Ulcerative disease Flashcards
What are causes of ulcerative disease in the dog and cat?
Dogs
* Infectious
* Mucocutaneous pyoderma
* Neoplastic
* Cutaneous epitheliotropic lymphoma
* Immune-mediated
* Vasculitis (rarely cats)
* Erythema multiforme, SJS and TEN (rarely cats)
* Facial and mucocutaneous DLE
* Traumatic
* Decubital ulcers
Cats
* Viral
* Feline herpesvirus infection
* Feline calicivirus infection
* Feline cowpox infection
* Immune-mediated / idiopathic
* Feline plasma cell pododermatitis
* Neoplastic
* Squamous cell carcinoma
How does the depth of ulcers and erosions differ? Why is it difficult to differentiate between both of these?
-
Ulcers are full-thickness wounds in the epithelium so that the dermis is exposed
- Painful – rather than itchy
- Blood cells and bleeding common
- Cytologically macrophages likely to be present
- Erosions are shallower wounds in the skin within the epithelium
- Crusts are common with both ulcers and erosions. It is sometimes difficult to see the difference without further examination
What are primary and secondary ulceration causes?
Primary ulceration
Diseases within the skin that result in epidermal loss
Due to
* Bacterial
* Viral
* Fungal
* immune-mediated
* Traumatic and idiopathic causes
Secondary ulceration
Common
Due to
* Localised trauma
* severe irritation / pruritus
* Secondary bacterial infections
* Esp. deep pyoderma
Always consider these causes as they are most common
How does feline herpes virus-1 usually present? What can trigger it? How is it diagnosed? WHat drug should you not use? What is the prognosis?
- May not have active or historical URTI signs
- Usually adults
- Facial lesions make a ‘mask’
- eyelids, muzzle and nose
- +/- elsewhere on body
- eyelids, muzzle and nose
- Triggers include stress or glucocorticoids
-
Diagnosis on histopathology
- eosinophilic +/- neutrophilic inflammation
- Important differential = allergic dermatitis (particularly head and neck pruritus and eosinophilic granuloma)
- DO NOT use steroids - immunosuppressive
- Prognosis for herpesvirus dermatitis guarded because recrudescence is common.
How does calicivirus usually present? What drug should you stay away from with this disease?
- Cutaneous signs rare
- Usually URTI
- ulcers and vesicles on mucous membrane, lips and nose
- A rare presentation involving highly virulent strain (VS-FCV) with severe cutaneous and systemic disease is reported
- Rare but important!
- Similar to FHV, allergic dermatitis DD may lead to inappropriate use of steroids or other immunosuppressant agents.
How should you treat URT viruses in cats?
Supportive care
* Fluids, and nutritional support
* Feeding (oesophageal) tube?
* Appetite stimulants e.g. mirtazapine
* Steam inhalation may assist decongestion
* Topical ocular medications are often needed in FHV-1 to treat pain and ulceration
* Lubricants
* Antibiotics
Specific antivirals
* May be useful in FHV-1
* Famciclovir for systemic use in severe cases
* Also described for calicivirus
* Lysine for FHV-1 is ineffective
* Feline interferon omega (by s/c injection or orally for FHV-1, but unknown clinical benefit.
* Antivirals such as trifluidine used for ocular disease in FHV-1
How is cow pox different from calici and FHV-1? Why is it difficult to manage? How are cats infected? What is the prognosis?
DNA virus of the Orthopoxvirus genus
Non-enveloped whereas other 2 are enveloped.
Properties
* resistant to chemical disinfection
* dry scabs and crusts may remain viable for long periods.
* In the home, bleach is the most available disinfectant (alcohol gels widely used in hospital settings are ineffective)
Transmission
* infections from bank vole, field vole & the wood mouse
* signs usually start around the head, sometimes the fore feet
* Virus is inoculated by a bite or scratch from the rodent prey
* crusted ulcerated area with central ulceration
* distinctive crater-edge in some
* Viral replication results in secondary papular crusting eruption after 7-14 days
Prognosis
* Spontaneous recovery occurs in around 4-5 weeks in most
* BUT in immunocompromised cats, replication in the chest can cause severe signs including pneumonia and exudative pleuritis. Generalised cowpox infections may be fatal in young kittens and in cats treated with corticosteroids
- Zoonosis and has been fatal in some immunocompromised people
How do you diagnose cow pox?
