Infectious Skin Diseases/Demodicosis/Immune-mediated/Ear Flashcards
Folliculitis/Clinical signs/Differentials
Folliculitis = infection of hair follicle by bacteria, demodex mites or dermatophytes fungi Clinical signs = hair follicle damage and inflammation #1 = bacterial infection (superficial pyoderma) #2 = Demodicosis #3 = Dermatophytosis (less common in dogs than cats) **all three are clinically indistinguishable in dogs
Canine Pyoderma - Definition, how does it develop
Staphlococcus pseudintermedius (lives on healthy host – skin, hair follicles, coat and mucocutaneous sites) Any age, sex or breed is susceptible
Clinical pyoderma develops secondary to:
- cutaneous damage
- inflammatory skin disease
- immune compromise (endocrine, neoplasia)
- immunosuppressive drugs
Has tendency to reoccur if the underlying cause is not addressed
Clinical signs for surface/superficial pyoderma
Surface Pyoderma
Erethema, alopecia, lichenification, pruritis, odor
Moist exudates <friction, tears, saliva, urine
Seen as mixed infection with Malassezia pachydermatis
Locations: folds of the lip, face, vulva, tail, neck, leg, and interdigital areas
Superficial Pyoderma
Ventral abdomen, axillary, inguinal regions
Papule, pustule, crust, epidermal collarette
Alopecia on dorsum/flanks
-short haired breed = moth eaten
-looks like dermatophytosis
Pruritis
How do you diagnose pyoderma? When?
Cutaneous cytology
- time efficient, easy, cheap
- presence and type of infectious agent/inflammatory cells
- direct impression smear or acetate tape
- used to assess treatment status
- when no more organisms on cytology = successful therapy treatment
*rods may mean gram negative bacteria (assume Pseudomonas)
– may be resistant to abx so be sure to culture and do a sensitivity test to confirm
What causes dermatophytosis?
Develop secondary to some predisposing factor – increased skin moisture, Cutaneous damage, inflammatory skin disease, immune compromise (drugs, endocrinopathy, neoplasia)
Viral disease = important underlying disease (FIV, FeLV, FIP) → infection is 3x more prevalent in cats with FIP
Need a cell mediated immune response for recovery from infection
Dermatophytosis - clinical signs
Variable
Pruritis is mild to severe
On the face (pinnae, periocular, dorsal muzzle) – alopecia, erythema, scaling, crusts, papules, pustules, epidermal collarettes
- classic “round” lesions are rare
- multifocal or generalized
- ingestion of hair = constipation, weight loss, anorexia, vomiting (esp long haired)
On the face (dorsal muzzle) – alopecia, crusts, papules, pustules
- superficial pustule dermatophytosis
- hunting dogs
- Trichophyton spp
- no nasal platum involvement, no loss of cobblestone (more likely PF, DLE)
- acantholysis seen on histopath
Face and Distal limb – nodules
- nodular dermatophytosis
- single > multifocal
- usually in dogs
Trunk, tail base – nodules
- dermatophytic pseudomycetoma
- multifocal > singular
- usually in Persians
Nailbed – chronic nail fragility and deformity
- onychomycosis
- can affect 1 or more digits (all are affected with canine lupoid onychitis)
Dermatophytosis - diagnosis
Culture is gold standard:
- dermatophytes use protein first → producing alkaline metabolites which increase the pH of the medium and turn it red within 5-14d
- saprophytes use carbs first → no color change and consume protein later which will then produce the color change 10-14d
- Microsporum take 7-14d to grow
- Trichophyton take up to 21d
- discard after 21d if no growth
Dermatophytosis - treatment(oral/topical)/duration of treatment
TOPICAL: Lime sulfur Enilconazole Miconazole - all have consistent antifungal therapy in the treatment of dermatophytosis
Schedule:
2x weekly whole body application
- lime sulfur and enilconazole should NOT be rinsed
- miconazole has a contact time of 10 min
ORAL:
Treatment of choice
Itraconazole – azole
-ptyalism, vomiting, diarrhea, anorexia, lethargy
