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Rosanna Marsella
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$ 99
Clinical approach to Feline Dermatologic Diseases
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Clinical approach to
Feline Dermatologic Diseases
R. Marsella
Feline Dermatologic Diseases
Cats are not small dogs and frequently they are forgotten in the literature. This book is intended to be an easy to use reference for practitioners and dermatology enthusiasts that only focuses on cats and their manifestations of skin disease. The emphasis will be on problem-based approach with numerous flowcharts and clinical images to provide examples of the various manifestations of skin disease in cats. The prominence is placed on clinically applicable information and experienced based clinical tips to help clinicians troubleshoot the various clinical presentations of skin disease in this species. Many dermatologic diseases may look similar and the purpose of this book is to help clinicians successfully diagnose the underlying disease rather than empirically treat symptoms. Particular emphasis will be placed on syndromes that are peculiar of cats and the special precautions that need to be taken when prescribing treatments in this species.
Clinical approach to Feline Dermatologic Diseases
Clinical Approach to Feline Dermatologic eBook available Diseases Clinical approach to
Rosanna Marsella
Clinical approach to
Feline Dermatologic Diseases
ISBN 978-88-214-5076-1
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€ 79
£ 79
$ 99
COVER MARSELLA UK_216X280_Ok.indd Tutte le pagine
This easy-to-use reference for practitioners and dermatology enthusiasts focuses on skin disease in cats. Its aim is to help veterinarians diagnose the underlying disease instead of empirically treating the signs. Along with a problem-based approach and graphic examples, this book provides clinically applicable information and experience-based tips to troubleshoot feline dermatologic diseases.
12/04/21 17:01
TARGET AUDIENCE:
✱ Small animal vets. Dermatology FORMAT: 21.6 × 28 cm ESTIMATED NUMBER OF PAGES: 200 approx. RETAIL PRICE NUMBER OF IMAGES: 260 approx. BINDING: hardcover ISBN: 978-88-214-5076-1 EISBN: 978-88-214-5077-8 ESTIMATED PUBLISHING DATE: May 2021
€79
Author ROSANNA MARSELLA DVM, DACVD. Full professor of small animal clinical sciences at the University of Florida, United States.
KEY FEATURES:
➜ ➜ ➜ ➜
Easy-to-use reference focused on skin disease in cats Logical, systematic problem-based approach Clinically applicable information for veterinary professionals Over 250 images
Presentation of the book Cats are not small dogs and they are frequently forgotten in the literature. This book is intended to be an easy-to-use reference for veterinary practitioners and dermatology enthusiasts that focuses only on feline dermatologic disease. This work takes a problem-based approach with numerous flowcharts and clinical images to provide examples of the various manifestations of skin disease in cats. With the aid of its clinically applicable information and experience-based tips, veterinary practitioners will be able to troubleshoot the different clinical presentations of skin disease in this species. Since many dermatologic diseases may look similar to each other, the purpose of this book is to help clinicians successfully diagnose the underlying disease instead of empirically treating the clinical signs. Particular emphasis is placed on syndromes that are peculiar to cats and the special precautions that need to be taken when prescribing treatments in this species.
Clinical Approach to Feline Dermatologic Diseases
The author Rosanna Marsella Dr Marsella received her degree in veterinary medicine from the University of Milan, Italy, in 1991. In 1996 she became a diplomate of the American College of Veterinary Dermatology, of which she has been president.
hkeita/shutterstock.com
Since 1997, Dr Marsella has been a faculty member at the University of Florida, United States, where she is currently a full professor of small animal clinical sciences and director of the laboratory of comparative dermatology.
