I am a ver student, how can you help me in this

Asking for Preferences
Asking for Preferences
Clinical case discussions - that's one of the best ways to learn veterinary medicine! Here's exactly how I can help you with that:

How I Can Help You - Vet Student (Clinical Cases)

1. Work through a case with you step by step
  • You present the signalment, history, and clinical signs
  • I help you build a problem list, generate a differential diagnosis list, and prioritize differentials
  • We discuss which diagnostics to run and why
2. Interpret diagnostics
  • Walk through CBC, biochemistry panels, urinalysis, imaging findings, cytology, histopathology
  • Explain what abnormalities mean and how they narrow your differentials
3. Treatment planning
  • Discuss treatment options with mechanisms of action
  • Drug dosages, protocols, and monitoring parameters
  • Supportive care rationale
4. Pathophysiology deep-dives
  • If a case involves a disease you don't fully understand, I can explain the underlying pathophysiology in detail
5. Post-case learning
  • After working through a case, I can summarize key learning points and give you similar cases to test yourself

To get started, just present a case! You can share:
  • Species, breed, age, sex
  • Chief complaint / history
  • Clinical findings
  • Any diagnostics already done
Throw a case at me and we'll work through it together!

Explain how to build a differential diagnosis list

Building a differential diagnosis (DDx) list is a core clinical skill. Here's a structured, practical approach:

Building a Differential Diagnosis List

Step 1 - Extract the Key Problems

Before listing differentials, identify your master problem list from the history and physical exam. Don't jump straight to a diagnosis - list the individual abnormalities first.
Example: A 6-year-old Labrador presenting with polyuria, polydipsia, pot-bellied appearance, and skin infection.
  • Problem 1: PU/PD
  • Problem 2: Pot-bellied abdomen
  • Problem 3: Recurrent pyoderma
Then pick your key problem (the one most specific and likely to narrow the list fastest) and build your DDx around it. You can then check if the other problems fit each differential.

Step 2 - Use a Systematic Framework (DAMNIT-V)

A mnemonic prevents you from missing categories. The most widely used in vet medicine is DAMNIT-V:
LetterCategoryExamples
DDegenerativeDegenerative joint disease, cerebellar abiotrophy
AAnomalous / AnatomicCongenital defects, portosystemic shunts
MMetabolicHypothyroidism, Cushing's, Addison's, hepatic disease
NNeoplasticTumors (benign or malignant)
NNutritionalDietary deficiencies, obesity
IInflammatory / Infectious / Immune-mediatedBacterial, viral, fungal, immune disease
TTraumatic / ToxicInjuries, toxin ingestion
VVascularThromboembolism, hypertension, infarction
Go through each category and ask: "Could anything in this category cause this problem in this patient?"

Step 3 - Apply Patient Filters (Narrow the List)

Once you have a broad list, filter it using patient-specific information. This is where the signalment and history become powerful:
  • Species - Cats don't get Addison's commonly; dogs do. Hyperthyroidism is common in cats, rare in dogs.
  • Breed - Boxers are prone to mast cell tumors. Dobermans to dilated cardiomyopathy. Bernese Mountain Dogs to histiocytic sarcoma.
  • Age - Young animals: congenital, infectious, nutritional. Middle-aged: metabolic, immune-mediated. Old: neoplastic, degenerative.
  • Sex / reproductive status - Intact female dog with PU/PD and vaginal discharge? Pyometra moves to the top immediately.
  • Vaccination / travel history - Unvaccinated puppy with hemorrhagic diarrhea? Parvovirus is #1.
  • Onset and progression - Acute vs. chronic, progressive vs. static, episodic vs. continuous.

Step 4 - Rank Your Differentials

Prioritize the list by two factors:
  1. Probability - What is most likely given this patient's signalment, history, and clinical findings?
  2. Consequence - What can you NOT afford to miss, even if less likely? (e.g., a toxic ingestion, a ruptured GDV, a pneumothorax)
A practical way to rank:
  • Rule-outs (R/O): Must be excluded because they are life-threatening or very likely
  • Likely: Fits the overall picture well
  • Less likely but possible: Don't discard; revisit if top differentials are excluded

Step 5 - Design Diagnostics to Discriminate

Each diagnostic test should be chosen to include or exclude a specific differential. Ask yourself:
"Which differential does this test help me confirm or rule out?"
  • CBC + biochemistry panel - screens broadly for metabolic, inflammatory, and organ disease
  • Urinalysis + urine culture - essential for PU/PD cases
  • Imaging (radiographs, ultrasound) - organ size, masses, effusions, structural abnormalities
  • Specific tests (ACTH stim, TLI, bile acids, FELV/FIV, PCR panels) - targeted once your top differentials are known
Avoid "shotgun" diagnostics - ordering everything at once without a reasoning framework is expensive and harder to interpret.

Step 6 - Revisit and Revise

A DDx list is not static. As results come back:
  • Cross off differentials that are excluded
  • Promote differentials that gain supporting evidence
  • Add new differentials if unexpected findings emerge
This iterative loop - problem → hypothesis → test → refine - is the core of clinical reasoning.

Quick Summary Framework

1. Build problem list from history + PE
2. Pick key problem(s)
3. Apply DAMNIT-V to generate broad DDx
4. Filter by signalment (species, breed, age, sex, history)
5. Rank by probability + consequence
6. Choose targeted diagnostics
7. Revise as results come in

Pro tip for exams and rounds: When presenting a case, always start with "My top differential is X because..." followed by "I also want to rule out Y because it is life-threatening / fits the presentation." This shows structured thinking and impresses supervisors.
Want to try working through an actual case using this framework?

Explain at least 10 so n diseases of digs and cats

Reading File
Finding Sources
Finding Sources
The library contains human medicine textbooks, not veterinary-specific ones. I'll draw on my veterinary knowledge to give you a thorough, accurate overview of 10+ important diseases of dogs and cats.

10 Important Diseases of Dogs and Cats


DOGS


1. Canine Parvovirus (CPV-2)

Category: Infectious (Viral)
Pathophysiology: CPV-2 targets rapidly dividing cells - specifically the intestinal crypt epithelium and bone marrow. Destruction of intestinal crypts leads to villous collapse, malabsorption, and breakdown of the mucosal barrier, allowing bacterial translocation into the bloodstream (septicemia).
Signalment most at risk: Unvaccinated puppies, 6 weeks - 6 months. Rottweilers, Dobermans, and American Pit Bull Terriers have higher susceptibility.
Clinical signs:
  • Profuse, hemorrhagic, foul-smelling diarrhea
  • Severe vomiting
  • Depression, anorexia
  • Fever (or hypothermia in severe cases)
  • Dehydration
Diagnosis:
  • SNAP ELISA fecal antigen test (in-clinic)
  • CBC: leukopenia (neutropenia + lymphopenia) is characteristic
  • PCR for confirmation
Treatment: Supportive only - IV fluids, antiemetics (maropitant), broad-spectrum antibiotics (ampicillin + enrofloxacin), nutritional support (early enteral feeding). No antiviral treatment available.
Prognosis: 85-95% survival with aggressive hospitalized care; <10% without treatment.
Prevention: Vaccination (core vaccine). Isolate affected animals - virus survives in the environment for months to years.

2. Canine Distemper

Category: Infectious (Viral - Paramyxovirus)
Pathophysiology: Morbillivirus spreads via respiratory secretions, causing viremia and infection of epithelial cells, lymphoid tissue, and the CNS. Demyelination occurs in the brain and spinal cord.
Clinical signs (multi-systemic):
  • Respiratory: Nasal/ocular discharge, pneumonia
  • GI: Vomiting, diarrhea
  • Neurological: Seizures, myoclonus (rhythmic muscle twitching - characteristic), ataxia, paresis
  • Skin: Hyperkeratosis of nose and footpads ("hard pad disease")
  • Teeth: Enamel hypoplasia in surviving puppies
Diagnosis: Clinical signs + PCR (conjunctival/nasal swab, CSF, blood), conjunctival inclusion bodies on cytology
Treatment: Supportive (no antiviral). Anticonvulsants for seizures. Prognosis guarded to poor once neurological signs appear.
Prevention: Core vaccination (part of the DHPPiL combo).

