Dermatologic manifestations of systemic disease

Question 1

Outline calcinosis cutis

Answer 1

Dystrophic calcification of the skin

• HAC (naturally­occurring and iatrogenic)
• Clinical diagnosis in cases with compatible Hx, characteristic skin appearance and location
• Erythematous papules, gritty plaques, ulceration, haemorrhagic crusts +/­ 2ary infections
• The grittyness is pathogmonic
• Areas of friction
• Dorsal cervical, axillary, inguinal, MM, tongue

Question 2

What would be the ddx for
- Paw pad hyperkeratosis & peri­oral crusting
dermatitis, Lethargy, PU/PD

Answer 2

• Superficial Necrolytic Dermatitis (hepatocutaneous syndrome)
• Pemphigus foliaceus
• Adverse Drug Reaction
• Erythema Multiforme
• Contact hypersensitivity/irritant
• Zinc­responsive dermatitis

Question 3

What do you see on skin biopsy in a case of superficial necrolytic dermatitis?

Answer 3

‘French flag’ pattern

• Pink (parakeratotic hyperkeratosis)
• White (keratinocyte pallor ­ degeneration)
• Blue (basal cell hyperplasia)

Question 4

What is superficial necrolytic dermatitis?

Answer 4

• Uncommon skin condition associated to systemic metabolic diseases
• Mostly 2ary to metabolic hepatic disease (cirrhosis, neoplasia, hepatic lipidosis, phenobarbital tx)
• Unique liver appearance on US (‘honeycomb’ or ‘Swiss cheese’)
• Other names: Hepatocutaneous Syndrome, Necrolytic Migratory Erythema
• Small number of cases 2ary to glucagonomas (most common cause in humans)
• Older dogs
• Footpad hyperkeratosis with fissures and crusting dermatitis at pressure points, muco­cutaneous junctions and paws.
• PU/PD common

Question 5

How do you treat superficial necrolytic dermatitis?

Answer 5

• Generally guarded­poor prognosis
• Parenteral aminoacid infusions, EFAs, high quality protein diets
• Manage 2ary pyoderma and/or Malassezia spp. overgrowth
• Potentially better prognosis if glucagon ­producing neoplasia identified and removed prior to metastases

Question 6

What are the main non-­neoplastic skin disorders associated with internal malignancy?

Answer 6

• Feline Thymoma ­associated exfoliative dermatosis
• Feline Paraneoplastic alopecia
• Testicular tumours
• Paraneoplastic pemphigus

Question 7

How does Feline thymoma­ associated exfoliative dermatosis present?

Answer 7

• Generalised exfoliative dermatitis with marked scaling
• Immune­mediated mechanism of graft­versus­host type reaction suspected
• Generally non­pruritic
• 2ary bacteria and Malassezia infections ++++

Question 8

What are the ddx for generalised exfoliative dermatitis with marked scaling?

Answer 8

• Dermatophytosis
• Cheyletiellosis
• Erythema multiforme
• Epitheliotropic T­-cell lymphoma

Question 9

How do you dx/manage Feline thymoma ­associated exfoliative dermatosis?

Answer 9

• Dx: histopathology of skin lesions, thoracic imaging
• Surgical resection of thymoma results in resolution of dermatosis
• Feline non­ thymoma associated exfoliative dermatosis clinically and histopathologically identical
• Response to immune­ suppressive therapy

Question 10

Outline feline paraneoplastic alopecia

Answer 10

• 2ary to pancreatic adenocarcinoma (others uncommonly)
• Bilaterally symmetrical, ventrally­ distributed alopecia
• Shiny skin (no fragility)
• Non­pruritic, unless 2ary Malassezia +++ common – brown greasy accumulations
• Dry, scaly or fissured footpads
• Skin lesions the 1st clinical sign noticed, no concurrent systemic signs
• Characteristic skin histopathology Æ recommend abdominal imaging
• Prognosis grave (metastasis)

Question 11

What skin signs may you see with canine testicular tumours?