Table of contents 1. Clinical approach to feline patients with skin disorders 2. Diagnostic tests in feline dermatology 3. Dermatologic therapy 4. Clinical approach to feline pruritus 5. Clinical approach to feline allergic skin diseases 6. Clinical approach to feline superficial fungal infections 7. Clinical approach to feline ectoparasites 8. Clinical approach to feline crusting dermatitis 9. Clinical approach to feline nodular dermatitis 10. Clinical approach to eosinophilic granuloma complex 11. Clinical approach to feline ulcerative diseases 12. Clinical approach to feline alopecia 13. Clinical approach to feline otitis 14. Clinical approach to feline facial dermatitis 15. Clinical approach to feline pododermatitis and nail diseases
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Rosanna Marsella
Clinical approach to
Feline Dermatologic Diseases
CHAPTER
8
Clinical approach to crusting dermatitis in cats
Crusts and scales are common secondary skin lesions with multiple causes in dermatology, coming from many underlying diseases. Since crusts and scales are non-specific, it is crucial for clinicians to identify “whenever possible” the primary lesions, thus providing a clue about the underlying primary disease. The clinical appearance of crusts and scales is frequently described under the term “seborrhea”. This is not an actual diagnosis but a mere description of a clinical appearance. Seborrhea can be described as “greasy” or “dry”. It should be kept in mind that, in
clinical practice, very few seborrhea cases are actually due to a primary keratinization disorder (also referred to as “primary seborrhea”). The vast majority of cases are secondary and the cause should be identified as there is no treatment that “fixes them all”. A large variety of mechanisms can lead to the formation of crusts and scales. In this chapter, details about the specific diseases and disorders will be discussed, explaining how to sort out the list of differential diagnoses developing a step-by-step logical and sequential approach to crusting dermatitis (Fig. 8.1).
Approach to crusting dermatitis Skin scraping
Positive
Cytology
Bacteria or yeast
Negative
Consider treating to rule out possibility using a broad spectrum product
Treat based on findings and reassess
Fungal culture
Treat based on assessment of cytological findings in combination with clinical signs and reassess
Negative
Positive: treat for dermatophytosis See chapter 6 for more details
Consider other DDX on the list based on distribution of signs
If negative for secondary infection: If parasites and dermatophytes have been ruled out, consider biopsy If acantholytic cells are found on cytology without bacteria, biopsy to confirm pemphigus foliaceous
Figure 8.1. Flow chart summarizing the diagnostic approach to crusting dermatitis in cats.
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Clinical approach to crusting dermatitis in cats
METABOLIC CAUSES Crusts can also be the effect of a direct insult like a spider bite, and scaling can be result of a metabolic problem like diabetes (Fig. 8.6). This is not a common differential in cats but should be considered in geriatric patients with concurrent illnesses.
NEOPLASIA Scaling and crusting may also be the result of accumulation of neoplastic cells like the case of cutaneous lymphoma (also known as mycosis fungoides). This
disease has many different manifestations but one is erythroderma, intense pruritus, particularly in older cats and even cats that never had a skin disease before nor a prior history of allergic disease. Diffuse silvery scaling and crusting is common (Figs. 8.7-8.8), together with thinning of the hair coat. These patients typically show weight loss and are generally unwell although early on in their disease they may seem very similar to an allergic patient posing a clinical challenge. Many may be considered potential food allergic cats as food hypersensitivity may start at any age and may be associated with pruritus that may not
Figure 8.6. Scaling dermatitis
and hair loss in a cat with diabetes. In these patients it is important to rule out D. cati due the immunosuppressive effects of diabetes, and to do a cytology for Malassezia, which can flourish under these conditions.
Figure 8.7. Crusting dermatitis on the head of a cat diagnosed with mycosis fungoides.
This patient was severely pruritic and also had a secondary bacterial infection.
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Figure 8.8. Same patient after clearing the infection. Note the intense erythema and some crusting that persisted and was linked to the underlying mycosis fungoides. Pruritus remained intense.
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respond to glucocorticoids. It is suggested to biopsy older pruritic crusty cats, minimally to rule out the possibility of cutaneous lymphoma before embarking into a lengthy food trial (8+ weeks) or other investigations for allergies. Thus, crusting and scaling in older cats should prompt the consideration of a possible neoplastic or metabolic condition. Indeed, scaling and alopecia may be a manifestation of an internal disease. This is the case of thymoma-associated dermatitis (Fig. 8.9). This is a syndrome in which scaling and hypotrichosis are associated with the presence of a thymoma. Diagnosis is made by skin biopsy and a thoracic radiograph showing a mediastinic mass.
frequently around the commissure of the mouth, nails, and face. It is frequently associated with pruritus and a history of a lack of responsiveness to standard antibiotic courses. Cytology again is a very important part of the evaluation of any dermatology cases and can provide a diagnosis in this case. Although there is no magic number of yeasts necessary to make a diagnosis of Malassezia dermatitis, the presence of yeasts on cytology in combination with the above described clinical signs is highly suggestive of this secondary infection. It is crucial to remember that Malassezia is a secondary cause in the vast majority of cases; thus, a diagnosis of Malassezia should prompt the clinician in the search of the underlying disease.
