-
What are the functions of skin?
- Protective barrier
- Regulates temp and BP
- Produces VitD
- Stores nutrients
- Innate and adaptive immunity
-
What structures make up the epidermis?
- Stratum corneum
- Stratum lucidum (most animals don't have)
- Stratum granulosum
- Stratum spinosum
- Stratum basale
-
What is the function of the subcutis?
- attaches dermis to muscle or bone
- contains adipose tissue, collagen and elastic fibers
-
What structures make up the adnexa?
- hair follicles
- sweat glands
- sebaceous glands
- specialized structures like hooves
-
What are the hair growth stages?
- anagen (active growth)
- catagen (transition)
- telogen (resting)
-
What stimulates good hair growth?
- photoperiod
- thyroid hormone
- growth hormone
-
What suppresses hair growth?
-
What causes poor quality hair growth?
- low protein diet
- protein-losing diseases
-
What types of hair follicles to cattle and horses have?
one large follicle (simple)
-
What kind of hair follicles to pigs have?
simple follicle grouped in clusters
-
What kind of hair follicles do goats have?
compound follicles or primary and secondary follicles
-
What kind of hair follicles do sheep have?
- simple follicles = hair
- compound follicles = wool
-
When would you use a KOH prep?
immediate dermatophyte dx
-
When would you use a skin scraping?
microscopic ectoparasites
-
When would you use an acetate tape prep?
Chorioptes dx
-
How can dermatophilus be dx?
- saline + crusts powdered and stained
- look for g+ railroads tracks
-
How would you dx microfilaria in cattle, sheep and goats?
- Punch biopsy of tissue
- Minced and incubated for 15 min
- Check for characteristic whiplash movement
-
What are some pruritic mediators?
-
What are some common ectoparasites of FA?
- flying insects
- lice
- Sarcoptes scabiei
- Psoroptes
- Chorioptes
-
What are some common causes of infectious nodules in FA?
- Corynebacterium pseudotuberculosis
- Hypoderma spp (warbles)
- Sporotrichosis
- Actinobacillosis
- Actinomycosis
-
What are some common causes of neoplastic nodules in FA?
- Squamous cell carcinoma (SCC)
- Fibroma or fibrosarcoma
- Epidermal inclusion cyst
-
What is the difference between an erosion and an ulcer?
Erosion heals without a scar
-
What are some common causes of immune-mediated erosions and ulcers in FA?
- Adverse drug reaction
- Contact irritant
- Contact hypersensitivity
- Photosensitivity
- Vasculitis
-
What are some common causes of infectious erosions and ulcers in FA?
- Dermatophilus congloensis
- Viral (IBR, Vesicular Stomatitis, Herpes Virus, FMD)
-
What are some common causes of neoplastic erosions and ulcers in FA?
SCC
-
What can cause a papule?
- Hypersensitivity (parasitic most common, drugs, food is rare)
- Parasites (horn flies)
- Infectious diseases
- Neoplasm
- Immune-mediated (rare e.g. pemphigus foliaceus)
-
What can cause a bulla?
- burn
- viral infections
- immune mediated diseases (bullous pemphigoid)
-
What are the most common causes of a papule, pustule or vesicle?
- Ectoparasites (papules)
- -Sarcoptes scabiei
- -Psoroptes cuniculi (goats)
- -Lice
- Infectious
- -viral (Vesicular stomatitis, FMD)
- -bacterial (Staphyloccocal pyoderma in goats)
-
What is parakeratosis?
Cornification with nuclear retention
-
What is orthokeratosis?
Cornification without nuclear retention
-
What are some common causes of non-pruritic scaling and crusting?
- Infectious disease (Dermatophilosis, Dermatophytosis, viral)
- Nutritional
- Toxic
- Immune-mediated (Pemphigus foliaceus, cutanenous filariasis)
- Photosensitization
- Irritant contact reactions
- Burns
-
What are some common causes of scaling and crusting?
- Ectoparasites (Sarcoptes scabiei in ruminants, Psoroptes cuniculi in goats, Psoroptes ovis in sheep, lice, Chorioptes spp in cattle)
- Infectious (Dermatophilus congolensis, Staphylococcal pyoderma, Dermatophytosis)
- Immune-mediated (Pemphigus foliaceus in goats)
- Nutritional (Zinc deficiency in ruminants)
-
What are the most common causes of alopecia?
- Dermatophytosis
- Alopecia areata (cattle)
- Drug reaction
- Congenital hypotrichosis
-
What are the most common causes of increased coat length?
