Bacterial pyoderma is more common in the dog than any other mammalian species.
Bacterial pyoderma is more common in the dog than any other mammalian species. Currently Staph virulence factors such as protein A, leukocidin, hemolysins, epidermolytic toxin have not been shown to be to play a role in canine pyoderma as opposed to humans w/Staph aureus infections. Studies have been unable to identify differences in toxin profiles were found between Staph from normal dogs and dogs with pyoderma. Because Staphylococcus intermedius is a normal commensal of the dog it appears that abnormal "host factors" are an important cause of pyoderma in dogs. These include hypersensitivities, endocrinopathies and cornification abnormalities.
Pyodermas can be classified based on the depth of the lesion(s). The different classifications are:
1. Surface pyoderma
2. Superficial bacterial folliculitis (SBF)
3. Deep pyoderma
Pyotraumatic dermatitis is diagnosed based on the appearance of the lesions (alopecia, crusts, erosions ± pain) w/a history of a peracute onset. Treatment for this lesion is sedation, clipping and scrubbing the lesion(s) gently w/a chlorhexidene based shampoo. This is followed by an injection of dexamethasone (2 mg/ml) – 2 mg/30# SQ and dispensing topical therapy using a moderately potent antibiotic/steroid cream (Panolog) bid for 5-10 days along w/continued (gentle) cleansing of the lesion. IDENTIFY and treat/eliminate (if possible) the underlying cause (flea allergy dermatitis (FAD), environmental allergen induced atopic dermatitis (atopy) or cutaneous adverse food reactions (CAFR). Please note that Golden Retrievers and Saint Bernards have a unique form of a pyotraumatic dermatitis involving the cheeks. This cheek "pyoderma" is NOT a surface pyoderma but rather a deep folliculitis and furunculosis and needs aggressive antibiotic therapy for 30 days along w/an e –collar to prevent self-trauma- NOT steroids!
Mucocutaneous pyoderma (the author feels a better name is "antibiotic responsive dermatitis" since bacteria are not seen histologically) is a crusting disease that may affect the lips, nasal planum (exclusively), the bridge of the nose, periocular region, genitals or anus. Clinically it is indistinguishable from DLE. There is no identifiable cause for this disease and the diagnosis is based on the signalment (adult dog, most commonly in German Shepard Dogs (or mixes)), clinical appearance and distribution of the lesions and most importantly response to antibiotic therapy. In the past it was differentiated from DLE based on histopathologic findings. DLE was diagnosed when a lichenoid lymphocytic to lympho-plasmocytic interface dermatitis with hydropic degeneration and/or individual necrotic keratinocyte involving the basal cell layer, pigmentary incontinence and a thickened basement membrane was present. Mucocutaneous pyoderma would be diagnosed histologically when a lichenoid plasmacytic to lymphoplasmocytic infiltration was present without an interface change and without basal cell damage. HOWEVER, this criteria has been called into question with a recent study that reported that histologically mucocutaneous pyoderma and DLE may be indistinguishable! In that study, dogs were separated, based on histologic findings, into 3 groups, ones with a lymphocytic lichenoid interface dermatitis with hydropic degeneration; ones with plasmacytic lichenoid dermatitis, and lastly ones with a mixture of the first 2 patterns- lymphoplasmacytic lichenoid, interface dermatitis with hydropic degeneration. The authors then evaluated whether the group responded to antibiotics or immunomodulating therapy. There was no statistical difference when histopathologic features were compared between the 2nd and 3rd groups! The author now believes that all cases of canine nasal dermatitis should have a 30 day course of cephalexin prior to immunomodulating therapy- in fact prior to biopsy a 3-4 week course of a cephalosporin is appropriate and may establish a diagnosis w/o needing to biopsy the lesion!
Impetigo is a NON-follicular surface pyoderma seen most commonly in puppies between 6 weeks and 4 months of age. This lesion is usually found as an incidental finding during a routine vaccination visit. An underlying cause is rarely identified but the puppy should be evaluated for intestinal parasites and the diet and environment of the puppy should be reviewed and changed if necessary. Diagnosis is based on signalment, clinical appearance and distribution of the lesions and response to topical ± systemic antimicrobial therapy. If systemic antibiotics are used they should used for 10-14 days passed clinical resolution of the lesions. Many times just an antimicrobial shampoo (containing chlorhexidene) ± a topical antimicrobial residual product (chlorhexidene containing spray or leave on conditioner or a Mupirocin containing ointment) for 10-14 days is sufficient.