MALASSEZIA OVERGROWTH
PRIMARY KERATINIZATION ALTERATION
Metabolic, endocrine and allergic diseases are associated with altered production of lipids and become predisposing causes of Malassezia overgrowth. This disorder manifests with brown crusting and scaling
Crusting can also be the result of a primary disease of keratinization. In this case, crusting and seborrhea are evident early on in life. Kittens are known for
Fig. 8.9. Hair loss and mild scaling on the pinnae of a patient diagnosed with thymoma.
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Clinical approach to crusting dermatitis in cats
having greasy skin at a very young age. Owners complain about the feel of their coat and the fact that they appear “dirty and greasy” even with frequent bathing. These cats are very prone to the development of secondary infections. Initially they are not pruritic but once they develop bacterial and yeast infections, they can become very pruritic. Typically, the course shows temporary improvement with the treatment of the secondary infections, but infections typically recur as soon as the treatment is discontinued. This is because the skin is not normal and it is very prone to repeated overcolonization by bacteria and yeasts. The ears are also affected and excessive wax production and ceruminous otitis are also common manifestations. A slang term of a presentation of primary seborrhea is “dirty face syndrome” in which kittens have crusting and greasy skin around their eyes, mouth and ears. This disease is genetically inherited and cannot really be cured. A faster mitotic rate and abnormal composition and mount of skin lipids are believed to be the result of primary seborrhea. This disease can be managed symptomatically dealing with the secondary recurrent infections and applying topical therapy with keratolytic agents like sulfur and salicylic acid to remove the crusts, scales and cut down on the number of bacteria and yeasts. It is important to remember that ingredients like tar (used as keratolytic and keratoplastic agent in dogs) and selenium disulfide, used to kill yeasts in
Figure 8.10. Crusting on the margin of the pinnae of a cat with Notoedres spp. Note the crusted papules on the pinnae. Notoedres is a superficial mite and the papules are the result of the mite burrowing in the skin. These papules are not oriented around the hair follicles. Superficial skin scrapings are indicated to diagnose this highly pruritic disease.
8
dogs and people are toxic to cats and should never be used in this species. Sulfur can be used in cats and can be used both as a shampoo or as a dip. The dip can be used also as a topical therapy to address dermatophytes and some mites (e.g., notoedric mange). Another option to degrease the skin and remove crusts is the use of benzoyl peroxide. This is antimicrobial and has the ability to both help with secondary bacterial infections as well degreasing the skin.
Distribution of crusting dermatitis lesions The distribution of some of these diseases can certainly overlap. For example, Notoedres spp., dermatophytes, Demodex spp., and pemphigus all frequently affect the face and ears. Yet, a trained eye can detect subtle changes that can help rank these differential diagnoses. For example, Notoedres spp. prefers the margins of the ears (Fig. 8.10) and is associated with great pruritus. Pemphigus usually affects the concave surface of the pinnae (Figs. 8.11-8.12), the chin (Fig. 8.13), the bridge of the nose (Figs. 8.14-8.15), the perinipple area (Figs. 8.168.17) and the nail folds (Figs. 8.18-8.20). So, a clinician should know which sites to check to help in the ranking of these diseases.
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Figure 8.11. Papules and pustules in the concave pinna of a cat with pemphigus foliaceous. The pustules are large and span multiple follicles. They are transient and quickly replace by yellow crusts.
Figure 8.12. Large yellow crusts
on the concave surface of the pinna of a cat with pemphigus foliaceus.
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Clinical approach to crusting dermatitis in cats
Figure 8.13. Large crusts on the chin of a cat with pemphigus foliaceous. This patient had been originally misdiagnosed as a “bad case of chin acne”. Cytology was useful to show large number of acantholytic cells.
Figure 8.14. Patient with
systemic severe pemphigus showing depression and crusts on the nose and preauricularly.