3. Hyperadrenocorticism (Cushing's Disease)

Category: Metabolic / Endocrine
Pathophysiology: Excess cortisol production. 85% are pituitary-dependent (PDH) - a pituitary adenoma secretes excess ACTH, driving bilateral adrenal hyperplasia. 15% are adrenal-dependent (ADH) - a functional adrenal tumor secretes cortisol autonomously.
Signalment: Middle-aged to older dogs. Poodles, Dachshunds, Boxers, Beagles predisposed.
Clinical signs (classic "PUPD + 3Ps"):
  • Polyuria / Polydipsia
  • Polyphagia
  • Pot-bellied abdomen (muscle wasting + hepatomegaly + fat redistribution)
  • Bilateral symmetrical alopecia
  • Skin thinning, calcinosis cutis
  • Recurrent infections (immunosuppression)
  • Muscle weakness
Diagnosis:
  • Screening: UCCR (urine cortisol:creatinine ratio), LDDS test (low-dose dexamethasone suppression)
  • Differentiating PDH vs. ADH: HDDS test (high-dose), abdominal ultrasound, endogenous ACTH
  • CBC: "stress leukogram" (neutrophilia, eosinopenia, lymphopenia), elevated ALP
Treatment:
  • PDH: Trilostane or mitotane (o,p'-DDD)
  • ADH: Adrenalectomy preferred

4. Canine Hip Dysplasia

Category: Degenerative / Developmental
Pathophysiology: Abnormal development of the coxofemoral joint leading to laxity, subluxation, cartilage erosion, and secondary osteoarthritis. Multifactorial - genetic predisposition + environmental factors (rapid growth, excessive exercise in puppies).
Signalment: Large and giant breeds - German Shepherds, Labrador Retrievers, Golden Retrievers, Rottweilers.
Clinical signs:
  • Hindlimb lameness (often bilateral)
  • "Bunny hopping" gait
  • Reluctance to rise, exercise intolerance
  • Pain on hip extension
  • Crepitus on joint manipulation
  • Muscle atrophy of hindquarters
Diagnosis: Orthopedic exam + radiographs (OFA or PennHIP views). Norberg angle assessment.
Treatment:
  • Conservative: weight management, physiotherapy, NSAIDs (meloxicam, carprofen), joint supplements
  • Surgical: triple pelvic osteotomy (young dogs), femoral head and neck excision (FHO), total hip replacement (THR)

5. Canine Gastric Dilatation-Volvulus (GDV)

Category: Emergency / Surgical
Pathophysiology: Stomach fills with gas and rotates on its mesenteric axis (typically 90-360° clockwise). Rotation traps gas, occludes the portal vein and caudal vena cava, causes ischemia of the gastric wall, and leads to distributive shock. Life-threatening within hours.
Signalment: Large, deep-chested breeds - Great Danes, German Shepherds, Standard Poodles, Weimaraners. Middle-aged to older males.
Clinical signs:
  • Non-productive retching (hallmark sign)
  • Distended, tympanic abdomen
  • Hypersalivation, restlessness
  • Rapid progression to collapse, shock (pale mucous membranes, weak pulse, tachycardia)
Diagnosis: Clinical suspicion + lateral abdominal radiograph ("double bubble" or "shelf sign" - pylorus displaced dorsocranially)
Treatment: TRUE EMERGENCY
  1. IV access (2 large-bore catheters), aggressive fluid resuscitation
  2. Gastric decompression (orogastric tube or trocarization)
  3. Emergency surgery: derotation, gastropexy, resection of necrotic stomach/spleen
  • Prophylactic gastropexy offered to at-risk breeds
Prognosis: 80-85% survival with prompt surgery. Worsens significantly with delay.

6. Canine Babesiosis

Category: Infectious (Protozoal)
Pathophysiology: Tick-transmitted (Rhipicephalus, Dermacentor spp.) hemoprotozoan. Babesia canis and B. gibsoni infect and destroy red blood cells, causing hemolytic anemia. Immune-mediated destruction compounds the direct parasitic damage.
Clinical signs:
  • Pale or icteric mucous membranes
  • Hemoglobinuria ("port-wine" colored urine)
  • Fever, weakness, collapse
  • Splenomegaly
Diagnosis: Blood smear (intraerythrocytic piriform parasites), PCR (gold standard), serology
Treatment: Imidocarb dipropionate (drug of choice for B. canis); atovaquone + azithromycin for B. gibsoni. Supportive care, blood transfusion if severely anemic.

CATS


7. Feline Hyperthyroidism

Category: Endocrine / Metabolic
Pathophysiology: Benign functional adenomatous hyperplasia of one or both thyroid lobes in >98% of cases. Excess thyroid hormones (T3/T4) cause a hypermetabolic state. Most common endocrine disease of cats.
Signalment: Middle-aged to older cats (>8 years). Siamese and Himalayan cats appear less predisposed.
Clinical signs:
  • Weight loss despite polyphagia (classic combination)
  • Hyperactivity, restlessness, aggression
  • Vomiting, diarrhea
  • Unkempt coat
  • Tachycardia, heart murmur, gallop rhythm
  • Hypertension (secondary)
  • Goiter (palpable thyroid nodule in ~90%)
Diagnosis: Elevated total T4 (tT4) is diagnostic in most cases. Free T4 by equilibrium dialysis if borderline. Technetium scan for surgical/I-131 planning.
Treatment options:
  • Methimazole (daily medication - medical management)
  • Radioactive iodine (I-131) - curative, treatment of choice
  • Surgical thyroidectomy - curative
  • Dietary iodine restriction (Hill's y/d)
Watch for: Masked renal disease - hyperthyroidism elevates GFR, and treating it can unmask pre-existing CKD.

8. Feline Lower Urinary Tract Disease (FLUTD) / Feline Idiopathic Cystitis (FIC)

Category: Urological / Inflammatory
Pathophysiology: FLUTD is an umbrella term. In cats <10 years, ~65% of cases are idiopathic (FIC), thought to be stress-related with neurogenic inflammation of the bladder wall. Other causes include urolithiasis (struvite, oxalate), urethral plugs (in males), and infection (less common in young cats).
Signalment: Indoor, overweight, middle-aged cats. Male cats at higher risk for urethral obstruction due to anatomy.
Clinical signs:
  • Dysuria, stranguria, pollakiuria
  • Hematuria
  • Periuria (urinating outside litter box)
  • In urethral obstruction: straining with no urine production, vocalization, collapse, bradycardia (life-threatening hyperkalemia)
Diagnosis: Urinalysis + urine culture, abdominal radiographs/ultrasound, contrast urethrogram if needed
Treatment:
  • FIC: stress reduction (environmental enrichment), increased water intake, urinary diets, pain management
  • Urethral obstruction: EMERGENCY - urethral catheterization, IV fluids, treat hyperkalemia (ECG monitoring)
  • Urolithiasis: dietary dissolution (struvite) or surgical removal (oxalate)

9. Feline Infectious Peritonitis (FIP)

Category: Infectious (Viral - Coronavirus mutation)
Pathophysiology: Feline coronavirus (FCoV) mutates within an individual cat to become FIPV (feline infectious peritonitis virus), which infects macrophages and causes a systemic pyogranulomatous vasculitis. Two forms:
  • Wet (effusive): Immune complex deposition in vessels leads to protein-rich effusions in body cavities
  • Dry (non-effusive): Granuloma formation in organs (CNS, eyes, liver, kidneys)
Signalment: Young cats (<2 years) and old/immunocompromised cats. Purebred cats at higher risk.
Clinical signs:
  • Wet: Distended abdomen (ascites) or pleural effusion, dyspnea, fever, weight loss
  • Dry: Neurological signs (ataxia, seizures), uveitis, chorioretinitis, organomegaly
Diagnosis: Challenging. Effusion analysis (high protein, high globulin, yellow color, Rivalta's test), serology, PCR on effusion or tissue. Histopathology is gold standard.
Treatment: GS-441524 (nucleoside analog antiviral) - now widely available and highly effective, transforming FIP from a nearly 100% fatal disease to a treatable one. 12-week treatment course.

10. Feline Chronic Kidney Disease (CKD)

Category: Degenerative / Metabolic
Pathophysiology: Progressive, irreversible loss of functional nephrons over time. Remaining nephrons undergo compensatory hypertrophy but eventually fail. Leads to uremia, hyperphosphatemia, hypertension, anemia, and metabolic acidosis. Most common cause of death in older cats.
Signalment: Cats >7 years. Abyssinians, Persians predisposed to polycystic kidney disease (PKD) as a specific cause.
Clinical signs:
  • PU/PD
  • Weight loss, muscle wasting
  • Vomiting, anorexia
  • Halitosis (uremic breath)
  • Pale mucous membranes (non-regenerative anemia)
  • Hypertension (retinal detachment, sudden blindness)
  • Dehydration, poor coat
Staging (IRIS system):
StageCreatinine (µmol/L)SDMA
I<140<18
II140-24918-25
III250-43926-38
IV>440>38
Treatment:
  • Renal diet (phosphorus restriction, moderate protein)
  • Phosphate binders (aluminum hydroxide, lanthanum carbonate)
  • Antihypertensives (amlodipine)
  • Erythropoiesis-stimulating agents for anemia (darbepoetin)
  • Sub-cutaneous fluids (home management)
  • Treat concurrent conditions (UTI, hypertension, proteinuria)

11. Feline Asthma (Chronic Bronchial Disease)

Category: Inflammatory / Immune-mediated
Pathophysiology: Allergen-driven Type I hypersensitivity reaction in the lower airways. Mast cell degranulation and eosinophilic inflammation cause bronchoconstriction, mucus hypersecretion, and airway remodeling. Reversible (early) to irreversible (chronic).
Clinical signs:
  • Episodic coughing (crouching, neck extended - classic posture)
  • Wheezing
  • Increased respiratory effort (abdominal breathing)
  • Acute respiratory distress during attacks
Diagnosis: Radiographs (hyperinflation, peribronchial cuffing, "donut" sign), bronchoscopy + BAL (eosinophilia), rule out heartworm, lungworm, cardiac disease
Treatment:
  • Acute attack: Oxygen, bronchodilators (terbutaline SC, albuterol inhaler)
  • Long-term: Inhaled corticosteroids (fluticasone via AeroKat spacer), inhaled bronchodilators (albuterol as needed)
  • Identify and eliminate allergen triggers

12. Canine/Feline Diabetes Mellitus

Category: Metabolic / Endocrine
FeatureDogsCats
TypeType 1-like (absolute insulin deficiency)Type 2-like (insulin resistance + beta cell exhaustion)
Sex predispositionIntact femalesNeutered males, obese cats
Remission possible?NoYes (20-30% if caught early + obesity corrected)
Insulin of choiceNPH, VetsulinPZI, Glargine
Common clinical signs in both species:
  • PU/PD, polyphagia
  • Weight loss
  • Cataracts (dogs - rapidly progressive)
  • Plantigrade stance (cats - diabetic neuropathy)
  • Recurrent infections
Monitoring: Blood glucose curves, fructosamine (reflects 2-3 week average glucose), urinalysis
Complication to know: Diabetic ketoacidosis (DKA) - a life-threatening complication requiring emergency hospitalization, IV fluids, insulin CRI, electrolyte correction.

