Skeletal muscles and skin Flashcards
You are called out to a farm to investigate a sad scene. 30% of 2 month old lambs are in a mob of 40. They are lying on their chest and rolling on to their sides. You see that they are weak and stiff, and they eventually die within a few days. What can we do to figure out what the pathological process was that resulted in these signs?
Necropsy on an acutely diseased lamb
You are called out to a farm to investigate a sad scene. 30% of 2 month old lambs are in a mob of 40. They are lying on their chest and rolling on to their sides. You see that they are weak and stiff, and they eventually die within a few days. Upon necropsy and skinning, you notice that the muscles are pale, dry, and firm. What pathological processes could account for this appearance?
- Degeneration/necrosis
- Inflammation and repair
- Circulatory disorder
- Disorder of growth
- Pigments and deposits
- Degeneration/necrosis
(2nd img: not as severe; streaks of white)
What are the etiologies of these pathologic changes (A, B, C, and D) resulting in pale skeletal muscle?
A: pale streaks, necrosis and mineralization, degenerative myopathy, canine X-linked muscular dystrophy, diaphragmn (left side), dog
B: localized pallor, necrosis, injection site of an irritant substance, semitendinosus muscle, cow. This irritant was injected just under they perimysium and caused necrosis and disruption of the myofibers. Some irritant seeped down between the fascicles to cause necrosis, but the fascicles of myofibers are still in place
C: overall pale muscle with pale streaks from collagen and fat infiltration, denervation atrophy, equine motor neuron disease, horse. Equine motor neuron disease muscle (right) compared with normal muscle (left)
D: enlargement and pallor, steatosis, longissimus muscles, neonatal calf. The majority of the muscles have been replaced by fat
What are the 4 main etiologies that makes skeletal muscle look white?
Fatty infiltration, calcification, degeneration/necrosis, fibrous connective tissue (scarring)
What is the gross morphological diagnosis?
- Skeletal muscle degeneration and necrosis
- Rhabdomyolysis
- Myonecrosis
- Zenker’s necrosis
Any of these are acceptable, but A. skeletal muscle degeneration and necrosis is more correct.
What is morphologically abnormal about this muscle histopathology? (muscle from the necropsied lambs)
Vacuolization of the sarcoplasm/cytoplasm and condensation of the cytoplasm with loss of striations
What do myofibers/myocytes do when they are hurt?
- They die
- Vacuolation of sarcoplasm
- Condensation of sarcoplasm (looks hyper-eosinophilic, and lose striations)
- Nuclear pyknosis
- Calcification (dystrophic)
- They regeneration
- Internalization of nuclei (satellite cells internalized from the endomecium that differentiate into myblasts > proliferate > more sarcoplasm)
- Macrophages infiltrate (to clean up dead material)
What types of causes incite this pattern of degeneration and necrosis?
Pathology report: polyphasic skeletal muscle degeneration and necrosis
Causes of polyphasic lesions : ongoing insults
- Nutritional deficiency- vitamin E/Se
- Ongoing toxicities
- Genetic defects in myocyte structural/metabolic elements
Polyphasic- myocytes are in different stages of injury and regeneration (both)
How does nutritional deficiency cause this mess?
Pathology report: polyphasic skeletal muscle degeneration and necrosis
Pathogenesis: vitamin E/Se deficiency > needed for enzymes like glutathione peroxidase/reductase > lack of ability to scavenge free radicals > oxidative damage (lipoperoxidation of cell membranes) > myocyte injury (free radicals go around punching holes in the cells)
What is the cause of vacuolization and condensation of muscle cells in a horse?
Pathology report: acute monophasic skeletal muscle degeneration and necrosis
Monensin toxicity (causes too much calcium to be released)
Monophasic- single insult at once
What are the causes of monophasic lesions: a single insult?
- Trauma (will be focal)
- Exertion, capture
- Toxin- ionophores (monensin; horses are really sensitive to this, given ruminant ration), plants (coffee senna)
What is the name of the disease caused by Vitamin E/Se deficiency?
White Muscle Disease (a nutritional myopathy)
- See lesions in the most active muscles
- Can see lesions in the heart with this condition and other metabolic/toxic myopathies of skeletal muscle
- Can also see lesions in the muscles of mastication and tongue (esp. neonates)
- Diaphragm
(2nd img: MDx: cardiac myonecrosis)
In a horse with single or multiple episodes, you see general signs of pain, anxiety, and cramping most prominently after exercise. Multiple muscle groups look like this; is this pattern of muscle necrosis monophasic or polyphasic?
Monophasic (no regeneration happening)
In a horse with single or multiple episodes, you see general signs of pain, anxiety, and cramping most prominently after exercise. Multiple muscle groups look like this; what types of causes typically incite this pattern of necrosis?
- Nutritional deficiency
- Acute toxicity
- Ongoing toxicity
- Exertion
- Trauma
B. Acute toxicity or D. Exertion
Not trauma because it is multifocal
What is the MDx of this muscle from a horse?
Exertional rhabdomyolysis (Typing up, azoturia)- necrosis/lysis of skeletal muscle
- Ionic events of contraction can produce an adverse environment when extreme (calcium released from sarcoplasm > lots of glycolysis > lots of lactic acid build up)
- May have underlying metabolic conditions which predispose, such as polysaccharide storage disease
Is this lesion monophasic or polyphasic? (long distance racing dogs)
Polyphasic
- Foci of skeletal muscle necrosis common in sled dogs, also observe in racing greyhounds
- Exertional? Vitamin E/Se deficiency involvement? Underlying myocyte metabolism issue?
- “Sled dog myopathy”- lethal, generalized lesions involving non-locomotory muscles (lethal because of lesions in the heart, severe lactic acidosis, myoglobinuric nephrosis > kidney failure, electrolyte derrangement)
What do you call an excess of nitrogen in the urine?
Azoturia
This muscle is form a 1-year-old deer with capture myopathy. Why is the kidney and urine abnormal?
Multifocal lesions of degeneration and necrosis, areas of palor, streaks of palor, dry to the touch, slightly swollen (muscles); kidney is dark in the cortex and the urine is red (myoglobinuria)
What is the disease in zoo and wild birds due to exertion, stress during capture/handling/transport, and whose pathogenesis is anaerobic glycolysis (too much lactic acid produced) > hyperthermia (from contraction of skeletal muscles), metabolic acidosis?
Capture myopathy
BOARD QUESTION
What is this other example of a metabolic condition predisposing to necrosis where the MDx is focal muscle degeneration and necrosis? What is the pathogenesis?
Malignant hyperthermia (affects pigs)
- Lumbar vertebral column; pale, slightly swollen, dry to the touch
- Pathogenesis: inherited defect in skeletal muscle ryanodine receptor > excessive Ca release and contraction when stimulated > heat production and myocyte necrosis
- Can be due to stress, excitation, or even anesthetics
Are the pale streaks in this muscle due to degeneration and necrosis?
No, because it is just fat (same color as the fat right next to it)
Does this calf have skeletal muscle degeneration and necrosis?
No, young animals store a lot of glycogen in their liver and skeletal muscles especially, so they will look more pale than usual.
- Not dry, not slightly swollen (cannot be tested on this)
You are called out to a farm where 34 of 120 yearlings are dead. Vaccines were not given. The farmer did not see any clinical signs and said that they just dropped dead suddenly. Upon necropsy and skinning, you notice hemorrhage, shiny and swollen fascia (edematous), areas of necrosis (pale and dry), and pockets of air (crepitus). What pathological processes could account for this appearance?
- Degeneration/necrosis
- Inflammation and repair
- Circulatory disorder
- Disorder of growth
- Pigments and deposits
- Degeneration/necrosis, 2. Inflammation and repair, 3. Circulatory disorder (hemorrhage)
* Histologically will see air pocks (emphysema), condensation of the sarcoplasm (more red), pyknotic nuclei, infiltrated leukocytes (neutrophils), edema, and fibrin
What is the morphologic diagnosis and name of the disease of this calf?