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Figure 8.15. Same patient of
Fig. 8.14 after starting therapy, showing a decrease of crusting on the nose.
Figure 8.16. Pemphigus patient showing intense erythema and perinipple crusting.
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Clinical approach to crusting dermatitis in cats
Figure 8.17. Pemphigus patient showing epidermal collarettes
in the perinipple area. This area is a common site for pemphigus in cats. Once the pustules break, epidermal collarettes can be commonly found.
Figure 8.19. Milder case of paronychia in a pemphigus case.
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Figure 8.18. Nail bed area filled with dry exudate in a cat with pemphigus foliaceus. The nail bed area is commonly affected. The material can be used for cytology to demonstrate neutrophils and acantholytic cells.
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Figure 8.20. Severe case
of paronychia and crusting involving the whole foot and footpad in a patient with pemphigus foliaceous. This patient was unable/unwilling to walk and was systemically ill as a consequence of the fare of pemphigus.
Clinical signs Pemphigus is not typically considered a pruritic disease, yet some cases can be pruritic. It can be linked to secondary infections as well as the fact that some patients have a strong eosinophilic component. Pemphigus patients are typically middle-aged cats that many times also waxe and wane and show a decreased appetite and lethargy. Not every patient shows all these signs, but it should be noted whether there are any other systemic manifestations. Crusts can be the result of pruritic diseases that simply lead to excoriations. If the history points towards the presence of pruritus, these cases need to be worked out for this cause. Many allergic cats can present with crusting on their faces (Fig. 8.21), sides and periocularly due to the self-trauma or actual mosquito bites (Fig. 8.22). These crusts lack the honey colored appearance of the crusts of autoimmune diseases and the characteristic crusting of the margin of the pinnae as seen in notoedric cats.
Diagnosis of crusting dermatitis In terms of addressing the possibility of parasitic diseases, when approaching a case of crusting dermatitis, wide, superficial scrapings for Notoedres spp. must also be considered, and not just deep skin scrapings for Demodex cati. It is important to remember that Notoedres spp. mites may not be present in all scrapings, and that empirical treatments may be necessary to rule out this disease when suspected. Drugs suitable for that approach are topical flurananer, which can address D. cati, D. gattoi and Notoedres spp.) or selamectin, which would address Notoedres spp. and D. gattoi. Another option to address Notoedres spp. and D. gattoi is the use of lime sulfur dips. This is more labor intensive but has the added benefit of being a strong antipruritic agent, as well as an effective treatment for a potential dermatophytosis. This is a choice that some clinicians may consider while waiting for fungal culture results, or when dealing with patients with intense pruritus. Based on the availability of products and patient considerations, a clinician can pick and choose which treatment to recommend. 13
Clinical approach to crusting dermatitis in cats
Figure 8.21. Erythema and excoriations due to self-trauma in a flea-allergic cat. Lesions are self-inflicted.
Figure 8.22. Primary nodular eruption in a cat with mosquito hypersensitivity. Lesions are primary and induced by the bite. The eosinophilic accumulation in the skin after the bite leads to damage of the skin and formation of crusts. Lesions can be pruritic and even painful. Skin damage develops even when trauma is prevented by using an e-collar.
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When a cytology is done from the nail bed of these patients it is common to find, besides inflammatory cells and some cocci, large round blue epithelial cells with a nucleus. These are acantholytic cells (Fig. 8.23). Since epithelial cells detach before complete keratinization, they do not present as polyhedral shaped squames with no nucleus (Fig. 8.24). Instead, they are smaller, still have a nucleus, and are round-shaped. Although acantholytic cells can be formed in other diseases besides pemphigus, this finding should be noted and pemphigus must be considered as a possible differential diagnosis. Such differential should be pursued with a skin biopsy. The reason why other disorders can also cause acantolytic cells is that any time there is a severe influx of neutrophils in the epidermis, and these cells release their proteolytic enzymes in the dermis, desmogleins can be damaged and acantholytic cells can
be generated in ways that are not autoimmune diseases but simply a severe inflammatory disease. This can be, for example, the case of a severe contact dermatitis or a severe dermatophytosis.
