Pruritic microbial skin disease Flashcards
Microbial infections causing pruritus and their significance
- Bacterial pyoderma (surface/superficial)
- Malassezia dermatitis
- Dermatophytosis (variably pruritic)
- Both bacterial pyoderma and Malassezia dermatitis very common in dog. Less common in cats
- Very rarely a primary problem
- Nonetheless essential to identify and treat, as may be significant contributor to patient’s clinical signs.
Pathogenesis of clinical disease
- Normal skin inhabited by diverse microbial communities (bacteria and fungi)
- Resident flora can aid in exclusion of pathogens but some are opportunist pathogens
(e.g. certain Staphylococci, Malassezia spp) - These may cause disease if:
– Compromise of cutaneous defences, e.g. mechanical damage to skin, defects in skin barrier function, changes to innate/acquired immunity
– Increased microbial adherence (e.g. with canine atopic dermatitis (CAD)
– Changes to skin microclimate
– Changes to skin microbiome - Now recognising role of dysbiosis: involves imbalance between types of organism in the microbiome, occurs with surface microbial overgrowths
- May develop with certain skin diseases: e.g. canine atopic dermatitis (CAD) (decreased bacterial/fungal diversity and increased proportion of Staph/Malassezia)
- Microbial numbers increase if CAD inadequately controlled -> clinical lesions
Organisms involved in bacterial pyoderma
- Coagulase-positive staphylococci
- Coagulase-negative staphylococci (CoNS)
- Non-staphylococci
Coagulase-positive staphylococci causing pyoderma (bacterium, species, primary reservoir)
- S. pseudintermedius
– dog: most common cause
– cat: most common cause
– man: low pathogenicity
– primary reservoir = domestic species - S. schleiferi subsp coagulans
– dog: 2nd most common
– cat: rare
– man: rare
– primary reservoir = dogs - S. aureus
– dog: uncommon
– cat: uncommon
– man: common
– primary reservoir: man - S. hyicus
– dog: rare
– cat: rare
– man: -
– primary reservoir: pigs
Coagulase-negative staphylococci (CoNS) causing pyoderma
- Previously thought all to be non-pathogenic, but opinions changing, so important to speciate CoNS if cultured
- Discuss relevance with microbiologist, especially as frequently show MDR (multi-drug resistant) pattern
Non-staphylococci causing pyoderma
- e.g. G-ve bacteria, non-Staph G+ve cocci
- Rare in superficial pyoderma (so culture if rods on cytology)
- More likely in surface pyodermas: treated topically so culture less relevant
Depth of infection
- Surface pyoderma = bacteria proliferate on epidermal surface
- Superficial pyoderma = bacteria invade epidermis
Examples of surface pyoderma
- Intertrigo (skin fold infection)
- Acute moist dermatitis, pyotraumatic dermatitis (‘hot spots’)
- Bacterial overgrowth syndrome
- Mucocutaneous pyoderma
- +/- Malassezia in some surface infections
Examples of superficial pyoderma
- Folliculitis
- Impetigo
- Exfoliative superficial pyoderma
Folliculitis
- Follicular pustules
- Most common form of pyoderma in dog
Impetigo
- Interfollicular pustules
- Common in: young dogs (3-5m), dogs suffering from immunosuppression (pustules may be large – ‘bullous impetigo - +/- pruritus)
Exfoliative superficial pyoderma
- Infection dissects through layers of
stratum corneum: due to exfoliative bacterial toxins - i.e. toxins produced split the surface off
Clinical signs of Canine intertrigo
- Mixed microbial overgrowth (cocci, rods, Malassezia) +/- neutrophilic inflammation
- In moist warm environment of skin folds, e.g. Facial and tail folds, Vulval folds, Intertrigenous (i.e. skin-skin frictional) areas, e.g. of obese animals
- May be exacerbated by inflammatory primary disease (e.g. CAD)
- May develop into superficial or deep pyoderma
- E.g. sausage dog armpits
Clinical signs of acute moist dermatitis
- Acute lesion caused by skin self-trauma
- Triggered by any irritant (flea bite, classically)
- Very rapid development of bacterial overgrowth – can -> to pyotraumatic folliculitis if not addressed rapidly (stop pruritus, cleanse and dry skin)
- Hair loss, sticky exudate, painful
- Fine 1 minute -> scratch -> big lesion suddenly
Clinical signs of bacterial overgrowth syndrome
