Pruritic microbial skin disease Flashcards

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1
Q

Microbial infections causing pruritus and their significance

A
  • 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.
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2
Q

Pathogenesis of clinical disease

A
  • 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
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3
Q

Organisms involved in bacterial pyoderma

A
  • Coagulase-positive staphylococci
  • Coagulase-negative staphylococci (CoNS)
  • Non-staphylococci
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4
Q

Coagulase-positive staphylococci causing pyoderma (bacterium, species, primary reservoir)

A
  • 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
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5
Q

Coagulase-negative staphylococci (CoNS) causing pyoderma

A
  • 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
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6
Q

Non-staphylococci causing pyoderma

A
  • 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
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7
Q

Depth of infection

A
  • Surface pyoderma = bacteria proliferate on epidermal surface
  • Superficial pyoderma = bacteria invade epidermis
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8
Q

Examples of surface pyoderma

A
  • Intertrigo (skin fold infection)
  • Acute moist dermatitis, pyotraumatic dermatitis (‘hot spots’)
  • Bacterial overgrowth syndrome
  • Mucocutaneous pyoderma
  • +/- Malassezia in some surface infections
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9
Q

Examples of superficial pyoderma

A
  • Folliculitis
  • Impetigo
  • Exfoliative superficial pyoderma
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10
Q

Folliculitis

A
  • Follicular pustules
  • Most common form of pyoderma in dog
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11
Q

Impetigo

A
  • Interfollicular pustules
  • Common in: young dogs (3-5m), dogs suffering from immunosuppression (pustules may be large – ‘bullous impetigo - +/- pruritus)
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12
Q

Exfoliative superficial pyoderma

A
  • Infection dissects through layers of
    stratum corneum: due to exfoliative bacterial toxins
  • i.e. toxins produced split the surface off
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13
Q

Clinical signs of Canine intertrigo

A
  • 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
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14
Q

Clinical signs of acute moist dermatitis

A
  • 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
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15
Q

Clinical signs of bacterial overgrowth syndrome

A
  • 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
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16
Q

Clinical signs of mucocutaneous pyoderma

A
  • Affect lips/perioral skin, nasal planum, nares
  • Occasionally eyelids, vulva, prepuce, anus
  • Especially GSDs and crosses
  • Ddx autoimmune disease
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17
Q

Clinical signs of bacterial folliculitis

A
  • 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
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18
Q

Clinical signs of short-coat pyoderma

A
  • Papules on short coated dogs (‘Short coated pyoderma’) -> ‘bumps’ on skin
  • Ddx: urticarial ‘hives’
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19
Q

Clinical signs of superficial pyoderma

A
  • 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
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20
Q

Clinical signs of exfoliative superficial pyoderma (ESP)

A
  • 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
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21
Q

Clinical signs of impetigo

A
  • 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
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22
Q

Pyoderma in cats

A
  • uncommon (or under diagnosed?)
  • pyoderma is a ddx for any of the 4 feline cutaneous reaction patterns, and focal/multifocal alopecia
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23
Q

Most common presentations of pyoderma in cats

A
  • 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)
24
Q

Diagnosis of pyoderma

A

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

25
Q

Cytology for surface pyoderma

A
  • Bacterial overgrowth
  • Increased numbers of bacteria but no (or minimal) inflammatory cell response
26
Q

Cytology of superficial pyoderma

A
  • Degenerate neutrophils
  • Intracellular cocci/bacteria
  • Cocci/bacteria/rods
27
Q

When to do C&ST

A
  • 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)
28
Q

How to do cytology of primary lesions

A
  • 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
29
Q

How to do cytology of secondary lesions

A
  • Sample under crusts (if moist beneath) or under rim of collarette, using saline-moistened swab
30
Q

How to do cytology if no primary or secondary lesions are present

A
  • 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
31
Q

General tx & management principles

A
  • 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
32
Q

Treatment for acute moist dermatitis (pyotraumatic dermatitis)

A
  • 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
33
Q

Topical vs systemic antibiotics

A
  • 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
34
Q

Surface pyoderma tx

A
  • 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

35
Q

Superficial pyoderma tx

A

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

36
Q

If superficial pyoderma unresponsive to topical treatment (or topical treatment not feasible or deep pyoderma present)

A

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)

37
Q

Chlorhexidine

A
  • 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
38
Q

Other antibacterial agents

A

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?
39
Q

Meticillin-resistant staphylococcal pyoderma

A
  • 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

40
Q

Main risk factors for development of clinical MRS infections

A
  • 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)
41
Q

MRSP vs MRSA

A

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

42
Q

Diagnosis of MRS infections

A
  • 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)
43
Q

Tx of MRS infections: surface/superficial infections

A
  • Topical therapy alone – as per meticillin-sensitive infections
  • Avoid systemic antibiotics if at all possible (selects for more resistance)
44
Q

Tx of MRS infections: deep infections

A
  • 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
45
Q

Tx of MRS infections - general

A
  • 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??
46
Q

Malassezia dermatitis

A
  • 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
47
Q

Malassezia dermatitis: Pathogenesis

A

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
48
Q

Malassezia dermatitis: Zoonotic potential

A
  • Can transiently colonise man
  • but risk of infection low unless immunocompromised
49
Q

Malassezia Dermatitis: Clinical signs

A

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

50
Q

Malassezia Dermatitis: Signalment

A

Any breed/age/sex, though some breeds favoured, e.g.
- Dogs: Bassets, cockers, WHWT
- Cats: Devon Rex

51
Q

Malassezia Dermatitis: Cytology

A
  • 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
52
Q

Malassezia Dermatitis: Culture, skin biopsy

A
  • May identify organisms but not used routinely currently
53
Q

Malassezia Dermatitis: management

A
  • 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
54
Q

Malassezia Dermatitis: Prevention

A
  • establish and tx primary cause
  • often need regular tx if primary cause can’t be fully controlled
55
Q

Ddx with any alopecia, especially if patchy

A
  • Pyoderma