equine skin dx 2 Flashcards
what are fungal spp cause dermatophytosis?
what are the clinical signs of dermatophytosis?
ringworm:
* Trichophyton equinum (+++) and Mycrosporum gypseum
**Primary lesions: **
* circular areas of alopecia with variable scaling and crusting. Occasional erythema on white skin areas
* Circular areas of erected hair (early disease)
* Occasionally mild pruritus: keratinases release or 2nd bacterial infection
Location: head, neck, lateral thorax and girth,
* might participate on “pastern dermatitis”
* might complicate lesions triggered by mites in lower limbs
What are the causes of crusting and scaling in horses?
- Bacteria
- D. Congolensis
- Staph/Strep folliculitis
- Dermatophytosis
- Trichophyton equinum
- Microsporum gypseum
- Pemphigus
- Parasites - Chronic
- Mites
- Lice
- Onchocerca
- Chronification
- Hypersensitivities
- Drug reactions
- Photosensitisation
What is the causeative agent of rain scale/rot in horses?
What are the risk factors?
How is it contracted?
Dermatophilosis (D. congolensis)
- Gram-positive facultative anaerobic actinomycete: railroad tracks
- Quiescent (dormant) form in horse skin> Skin damage and moisture
- Zoospores> infective form (motile and flagellate)
- Risk factors: poor hygiene (sweaty horses), high temperature and humidity, poor nutrition, low-immunity
- Zoospores might remain viable in crust for up to 2 months (disinfection)
- It is contagious with an incubation period of 2-15 days depending on host immunity
What is the apperance of dermatophilosis?
where are the lesions located?
- Tufted coalescing papules that become exudative>
- large oval lesions with a “paintbrush effect”
- thick crust with thin pus underneath. Painful but not pruritic
- “dribbling” or “scald line” : the dorsum and trunk
Location: Rump, saddle areas, face and neck and pastern coronet (associated with “mud fever” )
What is the management and treatment of dermatophilosis?
mild cases migh spontaneously regress within 4 weeks
Local treatment:
* Antiseptic washes: Chlorhexidine or povidone-iodine based daily for 1 week then once a week until resolution
* Daily application of 5% K-permanganate for 5 days
* Following washing and rinsing skin should be dry with a towel, or heat lamp
Systemic treatment: in highly exudative and painful cases with/without secondary infections (staph/strep)
* Penicillin for 3-5 days
* TMPS for 2 weeks
Management
* Rarely transmitted zoonotic BUT **WEAR GLOVES **
* Always CONTAGIOUS so isolate horses and clean tack
* Wash tack: rugs, saddle pads, brushes, etc @ 60 °C
* 50% Captan solution
* Keep horses dry after exercise
* Maintain the bedding clean and dry, avoid accumulation of manure
* Avoid sunlight in affected areas as it might aggravate irritation
* Use sunblock in affected white areas (factor >20)
* Correct diet, treat concurrent disease
What is the treatment of dermatophytosis?
- Rarely transmitted zoonotic BUT WEAR GLOVES
- Immunocompromised people and children
- Always CONTAGIOUS so isolate horses and clean tack
- Correct nutritional imbalances or primary immuno-suppressant disease
- Stop training/ridding and working animals until recovery
- Exposure to sunlight might be beneficial:
- Clean and disinfect tack with inorganic peroxide compounds
- If premises outbreak: K-monopersulphate on surfaces “fogging”
Local treatment: Multiple options
* Chlorhexidine 4% spray every day for 7 days
* Chlorhexidine 2% + Miconazole 2% spray or shampoo 2-3 times/week
* Clotrimazole 1% + Betamethasone 0.1% cream/lotion
* Lime Sulfur 5% dip
How is dermatophytosis spread?
what is the pathogenesis?
What horses are predominantly affected?
- Normally spread through contaminated girth, boots, clippers, brushes, etc
- **Invasion of hair follicle **is key on pathogenesis:
- keratinases facilitate invasion of hair shafts
- Anagen phase (active keratin production): active proliferation,
- Telogen phase limit the spread» self-limiting infection
- Spontaneous remission can occur within 3 months
- Young horses more likely to be affected: role of host immunity»but old horses with PPID?
