Approach to the Pruritic Pet
World Small Animal Veterinary Association World Congress Proceedings, 2015
M. Shipstone
School of Veterinary Science, University of Queensland, Stafford, QLD, Australia

Pathophysiology

Pruritus is a specific cutaneous sensation that is quite distinct from the other cutaneous sensations. No one mediator is responsible for the initiation of the sensation and it is most likely that the additive effect of multiple mediators summate to produce pruritus. This is highlighted by the fact that no single blocking agent is consistently effective in the elimination of pruritus in any mammalian species yet studied.

Modulation of Pruritus

"Gate theory" has been proposed to explain how central factors may modulate the sensation of itch, which may occur at or above the level of the spinal cord. Stress, anxiety, boredom, pain, touch temperature may all affect it. Environmental factors may increase skin sensitivity such that the response to a specific stimulus is increased.

"Threshold phenomenon". This proposes that a certain pruritic load may be tolerated without causing any clinical signs. A small increase in the stimuli, however, may push the individual over the threshold leading to the development of clinical signs. While some factors initiate pruritus, others may simply lower this threshold. Connected with this is the "summation effect", whereby pruritic stimuli from different mediators or coexistent skin diseases may add together to produce moderate to severe pruritus, where any individual factor would only produce mild or no effect at all.

Clinical Aspects

Clinical Manifestations

Pruritus is a sensation and is synonymous with itch. Animals generally display the sensation of itch clinically by scratching. However, it may also be manifested by licking, sucking, biting, chewing, rubbing, or rolling. It is important to list all of the manifestations to the client when trying to determine the history, severity and distribution of irritation, as frequently the client may not associate some of these (particularly licking) as a symptom of itch.

Pruritus is just a symptom and may be seen in a variety of diseases and pathologic changes. It may be caused by primary diseases, but may also be affected by modulating and or amplifying factors. The relative importance of all of these must be sorted out in each individual if successful management is to be achieved.

Causative factors of pruritus

Primary disease

Modulating factors

Amplifying factors

 Atopy

 Flea allergy

 Food adverse reaction

 Contact allergy/irritation

 Scabies

 Cheyletiella

 Demodicosis

 Dermatophytosis

 Neoplasia

 Autoimmune disease

 Dry skin

 Heat

 Boredom

 Anxiety

 Stress

 Bacterial infection

 Malassezia infection

 Psychogenic

Successful management involves determination of the following:

1.  What is the specific diagnosis or diagnoses?

2.  Are modulating or amplifying factors present, which may either increase pruritic load or lower pruritic threshold?

3.  What will the diagnostic and management plan involve?

4.  Are the clients aware of the investigative and treatment plan? Are they compliant?

Client education and compliance is critical if these animals are to be managed successfully long term and should be the most time consuming portion of the initial consult or second only after the history. Remember, pruritus is a symptom, not a disease, and the most successful treatment involves identifying and treating the cause.

Investigation

History and clinical signs are used to determine the differential diagnosis. The goal is to establish a chronology of the disease progression. At what age did it begin; what were the clinical signs initially versus now? Have they changed; is it getting worse?

Is it seasonal or nonseasonal - food adverse reactions may mimic atopy, but are generally nonseasonal. Atopy, insect bite hypersensitivity are more frequently seasonal.

Response to therapy? This will often give clues as to amplifying or modulating factors. For example, failure of antibiotics or steroids when they were previously effective may signal Malassezia infection. Failure of steroids may indicate pyoderma, bacterial overgrowth or Malassezia.

Recurrent otitis may indicate either atopy or food allergy. In fact, up to 30% of atopics or food allergic animals may present with otitis as the initial and sometimes only clinical sign.

Clinical Examination

Rule out the obvious; are ectoparasites present? Fleas, lice, ticks. Treatment and elimination will allow determination of their significance.

Pruritus and Lesions Present

Alopecia, scaling, hyperpigmentation may indicate Demodex, scaling, crusting, papules particularly on the pinnal margin, periocularly, elbows or ventrally may indicate scabies. Scabies also generally causes severe pruritus, such that the animal will scratch madly during the consult. It is one of the few diseases where the animals will continue to scratch in this fashion in the consult room. Cheyletiella is a pruritic disease that causes scaling which may be severe, particularly along the dorsum.

If Demodex is suspected, multiple deep skin scrapes are necessary. Scabies requires a much more extensive, superficial to identify the mites. Despite this, the sensitivity of skin scrapes have been reported as low as 20–40%. So, if scabies is suspected, trial therapy with ivermectin, milbemycin or topicals may be necessary.

If in doubt, skin scrape - there is no lesion that "couldn't possibly be mites" or "just doesn't look like mites".