MDx: acute necrotic and hemorrhagic myositis
Disease dx: “Black leg”
Comments: gram positive bacilli identified, consistent with Clostridium chauvoei infection
If this is just a bacterial infection of muscle, why did it kill so many cattle? And why are we seeing these other lesions such as serous pleural effusion and epicardial petechial hemorrhage?
Pathogenesis; ingestion of spores > dissemination to muscle via blood > latency > tissue hypoxia/acidosis > bacterial proliferation > production of exotoxins > myonecrosis and systemic endothelial damage > death from septicemic shock
- Start a vaccine program which includes Clostridium to cover incoming calves > good to go!
What causes outbreaks of Black leg?
- Parturition
- Handling- IM meds/vax, marking, shearing, etc.
- Trauma during confinement
- Soil disturbance
What are the types of causes inciting myositis?
KNOW THIS
- Necrotic/hemorrhagge- Clostridium chauvoei, C. septicum
- Suppurative- pyogenic bacteria
- Suppurative myositis in a horse with Pigeon fever caused by Corynebacterium pseudotuberculosis (not common)
- Lymphocytic- immune-mediated (do not usually see gross changes)
- Eosinophilic- active protozoal/parasitic infections or immune-mediated (especially type I hypersenstivity; seen at slaughter in cows, muscle is lavendar/gray/green due to eosinophils)
- Granulomatous (nodules; not common)
What kind of myositis is this?
Focal suppurative myositis
What is the MDx for a dog with “Masticatory myositis” (immune-mediated), active phase?
Diffuse eosinophilic myositis
What is the MDx and name of the disease of this dog?
MDx: chronic eosinophilic myositis and muscle atrophy
Disease name: end stage Masticatory myositis
What is the MDx of this dog?
MDx: Bilateral exophthalmus due to “Extraocular polymyositis”
Histological MDx: eosinophilic myositis of extraocular muscles (auto-immune)
What can be seen in this dog with eosinophilic myositis?
Intralesional protozoa in small animal- toxoplasma vs. neospora
What kind of parasite can be seen in eosinophilic myositis in a cow?
Sarcocystic spp. infection (latent) around myofibers
(in sheeps, it can be seen grossly; often do not have eosinophilic response)
What parasite is encysted in the skeletal muscle of a sheep? What is the MDx?
Cysticercus ovis
MDx: skeletal muscle parasitic cysts; +/- eosinophilic/ granulomatous myositis
You received another farm call regarding a “downer cow” that cannot be sent to slaughter because they wanted to make sure no diseases would affect other animals. What can we do to determine the pathological process responsible for this presentation?
Post mortem (necropsy)!
What is morphologically abnormal about the pectoral muscles at post-mortem?
There are discrete areas of muscle pallor bordered by reddened zones; no as wet, central area of depression and darkness.
What is the most appropriate morphological diagnosis?
- Skeletal muscle degeneration and necrosis
- Eosinophilic myositis
- Muscle infarct
- Muscle atrophy
- Muscle calcification
- Muscle infarct and 1. Skeletal muscle degeneration and necrosis
- Muscle infarct is a better answer because it was laying down (loss of blood circulation) and there were sharp lines of demarcation (often has a geometric shape)
- Center is more severe (dark area)
What is the pathogenesis of this leg from a “downer cow” (muscle infarct)?
Pathogenesis: recumbency > increased intramuscular pressure > poor perfusion > ischemia > infarction
- Pale/dry areas- necrosis; arterial infarct
- Dark/almost blue areas- vascular congestion; venous infarct
*Can see similar lesion post-anesthesia of large animals*
A melon headed whale that was stranded off of the Gold Coast died and the pathology report showed that the MDx was focal monophasic myonecrosis. Histologically, myofibers were fragmented and vacuolated, some were swollen, and cross striations could not be seen due to condensation. Is this lesion a cause or effect of the animal’s state?
An ischemic lesion (infarct) from beaching
Also consider: Trauma during transport to Sea World? Capture myopathy? vs. primary cause of beaching?
Pathogenesis: rapid muscle growth > period of increased circulation (exertional) > muscle swelling confined by fascia > impedes blood supply > low perfusion > ischemia > infarction. What is the name of the syndrome?
(other ways of infarcting a muscle)
Compartment Syndrome
(img: supermarket chicken breast, UK)
This gastrocnemius muscle of a 10-year-old male/neutered Rottweiler was friable and had an MDx of intramusclar hemorrhage. What is the etiology?
Trauma (especially penetrating wounds, fractures)
(img: underlying tibial bone mass in the medullary cavity; osteosarcoma with a pathological fracture)
What is the MDx and disease Dx of a piglet, puppy, or rabbit who since birth could not stand; limbs were abducted, had a flattened chest, but was otherwise normal? Histologically, the myocytes were smaller.
MDx: Myocyte hypoplasia
Disease Dx: “Splay leg” (piglets) or “Swimmer syndrome” (puppies)
What is the etiology and pathogenesis of “Splay leg” or “Swimmer syndrome”?
Pathogenesis unknown currently; may be caused by genetic predisposition, primary spinal/ neuromuscular disease?, underlying infections?, overfeeding mother?, slippery flooring?
Does myocyte HYPERplasia occur? Can myocytes proliferate?
Yes; myocytes increase in size (hypertrophy) by addition of myofilaments, but myocytes CANNOT proliferate
What are the causes of myocyte hypertrophy?
- Exercise conditioning (athletes)
- Compensatory
- Decreased number/size functional myocytes, increased load on remaining
What are the causes of myocyte hyperplasia “double muscling”?
- Inactivation of the regulatory gene myostatin (involved in myoblast cell progression to muscle fibers)
- They’re just born this way!
What pathological processes could account for this appearance in a puppy with “Splay legs”?
- Degeneration/necrosis
- Inflammation and repair
- Circulatory disorders
- Disorders of growth
- Deposits and pigmentations
- Disorders of growth/ developmental anomalies
What is morphologically abnormal with this horse? MDx? Etiology?
Muscles are lopsided (less on the left side)
MDx: regional atrophy
Etiology:
- Physiologic (disuse, aging)
- Cachexia/malnutrition (chronic inflammatory disease, cancer)
- Endocrine disease- myocytes have surface receptors for hormones (hypoT, hyperA)
- Denervation- myocyte maintenance requires trophic factors generated at neuromusclar junction; occurs quickly!
This case is severe, so most likely denervation.
(2nd img: the horse’s muscle would look like the right)
What is morphologically abnormal about this muscle from a horse?
White streaks = fibrosis and fatty infiltration (steatosis) often develop in long-standing atrophy. Notice that we can use the terms ‘atrophy’ and ‘hypertrophy’ when referring to muscle as a whole (grossly) or to the diameter of a myocyte (histologically)
T or F. Atrophy can be the end result of other pathological processes affecting the muscle.
True; end stage “Masticatory myositis”
BOARD QUESTION
This is a larynx from a horse clinically diagnosed with laryngeal paralysis. Note the left cricoarytenoideus dorsalis muscle; what is the etiology?
Damage to the left recurrent laryngeal nerve
Which cell type do neoplasms with striated muscle differentiation (‘rhabdomyoma/sarcoma’) derive from?
- Skeletal myocytes
- Fibroblasts
- Pluripotential stem cells
- All of the above
- None of the above
C. Pluripotential stem cells
(skeletal myocytes are already differentiated!)
What cell is this rhabdomyosarcoma in the rear leg from a dog derived from?
Satellite cells or stem cell anywhere else in the body (uncommon)
- Cannot see where it begins or ends
- Tan, fleshy mass
- Very invasive tumors
A 10-year old female mixed breed was euthanized due to a severe mammary tumor. Tan nodules were seen in the lungs and histologically (after PTAH stain), cross striations could be seen in the cytoplasm (during myoblast differentiation). What was the MDx?
Rhabdomyosarcoma
- Primitive cells seen in histopathology, so have to use immunohistochemistry to look for desmin (brown; only in striated muscles)
Where does hemangiosarcoma originate from?