Answer 11

• Linear preputial erythema with hyperestrogenism

- Tail gland and perianal gland hyperplasia with hyperandrogenism

Question 12

Outline paraneoplastic pemphigus

Answer 12

• Very rare (3 dogs, 1 cat)
• Reported with thymoma, thymic lymphoma and splenic sarcoma
• Severe autoimmune blistering skin disease
• Autoantibodies against several desmosomal components
• Erosions, ulcers on mucosae, mucocutaneous junctions +/­ haired skin
• Dx: characteristic skin histopathology Æ look for internal neoplasia
• Suprabasal clefting (as seen with PV)
• Lymphocytic interface dermatitis with basal and suprabasal apoptotic keratinocytes (as seen with EM)
• Grave prognosis
• Management of the underlying neoplasia
• No response to immune­suppressive therapy

Question 13

What would be the ddx for progressive generalised non­pruritic alopecia and scaling, PU/PD and weight loss, Generalised peripheral lymphadenopathy

Answer 13

Cutaneous lymphoma
SLE
Pemphigus foliaceus
Sebaceous adenitis
Endocrinopathy
Anagen/telogen effluvium
Infection
Leishmania

Question 14

Which viruses may show skin signs?

Answer 14

Leishmaniosis and other protozoal infections
Subcutaneous and deep mycoses (cryptococcosis, histoplasmosis, aspergillosis, etc)
Canine distemper virus
FIV/FeLV
Feline Poxvirus
Feline herpesvirus
FIP

Question 15

What is canine sterile nodular panniculitis

Answer 15

Single or multiple deep subcutaneous nodules (+/­ draining tracts, ulceration)
Trunk, head, neck, generalised
Inflammation of panniculus
Adult dogs (can also be seen in young), any breed
Dachshunds, Poodles, Australian shepherd dogs, Brittany spaniels, Chihuahuas, Dalmatians, Pomeranians
Diagnosis of exclusion
Rule out infectious and other non­infectious causes of nodular skin disease
Full thickness skin biopsies for histopathology + special stains + bacterial, fungal, and mycobacterial cultures
Immunosuppressive treatment with oral GC +/­ ciclosporin, tetracycline antibiotic and niacinamide

Question 16

What is canine renal cystadenocarcinoma and nodular dermatofibrosis?

Answer 16

Rare inherited syndrome of GSD (mainly)
Nodular dermatofibrosis (ND): cutaneous benign collagenous nodular disease
Multiple firm dermal and subcutaneous nodules affecting extremities +/­ other locations
Bilateral renal neoplasia develop months to years after cutaneous nodules
Cystadenocarcinoma or cystadenoma or uterine leiomyoma (less common)
Haematuria, PU/PD, weight loss, vomiting
Nodular dermatofibrosis historically considered as a paraneoplastic syndrome
TGF­b1 production by renal tumour cells
FLCN gene mutation encoding folliculin (tumour suppressor function suspected)
Autosomal dominant transmission

Question 17

How does coronavirus become FIP?

Answer 17

a mutation occurs, resulting in the ability of the virus to replicate within macrophages, and mutated viruses are disseminated from the intestine by macrophages throughout the body. Clinical signs result from the cat’s own immune reaction. FIP is an immune complex disease involving virus, antiviral antibodies and complement

Question 18

How does alopecia in curly coat retrievers present?

Answer 18

Young adults

follicular dysplasia

Question 19

What is syndrome I of zinc responsive dermatitis

Answer 19

identified in Siberian huskies, Alaskan malamutes, and occasionally other breeds. Affected dogs typically present with erythema followed by variable alopecia with fine silver scale that becomes adherent or develops into crusting involving the mucocutaneous junctions of the face (periocular, perioral), pressure points (elbows, hocks), and footpad margins
Diagnosis is based on signalment, typical cutaneous lesions, and histopathology of skin biopsies that shows marked follicular and epidermal parakeratotic hyperkeratosis. Therapy requires Zn supplementation with a recommended dosage of 2–3 mg/kg of elemental Zn in the form of zinc sulfate, zinc gluconate, or zinc methionine. There was not a detected difference between the different Zn salts in one study Clinical signs are typically improved within 4–6 weeks.