- Bacterial multiplication with no/minimal inflammation on cytology (?not a true pyoderma)
- Often highly pruritic
- Usually involves staphylococci
- Lesions may be greasy, malodorous, erythematous, alopecia -> hyperpigmentation, lichenification
- Subtle and often missed
Clinical signs of mucocutaneous pyoderma
- Affect lips/perioral skin, nasal planum, nares
- Occasionally eyelids, vulva, prepuce, anus
- Especially GSDs and crosses
- Ddx autoimmune disease
Clinical signs of bacterial folliculitis
- Variable clinical picture
- Papules -> pustules - primary lesions but short-lived -> often present as secondary lesions
– Crusts
– Small epidermal collarettes – peripheral scale +/- central post-inflammatory pigmentation
Clinical signs of short-coat pyoderma
- Papules on short coated dogs (‘Short coated pyoderma’) -> ‘bumps’ on skin
- Ddx: urticarial ‘hives’
Clinical signs of superficial pyoderma
- Obvious primary/secondary lesions sometimes not seen but infection results in loss of hair from follicle:
– multifocal patchy alopecia (+/- hyperpigmentation), e.g. in short-coat pyoderma - vague patchy thinning of hair in silky-coated breeds (e.g. Yorkshire terrier)
- thinning of undercoat in heavy-coated (e.g. Husky, Akita) or wire-haired breeds
- Concurrent corticosteroid use -> no visible inflammatory change with pyoderma, so may present only as alopecia
Clinical signs of exfoliative superficial pyoderma (ESP)
- Rapidly-expanding erythematous rings with peripheral peeling (epidermal collarettes) – may coalesce -> large collarettes
- Also central alopecia +/- hyperpigmentation
- Often highly pruritic
- NB no preceding pustule/papule
Clinical signs of impetigo
- Usually associated with immature immune system/ immunosuppression
– E.g. in puppies (‘puppy pyoderma’), HAC - ‘Bullous impetigo’
– Large flaccid pustules up to15mm diameter, often with erythematous rim
– May be non-pruritic
Pyoderma in cats
- uncommon (or under diagnosed?)
- pyoderma is a ddx for any of the 4 feline cutaneous reaction patterns, and focal/multifocal alopecia
Most common presentations of pyoderma in cats
- Feline acne
- Surface pyoderma superimposed on EGC lesions
- Folliculitis:
– Miliary dermatitis (small crusted papules)
– Larger crusts
– Alopecia with minimal inflammation, ddx dermatophytosis, demodicosis (D cati)
Diagnosis of pyoderma
Cytology
always
- impression smear (direct or indirect) or stained acetate tape strip
- Perform on papules/pustules/erosions, skin under crusts, under epidermal collarette rim
- NB Absence of surface bacteria does not rule out pyoderma – organisms may be within hair follicle
Culture and susceptibility testing occasionally
Cytology for surface pyoderma
- Bacterial overgrowth
- Increased numbers of bacteria but no (or minimal) inflammatory cell response
Cytology of superficial pyoderma
- Degenerate neutrophils
- Intracellular cocci/bacteria
- Cocci/bacteria/rods
When to do C&ST
- Superficial pyoderma unresponsive to initial empirical therapy
- History of repeated antibiotic use
- Previous isolation of a meticillin resistant Staphylococcus (MRS)
- Rods seen on cytology
- If deep pyoderma, draining sinus, nodular/granulomatous lesion present
- If suspect unusual organism (e.g. mycobacteria, actinomycetes)
How to do cytology of primary lesions
- best for cytology (if lesions present)
- Look for papules/pustule in groin axillae esp
- Burst pustule with sterile needle, or gently remove top of papule with edge of microscope slide/back of scalpel blade -> direct swab of exudate
How to do cytology of secondary lesions
- Sample under crusts (if moist beneath) or under rim of collarette, using saline-moistened swab
How to do cytology if no primary or secondary lesions are present
- Small punch tissue biopsy
- Gently blot surface with alcohol swab to remove contamination and allow to dry – do not prep in normal manner
- Submit in sterile glass tube +/- spot of sterile saline
General tx & management principles
- Approach to treatment of pyoderma changed since emergence of multi drug-resistant staphylococcci (MDRS), especially meticillin-resistant staphylococci (MRS)
- Address infection: immediate priority
- Use of antipruritic agents?