Skeletal muscle
“Rufus”, a 1-year-old male Golden Retriever presented with progressive generalized muscle weakness, atrophy, joint contractures and angular deformities. He was excercise intolerant and had excessive drooling and problems eating. Biopsy showed hypertrophy and atrophy of myocytes, fibrosis, vacuolation, and internalized nuclei (regeneration). What is the next best diagnositc stem? What is the MDx?
Muscle biospy
MDx: polyphasic myocyte degeneration and necrosis (primary process), chronic, with hypertrophy, atrophy and fibrosis.
“Rufus”, a 1-year-old male Golden Retriever presented with progressive generalized muscle weakness, atrophy, joint contractures and angular deformities. He was excercise intolerant and had excessive drooling and problems eating. Biopsy showed hypertrophy and atrophy of myocytes, fibrosis, vacuolation, and internalized nuclei (regeneration). What is the cause of this polyphasic lesion?
- Nutritional deficiency- vitamin E/Se
- Ongoing toxicities
- Genetic defects in myocyte structural/metabolic elements
- Genetic defects in myocyte structural/metabolic elements
- “Muscular Dystrophy”: an X-linked inherited myopathy reported in dogs and cats, especially Golden retrievers; defects in dystrophin gene- cytoskeletal protein
- Poor prognosis, no treatment :(
Important point: usually not possible to discern the cause of muscle injury with histopathology- supplemental tests, clinical history usually required!
Which 3 pigments and tissue deposits are observed in skeletal muscle?
- Lipofuscin
- Hemosiderin
- Metastatic calcification
- Dystrophic calcification
- Exogenous pigments
- Lipofuscin (because myocytes are long lived), 4. Dystrophic calcification (because so much calcium is stored in the the endoplasmic reticulum), 5. Exogenous pigments (from injections)
What is the MDx and etiology to White muscle disease?
MDx: polyphasic myocyte degeneration and necrosis
Etiology: vitamin E/Se deficiency
Note: calcification of myofibers secondary to degeneration/ necrosis
What is going on with these diaphragms of 600 sheep? Yellow plaques on peritoneal surface, below peritoneal surface, and body wall. Little round needles were seen histologically. Are these endogenous or exogenous deposits?
Exogenous; Barium injection intraperitoneally instead of SC
You were called in to investigate several deaths of ducks at a local pond. Some of the surviving birds were very weak. What can you do to figure out the pathological process that resulted in these signs?
Post-mortem exam
You were called in to investigate several deaths of ducks at a local pond. Some of the surviving birds were very weak. After sending out post-mortem samples, the pathology report came back with an open MDx and no lesions were identified in over 20 sections examined. Nothing was wrong with the muscle or nervous system. What is going on?
Botulism!
Pathogenesis: decaying organic matter > Clostridium botulinum thrives and elaborates exotoxin into environment > ingested > toxin inhibits Ach release from nerve terminals at neuromuscular junction > progressive generalized paralysis with death by cardiorespiratory failure
*Important point: some diseases with profound muscular signs do not have gross/histological lesions, BUT you can exploit the known pathogenesis to make a diagnosis
What are other “biochemical” pathological processes resulting in severe muscular clinical signs?
- Neuromusclar junction disorders- Botulism, myasthenia gravis, tick paralysis
- Electrolyte derangements- hypokalemia (cats), hypocalcemia (cattle)
- Misc. inherited disorders of muscle metabolism- myotonias (often involve ion channel defects- inability of fibers to relax)
A 7-year-old, castrated male, island mix developed severe skin lesions and became lame. The owner did not want to pursue further treatment so he was euthanized. How would you describe these lesions?
- Ulcers
- Papules
- Erythema (only a skin term)
What is a palpable elevation filled with clear fluid
Vesicle (fragile; easy for secondary pathogens to infect and form a pustule)
- Causes: auto-immune dermatoses, viral infections, chemical irritants, burns
- Pathological processes: degeneration/necrosis and inflammation & repair
(img: horse with vesicular stomatitis)
What is a palpable elevation filled with clear fluid >1 cm?
Bulla
- Causes: auto-immune dermatoses, viral infections, chemical irritants, burns
- Pathological processes: degeneration/necrosis and inflammation & repair
What kind of cellular changes can lead to the formation of a vesicle or bulla?
- Spongiosis- intercellular edema (epidermis starts to look like a sponge) KNOW THIS
- Hydropic degeneration- intracellular edema (loss of osmotic balance)
- Acantholysis- disruption of intercellular junctions of keratinocytes (ex. desmosomes; not spiny, they are just floating about by themselves; usually immune-mediated) KNOW THIS
Which levels in the skin do vesicles form?
- Subcorneal- the stratum corneum forms the roof of the vesicle (as in impetigo or pemphigus foliaceous)
- Suprabasal- a portion of the epidermis (stratum spongiosum) forms the roof (as in pemphigus vulgaris)
- Subepidermal- the entire epidermis separates from the dermis and forms the roof (as in bullous pemphigold)
What is a palpable elevation filled with pus?
Pustule (ex. zits)
- Cause: leukocyte infiltrate
- Pathological process: inflammation & repair
What is dried exudate, serum, blood, and scale that is adhered to the skin surface?
Crust
- Causes: severe disorder of keratinization, severe pustular dermatitis, secondary to ulcers
- Pathological process: degeneration/necrosis, inflammation & repair, and disorder of growth
How is a crust formed from a pustule?
Leukocytes (black dots) migrate from the perivacular dermis into the epidermis (exocytosis) > leukocytes migrate into the epidermis and accumulate to form a pustule > pustule dries to form a crust
What is a palpable, solid, elevated mass < 1cm in diameter (no fluid on the inside)?
Papules (ex. mosquito bite; something is being added)
- Causes: infiltrate of inflammatory cells, infiltrate of neoplastic cells, epidermal hyperplasia, deposit of mineral (ex. calcium)
- Pathologic processes: inflammation & repair, disorder of growth, and deposits & pigmentations
What is a palpable, solid, elevated mass >1 cm in diameter and deeper than a papule?
Nodule (ex. tumors)
- Causes: infiltrate of inflammatory cells, infiltrate of neoplastic cells, epidermal hyperplasia, deposit of mineral (ex. calcium)
- Pathologic processes: inflammation & repair, disorder of growth, and deposits & pigmentations
What do you call coalesced papules?
Plaques
- Causes: infiltrate of inflammatory cells, infiltrate of neoplastic cells, epidermal hyperplasia, deposit of mineral (ex. calcium)
- Pathologic processes: inflammation & repair, disorder of growth, and deposits & pigmentations
What do you call it when there is loss of epidermis with the exposure of dermis?
Ulcers (erosion is similar but less severe, just a partial thickness defect while ulcer is a full thickness defect)
- Causes: secondary to…
- Epidermal necrosis, inflammation, infarction, neoplasia
- Pathologic processes: degeneration/necrosis, inflammation & repair, circulatory disorders, and disorders of growth
What do you call an accumulation of loose keratinized cells?
Scale (ex. dandruff)
- Causes: disorders of keratinization, chronic dermatitis (most common cause of disorders of keratinization)
- Pathologic processes: inflammation & repair and disorder of growth
What is a circular rim of scale that occurs secondary to rupture of a vesicles, pustule, or papule?
Epidermal collarette (area around it is erythematous or has alopecia)
What do you call thickening and hardening of the skin?
Lichenification (“elephant skin”; extra wrinkles, dull looking, hyperpigmented)
- Causes: chronic irritation/inflammation
- Pathologic process: inflammation & repair
Explain this skin lesion with the new terms that you know.
Ulcerated plaque
Explain this skin lesion with the new terms that you know.
Crust and papule
Explain this skin lesion with the new terms that you know.
Plaques and crust covered pustules
Post-mortem artifact: biopsies
Which of the following should you NOT do when collecting a skin biopsy?
- Include crust
- Collect multiple samples, range of changes
- Biopsy the center of a lesion
- Be gentle
- Biopsy early, before treatment
- Biopsy the center of a lesion
ALSO DO NOT…
- Surgically prep the site
- Grasp with forceps (samples will be crushed, use a pin instead)
- Hold out on history/DDx
You are called out to an area that just had a period of rain and cold and had just become sunny. There is a flock of 300 merino ewes & lambs with skin lesions (mostly in areas with less hair) huddled around each other in the shade. How would you describe the lesions?
