide further information and to help rule out more esoteric causes of pruritus, such as cutaneous lymphoma. The author typically reserves biopsies for patients that did not respond to appropriate therapy or patients with atypical presentations (e.g., persistent diffuse erythema or scale, ulceration, involvement of mucocutaneous junctions).
1. Take a Thorough History
For evaluating a pruritic dog, a thorough medical history is invaluable. A good history can help point the veterinarian toward likely diagnoses and, of equal importance, away from unlikely diagnoses. TABLE 4 shows questions to ask when taking a dermatologic history, some follow-up questions, and a brief synopsis of information to be gained from the answers.
2. Perform Physical and Dermatologic Examinations
Every pruritic dog should undergo thorough physical and dermatologic examinations. It is beyond the scope of this article to cover all possible relevant findings; however, some areas are particularly important to evaluate. These areas are the dorsal and ventral interdigital skin, the claws and skin around the claw beds, the perianal and perineal skin, the elbow folds, and the ventral lip folds. In addition, a rectal exam is indicated for any patient with caudal pruritus since some patients with impacted anal sacs will lick or chew over the tailhead rather than scoot.19 Evaluation of areas demonstrating erythema, pustules, bronzing (especially on the claws), or moist or greasy dermatitis may be particularly useful. TABLES 1–3 list some of the more common differential diagnoses, the typical distribution of these conditions, and relevant diagnostic techniques.
3. Identify and Eliminate Infectious and Ectoparasitic Causes First
Although true that a significant percentage of pruritic dogs experience 1 or more types of allergic skin disease, it is often a better use of time to first evaluate the patient for infectious or parasitic causes of pruritus. With the exception of flea allergy (for which institution of aggressive flea control is always indicated), a workup for food allergy or atopic dermatitis may or may not be indicated at the first examination. If significant infection with fleas, bacteria, or yeast is found, elimination of these conditions may provide a better baseline assessment of the patient’s true condition.
Another reason to identify and eliminate infectious and ectoparasitic conditions first is because they are typically easier to identify and treat, whereas a thorough workup for allergic skin disease may be fairly expensive and lengthy. In addition, because pruritus can result from the combination of all factors present, failure to eliminate nonallergic conditions may interfere with an accurate assessment of the patient’s condition, potentially skewing the results of an allergy workup.1 Although the infectious and parasitic categories together represent a very large number of potential differential diagnoses, most of these conditions can be rapidly and inexpensively identified by using a relatively small number of diagnostic and therapeutic techniques (TABLES 1, 2). Should the pruritus persist after elimination of infections or parasites, an allergic skin disease workup would then be warranted.
At the first visit, institution of some form of anti-inflammatory therapy is generally indicated. Pruritic behaviors create cutaneous microtrauma, which causes the release of inflammatory mediators and favors the development and perpetuation of infection. Although anti-inflammatory medications could interfere with assessment of the patient’s condition in the short term, the decreased inflammation not only provides relief for the patient but also allows traumatized skin to heal and could facilitate elimination of secondary infections.
4. Treat and Reassess
Reassessment is an important part of the workup of the pruritic dog. All too often, the veterinarian sees a patient months after the initial diagnostics and treatment were performed and prescribed, only to be told that the therapy “didn’t work.” Sometimes the patient did improve after initial therapy but started to worsen again after the initially prescribed medication ran out. If the client takes no action at this point, the condition will most likely continue to degrade, and by the time the client again seeks veterinary care, the brief respite from pruritus may be long forgotten. The author recommends that clients come in for a recheck or check in by phone or email 2 to 3 weeks after the initial visit. If necessary, the veterinarian or veterinary nurse can initiate contact. Patients should also be rechecked before medication is finished to confirm resolution of the infection/infestation. If the patient has improved, it may then be possible to begin an allergic skin disease workup. If the patient has not improved sufficiently, workup may need to be delayed and the patient further evaluated (or re-evaluated) for the presence or recurrence of infectious or parasitic agents.
5. Perform Workup for Allergic Pruritic Skin Disease
As stated above, good flea control is important in the workup of any pruritic dog, regardless of whether flea allergy is considered to be a differential. Fortunately, modern flea control agents have made the elimination of fleas possible in all but the most challenging circumstances. Regardless of the agent(s) chosen, treatment of the patient and all in-contact animals must be maintained for a minimum of 12 weeks to be certain that the local flea population has been eliminated.1
Many “diagnostic tools” are marketed for the diagnosis of food allergy, including measurement of serum IgE, fecal IgE, or salivary food-specific IgE. Unfortunately, those modalities can neither reliably diagnose food allergy nor identify problematic or tolerated food items.20 Patch testing and lymphocyte stimulation tests may be of some use but are typically restricted to investigational settings or academic institutions.21,22 To date, the only practical method for the diagnosis of food allergy and identification of culprit foods is the dietary elimination trial.20
Elimination trials may be conducted by using either hydrolyzed diets (processed to minimize peptide size) or novel protein diets (commercial or home cooked). Both approaches are valid, but neither is guaranteed to succeed. If hydrolyzed protein diets are used for diagnostic purposes, ultrahydrolyzed diets (1- to 2-kilodalton fragments) are considered superior to semihydrolyzed diets (~10-kilodalton fragments).23 The small peptide fragments in ultrahydrolyzed diets makes clinical reactivity unlikely (but still possible) even if the protein from which that diet is sourced is one that the patient has been fed before. If desired, an ultrahydrolyzed diet could be selected from a different protein source (e.g., salmon-based diet for a patient previously fed chicken). However, even this approach has its limitations since recent work has demonstrated that allergenic cross-reactivity is possible between surprisingly disparate sources, such as fish and chicken.24
If a novel protein diet is selected, the patient’s dietary history should be reviewed to identify dietary items to which the patient has been exposed. Appropriate diets should consist of ingredients from sources phylogenetically distant from those in the patient’s previous diet. For example, a kangaroo-based or alligator-based diet might be a good empirical choice for a dog previously fed chicken. Again, cross-reactivity remains a potential limitation of these diets as well.