Quick Reference Summary Table

#DiseaseSpeciesKey Hallmark
1ParvovirusDogBloody diarrhea + leukopenia in unvaccinated puppy
2DistemperDogMyoclonus + multisystemic signs + hard pads
3Cushing'sDogPU/PD + pot belly + alopecia + high ALP
4Hip DysplasiaDogHindlimb lameness in large breed
5GDVDogNon-productive retching + tympanic abdomen = EMERGENCY
6BabesiosisDogHemolytic anemia + hemoglobinuria + tick exposure
7HyperthyroidismCatWeight loss + polyphagia + tachycardia in old cat
8FLUTD/FICCatDysuria + hematuria; obstruction = EMERGENCY in males
9FIPCatEffusions + fever + young cat; now treatable with GS-441524
10CKDCatPU/PD + weight loss + anemia in old cat; IRIS staging
11Feline AsthmaCatEpisodic cough with neck-extended posture
12DiabetesBothPU/PD + weight loss; cataracts in dogs; plantigrade in cats

Want me to go deeper on any of these - such as full diagnostic workups, treatment protocols, or case-based questions to test your knowledge?

I mean explain 10 skin diseases of dogs and cats

Finding Sources
Finding Sources
The library covers human medicine, so there are no dedicated veterinary dermatology textbooks in it. I'll give you a thorough, exam-ready breakdown from veterinary knowledge below.

10 Skin Diseases of Dogs and Cats


1. Canine Atopic Dermatitis (CAD)

Species: Dogs (also recognized in cats as feline atopic skin syndrome) Category: Allergic / Immune-mediated
Pathophysiology: A genetic predisposition leads to a defective skin barrier and an aberrant Th2-dominant immune response to environmental allergens (house dust mites, pollens, molds, storage mites). IgE sensitization occurs, and re-exposure triggers mast cell degranulation and eosinophilic/lymphocytic inflammation. Chronic scratching damages the skin further, allowing secondary bacterial and yeast infections.
Signalment: Young dogs (1-3 years onset). Predisposed breeds: West Highland White Terriers, Golden Retrievers, Labrador Retrievers, French Bulldogs, Boxers, Shih Tzus.
Clinical signs:
  • Pruritus (the primary sign) - often seasonal at first, becomes year-round
  • Erythema and self-trauma lesions at characteristic sites: face (periocular, perioral), ears (otitis externa), ventral abdomen, axillae, groin, interdigital spaces
  • Alopecia, lichenification, and hyperpigmentation with chronicity
  • Recurrent pyoderma and Malassezia otitis/dermatitis
Diagnosis:
  • Diagnosis of exclusion - must rule out flea allergy and food allergy first (Favrot criteria used clinically)
  • Intradermal allergy testing (IDAT) or serum allergen-specific IgE testing for identifying triggers
  • Skin cytology to identify secondary infections
Treatment:
  • Acute flares: corticosteroids (prednisolone), oclacitinib (Apoquel - JAK1 inhibitor), lokivetmab (Cytopoint - anti-IL-31 monoclonal antibody)
  • Long-term: allergen-specific immunotherapy (ASIT) - the only disease-modifying option
  • Skin barrier support: essential fatty acid supplementation, medicated shampoos
  • Treat secondary infections concurrently

2. Flea Allergy Dermatitis (FAD)

Species: Dogs and Cats - the most common skin disease in both Category: Allergic (Type I and Type IV hypersensitivity)
Pathophysiology: An allergic reaction to proteins in flea saliva. A single flea bite in a sensitized animal is enough to trigger intense pruritus. Both immediate (IgE-mediated) and delayed (T-cell-mediated) hypersensitivity components are involved.
Clinical signs:
  • Dogs: Intense pruritus over the dorsal lumbosacral area ("flea triangle"), tail base, caudal thighs, and flanks. Secondary lesions: papules, crusts, alopecia, hot spots (acute moist dermatitis)
  • Cats: Miliary dermatitis (tiny crusted papules all over the body, especially dorsal), symmetric self-induced alopecia (ventral abdomen, inner thighs), eosinophilic granuloma complex lesions
Diagnosis:
  • Clinical distribution + response to flea control
  • Finding fleas or flea dirt (comma-shaped reddish-brown specks) - note: may be absent in highly grooming cats
  • Intradermal test with flea antigen
Treatment:
  • Strict flea control on ALL pets in the household AND environment (premise sprays with IGR)
  • Fast-acting adulticides: afoxolaner (NexGard), fluralaner (Bravecto), sarolaner (Simparica)
  • Anti-pruritic therapy during acute phase (prednisolone, oclacitinib)

3. Canine Pyoderma (Bacterial Skin Infection)

Species: Primarily dogs Category: Infectious (Bacterial)
Pathophysiology: Staphylococcus pseudintermedius (coagulase-positive) is the main pathogen in dogs. It is an opportunistic commensal that invades when skin barrier is disrupted (by atopy, trauma, moisture, immunosuppression). Classified by depth:
  • Surface pyoderma: Skin fold dermatitis, hot spots (acute moist dermatitis), mucocutaneous pyoderma
  • Superficial pyoderma: Impetigo (puppies), superficial bacterial folliculitis (most common)
  • Deep pyoderma: Furunculosis, cellulitis, fistulous tracts
Clinical signs:
  • Superficial: papules, pustules, epidermal collarettes (pathognomonic - circular crusted lesion with peeling edge), alopecia, "moth-eaten" coat
  • Deep: nodules, draining tracts, crusted plaques, pain, fever
Diagnosis:
  • Skin cytology: intracellular cocci within neutrophils (confirms infection vs. colonization)
  • Culture and sensitivity (C&S): essential for recurrent/deep cases and suspected MRSP (methicillin-resistant S. pseudintermedius)
Treatment:
  • Superficial: topical antibiotics/antiseptics (chlorhexidine shampoos, sprays) ± oral antibiotics (amoxicillin-clavulanate, cefalexin) for 3-4 weeks
  • Deep: 6-8+ weeks antibiotics guided by C&S
  • Always investigate and treat the underlying cause

4. Malassezia Dermatitis

Species: Dogs primarily; less common in cats Category: Infectious (Fungal/Yeast)
Pathophysiology: Malassezia pachydermatis is a commensal lipophilic yeast. Overgrowth occurs when skin conditions change (increased moisture, sebum production, disrupted barrier from atopy). It triggers a hypersensitivity reaction in predisposed dogs, amplifying pruritus beyond what the organism numbers alone would explain.
Signalment predisposed breeds: Basset Hounds, West Highland White Terriers, Cocker Spaniels, Shih Tzus, Dachshunds.
Clinical signs:
  • Intense pruritus, greasy/oily skin
  • Characteristic "rancid" or "corn chip" odor
  • Erythema, hyperpigmentation, lichenification (elephant skin appearance in chronic cases)
  • Distribution: skin folds, ventral neck, axillae, groin, interdigital spaces, ears (otitis)
  • Yellow-brown waxy debris in ear canals
Diagnosis:
  • Skin cytology (tape strip or cotton swab - Diff-Quik stain): peanut-shaped or "footprint"-shaped yeast organisms (>2/high-power field is significant)
Treatment:
  • Topical: miconazole/chlorhexidine shampoos (leave-in contact 10 minutes), leave-on mousses
  • Systemic: ketoconazole or itraconazole for 3-4 weeks in widespread/refractory cases
  • Treat underlying disease (usually atopy)

5. Dermatophytosis (Ringworm)

Species: Dogs and Cats - cats are particularly important as reservoir hosts Category: Infectious (Fungal) - ZOONOTIC
Pathophysiology: Microsporum canis (most common in cats and dogs), M. gypseum, and Trichophyton mentagrophytes invade keratinized tissues (stratum corneum, hair shafts, claws). The fungus produces keratinases, causing hair breakage and follicular inflammation.
Clinical signs:
  • Classic: circular patches of alopecia with scale and crusting (hence "ringworm" - no actual worm)
  • Cats: often asymptomatic carriers (especially longhaired cats) or show patchy alopecia on face, ears, and forelimbs. Kerion (inflammatory nodule) in some cases
  • Dogs: more obviously inflamed lesions; generalized form possible in immunocompromised animals
Diagnosis:
  • Wood's lamp: M. canis fluoresces apple-green (only ~50% of strains fluoresce - negative result does not rule out)
  • Direct microscopy (KOH prep or fungal stain): hyphae and arthrospores around hair shafts
  • Fungal culture on DTM (Dermatophyte Test Medium): red color change + colony growth (gold standard, takes 1-3 weeks)
  • PCR: fastest and most sensitive
Treatment:
  • Topical: miconazole/chlorhexidine shampoo (twice weekly) or lime sulfur dips
  • Systemic: itraconazole (drug of choice for cats), terbinafine, or griseofulvin
  • Environmental decontamination: vacuum, disinfect with dilute bleach (1:10), wash bedding
  • Treat until two consecutive negative cultures