Terbinafine –allylamine
-vomiting
*Both inhibit the development of ergosterol in the fungal cell wall
DURATION OF TX:
- don’t rely on clinical appearance
- culture monitoring q2-4wks
- mycological cure = 2-3 consecutive negative cultures obtained bi-weekly and resolution of clinical signs
Malassezia Dermatiti - causes
Part of normal Cutaneous microflora – colonizes skin, external ear canal, anal sacs, rectum, vagina
Dermatitis develops secondary to predisposing factor:
- Cutaneous damage
- inflammatory skin disease
- immune compromise
- immunosuppressive drugs
- abx treatment
*tendency to reoccur if underlying issue is not dealt with
Malassezia Dermatiti - clinical signs
Pruritis – moderate to severe
Odor
Dogs: alopecia, erythema, greasy brown macules, lichenification
-ventral neck, medial thigh, axillae, inguinae, perianal, interdigital space, lip folds, ear pinnae
-paronychia common with dark brown nailbed discharge
Cats: alopecia, erythema, crusting/greasy adherent scales
-face, ventral neck, abdomen, chin, ear pinnae, interdigital space, nailbed
Malassezia Dermatiti - treatment
TOPICAL:
Topical antifungal therapy is treatment of choice
Miconazole
Chlorhexidine
-both require 10 min of contact time
Shampoo 2x weekly until clinical improvement, then reduce to every 10-14d for maintenance
ORAL: 7-10d Needed in severe generalized cases Ketoconazole – azole -vomiting, diarrhea, anorexia, lethargy *More likely to cause living toxicity compare to itraconazole Itraconazole – azole -ptyalism, vomiting, diarrhea, anorexia, lethargy Terbinafine –allylamine -vomiting
Canine Demidecosis - Cause/Advice to breeders
Predisposing factors:
- young dogs → malnutrition, debilitation
- adult dogs → immunosuppressive drugs (glucocorticosteroids, azathioprine, chemo), underlying diseases (hyperadrenocorticism, hypothyroidism, neoplasia)
Advice to Breeders – should demodicosis dogs be bred?
- all dogs should be eliminated from breeding pool (no clear differentiation between generalized and localized demodicosis)
- specifically treat the dog for demodicosis before breeding
- 1-2 localized areas – can use shampoo instead of miticidal therapy
- if disease progresses to point where miticidal therapy is needed – neuter animal!
- stress of Sx may promote disease progression
Canine Demodicosis - Prognosis
- good – majority of cases reach long term remission
- some with incurable or poorly controlled infection – may never be cured and may need long-term therapy (monthly rises or weekly ivermectin)
- a relapse within the first 1-2 yrs after remission occurs in some dogs → most are cured with a bout of the same treatment used the first time, or another therapy
- watch dog closely for reoccurrence for the first 12 mo after treatment has been discontinued
Canine Demodicosis - Clinical Signs
Alopecia, scaling, follicular casts, papules, comedones
Erythema, crusts, hyperpigmentation, lichenification, nodules
Lesions begin on face (periocular)
And thoracic limbs and may progress to other places (trunk)
D. canis – non=pruritic initially
→Secondary bacterial infection leads to pruritis (seen in generalized cases)
→Bilateral ceruminous otitis externa
→May only be localized to ears (otodemodicosis)
→Pedal demodicosis associated with interdigital swelling (pododemodicosis) – larger dogs extremely painful and lame
D. cornei – often pruritic
Severe Demodicosis:
-follicular pustules, furunculosis with crusts, exudation, ulceration, draining tracts, pain, swelling
*Systemic signs only seen with severe generalized cases (fever, lethargy, lymphadenopathy)
Canine Demodicosis - Treatment & treatment duration
LOCALIZED:
- resolves spontaneously within 1-2mo
- simple monitoring for further progression
- topical antiseptic shampoos if owner wants to treat (benzol peroxide of chlorhexidine
-DON’T use any topical glucocorticosteroid treatment – could favor disease generalization
- DO NOT USE MITICIDAL THERAPY!