Crusting, erythema, alopecia, edema, ulceration
If skin lesions indicate something is injuring the epidermis, the pathological process is likely epidermal ________________________ or _______________________.
Degeneration & necrosis or Inflammatory (infectious)
You are called out to an area that just had a period of rain and cold and had just become sunny. There is a flock of 300 merino ewes & lambs with skin lesions (mostly in areas with less hair) huddled around each other in the shade. What will be on your differential diagnosis list?
KNOW THIS
DDx: Photosensitization, dermatophilus, viral infections (Bluetongue, pox (orf), vesicular disease (FMD, VS)
You are called out to an area that just had a period of rain and cold and had just become sunny. There is a flock of 300 merino ewes & lambs with skin lesions (mostly in areas with less hair) huddled around each other in the shade. What can we do to determine the cause?
Biopsy, culture, IFA
- Serum chemistry (for overall health): NSF
- Serum ELISA for bluetongue: negative
- Virus isolation from crust: negative
- Plant identification: St. Johns Wort > causes type I photosensitization
- Histopathology results
- MDx: epidermal necrosis and ulceration (etiology uknown); comment: bacterial dermatitis which appears to be secondary
(2nd img: pink in the epidermis = necrosis
What is the pathogenesis of primary photosensitization?
UV light absorbed by photodynamic chemicals in skin > free radical damage > epidermal necrosis of lightly pigmented or sparsely haired skin
- Melanin protects against UV light
What causes type I (exogenous) primary photosensitization?
- Consumption of plants containing photosensitive chemicals
- St. Johns Wort, lucerne, perennial ryegrass
- TMS, quinolones, griseofulvin
What causes type II (intrinsic) primary photosensitization?
- Porphyria (a rare hereditary disease when blood pigment hemoglobin is metabolized)
- Inherited deficiency of proporphyrinogen III cosynthetase > defect in heme synthesis > build up of porphyrins
What is the pathogenesis of secondary photosensitization?
Light activates agents > free radical damage > epidermal necrosis of lightly pigmented or sparsely haired skin
What causes type III, hepatogenous secondary photosensitization?
- Poor hepatic clearance of phylloerythrin (product of rumenal chlorophyll transformation)
- Toxins causing biliary obstruction:
- Lantadenes- Red Lantana
- Steroidal saponins- Tribulus, Pancium
- Sporodesmin (Facial Eczema)- Lolium perenne + Pithomyces chartarum > sporodesmin toxicosis
- Other hepatotoxins: Pyrrolizidine alkaloids, aflatoxin, phomopsin
- Caution, liver may look normal!
What would you do to treat the flock of sheep with epidermal necrosis and ulceration?
Move the mob to another paddock with shade cover and no St. Johns Wort, treat animals with severe lesions which may have secondary infections > healed within a month
T or F. Most degeneration & necrosis skin cases have features such as epidermal necrosis/ulceration, leukocyte infiltration, thrombosis, and a secondary bacterial infection.
True!
Do you remember wound healing by first and second intention?
REVIEW
What is solar injury caused by?
Excessive acute UV light exposure (‘sunburn’)
- Erythema > blistering/vesicles > sloughing of necrotic skin
- Potentially due to UV-mediated endothelial damage and cytokine production
(img: MDx: Chronic locally extensive cutaneous ulcer)
What does chronic (years) UV light exposure lead to?
Solar/actinic keratosis
- Chronic injury leads to epidermal hyperplasia and dermal fibrosis and elastosis (‘saggy neck skin’)
- Comedones- blown out follicles filled with keratin due to dermal fibrosis
- Increased risk for neoplasia due to direct DNA injury and subsequent mutations > can turn into squamous cell carcinoma
- Usually on the ventrum (papules to plaques, erythema)
(img: dermal elastosis)
Is this describing a 1st degree, 2nd degree, or 3rd degree thermal burn?
- Epidermis and dermis
- Vesicle formation
- Some adnexa are preserved allowing epidermal regeneration with some scarring
2nd degree
Is this describing a 1st degree, 2nd degree, or 3rd degree thermal burn?
- Epidermis
- Reddened/darkened necrotic epidermis
- Complete healing
1st degree
Is this describing a 1st degree, 2nd degree, or 3rd degree thermal burn?
- Full thickness epidermis and dermis +/- subcutis (even muscle)
- Sloughing of necrotic tissue, followed by granulation tissue
- Scar; life threatening (fluid/protein loss and portal for sepsis)
3rd degree
Are these 1st degree, 2nd degree, or 3rd degree burns?
3rd degree
What do you call burns caused by body or wound secretions, application of drugs, exposure to acids, alkalies, soaps, detergents, or irritant plants?
Chemical burns (not common)
- Most cases mild (‘irritant’)
- Exposure via direct application: must penetrate hair and protective epidermal layers; adsorptive medium may facilitate
- Main issue differentiating vs. contact hypersensitivity dermatitis
What are Erythema Multiforme and Toxic Epidermal Necrolysis?
Skin lesions with a pathogenesis thought to involve type IV hypersensitivity towards antigens or the surface of keratinocytes inducing apoptosis
- Induced via antigenic mimicry from drug administration, underlying infection, neoplasia, dyes/preservatives in pet foods?
- Histologically distinct
- Widespread coalescing erythematous macules (spot that is a different color; ring-like or snake-like) > vesicles and ulcers
What is the histo MDx of this dog with solar/actinic keratosis?
Histo MDx: epidermal hyperplasia, dermal fibrosis, +/- chronic dermatitis
Years later, it turned into squamous cell carcinoma :(
What are the early gross features of dermatitis (inflammation & repair)?
Edema, erythema, +/- pustules, crust, vesicles
What are the later gross features of dermatitis (inflammation & repair)?
Epidermal hyperplasia, scaling, ulceration, alopecia (due to cytokines), lichenification, pigmentary change (hyperpigment of melanin), fibrosis/scarring
Do you remember all of your immune-mediated hypersensitivity reactions?
REVIEW
Type I: allergy
Type II: auto-immune
What do you call ‘pus in the skin’, usually with the involvement of bacterial infection?
Pyoderma
Are the following examples of deep or superficial pyoderma?
- Bacterial furunculosis
- Abscesses
Deep- deep dermis
- Bacterial furunculosis- when hair ruptures and causes a suppurative inflammatory response against the hair (like a zit)
- (img: dog with chin acne, a deep pyoderma with bacterial furunculosis)*
Why are bacterial skin infections so common in dogs?
- Really thin stratum corneum
- Lack of lipid seal of hair follicles
- High skin pH
- Often involve Staphylococcus spp.
- Exception: opportunistic gram negatives, and cases of dermatophilosis
- Produce exfoliative toxins that cause intraepidermal splitting
What is another word to describe superficial pustular dermatitis?
Impetigo
- Nonfollicular pustules which develop into crusts
- Prepubescent puppies- healthy otherwise
- Adults- look for underlying disease
What is another word to describe skin fold pyoderma?
Intertrigo
- Pathogenesis: closely apposed skin surfaces > frictional trauma > moisture > opportunistic infections
- (img: MDx neutrophilic dermatitis)*
What is pyotraumatic dermatitis?
‘Hot spots’
- Very common in dogs
- Self trauma > bacterial infection
- Alopecic, slightly raised, red well-circumscribed lesions > ulceration/crusting
- Underlying pruritus- especially flea allergy dermatitis!
What skin disease is fatal in neonatal pigs, caused by Staphylococcus hyicus?
Greasy Pig Disease (Exudative Epidermitis)
- Gross: erythema > pustules > crusts
- Predisposing factors: other skin lesions, poor nutrition/husbandry, lacerations (too crowded)
What is the infection caused by Dermatophilus congolensis (gram positive) that forms lesions on the back or distal extremities?