– Surface pyoderma: drugs to control pruritus (including corticosteroids) indicated
– Superficial pyoderma
traditionally advised against concurrent use of any drug that may hamper the host’s immune response, especially corticosteroids. But, short course (e.g. 3-5 days) now considered acceptable in cases where underlying inflammatory process likely to be driving infection (e.g. pyoderma secondary to atopic flare). - Deep pyoderma: drugs that may hamper host’s immune system (e.g. corticosteroids, oclacitinib) contraindicated
- Address underlying disease: essential for long term resolution of secondary infection
Treatment for acute moist dermatitis (pyotraumatic dermatitis)
- Clip lesions (under sedation/GA if painful)
- Treat with topical antimicrobial – e.g. chlorhexidine, fusidic acid*
- Control pruritus – corticosteroids* usually
- *(in ‘Isaderm’)
- BUT if satellite lesions present, infection may be deeper (pyotraumatic folliculitis/furunculosis) so avoid corticosteroids
Topical vs systemic antibiotics
- Surface pyoderma:
– always topical - Superficial pyoderma:
–Topical alone whenever possible
– Add systemic first tier antimicrobial drugs if severe or extensive
– NB accurate dosing, target the specific organism, use narrow-spectrum drugs where possible
Surface pyoderma tx
- Topical tx only
- 2-4% Chlorhexidine or other antiseptics q1-3d
If not responsive or very severe:
- Fusidic acid +/- glucocorticoid (cocci) = Isaderm
- Silver sulphadiazine (if rods, poor efficacy for gram negative bacteria
Superficial pyoderma tx
Topical tx only is appropriate, review after 2-3w and continue until underlying cause controlled
- 2-4% chlorhexidine q1-3d
If non-responsive to topical antibiotic therapy
- Clindamycin (1st choice as narrowest spec)
- TMPS (no oral product now licensed for dog, cat)
- Cefalexin
- Amoxiclav
Systemic antibiotics always in combination with topical antiseptics (q1-3d).
Treat for 2w then reassess.
If poor response investigate resistance (cytology, C&ST).
Use doses at upper end of range (get less resistance this way).
Always culture if there’s a history of MRSP/MRSA or prior antibiotic courses or if rods are seen on cytology
If superficial pyoderma unresponsive to topical treatment (or topical treatment not feasible or deep pyoderma present)
Dogs:
- Clindamycin (5.5-10mg/kg q12-24h)
- Amoxiclav (12.5-25mg/kg q12h)
- Cephalexin (15-25mg/kg q24h)
- TMPS (15-30mg/kg q12h)
– many doses off label and require informed consent
Cats:
- amoxiclav > clindamycin > cephalexin
Treat until 1 week beyond clinical cure for superficial pyoderma and 2 weeks beyond clinical cure for deep pyoderma (usually at least 3-4w)
Chlorhexidine
- The most proven antiseptic for dermatological use
- 2-4% chlorhexidine shampoo
- Active vs Staphs and Malassezia
- Usually effective against meticillin-sensitive Staphs (MSS) and MRS
- Cheaper than systemic antibiotics
- Hibiscrub: Chlorhexidine 4% surgical scrub, cheapest, but drying & low persistence
- Malaseb: Chlorhexidine 2%, miconazole 2%, most expensive, drying, good persistence, POM-V, efficacy well-proven
- Clorexyderm, etc: Chlorhexidine 3-4% + moisturisers, intermediate cost, good persistence, not licensed but widely accepted as effective
- Spot gel
- Foams/mousses
- Wipes/pads, e.g. CLX wipes: lower concentration of chlorhexidine but combined with TrizEDTA
-> potentiates activity of antibiotics/antiseptics by increasing membrane permeability of bacterial cell walls - Wipes: good for facial folds, especially near the eye
Other antibacterial agents
Many exist but efficacy poorer or unproven – consider if chlorhexidine not effective/appropriate
- Hypochlorous acid
- Medical honey
- Chloroxylenol
- Ethyl lactate
- Povidone-iodine
- Triclosan
- Natural host defence peptide products (antimicrobial peptides)
- Essential oils?
Meticillin-resistant staphylococcal pyoderma
- Meticillin not used clinically but used as marker for multi-drug resistance (MDR) in coagulase +ve Staphs
- Resistance, encoded on mecA gene.
