Lecture 4 - Bacterial Skin Diseases

Lecture 4 - Bacterial Skin Diseases
A. Resident microflora
Colonize normal skin and may be found in the superficial epidermis and hair follicles
of normal skin. These commensal microflora play an important role in inhibiting
colonization by pathogenic organisms.
B. Skin infection: Pathogenic bacteria are causing clinical signs in the host.
A. Pathogenic bacteria: Staphylococcus intermedius is most common
1. Dog
a. The primary skin pathogen is Staph. intermedius. In severe,
complicated, or deep pyodermas, other organisms may also be
causative (Pseudomonas, Proteus, etc.).
b. Staphylococcus aureus and Staphylococcus schleiferi
An increasing prevalence of Staph aureus and the emergence of a new
species (Staph schleiferi) has been noted in dogs. Both species are
pathogenic, have the ability to develop multidrug resistance, and are
of zoonotic concern.
2. Cat
Whereas bacterial skin infections are quite common in the dog, Staph
pyodermas are uncommon in the cat. The most common skin infection in the
cat is the bite wound abscess.
B. Classification of pyoderma
1. Primary pyoderma: skin infection that occurs in healthy skin with no apparent
cause. Uncommon.
2. Secondary pyoderma: skin infection that has an underlying cause or occurs in
diseased skin.
a. Most pyodermasare secondary in nature.
b. Underlying causes: include allergies (approximately 80% of allergic
dogs have a secondary pyoderma at time of diagnosis), mites,
dermatophytes, seborrhea, and endocrine disorders.
c. Diseased skin: trauma, moisture, immunocompromise, and altered
normal flora predispose.
3. Depth of infection: pyodermas are characterized as surface, superficial, or
deep (see later).
C. Diagnosis
1. History and physical exam
The diagnosis of pyoderma is made on exam based on clinical appearance of
skin lesions. However, a meticulous history and complete physical exam
is crucial in determining likely contributory causes (remember, most
pyodermas are secondary!).
2. Basic tests used in the evaluation of all patients with pyoderma
a. Thorough dermatologic exam: to evaluate for contributory causes.
b. Skin scrapings: to look for mites.
c. DTM culture: to evaluate for dermatophytes.
d. Cytology (Diff-Quik): needle aspirate (of pustule, papule, nodule), or
imprint of exudate.
To evaluate for inflammatory cells (neutrophils, eosinophils) and
microorganisms (bacteria, yeast, etc.). *Q: How can you differentiate
between colonization and infection? Infection is associated with
inflammatory cells and intracellular bacteria, colonization is not.
3. Tests pursued in deep, non-responsive, or recurrent pyodermas
Skin biopsy: invaluable test in refractory, non-responsive pyoderma or
i. Technique: obtain multiple skin biopsy samples (Baker biopsy
punch often utilized). Collect intact primary lesions (ex: papule,
vesicle) as well as samples with a border of normal:diseased skin.
ii. Purpose: to obtain histopathologic diagnosis and look for causative
b. Skin culture and sensitivity: to identify causative organism(s) and
sensitivity pattern
i. Biopsy: historically considered technique of choice (reduces
likelihood of harvesting contaminants). The superficial skin is
cleansed with an antiseptic and a punch biopsy is obtained and
placed in a sterile vial containing transport media.
ii. Skin swab: recent study (Evaluation of aerobic bacteriologic culture
of epidermal collarette specimens in dogs with superficial
pyoderma - JAVMA March 2005) indicates that swab technique was
a simple and reliable method for identification of S. intermedius in
c. Rule out contributory hypersensitivities *Q: How would you do this?
d. Rule out underlying metabolic disease: CBC, profile, UA.
e. Rule out underlying endocrine or immunologic disease: testing as
D. Treatment of skin infections
1. Address underlying cause: key to successful treatment
2. Antibacterial shampoos
a. Purpose
Removes tissue debris and aids in eliminating bacteria in the more
superficial layers of the skin (where antibiotic levels tend to be lower).
b. Frequency of shampoo application:
i. For active infections, provide shampoo therapy 2 - 3 times weekly.