Figure 8.23. Cytology from the patient in Fig. 8.20 showing
Figure 8.24. Cytology showing neutrophils and clusters of acantholytic cells (indicated by red arrows) and a couple of desquamated keratinocytes (no nucleus, polyhedral shape, indicated by black arrows). Desquamated keratinocytes are common in skin cytology, while acantholytic cells point out towards some form of disruption of the epidermis, either due to an autoimmune disease like pemphigus or some severe inflammatory response in the epidermis which leads to premature separation of keratinocytes before they have undergone the process of keratinization which would include the loss of nucleus and the change of shape from round to polyhedral.
acantholytic cells (large circular blue cells with a nucleus, derived from premature separation of keratinocytes in the epidermis).
Treatment of crusting dermatitis Milder options for dry seborrhea include the use of emollients and moisturizers like ceramides and phytosphingosine, a precursor of ceramides. Some of these products are combined with antimicrobial agents like chlorhexidine. Typically, shampoos are more difficult to use in cats compared to leave-on-type conditioners. Sprays are also difficult to apply and may need
15
Clinical approach to crusting dermatitis in cats
to be applied on a gauze before being applied to the animal. Another good option is also the application of sphingolipid emulsions or essential fatty acid-type preparations in the form of a spot-on. These products are applied between the shoulder blades and diffuse in the surrounding areas providing essential fatty acids which improve the coat condition and potentially the patients’ skin barrier function. More knowledge in this regard has been obtained in canine patients compared to feline patients. Nevertheless, some clinicians choose this option as it is considered safe and moderately effective for cases of dry skin.
Pemphigus foliaceous Pemphigus foliaceous is the most common cutaneous autoimmune disease in cats. It can occur for a variety of reasons. In some cases it is possible to identify a triggering antigen against which the immune system is mounting a response ranging from vaccines to drugs and even some flea products. This immune response cross reacts with desmogleins in the upper epidermis and the antibody, which were intended for another allergen, attacks the desmogleins as an innocent bystander. This is an IgG-mediated response. It is a type II-hypersensitivity, a cytotoxic reaction that triggers the accumulation of inflammatory cells like neutrophils, and even eosinophils. The result is the breakage of the connection between epidermal keratinocytes and the formation of pustules. In some cases it is possible to identify the trigger. This is very important to do in very young animals that otherwise would not be in the “right age” for autoimmune diseases. It is important to question the vaccination history, and any drug or supplement that was given to the animal. This is because the majority of the so-called “idiopathic” autoimmune cases (aka “cases in which a triggering cause cannot be identified”) are typically middle-aged. In those cases, it is almost accepted that the immune system is attacking self for no obvious cause. It is important to remember that, in order to build an immune response to an antigen, the patient could have been exposed to it without any problems for a while. So, rather than ruling out vaccines, flea products or drugs that have been used in the past without any problem, anything should be carefully considered. Particular attention must be payed to treatments that 16
were administered in the 4-6 weeks prior to the development of signs. Some have a very good prognosis once the “aberrant” immune response is suppressed and no additional exposure to the offending allergen occurs. Some cases, however, are self-perpetuating and can continue to develop lesions even when the offending allergen is removed and require long-term immune suppression, just like an idiopathic case would require. In older patients, triggers like neoplasia must be considered as they are “too old” for the idiopathic form for the disease. In these cases the immune system is also reacting to an antigen related to the tumor, which happens to cross-react with an epidermal epitope leading to an autoimmune response. Failure to identify the triggering cause or dealing with a triggering cause that cannot be removed or avoided, makes treatment particularly challenging and worsens the prognosis. Having said this, the author has seen pemphigus in patients of all ages. Some cases are patients with a previous history of allergies, and then the owners report a “change in signs”. These cases may be more subtle to diagnose as they have had skin disease all their lives but the disease changes from being well controlled with anti-inflammatory doses of glucocorticoids or cyclosporine to being more recalcitrant and being associated with crusting and malaise. A drug eruption should always be considered whether in the form of pemphigus or erythema multiforme. It is also important to consider that chronic skin trauma can actually, sometimes, expose the immune system to antigens that were otherwise protected. This is one speculation of why allergic patients may later on in life develop autoimmune skin diseases. This is proposed to be a result of chronic trauma and the formation of autoantibodies. Generally speaking, a predisposition towards females is reported for autoimmune diseases. In terms of clinical manifestations of pemphigus, they vary greatly. Some patients have localized and mild disease for a long time. They are sometimes misdiagnosed as cases of chin acne that does not improve with standard treatment for acne. In these cases, lesions are papules, pustules and crusts on the chin. Frequently, the disease eventually unfolds into a pustular eruption on the pinnae and bridge of the nose as well as periocularly (Fig. 8.25). This pattern is sometimes described as a “butterfly” pattern. The lesions are pustules, frequently large and spanning multiple follicles, intermixed with honey-colored crusts. Sometimes on histopathology
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Figure 8.25. Swelling, erythema and erosions on the face of a patient with herpes dermatitis.