Selecting the diet is only part of a dietary elimination trial. The client must also ensure that the dog does not receive food or food-based items from other sources, which may include foods eaten by other animals in the house, table scraps, dropped food, pill pockets, food-based chew toys (rawhides, hooves), and treats. Commonly overlooked food sources are chewable medications (including heartworm and flea preventives), animal feces, licking other animals’ food bowls, and dirty dishes in the sink.1
There is no consensus on the required length of a diet trial. A recent review article recommended a minimum of 8 weeks to identify 95% of food-allergic patients; in a small number of dogs, food allergy was not identified until 13 weeks.25 For at least the first few weeks of the trial, it may be prudent to provide 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.26 Ideally, all elimination diets should be followed by rechallenge with the dog’s previous diet even if the dog does not become asymptomatic. Exacerbation of clinical disease after the challenge both confirms the diagnosis of food allergy in asymptomatic dogs and suggests a food allergy component in dogs demonstrating only partial improvement during the trial. Resolution of clinical flare after reinstitution of the elimination diet further solidifies the diagnosis.
Atopic dermatitis may be best thought of as a syndrome rather than a specific diagnosis. The condition is generally associated with hypersensitivity to environmental allergens. In addition, the additive nature of pruritus means that the presence of other irritating or allergic factors (e.g., infections, fleas, food allergy) can trigger clinical flares of atopic dermatitis.1,27 This hypersensitivity may be IgE mediated, although for some patients that are otherwise identically affected, allergen-specific IgE cannot be demonstrated by serology or intradermal testing. These patients are referred to as having “atopic-like dermatitis.”28
Recently, 2 sets of criteria have been developed to help veterinarians diagnose atopic dermatitis (BOX 1).8 By themselves, these criteria do not prove that a patient does or does not have atopic dermatitis, and they do not replace an appropriate workup to identify and eliminate other potential causes of atopic dermatitis. However, they do provide useful information about which clinical signs (and combination of signs) may best support a diagnosis of atopic dermatitis. Either set of criteria may be used. The first set is relatively sensitive and has moderate to high specificity; the second set is not sensitive but is highly to very highly specific.
Because of the many potential contributing factors, it is prudent to ensure that all reasonable differentials are ruled out or (in the case of concurrent allergic skin disease) under control before the diagnosis of atopic dermatitis is made. For this reason, atopic dermatitis is considered to be a clinical diagnosis of exclusion. Although allergy testing (serology or intradermal) is often used to “diagnose” atopic dermatitis, these diagnostics cannot reliably discriminate between healthy and atopic dogs and can only support a clinical diagnosis of atopy.29
Although allergy testing alone cannot diagnose atopy, it is useful for identifying potential allergenic triggers so that desensitization can be attempted.1 The preferred diagnostic test is generally intradermal testing because it mimics the interaction between the allergen and the patient. However, intradermal testing is not always possible or practical, in which case a good serologic test can provide useful information. Because variations in laboratory methods can significantly affect serologic assay results,30 consulting a veterinary dermatologist before selecting a laboratory is recommended.
- The number of differential diagnoses for pruritus in dogs can seem overwhelming. However, following a few simple guidelines can greatly facilitate the workup.
- Get a good history—ask questions rather than assume that the client has told you everything of relevance.
- First screen the patient for infectious or parasitic causes of pruritus before leaping into an allergic skin disease workup.
- Treat and reassess—evaluate the response to initial treatment to help avoid basing decisions on client memory (lapses) and to get a better idea of the patient’s true baseline.
- Leave atopic dermatitis for last. Unless the patient demonstrates purely seasonal pruritus, investigate infections, ectoparasitism, and food allergy first. Even patients with purely seasonal pruritus should be evaluated for the possible presence of seasonally influenced parasites, such as fleas and chiggers.
1. Hensel P, Santoro D, Favrot C, et al. Canine atopic dermatitis: detailed guidelines for diagnosis and allergen identification. BMC Vet Res. 2015;11:1–13.