6. Canine Demodicosis (Demodex)

Species: Dogs; feline demodicosis is much rarer (Demodex cati, D. gatoi) Category: Parasitic (Mite)
Pathophysiology: Demodex canis is a normal commensal of canine skin, living in hair follicles. Overgrowth occurs when cell-mediated immunity (specifically T-lymphocyte function) is impaired - either due to genetic immunodeficiency (juvenile demodicosis) or acquired immunosuppression (adult-onset demodicosis - always investigate underlying disease: neoplasia, hypothyroidism, immunosuppressive drugs, hyperadrenocorticism).
Classification:
  • Localized: <5 patches, young dogs, 90% self-resolving
  • Generalized: >5 patches OR affects entire body/body region; requires treatment
Clinical signs:
  • NON-PRURITIC (or mildly pruritic) alopecia - key differentiating feature from allergic diseases
  • Erythema, scaling, comedones, follicular casts
  • Deep demodicosis: furunculosis, draining tracts, secondary bacterial infection (very pruritic at this stage), systemic illness
Diagnosis:
  • Deep skin scraping: multiple sites, scrape until capillary bleeding, look for mites under microscopy. Finding ANY mites is significant (except on face/feet where low numbers are normal)
  • Hair pluck/trichogram: useful for paws and face
  • Skin biopsy for refractory cases
Treatment:
  • Localized: often monitor; topical amitraz if treatment desired
  • Generalized: isoxazoline class (afoxolaner, fluralaner, sarolaner) - now first-line, highly effective. Amitraz dips (second-line). Treat until 2 negative scrapings one month apart.
  • Always treat secondary pyoderma and investigate underlying cause in adult-onset cases

7. Sarcoptic Mange (Scabies)

Species: Dogs primarily; rarely cats (Notoedres cati is the feline equivalent) Category: Parasitic (Mite) - ZOONOTIC (causes self-limiting rash in humans)
Pathophysiology: Sarcoptes scabiei var. canis is a highly contagious burrowing mite. Females tunnel into the stratum corneum to lay eggs. The mite and its feces trigger an intense Type I and Type IV hypersensitivity reaction causing extreme pruritus.
Clinical signs:
  • INTENSELY PRURITIC - often described as the "most pruritic disease" in dogs
  • Starts at sparsely haired areas: ear margins, elbows, hocks, and ventral abdomen
  • Erythematous papules, thick yellow/grey crusts
  • Alopecia, excoriations, secondary pyoderma with chronicity
  • Pinnal-pedal reflex: scratching response when ear margin is rubbed - 75-90% sensitive for sarcoptes
Diagnosis:
  • Skin scrapings: mites found in only ~50% of cases (superficial scraping of multiple sites)
  • Serology (ELISA): useful when scrapings negative
  • Diagnosis often made clinically + response to treatment (therapeutic trial)
Treatment:
  • Isoxazolines (afoxolaner, fluralaner, sarolaner) - highly effective, now preferred
  • Selamectin (Revolution) - 2 doses 4 weeks apart
  • Amitraz dips (older protocol)
  • Treat ALL in-contact dogs. Environmental treatment generally unnecessary (mite survives only days off host)

8. Feline Eosinophilic Granuloma Complex (EGC)

Species: Cats Category: Immune-mediated / Allergic reaction pattern
Pathophysiology: EGC is not a single disease but a reaction pattern - an eosinophil-driven response to an underlying trigger (most commonly FAD, food allergy, or atopic skin syndrome). Three distinct clinical presentations exist, all characterized by tissue eosinophilia.
Three forms:
FormAppearanceCommon Location
Indolent ulcer (rodent ulcer)Well-demarcated, raised, ulcerated, brownish lesion. NOT painful, NOT pruriticUpper lip, unilateral
Eosinophilic plaqueRaised, moist, erythematous, well-defined plaques; intensely pruriticVentral abdomen, inner thighs
Eosinophilic granulomaLinear streaks or nodular masses; may affect oral cavity (palate, tongue - cause dysphagia)Caudomedial thigh, oral cavity
Diagnosis:
  • Clinical appearance is often diagnostic
  • Cytology (fine needle aspirate): eosinophils, mast cells, occasionally collagen degeneration
  • Biopsy for confirmation and to rule out neoplasia
  • Identify and test for underlying allergy
Treatment:
  • Treat the underlying trigger (flea control, diet trial, environmental allergy management)
  • Immunosuppressive doses of prednisolone for acute lesions
  • Refractory cases: ciclosporin, chlorambucil, megestrol acetate (last resort)

9. Canine Sebaceous Adenitis (SA)

Species: Dogs (rare in cats) Category: Inflammatory / Immune-mediated
Pathophysiology: An immune-mediated destruction of sebaceous glands. Without sebum, the skin loses its lipid component, leading to progressive hyperkeratosis and follicular plugging. Exact etiology unknown; suspected genetic component.
Signalment predisposed breeds: Standard Poodles, Akitas, Samoyeds, Vizslas, Havanese.
Clinical signs:
  • Two forms based on coat type:
    • Long-coated breeds (Poodle): Tightly adhered silver-white scales along hair shafts (follicular casting), dull/brittle coat, progressive alopecia, musty odor
    • Short-coated breeds (Akita, Vizsla): Circular, moth-eaten alopecia with fine scaling, less follicular casting
Diagnosis:
  • Skin biopsy: absence or destruction of sebaceous glands (nodular granulomatous inflammation around glands in early disease; complete absence in end-stage)
Treatment:
  • Emollient therapy: essential fatty acid supplementation, oil sprays/soaks before bathing (baby oil or coconut oil), antiseborrheic shampoos
  • Immunosuppression: ciclosporin (most effective systemic treatment)
  • Retinoids (isotretinoin, acitretin) in some cases

10. Canine/Feline Pemphigus Foliaceus (PF)

Species: Dogs and Cats - most common autoimmune skin disease in both Category: Autoimmune
Pathophysiology: Autoantibodies (IgG) target desmoglein-1, a desmosomal adhesion protein in the superficial epidermis (stratum granulosum). Loss of keratinocyte adhesion (acantholysis) leads to intraepidermal cleft formation and pustule development just beneath the stratum corneum.
Signalment: Middle-aged dogs; Akitas, Chow Chows, Dobermans, Bearded Collies predisposed. Drug-triggered PF seen with topical flea medications.
Clinical signs:
  • Primary lesions: large, fragile superficial pustules (often already ruptured by the time of examination)
  • Secondary lesions: crusts and erosions - often thick, yellow-honey colored crusts
  • Characteristic distribution: face (nasal planum, periocular), pinnae, and footpads (footpad hyperkeratosis and crusting is a hallmark, especially in cats)
  • May be pruritic or non-pruritic
  • Nasal planum involvement commonly causes loss of normal cobblestone architecture
Diagnosis:
  • Cytology of intact pustule or underside of crust: acantholytic keratinocytes (large, round keratinocytes with central nuclei surrounded by neutrophils) - highly suggestive
  • Skin biopsy: subcorneal pustule with acantholytic keratinocytes (confirmatory)
  • Immunofluorescence or immunohistochemistry to demonstrate autoantibody deposition
Treatment:
  • Immunosuppressive doses of prednisolone (2-4 mg/kg/day) initially
  • Steroid-sparing agents added for long-term control: azathioprine (dogs), chlorambucil (cats - azathioprine is toxic to cats), ciclosporin, mycophenolate mofetil
  • Lifelong treatment usually required; aim for lowest effective immunosuppressive dose

Quick Reference Summary Table

#DiseaseSpeciesKey FeatureDiagnosis Tool
1Atopic DermatitisDog (+Cat)Pruritus - face, ears, feet, groinFavrot criteria + allergy testing
2Flea Allergy DermatitisDog + CatLumbosacral pruritus (dog); miliary dermatitis (cat)Flea dirt + response to flea control
3PyodermaDogEpidermal collarettes, pustulesCytology (intracellular cocci)
4Malassezia DermatitisDogGreasy, smelly, lichenified skinCytology (peanut-shaped yeast)
5DermatophytosisDog + CatCircular alopecia, zoonoticDTM culture / PCR
6DemodicosisDogNON-pruritic alopecia, follicularDeep skin scraping
7Sarcoptic MangeDogINTENSE pruritus, ear margins, zoonoticScraping / therapeutic trial
8Eosinophilic Granuloma ComplexCat3 forms: ulcer, plaque, granulomaCytology / biopsy
9Sebaceous AdenitisDogFollicular casting, destroyed sebaceous glandsBiopsy
10Pemphigus FoliaceusDog + CatCrusts on face + footpads, acantholytic cellsBiopsy

Key exam tip: Always think in three categories when approaching any skin case:
  1. Is this allergic? (atopy, FAD, food allergy) - pruritus is the driver
  2. Is this infectious? (bacteria, yeast, fungus, parasites) - often secondary to allergic disease
  3. Is this immune-mediated or neoplastic? - consider if distribution is atypical or lesions don't respond to standard treatment
Want me to quiz you on any of these, or go deeper on diagnosis and treatment for a specific disease?

I mean explain 10 skin diseases of dogs and cats

It looks like my previous response already covered exactly that - 10 skin diseases of dogs and cats in full detail! Here's a quick recap of what was covered:

The 10 Skin Diseases Already Explained

#DiseaseSpecies
1Atopic DermatitisDogs (+Cats)
2Flea Allergy Dermatitis (FAD)Dogs + Cats
3Canine PyodermaDogs
4Malassezia DermatitisDogs
5Dermatophytosis (Ringworm)Dogs + Cats
6Demodicosis (Demodex mange)Dogs
7Sarcoptic Mange (Scabies)Dogs
8Feline Eosinophilic Granuloma ComplexCats
9Sebaceous AdenitisDogs
10Pemphigus FoliaceusDogs + Cats

Each disease above was explained with:
  • Pathophysiology
  • Signalment (who gets it)
  • Clinical signs
  • Diagnosis
  • Treatment
Scroll up to see the full detailed explanations.