Dermatophilosis (“Lumpy Wool’)
- Filamentous bacteria which subdivide longitudinally and transversely
- Stimulate neutrophilic exocytosis: pustules > exudate > matting of hair/wool > alopecia
- Predisposing factors: wet weather in humid climates (‘rain rot’), prolonged wetting of skin/hair/wool allows penetration of epidermis by ‘zoospores’
- Diagnosis is in the crust
What is usually a secondary bacterial infection of superficial follicles and adjacent skin?
Canine superficial spreading pyoderma
- Gross: scaling, erythematous macules (often circular > ring shaped), papules, pustules, crusts, epidermal collarettes, alopecia
- Folliculitis
- DDx: Dermatophytosis (‘ring worm’), Demodicosis
- Diagnostics: cytology of pustule/crust (neutrophils with cocci), Woods lamp, fungal culture, skin scraping
What is a condition that is indistinguishable from Canine Superficial Spreading Pyoderma caused by Demodex spp. mites?
Demodicosis
- Lesion vary by host/mite species
- Distribution on body
- Neutrophilic to granulmatous (exudative vs. nodular grossly)
- Folliculitis: erythmatous macules > alopecia and scaling
- In dogs:
- Localized form in the face and forelegs (self-limiting)
- Generalized form
- Adult-onset demodicosis is often associated with systemic disease such as neoplasia, endocrinopathy, or immunosuppressive therapy
What is another condition that is indistinguishable from Canine Superficial Spreading Pyoderma caused by Epidermophyton, Microsporum, and Trichophyton spp. (keratinophilic fungi)?
Dermatophytosis (Ringworm)
- Contagious- acquired by contact with scales shed from infected animals
- Colonize keratin, do not need to invade tissue to cause disease
- Self-limiting in healthy animals, can become chronic/generalized in immunocompromised animals
- Predisposing factors: young or immunosuppressed animals, hot/humid environments
- Folliculitis: erythematous macules > alopecia and scaling
- In cattle: thick plaques that look gray and chunky
- Silver stain to see fungus
A 5 year old FS dog has acutely developed some nasty skin lesions, how do we describe these changes? What can we do to determine the pathological process and cause?
- Pustules, crust, alopecia, erythema
- Skin scraping, cytology of crust or pustule, aspirate, culture, biopsy
There is leukocyte infiltrate of the epidermis so you determine that the pathological process is likely inflammatory. What is the differential diagnoses? What can we do to determine the cause?
- Skin scraping: no mites or fungus seen
- Wood’s lamp: no fluorescence
- Fungal culture: no growth
- Cytology of a pustule: eosinophils, some bacteria, but not within cytoplasm of leukocytes, and not many neutrophils
The pathologist sent you this from the dog skin case (MDx eosinophilic pustular dermatitis with intralesional acantholytic keratinocytes) and said that it is consistent with Pemphigus foliaceous. What is that?
Pemphigus foliaceous
- “Pemphigus”- group of auto-immune diseases involving type II hypersensitivity against cell adhesion proteins (desmosomes)
- PF is the most common and milder form of pemphigus (reported in horses, dogs, cats and goats)- others are rare
- Often involves face, ears, footpads, clawbeds
- Vesicles, pustules, crusts, ulcers
- Can be spontaneous, drug-induced, or associated with allergic skin disease
Piglets at a zoo display have come down with skin lesions. How do we describe these changes?
Papules
Something is being added to the epidermis so you determine that the pathological process is likely a disturbance of growth or inflammatory. What is your differential diagnoses? What can we do to determine the cause?
- Skin scraping: no mites or fungus seen
- Cytology (aspirate a papule): a few lymphocytes, some keratin
- Culture of the crust: Staph. spp.
The histopathology report from the piglets came back with MDx as proliferative dermatitis with ‘ballooning degeneration’ and intracytoplasmic inclusion bodies. What is your diagnosis?
Swine-pox infection
- Sequence of lesions: macule > papule > superficial vesicle > umbilicated (depressed centers) pustule > crust > scar
- Poxviruses have a gene whole product is similar to epiderma growth factor > epidermal hyperplasia
- Many cutaneous lesions only, some systemic and fatal
- Some are foreign animal diseases
- Can become systemic
Describe this lesion.
Lamb with contagious exanthema (reddening), early papular to vesicular phase > Orf virus; zoonotic
Describe this lesion.
Lamb with contagious exanthema, late crusty phase > Orf virus; zoonotic
You see lameness, anorexia, ptyalism in some backyard livestock (pig, sheep, goat), what is your morphological diagnosis?
Vesicular stomatitis (bulla) and interdigital or vesicular dermatitis
You notice that something is injuring keratinocytes, so you determine that the pathological process is likely degeneration and necrosis or inflammatory. What is your differential diagnosis?
Viruses!
- Early herpesvirus (these can cause cutaneous vesicles!)
- Early poxvirus
- Vesicular diseases- FMD (foot and mouth disease), VSV (vesicular stomatitis virus), SVD (swine vesicular disease), VES (vesicular exanthema of swine)
(2nd img: Herpes simplex (cold sores) and Herpes zostar (chicken pox and shingles)
Your differential diagnosis for these cows, pigs, and goats was a virus, so what is the next best step in your diagnostic process?
The only sure way to distinguish these diseases is by laboratory testing.
- Producers and private practicioners are the first line of defense against these economically devastating diseases
- Whenever you see ulcers, look for vesicles!
What is this ulcerative facial dermatitis (cat) caused by?
Feline herpes virus-1
What is this vesiculo-ulcerative dermatitis caused by (cow)?
Bovine herpes virus-2 (Pseudo-lumpy skin disease)
- All over body caused by flies
What is this vesiculo-ulcerative mammilitis caused by?
A strain of Bovine herpes virus-2 (Herpesviral mammilitis)
A 4-year-old mixed breed presented with multiple skin lesions. How would you describe the lesions and what is the most likely pathological process?
- Papules, plaques, and nodules in multiple foci > something being added to the epidermis
- Pathological process: disturbance of growth or inflammatory
You predict that this is a pathological process of inflammation or a disturbance of growth. What is on your differential diagnosis list and what can you do to determine the cause?
- Skin scraping: not mites or fungus seen (is this really helpful in a nodular disease? NO, epidermis looks fine)
- Cytology (aspirate a papule): macrophages; inflammatory, cause not apparent
- Bacterial culture: Staph. spp.
The histolopathology report came back saying:
“MDx multifocal granulomatous dermatitis; no infectious agents or foreign material seen with special stains”
What is your next step?
- Fungal culture (1 month later): negative
- Mycobacterial culture (6 weeks later): negative
What is the pathogenesis of Idiopathic sterile granuloma and pyogranuloma syndrome?
- Rare
- Esp. dogs
- Cause unknown: caused by fastidious unrecognized organism? abnormal immune response to unidentified microbial antigen? variant of histiocytic neoplasia?
- Diagnosis of exclusion
What is the infectious granulomatous disease common in humid areas that is called “Swamp Cancer” because it clinically resembles a neoplasia?
Fungal dermatitis
- Uncommon
- Pythium, Lagenidum spp.
- Invasive lesions, involvement of regional lymph nodes
- Diagnose with culture + PCR because it’s fast
What is the infectious granulomatous disease that can form large clumps (grossly evident as ‘sulfur granules’) and is caused by bacteria introduced by traumatic injury?
Actinomycete Mycetomas
- Nocardia and Actinomyces sp.
- Gross: nodules, ulceration, draining sinuses, involvement of underlying bone
- MDx: pyogranulomatous dermatitis
What is the infectious granulomatous disease that is common amongst debilitated cats in cold, wet areas, and does not grow in culture?
Mycobacterial dermatitis (Feline leprosy)
- Mycobacterium lepraemurium: obligate intracellular organism (potentially other strains)
- Transmission uknown: biting insects?
- FIV/debilitation may be predisposing factors
- Numbers of mycobacteria in lesions can be low- might not see on histo
- DOES NOT GROW IN CULTURE so must use PCR and can not get sensitivity results
- MDx: granulomatous dermatitis
What is the infectious granulomatous disease that is caused by ‘atypical mycobacteria’ (a facultative saprophyte), and tends to occur via wound contamination or traumatic implantation?