it is possible to see the various layers of pustules and acantholytic cells and this is the reflection that this disease has a classic course of waxing and waning flares. During the flares, the patient does not feel well; it stops eating, and may run a fever. This is typically associated or shortly followed by a new eruption of pustular lesions. With each “wave” the disease tends to become worse, more aggressive and more generalized. If the patient has been exposed on and off to suboptimal doses of glucocorticoids, the disease also becomes progressively more resistant to glucocorticoids. The typical scenario is that the first few rounds of steroids provided some improvement although temporary and not complete and eventually stop helping. This is a very important reason for which it is crucial to make a timely diagnosis and treat these patients with the appropriate dose of glucocorticoids as well as other steroid sparing agents. When we think of diseases that become resistant to treatment we tend to think of bacterial infections. Yet, autoimmune diseases can do this as well, creating a major challenge for the management. Sometimes, what happens in real life is that either owners or veterinarians are hesitant to biopsy, so clinicians empirically prescribe some glucocorticoids. As they are not sure about the diagnosis, typically anti-inflammatory doses or low immune-suppressive are prescribed for a short period. Glucocorticoids are hardly ever associated with a steroid sparing agent. Then, as soon as the tapering schedule of the glucocorticoid is done, lesions come back with vengeance. At this point, higher doses are needed or a different glucocorticoid
is necessary typically moving from milder and safer choices to more long lasting powerful agents, with more potential for adverse effects. So, when dealing with a case with a history of recurrent pustular/crusting eruption affecting the face, it is important to consider pemphigus foliaceous on the list of differential diagnoses and consider a skin biopsy than to attempt glucocorticoid therapy without having a diagnosis. Other areas that are commonly affected are the nail folds, the perinipple area and the footpads. The nail themselves are typically not affected. This is important because if they are, dermatophytosis should become a priority in the rule outs. Affected patients are reluctant to walk and lethargic. One area that is not affected in pemphigus foliaceous patients is the oral cavity. It should be noted that pemphigus foliaceous is a cutaneous disease and not a disease of the mucous membranes like other autoimmune diseases such as pemphigus vulgaris or bullous pemphigoid. As mentioned before, besides skin scraping (both superficial and deep) and fungal culture, cytology is an integral component of the basic dermatology workup. The detection of acantholytic cells is easier in those patients that are actively flaring and have not been recently exposed to glucocorticoids. In order to confirm the diagnosis of pemphigus it is strongly recommended to follow up with a skin biopsy. The best lesion to biopsy is a pustule or an area with crusts. The worst area to biopsy is an ulcerated area as the disease is in the epidermis. It is beneficial to clip the areas surrounding the affected regions and search for new, fresh lesions. Sometimes, the less obvious and severe lesions are the best area to obtain an answer. Care should be taken not to damage any lesion when doing the biopsy. There should be no scrubbing or prepping of the area as it is crucial to preserve the pustules or the crusts. If not active lesions are present it is acceptable to submit crusts to be processed for histopathology. A regular histopathology is sufficient and it is not customary to ask for immunofluorescence or immunohistochemistry. The pustules typically span multiple follicles and are filled with neutrophils, eosinophils and acantholytic cells. The presence of bacteria can sometimes make the diagnosis of pemphigus a little more difficult and this is why, if possible, it is best to treat infections before the biopsy. The concurrent use of glucocorticoids also interferes with the ability to make a diagnosis and that is why it is important to 17
Clinical approach to crusting dermatitis in cats