- History and clinical signs are consistent
- Younger, hunting rural cat
- Onset of a single crusted ulcerated lesion
- followed by smaller lesions
- Possible confusion with
- Allergic skin disease – pruritus?
- Herpes and calicivirus – respiratory disease, ocular discharge?
- Trauma?
- Diagnosis by PCR &/or biopsy
How should cowpox be treated?
- Steroids/immunosuppressants must not be used
-
Supportive therapy
- Fluids, appetite stimulation / high energy food / enteric feeding, tube feeding if oral lesions
- Recombinant interferon-omega (Virbagen Omega [Virbac])
-
Manage co-morbidities
- Feline **respiratory disease **
- e.g. Bordetella bronchiseptica ± Mycoplasma infection, Feline herpes or calicivirus
- A poor prognosis
-
Bacterial: Secondary bacterial skin infection
- Manage with suitable topical or systemic antibiosis and topicals (be mindful of pain)
- Feline **respiratory disease **
What causes plasma cell pododermatitis? What clinical signs are associated? How is it diagnosed? How is it treated?
Background
* Unknown aetiology - ? immune-mediated
* Strong relationship to FIV in some studies
* Not uncommon
Clinical signs
* Soft, swollen pads with scaling
* ulceration centrally in some
* Some cats have gingivitis-stomatitis or nasal lesions
* May be associated with glomerulopathy and/ or FIV
Diagnosis
* FNA shows plasma cells (often scant)
* Biopsy may be needed to confirm diagnosis in some cases
Treatment
* Spontaneous regression
* Prolapsed material needs surgical repair
* Immune-modulation
* Steroids, ciclosporin
* Doxycycline commonly used (poor antibiotic stewardship)
* Prognosis
* Usually good unless other underlying disease
What are the different types of cutaneous lupus in the dog?
Facial discoid lupus erythematosus - FDLE
Mucocutaneous lupus erythematosus - MCLE
What clinical signs are associated with FDLE? WHat is it difficult to differentiate it from?
- GSD’s / 7y onset (& many other breeds, but much less common)
- most common form of lupus
- Nasal planum / nares
- Erythema, depigmentation, scaling-> erosions/ulcerations, loss of architecture of nasal planum +/- crusting
- Diagnostic dilemma with mucocutaneous pyoderma
- Need to give 3-4 weeks antibiotics to perform histopath
What clinical signs are associated with MCLE? What is it difficult to differentiate from?
- German Shepherd dogs
- Females>males / 6y onset
- Perimucosal ulcerated skin lesions / pain on urinating/defaecating
- Anus, perigenital region, lips, periocular / symmetrical
- Diagnostic dilemma with mucocutaneous pyoderma
- Need to give 3-4 weeks antibiotics to perform histopath
How should you treat cutaneous lupus?
Topical
* Use where possible
* Good antimicrobial cover
* Topical antiseptics
* Chlorhexidine wipes, sprays and shampoo
* Hypochlorous spray
* Topical steroid creams / sprays
* Tacrolimus
Systemic
* Avoid as risk of adverse effects
* Immunosuppression
* Prednisolone 2-4mg /kg PO daily
* Ciclosporin 5 mg /kg PO daily
* Adjunctive
* Azathioprine
* Chlorambucil
* Avoid chronic intermittent use of oral antibiotics
What are the clinical features of mucocutaneous pyoderma? How is it treated?
Clinical features
* Erythema, swelling and crusting
* Depigmentation, fissuring and erosions (primarily involving the lips and perioral skin)
* Resolves with relatively short courses of antibiotics
* Long-term management may be needed as lesions may recur
* Confusion with CLE and lip fold intertrigo
* Considerable overlap with FDLE and MCLE on histopathology
Treatment
* Acute
* Anti-staphylococcal antibiotics and chlorhexidine washes for 3-4 weeks
* Steroids may be useful, in reducing disease severity, but may complicate histopathology
* Chronic
* Frequent and chronic antiseptic use
* Many dogs require intermittent topical steroids
What is cutaneous epitheliotropic lymphoma? What clinical signs are associated? How should it be treated?
- Disease of older dogs
- Very variable presentation
- Lymphocyte invasion of epidermis causes depigmentation, ulceration and plaques and as hair follicles are involved alopecia is common
- Oral lesions are common
- CEL can be very pruritic as T-cells may produce IL-31.