ii. For ongoing management, provide shampoo therapy 1 - 2 times
Work up good lather and allow minimum of 10 - 15 minutes
contact time. Most effective if hair is clipped short and washed
c. Antibacterial shampoo options (see table)
i. Benzoyl peroxide
Most effective antibacterial shampoo. Also has keratolytic,
antipruritic, degreasing and follicular flushing action. Can be
irritating (drying) to the patient with inflamed or sensitive skin. Use
of humectant spray or rinse after shampoo may be helpful.
ii. Chlorhexidine
Also an effective antibacterial shampoo that is less irritating for the
patient with dry skin. Chlorhexidine is a good antiseptic (kills
microbes on tissues) as well as disinfectant (kills microbes on
inanimate objects). No degreasing activity, not keratolytic.
iii. Ethyl lactate
Similar to chlorhexidine in regards to efficacy. Antibacterial,
rehydrating, keratoplastic, and has mild follicular flushing activity.
iv. Other: sulfur containing shampoos (sulfur has both antibacterial
and antifungal activity).
d. Table of shampoos: adapted in part from: Practical Topical Therapy for
Skin Infections Proceedings - WVC 2004 Karin M. Beale, DVM, DACVD
Shampoo Name
Comments (K = keratolytic)
Benzoyl Peroxide 2.5%
Oxydex® DVM
Deep pyoderma, folliculitis, can
be drying, K
Benzoyl Peroxide 3%
Pyoben® Virbac
As above, slow release
Benzoyl Peroxide 2.5%,
Sulfur 2%
SulfOxydex® DVM
As above, also keratoplastic
Benzoyl Peroxide 2.5%
Micro Pearls
Benzoyl Plus®
As above, also contains
Benzoyl Peroxide 2.5%,
Sulfur 1 %
As above, also contains
humectant, Salicylic acid 1%
Acetic acid 2%, Boric
acid 2%,
Pyoderma, Malassezia, also in
wipes, spray
Chlorhexidine 2%
Chlorhexidine 4%
Maximum® DVM
Pyoderma, Malassezia
Chlorhexidine 2%, Sulfur Seba-Hex® EVSCO Pyoderma, Malassezia
Salicylic acid2%
Ethyl lactate10%
Etiderm® Virbac
Pyoderma, rehydrating,
Ketoconazole 1%,
Chlorhexidine 2%
KetoChlor® Virbac
Pyoderma, Dermatophytes,
Miconazole 2%,
Chlorhexidine 2%
Malaseb® DVM
Pyoderma, Dermatophytes,
3. Soaks and hydrotherapy (whirlpool bath)
a. Purpose
Helpful in the initial management of deep pyoderma to remove crusts
and decrease surface bacteria. Clip hair in affected area, and apply
soaks or whirlpools until drainage abates.
b. Agents: dilute solutions of chlorhexidine or povidone-iodine are good
4. Topical antibacterial lotions, gels, wipes, spray: for localized lesions (table
adapted from WVC 2004 Karin M. Beale DACVD)
1. Bactoderm
ointment, Pfizer
preferred topical
antibiotic for Staph
2. Malaseb wipes, Miconazole 2%, chlorhexidine 2% Pyoderma,
3. Resi-Chlor,
Chlorhexidine 2% lotion
Localized pyoderma,
4. Chlorhexiderm
Chlorhexidine 4% spray
Localized pyoderma,
5. Gentocin spray, Gentamycin, betamethasone
6. Tresaderm
Thiabendazole, dexamethasone,
neomycin (neomycin less
effective for pyoderma)
7. Oxydex gel,
5% Benzoyl Peroxide gel
8. Silver
Localized pyoderma with
sulfadiazine cream Pseudomonas spp.
9. Polymixin B,
Localized pyoderma,
contains steroid
Focal deep pyoderma,
acne, can be drying
Localized pyoderma with
Pseudomonas spp.
Inactivated by purulent exudates, Inactivated by purulent
poor penetration
exudates, poor
5. Oral antibiotics
a. Role
Oral antibiotics are necessary to reach effective antibiotic levels in the
skin in most pyodermas (as stratum corneum is a major barrier to
effective topical penetration).
b. Dose and duration of therapy
i. Use maximal therapeutic dose
Antibiotic levels in skin are often much less than that in blood.