refrain from starting any treatment before the biopsy, if at all possible. In order to speed up ruling out dermatophytes, some clinicians may ask for special stains for dermatophytes if there is evidence of folliculitis as typically the histopathology report is available in shorter times that the time required for dermatophytes to grow and for microbiology labs to provide final fungal culture results back. Once the diagnosis of pemphigus is confirmed through histopathology, immunosuppressive therapy is initiated. This involves a combination of glucocorticoids and a steroid sparing agent. Many of these cases are also placed on a systemic antibiotic both because they may already have an infection and also to minimize future infections. In the author’s experience, very few cases can be managed just with the use of glucocorticoids and a vast majority require a steroid sparing agent to allow sufficient tapering of the glucocorticoids and minimize the severity of the adverse effects. The vast majority of idiopathic cases requires treatment for life, and the ones where there is a concurrent allergy tend to have flares of their pemphigus during their allergy season. Importantly, any form of stress, emotional or due to other illnesses, can lead to a flare of the autoimmune disease requiring increases of the medications necessary to control the pemphigus. The treatment is typically designed as composed by an “induction period” of 10-14 days followed by a “maintenance period”. In the induction period the remission of the disease is largely dependent on the use of glucocorticoids due to their strong ability to suppress inflammation. In the more chronic period, the remission is maintained by the steroid sparing agent. The steroid sparing agent typically has a lag phase of several weeks (2-6 weeks depending on the agent used). During this period of time adverse effects can already occur but minimal effect in the control of pemphigus exists. This is why the tapering of the glucocorticoids is done in a way to allow sufficient time for the steroid sparing agent to kick in. In terms of glucocorticoids, a common starting medication is prednisolone. For those cats with excessive polyuria and polydipsia when using prednisolone, methylprednisolone can be used. A common starting immunosuppressive dose for prednisolone is 3.3-4.4 mg/kg orally twice daily. If methylprednisolone is used 1.5-3 mg/kg twice daily can be a good induction. Other options for glucocorticoids can be oral dexamethasone 18
and triamcinolone. These are more powerful and longer lasting glucocorticoids that are typically only used when prednisolone or methylprednisolone are not good options. This is usually the result of developed resistance of the disease. Dexamethasone (induction dose of 0.2-0.4 mg/kg twice daily) and triamcinolone (induction dose of 0.4-0.8 mg/kg twice daily) can be used instead, but they induce adverse effects more quickly ranging from diabetes to increased liver enzymes, from cutaneous atrophy, skin fragility, propensity to infections (both cutaneous and urinary). The least desirable choice for glucocorticoids when managing pemphigus is the use of injectable long lasting preparations like DepoMedrol. These preparations are not amenable to the concept of alternating regimens for the sake of safety and to minimize adrenal suppression and it is very common to require more and frequent administration obtaining less and less control of the disease overtime while accumulating more and more adverse effects. For patients that cannot tolerate glucocorticoids altogether due to diabetes, for example, other options can be oral cyclosporine or, off-label oral oclacitinib. Cyclosporine is usually not an effective treatment for pemphigus as monotherapy but it can be used as adjunctive therapy either as a substitution of the glucocorticoids or as a steroid sparing agent. The dose of cyclosporine as adjunctive treatment is the same used for allergic skin diseases (7 mg/kg orally once daily or every other day during maintenance). Due to the metabolism of cyclosporine through cytochrome P450, it is important to consider other medications that are prescribed to the patient to minimize adverse drug interactions. Cyclosporine can induce adverse gastrointestinal effects in many patients like vomiting, diarrhea, nausea and decreased appetite. In many patients the dose can be decreased once the disease is in remission. The use of oral oclacitinib, a JAK inhibitor approved for use in dogs, has been adopted in some feline cases, both for the treatment of allergies and as adjunctive therapy for autoimmune diseases. Some cats may show positive response while others may not benefit from this approach. It appears that cats require larger doses than dogs, as it is the case for other medications so it is common to start with doses like 0.6 mg/kg twice daily for the first couple of weeks and then taper. The effect, if positive, is typically immediate. It is important to remember that oclacitinib is not anti-inflammatory per se like glucocorticoids are. The way this medication is
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