2. Miller WH Jr, Griffin CE, Campbell KL. Diagnostic methods. In: Miller WH Jr, Griffin CE, Campbell KL, eds. Muller and Kirk’s Small Animal Dermatology. St. Louis, MO; Elsevier Mosby; 2013:57–107.
3. Bond R, Morris DO, Guillot J, et al. Biology, diagnosis and treatment of Malassezia dermatitis in dogs and cats; clinical consensus guidelines for the World Association for Veterinary Dermatology. Vet Dermatol. 2020;31(1):73–77.
4. Moriello K. Feline dermatophytosis: aspects pertinent to disease management in single and multiple cat situations. J Feline Med Surg. 2014;16(5):419–431.
5. Moriello KA, Coyner K, Paterson S, Mignon B. Diagnosis and treatment of dermatophytosis in dogs and cats. Vet Dermatol. 2017;28(3):266–e68.
6. Miller WH Jr, Griffin CE, Campbell KL. Parasitic skin disease. In: Miller WH Jr, Griffin CE, Campbell KL, eds. Muller and Kirk’s Small Animal Dermatology. St. Louis, MO: Elsevier Mosby; 2013:284–342.
7. Olivry T, Mueller RS. Critically appraised topic on adverse food reactions of companion animals (7): signalment and cutaneous manifestations of dogs and cats with adverse food reactions. BMC Vet Res. 2019;15(1):140.
8. Favrot C, Steffan J, Seewald W, Picco F. A prospective study on the clinical features of chronic canine atopic dermatitis and its diagnosis. Vet Dermatol. 2010;21(1):23–31.
9. Hill PB, Lo A, Eden CAN, et al. Survey of the prevalence, diagnosis and treatment of dermatological conditions in small animals in general practice. Vet Rec. 2006;158(16):533–539.
10. Scott DW, Paradis M. A survey of canine and feline skin disorders seen in a university practice: Small Animal Clinic, University of Montréal, Saint-Hyacinthe, Québec (1987-1988). Can Vet J. 1990;31(12):830–835.
11. Chiu IM. Infection, pain, and itch. Neurosci Bull. 2018;34(1):109–119.
12. 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.
13. Pucheu-Haston C. The flea-infested pet: overview of current products. Todays Vet Pract. 2017;7(3):90-95.
14. Rust MW, Dryden MW. The biology, ecology and management of the cat flea. Annu Rev Entomol. 1997;42:451–473.
15. Gross TL, Ihrke PJ, Walder EJ, Affolter VK. Perivascular diseases of the dermis. In: Gross TL, Ihrke PJ, Walder EJ, Affolter VK, eds. Skin Diseases of the Dog and Cat: Clinical and Histopathologic Diagnosis. Oxford, UK: Blackwell Science; 2005:200–237.
16. Rybnicek J, Lau-Gillard PJ, Harvey R, Hill PB. Further validation of a pruritus severity scale for use in dogs. Vet Dermatol. 2009;20(2):115–122.
17. Griffin CE, DeBoer DJ. The ACVD task force on canine atopic dermatitis (XIV): clinical manifestations of canine atopic dermatitis. Vet Immunol Immunopathol. 2001;81(3-4):255–269.
18. Mueller RS, Olivry T. Critically appraised topic on adverse food reactions of companion animals (6): prevalence of noncutaneous manifestations of adverse food reactions in dogs and cats. BMC Vet Rec. 2018;14(1):341.
19. James DJ, Griffin CE, Polissar NL, Neradilek MB. Comparison of anal sac cytological findings and behaviour in clinically normal dogs and those affected with anal sac disease. Vet Dermatol. 2011;22(1):80–87.
20. 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.
21. Bethlehem S, Bexley J, Mueller RS. Patch testing and allergen-specific serum IgE and IgG antibodies in the diagnosis of canine adverse food reactions. Vet Immunol Immunopathol. 2012;145(3-4):582–589.
22. Fujimura M, Masuda K, Hayashiya M, Okayama T. Flow cytometric analysis of lymphocyte proliferative responses to food allergens in dogs with food allergy. J Vet Med Sci. 2011;73(10):1309–1317.
23. 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.
24. Bexley J, Kingswell N, Olivry T. Serum IgE cross-reactivity between fish and chicken meats in dogs. Vet Dermatol. 2019;30(1):25–e8.
25. 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.
26. 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.
27. Olivry T, DeBoer DJ, Favrot C, et al. Treatment of canine atopic dermatitis: 2015 updated guidelines from the International Committee on Allergic Diseases of Animals (ICADA). BMC Vet Res. 2015;11:210.
28. Halliwell REW. Revised nomenclature for veterinary allergy. Vet Immunol Immunopathol. 2006;114(3-4):207–208.
29. Lauber B, Molitor V, Meury S, et al. Total IgE and allergen-specific IgE and IgG antibody levels in sera of atopic dermatitis affected and non-affected Labrador- and Golden retrievers. Vet Immunol Immunopathol. 2012;149(1-2):112–118.
30. Plant JD, Neradelik MB, Polissae 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.