Question 20

What is zinc repsonsive dermatitis syndrome II?

Answer 20

occurs in rapidly growing puppies that are being fed a poor-quality dog food or are being oversupplemented with calcium. These dogs are thought to have a relative Zn deficiency caused by a combination of low Zn intake and calcium or cereal phytate binding of Zn. Affected dogs have generalized crusting plaques with extensive crusting and fissuring of the foot pads. Diagnosis is based on compatible history, clinical signs, and histopathology (similar to those of syndrome I). Response to Zn supplementation is dramatic but is not needed once the dog has reached maturity, unlike most syndrome I dogs. Many dogs will respond to a higher quality diet.

Question 21

What is lethal acrodermatitis?

Answer 21

autosomal recessive disease seen in white bull terriers.
The homozygously affected puppies show clinical signs in the first few weeks of life and have a median survival of 7 months, typically succumbing to bronchopneumonia and sepsis. Bull terriers that are heterozygously affected may have increased risk for pyoderma.
progressive crusting dermatitis of the distal extremities and mucocutaneous junctions. Abnormal keratinization of paw pads can result in splaying of the feet. Claw dystrophy and paronychia may also be present.
There is no therapy

Question 22

How do cutaneous xanthomas present?

Answer 22

present as multiple pale yellow to white plaques, papules, or nodules with erythematous borders. They often are located on the head, particularly the preauricular area or pinnae. Lesions can develop in paw pads and over boney prominences on limbs
occur when there is underlying hereditary defects in lipid metabolism or acquired dyslipoproteinemia secondary to diabetes mellitus, or use of megestrol acetate.

Question 23

How do you ix/ tx cutaneous xanthomas

Answer 23

Histologic evaluation of skin biopsies shows large foamy macrophages and giant cells. Serum biochemistry evaluations for diabetes mellitus, hypercholesterolemia, and hypertriglyceridemia should be obtained. Feeding of a low-fat diet and identification and correction of the underlying disturbance in lipid metabolism is recommended for patients that have had cutaneous xanthomas identified.

Question 24

How may deep or systemic mycoses appear?

blastomycosis, coccidioidomycosis, cryptococcosis, histoplasmosis, aspergillosis

Answer 24

papules, nodules, draining tracts, and ulceration and typically result from hematogenous dissemination of the fungal organism to the skin.
Nasal aspergillosis can cause depigmentation and ulceration often beneath the nares as a result of a drainage board effect from the chronic nasal discharge

Question 25

How can distemper affect the skin?

Answer 25

Hard pad disease

Dogs develop excessive keratinous material on the foot pads and nasal planum

Question 26

How can feline herpes virus affect the skin?

Answer 26

ulcerative dermatitis typically involves the dorsal muzzle, but lesions may extend to involve the nasal planum. Cats do not have to have concurrent ocular or upper respiratory tract signs. Histologically, the lesion is a necrotizing, ulcerative dermatitis most often with a concurrent marked eosinophilic inflammation, but the inflammatory pattern may be strongly neutrophilic in some cases

Question 27

What is SLE?

Answer 27

Systemic lupus erythematosus (SLE) is a multisystemic autoimmune disease. The collie, Shetland sheepdog, German shepherd dog, spitz, and poodle are reported to be at increased risk. Skin disease occurs in less than 20% of SLE cases. Fever, polyarthritis, protein-losing nephropathy, anemia, and thrombocytopenia are more common clinical signs seen with SLE. Organ-specific and non–organ-specific autoantibodies target a variety of tissue antigens in SLE. Resultant tissue damage occurs when there is immune complex deposition (as occurs in glomerulonephritis) or can occur because of direct cytotoxic effects or cell-mediated immunity.