→potential side effects that are risky to patients that may cure on their own
→enables us to ID dogs that develop generalized demodicosis and eliminate them from breeding (genetic basis)
Amitraz Dip Side Effects: - toxicity attributable to alpha 2 adrenergic activity → sedation → lethargy → bradycardia → decreased body temp → hyperglycemia → ataxia → polyphagia, polydipsia → vomiting, diarrhea *Don’t use this dip and macrocyclic lactones
General Guidelines for Treatment Duration
- don’t rely on clinical appearance as end result
- clinically normal dogs may still be infected
- multiple negative skin scrapings and resolution of clinical signs = therapeutic end point
- repeatedly scrape 3-5 of the worse infected areas and any new lesions MONTHLY until all areas are negative
- continue 1 mo past the second negative scraping – just to be sure
- if dog responds slowly to treatment – extend the therapy even further
Macrocyclic Lactones
Ivermectin, abamectin, doramectin, eprinomectin, selamectin, milbemycin, moxidectin
Macrocyclic Lactones - side effects
Side Effects – mostly seen in collies (70%)
Lacking PGP or being given a drug that inhibits it → greater oral bioavailability and accumulate higher substrates n the brain
ML and ivermectin in particular can cause severe neurotoxicosis → lethargy, muscle tremors, mydriasis, seizures, coma, death, blindness
REMEMBER it is off-label and side effects may occur
Have an owner sign a consent form outlining all this
Macrocyclic Lactones - side effect signs
- Mydriasis (dilation) = early sign of neurotoxicity
- Ptyalism (hypersalivation)
- Lethargy
- Ataxia
- Muscle tremors
- Edematous wheals
- Discontinue use if any of these signs appear
Pemphigus foliaceus - Clinical signs (dogs vs cats)
Primary lesions are transient (Large confluent pustules) – rupture easily
Secondary lesions (crusting) – seen more often
-bilateral and symmetrical crusting
Start on face – dorsal muzzle, nasal platum, periocular area, ear pinnae
Predilection of lesions for footpads (seen in 1/3 of the patients – some this is the only place it is found)
Mucosal lesions are rare
Total body involvement can occur
Waxing and waning course
Systemic lesions only seen in dogs with widespread erosive lesions (anorexia, lethargy, fever, weight loss)
CATS: Sterile paronychia (inflammation of nailbed) with thick caseous discharge in ungual folds of claws and common involvement of the nipples
Pemphigus foliaceus -Diagnosis
Must demonstrate acantholytic keratinocytes by impression smear of intact pustules
- usually clustered together with nondegenerative neutrophils and rare eosinophils commonly seen
- large free floating rounded keratinocytes with central nucleus, stained cytoplasm (5x the size of neutrophils) → can tell they are from a deeper layer b/c they still have their organelles
NOTE: will NOT see intra/extracellular bacteria with degenerative neutrophils
No pustules? Collect sample from exudate under a recent crust
Pemphigus foliaceus - Treatment
Oral therapy – suppression of immune system with glucocorticosteroids (GC) → prednisone (dog) or prednisolone (cats)
→if lesions decrease in extent and severity – reduce dose/administration frequency
GOAL: alternate day therapy
In many cases GC are incapable of stopping or slowing lesions
May need the addition of cytotoxic drugs – Azathioprine (dog) (causes neutropenia and thrombocytopenia in cats – lower activity of thiopurine methyltransferase; which metabolizes the drug - DON’T USE!) or chlorambucil (cat)
Pemphigus foliaceus - Adjuvant cytotoxic drugs
Adjuvant Cytotoxic Drugs:
- used to reduce overall GC used in case you can’t get the concentration down to safe long-term levels
- used in combo with GC in more refractory case
- can use as sole therapy
→azathioprine (dogs)
- 4-8 wk lag phase – slow onset to see effects
- mylosuppression, increased risk of infection, diarrhea (severe, hemorrhagic), vomiting, pancreatitis, hepatotoxicity
- monitor via CBC q2-3wks for first 3mo then q3mo
- serum biochem q2-3mo until remission
- q6mo for CBC and biochem once remission
→chlorambucil (cats and small dogs)
- 3-6wk lag phase
