Pruritus is defined as an unpleasant sensation within the skin that provokes the desire to scratch.
Pruritus may be well or poorly localized. It may manifest as a sharp or diffuse, burning sensation. Although the skin is richly innervated, there are no known specialized pruritus receptors. The sensation of itch is transmitted via a specialized set of afferent fibers. Myelinated fibers that conduct sensations at 10–20 m/sec carry the well-localized pricking itch sensation. In contrast, the sensation of burning itch is transmitted via nonmyelinated fibers that conduct sensations at 2 m/sec. Both of these fibers enter the dorsal root of the spinal cord, ascend through the dorsal column, and cross into the lateral spinothalamic tract. From there they go to the thalamus and on to the sensory cortex.
The mediators of pruritus are controversial and may vary depending on the species. These putative mediators include histamines (released from mast cell degranulation), proteolytic enzymes (proteases), and leukotrienes. Proteases are released by fungi, bacteria, and mast cell degranulation, and during antigen-antibody reactions. Leukotrienes, prostaglandins, and thromboxane A2, which are broken down from arachidonic acid, are pro-inflammatory. Essential fatty acids, particularly glinolenic acid, have been used to counter the inflammation mediated by leukotrienes and thromboxane A2. The sensation of pruritus may be affected by a variety of factors, including boredom, competing sensations, and anxiety. Stress may potentiate pruritus via the release of opioid peptides.
Pruritus is a clinical sign and not a diagnosis or specific disease. In general, the most common causes of pruritus are parasites, infections, allergic skin diseases, and miscellaneous causes (eg, cutaneous neoplasia). Many diseases that are nonpruritic (eg, endocrinopathies) become pruritic when the patient develops secondary bacterial or yeast infections.
A thorough dermatologic history and physical examination should be performed. Parasitic causes of pruritus, including Demodex, fleas and ticks, contagious mites, and lice, should be excluded, because they are most common. Skin scrapings can exclude (or include) various mite infestations, including Demodex. However, some mite infestations (eg, Sarcoptes, Cheyletiella, Psoroptes, Chorioptes) might be missed on skin scrapings. If a mite infestation is suspected, a response to therapy trial should be undertaken. The most commonly used drug in these cases is ivermectin. Fleas can be excluded or included based on a history of flea control, response to flea control, or finding evidence of flea infestation via a flea combing. Flea control practices can also exclude louse infestations.
The next most important group of pruritic diseases to exclude is infectious causes of skin disease. These include bacterial infections (primarily staphylococcal infections, Malassezia overgrowth, and dermatophytosis). A fungal culture should be performed in any cat presented for pruritus. It is also highly recommended in dogs that are newly acquired, any animal with a possible history of exposure and/or compatible clinical signs, or when there is a history of people with skin disease. Concurrent bacterial and yeast infections are increasingly recognized as a common cause of pruritus in dogs, cats, and large animals. Bacterial pyoderma is underdiagnosed in cats, and a response to therapy trial may be needed to exclude or include it.
Infectious causes of pruritus commonly induce clinical signs of hair loss, scaling, scales piercing hairs, odor, and/or greasy seborrhea. Marked pedal pruritus and facial rubbing are common in animals with concurrent yeast and bacterial infections. Before pursuing allergies as a cause of pruritus or performing skin biopsies or other more expensive and/or invasive diagnostic testing, a concurrent bacterial and yeast infection should be excluded. A 21–30 day concurrent course of an antibiotic effective against Staphylococcus spp (eg, cephalexin 30 mg/kg, PO, bid) and a systemic antifungal (eg, ketoconazole, itraconazole, or fluconazole 5–10 mg/kg/day, PO) should be prescribed. If the pruritus resolves, then existing pruritus was due to a microbial infection.
It is possible that the initial trigger has long passed or is seasonal. However, if the animal's pruritus is unchanged or only somewhat better, the most likely underlying cause is allergic (assuming parasitic causes have been excluded). The most common causes of allergic pruritus are insect bite hypersensitivity (eg, flea allergy, mosquito bite allergy, fly bite), food allergy, and atopic dermatitis. Flea allergy dermatitis and insect bite hypersensitivity are excluded based on response to insect control. Animals that do not have insect bite hypersensitivity but are seasonally pruritic most likely have atopic dermatitis. Animals with year-round allergic pruritus have atopic dermatitis and/or food allergy. Food allergy is excluded or included based on response to a diet trial and provocative challenge. Atopic dermatitis is a clinical diagnosis; in vitro allergy testing and intradermal skin testing show only antigen exposure patterns. These tests are used to determine the contents of an immunotherapy vaccine.
Successful therapy depends on identification of the underlying cause. Patients with idiopathic pruritus or those in which treatment of the underlying disease does not eliminate the pruritus (eg, atopic patients) require medical management of pruritus. Currently, evidence-based reviews of antipruritic do not support the use of antihistamines to control pruritus.
Essential Fatty Acids:
Essential fatty acids are rarely effective as sole antipruritic agents and are not suitable for acute flares of pruritus. If they are beneficial, it is a longterm therapy.
Glucocorticoids are the most effective drugs in the management of pruritus. However, they cannot be used safely for longterm management because of adverse effects (eg, suppression of adrenal function, risk of development of diabetes mellitus, risk of secondary urinary tract infections). In addition, owners can rarely tolerate the common adverse effects (polydipsia, polyuria, polyphagia, and panting) for long periods. Anti-inflammatory dosages range from 0.5–1.0 mg/kg/day, PO, for 5–10 days and then every other day. Topical spray formulations of triamcinolone acetate are highly effective and good alternatives to oral steroids.
Other Systemic Antipruritic Agents:
Cyclosporine modified is a highly effective nonsteroidal drug for control of pruritus. The only formulation that can be used is modified cyclosporine. The dosage is 5 mg/kg for dogs and 7 mg/kg for cats. Maximal benefit can take as long as 30 days to observe. Once efficacy is established, dose tapering to every other day can be attempted. Common adverse effects include vomiting and diarrhea (common) and gingival hyperplasia (less common). s. Another new drug for control of pruritus in dogs is oclacitinib, a Janus kinase (JAK) inhibitor that provides rapid relief from pruritus and inflammation in dogs with short- and longterm allergic skin disease.
Last full review/revision June 2013 by Karen A. Moriello, DVM, DACVD