Must insure complete surface (look at) as well as deep (palpate)
healing before discontinuing antibiotics.
ii. First-time pyoderma
Treat for minimum of 3 weeks (at least one week past clinical
iii. Complicated or deep pyoderma
Typically treated for minimum of 8 weeks (at least 2 weeks past
clinical cure). Early relapses (< 7 days) are likely due to
inadequate initial treatment. Later relapses (weeks to months) or
likely due to unresolved underlying cause.
c. Selection of appropriate antibiotics (see table)
i. First line antibiotics: used initially in the treatment of most
superficial pyodermas. These antibiotics are typically narrow
spectrum, preserve endogenous flora, and are effective against
Staph intermedius (B-lactamase producer).
ii. Second line antibiotics: used in recurrent, deep, or nonresponsive pyodermas. These antibiotics are often effective against
resistant Staphylococcus and have an extended spectrum (to
include gram negatives). Culture and sensitivity is best means by
which to determine antibiotic selection.
First line
Active ingredient
1. Keflex®
30 mg/kg PO BID
or 22 mg/kg PO
2. Cefa-Tabs®
30 mg/kg PO BID
or 22 mg/kg PO
30 mg/kg PO BID
4. Primor®
27.5 mg/kg BID for
one day, then SID
5. Others
Clindamycin, Erythromycin,
Second line
Active ingredient
1. Clavamox®
Amoxicillin/Clavulanic acid
14 - 22 mgs/kg PO
2. Baytril®
5 - 10 mgs/kg PO
3. Simplicef®
Cefpodoxime Proxetil
5 - 10 mg/kg PO
4. Zeniquin®
5.5 mgs/kg PO SID
5. Orbax®
2.5 - 7.5 mg/kg
**Important note: not all antibiotics noted above are approved for use in the
cat. Consult drug insert prior to use. Significant side effects (and precautions)
may be associated with use.**
6. Immunostimulation therapy
May be helpful in the treatment of idiopathic recurrent pyoderma (no
underlying causative factors identifiable). Staphage Lysate is a bacterialderived product given by injection (on a longterm basis - detailed protocol)
and may help boost CMI to resolve pyoderma. Controversial benefit.
A. Definition
Bacterial colonization or overgrowth is present on the skin surface - but the skin is
not infected.
B. Intertrigo (skinfold pyoderma)
1. Etiology
Occurs in breeds with excess skin folds and is due to irritation (skin rubbing
against skin). Bacterial multiplication is encouraged by moisture, obesity, and
secretions (urine, saliva).
2. Clinical signs
a. Skin lesions occur in regions of the body with excessive folds and are
characterized by local erythema, oozing, erosion, and odiferous
b. Predisposed sites include lower lip (Spaniel, St Bernard), facial folds
(brachycephalic breeds), vulvar fold (older obese female), tail fold
(Pug, etc.) or body folds (Shar Pei). *Q: What may be another
deleterious result of facial fold dermatitis?
3. Treatment: reduce obesity, antibacterial shampoos, topical antimicrobial
products (mupirocin, Malaseb wipes, benzoyl peroxide gels) and surgical
excision of excessive skin folds (if possible).
A. Overview
1. Definition: bacterial infection of the skin that involves the epidermis and/or
intact hair follicles.
2. Clinical lesions: can be variable
Lesions often consist of papular to pustular eruptions (centered around the
hair follicle), epidermal collarettes, and crusts. Many alternate clinical
presentations also occur (see below).
B. Impetigo (puppy pyoderma)
1. Clinical signs
Mild superficial pustular rash and crusts in hairless inguinal and axillary region
of young puppies (< 1 year). May be idiopathic or associated with dirty
environment, poor nutrition, or parasitism.
2. Treatment
Most cases are self-limiting and respond to topical antimicrobial shampoo
therapy, systemic antibiotics are rarely needed.
C. Bullous impetigo
1. Clinical signs
Superficial pyoderma with large flaccid pus-filled bullae often noted in
inguinal/axillary region. Occurs in adult dog and may be associated with
underlying disease, immunosuppression (HAC, diabetes mellitus, etc).
2. Treatment: antimicrobial shampoo therapy, systemic antibiotics, look for
D. Superficial folliculitis: most common form of canine pyoderma (rare in
1. Predisposing factors: most pyodermas are secondary.
Staph intermedius is the primary cutaneous pathogen (other possible bacteria
include E. coli , Proteus mirabilis, and Pseudomonas spp). Common
predisposing conditions include demodicosis and dermatophytosis.