- mylosuppression, increased risk of infection, vomiting, diarrhea, anorexia
- monitor same as azathioprine
Discoid Lupus Erythematosus - Clinical Signs
Nasal platum and dorsal muzzle
Acute signs = erythema and depigmentation – replaced by erosions, crusting and ulcers
Deep nasal ulcers can cause hemorrhage and pain
Lesions heal with atrophic scars (lose cobblestone appearance)
Other body parts less commonly affected (periocular area, ear pinnae, mucocutaneous junction, footpads)
Lesions start/more severe in summer – sunlight, UV exposure
No systemic disease (otherwise would be called systemic lupus erythematosus → polyarthritis, anemia, glomerulonephritis)
Canine Post Rabies Vaccination Panniculitis - General
Idiosyncratic immunologic reaction to rabies Ag
Common
Seen in toy-breed dogs
Canine Post Rabies Vaccination Panniculitis - Clinical Signs
Localized circular area of alopecia, erythema and mild scaling
2-10cm around/below vaccination site (lateral thigh, shoulder, dorsum)
Plaque
Hypo/hyperpigmentation
Temporal association with rabies vaccination
Develops within 2-3mo, sometimes longer
Occasional hyperthermia, lethargy
*Hair will not grow back without treatment (cosmetic Tx only)
Canine Post Rabies Vaccination Panniculitis - Histological Findings
Cell poor vasculitis, follicular atrophy, follicular and dermal apoptotic cells, subepidermal vesicles, mild diffuse dermatitis, diffuse dermal palor, no lichenoid interface dermatitis, Cutaneous skeletal myositis
Moderate – severe panniculitis
Amorphic, basophilic foreign material (vaccine product)
Cell poor vasculitis affects dermis and panniculus
The Difference Between Dogs and Cats – Tympanic Cavity
- Septum bulla is in the middle ear of dog and cat (bony)
- Size of this septum bulla in dog vs cat is significant when it comes to treating and managing the middle ear disease
- In the DOG, this septum bulla is an incomplete ridge – large opening btwn the tympanic cavity proper and ventral cavity – therefore, you can flush the entire tympanic cavity
- In the CAT the septum bulla is a lot more developed – separates tympanic cavity into to sections → dorsolateral epitympanic cavity (pars tympanica) and the ventromedial tympanic cavity (pars endotympanica) → the separation is almost complete, with only communication through small openings. Therefore, can ONLY flush the dorsolateral compartment. In most cases of middle ear infection in the CAT – surgical management is necessary
- Avoid using ointment in a CAT with a ruptured tympanic membrane b/c it may get trapped in the ventromedial compartment
Classification of Causes of Otitis Externa
a. Hypersensitivity disorders
b. Ectoparasites
c. Obstruction (neoplasia, cysts, polyps)
* *Neoplasia is unilateral ear disease seen in older dogs/cats
d. Foreign Bodies
e. Immune mediated skin diseases
f. Keratinization disorders
g. Endocrinopathies
h. Fungal
Ectoparasites causing Otitis Externa
i. Otodectes cynotis – ear mite – otoacariasis → 50% of cases of otitis externa in cats and 5-10% in dogs
ii. Exudates is dark brown to black
iii. Chronic cases secondarily infected with yeast or bacteria → exudates becomes ceruminous or purulent
iv. Demodex canis and catii may uncommonly cause ceruminous exudates in dogs and cats w/ or w/o skin lesions
Obstructions causing Otitis Externa
i. Tumors are relatively uncommon, and arise from ceruminous glands of external canal
ii. Dog tumors = benign (ceruminous gland adenoma)
iii. Cat tumors = malignant (ceruminous gland adenocarcinoma)
iv. Obstructive masses → accumulation of cerum and debris and lead to secondary infections
* *Aural polyps associated with unilateral otitis
v. Commonly seen in younger cats (any age possible)
vi. 2nd most common cause of otitis in cat
vii. Infectious cause or chronic inflammation are thought to be cause
viii. Comprised of mixed inflammatory cells with an epithelial layer
Foreign bodies causing Otitis Externa
i. Acute, unilateral and painful
ii. Chronic if overlooked
iii. Dangerous if tympanic membrane perforation
iv. Plant material
v. Dirt, sand
vi. Dried medication
vii. Ceruminoliths (wax balls)
viii. Dead insect