Mycobacterial dermatitis
-
Facultative saprophyte- inhabitants of soil, water, and decomposing vegetation
- Rapid-growing (more common)- M. fortuitum, M. smegmatis, M. chelonae, M. abscessus, M. thermoresistible [FYI]
- Slow-growing- M. avium-intracellulare complex, M. kansasii, M. ulcerans [FYI]
- Usually localized, but can disseminate
- Can do culture and sensitivity (easy)
- Organism more often found extracellularly
- ACID FAST STAIN
What is the infectious granulomatous disease causing nodules (and plaques) involving the dorsal pinna (less commonly in other distal extremities) in short coated breeds, especially Boxers?
Mycobacterial dermatitis (Canine Leproid Granuloma)
- Caused by a saprophytic mycobactreria
- Transmission: fly bites?
- Self-limiting in immunocompetent dogs but may last months
- Difficult to culture, may need PCR; but usually can find organisms with histo
- ZN stain will show acid fast bacillin within macrophages
What sterile granulomatous disease occurs in puppies less than 4 months old (one or more in a litter) where you see pustules, nodules, and swelling of the face, ears and mucocutaneous junctions?
Puppy Strangles (Juvenile sterile granulomatous dermatitis)
- Pathogenesis unknown
- Histo: (pyo) granulomatous dermatitis and panniculitis +/- lymphadenitis
- Fever, joint pain
- MDx: pyogranulomatous dermatitis
What infectious ‘granulomatous’ disease is common in dogs where they persistently lick and chew at their extremities?
‘Lick granuloma’ (Acral lick dermatitis)
- Histo: NOT REALLY A GRANULOMA; it is epidermal hyperplasia, granulation tissue, dermal fibrosis
- Underlying factors: boredom? sensory polyneuropathy?
- Gross: extremities, circumscribed, hairless, and ulcerated
A 3-year-old mixed breed presented with constant itching, especially in the middle of the night. How would you describe the lesions and what is the most likely pathological process?
- Erythema, alopecia, scaling
- Pathological process: inflammatory
What diagnostic steps would you take for this case?
- Skin scraping: no mites or fungus seen
- Bacterial culture: Staph. spp.
- Fungal culture (hair pluck): negative
(2nd img: skin biopsy)
The histopathology report came back with “eosinophilic dermatitis with epidermal hyperplasia; no cause evident”. What diagnosis is this most consistent with?
Allergic Skin Disease
What does an allergic skin disease look like grossly and histologically?
- Gross:
- Lesions due to self-inflicted trauma: erythema, alopecia, excoriation (deep scratch)
- Lesions due to secondary pyoderma: papules, pustules, crusts
- Lesions due to chronicity: lichenification, hyperpigmentation, scaling
- Hist: lymphocytic and esosinophilic dermatitis
Which allergic skin disease is distributed around the ventrum, face, and distal extremities from type I hypersensitivity to environmental allergens (“inhalant allergy”)?
Atopy
- Affects 10-15% of dogs
- Diagnose with intradermal skin testing
- Can try to change diet, etc.
(img: Golden Retreiver with atopic dermatitis, erythemia, alopecia, and erosions in the skin around the eye and muzzle; the lesions are caused by self-trauma from rubbing and scratching as a result of pruritus)
Which allergic skin disease is often in poorly haired areas from type IV hypersensitivity due to direct contact with objects such as plastics in food bowls, dyes in carpets, and plant residues in bedding?
Contact dermatitis
- Low molecular weight haptens present in chemicals require binding to cell-associated proteins prior to being recognized by CD8+ (cytotoxic) T lymphocytes
- Distribution depends on site of contact
Which allergic skin disease often causes papules in areas favored by insects due to type I and/or type IV hypersensitivity reactions?
Insect bite hypersensitivity
- Examples:
- Culicoides saliva: horses
- Flea saliva: dogs and cats
- Mosquito saliva: cats
- Distribution:
- Culicoides: tail base, withers, head
- Fleas: tail base (dog), neck (cats)
- Mosquito: nose and fase
- Histo: may have eosinophilic pustules, folliculitis, or granulomas
(1st img: dog with flea bite hypersensitivity; pyotraumatic dermatitis [secondary self-trauma associated pyoderma] is very common with this condition)
T or F. “Miliary dermatitis” is a disease commonly seen in cats already with an allergic skin disease.
False! Miliary dermatitis is not a disease, it is a pattern of lesions
- Small crusty erythematous papules
- Commonly seen in cats with allergic skin disease
What are other PATTERNS OF LESIONS (NOT a disease) commonly seen in cats with allergic skin disease?
Eosinophilic granuloma complex
- Indolent ulcer- ulcers on upper lips
- Eosinophilic plaque- discrete red to ulcerated plaques on abdomen or medial thighs
- Eosinophilic granuloma- nodules (may be ulcerated) on thighs, face or mouth
What are causes of eosinophilic granulomas?
Parasite reaction, insect bite hypersensitivity, foreign body reaction, underlying mast cell neoplasia
- Grossly similar to non-eosinophilic granulomas
- Often see collagenolysis- due to proteolytic enzymes of eosinophil granules?
What is the condition in this cow with cutaneous eosinophilic granulomas caused by larval migration of Habronema or Draschia sp. deposited into a wound by house or stable flies?
Cutaneous habronemiasis (Summer sores)
What is the 2nd most common autoimmune skin disease that is induced/exacerbated by UV light, usually on the dorsal nose and nasal planum?
Discoid Lupus Erythematosis
- Interface dermatitis (between epidermis and dermis where melanocytes are > hypopigmentation)
- Dorsal nose and nasal planum > pinnae, lips, periocular region > oral mucosa
- Gross: depigmentation, erythema, scaling, erosion, ulceration, and crusting
- Histo: interface dermatitis
- MDx: ulcerative dermatitis
- DDx: Uveodermatologic syndrome: auto-immune disease against dermal and uveal melanocytes, esp. arctic breeds; or dermatomyositis
- *1st most common is Pemphigous foliaceous
What are the 4 main mechanisms of subcutaneous edema?
Edema: shiny, yellow, gelatinous, thickened
- Increased vascular permeability
- Reduced oncotic pressure
- Increased hydrostatic pressure (hypertension, chronic congestion)
- Lymphatic obstruction
What is the MDx and etiology?
MDx: multifocal cutaneous ecchymotic hemorrhages (discrete and bright red compared to congestion)
Etiology: primary hemostasis defect (vasculitis vs. thrombocytopenia)
(Hematomas > coagulopathies)
What is the MDx and etiology?
Pig with “Diamond Skin Disease”
MDx: cutaneous infarcts
Etiology: E. rhusiopathiae bacteremia, associated thrombosis and vasculitis (occlusion of blood supply to skin > area goes dark blue to black (dry gangrene) due to lack of blood supply; compare to photosensitization, where ulcers and crusts are formed)
(2nd img: epidermis and dermis are necrotic from infarction; the only normal dermis and epidermis are at the extreme left, H&E stain; arrow = thrombosis of the vessel)
What is the MDx and etiology?
Pig with “Diamond Skin Disease”
MDx: cutaneous ecchymotic hemorrhages (maybe early infarct, can’t really tell)
Etiology: E. rhusiopathiae bacteremia and associated vasculitis
This horse has red or purple macules/patches (hemorrhage or infarct) in the skin or mucous membranes due to type III immune-mediated vasculitis. What is the condition and cause?
Purpura hemorrhagica
Etiology: Streptococcus equi infection (rarely with other infections or vaccinations)
(img: ecchymotic hemorrhages and subcutaneous edema)
This goat was out in cold temperatures for a while and the distal half its ear got dry gangrene. What is this called and what is the pathogenesis?
Frost bite
Pathogenesis: formation of ice crystal that physically disrupt cells > vasoconstriction and endothelial damage > reduced blood flow > thrombosis > infarction
(Dry gangrene = coagulative necrosis, can see in patients with diabetes)
What happens when an animal gets a snake or spider bite (envenomation)?
- Spider bites (Brown recluse spider) > dermal necrosis, hemorrhage, edema, neutrophilic vasculitis, and arterial wall necrosis
- Snake bites > pain, edema, erythema, necrosis
A goat ingested Claviceps purpurea (fungus) and showed these lesions. What happened?
