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Pruritus

Definition

Pruritus is an unpleasant sensation that provokes the desire to scratch. It is designated a primary cutaneous sensation, along with heat, cold, pain, and touch. There are two broad categories of pruritus.

Physiologic or spontaneous itch is a sharp, well- defined, pruritic sensation that is sufficiently intense to prompt scratching but does not result in significant irritation of the skin; this is a frequent daily occurrence in normal individuals. Pathologic itch is the less well-defined pruritus that occurs in a variety of primary and secondary skin disorders and in systemic diseases. It is an intense cutaneous discomfort that provokes vigorous scratching.6

Mechanisms of Pruritus

The investigation of the mechanism of pruritus has been primar­ily in laboratory animals and humans. It is presumed that much of this knowledge is applicable to other animal species. Pruritus is a distinct sensory quality transmitted from an arborizing network of nerve endings situated at or near the dermoepidermal junction. The sensation is carried to the spinal cord through small, unmyelinated C fibers. The fibers enter the dorsal root of the spinal cord and ascend in the ventrolateral spinothalamic tract through the posterior ventral nucleus of the thalamus to the sensory cortex. The pruritic sensation may be modified in the sensory cortex by behavioral factors or competing stimuli.7,8

Many physical and chemical stimuli can evoke pruritus, and many substances have been implicated as mediating pruritus in humans. Examples of these mediators, which are assumed to have importance in domestic animals as well, include the following8:

• Histamine. Histamine has been regarded as the classic mediator of pruritus. Histamine is present in mast cells in the dermis and in blood basophils. An intradermal injection of histamine produces pruritus within 20 to 50 seconds.

Because many pruritic disorders respond poorly to antihistamines given either therapeutically or prophylactically, histamine is not believed to be the sole mediator of pruritus.

• Endopeptidases. Examples include trypsin, papain, and kallikrein.

• Prostaglandins (E series and endoperoxidases). Prostaglandins induce pruritus by potentiating the release of proteases from keratinocytes and leukocytes and by lowering the threshold and increasing the duration of histamine-induced pruritus.

• Endogenous opioid peptides. Opiates may potentiate preexisting pruritus. The opiate antagonist naloxone hydrochloride has an attenuating effect on the histamine-induced component of pruritus.

• Substance P. Substance P is a neurotransmitter found in the central and peripheral nervous systems. When introduced intradermally, it elicits a pruritic response.

Many factors can potentiate existing pruritus. Neurologic factors such as boredom and fatigue can potentiate a pathologic itch and possibly transform a physiologic itch into a pathologic itch. Local axonal reflexes can potentiate pruritus; that is, if a second stimulus is applied to an area close to one that is pruritic, the second stimulus, irrespective of its type, is perceived as an itch. In addition, skin with chronic dermatitis has limited perception of stimuli, and any stimulus applied to the affected region may be perceived as either a burning sensation or an itch. This phenomenon is known as “conversion itch.” Second­ary bacterial infections, vasodilatation, and inflammation result in a local increase in proteases that potentiate pruritus.7

Pruritus can be diminished by several nonpharmacologic mechanisms, the most common being application of competing stimuli. Pruritus is a minor sensation compared with the other primary sensations of heat, cold, touch, and pain; thus local application of a competing stimulus to a pruritic area often suppresses the pruritic sensation. Scratching is an example of a competing stimulus.

Scratching may relieve pruritus by disturbing the rhythm of afferent impulses traveling toward the central nervous system. An alternative theory is that scratching may cause transient damage to nerve fibers that convey the pruritic sensation. Unfortunately, the effect is short lived because the epidermal damage induced by scratching causes the release of epidermal proteases that may later increase the degree of pruritus. Centrally acting factors such as diversions or distractions can also diminish the perception of pruritus by providing competing stimuli directly to the cortex rather than locally to the skin.7

Approach to Diagnosis of Pruritus

Pruritus is the most common sign of cutaneous disease. Most often in large animals, it is caused by ectoparasites or a hyper­sensitivity reaction, or both (e.g., Culicoides hypersensitivity); it may also be caused by cutaneous bacterial or fungal infections (e.g., dermatophytes, Malassezia species) (Box 11.1). Because pruritus may be a feature of a more generalized disease process,

■ BOX 11.1

Most Common Causes of Pruritus in Horses and Ruminants

Ectoparasites

Culicoides species (horses)

Other flying insects

Lice

Psoroptes cuniculi (goats)

Psoroptes ovis (sheep)

Sarcoptes scabiei (ruminants)

Chorioptes species (horses and cattle)

Hypersensitivity (Horses)

Atopic dermatitis

Infectious

Staphylococcal pyoderma (horses)

Dermatophytes

it is important to take the patient's general health into account. Hypersensitivity reactions, which are commonly pruritic, may or may not be limited to the skin. For example, anaphylaxis is a life-threatening hypersensitivity reaction that may manifest as pruritus in its early stages. Other pruritic skin diseases include immune-mediated diseases such as atopic dermatitis or pemphigus foliaceus; direct irritation by chemicals; and photoactivated dermatoses. It is helpful to formulate a differential diagnosis by considering each of these broad categories of diseases and using historic information, other cutaneous signs, and appropriate diagnostic tests to narrow the list of differential diagnoses.

The following steps are a guide to the diagnosis of pruritus in the horse and ruminant:

1. History and physical examination (see Fig. 11.1).

a. Determine if the pruritus is a seasonal or year-round problem. A seasonally recurrent pruritic disease tends to suggest either seasonal exposure to a parasite (e.g., lice in the winter, flies in the summer) or a seasonal environmental allergen (e.g., pollens) as the cause. Determine the level of fly exposure for the animal that is pruritic in the warmer months.

b. Determine if the pruritus is generalized or localized and, if localized, what areas of the body are affected. For example, photoactivated dermatoses are limited to the white-haired regions.

c. Determine if contact animals of the same and/or different species are affected or unaffected. The presence of multiple pruritic animals is suggestive of a contagious disease (e.g., dermatophytes, ectoparasites) or a disease of common exposure (Culicoides). A single pruritic animal among a group of unaffected animals is more likely to be experienc­ing a hypersensitivity reaction (drug or environmental).

d. Determine what topical and systemic medications were given to the animal both before and after the onset of the problem. Medications given before onset may be the cause of the pruritus, and those given after onset may interfere with the results of diagnostic tests.

e. Determine whether all the cutaneous lesions can be attributed to self-trauma or if primary cutaneous changes are present (e.g., wheals, nodules, pigmentary changes).

f. Determine whether, on close inspection, the coat shows evidence of small but grossly visible parasites such as lice or their eggs.

2. The most useful diagnostic tests are skin scrapings, acetate tape preparations, dermatophyte culture plus KOH preparation, Dermatophilus preparation, microfilarial preparation, biopsy for routine histopathologic examination, and intradermal testing (see Chapter 40).

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Source: Smith Bradford P., Van Metre David C., Pusterla Nicola (eds.). Large Animal Internal Medicine. Part 1. 6th edition. — Elsevier,2020. — 2279 p.. 2020

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