Pruritus is a clinical sign rather than a diagnosis or disease and may have a multitude of causes. Broadly speaking, however, there are three main causes of pruritus that the clinician should consider when faced with a pruritic patient: parasites, infections and allergies. Additionally, some diseases that are primarily non-pruritic may become pruritic when secondary infection is present (eg an endocrinopathy such as hypothyroidism with secondary bacterial pyoderma).
Approaching the puritic case
Investigation of pruritus necessitates a thorough dermatological history and clinical examination, and successful treatment outcomes depend on making an accurate diagnosis and managing the various components of the disease in the individual patient (Favrot et al., 2010). Rushing to address the pruritus without due care and attention to the various factors at play can result in poor response to treatment or even exacerbation in clinical signs, not to mention a frustrated client.
The challenge we frequently encounter is that atopic patients commonly present to the clinician with concurrent secondary infections (due to self-trauma and skin barrier defects) and many suffer from food-induced flares or a combination of food and environmental allergies. Furthermore, some patients can have hypersensitivities to micro-organisms, which further complicates the disease process (Marsella et al., 2011; 2012).
In the context of the factors contributing to pruritus, it can be useful to refer to the pruritus threshold theory (Marsella and Sousa, 2011). This theory illustrates the fact that each individual patient has a personal threshold at which clinical signs of pruritus are evident (ie scratching, nibbling, chewing, rubbing) and, in the majority of cases, there are several factors that may contribute to the level of pruritus at any one time. It can be useful to think of these factors as “building blocks” that add up to push the patient over the threshold, with each building block having its own “height” or “weighting”. So, for example, a dog with a low-grade environmental allergy may be asymptomatic until it develops a secondary pyoderma, and by treating the secondary pyoderma, we can keep this patient below its pruritic threshold for most of the time. Teasing out the major components of each individual patient’s disease takes time but investing time in identifying these components can pay dividends in the longer term.
The diagnostic process
The diagnostic process should be logical and comprise a detailed history-taking exercise followed by a full clinical examination, a detailed dermatological examination and then basic screening tests (see Figure 1).
It is worth emphasising the importance of going back to basics when it comes to the initial investigations as the indiscriminate use of a wide variety of irrelevant tests too early on can lead the clinician into a maze of false positive and false negative results, resulting in an incorrect diagnosis and inappropriate treatment recommendations.
This is why allergy testing has no role in the “diagnosis” of allergy. Allergic skin disease is a diagnosis of exclusion; allergy testing should only be undertaken to identify allergens for avoidance and allergen-specific immunotherapy.
The history-taking exercise is an important first assessment of the presenting problem and often gives vital clues as to the underlying cause of the pruritus. Using a history-taking sheet can keep things streamlined and consistent and allows a certain amount of “staying in control” during the consultation. Key information such as general health, family history of skin disease, diet, lifestyle, travel history, history of contagion, medical history and how the skin disease has progressed over time or responded to treatment are all important to determine.
Specifically, the date and age of onset, distribution of the problem at onset, initial appearance, progression/regression of lesions over time, seasonality and pruritus score are vital to establish. It is also very helpful to determine (if possible) whether the pruritus preceded the development of skin lesions (common in allergic skin disease) or whether skin lesions preceded pruritus (common in pyoderma).
The clinical examination comes next and should begin with gaining an overall impression of the patient: demean-our, attitude and general distribution of lesions if obviously visible. A full clinical examination should be performed to assess the general health of the patient and include palpation of peripheral lymph nodes, abdomen and testicles (if present). The detailed dermatological examination should follow with an initial assessment of skin and coat quality and then a detailed examination of the entire skin for lesions, distribution patterns and presence of ectoparasites – not forgetting those hard-to-reach areas such as facial folds and interdigital skin (see Figure 2). Clipping of the haircoat may be necessary to visualise lesions in some cases.
It can be useful to annotate a body map with location of primary and secondary skin lesions. Establishing the distribution and configuration of lesions may help prioritise certain differential diagnoses. For example, bilateral and symmetrical patterns often suggest a systemic cause (such as endocrine or allergy), whereas asymmetrical patterns may suggest infection or neoplasia.
Furthermore, certain breed-associated phenotypes have been recognised for canine atopic dermatitis (Wilhem et al., 2011). Some of these differences may be due to genetic variability while others are likely to be associated with variations in environmental factors.
Otoscopy should form part of the dermatological investigation and include examination of the pinnae and external ear canal plus assessment of discharge (if present) and the tympanic membrane. Even if the problem appears to be very localised (for example, pedal furunculosis or otitis), the clinician should be urged to look further and assess the skin in its entirety to look for other, perhaps more subtle, signs that may suggest a more generalised problem, such as allergy.
It is worth noting that cats show a much greater variety of clinical signs compared to dogs, and distribution patterns are often not quite so distinct (Hobi et al., 2011). Pruritus in cats is generally displayed as overgrooming and cats are usually quite secretive in their behaviour, which means that owners are not often aware that they are pruritic. Four cutaneous reaction patterns exist in cats, each of which represents a manifestation of pruritus: self-induced symmetrical alopecia, miliary dermatitis, head and neck pruritus and eosinophilic dermatitis. These different presentations often occur together in the same patient (see Figure 3).
A well-thought-out differential list should be developed and listed in order of most likely to least likely, taking into account incidence and prevalence of disease in relation to age of onset, breed, gender and geographical location. This will direct the use of appropriate tests and investigations so that a definitive diagnosis can be made.
Basic screening tests and therapeutic trials
Simple and inexpensive screening tests are very helpful in confirming or ruling out the main differentials of pruritus and can usually be performed during the consultation. Flea comb/coat brushings, skin scrapes, hair plucks and cytology form the “bread and butter” of any pruritus work-up and only require a basic dermatology work-up kit.
If parasites are identified or suspected, a treatment trial should be performed for at least three to four weeks. Any infection identified on cytology should also be treated. Often, these are done at the same time with an appropriate ectoparasiticide and a topical antimicrobial agent (sometimes systemic antimicrobial agents are required).
If pruritus persists and is non-seasonal, then a food trial should be undertaken. This can be more challenging in cats due to their lifestyle and risks of hepatic lipidosis if the patient refuses to eat the diet for more than a day or so. Owners require detailed instructions to ensure that the food trial is conducted reliably, and compliance is good.
The choice of trial diet should be based upon knowledge of prior dietary history, although recent studies have shown that the mislabelling of pet foods is common, even in those claiming to contain “novel” or “limited” ingredients (Olivry and Mueller, 2018). The author prefers to use a hydrolysed diet containing proteins that have not been previously fed if possible. The trial should be eight weeks long; diagnosis of food allergy is made by noting a marked improvement over the period of the diet trial followed by a period of relapse within a week or two of reintroducing the previous diet.
Atopic dermatitis is a diagnosis of exclusion and once the other causes of pruritus have been ruled out, the clinician can be relatively confident if the history and clinical presentation is consistent (Hensel et al., 2015). Once the diagnosis is made, the next step is the individualisation of the treatment plan (Olivry et al., 2015).
The multimodal approach consists of a combination of some of the following: allergen avoidance, immunotherapy, infection control, essential fatty acids (or diets enriched in essential fatty acids), antihistamines, glucocorticoids, oclacitinib, ciclosporin and lokivetmab, with the principle that the smallest amount of therapy should be used to minimise side effects. The patient should be regularly assessed, treatment should be modified if necessary and compliance should be maintained through good communication.
