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COLUMN EDITOR COLUMN EDITOR Craig E. Griffin, DVM, DACVD Animal Dermatology Clinic, San Diego, California
COLUMN EDITOR COLUMN EDITOR Wayne S. Rosenkrantz, DVM, DACVD Animal Dermatology Clinic, Tustin, California
Overview of Flea Allergy Dermatitis ❯❯ Andrea Lam, DVM
❯❯ Anthony Yu, DVM, MS, DACVDa
University of California Davis Veterinary Medical Teaching Hospital
F
lea allergy dermatitis, or flea-bite hypersensitivity, is the most common small animal dermatologic condition.1–3 In some regions of the world, it is the most commonly seen canine disease. This disease does not exist in locations that are inhospitable to fleas, such as those at elevations above 1500 ft or with low humidity (e.g., the desert). Although there are more than 2000 documented species and subspecies of fleas, the cat flea (Ctenocephalides felis felis) is the species most frequently found infesting dogs, cats, and all caged pets in North America.
Flea Facts
At a Glance Flea Facts Page 220
Pathogenesis Page 220
Diagnosis Page 222
Treatment Page 223
Flea Control Products Page 224
a Dr. Yu discloses that he has received financial support from Greer Laboratories, Iams, Novartis Animal Health, and Pfizer Animal Health.
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The life cycle of the flea ranges from as few as 12 to as many as 190 days, with an average of 21 days. The time needed for development depends heavily on environmental conditions, particularly temperature and humidity. The optimal environment is a low-altitude geographic location, a temperature of 75°F (23.8°C), and a relative humidity of 78%. An adult flea takes its first blood meal from a host within minutes of contact. Female fleas lay their first egg 24 to 36 hours after this blood meal. Flea eggs are smooth and slick. Only 30% of eggs remain on the haircoat; the remainder fall off the host into the environment. Hatching takes place within 1 to 10 days, again depending on humidity and temperature. A single female flea can lay 1000 eggs within 30 days, and most average 2000 eggs during their life. Although eggs can hatch anywhere in the environment, development of the larvae that emerge from the eggs must take place off the host because mammalian body temperatures are too high for survival. Larvae are highly sensitive to heat and desiccation and therefore tend to move downward and away from direct light
University of Guelph Ontario Veterinary College
sources. The larvae feed on adult flea feces (partially digested blood) in the environment. Within 5 to 11 days, a larva undergoes two separate molting stages before forming a pupa. The pupal stage is the most resilient of all stages because the cocoon is highly resistant to desiccation. It also has a sticky surface that helps to prevent premature removal from the environment and that accumulates dust and other household particulates to provide protection. On average, the pupal stage lasts 8 to 9 days; however, fleas can pupate for up to 6 months if the environmental conditions are not ideal for emergence. Only with proper environmental stimuli, such as an increase in carbon dioxide, warmth, physical pressure, and vibration, will an adult flea emerge from its cocoon. After emerging from the cocoon, adult fleas search for an appropriate host. Adult fleas are attracted to light and tend to migrate upward toward surfaces where contact with an appropriate host is more likely. Once a host is found, feeding and mating take place within 8 to 24 hours. Female fleas can consume 15 times their body weight in blood per day. Adult fleas act as obligate, permanent ectoparasites, preferring to remain on a host rather than in the environment.
Pathogenesis Flea saliva contains histamine-like compounds, proteolytic enzymes, and anticoagulants. These proteins are released into the host during feeding and can act as inflammatory or antigenic stimuli in sensitive animals. Various immunologic responses are provoked, including immediate and delayed hypersensitivity reactions,4 late-phase IgE-mediated responses, and cutaneous basophil hypersensitivity reactions.5 Dogs with atopic dermatitis appear to be predisposed to the development of flea allergy dermatitis.6,7
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Dr. Yu (shown here with his dogs [from left to right] Timmy, Joey, and Bitsy) is associate professor of dermatology at The University of Guelph Ontario Veterinary College in Canada.
WEB EXCLUSIVE An extended version of this article is available on
CompendiumVet.com.
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FIGURE 1
FIGURE 2
Typical distribution pattern of flea allergy dermatitis affecting the caudodorsolumbar region and caudal thighs (caudal to the “waistline”).
A fibropruritic nodule, a benign hyperplastic reaction to severe flea allergy dermatitis, on a dog.
Diagnosis
QuickNotes History and physical examination findings are the keys to making an appropriate diagnosis of flea allergy dermatitis.
History and physical examination findings are the keys to making an appropriate diagnosis of flea allergy dermatitis. There is no breed or sex predilection, and flea allergy dermatitis can develop in animals of any age. Patients may exhibit seasonal or year-round pruritus, depending on their geographic location. The owner may report an increase in pruritus following the introduction of a new pet or a visit to a boarding or grooming facility. Often, clinical signs manifest on the caudal aspect of the animal, especially in dogs (FIGURE 1). Evidence of self-induced alopecia; erythema; pyotraumatic dermatitis; dull, coarse
FIGURE 3
“Hot spot” or acute moist traumatic dermatitis. One of the common underlying etiologies of this condition is flea allergy or flea-bite hypersensitivity.
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haircoat; hyperpigmentation; and/or lichenification may be observed affecting the dorsal lumbosacral region, tail base, caudomedial thighs, inguinal region, and umbilical fold.1 Other physical examination findings include papules or encrusted papules, crusting, scaling, and, occasionally, fibropruritic nodules (FIGURE 2) in association with affected areas. Secondary superficial to deep pyodermas are common (FIGURE 3). Close examination of the skin and haircoat using a flea comb may reveal flea dirt or adult fleas (FIGURE 4). Some pets may even exhibit clinical anemia as a result of severe flea infestation (FIGURE 5). Pets that are fastidious groomers can ingest adult fleas
FIGURE 4
Flea comb. This is a useful tool to demonstrate fleas and flea dirt to clients who are in denial about the presence of fleas on their pet.
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carrying the tapeworm Dipylidium caninum and may have segments of D. caninum in their feces. Clinical manifestations of flea allergy dermatitis in cats can include miliary dermatitis, eosinophilic granulomas or plaques, or self-induced alopecia without active lesions (FIGURE 6). Affected areas may include the dorsum, inguinal region, caudomedial thighs, head, and neck. A lack of fleas or flea dirt is commonly reported by owners and should not override a diagnosis of flea allergy dermatitis if clinical suspicion is high. Intradermal skin testing with flea allergen may reveal wheal formation with immediate and delayed hypersensitivity. Serum in vitro testing for flea-specific IgE has variable accuracy and does not identify animals with delayed hypersensitivity reactions. Histopathology is nonspecific and reveals a superficial perivascular inflammation, often containing eosinophils—a pattern that can be seen in other hypersensitivity reactions.