Superficial bacterial infection of the hair follicle (folliculitis) (SBF) is the most common presentation for dogs w/a bacterial skin infection. Staphylococcus intermedius and, less commonly, Staphylococcus aureus have been the most commonly isolated pathogens in dogs w/SBF. Recently another Staphylococcus organism has been associated w/bacterial pyodermas. This staphylococcus - Staphylococcus schleiferi may be either coagulase positive (Staphylococcus schleiferi coagulans) or coagulase negative Staphylococcus schleiferi (schleiferi). Because of zoonotic potential and the identification of methicillin resistant strains it is important that laboratories identify coagulase negative Staphylococcus down to the species level (to ddx nonpathogenic S. epidermidis from pathogenic Staphylococcus schleiferi). In addition, when submitting cultures from the skin be sure that the laboratory will differentiate Staphylococcus intermedius from Staphylococcus schleiferi coagulans.
Dogs w/SBF may be non-pruritic or pruritic (from mild to intensely). Clinically SBF appears differently in different breeds of dogs. Most dogs will have multifocal areas of alopecia, follicular papules or pustules, epidermal collarettes, and serous crusts involving the trunk, abdomen and axillary areas. Short-coated breeds often present with a moth eaten appearance to the hair coat due to multiple superficial follicular papules. Clinically these dogs will appear similar to dogs w/urticaria. These may be the only lesions present. Cocker Spaniels have their own special presentation, vegetative plaques. These plaques are frequently mistaken for seborrheic plaques. Clinically and histologically they can be quite similar, so if plaques are found in a Cocker, the dog should be treated for a bacterial pyoderma before condemning the dog to "idiopathic seborrhea". The diagnosis of SBF is usually based on clinical signs—alopecia, papules, pustules, and epidermal collarettes. Differential diagnoses for lesions (follicular papules) that resemble SBF include demodicosis, Malassezia dermatitis and dermatophytosis. If non-follicular papules, add insect bites to the differential diagnosis list. If epidermal collarettes or pustules are present pemphigus foliaceus should be considered.
Primary lesions seen in deep bacterial pyoderma include nodules, hemorrhagic bullae, and draining tracts consisting of a serosanguineous to purulent exudate. Distribution of these lesions includes the bridge of the nose, chin, elbows, hocks and interdigital areas. In some dogs lesions may also include the lateral stifles or the trunk. Acral lick dermatitis is a subset of deep pyodermas usually affecting the carpus, metacarpus or metatarsal regions.
Any time a pyoderma is diagnosed in a dog it is essential that you approach the problem in a systematic manner but this is especially true for SBF and deep pyodermas. It is critical to remember that there is NO such thing as a primary bacterial pyoderma in the dog- you must always remember that it is "due to" something else. A dog presented for the first time w/a SBF may only need to have limited diagnostics performed while a recurrent or chronic case of SBF or a dog presented ANY time w/a deep bacterial pyoderma will need to have the underlying cause aggressively pursued. Causes of SBF (deep pyoderma causes are marked w/an *) include
1. Hypersensitivities (atopy; cutaneous adverse food reactions; FAD)
2. Endogenous (hyperadrenocorticism) or exogenous steroid exposure;
5. Follicular dysplasias (eg color dilution alopecia, Chinese crested dogs);
6. Cornification abnormalities (sebaceous adenitis, ichthyosis)
In approaching a dermatologic case, the first step is to review the signalment. Age and breed can help point you in the right directions.
The next step may be the most important one, obtaining a detailed history! This starts by getting a copy of the dog's medical record. If the dog has had previous skin or ear disease, getting a copy of the medical records may help tremendously in developing a differential diagnosis list. Questioning the owner can help pinpoint the primary cause of the pyoderma. Questions that should be asked include:
1. Distribution of lesions initially and currently.
2. When did these symptoms first occur?
3. Has the dog had previous ear or skin disease before and if so when did it occur and how was it treated?
4. Where does the dog live- indoor, outdoors, both?
5. Which, if any heartworm and flea preventative is being used and how is it used
6. Are there any other pets in the household? If so, what kind and are they symptomatic.
7. Are any of the humans in the household showing "new" skin problems? If so, what kind
8. Do they board the dog, take him to obedience school, training or to the groomers?
9. What does the dog eat?
10. Is the dog pruritic
11. Is today's clinical presentation the best, worse or average since the problem began?
12. How was the progression of the lesions? Gradual or sudden?
13. If the dog is pruritic was there a "rash" first or itching first? Or did they occur simultaneously?
After reviewing signalment and thoroughly questioning the owner, the next step is to do a complete physical exam.