If you meant something different - for example:
  • A different set of 10 skin diseases
  • Diseases explained in a different format (e.g., shorter notes, table only, or focused on one species)
  • A specific category of skin disease (e.g., only parasitic, only fungal, only autoimmune)
Just let me know and I'll tailor it for you!

Act as a world-class veterinary clinician, veterinary , dermatologist pharmacologist, veterinary pathologist, and infectious disease specialist and start a 4 month journy to cover animals diseases and their treatmens. I am a veterinary student and want help specifically with animal diseases, diagnosis, treatment, and medicines. For every disease, provide: Definition and causative agent. Species affected. Epidemiology and transmission. Pathogenesis (step-by-step). Clinical signs. Differential diagnoses. Diagnostic tests and interpretation. Treatment protocols with drug names, drug class, mechanism of action, dosage (when appropriate and safe), route, duration, contraindications, adverse effects, withdrawal periods, and resistance concerns. Prevention, vaccination, biosecurity, and control measures. Prognosis and economic importance. Zoonotic significance (if any). For every medicine, provide: Drug class. Mechanism of action. Spectrum of activity. Indications. Dosage by species (if available). Adverse effects. Contraindications. Drug interactions. Withdrawal period for food-producing animals. Comparison with alternative drugs. Use evidence-based veterinary medicine and reference standard veterinary sources such as the Merck Veterinary Manual, Plumb's Veterinary Drugs, and peer-reviewed literature when possible. Present information in easy language first, then detailed scientific explanation, followed by summary tables, mnemonics, exam points, viva questions, and clinical case scenarios. Correct any misconceptions in my questions and explain the reasoning. Assume I am preparing for veterinary professional examinations and future clinical practice.

Asking for Preferences

Explain 10 skin diseases in tabular form with more focus on differentials

10 Skin Diseases of Dogs & Cats — Tabular Format with Differential Focus


MASTER COMPARISON TABLE — All 10 Diseases at a Glance

#DiseaseSpeciesPrimary LesionDistributionPruritus LevelKey Differentiating Feature
1Atopic DermatitisDog > CatErythema, alopeciaFace, ears, feet, axillae, groin+++++Seasonal onset, young dog, responds to steroids
2Flea Allergy DermatitisDog + CatPapules, crustsLumbosacral, tail base (dog); miliary (cat)+++++Flea dirt present, dramatic response to flea control
3Superficial PyodermaDogPustules, epidermal collarettesTrunk, groin++Collarettes pathognomonic; intracellular cocci on cytology
4Malassezia DermatitisDog > CatGreasy scale, lichenificationSkin folds, ventral, ears++++Rancid odor, yeast on cytology, responds to antifungals
5DermatophytosisDog + CatCircular alopecia, scaleFace, ears, limbs+ (usually)Positive DTM culture; zoonotic
6DemodicosisDogFollicular alopecia, scalePeriocular, muzzle, feet → generalized+ (unless deep)NON-pruritic alopecia; mites on deep scraping
7Sarcoptic MangeDogPapules, thick crustsEar margins, elbows, hocks+++++Pinnal-pedal reflex; zoonotic
8Pemphigus FoliaceusDog + CatPustules → crustsFace, nasal planum, footpads, pinnae+/++Acantholytic cells on cytology; footpad involvement
9Eosinophilic Granuloma ComplexCatUlcer / plaque / noduleUpper lip, abdomen, thighs++ (plaque)Eosinophils on cytology; 3 distinct clinical forms
10Sebaceous AdenitisDogFollicular casts, alopeciaDorsum, face, ears+Silver-white follicular casts; absent sebaceous glands on biopsy

DIFFERENTIAL DIAGNOSIS FOCUS — By Presenting Complaint


🔴 COMPLAINT 1: Intense Pruritus

FeatureAtopic DermatitisFlea Allergy DermatitisSarcoptic MangeMalassezia Dermatitis
OnsetGradual, seasonal → year-roundYear-round (worse summer/fall)Acute, rapid spreadGradual
AgeYoung (1-3 yrs)Any ageAny ageAny age
DistributionFeet, face, ears, axillae, groinLumbosacral, tail baseEar margins, elbows, hocks, ventralSkin folds, ventral, ears
Primary lesionsErythema, papulesPapules, crustsPapules, thick crustsGreasy scale, erythema
Flea dirtAbsentPresentAbsentAbsent
Pinnal-pedal reflexNegativeNegativePositive (75-90%)Negative
Skin scrapingNegativeNegativeMay find mites (50%)Negative
CytologyBacteria/yeast (secondary)Bacteria (secondary)NegativePeanut-shaped yeast
Response to steroidsGoodPartialNonePartial
Response to flea controlNoneDramaticNoneNone
Contagious?NoNoYES (to humans)No
Key distinguishing testAllergy testing (IDAT/serology)Therapeutic flea control trialScabicidal therapeutic trialCytology + antifungal response

🟠 COMPLAINT 2: Alopecia (Hair Loss)

FeatureDemodicosisDermatophytosisSuperficial PyodermaSebaceous AdenitisHypothyroidism*
PruritusNone to mildNone to mildMild-moderateMildNone
AgeYoung (<18 mo) or oldAny (young more common)AnyMiddle-agedMiddle-aged/old
Lesion typeFollicular alopecia, scaling, comedonesCircular patches, broken hairsCollarettes, pustulesFollicular casts, dull coatBilat. symmetrical alopecia
DistributionPeriocular, muzzle → generalizedFace, ears, limbsTrunk, groinDorsum, faceTrunk, tail ("rat tail")
Coat textureDull, scalyBroken stubsMoth-eatenDull, brittleDry, brittle
Scale characterFine, greyWhite, powderyYellow crusts (collarettes)Silver-white follicular castsDiffuse fine scale
InflammationMild early; severe if deepMildModerateMildNone
DiagnosisDeep skin scrapingDTM culture / PCRCytologySkin biopsyThyroid panel (T4, TSH)
Zoonotic?NoYESNoNoNo
Key featureMites in hair folliclesArthrospores on hair shaftIntracellular cocciAbsent sebaceous glandsConcurrent systemic signs
*Hypothyroidism included as important DDx for alopecia

🟡 COMPLAINT 3: Pustules and Crusts

FeatureSuperficial PyodermaPemphigus FoliaceusDermatophytosisDemodicosis (deep)
PathogenesisBacterial infectionAutoimmune (anti-desmoglein IgG)Fungal invasionMite-induced folliculitis
Pustule depthSubcorneal-superficialSubcorneal (very superficial)FollicularDeep follicular/furunculosis
Crust colorYellow-honeyYellow-honeyWhite-greyHaemorrhagic/brown
DistributionTrunk, groin, chinFace, nasal planum, footpads, pinnaeFace, ears, limbsFace, feet → generalized
Footpad lesionsRareCommon (hyperkeratosis + crusts)RareRare
Nasal involvementRareCommon (loss of cobblestone pattern)OccasionalRare
CytologyIntracellular cocci + neutrophilsAcantholytic keratinocytes + neutrophilsHyphae/arthrosporesMites, eggs
Response to antibioticsExcellentNone (worsens if only antibiotics given)NoneAntiparasitic needed
Response to steroidsWorsens (immunosuppression)Good (required)Worsens significantlyWorsens
Gold standard DxCulture & sensitivitySkin biopsy + immunohistochemistryDTM culture / biopsyDeep skin scraping
Exam trapPF pustules look exactly like pyoderma — ALWAYS do cytologyAcantholytic cells are keyWood's lamp negative in 50%Scraping negative doesn't rule out

🟢 COMPLAINT 4: Facial + Nasal Planum Lesions (Crucial for Differentials)

FeaturePemphigus FoliaceusDiscoid Lupus Erythematosus (DLE)Zinc-Responsive DermatosisNasal PyodermaDermatophytosis
Nasal planumCrusted, loss of cobblestone textureDepigmentation, erosion, cobblestone LOSTCrusting, hyperkeratosisPustules, crustsScaling, crusting
Facial skinPeriocular, pinnae crustsPeriocular, nasal bridgeAround eyes/mouthMuzzle foldPatchy alopecia
FootpadsYES - hyperkeratotic crustsRareYES - fissured, hyperkeratoticNoRare
PhotosensitivityMildYES - worsens in sunlightNoNoNo
DepigmentationSometimesClassic signNoNoNo
CytologyAcantholytic cellsNon-specific inflammationParakeratosisCocci/neutrophilsHyphae/spores
Biopsy patternSubcorneal pustule, acantholysisHydropic interface dermatitisDiffuse parakeratosisSuppurative folliculitisFungal elements in follicle
ANA testNegativeSometimes positive (low titer)NegativeNegativeNegative
TreatmentImmunosuppressionTopical tacrolimus/steroids, sun avoidanceZinc supplementationAntibioticsAntifungals