Treatment Based on current knowledge of flea biology, topical or systemic flea adulticide therapy may be the only management required to establish adequate control over flea infestations. Many prescription flea control products are currently available (TABLE 1). Ideally, integrated pest management, including the use of flea adulticides along with insect growth regulators
(IGRs) or insect development inhibitors (IDIs), should be used as a long-term management program to effectively eradicate infestation while minimizing potential drug resistance. If the environment is heavily burdened with various stages of fleas, environmental control is also warranted. Vibrations from a vacuum cleaner help stimulate emergence of the adult flea from the impervious pupa and, hence, increase the likelihood of effective environmental ectoparasiticide control. One to two applications of a synthetic pyrethroid or fipronil as an environmental spray every 7 days should be sufficient, although the addition of a household IGR such as methoprene or pyriproxyfen and/or sodium polyborate in carpeted areas would produce the best results in the house. To avoid any potential adverse reactions, it is best to remove pets from the treated environment until the products have dried; therefore environmental treatment is often done in stages. Professionally licensed exterminators should be considered for yards and households that are heavily infested. All blankets, bedding, and rugs that are favored by the affected pet should be laundered. All carpeted areas and furniture that can house preadult fleas should be vacuumed, and the vacuum bag should be disposed of immediately. All household pets should be prevented access to flea-dense areas, such as porches, garages, and crawl spaces. Contact
QuickNotes A lack of fleas or flea dirt should not override a diagnosis of flea allergy dermatitis if clinical suspicion is high.
FIGURE 5 Severe flea infestation.
Fleas on a dog before treatment.
When the dog was bathed, the water turned red from the extreme amount of flea dirt in the haircoat.
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TABLE 1
Flea Control Products Approved by the US Environmental Protection Agency and/or the US Food and Drug Administrationa Product (Manufacturer)
Active Flea Control Ingredientsb
Species and Minimum Age
Program/Sentinel (Novartis Animal Health)
Lufenuron
Dogs: 4 weeks
Frontline Plus (Merial)
Fipronil
Dogs: 8 weeks
S-Methoprene
Cats: 8 weeks
Cats: 6 weeks
Dosage/Administration
Mode of Action
Monthly oral; also injectable q6mo feline product
Inhibitor of chitin biosynthesis
Monthly spot-on
Fipronil: GABA-gated chloride channel antagonist S-methoprene: Juvenile hormone analogue (IGR)
Advantage (Bayer Animal Health)
Imidacloprid
Advantage Multi (Bayer Animal Health)
Imidacloprid
K9 Advantix (Bayer Animal Health)
Imidacloprid
Dogs: 7 weeks Cats: 8 weeks Dogs: 7 weeks
Monthly spot-on; can be used weekly
Nicotinic acetylcholine-receptor antagonist
Monthly spot-on
Nicotinic acetylcholine-receptor antagonist
Monthly spot-on
Nicotinic acetylcholine-receptor antagonist
Cats: 9 weeks (do not use canine product on cats) Dogs: 7 weeks
Permethrin
Permethrin: Sodium channel modulator Revolution (Pfizer Animal Health)
Selamectin
ProMeris for dogs (Fort Dodge Animal Health)
Metaflumizone
ProMeris for cats (Fort Dodge Animal Health)
Dogs: 8 weeks
Monthly spot-on
Chloride channel activator
Dogs: 8 weeks
Monthly spot-on
Voltage-dependent sodium channel blocker
Metaflumizone
Cats: 8 weeks
Monthly spot-on
Voltage-dependent sodium channel blocker
Comfortis (Eli Lilly)
Spinosad
Dogs: 14 weeks
Monthly chewable tablet
Nicotinic acetylcholine-receptor agonist (spinosyn)
Capstar (Novartis Animal Health)
Nitenpyram
Dogs: 4 weeks and 2+ lb
One tablet prn or daily/EOD
Nicotinic acetylcholine-receptor antagonist
Vectra 3D for Dogsc (Summit VetPharm)
Dinotefuran
Monthly spot-on
Dinotefuran: Nicotinic acetylcholinereceptor antagonist
Cats: 8 weeks
Cats: 4 weeks and 2+ lb Dogs: 7 weeks
Permethrin
Permethrin: Sodium channel modulator
Pyriproxyfen
Pyriproxyfen: Juvenile hormone analogue (IGR) Vectra for Cats & Kittens (Summit VetPharm)
Dinotefuran
Cats: 8 weeks
Monthly spot-on
Pyriproxyfen
Dinotefuran: Nicotinic acetylcholinereceptor antagonist Pyriproxyfen: Juvenile hormone analogue (IGR)
a
Adapted with permission from Mark Grossman and Carol Foil, Veterinary Information Network 2008. For the complete chart, visit www.vin.com/Link.plx?ID=37277. (EOD = every other day; prn = as needed)
b
Ingredients active against other parasites not listed.
c
This chart reflects the latest revision by VIN in September 2008. Please note that the following product has since become available: Vectra for Dogs and Puppies.
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FIGURE 6 Common reaction patterns associated with underlying flea allergic dermatitis in cats.
QuickNotes
Miliary dermatitis of the dorsum.
Self-induced alopecia of the ventral abdomen.
with feral cats, wildlife, and other unknown neighborhood animals should be prevented. Eliminating all secondary bacterial and Malassezia infections provides short-term relief of pruritus. Shampoo therapy and short courses of oral corticosteroids are good adjunctive
therapies. Antihistamines and essential fatty acids are not effective in flea-allergic patients. Finally, all animals in the household must be treated with ectoparasiticide therapy to prevent reestablishment of flea populations and perpetuation of disease.
Topical or systemic flea adulticide therapy may be the only management required to establish adequate control over flea infestations.
References 1. Scott DW, Miller WH, Griffin CE. Skin immune system and allergic skin disorders. In: Scott DW, Miller WH, Griffin CE, eds. Muller and Kirk’s Small Animal Dermatology. 6th ed. Philadelphia: WB Saunders; 2001:543-666. 2. Cole LK. Fleas and flea allergy dermatitis. 6th Proc World Congr Vet Dermatol 2008:119-125. 3. Dryden MW. Flea and tick control in the 21st century: challenges and opportunities. Vet Dermatol 2008;19(suppl 1):12. 4. Gross TL, Halliwell RE. Lesions of experimental flea bite hyper-
APPLIED DERMATOLOGY WEB EXCLUSIVE
sensitivity in the dog. Vet Pathol 1985;22:78-81. 5. Halliwell RE, Preston JF, Nesbitt JG. Aspects of the immunopathogenesis of flea allergy dermatitis in dogs. Vet Immunol Immunopathol 1987;17:483-494. 6. Kwocka KW. Fleas and related disease. Vet Clin North Am Small Anim Pract 1987;17:1235-1262. 7. Reedy LM, Miller WH. In: Reedy LM, Miller WH, eds. Allergic Skin Diseases of Dogs and Cats. Philadelphia: WB Saunders: 1989:171-187.