2. Clinical signs: lesions are variable
a. Lesions
Bacterial folliculitis = infection confined to hair follicle. The classic
primary lesion is a tiny intact papule or pustule with a hair emanating
from the center Lesions are often concentrated on the ventrum and
b. Papulo-pustular rash
May note papules, pustules, crusts, epidermal collarettes, and
hyperpigmented or erythematous macules.
c. Moth-eaten alopecia
In other dogs, may note "surface bumps" covered by hair. Focal
"moth-eaten" alopecia occurs as these hairs fall out.
3. Diagnosis: pursue appropriate tests (see above) - must answer question: Why
is infection present?
4. Treatment
a. Address underlying cause.
b. Topical antibacterial (and sometimes anti-seborrheic) shampoo therapy
(see table above).
c. Oral antibiotics: institute therapy with a "first-line antibiotic." *Q:
What is the minimum length of therapy? *Q: How do you determine
when therapy is complete? Avoid concurrent use of glucocorticoids.
d. Recurrence of disease: If pyoderma is pruritic and recurrent, consider
underlying disease (*Q: Such as?). If pyoderma is recurrent and nonpruritic, consider other underlying diseases (*Q: Such as?)
E. Pyotraumatic folliculitis (hot spot)
1. Etiology
Peracute skin lesion caused by self-trauma that is triggered by a painful or
pruritic event.
2. Clinical signs: most common in large breed, heavy coated dogs in warm
humid climates.
a. Initial lesions (pyotraumatic dermatitis) are well demarcated, painful,
erythematous, moist, and have a yellowish center covered with a
proteinaceous exuduate. Surface colonization of bacteria is present.
b. Lesions rapidly progress to deeper involvement (pyotraumatic
folliculitis) heralded by satellite papules and bacterial invasion of hair
3. Treatment
a. Eliminate trigger, clip hair (may require sedation, lesions can be
painful), and remove exudate with antibacterial shampoo. Elizabethan
collar may be necessary.
b. Topical antibacterial ointment (such as mupirocin): acts as a wound
barrier and helps to address bacterial infection.
c. Systemic therapy: first-line oral antibiotics for folliculitis (see above)
and oral glucocorticoids at anti-inflammatory doses for 3 to 5 days
to alleviate associated inflammation and pruritis.
G. Juvenile cellulitis (juvenile pyoderma, puppy strangles)
1. Pathogenesis
This is a sterile granulomatous and pustular disease of puppies that closely
mimics superficial pyoderma. Cause unknown - may be heritable.
2. Clinical signs
Acute swelling of the face and submandibular LN's followed by papules,
pustules, oozing serum or pus, and crust formation. Systemic signs of illness
are usually present.
3. Diagnosis: biopsies reveal granulomas and cellulitis, skin cultures are usually
4. Treatment: immunosuppressive doses of glucocorticoids (most
important), and oral antibiotics (to address secondary bacterial infection).
A. Overview
1. Definition
Skin infection is deeper and often serious, extending further down into
the hair follicle, dermis or subcutis. May be associated with systemic signs of
illness. Less common than superficial pyoderma. Rare in cat.
2. Pathogenesis
Deep pyodermas do not occur spontaneously - they usually are a continuation
of superficial pyoderma associated with underlying disease.
3. Skin lesions
Several clinical syndromes exist, but characteristic lesions include red/purple
nodules, hemorrhagic bullae, ulcerative lesions, and draining purulent
fistulous tracts.
a. Furunculosis: rupture of an infected hair follicle with release of
keratin and bacteria in dermis, often associated with a
pyogranulomatous response.
b. Bacteria: Staph intermedius, and other potential invaders (Proteus
spp, Pseudomonas, E. coli).
c. Bacteremia and sepsis are potential systemic complications of deep
4. Treatment principles (applies to clinical syndrome's noted below)
a. Identify and treat underlying disease (see above)
b. Whirlpool soaks with antiseptic agents (where applicable)
c. Antibacterial shampoos (particularly those shampoos with follicular
d. Appropriate antibiotic therapy (second line antibiotic) for a minimum
of 8 - 10 weeks and at least two weeks beyond clinical cure.
e. Surgical excision of focal lesions, or debridement as indicated.
f. Biopsy and culture (aerobic, anaerobic and fungal) should be pursued
in all non-responsive cases.