- In early stage often mistaken for cAD, but the older age of onset should be a red flag
- Variable response to chemotherapy
- Lomustine / Masitinib
- Can just treat signs of itch
What causes vasculitis? Where are lesions commonly found? How is it diagnosed?
- Immune-mediated damage of cutaneous blood vessels, but systemic involvement needs to be considered
- Uncommon, but important group of diseases in dogs and cats.
- Many causes, including infections (e.g. Leishmaniasis), food hypersensitivity, insect bites, neoplasia, and drugs (e.g. high dose itraconazole)and idiopathic
-
Lesions are often on dependent areas
- pinnae, tail tip, pads and nails
- elbows and other areas of wear and tear.
- In severe cases oral and more generalised lesions are noted.
-
Diagnosis: rule out 1˚ disease & biopsy.
- Late biopsies often give equivocal results
What clinical signs are associated with acute and chronic vasculitis? How is it treated?
-
Acute signs
- palpable purpura
- erythematous to purpuric plaques
- haemorrhagic bullae,
- crateriform ulcers
- pitting oedema, and occasional localised cyanosis.
-
Chronic
- Non-healing wounds and ulceration with tissue loss
- Reduced blood flow to skin resulting in
- Alopecia and thin skin
- Scarring
-
Treatment (proportional to damage)
- Identify underlying cause if possible
- Immunosuppressive agents (e.g. steroids)
- Perfusion enhancing drugs (e.g. propentofylline)
- Surgery sometimes needed for tail and ear lesions
What causes erythema multiforme? What clinical signs are associated?
Causes
* Acute onset of a cutaneous inflammatory reaction
* Rare to uncommon, no age or breed predisposition
* Aetiology: different possible triggers identified including drug reaction, idiopathic, bacterial & viral infections, systemic diseases, neoplasia and adverse food reaction
* T-cell mediated attack of keratinocytes leading to cell death
Clinical signs
* Acute symmetrical onset of erythematous macules or papules that spread peripherally producing annular or arciform patterns – plaques and bullae resulting in ulcers
* Target lesions common in people, not dogs where lesions are less well defined
Lesions
* Erythematous macules
* Papules, plaques & wheals
* Annular, arcuate, or polycyclic patterns
* Marked scaling and crusting
Distribution
* Trunk, ++ axillary and inguinal
* Mucocutaneous
* Head
* Generalised
* Mucosal involvement: possible
* Epidermal detachment: rare and not extensive (<10% of body surface)
How is erythema multiforme diagnosed? What differential diagnoses should you consider?
Diagnosis
* Acute onset is very useful, biopsy is needed for definitive diagnosis as mimics other problems
* If > 10% epidermal detachment, more serious SJS† and >30% TEN†
* Skin scrapings / Hair plucks
* Ear examination and cytology ± bacteriology (2˚ bacterial ear disease common)
* Haematology, biochemistry and urine analysis
* Consider chest and abdominal imaging
* Biopsy for definitive diagnosis
Differential diagnoses
- Urticaria – as wheals
- Bacterial folliculitis, demodicosis, PF – as crusts
- Cutaneous adverse drug reactions (other forms e.g. Wells-like) – as ulcerations/erosions
How should you treat erythema multiforme?
**Mild **
* EM may run a mild course
* Spontaneous regression possible
* Common in people with viral causes
* Look for underlying cause and correct it
* Stop any drug therapy
* Diet trial
* Suspect very mild cases are just ignored by owners and resolve
Extensive
* Severe vesiculobullous cases require supportive care and immunosuppressive drugs
* Glucocorticoids
* Ciclosporin
* Azathioprine
* IVIG
* Pentoxifylline – anecdotal benefit
* In severe cases and especially with more extensive skin involvement 2˚ skin infections need to be carefully managed
What is cutaneous and renal glomerular vasculopathy (alabama rot)? How should it be treated?
History and clinical signs
* CRGV is a rare
* potentially life-threating
* unknown aetiology
* often characterised by ulceration of the distal extremities in dogs.
* Variably associated with clinically significant renal azotaemia due to acute kidney injury (AKI)
* 91% between November & May
* Dogs have generally been walked in woodland.
Pathophysiology
* An unknown toxin, is acquired by ingestion or another route (currently unknown).