Otitis externa is another common, often frustrating, dermatologic condition. Visit CompendiumVet.com for one expert’s approach to canine otitis externa, “A Practical Approach to Diagnosing and Managing Ear Disease in Dogs,” by Paul Bloom, DVM, DACVD, DAVBP (Canine and Feline).
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SERIES EDITOR Craig E. Griffin, DVM, DACVD Animal Dermatology Clinic, San Diego, California
SERIES EDITOR Wayne S. Rosenkrantz, DVM, DACVD Animal Dermatology Clinic, Tustin, California
Diagnosing the Cause of Feline Pruritus ❯❯ Rudayna Ghubash, DVM, DACVD Animal Dermatology Clinic Marina del Rey, California
D
iagnosing the underlying cause of pruritus in cats can be considered. Food allergy can start at any age. be difficult because of the variations in clinical pre- Some breeds are predisposed to certain diseases, such as Persians (dermatophytosis) and sentation and numerous possible etiologies. Many own- Siamese (food allergies)1–3 (FIGURE 1). ers are not aware of how much their cats lick and groom themselves, making it difficult to assess the cat’s degree Environment of pruritus. The ability to interpret historical information, Outdoor cats have greater exposure to mosquitoes (FIGURE 2), parasites (e.g., fleas, Notoedres identify and understand the significance of clinical lesions, mites), and infectious agents (e.g., dermatand appropriately use diagnostic tests aids in the diagnosis ophytes, viruses). Knowing whether other animals or people are affected can indicate and management of feline pruritus. Historical Information Signalment
At a Glance Historical Information Page 352
Physical Examination Page 353
Common Diagnostic Differentials for Feline Pruritus Based on Lesion Location
Breed and age at onset of clinical signs provide clues to underlying etiologies. Pruritus in patients younger than 6 months is most commonly caused by parasites (Notoedres, Cheyletiella, and Otodectes spp), allergies (especially flea and food), and dermatophytosis. When pruritus begins in middle age, the differentials are the same, but allergic disease (food allergy, atopic dermatitis) becomes more probable. When pruritus begins in older animals with no history of skin disease, conditions such as epitheliotropic lymphoma, pemphigus foliaceus, Bowen’s disease, and paraneoplastic syndrome should also FIGURE 1
whether a contagious or zoonotic disease is present (e.g., dermatophytosis, cheyletiellosis, scabies). Psychogenic pruritus can be triggered by environmental changes, such as construction, remodeling, moving, or introduction of a new pet or person into the household. Siamese cats and Siamese crosses seem to be at risk for psychogenic disorders; however, psychogenic pruritus should not be assumed based on breed and is diagnosed only after all other causes of pruritus have been excluded.4
Concurrent and Previous Disease In cats with concurrent histories of pruritus and gastrointestinal disease (e.g., inflammatory bowel disease), food allergy should be FIGURE 2
Page 353
Diagnostic Tests Page 356
Facial pruritus in a food-allergic Siamese cat.
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Facial and pinnal involvement in a cat with mosquito bite hypersensitivity.
Compendium: Continuing Education for Veterinarians® | August 2009 | CompendiumVet.com
FIGURE 3
TABLE 1
Common Diagnostic Differentials for Feline Pruritus Based on Lesion Location Lesion Location Diagnostic Differentials
Pemphigus foliaceus with secondary bacterial pyoderma around the claw folds in a cat.
Ear canals
Food allergy Atopic dermatitis Notoedres infection Otodectes infection
Head and neck
Food allergy Atopic dermatitis Flea allergy Notoedres infection Mosquito bite hypersensitivity Otodectes infection Viral dermatoses Idiopathic facial dermatitis (“dirty face” syndrome) Drug reaction
diligently investigated. Atopic dermatitis should be strongly considered in pruritic animals with concurrent airway disease or asthma. Viral dermatoses should be suspected in cats with a history of upper airway viral disease and erosive facial lesions. A detailed drug history is critical because certain drugs and vaccines can trigger erythema multiforme and pemphigus foliaceus.5 Nasal planum
Mosquito bite hypersensitivity Viral dermatoses Squamous cell carcinoma Pemphigus foliaceus Cryptococcus infection
Dorsal cervical region
Flea allergy Atopic dermatitis Food allergy Injection-site reaction
Physical Examination Lesion Distribution Observing the distribution of lesions, especially in the initial stages of the underlying disease, can be helpful in narrowing the differential diagnosis. Flea allergy lesions are typically more severe in the lumbosacral, groin, and dorsocervical areas, whereas food allergy lesions are more common on the head. The clinical signs of atopic dermatitis vary but can mimic those of food and flea allergies. Cheyletiellosis lesions (scale, papules, crusts) tend to be distributed dorsally. Dermatophytosis can be localized to a specific site or can be generalized. Some cats may be asymptomatic carriers of Cheyletiella mites or dermatophytes. Pemphigus foliaceus usually targets the pinnae, bridge of the nose, claw folds (FIGURE 3), and perimammary areas but can also be generalized. TABLE 1 lists some common diagnostic differentials based on lesion distribution.
Lesion Appearance The ability to recognize and identify lesion types can provide valuable information in the evaluation of a pruritic cat. Excoriations, a nonspecific sign of self-trauma typically associated with pruritus, are characterized by their linear shape and are most prevalent on the head and neck. Erosions are superficial
QuickNotes Observing the distribution of pruritic lesions, especially in the initial stages of the underlying disease, can be very helpful in narrowing the differential diagnosis.
Dorsal and lumbar Flea allergy region Cheyletiellosis Claw folds
Pemphigus foliaceus Bowen’s disease
Ventral abdomen
Demodex gatoi infection Food allergy Atopic dermatitis Flea allergy Psychogenic pruritus
Generalized
Dermatophytosis Food allergy Atopic dermatitis Flea allergy Pemphigus foliaceus Epitheliotropic lymphoma Drug reaction Paraneoplastic syndrome Erythema multiforme
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FIGURE 4
Indolent ulcers in a cat with flea allergy dermatitis.