Question 28

What cutaneous lesions may be seen with SLE?

Answer 28

erythema, scaling, crusting, depigmentation, alopecia, and ulcerations. Lesions often involve the face, pinnae, and distal extremities. Lesions may be present on mucocutaneous junctions and within the oral cavity. Ulcers and erosions are rarely diagnostic lesions to biopsy, because an intact epidermis is needed to make a definitive diagnosis. The histopathologic findings are variable, but classic lesions include apoptosis of basal cells and basal cell vacuolation, which lead to dermo-epidermal separation and consequent ulceration.

Question 29

How does erythema multiforme present?

Answer 29

often pleomorphic with an acute onset of erythematous plaques and macules that often become annular or serpiginous as they coalesce or they may appear targetoid. Progression to ulcerations is common, and lesions may become variably crusted. Lesions often are generalized but are most commonly found on the ventrum, axillae, inguinal region, mucocutaneous junctions, oral cavity, and pinnae. Biopsies should be obtained from areas of erythema without ulceration or crusting because an intact epidermis is needed for the diagnosis. Histologically, apoptosis with lymphocyte satellitosis is the characteristic microscopic lesion of EM.

Question 30

What may lead to an unkept haircoat in cats?

Answer 30

Hyperthyroidism
Reduced ability to groom - OA, obesity, oral pain, lethargy, malaise
Nutritional deficiencies

Question 31

When may cats get demodex

Answer 31

diabetes mellitus, FIV, feline leukaemia virus (FeLV) infection, systemic lupus erythematosus (SLE), Mycoplasma haemofelis infection, hyperadrenocorticism, and systemic or topical inhalant (fluticasone) steroid therapy

Question 32

What is FeLV giant cell associated dermatitis

Answer 32

very rare scaling, alopecic and crusting dermatitis, with some pruritus
The head is generally affected (pinnae, preauricular, perioral), along with variable involvement of feet, footpads and other mucocutaneous areas
Histopathology changes in skin biopsies reveal characteristic ballooning of epidermal and follicular epithelial cells (giant cells). FeLV infection in a cat with unexplained, poorly responsive or atypical pruritic dermatitis may raise suspicion for this differential

Question 33

Outline cutaenous horns in cats

Answer 33

conical or cylindrical collections of keratin – are rare, and most often reported on the footpads, although they occasionally arise on the nasal planum or eyelids. They may be associated with FeLV infection (multiple horns), or may constitute localised cutaneous disease only (single or multiple, due to papillomavirus, actinic keratosis, squamous cell carcinoma [SCC] in situ, SCC, keratinising acanthoma). Screening for FeLV status is warranted in cats presenting with cutaneous horns

Question 34

What are the most likely ddx for multifocal erosions and ulceration in a cat?

Answer 34

Erythema multiforme, paraneoplastic pemphigus, drug reactions (no recent history), cutaneous vasculitis and systemic lupus erythematosus

Question 35

How do SCCs in situ present?

Answer 35

middle-aged to older cats of varying breeds as localised single or multifocal melanotic scaly plaques, progressing to ulcerative and crusted plaques and nodules
Some forms are associated with papilloma virus

Question 36

What is erythema multiforme?

Answer 36

characterised by multifocal keratinocyte death (apoptosis), resulting in multifocal to coalescing areas of erythema to ulceration of the skin and mucosa. There is a spectrum of severity, from mild erythematous lesions to full thickness ulceration, affecting localised to extensive skin and mucosal areas. Classical ‘target’ lesions, consisting of erythematous macules that spread peripherally and clear centrally, may be present.
Concurrent malaise and pyrexia are common

Question 37

What are the main causes of infectious nodules in cats?

Answer 37

Nocardia
Leprosy
Mycobacteria
Environmental fungi
Protozoa (e.g. leishmania)