🔵 COMPLAINT 5: Cat-Specific Skin Presentations

FeatureFlea Allergy DermatitisFeline Atopic Skin SyndromeFood AllergyEosinophilic PlaquePemphigus Foliaceus
PatternMiliary dermatitis, self-induced alopeciaSelf-induced alopecia, head/neck pruritusAny of the above patternsRaised moist plaquesCrusts, face/footpads
Pruritus++++++++++++++++/++
DistributionDorsum, caudal bodyHead, neck, ventral abdomenNon-seasonal, any siteVentral abdomen, inner thighsNasal planum, pinnae, footpads
Lesion typeCrusted papules (miliary)Alopecia, excoriationsVariableRaised, erythematous, moistThick yellow crusts
Flea dirtPresentAbsentAbsentAbsentAbsent
SeasonalityYear-round (worse summer)Seasonal or year-roundYear-roundDepends on triggerYear-round
Diet trial responseNoneNoneExcellent (8-12 wks)If food is trigger: yesNone
CytologyEosinophils/bacteriaEosinophils/bacteriaVariableEosinophils (predominant)Acantholytic cells
Key diagnostic stepFlea control trialAllergy testing after exclusionsStrict hydrolyzed/novel protein diet trialCytology + rule out triggersSkin biopsy

DIFFERENTIAL DIAGNOSIS DECISION TREE

PRURITIC SKIN DISEASE?
│
├── YES ──► Is distribution LUMBOSACRAL / TAIL BASE?
│           ├── YES + flea dirt ──► FLEA ALLERGY DERMATITIS
│           └── NO ──► Is distribution FEET/FACE/EARS/GROIN?
│                       ├── YES ──► ATOPIC DERMATITIS (rule out FAD + food allergy first)
│                       └── EAR MARGINS + ELBOWS + HOCKS?
│                           └── YES + pinnal-pedal reflex ──► SARCOPTIC MANGE
│
└── NON-PRURITIC (or mild) ALOPECIA?
    ├── Deep skin scraping POSITIVE ──► DEMODICOSIS
    ├── DTM culture POSITIVE ──► DERMATOPHYTOSIS
    ├── Silver follicular casts + Poodle/Akita ──► SEBACEOUS ADENITIS
    └── Systemic signs (obesity, bradycardia) ──► HYPOTHYROIDISM / HYPERADRENOCORTICISM

PUSTULES + CRUSTS?
├── Cytology: intracellular cocci ──► PYODERMA
├── Cytology: acantholytic cells ──► PEMPHIGUS FOLIACEUS
├── Footpad + nasal planum + pinnae ──► PEMPHIGUS FOLIACEUS (first choice)
└── Culture: dermatophyte ──► DERMATOPHYTOSIS

CAT with EOSINOPHILIC LESION?
├── Upper lip ulcer ──► INDOLENT ULCER (EGC)
├── Moist raised plaque on abdomen ──► EOSINOPHILIC PLAQUE (EGC)
└── Linear thigh lesion / oral nodule ──► EOSINOPHILIC GRANULOMA (EGC)
    └── In all 3 ──► FIND THE TRIGGER (FAD > food allergy > atopy)

KEY EXAM MNEMONICS

"SAD MAP FDP" - remember all 10 diseases:
  • Sarcoptic mange
  • Atopic dermatitis
  • Demodicosis
  • Malassezia dermatitis
  • Autoimmmune (Pemphigus Foliaceus)
  • Pyoderma
  • Flea Allergy Dermatitis
  • Dermatophytosis
  • Pemphigus... (EGC for cats)
  • Sebaceous adenitis

"ITCH SCALE" - Pruritus ranking (highest to lowest):
Sarcoptes > FAD = Atopy > Malassezia > Pyoderma > Pemphigus > EGC > Dermatophytosis = Demodicosis > Sebaceous Adenitis

CRITICAL EXAM TRAPS & MISCONCEPTIONS

TrapCorrect Answer
"Demodicosis is always pruritic"FALSE - it is NON-pruritic unless deep/secondary pyoderma develops
"Negative Wood's lamp rules out ringworm"FALSE - only ~50% of M. canis strains fluoresce
"Pemphigus and pyoderma look different"FALSE - both produce superficial pustules; CYTOLOGY is the differentiator
"Sarcoptes mites are always found on scraping"FALSE - found in only ~50% of cases; treat empirically
"FAD requires many fleas to cause signs"FALSE - ONE flea bite causes reaction in sensitized animals
"Sebaceous adenitis is caused by infection"FALSE - it is immune-mediated destruction of sebaceous glands
"Treat EGC with steroids alone"INCOMPLETE - must identify and eliminate underlying trigger
"Azathioprine is safe in cats"FALSE - cats lack thiopurine methyltransferase; causes fatal bone marrow suppression

TOP VIVA QUESTIONS

  1. How do you differentiate superficial pyoderma from pemphigus foliaceus on cytology?
  2. What is the pinnal-pedal reflex and which disease is it associated with?
  3. Why must you investigate for underlying disease in adult-onset demodicosis?
  4. Name the three forms of eosinophilic granuloma complex in cats and their locations.
  5. Why can treating feline hyperthyroidism unmask renal disease? (bonus systemic question)
  6. What is the gold standard for diagnosing sebaceous adenitis?
  7. Which immunosuppressive drug is contraindicated in cats and why?
  8. Name two zoonotic skin diseases of dogs and their causative agents.
  9. What does a positive Rivalta's test indicate in a cat with ascites? (links to FIP)
  10. What is the mechanism of action of oclacitinib (Apoquel)?

Ready to go deeper on any of these diseases, or shall we begin the 4-month structured journey starting with Disease #1 in full clinical detail?

Most of your focus should be on clinical signs and their differntials

10 Skin Diseases — Clinical Signs & Differentials (Deep Focus)


PART 1: CLINICAL SIGNS IN DETAIL — Disease by Disease


DISEASE 1: Atopic Dermatitis (AD)

Clinical Signs — Easy Language First

The dog licks its paws, rubs its face on the carpet, and scratches its ears constantly. The skin looks red and irritated in the armpits, groin, belly, and between the toes. Over time the skin becomes thick, dark, and leathery from all the scratching.

Clinical Signs — Scientific Detail

Primary signs (directly from the disease):
SignDescriptionWhy it happens
PruritusIntense, often the ONLY early signIL-31 release from Th2 cells activates itch neurons
ErythemaRedness at predilection sitesVasodilation from mast cell mediators
PapulesSmall red bumpsEarly inflammatory infiltrate
Self-traumaExcoriations, alopecia from licking/scratchingResponse to itch
Secondary signs (from chronicity + infection):
SignDescriptionSignificance
LichenificationThick, elephant-like skinChronic rubbing/trauma
HyperpigmentationDarkening of skinMelanocyte stimulation from chronic inflammation
AlopeciaHair loss at affected sitesSelf-trauma + follicular damage
SeborrheaGreasy or flaky skinAltered skin barrier lipids
Otitis externaWaxy brown discharge, head shakingSecondary Malassezia + bacterial overgrowth
PyodermaPustules, collarettesSecondary Staph. pseudintermedius
PododermatitisInterdigital redness, "rust-brown staining" of pawsChronic licking (porphyrin staining)
Predilection sites (MUST memorize):
FACE:     Periocular (raccoon eyes), perioral, chin
EARS:     Pinnae, ear canal (otitis externa)
FEET:     Interdigital spaces, paw pads, dorsum of paws
BODY:     Axillae, groin, ventral abdomen, perineum
Chronological progression:
Early: Seasonal pruritus, mild erythema, face/feet
↓
Intermediate: Year-round, otitis, pododermatitis, secondary infections
↓
Chronic: Lichenification, hyperpigmentation, permanent skin changes

DISEASE 2: Flea Allergy Dermatitis (FAD)

Clinical Signs — Easy Language First

The dog scratches violently at its back end - the area just in front of the tail - and bites at the base of the tail. You may notice tiny black specks (flea dirt) in the coat. In cats, you see tiny crusted bumps all over the body, and the cat may pull out fur from the belly.

Clinical Signs — Scientific Detail

In DOGS:
SignLocationDescription
PruritusLumbosacral area, tail base, caudal thighs, flanksMost intense at tail base - "flea triangle"
PapulesDorsal trunk, tail baseSmall, erythematous, topped with crust
AlopeciaLumbosacral, tail baseSelf-trauma
Hot spots (acute moist dermatitis)Anywhere, often rump/cheekRapidly expanding moist, painful erosion
Secondary pyodermaAnywhereFrom self-trauma + bacterial colonization
HyperpigmentationLumbosacralChronic cases
In CATS — 4 reaction patterns:
PatternDescriptionLocation
Miliary dermatitisHundreds of tiny crusted papules ("millet seeds")Dorsum, neck, base of tail
Self-induced alopeciaSymmetric hair loss from over-groomingVentral abdomen, inner thighs, flanks
Eosinophilic granuloma complexUlcer / plaque / granulomaUpper lip, abdomen, thighs
Head & neck pruritusExcoriations around face/neckHead, neck, pinnae
Critical clinical clue:
Finding flea dirt (reddish-brown comma-shaped specks that turn red on wet cotton) confirms flea exposure. BUT in cats that over-groom, fleas may be completely absent despite active infestation.

DISEASE 3: Superficial Pyoderma (Bacterial Skin Infection)

Clinical Signs — Easy Language First

You see ring-shaped crusty patches on the belly and trunk — like circular peeling patches with a red ring around them. The dog may scratch but not intensely. Sometimes you see actual pus-filled bumps. The coat looks "moth-eaten" with patchy hair loss.