After your examination you should have a list of differential diagnoses for the underlying cause of the SBF (or a deep pyoderma) in the patient. ALL dogs w/lesions consistent w/SBF or deep pyoderma need to have deep skin scrapings performed for to identify demodex mites if present. More recently a superficial demodectic mite has been identified in dogs- Demodex cornei. This short-bodied canine mite inhabits the surface layer of the skin as does the similar Demodex gatoi of cats. The biology of this new canine mite and its pathogenesis is poorly defined. It has been associated with a pruritic dermatitis. An impression smear of a lesion should be evaluated for infectious agents, inflammatory cells and acantholytic keratinocytes (found in pemphigus foliaceus pustules). Dermatophyte cultures should be considered depending on the signalment, distribution of the lesions and the extent of the lesions.
Culture and susceptibility testing should be performed on poorly responsive (NOT recurrent) SBF. If a deep pyoderma has exclusively rods on cytology, has been treated w/antibiotics recently or the dog is systemically ill then a culture and susceptibility test should be performed. If a c/s is submitted, the MIC (broth microdilution technique) method should be used to determine the susceptibility rather than the disc diffusion method (Kirby-Bauer). The disk-diffusion susceptibility test (DDST) is semiquantitative in that the drug concentration achieved in the agar surrounding the disc can be roughly correlated w/the concentration achieved in the patient's serum. It will only report the organism's susceptibility (susceptible, intermediate or resistant) based on an approximation of the effect of an antibiotic on bacterial growth on a solid medium. Tube dilution (MIC) is quantitative, not only reporting SIR but also the amount of drug necessary to inhibit microbial growth. This allows you to not only decide susceptible or resistant but also the proper dosage and frequency of administration of the antibiotic. Please be aware that a susceptible designation alone does not necessarily imply efficacy. The advantage of the MIC method is that not only does it indicates susceptibility, but it also implies the relative risk of emerging resistance and thus the need for a high dose.
Samples from a pustule or intact nodule should be used for culturing however, if an intact pustule is not available culturing an epidermal collarette has also been shown to be reliable for sampling a SBF while using a minitip culturette to sample deep into a draining tract or a macerated tissue sample are acceptable for deep pyodermas.
When interpreting susceptibility be aware that if the Staphylococcus is reported to be resistant to oxacillin then it will be resistant to ALL of the beta lactams.
Recently the effectiveness of clindamycin against MRSA has been questioned. This concern is related to 2 genes, the msrA and the erm that are responsible for S.aureus' resistance to different antibiotics. The msrA gene accounts for the resistance to beta lactams while the erm gene codes for clindamycin resistant. The erm gene may be constitutive which means that it will be present in the bacteria from the onset and the culture will report resistance to clindamycin. It may be inducible in which case the MRSA will be initially susceptible to clindamycin and therefore reported as such. When MRSA has the inducible gene there is a potential for resistance to clindamycin to develop WHILE on treatment. As the susceptibility pattern to clindamycin of MRSA isolates possessing msrA gene (truly susceptible to clindamycin) or the inducible erm gene (potentially resistant) are the same, it is important to distinguish between these phenotypes. This is accomplished by an additional culture technique called the Double-disc diffusion D-test. This test will detect the occurrence of the inducible erm gene. Since no commercial lab is currently doing this additional culture, resistance to erythromycin may be used as a clue to this inducible gene. This is because the msrA gene and the erm gene also encode Staphylococcus resistance to erythromycin. So if the Staphylococcus is resistant to erythromycin, there is a potential for the presence of the inducible erm gene. In a recent study, 97.3% of erythromycin-resistant isolates of MRSA were truly resistant to clindamycin despite only 25.5% demonstrating clindamycin resistance by routine laboratory testing. Therefore it would prudent to avoid clindamycin on all Staphylococcus infections that report resistance to erythromycin.
When treating a dog w/a SBF use an antibiotic for at least 21 days, or 14 days past YOUR clinical examination that the infection has resolved, whichever is LONGER. For dogs w/deep pyoderma, treat for at least 6 weeks or 21 days beyond clinical resolution, whichever is longer. In SBF don't use GC for cases where the pruritus is only at the lesions or when the pruritus is only mild at the nonlesional areas. If a dog w/a SBF has intense pruritus at nonlesional areas then a tapering 21 days course of prednisone may be dispensed. Using GC in the presence of a pruritic pyoderma makes interpretation of response to therapy impossible (was it the steroid or the antibiotic/antifungal therapy that resolved the pruritus?). It also makes it more difficult to resolve the infection. NEVER use GC in deep pyodermas!!