MRS:
- Have same virulence and lesions as meticillin-sensitive staphs but much wider antimicrobial resistance (AMR) pattern (especially MRSP)
- Present in normal cutaneous microflora
- Organisms can survive in environment, though susceptible to routine cleaning agents
- Can be involved in any infection as per meticillin-sensitive Staphs
- MRS organisms not host-specific but have host preferences: organisms can be exchanged (in both directions) between pets and man -> source of opportunist infections
Main risk factors for development of clinical MRS infections
- Previous antimicrobial therapy
- Repeated visits to vet surgery
- Invasive procedures
- Suspect involvement if pyoderma seen in patient with history of risk factors or unresponsive to therapy (especially if antibiotics used)
MRSP vs MRSA
MRSP:
= meticillin-resistant Staphylococcus pseudintermedius
- Host preference: dogs
- Spread between pets: easy- direct and indirect contact (nosocomial infection)
- Transfer dog->man: rare
MRSA:
= meticillin-resistant Staphylococcus aureus
- Host preference: man (usual source of MRSA infection for dogs, cats)
- Spread between pets: slow
- Transfer dog->man: easy
Diagnosis of MRS infections
- Bacterial culture: request MRSA/MRSP screening – important that lab is capable of speciating organism
- Susceptibility pattern shows MDR, including all beta-lactams (NB amoxiclav may show false susceptibility)
Tx of MRS infections: surface/superficial infections
- Topical therapy alone – as per meticillin-sensitive infections
- Avoid systemic antibiotics if at all possible (selects for more resistance)
Tx of MRS infections: deep infections
- Systemic antibiotics, using lowest EMA Category drug shown to be effective (NB never amoxyclav, even if test indicates susceptibility) – seek specialist advice if no susceptibility to authorised drugs
- Plus topical therapies
Tx of MRS infections - general
- Strict hygiene measures in home and surgery are required, and owners need to be advised of zoonotic risk – advise they check with doctor as precaution
- Establish and address underlying cause
- Carriage (on skin/mucosae) of MRS frequently remains after lesion resolution
- May resolve naturally if further antibiotics avoided but may persist >1yr
- Is source of spread to other animals/man/environment
- So continue infection control until at least 1 carriage site is MRS-negative??
Malassezia dermatitis
- Malassezia is a commensal – carriage sites: ear canal, anal sacs, interdigital skin, mucocutaneous junctions.
- Predominant species on normal skin: M globosa, M restricta (highly lipid-dependent)
- But is opportunist pathogen -> Malassezia infection (common in dogs, uncommon in cats)
- On clinically-affected skin predominant species is M pachydermatis (less lipid-dependent than above strains), more pathogenic strains involved
Malassezia dermatitis: Pathogenesis
Host factors -> dysbiosis (surface overgrowth) via
- Anatomical features (skin folds, pendulous lips, hairy feet) -> warm lipid-rich environment
- Underlying disease (especially allergies, endocrinopathies, keratinisation disorders)
– Alter barrier function/lipids/humidity of skin
– Favour adhesion of organisms and ?predominance of more virulent strains
- Breed – e.g. Bassets + Devon Rex cats with high normal mucosal populations
- NB Use of corticosteroids/ciclosporin do not affect Malassezia populations
- Also Malassezia hypersensitivity may develop in atopic dogs – uncommon
Small number of organisms may -> large effect
Malassezia dermatitis: Zoonotic potential
- Can transiently colonise man
- but risk of infection low unless immunocompromised
Malassezia Dermatitis: Clinical signs
Pruritus varies:
- mild to severe (NB severe pruritus may be seen with minimal lesions)
- Initially erythema with greasy exudate, scale, crust -> lichenification, alopecia, hyperpigmentation
-Focal/multifocal/generalised - Common sites: ears, lips, muzzle, i/dig skin, flexor surfaces, ventral neck/body, axilla, medial limbs, perineum!
- +/- rancid malodour
- May cause waxy educate in claw fold and brown discolouration of claw
A common trigger for flares of allergic skin disease
Malassezia Dermatitis: Signalment
Any breed/age/sex, though some breeds favoured, e.g.
- Dogs: Bassets, cockers, WHWT
- Cats: Devon Rex
Malassezia Dermatitis: Cytology
- Stained acetate tape strip
- Direct/indirect impression smear if moist/wax
-Peanut/snowman/footprint/Russian doll appearance – may be mixed with bacterial overgrowth - May be clustered/adherent to keratinocytes (esp cats), so need to examine wide area
- No fixed number for significance – interpret in light of clinical signs - final diagnosis depends on response (clinical + cytological) to treatment
Malassezia Dermatitis: Culture, skin biopsy
- May identify organisms but not used routinely currently
Malassezia Dermatitis: management
- Reduce number of organisms
- Topical treatment very effective - often aimed at Malassezia AND bacterial pyoderma
– Miconazole/chlorhexidine shampoo
– 2-4% chlorhexidine shampoo/foam
– TrizEDTA/chlorhexidine wipes - Systemic treatment (Itraconazole / ketoconazole) if topical fails
Malassezia Dermatitis: Prevention
- establish and tx primary cause
- often need regular tx if primary cause can’t be fully controlled
Ddx with any alopecia, especially if patchy
- Pyoderma