lesions that are similar to, but often wider than, excoriations. Erosions caused by scratching tend to be linear, whereas those associated with licking tend to be circular. Erosions are often associated with eosinophilic plaques. Ulcers can appear as focal, nonpruritic lesions on the upper lip, known as rodent or indolent ulcers (FIGURE 4). These lesions are one of the components in the eosinophilic granuloma complex (EGC) triad. EGC lesions are reaction patterns that typically indicate an underlying allergy or hypersensitivity reaction, not a specific disease.6 Other conditions that can create skin ulcers with variable degrees of pruritus include vasculitis, autoimmune diseases, drug reactions, and neoplasia. Papules are small (1 to 5 mm), raised lesions that are often associated with crusts and are the most common lesions seen in miliary dermatitis. Like EGC lesions, miliary dermatitis is a sign of an underlying disease. It can be associated with flea allergy dermatitis (most common), atopic dermatitis, food allergy, bacterial folliculitis, cheyletiellosis, dermatophytosis, pemphigus foliaceus, and drug reactions. Plaques appear as moderate to well-defined elevations of the skin with erythema. Eosinophilic plaques, one of the EGC variants, are most commonly associated with underlying allergic disease (FIGURE 5). Eosinophilic granulomas, the third component of the EGC complex, are firm, sometimes ulcerated, raised areas that are often found in the mouth or in a linear pattern on the body (FIGURE 6). Alopecia that is associated with pruritus usually presents as broken off, barbered hairs from overgrooming, scratching, or rubbing. Other lesions of pru-
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FIGURE 5
FIGURE 6
Eosinophilic plaques in a cat with atopic and flea allergy dermatitis.
ritus are often present with alopecia; however, in some cases, broken or barbered hair is the only clue that the cat is pruritic. Thin flakes of shed epidermis characterize scale, a nonspecific sign that is commonly seen in cheyletiellosis.
QuickNotes Various allergies look the same on histopathology, so biopsy is usually not used to diagnose allergy and is never used to differentiate allergic reactions.
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Diagnostic Tests Cytology/Skin Scrapings Used appropriately, dermatologic diagnostic tests can be powerful tools. Skin scrapings are one of the easiest and most important of these tests and should be conducted for all pruritic cats except those with seasonal signs. Some of the more common parasites that can be identified on skin scraping samples include Cheyletiella blakei, Otodectes cynotis, Lynxacarus radovskyi, Trombicula autumnalis, Felicola subrostratus, Notoedres cati, Demodex cati, and Demodex gatoi. Cytology can be used to assess samples for the presence of bacteria, inflammatory cells, fungal spores and hyphae, acantholytic cells, and neoplastic cells. Cytology should be conducted for any pruritic cat with dermatologic lesions other than noninflammatory alopecia. True pyoderma cases should demonstrate intracellular bacteria, usually within neutrophils and, sometimes, within eosinophils. Eosinophils are inflammatory cells that are common in a variety of disorders, but they are most commonly associated with ectoparasites, allergies, and some forms of EGC lesions. Fungal spores and hyphae are common in cases of dermatophytosis. A fun-
Oral eosinophilic granulomas in a cat with concurrent indolent ulcers.
gal culture should always be performed for speciation. Cytology can also be of value in identifying some forms of cutaneous neoplasia. On rare occasions, it can identify ectoparasites such as Cheyletiella, especially when adhesive tape is used to collect the sample. Acantholytic cells suggest pemphigus foliaceus, although they can also be seen in dermatophytosis. Using a fine-tooth comb on the entire haircoat for several minutes to collect dander and scale for microscopic examination is considered the most reliable method to find Cheyletiella mites in both symptomatic and asymptomatic animals.7
Fungal Culture Fungal culture using dermatophyte test medium (DTM) is considered the gold standard for identifying dermatophytes. Dermatophyte infections can present as pruritic infections with any lesion type. When cultured on DTM, dermatophytes produce an alkaline by-product that changes the color of the medium from yellow to red. However, saprophytic contaminants may also turn the medium red under certain conditions. Therefore, DTM should be inspected daily for color change, and any growth must be examined microscopically for evidence of microconidia and macroconidia. Suspected fungal growth can be lifted with clear adhesive tape, stained with lactophenol cotton blue, and examined microscopically. Speciation of the dermatophytes should always be performed to determine the source of infection and help prevent future reinfection.
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Hair Examination use this product daily to every other day for the Hair examination using a Wood lamp can be 4- to 6-week period.9 However, this method can helpful in suspected cases of dermatophytosis, be expensive and is difficult in cats that are hard but fluorescence is seen in only a small percent- to pill. Another option is to use a topical formuage of cases of Microsporum canis infection. lation of a flea control product that is approved Hairs that fluoresce should be plucked for cul- for cats every 2 weeks for a 4- to 6-week period. ture for definitive diagnosis.1 Direct microscopic Some of these products are labeled for more freexamination of the hair can also identify der- quent than monthly application. matophytosis. Hyphae and spores can often be seen when the condenser lens is turned down, Food Elimination Trials although culture should always be performed When evaluating a cat for food allergy derto confirm the diagnosis. In cases of alopecia matitis, a food elimination trial must be conin which the degree of pruritus is unknown, ducted, as serologic testing is unreliable and conducting trichograms to examine the tips of inaccurate in domestic animals.10 Food-allergic plucked hairs can help determine if the alopecia cats can have the same clinical signs as aniis caused by self-trauma, in which case, the hair mals with atopic dermatitis or flea allergy, but they commonly present with severe pruritus tips appear fractured and jagged. of the head and neck. The only way to diagSkin Biopsy nose food allergy is to feed an elimination diet Skin biopsy can be a powerful tool when used for an 8- to 12-week period. I prefer a trial appropriately. Many specific infectious, para- consisting of a home-cooked diet or a novel sitic, autoimmune, and neoplastic diseases can limited protein–based commercial diet. I typibe diagnosed using biopsy. Biopsy is indi- cally only use a hydrolyzed diet if the other cated for unusual lesions or clinical presen- diets are not eaten. Owners who are willing to tations or when a case does not respond to make a home-cooked diet can be directed to standard treatment. However, samples taken balanceit.com, where they can purchase recifrom lesions of allergic disease look the same pes and supplements, or should contact a veton histopathology, so biopsy is not usually erinary nutritionist for a consultation. Because used to diagnose allergies and is never used cats have unique nutritional needs, it is imperto differentiate them. ative that home-cooked diets be balanced, as feeding an unsupplemented diet for more than Flea Control Trials 4 weeks can lead to nutritional deficiencies.11 If all nonallergic differentials have been ruled At the end of the 8- to 12-week trial period, the out, a systematic approach to allergies must be cat is rechallenged with the original diet and pursued. Atopic dermatitis, flea allergy, and food observed for exacerbation of clinical signs. allergy can look identical. Flea allergy is the most common allergy in cats in flea-endemic Allergy Testing locations, and flea control trials should be con- The diagnosis of atopic dermatitis is made primarily on the history and physical findings after ducted to eliminate this differential.8 The goal of a flea control trial is to keep the ruling out all other pruritic diseases. Once atopic cat free of fleas, optimally for 4 to 6 weeks, and dermatitis is diagnosed, allergy testing is used evaluate the degree of subsequent resolution of to determine the specific allergens to which the pruritus. If the environmental flea burden is high, patient is sensitive, typically to start immunothe first step should be to suggest that the owner therapy. Intradermal skin testing, although conconsult an exterminator about treating the indoor sidered the gold standard of allergy testing, is and outdoor environments. The option of keeping difficult to conduct in cats. Feline skin is thinner the cat exclusively indoors during the flea control than canine skin, making intradermal injections trial should always be discussed, although it is harder to perform.12 Furthermore, the degree not always feasible. Because studies in cats have of reactivity at the injection sites is often flatfound oral nitenpyram to have 100% efficacy ter, producing false-negative results.12 In vitro against adult Ctenocephalides felis fleas within allergy tests are available and provide a reason3 hours, an ideal method of performing a flea able alternative to skin testing. Some specialists control trial, especially in outdoor animals, is to prefer this method of allergy testing in cats.