SUMMARY- if the dog has papules, pustules and/or epidermal collarettes then deep skin scrapings, skin cytology ± fungal culture should be performed. Antibiotics and shampoo therapy are prescribed as mentioned below. RECHECK the dog after 14-21 days of antibiotics to access response. Treat any identified underlying disease.
1. Antibiotics- Remember for SBF 21 days is the minimum and 6 weeks is the minimum treatment time for dogs w/deep pyoderma.
a. Appropriate antibiotics include: Cephalexin (10-15 mg/# bid-tid), cefpodoxime proxetil- Simplicef® (5-10 mg/kg sid), clindamycin- Antirobe® (5.0 – 11 mg/# bid), amoxicillin/clavulanic acid – Clavamox® (10 mg# bid), trimethoprim/sulfonamide- Tribrissen® (10-15 mg/# bid). Reasons NOT to use fluoroquinolones in SBF are:
I. Information from the CDC website- " that none of the fluoroquinolones are FDA-approved for treatment of MRSA infections. A major limitation of fluoroquinolones is that resistant mutants can be selected with relative ease, leading to relapse and treatment failure. MRSA strains are especially adept at developing fluoroquinolone resistance, and such resistance is already found among MRSA isolated from patients with CA-MRSA infections
II. Because the incidence of MRSA is associated w/fluoroquinolone
b. My initial antibiotic will be either cephalexin or Simplicef®
I. Since any beta lactam will also select for MRSA (but not as intensely) I am strongly considering using clindamycin as a first choice in superficial bacterial pyoderma rather than a beta lactam
II. If there is no response to the initial appropriate anti-Staph antibiotic, given at an appropriate dose and frequency, then culture and susceptibility testing should be performed. Pending results the author will dispense clindamycin 5-10 mg/# bid if it has not already been used.
2. Antimicrobial ± antifungal shampoo is helpful
If the dog was pruritic along w/the SBF and the pruritus and lesions resolve when you have only treated the secondary infections continue the antibiotic for 14 more days. In this case the SBF was the major cause of the CURRENT pruritus (was only symptomatic when the secondary infection was present – "threshold theory") and it was secondary to one of the following:
a. Seasonal atopy and the season has changed;
b. An endocrinopathy
If the dog was pruritic w/the SBF and the pruritus did NOT resolve w/antibiotics but the lesions did, then continue the antibiotic for 14 more days. Atopy, CAFR or ectoparasites need to be pursued as the underlying cause in this situation.
If the dog was pruritic w/the SBF and the pruritus and lesions did NOT resolve w/antibiotics, ectoparasiticidal therapy, fungal culture and bacterial culture and susceptibility testing should be performed (and/or biopsy). Pending results the author will dispense clindamycin 5-10 mg/# bid
If the dog was NOT pruritic in the face of the SBF then either the dog has seasonal atopy and the season has changed or the dog has an endocrinopathy. Rarely CAFR or nonseasonal atopy may present w/recurrent non-pruritic SBF. If the lesions resolve w/antibiotics then continue the antibiotics for 14 more days and continue to investigate the underlying cause. If the lesions DON'T resolve w/antibiotics then fungal culture and bacterial culture and susceptibility testing should be performed (and/or biopsy). Pending results the author will dispense clindamycin 5-10 mg/# bid.
Unfortunately there will be cases of recurrent SBF that have been properly worked up and managed. In recurrent cases with no definable cause the author will treat w/antibiotics for a minimum of 6 weeks and begin immunotherapy w/Staph Phage Lysate (SPL) (Delmont Labs, Swarthmore, PA, USA). However the following criteria need to be met to maximize the success of SPL
1. The disease responds to antibiotic and topical antimicrobial therapy ALONE (NO steroids have been used)
2. The dog should have a history of recurrent SBF that has been treated appropriately (14 days past clinical resolution – minimum of 21 days)
3. All underlying causes should be ruled out (i.e., demodicosis, flea allergy dermatitis, CAFR, hyperadrenocorticism (iatrogenic and spontaneous) and hypothyroidism).
If in spite of these therapies the SBF continues to recurrent the author will "admit defeat" and treat w/a long term, low dose antibiotic therapy. The risk w/this treatment is the possibility of developing a resistant infection, even though this has not been recognized in cases managed by the author in this manner.
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