Ergot poisoning
- Toxic alkaloid
- Ergotamine > marked peripheral arteriolar vasoconstriction and damage to capillary endothelium (stimulation of adrenergic nerves) > thrombosis and ischemic necrosis
- Tall fescue grass infected with Neotyphodium coenophialum
This is a 12-year-old ThouroughBred gelding with acute onset of ‘welts’. How do we describe these changes?
Wheal
(Transient elevations that expand out > dissipate > disappear > more forms)
We agree that something has been added to the dermis (wheal), so the pathological process is a vascular disorder. What can we do to determine the causes?
NO BIOPSY because we know it’s going to be congestion and edema; don’t waste your time! Look at the history for triggers (type 1 and III hypersensitivity)
What do you call an elevated, irregular-shaped area of cutaneous edema (solid and transient)?
Wheal
Why do dogs and horses get urticaria (“hives”)?
Triggers: food, drugs, antisera, insect stings
- Pathogenesis: type I and III hypersensitivity
- Histo: subtle so don’t waste your time!
What is the MDx on this dog with a suspected centipede bite reaction?
MDx: multifocal cutaneous edema and congestion (wheals)
What do you call the hereditary (most common) condition in which an animal has less than the normal amount of hair?
Singy calf due to in utero BVD infection
MDx: hypotrichosis
- More susceptible to environmental extremes and infections
- Can be bred purposely
What is this condition in which the skin is hyperextensible?
Cutaneous Asthenia, Dermatosparaxis, Ehlers-Danlos
MDx: collagen dysplasia
- Collagen bundles are irregular in size and shape and are arranged haphazardly
What is this condition in a calf where the skin fails to develop in a segment?
Epitheliogenesis imperfecta (dermis and cutis exposed > secondary infections)
What is this congenital defect in cornification, calf?
Ichthyosis (“fish-like”), stratum corneum is extra thick > skin cracks
Pathogenesis: keratinocytes adhere to one another
What are some disorders with alopecia?
- Endocrine disorders (bilaterally symmetrical alopecia, hyperkeratosis, cutaneous hyperpigmentaiton): hypothyroidism, hyperadrenocorticism, hyperestrogenism (sertoli cell tumor), Alopecia X
- Hair cycle abnormalities: postclipping alopecia, Telogen effluvium, antimitotic drugs (chemotherapeutics, immunosuppressants)
- Self-trauma (pruritus, most common): ectoparasites, dermatitis of any cause, but particularly allergic skin disease
- Autoimmune: alopecia areata (Ab made against hair follicle, type II hypersensitivity, biopsy helpful!)
- General poor nutrition (bilaterally symmetrical): hairs are produced weak
- Hyperkeratosis: interferes with hair follice decreasing hair production
- Cicatricial alopecia (scar)
What is the difference between acanthosis and hyperkeratosis, which are both epidermal hyperplasias?
- Acanthosis: increased thickness of straum basale and spinosum, lichenification grossly
-
Hyperkeratosis: increased thickness of stratum corneum, scaling grossly
- Parakeratotic: nuclei retained
- Orthokeratotic: anuclear
What is the inherited disorder of keratinization/ cornification where it is thought to involve hyperproliferation of the epidermis, hair follicle infundibulum, and sebaceous glands?
Primary idiopathic seborrhea
- Dry form (seborrhea sicca) > dry skin and white-to-gray scales that exfoliate
- Greasy form (seborrhea oleosa) > excessive brown to yellow lipids
- Can’t really treat
What is the condition where there is scaling around the mouth, chin, eyes, pressure points, pawpads commonly in artctic and rapidly growing large-breed dogs?
Zinc responsive dermatosis
- Arctic breeds: inherited defect in zinc absorption
- Rapidly growing large-breed dogs: fed low zinc diet
What is the highly contagious and zoonotic condition caused by Sarcoptes scabiei?
Sarcoptic Mange
- Pathogenesis: burrow into stratum corneum > intense pruritis through hypersensitivity-like mechanism > self trauma, chronic, irritation > hyperkeratosis, lichenification, alopecia (eosinophilic dermatitis)
- Wild animals > can stop eating from the stress of scratching so much
- MDx: chronic dermatitis
What is the MDx of this dog with Sarcoptic Mange?
MDx: chronic dermatitis
What do you call a raised, irregular patch of thickened skin developing from chronic friction, usually over pressure points?
Callus
- Histo: epidermal hyperplasia
- May develop secondary pyoderma
What is the MDx and etiology?
Pig with Diamond Skin Disease
MDx: multifocal cutaneous infarcts
Etiology: Erysipelothrix rhusiopathiae
DDx: Salmonellosis (+ African swine fever, hog cholera viruses)
Which skin tumors (benign) are NOT true neoplasms?
- Nodular hyperplasia (ex. nodular sebaceous hyperlasia)
- Hamartoma: redundant disorganized tissue normally present at the site (usually collagenous, ex. skin tag)
- Cysts (ex. follicular cyst)
How do we describe these changes from an 8-year-old MN lab?
Nodular, ulcerated mass
What can we do to determine the pathological process and cause of this growth from an 8-year-old MN lab?
Aspirate, smear (cytology), biopsy
We agree that something is being added to the epidermis of the 8-year-old MN lab, so what is the pathological process and DDx? What can we do to determine the cause?
DDx: granulomatous nodule, bengin hyperplastic nodule, neoplasm
- Cytology: low numbers of spindle cells, some mixed leukocytes (probably not a round cell tumor or carcinoma)
- Biopsy: excisional vs. incisional, 1 cm margin, 1 fascial plane under growth, surgical margin assessment
- Histopathology
- Culture
What are spindle cell tumors?
Cutaneous Soft Tissue Sarcomas
- Very common in dogs
- Types: Fibrosarcoma, Nerve sheath tumor, Malignant fibrous histiocytoma, Liposarcoma, Myxosarcoma
- Have overlapping histiological features and similar prognosis (TREAT THE SAME)
- Prognosis predicted by grade and margins
- Locally invasive, slow to metastasize
What is your diagnosis on a cow with hyperkeratotic, horny cauliflower-like masses on its body?
Papillomas
- Caused by papilloma virus
- Pathogenesis: viral genes inactivate tumor-suppressor proteins
- Benign, spontaneously regress
What is your diagnosis for this nodular to plaque/wart-like lesion, composed of both epithelial and dermal components on a young adult horse?
Equine Sarcoid
- Thought to be caused by bovine papilloma virus
- Frequently involve sites of previous wounds
- Invasive, high rate of recurrence, but do not metastasize
- Histo: composed of both epithelial and dermal components- NEED A BIOPSY THAT IS NOT ULCERATED TO DIAGNOSED
- Don’t get it confused for proud flesh
What is your diagnosis for this verrucous and ulcerated lesion in poorly pigmented areas that was either due to solar radiation (ex. in cows) or a chronic injury, like fly strike (ex. in sheep)?
Squamous cell carcinoma
- Pathogenesis: solar radiation, chronic injury commonly involved
- Poorly pigmented, sparsely haired areas
- Histo: keratinizing squamous cells GONE WILD
- Can become ulcerated
What is your diagnosis for this white-yellow, greasy cauliflower-like lesion on a dog?
Sebaceous adenoma
- Benign growth of dogs
What is your diagnosis for this fatty nodule on a dog or a cat?
Lipoma
- Benign growth of dogs >>> cats
- Looks and feels like fat, only forming a nodule
- Histo: looks like normal fat
What is your diagnosis for this inflammatory-like lesion that is potentially malignant in dogs, but bengin in cats and horses?
Mast cell tumor
- Dog (more common): behavior varies with grade but all considered potentially malignant
- Can look like anything
- Often resembles inflammation
- Histo: will see lots of granules
What is your diagnosis for this dome-shaped lesion on a young dog that is of Langerhans’ cell origin?