QuickNotes If a diagnosis of atopic dermatitis is made, allergy testing is used to determine the specific allergens to which the patient is sensitive, typically to start immunotherapy.
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Conclusion Pruritus in cats can be difficult and frustrating to treat. However, with a methodic approach and appropriate diagnostic tests, practitioners can significantly decrease the severity of pruritus and improve the quality of life for most cats without chronic use of long-term repository steroids.
TO LEARN MORE
For a more detailed discussion of flea allergy dermatitis, see the May 2009 Applied Dermatology article, “Overview of Flea Allergy Dermatitis,” on CompendiumVet.com.
References 1. Scott DW, Miller WH, Griffin CE. Fungal skin diseases. In: Scott DW, Miller WH, Griffin CE, eds. Muller & Kirk’s Small Animal Dermatology. 6th ed. Philadelphia: WB Saunders; 2001:336-442. 2. Carlotti DN, Remy I, Prost C. Food allergy in dogs and cats: a review and report of 43 cases. Vet Dermatol 1990;1:55. 3. Rosser EJ. Food allergy in the cat. A prospective study of 13 cats. In: Ihrke PJ, Mason IS, White SD, eds. Advances in Veterinary Dermatology II. New York: Pergamon Press; 1993:33. 4. Waisglass SE, Landsberg GM, Yager JA, Hall JA. Underlying medical conditions in cats with presumptive psychogenic alopecia. JAVMA 2006;228(11):1705-1709. 5. Scott DW, Miller WH, Griffin CE. Immune-mediated disorders. In: Scott DW, Miller WH, Griffin CE, eds. Muller & Kirk’s Small Animal Dermatology. 6th ed. Philadelphia: WB Saunders; 2001:667-779. 6. Scott DW, Miller WH, Griffin CE. Miscellaneous skin diseases. In: Scott DW, Miller WH, Griffin CE, eds. Muller & Kirk’s Small Animal Dermatology. 6th ed. Philadelphia: WB Saunders; 2001:1125-1183. 7. Moriello KA. Cheyletiellosis. In: Griffin CE, Kwochka KA, Mac-
Donald JM, eds. Current Veterinary Dermatology: The Science and Art of Therapy. St Louis: Mosby; 1993:90-95. 8. Scott DW, Miller WH, Griffin CE. Skin immune system and allergic skin diseases. In: Scott DW, Miller WH, Griffin CE, eds. Muller & Kirk’s Small Animal Dermatology. 6th ed. Philadelphia: WB Saunders; 2001:543-666. 9. Schenker R. Tinembart O, Humbert-Droz E, et al. Comparative speed of kill between nitenpyram, fipronil, imidacloprid, selamectin and cythioate against adult flea Ctenocephalides felis (Bouche) on cats and dogs. Vet Parasitol 2003;112:249-254. 10. Jeffers JG, Shanley KJ, Meyer EK. Diagnostic testing of dogs for food hypersensitivity. JAVMA 1991;198(2):245-250. 11. Mueller RS, Jackson H. Atopy and adverse food reaction. In: Foster AP, Foil CS, eds. BSAVA Manual of Small Animal Dermatology. 2nd ed. Gloucester, England: BSAVA; 2003:125-136. 12. Gilbert S. Feline pruritus therapy. In: Bonagura JD, Twedt DC, eds. Kirk’s Current Veterinary Therapy. 14th ed. St. Louis: Saunders Elsevier; 2009:405-410.
Research Recap Selected abstract from Veterinary Therapeutics
Effect of Intraarticular Injection of Autologous Adipose-Derived Mesenchymal Stem and Regenerative Cells on Clinical Signs of Chronic Osteoarthritis of the Elbow Joint in Dogs* Black LL, Gaynor J, Adams C, et al. Vet Ther 2008;9(3):192-200. Autologous adipose-derived mesenchymal stem cell (AD-MSC) therapy involves harvesting fat from the patient, isolating the stem and regenerative cells, and administering the cells back to the patient. Autologous AD-MSC therapy in veterinary regenerative medicine has been commercially available since 2003. Previously reported results from a blinded, controlled trial in dogs with chronic osteoarthritis of the coxofemoral (hip) joint demonstrated efficacy of a single intraarticular injection of autologous AD-MSC therapy. The primary objective of the current study was to evaluate the effectiveness of this therapy in
dogs with chronic osteoarthritis of the humeroradial (elbow) joints and to determine the duration of effect. Fourteen dogs were recruited. Veterinarians assessed each dog for lameness, pain on manipulation, From the range of motion, and functional disability Fall 2008 issue using a numeric rating scale at baseline and specified intervals up to 180 days after treatment. Statistically sigTO nificant improveLEARN ment in outcome MORE measures was For more Veterinary Therapeutics abstracts, visit the archives at demonstrated.
VeterinaryTherapeutics.com *This study was sponsored by Vet-Stem, Inc. Poway, California.