Clinical Signs — Scientific Detail

Primary lesions:
LesionDescriptionSignificance
PustulePus-filled raised lesion within or around a hair follicleEarly lesion; fragile, easily ruptured
PapuleSmall red elevated lesionVery early, pre-pustular
Secondary/evolving lesions (what you usually find):
LesionDescriptionSignificance
Epidermal collarettePATHOGNOMONIC - circular peeling ring of stratum corneumRemnant of ruptured pustule; virtually diagnostic
CrustsDried exudateRuptured pustule/papule
Alopecia"Moth-eaten" patchy hair lossFollicular damage
Erythematous macules/patchesRed spots/patchesSuperficial inflammation
Target lesionsBull's-eye patternExpanding collarette
Distribution by pyoderma type:
TypeLocationKey lesion
Impetigo (puppies)Glabrous skin - groin, axillaePustules, no follicular involvement
Superficial folliculitisTrunk, dorsum, pressure pointsCollarettes, papules
Mucocutaneous pyodermaLips, periocular, nares, vulvaErosions, depigmentation
Skin fold pyodermaFacial/lip/body/vulvar/tail foldsErosion, maceration, odor

DISEASE 4: Malassezia Dermatitis

Clinical Signs — Easy Language First

The dog has extremely smelly skin — like rancid cheese or corn chips. The skin is greasy and dark, especially in the ear canals, armpits, groin, and neck folds. The dog scratches intensely. The more it scratches, the darker and thicker the skin gets.

Clinical Signs — Scientific Detail

The 5 cardinal signs of Malassezia dermatitis:
#SignDescription
1PruritusIntense; disproportionate to lesion severity
2ErythemaDiffuse redness at predilection sites
3Greasy/oily seborrheaYellow-brown waxy scale or greasy film
4Rancid odorDistinctive "musty/yeasty/corn chip" smell
5Lichenification + hyperpigmentationElephant-skin appearance in chronic cases
Predilection sites:
Ventral neck → Axillae → Groin → Perineum
Ear canals (brown waxy debris)
Interdigital spaces
Lip folds, facial folds
Ventral tail
Progression:
Acute: Erythema + mild scale + mild pruritus
↓
Subacute: Greasy scale + moderate pruritus + early lichenification
↓
Chronic: Severe lichenification + hyperpigmentation + alopecia (elephant skin)
In CATS: Less common; associated with paraneoplastic syndrome (thymoma, pancreatic carcinoma) or FIV; presents with generalized exfoliative dermatitis.

DISEASE 5: Dermatophytosis (Ringworm)

Clinical Signs — Easy Language First

You see round bald patches, especially on the face, ears, and legs. The patch has broken stubby hairs at the edges and a scaly center. It looks like a ring — red at the edges, clearing in the middle in some cases. Cats often carry the fungus without any symptoms at all.

Clinical Signs — Scientific Detail

Classic lesion characteristics:
FeatureDescription
ShapeCircular/oval patch — the "ring"
AlopeciaBroken hair stubs at periphery (not pulled out)
ScaleGrey-white, powdery scale within the patch
ErythemaMild to moderate at the edge
CrustingPresent in inflamed cases
PruritusMild or absent (key differentiator from allergic disease)
Clinical presentations by species:
Dogs:
FormDescription
ClassicCircular alopecia with scale on face, trunk, limbs
KerionRaised, boggy, nodular inflammatory lesion; painful; usually single
OnychomycosisBrittle, deformed claws; very refractory
GeneralizedImmunocompromised dogs; widespread lesions
Cats:
FormDescription
Asymptomatic carrierMost common in longhaired cats — NO visible lesions but culture positive
Focal alopeciaFace, ears, forelimbs; classic presentation
Miliary lesionsCrusted papules (mimics FAD)
PseudomycetomaDeep nodular; Persian cats; rare

DISEASE 6: Demodicosis

Clinical Signs — Easy Language First

The dog loses hair in patches, especially around the eyes, muzzle, and front legs. The skin looks scaly and red but the dog barely scratches — this is the big clue. In severe cases the skin becomes infected, swollen, and painful.

Clinical Signs — Scientific Detail

LOCALIZED demodicosis:
SignDescription
Focal alopecia1-5 discrete patches, <2.5 cm each
Scale/comedonesFollicular plugging, grey scale
ErythemaMild
SitesPeriocular (spectacle sign), muzzle, forelimbs
PruritusABSENT to minimal
GENERALIZED demodicosis:
SignDescription
Widespread alopeciaMultifocal → confluent hair loss
Follicular castsWaxy debris around hair follicles
ComedonesDilated follicles with dark plugs
HyperpigmentationChronic cases
Secondary pyodermaAdds pruritus, pain, odor
Deep furunculosisNodules, draining tracts, hemorrhagic crust
PododermatitisSevere interdigital swelling and pain — most refractory form
LymphadenopathyGeneralized cases with secondary infection
Systemic illnessFever, lethargy in severe deep demodicosis
KEY CLINICAL RULE:
If demodicosis is generalized AND the dog is >4 years old at first presentation → ALWAYS investigate for underlying immunosuppressive disease (hyperadrenocorticism, hypothyroidism, neoplasia, long-term steroid use, diabetes mellitus)

DISEASE 7: Sarcoptic Mange

Clinical Signs — Easy Language First

The dog is scratching so violently it cannot sleep. The ear edges are crusty and thickened. The elbows and hocks have thick greyish crusts. The dog loses hair in those areas. The owner may also have a rash on their arms (zoonosis).

Clinical Signs — Scientific Detail

Chronological progression of signs:
WEEK 1-2:   Intense pruritus, erythematous papules on ear margins and elbows
↓
WEEK 3-4:   Crusting of ear margins (pathognomonic), excoriations, alopecia
↓
WEEK 5-8:   Spreads to hocks, ventral chest, lateral elbows, face
↓
CHRONIC:    Thick grey/yellow crusts, widespread alopecia, lichenification,
            lymphadenopathy, emaciation in neglected cases
Primary and secondary signs:
SignLocationClinical importance
Pruritic papulesEar margins, elbows, hocks, ventral abdomenFirst signs
Thick yellow-grey crustsEar margins, pressure pointsHighly characteristic
AlopeciaEar margins → generalizedSelf-trauma
ExcoriationsWidespreadScratch marks
Pinnal-pedal reflexElicited by rubbing ear margin → dog scratches with hindleg75-90% sensitive; pathognomonic behavior
Secondary pyodermaAny siteBacterial complication
LymphadenopathyGeneralizedReactive from inflammation
EmaciationGeneralizedChronic neglected cases

DISEASE 8: Pemphigus Foliaceus (PF)

Clinical Signs — Easy Language First

The dog or cat develops pus-filled blisters, especially on the face and nose, that quickly burst and leave thick yellow crusty patches. The nose loses its normal bumpy texture. The footpads become thick and crusty. Unlike a bacterial infection, antibiotics don't help.

Clinical Signs — Scientific Detail

Primary lesion (rarely seen — very fragile):
LesionDescription
PustuleLarge, superficial, flaccid (easily ruptured)
LocationFace, nasal planum, pinnae, footpads
Secondary lesions (what you actually find on exam):
LesionDescriptionSignificance
CrustsThick, yellow-honey coloredRuptured pustule remnant
ErosionsShallow ulcerationsPost-pustular
AlopeciaAt crusted sitesSecondary
ScaleFine to thickEpidermal disruption
HALLMARK DISTRIBUTION — The "PF Triangle":
Nasal planum ──────► Loss of normal cobblestone texture (PATHOGNOMONIC)
Pinnae (ear flap) ──► Thick crusting on inner pinna surface
Periocular ─────────► Crusted patches around eyes
Footpads ───────────► Hyperkeratosis + crusting (especially in CATS)
Additional signs:
SignDescription
Nikolsky signGentle pressure slides superficial epidermis — positive in active disease
PruritusVariable - mild to moderate (unlike pyoderma which is mild)
Nasal depigmentationSecondary; may mimic DLE
Systemic signsFever, lethargy, anorexia in severe/generalized cases
LymphadenopathyIn active generalized disease
Cats specifically: Footpad crusting is extremely prominent and may be the presenting complaint.

DISEASE 9: Feline Eosinophilic Granuloma Complex (EGC)

Clinical Signs — Easy Language First

EGC is not one disease but THREE different-looking skin reactions in cats, all caused by the same allergy problem underneath. Think of them as three different "faces" of the same condition.

Clinical Signs — Three Forms in Detail:

FORM 1: Indolent Ulcer (Rodent Ulcer)
FeatureDescription
AppearanceWell-demarcated, raised, shiny, ulcerated lesion; brownish-red center
SurfaceSmooth, glistening, NOT painful, NOT pruritic
LocationUpper lip (unilateral or bilateral) - virtually always
SizeFew mm to several cm
Feel on palpationFirm, indurated edges
Cat's behaviorNormal - not bothered by it (absence of pain/itch is striking)
Danger signCan become large and disfiguring; rare malignant transformation reported
FORM 2: Eosinophilic Plaque
FeatureDescription
AppearanceRaised, well-demarcated, moist, erythematous, erosive plaques
SurfaceGlistening, oozing, may be ulcerated
LocationVentral abdomen, inner thighs, axillae
PruritusINTENSE (+++++) — most pruritic of the three forms
Cat's behaviorConstant licking at the site
Size1-5 cm; may coalesce
FORM 3: Eosinophilic Granuloma (Collagenolytic Granuloma)
FeatureDescription
Appearance on skinLinear streak of yellowish-pink raised tissue ("linear granuloma")
Appearance in mouthNodular masses on palate, tongue — may cause dysphagia
Appearance on chin"Fat chin" or "pouty lip" — swollen, thickened
Location on bodyCaudomedial thigh (linear streak), face, oral cavity, paw pads
PruritusMild
TextureFirm, nodular, well-defined
Cat's behaviorMay paw at mouth if oral involvement

DISEASE 10: Sebaceous Adenitis (SA)

Clinical Signs — Easy Language First

The dog's coat loses its shine and develops tightly stuck white scales along each hair shaft. The coat feels dry and brittle. Areas of hair loss appear on the top of the head, face, and back. There is a musty, unpleasant smell. The dog doesn't scratch much.