* CRGV is characterized histopathologically as a thrombotic microangiopathy (TMA)
* TMAs
* endothelial injury leading to loss of physiological thromboresistance, which allows widespread deposition of microthrombi in small vessels
* Leads to vessel damage
Treatment
* Supportive care
* Therapeutic plasma exchange (TPE or plasmapheresis)
* Severe AKI: poor prognosis
What are decubital ulcers? What are the different stages? How are they treated?
Background
* Result from prolonged application of pressure
* Over a boney prominence
* Under a bandage
* In very heavy or debilitated animals
* Not uncommon in small animal practice
* Can be very difficult to manage if neglected
Stages
* Stage I
* Redness of the skin
* Erosions and possibly ulceration
* Stage II
* Ulceration into the subcutis
* Stage III
* Ulceration into underlying tissues
* Stage IV
* Ulceration to level of bone
- Treatment
- Prevention is paramount
- Recumbent animals need to be placed on a waterbed or ‘egg-crate’ foam, turned regularly
- If sore develops
- Clean – antiseptics
- Protect – can ring bandaging or similar be used?
- Treat infection (n.b. cytology & culture)
- Surgically remove when animal standing
What are the steps of an immunosuppressive treatment plan?
- control - aim for complete control
- titrate - reduce the dose to the lowest level
- maintain - don’t keep trying to titrate
- monitor - ensure that the case is checked for iatrogenic adverse effect
How does an immunosuppressive induction therapy differ when treating humoral immune responses compared to cell-mediated immune responses?
Humoral immune-responses (and more acute CMI led diseases)
* Prednisolone is the mainstay of therapy in humoral diseases (e.g. canine pemphigus foliaceus)
* start 1.1mg/kg twice daily or 2.2mg/kg once daily in dogs (sometimes higher in severe disease)
* expect positive response (not cure) in 7- 10 days
Cell-mediated immune-responses
* Ciclosporin is the mainstay therapy in cell-mediated disease (e.g. cutaneous lupus erythematosus)
* Start 5mg/kg once daily in dogs and 7mg/kg once daily in cats
* BUT Very slow response (so often combined with steroids early in therapy)
What adjuvant drugs can you add to immunosuppressive therapy?
- Azathioprine (dogs only), chlorambucil, mycophenolate mofetil, and topical agents such as steroid sprays and creams and tacrolimus
- Increasingly oclacitinib is used ‘off-licence’ for immune-mediated disease
How should you monitor immunosuppressive therapies?
- Haematology, biochemistry, urinanalysis
- Regular (and frequent) clinical examinations
What is the transition phase of immunomodulatory therapy?
- Tapering of dose
- Observing for mild / slight recurrence to set maintenance level
- Aims differ in different patients
- Complete remission versus lesional but comfortable
- Define these aims with owner
- Sometimes more lesional than ideal - but need to avoid excessive adverse effects
- Treat the animal – not the owners wishes!
How do you decide on the maintenance dose of immunomodulatory therapy?
- Using the established dose found at the end of tapering for months to years
- Depends on attitude of owner
- Consequences of having to re-introduce higher dose therapy
- Sometimes maintenance dose is nothing = cure
- Judging the maintenance dose can be very hard. The slower the reduction during the transition period the easier to see the correct dose, but this comes with an increased risk of adverse effects
What are the side effects of azathioprine?
- myelosuppression
- 90% of patients show signs of anaemia and lymphopenia
- This is (if mild) expected - not necessary to discontinue treatment in many cases and is considered by some to be a marker of an adequate dose
- Pancreatitis
- usually concurrent steroids resolves with steroid withdrawal
- Hepatotoxicity- may not resolve with steroid withdrawal.
- Azathioprine is NOT used in cats
What side effects are common with chlorambucil? How should it be monitored? What conditions is it used in?
Haematology & biochemistry monitoring- 2-4 weeks
Side effects
* Anorexia
* Vomiting
* Diarrhoea
* usually only seen at daily dosing.
* 2 mg and 5mg tablets → suits small dogs & cats
Drug of choice in the cat as secondary immunosuppressive agent
Uses
* Pemphigus complex
* Bullous pemphigoid
* DLE & SLE
* Immune-mediated vasculitis
* Cold aggluttinin disease
* Lymphocyte & plasma cell malignancies