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SERIES EDITOR Craig E. Griffin, DVM, DACVD Animal Dermatology Clinic, San Diego, California
SERIES EDITOR Wayne S. Rosenkrantz, DVM, DACVD Animal Dermatology Clinic, Tustin, California
Otitis: Anatomy Every Practitioner Should Know ❯❯ Craig E. Griffin, DVM, DACVDa Animal Dermatology Clinic San Diego, California
C
hronic otitis externa is a difficult, frustrating problem. ear, which are enclosed by bones of the skull. Four etiologic components must be considered: primary Some giant-breed dogs have ear canals up to 11 cm long. More detailed descriptions of and secondary causes and perpetuating and predisposing the ear canal are given elsewhere.2 The tymfactors.1 Usually, these cases are complex and involve more panic membrane and medial end of the ear than one component. Perpetuating factors are changes in the canal are located ventral and caudal to, but anatomy and physiology of the ear that occur in response to almost on the same medial-to-lateral plane as, the eye (FIGURE 2). The most important anainflammation in the ear canal and the perpetuating factors tomic structures with regard to otitis are the already present. They are self-perpetuating, are not disease external ear canal, tympanic membrane, and specific, and include failure of self-cleaning mechanisms and middle ear. proliferative changes that create folds and stenosis of the External Ear lumen of the ear canal. Elimination of perpetuating factors The external ear is formed from two pieces of often requires aggressive cleaning of the ear and long-term cartilage and a bony canal that are covered by therapy. It is important to avoid damaging key structures skin. It ends medially at the thin tympanic membrane. The epithelium of the ear canal is conwhile aggressively cleaning the ear. Therefore, to adequately tinuous with the epithelium of the lateral aspect diagnose and manage perpetuating factors, veterinarians of the tympanic membrane so that the complete must recognize normal ear anatomy and physiology. FIGURE 1
Anatomy
At a Glance Anatomy Page 504
Physiology Page 510
aDr.
Griffin discloses that he has financial relationships with Efficas, Intervet/Schering-Plough Animal Health, Novartis Animal Health, Pfizer Animal Health, Sogeval, and Teva Animal Health.
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The ear (auris) is the vestibulocochlear organ. It is divided into three major portions: external, middle, and inner (FIGURE 1). The external ear consists of the pinna (auricle) and ear canal (external acoustic meatus). The shape of the pinna varies widely among breeds. For the purpose of describing anatomy, this article considers the erect-eared pinna (as seen on German shepherds) as it projects dorsally and laterally, with its concave surface facing rostrally. Numerous muscle attachments allow the pinna to move and thereby improve its function of helping collect sound waves. The sound waves enter the ear as they pass through the external orifice of the ear canal, located at the base of the pinna. The ear canal, which can be 5 to 10 cm in length, travels to the tympanic membrane and middle
Illustration showing a cross-section of the ear and its major components. With permission from Pfizer Atlas of Infection in Dogs and Cats. Wilmington, DE: The Gloyd Group, Inc; 2008.
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FIGURE 2
FIGURE 3 Straightening the pinna to perform the ear examination.a
QuickNotes
The auricular projection before the pinna is straightened.
Illustration of the relative locations of the ear canal and middle ear. With permission from Pfizer Atlas of Infection in Dogs and Cats. Wilmington, DE: The Gloyd Group, Inc; 2008.
ear canal is lined with epithelium. The larger portion of cartilage (the auricular cartilage) forms the pinna and most of the ear canal. The pinna rolls onto itself at the external orifice of the external ear canal (FIGURE 1). From the external orifice, the canal travels ventrally and slightly rostrally. This is the vertical canal. In the vertical canal, a projection of auricular cartilage emerges from the medial surface under the skin. This projection is unnamed, and its size varies between breeds and between individuals of the same breed. However, it is recognizable when examining the ear with an otoscope because it creates a “corner” around which the examiner must proceed to gain access to the canal. To prevent the auricular projection from blocking access to the ear canal lumen during otoscopic examination, pull the pinna dorsally and laterally. The tension created partially reduces the projection and straightens the ear canal lumen, allowing better access with the otoscope (FIGURE 3). At its ventral end, the ear canal bends
Aggressive cleaning is often needed to manage perpetuating factors, but care must be taken to avoid damaging key anatomic structures.
View of the ear canal after the pinna has been straightened. Note the auricular projection at top left. a
All photographs are copyright of Craig E. Griffin.
medially and continues until it reaches the tympanic membrane. This section, from the bend to the tympanic membrane, is the horizontal ear canal. The skin of the horizontal canal is surrounded by cartilage: the auricular cartilage surrounds the lateral portion, while the smaller anular cartilage, which extends between the auricular cartilage and the external portion of the bone of the external acoustic
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FIGURE 4
FIGURE 5
The anular cartilage (blue arrows) is overlapped by the distal end of the auricular cartilage (white arrows). Note how the anular cartilage overlaps or inserts within the bone of the external acoustic meatus (green arrows).
QuickNotes
FIGURE 6
When otitis is present, the skin covering the auricular projection is often inflamed. The pressure of an otoscope cone, especially the edge of the cone, may result in pain and resistance to examination.
A normal canine medial horizontal canal, ending at the tympanic membrane. Note the tuft of hairs (white arrow) adjacent to the ventral portion of the tympanic membrane. The blue arrow is on a dilated, distended pars flaccida with its prominent vasculature. Note the manubrium of the malleus (A) and the pars tensa (B).
VIDEO
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meatus, surrounds the medial portion (FIGURE 4). The anular cartilage and bony external acoustic meatus overlap so that dorsally, the cartilage lies inside the bone of the orifice, but ventrally, the bone is inside the cartilage. The size of the bony external acoustic meatus varies; in midsize dogs, it is about 1 cm long (FIGURE 5). Unlike the skin lining the cartilaginous canal, the skin lining the acoustic meatus lies on bone and therefore is not subject to
The bony external acoustic meatus of a dog skull. The blue arrowheads point to the ventral wall of the lateral and medial edges. The medial arrowhead is where the ventral portion of the pars tensa of the tympanic membrane would attach. The blue line indicates the portion of the horizontal canal where the skin would lie over bone rather than cartilage.
movement and massage. The change from cartilage to bone can be palpated with an angled Buck curette. The medial ring of the acoustic meatus is the location of the tympanic membrane. Often, larger primary hairs grow adjacent to the tympanic membrane (FIGURE 6), commonly on the ventral wall of the lumen. These hairs are a helpful landmark for locating the ventral tympanic membrane when an ear is diseased and the tympanic membrane is not readily apparent.
Tympanic Membrane The tympanic membrane consists of internal and external epithelial surfaces enclosing a thin layer of connective tissue that includes the manubrium of the malleus. It separates the external ear from the middle ear tympanic cavity. The tympanic membrane of the dog is made up of the pars flaccida and pars tensa (FIGURE 7). The pars flaccida, a small area of the dorsal to rostrodorsal aspect, is relatively flaccid and quite vascular. This structure may
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bulge out, can appear cystlike, and can hide the manubrium. Most of what is seen of the tympanic membrane when it is examined through an otoscope is the large pars tensa. A normal pars tensa is translucent, with striations that extend from the manubrium of the malleus out to the periphery. A whitish area with a line or ragged margin can sometimes be seen through the lower to middle section of the pars tensa. This whitish structure is best seen with a strong light source, such as a video otoscope. It represents a structure in the middle ear: the free edge of the septum bulla, which separates the tympanic cavity into dorsolateral and ventromedial parts (FIGURE 7). In dogs, the manubrium of the malleus is C shaped. It is located near the middle of the dorsal part of the pars tensa and points in a rostrocaudal direction. The concave aspect of the C faces rostrally, toward the nose. A perpendicular line from the top of the manubrium would point ventrally. Tension on the manubrium gives the tympanic membrane a mildly concave outer contour.2 The tympanic membrane is oriented at about a 30˚ to 45˚ angle from a dorsal-to-ventral plane. This creates a pocket or groove on the ventral floor of the horizontal canal, adjacent to the tympanic membrane, where small amounts of wax can accumulate. The tympanic membrane moves in response to pressure such as that generated by flushing and cleaning the ear canal. In cats, the tympanic membrane also consists of a pars tensa and pars flaccida, but to date, I have not observed a dilated pars flaccida in a cat. The manubrium of the malleus is relatively larger, is much straighter, and points more rostrally in cats than in dogs (FIGURE 8). In cats and dogs, when myringotomy is performed, the incision should be made in the caudal ventral quadrant of the tympanic membrane (i.e., ventral and caudal to the tip of the manubrium; FIGURE 9).