What are the three types of photosentisiation in horses
What are the clinical signs?
What is the teatment?
Abnormal reaction of the skin when exposed to UV-radiation
Non –pruritic crust in white areas
Type I: ingestion of photodynamic agent: plants. St. John’s wort, Perennial ryegrass
Type II: congenital disease: abnormal metabolism of porphyrins
**Type III: **liver failure (most common) liver normally incorporates to bile chlorophyll degradation products (phylloerythrin and porphyrins) if not cleared into bile reach skin and acts as photodynamic agents in white areas
TREATMENT: Treat primary problem, remove from pasture, apply sunscreen (>50+), cover affect areas until healing
What is pemphigus in horses?
What are the suggested cuases?
What ar ethe differnt types?
how is it diagnosed?
- Exfoliative dermatitis due to a type II hypersensitivity with antibodies directed epidermal cells. No breed or sex predisposition, wide range of ages at first diagnosis.
- Pemphigus antigens poorly understood in the horse:
- desmoglein protein?
- environmental triggers?
- food ingredients?
Types:
Foliaceous: more scaling and severe diffuse crusting:
Vulgaris/Bullous: mucocutaneous junctions with ulceration and bulla formation in the oral mucosa primarily
Diagnosis: Biopsy: acantholysis and Ab deposition
What is the treatment for pemphigus in the horse?
- Long-term glucocorticoid administration (prednisolone or dexamethasone): immunosuppressive doses
- Omega fatty acids
- Vitamin E supplementation (5000IU/500kg horse)
- Sunlight restriction: avoid exacerbation
- Addressing any underlying triggering factors?
- (fly bite allergies, drug administration, and diet…)
What is onchocerca?
What is the prevalence?
Where are the locations of the lesions? what is the apperance?
What is the treatment?
- Microfilaria parasite prevalent in warm climates; Threadworms
- Low prevalence due to regular use of macrocytic lactones as wormers (ivermectin/ moxidectin)
- Warm weather exacerbation: moving from deep dermis to superficial
- Adults live in nuchal ligament
Location : head, neck, ventral chest/abdomen, rarely ocular lesions. Alopecic flat crusts, mildly raised
Treatment: macrocytic lactones; permanent leukoderma possible
What is pastern dermatitis?
What are the causes?
what is the prognosis?
- Multifactorial syndrome affecting caudal aspect of the pasterns
- Environmental conditions (moisture, dirt) , parasitic, fungal and bacterial pathogens, potentially complicated with breed predisposition
- Staphylococcus aureusandDermatophilus congolensis primary pathogens»fungi secondary (Malassezia and Trichophyton)
- High prevalence and recurrent problem: Long term management
What is Chronic Proliferative Lymphoedema (CPL)? what breeds suffer from CPL?
- Shires, Clydesdales, and Belgian Draft
- Elastin dysfunction in distal lymphatic vessels
What is the diagnostic approach and management of pastern dermatitis?
- Take samples and clip hair: Chronic lesion less likely to yield Dx
- Clean with warm water and neutral soap: depending on primary agent Chlorhexidine might be indicated but might perpetuate dysbiosis in chronic cases
- Dry thoroughly with a soft towel and keep in a dry environment
-
Avoid bandaging BUT sometimes necessary
- Unable to provide dry/clean environment
- Very exudative/infected/painful lesions: avoid self-trauma
- **Treat primary problem **
-
Warn owner: Long term and environmental management mandatory
- Avoid frustration (Vet-Owner) and re-occurrence
What are the causes of ulcerative and erosive lesions?
- Viral - EHV3, Vesicular stomatitis
- Neoplasia - SCC
- Summer sores - Habronemiasis
What are the characteristics of lesions caused by EHV-3?
how is it transmitted?
What are the clinical signs?
how is it diagnosed?
- Lesions on the vulva, perineum, penis, prepuce and testicles
- Oral and lip ulcers
- Transmitted through direct contact during sexual intercourse or sniffing (naso-genital)
- Reluctance to breed, ptyalism…
- Serology (rising titre)