B. Localized forms of deep pyoderma
1. Callus pyoderma: occurs when calluses become secondarily infected.
2. Nasal folliculitis and furunculosis (nasal pyoderma)
Painful, localized, deep infection of the nose found most often in German
Shepherds and other dolichocephalic breeds. May be associated with "rooting"
behavior. Uncommon.
3. Muzzle folliculitis and furunculosis (canine chin acne)
a. Initial sterile inflammatory folliculitis that may progress to a deep
bacterial furunculosis. Found most often in short-coated breeds.
b. Follow treatment principles noted above. Local benzoyl peroxide
shampoo and topical antibacterial therapy (such as mupirocin).
4. Acral lick furunculosis: infected lick granuloma
Initial lesions often incited by boredom or other underlying trigger. Infected
lesions are more likely to exhibit surface ulceration.
5. Pododermatitis (interdigital pyoderma)
a. Clinical signs
Painful, red, swollen feet with nodules and exudative draining fistulas.
Variable pruritis, lameness, and lymphadenopathy. Males of shortcoated breeds are predisposed.
b. Etiology: *Q: What other diseases may cause these signs? What if
only one foot is affected?
Bacterial infections are secondary - look for underlying cause (mites,
FB's, allergies, etc.). Many cases are idiopathic. *What additional
diagnostics should be pursued if only one foot is infected?
C. Generalized forms of deep pyoderma
1. Deep folliculitis, furunculosis, and cellulitis.
a. Clinical signs
Note folliculitis, nodules, crusts, and open deep purulent fistulas with
ulceration. Lesions may be found distributed over trunk, abdomen, and
pressure points.
b. Deep pyoderma of G. Shepherds
i. Clinical signs as above but occurs in middle-aged German shepherd.
Initial lesions frequently noted over rump and lumbosacral area.
ii. Pruritis, regional lymphadenopathy, pain, and fever may be
iii. Evaluate for underlying disease (particularly hypothyroidism,
allergies, etc.)
2. Anaerobic cellulitis
a. Deep suppurative infection within subcutaneous tissue planes often
initiated by trauma or FB's, and secondary inoculation of microbes.
Systemic illness, fever, crepitant cellulitis (gas-producing anaerobes),
tissue discoloration and malodor may be present.
b. Treatment: surgical debridement, antiseptic lavage and appropriate
3. Cat bite abscess (less common in dogs)
a. Etiology
i. Bite wound abscesses are most frequently noted in head or tail
region. The skin seals over puncture site trapping bacteria inside,
and abscess develops within 2 - 4 days (causative organisms are
usually anaerobes from oral microflora).
ii. Commmon inoculated oral microflora include Pasteurella multocida
(also B-hemolytic Strep., Bacterioides, and Actinomyces spp.).
b. Treatment
Surgical debridement, antiseptic lavage, and appropriate antibiotics
(penicillin, amoxicillin, cephalosporins for 1 - 2 weeks). *Q: How is
this disease prevented? *Q: What other disease(s) may be transmitted
by this behavior?
A. Overview
1. Clinical presentation
a. Single to multiple cutaneous nodules are noted on exam. Some
nodules may ulcerate and form fistulous tracts with draining exudate.
b. Lesions are often indistinguishable from that due to the common
bite wound abscess, sequestered foreign body, subcutaneous mycosis
(see lecture 3), or isolated neoplasm.
2. Diagnostic evaluation
a. Biopsy for histopathology and culture (aerobic, anaerobic, and
fungal) to establish definitive diagnosis. Utilize special stains (fungal,
mycobacterial) to ascertain causative etiology.
b. Patients undergoing treatment for presumptive bite wound abscess
should have biopsy/cultures performed if non-responsive to treatment.
3. Treatment
a. For single lesions, surgical excision may be curative.
b. For multiple lesions, specific antibiotic or chemotherapeutic protocols
are often necessary (based on biopsy, culture/sensitivity results).
B. Etiologic agents
1. Bacteria: may originate from the mouth (commensals) or soil (saprophytes).
Organisms are typically inoculated into cutaneous wounds or traumatized
skin. Causative agents include Actinomycosis and Actinobacillosis (oral
microflora), and Nocardia (soil saprophyte).