Histiocytoma
- Dogs, mostly young, but any age
- Head, ears, neck, distal forelegs
- Epidermal dendritic antigen-presenting cell
- Benign, often spontaneously regress
- Histo: good to see with epidermis and dermis; will see round cells
What is your diagnosis for this dark brown lesion that had “junctional changes” when you sent it in for biopsy (nonulcerated)?
Melanoma
- Dog, horse, angora goat
- Usually dark brown
- Location, size, mitotic index, and cell morphology may help predict behavior
- Canine: oral, mucocutaneous, subungual, often malignant; haired skin often benign
- Gray horses: usually progressive and multicentric (can’t stop it)
What is your diagnosis for this lesion in a young adult dog that was due to solar radiation?
Hemangioma/Hemangiosarcoma
- Hemangiosarcoma
- Not as malignant as visceral counterparts
- Primary to skin or metastatic from visceral tumor
- Metastatic potential may vary with depth of tissue invasion
- Try to aspirate it > blood everywhere
(img: hemangiosarcoma; 2nd img: hemangioma)
What are the different forms of cutaneous lymphomas?
- Epitheliotropic: T cells
- Nonepitheliotropic: T or B cells
Many species are affected, especially dogs; ulcerations, poor prognosis
What are the factors that influence the production of melanin?
Hormones (ex. MSH from PTH), genes, age, inflammation, UV light exposure
(melanin- the pigment which imparts skin color)
What causes generalized hyperpigmentation?
Usually endocrine-related
- Endocrine dermatosis: Cushing’s, Hypothyroidism, Hyperestrogenism
- Acanthosis nigricans: genetically determined disease of young dachshunds
What causes localized hyperpigmentation?
- Chronic inflammation or physical irritation (rubbing/friction)
- Chronic flea allergy dermatitis (regional hyperpigmentation)
- Congenital (freckles)
What are the causes of hypopigmentation?
Acquired:
- Copper deficiency
- Destruction of melanocytes or melanin-containing keratinocytes (“pigmentary incontinence”): scars, autoimmune dermatosis, vitiligo, freeze-burn
- MDx: Leukoderma/Leukotrichia
Congenital:
- Inherited lack of melanocytes: horses, dogs, cats; associated with deafness (Foals with Lethal White syndrome)
- Piebaldism: foci of lack of melanocytes (anti-freckle)
- Albinism: melanocytes are present but defect to synthesize melanin (usually tyrosinase gene); color dilution is a mild form
What cutaneous calcification condition occurs in young, rapidly-growing, large-breed dogs and is grossly described as a single hard SQ nodule, usually over pressure points or at previous sites of trauma/injection?
Calcinosis circumscripta
What cutaneous calcification condition is associated with hyperadrenocorticism and looks like erythematous to white gritty plaques/foci and nodues?
Calcinosis cutis
- Pathognomonic for hyperadrenocorticism (Cushing’s)
What is your diagnosis for this thickened/puffy gelatinous skin lesion usually seen in Chinese Shar-Peis?
Mucinosis (mucin is normally in the dermis; protein bound to hyaluronic acid)
- If severe, can exude viscous fluid when pricked with needle
- Prone to injury
- Seen with:
- Inherited mucinosis in the Chinese Shar-Pei
- Myxedema with hypothyroidism
- MDx: cutaneous mucin
________________ is an idiopathic acquired melanocytopenis hypomelanosis in horses.
Vitiligo
- “Arabian Fading Syndrome”
- MDx: focal leukoderma
- Gradually expanding pale macules, often symmetrical
- Genetic inheritance
- Pathogenesis of melanocyte death?
- (Michael Jackson had this)
Finally! Which of the following is mostly likely the primary pathological process in our unknown case? (keratinization and fibrosis seen histologically)
- Degeneration and necrosis
- Inflammation and repair
- Circulatory disorder
- Disturbance of growth
- Pigments and deposits
- Disturbance of growth > neoplasia > squamous cell carcinoma (light parts of skin, ulcerations, cuboidal epithelial cells, plaques, secondary pyoderma) = actinic keratosis (erythemaous ventrum) with secondary squamous cell carcinoma
A 6-month-old bighorn sheep has been rejected by its ewe. The sedated ewe of the lamb in the preceding image is being examine by a biologist. What is morphologically abnormal? MDx? EtDx? Most likley cause?
- Crust, ulceration, pustules, papules
- DDx: Foot and Mouth Disease, Orf (Scabby Mouth), Vesicular disease, photosensitization, Dermatophilus congolensis (gram + bacteria)
- Since mom and baby both have it, we’re thinking viral, so Orf
- EtDx: poxviral dermatitis
- Cause: Orf virus
What is morphologically abnormal? MDx? Most likely cause?
- Lack of pigment of hair and skin
- MDx: hypopigmentation or leukoderma/leukotrichia
- Cause: albinism (genetic problem with tyrosinase enzyme; will have normal number of melanocytes)
Skin of an adult horse. What is morphologically abnormal? Most likely pathological process? MDx?
- Ulcerated plaque (a little elevated)
- Pathological process: Inflammation or neoplasia
- DDx: sarcoid, Swap Cancer (fungal), squamous cell carcinoma, summer sores (Habronema), proud flesh (exuberant granulation tissue)
- MDx: granulomatous dermatitis or sarcoid (viral); need to do biopsy
- Cause: bovine papilloma virus (sarcoid)
Skin of an adult horse. What is morphologically abnormal? Most likely pathological process? MDx?
- Pigmented, multi-nodular mass
- Pathological process: neoplasia or granuloma
- DDx: melanoma (grey horse, perineum)
- Cause: melanoma
A puppy has facial pustules and lymphadenomegaly. What is the most likely disease diagnosis?
- Pathogenesis: idiopathic infection
- Cause: Puppy strangles
What is morphologically abnormal? Most likely pathological process? MDx?
- Dark, discrete area (sharp line of demarcation = infarct), loss of digits (sloughed), dry, sunken
- Pathological process: necrosis (dry gangrene)
- MDx: cutaneous infarct
- Cause: Frost bite (occlusion of vessel from vasoconstriction, crystals form in vessel)
What is morphologically abnormal? MDx?
- Erythema, hyperpigmentation, lichenification
- MDx: chronic dermatitis
- DDx: Cushing’s disease, hyperestrogenism, allergy
We are concerned this is an estrogen producing sertoli cell tumor in a retained testicle. What are some expected associated skin lesions?
- Hyperestrogensim: hypermelanosis, bilaterally symmetrical alopecia, hyperkeratosis (scales)
3 dogs with similar lesions. What is morphologically abnormal? MDx? 3 potential causes?
- Epidermal collarettes (rim of scale; pustule has ruptured), pustule, erythematous macule, alopecia
- 3 potential causes: superficial spreading pyoderma, demodex, dermatophytosis (all are inflammatory around the hair follicles = folliculitis)
What is this disease?
Greasy Pig Disease caused by Staphylococcus hyicus
- Poor nutrition, poor environment, crowding
- Exudative (neutrophils) inflammation
Most likely pathological process?
- Ulcerated mass
- DDx: neoplasia or inflammation
- Etiology: Squamous cell carcinoma caused by vaccine reaction
Sheep. What is morphologically abnormal? MDx? Potential causes?
- Crusty nose
- MDx: exudative dermatitis or rhinitis
- Potential causes: vesicular viruses (Foot and Mouth Disease, vesicular stomatitis, Orf), photosensitization, dermatophilus
- Cause: Foot and Mouth Disease
Cat. What is morphologically abnormal? MDx?
- Plaques (edematous because they look shiny), alopecia, erythematous, discrete edges
- MDx: eosinophilic plaque (due to hypersensitivity/allergic skin disease)
What is the etiology?
Photosensitization (edema around affected tissue)
- Hepatogenous: any hepatoxin from cholestasis
- Exogenous: specific plants or drug
- Intrinsic
What is morphologically abnormal? MDx? Potential cause; Dx steps?
- Crust, alopecia, some ulceration
- MDx: exudative/pustular dermatitis
- Dx steps: skin scraping (mites, fungus), biopsy, cytology on crust, Wood’s lamp
- Cause: Demodex; crust from self trauma and secondary bacterial infection
