Pruritic microbial skin disease

• What microbial infections cause pruritus?

  Bacterial pyoderma (surface/superficial).

  Malassezia dermatitis

  Dermatophytosis - variably pruritic
• What is dysbiosis?

  Involves imbalance between types of organism in the micro biome.

  Occurs with surface microbial overgrowths.

  May develop with certain skin diseases:

  • Canine atopic dermatitis (CAD)
• What is the most common organism cause of pyoderma?

  S.pseudintermedius

  Most common cause in cats and dogs
• What is a surface pyoderma?

  Bacteria proliferate on epidermal surface, technically not an infection but an overgrowth.
• What are the clinical signs of surface pyoderma?

  Intertrigo (skin fold infection).

  Acute moist dermatitis, pyotraumatic dermatitis (hot spots)

  Bacterial overgrowth syndrome

  Mucocutaneous pyoderma

  +/- Malassezia in some surface infections.
• What are the clinical signs of folliculitis?

  Follicular pustules.

  Most common form of pyoderma in dog.
• What are the clinical signs of impetigo?

  Interfollicular pustules.

  Common in:

  • Young dogs (3-5 months).
  • Dogs suffering from immunosuppresion (pustules may be large - bullous impetigo +/- pruritus).
• What are the clinical signs of exfoliative superficial pyoderma?

  Infection dissects through layers of stratum corneum - duse to Exfoliative bacterial toxins. Manifests as scale coming off the skin.
• Canine intertrigo - skin fold infection

  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.
• Acute moist dermatitis (pyotraumatic dermatitis)


  Acute lesion caused by skin self-trauma.

  Triggered by any irritant (flea bite, classically), can get around the backends as they try to get to their anal glands.

  Very rapid development of bacterial overgrowth - can lead to pyotraumatic folliculitis if not addressed rapidly (stop pruritus, cleanse and dry skin).
• What is bacterial overgrowth syndrome?

  Bacterial multiplication with no/minimal on cytology.

  Often no highly pruritic.

  Usually involves staphylococci.

  Lesions may be greasy, malodorous, erythematous, alopecia leading to hyperpigmentation and lichenification.
• What is mucocutaneous pyoderma?

  Affect lips/perineal skin, nasal planum, nares.

  Occasionally eyelids, vulva, prepuce, anus.

  Especially GSDs and crosses.

  Differential diagnoses is autoimmune disease.
• What are the clinical signs of Exfoliative superficial pyoderma?

  Rapidly-expanding erythematous rings with peripheral peeling (epidermal collarettes) - may coalesce -> large epidural collarettes.

  Also central alopecia +/- hyperpigmentation.

  Often highly pruritic
• Bacterial pruritus in cats

  Bacterial pyodermas in cats are rare.

  Most common presentations:

  • Feline acne can sometimes be a superficial pyoderma.
  • Surface pyoderma superimposed on EGC lesions.
  • Folliculitis ->
  • Miliary dermatitis (small crusted papules)
  • Larger crusts.
  • Alopecia with minimal inflammation - d/d/ dermatophytosis, demodicosis
• When do you do culture and susceptibility testing?

  Superficial pyoderma unresponsive to initial empirical therapy.

  History of repeated antibiotic use.

  Previous isolation of a meticillin resistant Staphylococcus (MRS).

  Rods seen on cytology - unusual to see so need to know what the rods are.
• What is the cytology of surface pyoderma’s?

  Bacterial overgrowth.

  Increased numbers of bacteria but no inflammatory cell response.

  
• What is the cytology of a superficial pyoderma?

  Degenerate neutrophils, high numbers of cocci.

  
• What anti-pruritic agents are indicated for surface pyoderma?

  Drugs to control pruritus (including corticosteroids) indicated.
• What anti-pruritic agents are indicated for superficial pyoderma?

  Traditionally advised against concurrent use of any drug that may hamper the host’s immune response, especially corticosteroids.

  However, short course (e.g. 3-5 days) now be considered acceptable in cases where underlying inflammatory process (e.g. allergies) likely to be driving infection (e.g. pyoderma secondary to atopic flare).
• What anti-pruritic agents are indicated for deep pyoderma?

  Drugs that may hamper the host’s immune system (e.g. corticosteroids, oclacitinib) contraindicated. DO NOT GIVE!!
• What is the treatment for a surface pyoderma?

  Clip lesions (under sedation/GA if painful)

  Treat with topical antimicrobial - e.g. chlorhexidine, fusidic acid.

  Control pruritus - corticosteroids (however is sattelite lesions present, the infection may deeper (pyotraumatic folliculitis/furunculosis) in which case you would avoid corticosteroids).
• Addressing infection - topical vs systemic

  Surface pyoderma - always topical

  Superficial pyoderma:

  • Topical alone whenever possible
  • Add systemic first tier antimicrobial drugs if severe or extensive - accurate dosing, target the specific organism, use narrow-spectrum drugs where possible.
• What topical treatments are available for surface pyoderma’s?

  2-4% chlorhexidine or other antiseptics q1-3d.

  If not responsive to this or very severe:

  • Fusidic acid +/- glucocorticoid (cocci)
  • Silver sulphadiazine (if rods)
• What is the treatment for superficial pyoderma?

  Topical treatment ONLY is appropriate:

  Review after 2-3 weeks and continue until underlying cause controlled:

  • 2-4% chlorhexidine q1-3d.