Clinical Signs — Scientific Detail

Two forms based on coat type:
LONG-COATED BREEDS (Standard Poodle, Akita, Samoyed):
SignDescription
Follicular castingSilver-white scales tightly adherent to hair shafts — PATHOGNOMONIC
AlopeciaProgressive; starts on dorsal planum of nose, top of head, pinnae, dorsum
Coat textureDull, brittle, dry - loss of normal sheen
OdorMusty, unpleasant (secondary infection)
ScaleWhite-silver, diffuse
Secondary pyodermaBacterial folliculitis due to absent sebum defense
PruritusAbsent or mild (unless secondary infection)
SHORT-COATED BREEDS (Vizsla, Dachshund):
SignDescription
AlopeciaCircular, moth-eaten pattern
ScaleFine, diffuse, less conspicuous than in long-coated
ErythemaMild
Follicular castingLess prominent
PruritusMild

PART 2: MASTER DIFFERENTIAL DIAGNOSIS TABLES


TABLE A: Differentiating by PRURITUS LEVEL

Pruritus LevelDiseaseKey Clinical Clue
+++++ EXTREMESarcoptic MangeEar margin crusts + pinnal-pedal reflex
+++++ EXTREMEFlea Allergy DermatitisLumbosacral distribution + flea dirt
+++++ EXTREMEEosinophilic Plaque (EGC)Cat + raised moist abdominal plaque
++++ SEVEREAtopic DermatitisFace/feet/ears/groin distribution
++++ SEVEREMalassezia DermatitisRancid smell + greasy skin + yeast on cytology
+++ MODERATEPyodermaEpidermal collarettes + intracellular cocci
++ MILD-MODPemphigus FoliaceusFacial/footpad crusts + acantholytic cells
+ MILDDermatophytosisCircular alopecia + DTM positive
+ MINIMALDemodicosisNON-pruritic alopecia + mites on scraping
+ MINIMALSebaceous AdenitisFollicular casts + absent sebaceous glands

TABLE B: Differentiating by LESION TYPE

Primary LesionDiseaseDistinguishing Detail
PustulePyodermaFollicular; intracellular cocci
PustulePemphigus FoliaceusSubcorneal; acantholytic cells
PapuleFAD / AtopyErythematous; at predilection sites
PapuleSarcoptic mangeEar margins, elbows
CollarettePyodermaPATHOGNOMONIC for pyoderma
UlcerEGC - Indolent ulcerUpper lip; NOT painful
PlaqueEGC - Eosinophilic plaqueMoist; ventral abdomen; intensely pruritic
Nodule/linearEGC - GranulomaThigh; oral cavity
Follicular castsSebaceous adenitisSilver-white; adherent to shaft
Circular alopeciaDermatophytosisBroken hair stubs; scale
Diffuse alopeciaDemodicosisNon-pruritic; periocular start
LichenificationAtopy / MalasseziaChronic rubbing; skin fold sites
CrustsPemphigus / Sarcoptes / FADSee distribution to differentiate

TABLE C: Differentiating by DISTRIBUTION

Body SiteFirst Think OfAlso Consider
Ear margins (pinnae edges)Sarcoptic mangeVasculitis, fly strike
Lumbosacral / tail baseFlea Allergy DermatitisAtopy (rarely), contact allergy
Face + nasal planum + footpadsPemphigus foliaceusDLE, zinc deficiency
Periocular + muzzle (young dog)DemodicosisAtopy, ringworm
Face + ears + feet + groinAtopic DermatitisFood allergy
Skin folds + ventral + ear canalMalassezia dermatitisPyoderma, atopy
Trunk (collarettes)PyodermaDermatophytosis, pemphigus
Upper lip (cat)Indolent ulcer (EGC)SCC, trauma
Ventral abdomen (cat)Eosinophilic plaque (EGC)FAD, food allergy
Caudomedial thigh (cat)Eosinophilic granulomaFA, food allergy
Dorsum + follicular castsSebaceous adenitisHypothyroidism

TABLE D: THE MOST CRITICAL DIFFERENTIALS — Pyoderma vs PF vs Demodicosis

(These three are the most commonly confused in exams and clinics)
FeaturePyodermaPemphigus FoliaceusDemodicosis
CauseStaph. pseudintermediusAutoantibody vs desmoglein-1Demodex canis mite
Pustule depthIntrafollicular / subcornealSubcorneal (very superficial)Deep follicular
PruritusMild-moderateMild-moderateNONE (unless secondary pyoderma)
Footpad lesionsRareCommon + hyperkeratosisUncommon
Nasal planumRareCommon (loss of cobblestone)Rare
Systemic signsAbsentFever/lethargy in severe casesAbsent (unless deep infection)
CytologyIntracellular cocci in neutrophilsAcantholytic keratinocytesMites, eggs, larvae
Responds to antibioticsYESNONO
Responds to immunosuppressionWORSENSYESWORSENS
Gold standard testCulture + sensitivitySkin biopsyDeep skin scraping
Exam trapNever treat without cytologyPF looks identical to pyoderma grosslySuperficial scraping is inadequate

TABLE E: CYTOLOGY — The Most Powerful In-Clinic Differentiator

Cytology FindingDiagnosis
Intracellular cocci within neutrophilsBacterial pyoderma (Staph. spp.)
Peanut/footprint-shaped budding yeastMalassezia dermatitis
Acantholytic keratinocytes + neutrophilsPemphigus foliaceus
Mites, eggs, larvae (adult = 4 pairs legs)Demodicosis
Eosinophils predominantEGC / Allergic reaction / Parasites
Hyphae + arthrospores around hair shaftDermatophytosis
Degenerate neutrophils + rodsDeep infection / gram-negative
No organisms + mild inflammationAllergic/sterile

TABLE F: ZOONOTIC RISK SUMMARY

DiseaseZoonotic?Human SignsPrecautions
Sarcoptic MangeYESIntensely pruritic papular rash on forearms, trunk; self-limitingGloves, treat pet promptly
DermatophytosisYESCircular red scaly itchy rings on skin; nail infectionGloves, decontaminate environment
DemodicosisNONot zoonotic (D. canis is host-specific)None
PyodermaVery low riskMRSP theoretical risk in immunocompromisedHygiene
All othersNOStandard hygiene

CLINICAL CASE SCENARIOS FOR EXAM PRACTICE


CASE 1:
A 2-year-old male Golden Retriever presents with redness and hair loss between all four paws, red ears with dark waxy discharge, and a rancid odor. The pruritus is scored 8/10. He was diagnosed with "ear infection" twice in the past year. His littermate has similar signs.
What is the most likely diagnosis and differentials?
  • Primary: Atopic Dermatitis with secondary Malassezia otitis/pododermatitis
  • DDx: Food allergy (identical presentation), FAD (check for flea dirt)
  • Next step: Rule out FAD (flea control trial 3 months) → Rule out food allergy (diet trial 8-12 weeks) → If eliminated, diagnose atopy and pursue allergy testing

CASE 2:
A 7-year-old intact female Akita presents with circular patches of hair loss on the dorsal neck and top of head. White scales are tightly stuck to the hair shafts. The dog is not pruritic. The owner says the coat has been getting dull for the past 2 years.
What is the most likely diagnosis and differentials?
  • Primary: Sebaceous adenitis
  • DDx: Hypothyroidism (check T4), demodicosis (skin scraping), dermatophytosis (DTM culture)
  • Gold standard: Skin biopsy showing absent/destroyed sebaceous glands

CASE 3:
A 5-year-old DSH cat presents with a painless, shiny ulcer on the upper right lip that has been present for 3 months. The cat eats normally and is not distressed. You find no fleas. The owner has two other cats with no skin problems.
What is the most likely diagnosis and differentials?
  • Primary: Indolent ulcer (EGC)
  • DDx: Squamous cell carcinoma (older cats, sun-exposed), trauma, eosinophilic plaque (but that is pruritic and on abdomen)
  • Next step: Cytology/biopsy → identify underlying trigger (start with strict flea control even if no fleas seen, then food trial)

VIVA QUESTIONS — Clinical Signs Focus
  1. What is the "pinnal-pedal reflex" and what does a positive result suggest?
  2. Name three skin diseases where footpad lesions are a prominent feature.
  3. What is the difference in pruritus level between demodicosis and sarcoptic mange and why?
  4. A cat presents with symmetric hair loss on the ventral abdomen. Name 4 differentials.
  5. What does an epidermal collarette represent histologically?
  6. How do you distinguish between indolent ulcer and squamous cell carcinoma in a cat?
  7. Why does Malassezia dermatitis cause disproportionate pruritus relative to the organism numbers?
  8. Name the three forms of EGC and their classic locations.
  9. What clinical sign in pemphigus foliaceus differentiates it from discoid lupus erythematosus?
  10. A dog presents with non-pruritic alopecia periocularly. What is your #1 differential and what test confirms it?

Would you like to go deeper on a specific disease from this list, or shall we move on to the next group of diseases in our 4-month journey?
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