Pruritus is defined as an unpleasant sensation that provokes the desire to scratch. In veterinary medicine, this sensation is impossible to differentiate from other stimuli such as burning, since the animal’s responses to these stimuli are similar. Self-mutilation is a common sequela to offensive stimuli in the skin of small animals.

Pruritus should be regarded as one of five primary cutaneous sensations—heat, cold, pain, and touch being the other four. Pruritus is an epidermal sensation, whereas pain can also be perceived from denuded skin. The sensory receptors are naked nerve endings located in the epidermis. The axons that carry pruritic sensation are small unmyelinated C fibers. They ascend in the ventrolateral spinothalamic tracts via the thalamus to the cerebral cortex. Certain areas of the skin may have increased numbers of “itch” receptors or are more sensitive to pruritic stimuli. Although fewer nerve endings are present in chronic dermatitic skin, those present have a lower threshold for causing a pruritic sensation.

Mediators of Pruritus

There are numerous endogenous compounds capable of stimulating pruritus including proteases, leukotrienes, histamine, and peptides. These compounds are prominent mediators of inflammation. Proteolytic enzymes (proteases) are most likely the major mediators of pruritus in dogs and cats. These enzymes may be released from bacteria, fungi, mast cells, epidermal cells (cathepsin), leukocytes (leukopeptidases), or may leak from plasma (plasmin) following capillary dilatation. Although pruritus is a common feature of allergic skin disease, many other diseases cause pruritus through the release of proteolytic enzymes. Factors that can initiate pruritus include physical factors such as heat and cold, vasodilation, proteolytic enzymes such as histamine, serotonin, and bile acids, and asteatosis (dry skin).

Factors Affecting Pruritus

Certain conditions may potentiate the pruritic sensation or decrease the tolerance threshold. Boredom may increase the cerebral response to physiologic itch stimuli and convert the sensation to a pathologic state. This mechanism may play a limited role in the etiology of acral pruritic nodules, feline lick granuloma, feline hyperesthesia syndrome, and idiopathic acute moist dermatitis (“hot spots”). Chronically diseased skin has limited perception because of decreased pruritic receptors; however, stimuli applied to this skin are perceived as either a burning sensation or itch. Thus, stimuli not usually considered noxious may be converted to pruritus (conversion itch). In addition, the remaining nerve endings may have a lower threshold for pruritic sensation. Chronic inflammation and secondary bacterial infections potentiate pruritus by increasing the accessibility of proteases to the nerve endings.

Scratching is the primary physiologic response for the control or temporary relief of pruritus. Temporary relief occurs because other stimuli (heat, cold, touch, pain) suppress the sensation of itch by competing for neuronal circuits within the internuncial sensory neuronal pool in the spinal cord. To be effective, the competing stimulus must be applied to the same dermatome from which the pruritic sensation originated. Scratching can potentiate pruritus since the induced epidermal damage (excoriations) releases additional proteolytic enzymes. This potentiates the itch–scratch–itch cycle common in many skin diseases.

Pruritus is frequently associated with primary skin lesions; however, the associated scratching may destroy these lesions. Primary skin lesions include papules, pustules, vesicles, and hyperemia. Secondary skin lesions observed in pruritic animals include excoriations, scales, crusts, lichenification, and hyperpigmentation. The nature of these lesions, their distribution pattern, and the degree of pruritus are important factors to consider in formulating the initial plan for dermatologic conditions.

The desire to stop pruritus and its associated self-mutilation must be tempered by the desire to establish a correct diagnosis. Unfortunately, glucocorticoid drugs are frequently given to control pruritus without finding the underlying cause. The dermatologic history and physical examination should answer at least these five basic questions: (1) Is the condition pruritic? (2) What are the basic skin lesions? (3) What is the distribution pattern of lesions? (4) Is the condition contagious to other animals or to humans? and (5) Are other body systems involved?

A problem-specific database should include a complete history, a description of the dermatologic lesions and their pattern, analysis of multiple skin scrapings, a trichogram, and results of Wood’s light examination. This database should be expanded to include a variety of other procedures on the basis of the dermatologic findings. The expanded database might include fungal and bacterial cultures, intradermal skin tests, histopathology and direct fluorescent antibody, and dietary food trials.