2. Mycobacterial granulomas: caused by acid-fast mycobacteria
a. True tuberculosis: rare disease in dogs and cats
Usually due to infection with M. bovis or M. tuberculosis (obligate
pathogens acquired by exposure to infected people, milk or meat).
True tuberculosis is usually associated with systemic signs of illness
(GI, respiratory disease) and treatment is not recommended due to
zoonotic concerns.
b. Feline leprosy (M. lepraemurium may be causative agent)
Mode of transmission is unknown - insects may serve as vectors.
c. Opportunist (atypical) mycobacterial infections
These are saprophytes (M. fortuitum, M chelonei, others) found in the
environment and likely introduced by wound contamination. Noted
more often in the cat with lesions typically in ventral inguinal area.
3. Idiopathic sterile granuloma/pyogranuloma
a. Etiology: suspected immune-mediated pathogenesis. Uncommon in
dogs and rare in cats
Lesions are characterized by firm, painless cutaneous nodules,
plaques, or papules that sometimes ulcerate and drain. Secondary
infection is uncommon.
b. Treatment: surgical excision (solitary lesions), immunosuppressive
doses of glucocorticoids (multiple lesions). Glucocorticoid therapy may
need to be continued long-term.
4. Panniculitis: uncommon in dogs and cats
Etiology: sterile inflammatory nodules of the subcutaneous fat - usually
Lesions may ulcerate and drain an oily, yellowish-brown to bloody discharge.
Multiple nodular form may be accompanied by fever and systemic signs.
a. Treatment
Surgical excision for solitary lesions and immunosuppressive doses of
glucocorticoids for animals with multiple nodular form of disease.
Anecdoctal reports suggest that oral cyclosporine (Atopica®) (in
combination with glucocorticoids) is beneficial in treatment.
Goals of Lecture 4 - Bacterial skin diseases
References (for all dermatology lectures): Muller & Kirk's Small Animal Dermatology
5th edition 1995. Kirk's Current Veterinary Therapy XII. Bonagura. W.B. Saunders
Co. 1996. WB Saunders Co. Selected excerpts from ACVIM 1995 and 1996
proceedings, and JAVMA, JIVM, and Compendium 1992-2006. Small Animal
Dermatology Secrets: Karen L. Campbell 2004. Skin Diseases of the Dog and Cat
Richard Harvey, Patrick McKeever 2003. Small Animal Dermatology A Color Atlas and
Therapeutic Guide Linda Medleau, Keith Hnilica 2001 and Small Animal Ear Diseases
An Illustrated Guide 2nd edition. Gotthelf 2005. Supplemental information also
provided courtesy of Dr. Danny Scott and Dr. Miller, Cornell University.
1. What is the difference between resident microflora and pathogenic microflora
on the skin?
2. What is the primary skin bacterial pathogen in the dog? How is the cat
different? (A.2.) What is meant by a primary pyoderma? Secondary
pyoderma? Which is more common? What underlying conditions predispose to
development of pyoderma? (2.b.)
3. Be familiar with how to treat the patient with a pyoderma (D.1.2.) What
shampoos are particularly effective? (c.i.ii.) When are oral antibiotics
indicated? What type should be used? For how long? (5.a. b.i.ii. iii. C. i.ii.).
What antibiotics are commonly used as first line agents? (Cephalosporins,
Tribrissen). Second line agents? (Fluoroquinolones, Clavamox, Simplicef)
4. Be able to define surface, superficial and deep pyoderma.
5. Very briefly, be able to recognize and treat the following given a clinical
description: patient with skin fold intertrigo, puppy pyoderma, hot spot
6. Be able to recognize and treat superficial folliculitis (know this disease) and
briefly, how treatment is different for juvenile cellulitis (strangles) (4.)
7. Be familiar with information in V.A. If given a clinical description, be
able to recognize and treat the following forms of deep pyoderma (basic
treatment principles as outlined in V.4.): callus pyoderma, muzzle folliculitis,
interdigital pyoderma, generalized deep pyoderma, and cellulitis.
8. What are the clinical signs of the cat bite abscess? Likely causative
organisms? Treatment recommendations?
9. What types of other nodular diseases may mimic the patient with a deep
pyoderma? (VI. 1.b., atypical bacteria, mycobacteria, and panniculitis). What
is the most effective diagnostic approach? (2.a.b.)