  If non-responsive to topical antibiotic therapy.

  • Clindamycin
  • Trimethroprim sulphanomide
  • Cefalexin
  • Amoxicillin/clavulanate
• What is Chlorhexidine useful for?

  Active vs Staphs and Malassezia.

  Usually effective against meticillin-sensitive Staphs (MSS) and MRS.

  Cheaper than systemic antibiotics.
• Meticillin-resistant staphylococcal (MRS) pyoderma

  Have same virulence and lesions as meticillin-sensitive Staphs but wider Antimicrobial resistance (AMR) pattern (especially MRSP).

  Present in normal cutaneous microflora.

  Present in normal cutaneous microflora.

  Organisms can survive in environment, though susceptible to routine cleaning agents.

  Can be involved in any infections as per meticillin-sensitive Staphs.
• What is the treatment for MRS surface/superficial infection?

  Topical therapy alone - as per meticillin-sensitive infections.

  Avoid systemic antibiotics if at all possible (selects for more resistance).
• What is the treatment for MRS deep infections?

  Systemic antibiotics, using lowest EMA category drug shown to be effective (NB never amoxyclav, even if test indicates sensitivity).

  Plus topical therapies.
• What are the clinical signs of malassezia dermatitis?

  Signalment:

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

  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: ear, lips, muzzle, interdigital skin, flexor surfaces, ventral neck/body, axilla, medial limbs, perineum!

  +/- rancid malodour
• What are the diagnostic tests for malassezia dermatitis?

  Stained acetate tape strip

  Direct/indirect impression smear if moist/waxy.

  Peanut/snowman/footprint/Russian doll appearance - may be mixed with bacterial overgrowth.

  May be clustered/adherent to keratinocytes (especially cats), so need to examine wide area.

  No fixed number for significance - interpret in the light of clinical signs - final diagnosis depends on response (clinical + cytological) to treatment.

  
• What is the management and prevention for malassezia dermatitis?

  Management is to reduce the number of organisms.

  • Topical treatment very effective - often aimed at Malassezia AND bacterial pyoderma e.g. Micanazole/chlorhexidine shampoo.
  • Systemic treatment (Itraconazole/ketocanazole) if topical fails.

  Prevention - establish and treat the primary cause.

  • Often need regular treatment if primary cause can not be fully controlled.
• What are the triggers of allergic skin disease?

  Environmental allergens:

  • Environmental atopic dermatitis - dog
  • Feline atopic skin syndrome (FASS) - cat

  Foods:

  • Food-induced atopic dermatitis (‘food allergy’) - dog
  • Feline food allergy (FFA) - cat

  Ectoparasites:

  • Flea allergic dermatitis
  • Insect bite hypersensitivity
  • Mite hypersensitivity - especially Sarcoptes

  Contact allergens

  Micro-organisms e.g. Malassezia hypersensitivity

  Drugs
• What is canine atopic dermatitis (CAD)

  A common chronic, relapsing, pruritic and inflammatory skin syndrome with characteristic clinical features.

  Traditionally associated with IgE antibodies to environmental allergens
• What is the diagnostic criteria for CAD?


  Age at onset <3 years

  Living mostly indoors

  Glucocorticoid-responsive pruritus.

  Non-lesional pruritus (itch before the lesion manifests).

  Affected front feet and/or pinnae.

  Unaffected ear margins (sarcoptic mange create crusty ear margins).

  Unaffected dorsal/lumbar area.
• What is the signalment for canine atopic dermatitis?

  Breed disposition - varies with location, commonly:

  • Golden/Labrador retriever
  • WHWT/other terriers
  • English/French bulldog, Pug, Boxer, Lhasa Apso, GSD, Shar Pei
• What is the history of canine atopic dermatitis?

  Nearly always pruritic - very occasionally present as pyoderma that is 100% responsive to therapy.

  Scratch, lick, rub, scoot.

  Onset usually 6m-3y.

  May start seasonally -> year round.

  Most will respond to anti-inflammatory dose of corticosteroids.
• What are the clinical signs of canine atopic dermatitis?

  Affected areas commonly:

  • Face, ears (concave pinnae, ear canals).
  • Axillae, ventral abdomen, inguinum, perineum.
  • Carpi/tarsi, feet.

  Uncomplicated case:

  • Erythema
  • Self-induced alopecia, excoriations.
  • Primary popular eruption.

  With chronicity:

  • Lichenification, hyperpigmentation
• How does food-triggered atopic dermatitis present?

  Can develop at any age, but majority start less than 1 year.

  The sensitisation is not associated with diet change.

  The skin signs are clinically indistinguishable from environmental CAD.

  +/- Concurrent clinical signs:

  • GI signs
  • Urticaria/angiodema
  • Malassezia dermatitis
• What are the 4 cutaneous reactions patterns of the cat?

  Face, head, neck pruritus.

  Self-induced alopecia

  Miliary dermatitis

  Eosinophilic granuloma complex
• How do drug eruptions present dermatologically?

  Can manifest as almost any type of cutaneous lesion or reaction pattern.

  Should be remembered but are rare!

  Any of type I, II, III, IV hypersensitivity mechanisms can be involved.

  Antibiotics most frequently implicated - especially potentiated sulphonamides.