Are other lesions present? - e.g., erythema, lichenification, hyperpigmentation, greasiness, scaling, crusting, papules, pustules, epidermal collarettes, annular areas of hyper or hypopigmentation, "footprint" lesions, and "moth eaten" alopecia more commonly suggest bacterial involvement.

Lichenification, hyperpigmentation, erythematous plaques, yellow greasy crust, waxy follicular casts, particularly in the fold regions, and scaly mild paronychia may all suggest Malassezia.

Cytology is critical. I don't think it is much of an overstatement to say that it should be performed in areas of irritation on every animal regardless of the presence of lesions. Cytology must also be collected from several sites as the infection present may be quite regional in its distribution.

If abnormal numbers of organisms are identified, trial treatment is necessary to determine to what extent (if any) the infections are contributing (amplifying) the itch. A clear distinction must be made to the client between resolution of the lesions and resolution of the itch. It may be that treatment with antibiotics leads to resolution of lesions but no or minimal change in pruritus an individual, yet both resolution of lesions and near complete resolution of pruritus in another.

Once the infection has been eliminated, the animal is reassessed for its remaining level of pruritus.

Lesions Resolve, Pruritus Remains

Any reduction in pruritus allows a determination of the contribution of the infection.

The differentials thus are narrowed to insect bite hypersensitivity, food adverse reaction and atopy.

Insect bite hypersensitivity is diagnosed on the basis of appropriate clinical signs along with a positive response to an insect elimination trial. The 4 products I use for an insect elimination trial are

1.  Comfortis (spinosad) - 0, 2 and 4 weeks

2.  Frontline (fipronil) - Spray applied at 0, 2 and 4 weeks

3.  Capstar (nitenpyram) - Daily (dogs), every second day (cats) for 4 weeks

4.  Permoxin (permethrin) - Applied daily (to saturation) for 3–4 weeks (NB dogs only). Response to the trial is made at a 4 week recheck.

Food elimination trial involves the feeding of a novel (or hydrolysed) protein for at least 6–8 weeks. If there is an improvement, the diagnosis is then made by relapse on rechallenge with the old diet. A smorgasbord of all of the old diet is fed for 7–10 days. If the animal is sensitive to anything in the diet, it will react within this time (most in the first 3 days). If a flare in itch is seen, a sequential rechallenge is performed to determine precisely what component of the diet the animal is sensitive to.

If there is no response to the food elimination trial or insect elimination trial and the animal has clinical signs consistent with atopy, a diagnosis of atopy can be made. The detail of this can be found in the notes "Atopy - More Than Just Allergy" of these proceedings.

Lesions Resolve, Itch Resolves

The reason that the animal developed secondary infections needs to be identified. In older dogs, endocrinopathies, most commonly hypothyroidism or hyperadrenocorticoidism, is responsible and needs to be investigated with appropriate tests. In younger dogs (or old dogs with a long standing history dating from a younger animal), atopy may present as chronic or chronic relapsing pyoderma. In some breeds; e.g., the British Bulldog, atopy is not generally pruritic but presents as erythema in classic areas (e.g., interdigitally, axillae, groin, face, pinnae).

Diagram 1
Figure 1

 

Pruritus Present, No Lesions Present

The differential list includes Sarcoptes incognito, atopy, food adverse reactions, insect bite hypersensitivity, intestinal parasite hypersensitivity, contact hypersensitivity, contact irritant reaction, neoplasia.

Investigation involves trial therapy and elimination trials as previously described. Particularly in older dogs, investigation for neoplasia should be done.

A biopsy may allow the identification of contact reactions, neoplasia, vasculitis and a nonspecific reaction pattern suggestive of hypersensitivity.

Once a diagnosis has been made and the importance of both modulating factors and amplifying factors has been determined, a treatment plan can be formulated and implemented.

Diagram 2
Figure 2

 

References

1.  Bernhard JD. Clinical aspects of pruritus. In: Fitzpatrick TB, Eisen AZ, Wolff K, et al., eds. Dermatology in General Medicine. 4th ed. New York: McGraw Hill.

2.  Favrot et al. Vet Dermatol. 2010;21:23–30.

3.  Griffin CE. Diagnosis and management of pruritus in the dog. In: 14th Proceedings from the American Academy of Veterinary Dermatology (AAVD)/American College of Veterinary Dermatology (ACVD) meeting. San Antonio, TX; 1998:5–10.

4.  Ihrke PJ. Pruritus. In: Ettinger SJ, Feldman EC, eds. Textbook of Veterinary Internal Medicine. 4th ed. Philadelphia, PA: WB Saunders; 1995:214–218.

5.  Shanley KJ. Pathophysiology of pruritus. Vet Clin North Am Small Anim Pract. 1988;18:971.

  

Speaker Information
(click the speaker's name to view other papers and abstracts submitted by this speaker)

M. Shipstone
University of Queensland
School of Veterinary Science
Stafford, QLD, Australia


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