Middle Ear The middle ear consists of the tympanic cavity and the medial wall of the tympanic membrane; the auditory ossicles and their associated ligaments, muscles, and nerves; and the auditory (eustachian) tube. Normally, the only communication from the middle ear cavity to the outside environment is through the auditory tube, which opens into the nasopharynx and
FIGURE 7
Normal left tympanic membrane with the pars tensa and the vascular pars flaccida. Vessels extend down along the manubrium of the malleus. Note the shadow of the septum bulla (A) seen behind the pars tensa.
serves to equalize pressure on either side of the tympanic membrane. The tympanic cavity may be divided clinically into three parts: dorsal, middle, and ventral. The dorsal part, also called the epitympanic recess, is the smallest and contains the head of the malleus and its articulation with the incus. The middle part, or tympanic cavity proper, is adjacent to the tympanic membrane rostrally and laterally. The prominent structure on the caudal medial aspect of the tympanic cavity proper is the promontory of the petrosal part of the temporal bone (FIGURE 10). The barrel-shaped promontory is situated roughly opposite to the mid-dorsal aspect of the tympanic membrane. At the caudal end of the promontory is the cochlear window, which communicates with the cochlea of the bony labyrinth (FIGURE 11). This structure must be avoided when a myringotomy is performed and the middle ear is flushed. The caudal opening of the auditory tube lies in the rostral-medial part of the middle tympanic cavity. The middle portion of the tympanic cavity communicates freely with the ventral portion, contained in the egg-shaped tympanic bulla. The ventral portion is the largest portion of the tympanic cavity. A ridge of bone, the septum bulla, projects from the medial wall of the tympanic bulla into the cavity between its middle and ventral components. The septum bulla is readily seen just ventral and caudal to the promontory and cochlear window (FIGURE 12) and
QuickNotes In an abnormal ear, tympanic movement is helpful in identifying the tympanic membrane.
VIDEO
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FIGURE 8 Anatomy of the feline middle ear.
Needle A is inserted into the auditory tube. Needle B goes into the tympanic cavity up through a ventral bulla osteotomy opening.
QuickNotes
The needle (A) can be seen in the middle ear. Note that the manubrium (C) is relatively larger than that in the canine ear, and the long axis points rostroventrally, not ventrally as in dogs.
When possible, the middle ear anatomy of cats should be avoided when cleaning.
The needle (B) is inserted through the auditory tube. This view is through the external acoustic meatus.
often has many bony ossicles or “knobbed spicules” along the free edge in the tympanic cavity2 (FIGURE 13). This ridge makes passing catheters or tubes into the ventral bulla very difficult. When the middle ear is flushed, the goal is to direct fluid pressure below the septum bulla. The inner ring of the osseous external acoustic meatus is a helpful landmark because it is the attachment site of the tympanic membrane. If the ventral inner edge can be palpated with an ear loop, then the tympanic membrane is either ruptured or out of
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The needle is pointing from the dorsal portion of the ventral bulla into the ventral portion. Fluid that reaches the ventral portion is trapped by the septum. This ventral-to-dorsal view looks through a hole in the ventral bulla.
its normal anatomic position (FIGURE 14). Once the ventral medial edge of the osseous external acoustic meatus is reached, the cochlear window is a short distance (5 to 8 mm) medially. Care should be taken to stay caudal and ventral to the cochlear window. The middle ear in cats is very different from that in dogs in that the septum bullae is very large and nearly divides the ventral portion of the tympanic cavity into a small dorsolateral and a large ventromedial part—the pars tympanica and pars endotympanica, respectively. These
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FIGURE 9
FIGURE 10
A tomcat catheter in the left external ear canal, pointing to the optimal site for performing a myringotomy. The incision is made in the caudal ventral quadrant of the pars tensa of the tympanic membrane (blue lines). This site is caudal to the convex surface and below the tip of the manubrium.
View through the left external acoustic meatus of a dog skull. An orange feeding tube (A) enters the middle ear from the auditory tube. The septum bulla (B), promontory (P), and opening in the promontory to the cochlear window (C) can be seen.
FIGURE 11 Ventral to dorsal view through an opening in the ventral wall of the bulla of a dog skull. Note the metal rod (A) passing through the lateral margin of the bony external acoustic meatus (B). C indicates the medial edge of the bony external acoustic meatus. The tip of the metal rod (arrow) is through the cochlear window. This site must not be touched or subjected to direct pressure during procedures such as flushing the middle ear.
S indicates the septum bulla.
QuickNotes When the tympanic membrane is ruptured, ear medications and cleansers should be used cautiously and be nonototoxic.
The white lines indicate the lateral ventral edge and medial ventral edge of the bony external acoustic meatus. The distance between the lines varies from 7 to 15 mm and is narrower on the rostral side.
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FIGURE 12
FIGURE 13
Close-up view of the septum bulla showing the bony ossicles (arrows) on the free margin. FIGURE 15 View of the middle ear through the external acoustic meatus. P = promontory, S = septum bulla, C = cochlear window. FIGURE 14
Feline skull showing a needle going through the auditory tube into the tympanic cavity proper. The large, almost complete septum is seen ventral to the manubrium of the malleus.
two parts of the tympanic cavity communicate through a small opening in the caudal medial quadrant near the promontory and cochlear window (FIGURES 15 AND 16). Liquid medications instilled into the feline tympanic cavity are difďŹ cult to remove because they are trapped once they enter the ventromedial portion. View of the left middle ear from the ventral bulla, with an ear loop just over the medial ventral edge of the external acoustic meatus (E). If the tip of the ear loop drops over this edge, it has passed the normal attachment site of the ventral edge of the pars tensa on the tympanic ring. Note the promontory (P) and the cochlear window (C).
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Physiology The skin lining the ear canal is relatively smooth. Similar to the skin in most body regions, it has a thin epidermis and a dermis that contains adnexa (hair follicles and sebaceous and apocrine glands). The vertical canal has relatively more
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adnexa than the horizontal canal. To date, breed differences in the number of sebaceous glands have not been shown, although apocrine gland and hair follicle densities differ.3 The skin and adnexa constantly produce exfoliating corneocytes, intercellular material, and glandular secretions. This material forms cerumen (earwax), which is thought to play a protective role. IgA, IgG, and IgM have been identified in canine cerumen.4 IgG is the predominant immunoglobulin in both normal and inflamed ears. Its relative concentration increases significantly in the presence of disease. Cerumen also contains a wide variety of lipids, which may have some antimicrobial effects5; however, bacteria and yeast are present in normal ears. Cerumen is constantly being produced throughout the ear canal, and if it were to build up, blockage could result. However, there is a normal clearing mechanism: the movement of the epidermis. Epithelial migration, in which the surface of the skin lining the ear canal constantly moves from the tympanic membrane laterally to the external orifice of the ear canal (FIGURE 17),
FIGURE 16
Close-up photo of a feline middle ear viewed through the external acoustic meatus. Note the opening (O) in the septum that communicates with the larger ventromedial part of the tympanic cavity, the endotympanic part of the temporal bone. C = cochlear window, P = promontory.
has been shown in humans and guinea pigs.6 It seems likely that besides removing the cerumen, this process also facilitates the removal of sur-
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FIGURE 17 Illustrations depicting the migration of cerumen and surface epithelial cells from the deep ear canal to the external orifice.
This process must function for an ear canal to remain healthy. With permission from Pfizer Atlas of Infection in Dogs and Cats. Wilmington, DE: The Gloyd Group, Inc; 2008.
face microorganisms and even small particulate dog and cat ears at 1000× magnification,1 I debris trapped in the sticky cerumen. consider bacteria excessive when more than Cytologic studies of normal ear cerumen five cocci or one rod per 1000× (oil immerhave produced variable results in numbers of sion) field is found. Normal numbers of yeast bacteria and yeast but have found essentially are even more controversial, although I conno inflammatory cells.7,8 These studies evalu- sider more than three organisms in dogs or ated samples at 400× dry field magnification, more than one in cats per oil immersion field not by oil immersion (1000×), which is my pre- to be increased. Rarely, up to 20 organisms per ferred magnification. It has been stated that 1000× field can be normal for an individual dog 400× magnification is not sufficient to identify or cat. However, these numbers are irrelevant all bacteria.9 Based on a published, non–peer- once multiple inflammatory cells are present, reviewed evaluation of cerumen from normal as this finding is abnormal. References 1. Scott DW, Miller WH Jr, Griffin CE. Muller and Kirk’s Small Animal Dermatology. 6th ed. Philadelphia: WB Saunders; 2001. 2. Evans H. Miller’s Anatomy of the Dog. 3rd ed. Philadelphia: WB Saunders; 1993. 3. Stout-Graham M, Kainer RA, Whaler LR, Macy DW. Morphologic measurements of the external horizontal ear canal of dogs. Am J Vet Res 1990;51(7):990-994. 4. Huang HP, Little CJ, Fixter LM. Effects of fatty acids on the growth and composition of Malassezia pachydermatis and their relevance to canine otitis externa. Res Vet Sci 1993;55(1):119-123. 5. Huang HP, Fixter LM, Little CJ. Lipid content of cerumen from
normal dogs and otitic canine ears. Vet Rec 1994;134(15):380-381. 6. Johnson A, Hawke M. An ink impregnation study of the migratory skin in the external auditory canal of the guinea-pig. Acta Otolaryngol 1986;101(3-4):269-277. 7. Ginel PJ, Lucena R, Rodriguez JC, Ortega J. A semiquantitative cytological evaluation of normal and pathological samples from the external ear canal of dogs and cats. Vet Derm 2002;13(3):151-156. 8. Tater K, Scott DW, Miller WH Jr, Erb HN. The cytology of the external ear canal in the normal dog and cat. J Vet Med 2003;50:370-374. 9. Angus JC. Otic cytology in health and disease. Vet Clin North Am Small Anim Pract 2004;34(2):411-424.
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Successful Use of Probiotics in a Dog with Chronic Diarrhea Teresa A. Bessler, DVM Buffalo Veterinary Clinic Buffalo, Wyoming
Patient: Kodi, a 14-year-old American Eskimo dog History: When Kodi became my patient in August 2007, he had a 2-year history of kidney disease and was eating Purina Veterinary Diets® NF Kidney Function® canine formula to help manage his condition. He also had a long history of frequent bouts of watery diarrhea. Therapy Plan: Because of Kodi’s chronic kidney disease, I instructed the owners to continue feeding NF. I also prescribed 1 g of sucralfate twice daily for 5 days to treat a brief episode of anorexia and 250 mg of metronidazole twice daily for 5 days to resolve the diarrhea; metronidazole helped briefly, but the diarrhea returned. In October 2007, Kodi’s owners made an appointment to have him euthanized because of the chronic diarrhea. Kodi was having fecal accidents in the house, and the owners did not wish to pursue expensive diagnostics. I talked to them about Purina Veterinary Diets® FortiFlora® Canine Nutritional Supplement, and they agreed to try it. Kodi was given FortiFlora once daily, and Purina Veterinary Diets ® Gentle Snackers TM were allowed as treats. Outcome: Two weeks after adding FortiFlora to the diet, Kodi’s diarrhea had transformed into fairly firm stools. FortiFlora helped resolve the problem. At Kodi’s last evaluation, the chronic diarrhea hadn’t returned. This information has not been peer reviewed and does not necessarily reflect the opinions of, nor constitute or imply endorsement or recommendation by, the Publisher or Editorial Board. The Publisher is not responsible for any data, opinions, or statements provided herein.
Veterinarian’s Comments I have been recommending Purina Veterinary Diets® FortiFlora® as a nutritional supplement for the past 2 years. I find it to be very effective in cases of acute and chronic diarrhea and in patients on long-term antibiotic therapy. I estimate that I have used FortiFlora in at least 40 patients with a 90% success rate. I explain to owners that FortiFlora is a nutritional supplement that contains beneficial bacteria and promotes intestinal health. Owners appreciate that FortiFlora comes in premeasured packages and is simply sprinkled on top of the pet’s food. FortiFlora delivers good clinical results, and dogs and cats find it palatable; I have not had one owner tell me that his or her pet would not eat it. Kodi’s owners were very happy with the positive results obtained with FortiFlora. They told me the nutritional supplement had changed their lives and Kodi’s as well, and they wished they had known about FortiFlora sooner. Sponsored by