Congenital hypertrichosis
-
How can hypopigmentation happen?
- decreased melanin production
- decreased dispersion of melanin granules
- increased loss of melanin
-
What is leukotrichia?
acquired loss of melanin from the hair shaft, actual factors are unknown
-
What is albinism?
Recessive genetic defect in which a normal complement of melanocytes is present but a biochemical defect results in lack of ability to synthesize tyrosinase, so that melantoin is not produced. In true albinos there is a lack of pigment in all tissues
-
What is the most common cause of loss of pigmentation in FA?
- Burns & other traumas
- *Copper deficiency*
-
What is the most common cause of increased pigmentation in FA?
-
What does C. pseudotuberculosis cause?
- Sheep & goats: caseous lymphadenitis (CLA)
- Cattle: cutaneous granuloma
- Horses: ulcerative lymphangitis
-
What is CLA or concern in sheep?
- Condemnation of carcass (3-5% of mutton, 0.02-0.03% of lambs)
- Downgrading of carcasses
- Decreased wool production in Merino sheep
- Decreased growth rates
-
What are the characteristics of C. pseudotuberculosis?
- Facultative intracellular gram+ coccobacillus
- Infects macrophages & monocytes
- Soil borne, survives for months-years; even in sunlight
-
What is the pathogenesis of C. pseudotuberculosis?
- Phospholipase D is a potent exotoxin & key virulence factor
- -hydrolyzes sphingomyelin
- -impairs chemotaxis of neutrophils
- Increased vascular permeability
- Leakage of plasma from vessels into tissue & lymphatics
- Spread of organism regionally & systemically
- Mycolic acid has local cytotoxic properties
- -degenerative changes & death in phagocytozing leukocytes
- -protection from hydrolytic enzymes within lysosomes→ survives phagocytosis → exists facultative intracellular → transport to local LN
- -helps survival in the environment
-
What are the CS of internal CLA?
- Hematogenous or lymphogenous spread
- In sheep visceral lesions esp. lung
- Lung parenchyma, mediastinal & bronchial LN Can lead to bronchopneumonia & pleuritis
- Chronic ill thrift
-
What are the CS of external CLA?
- Superficial LN involvement
- Submandibular, prescapular, prefemoral, supramammary LN
- Goats: Head & neck LN more often involved
- Sheep: torso
- Cattle: Cutaneous excoriated granuloma (looks like the cow has been shot)
-
How can CLA be dx?
- PE: Abscessed external lymph nodes, often several animals in a flock affected
- U/S: Internal abscesses
- TTW
- Radiographs
- Serology
- Culture (but few viable bacteria in chronic abscesses, synergistic lysis with R. equi)
-
What is the SHI test?
- Serological test for CLA
- Synergistic hemolysis inhibition test
- Dilute patient serum & incubate with CLA sphingomyelinase & R. equi exotoxin
- Look for resumption of hemolysis when antibodies are diluted out
-
How do you interpret the SHI test?
- Titer interpretation
- <1:8 not significant
- >1:256 likely internal abscess formation
-
Why could a SHI test titer interpretation be normal in a positive CLA cow?
- titer could be rising
- acute onset
- thick capsule around abscess
- consumption of antibody during acute infection
-
What is the tx for CLA in sheep and goats?
- Lance & flush: avoid contamination of the environment, isolate from herd
- Surgical removal: remove with capsule, likely recurrence, expensive
- Antibiotics: long term treatment, difficult to treat internal abscesses, may reduce size
- Cull: not always economical or desirable
-
What is the tx for CLA in cattle?
- Investigate facilities if an outbreak occurs in similar location in different animals
- Clean & debride
- Antibiotics don't help
- 2-4 weeks spontaneous recovery
- Usually no vaccination
-
What are the CLA vx, and when should you give them?
- Commercial & autogenous types
- Goats: pre-breeding
- Kids: before exposure to potentially infected adults or at 10 weeks of age
-
What are the two types of contact dermatitis?
-
What is allergic contact dermatitis?
- Cutaneous reaction in a sensitized animal to a non-irritating concentration of the offending agent
- Delayed hypersensitivity (Type IV) reaction
- Prior exposure to allergen is necessary
-
What is an irritant contact dermatitis?
- Cutaneous reaction to an irritating concentration of an offending agent
- Predisposing factor is moisture e.g. urine, feces, wounds, acids, alkaline substances, crude oil, fuel, sprays, wood preservatives, bedding, filth
-
What are the CS of contact dermatitis?
Erythema, edema, vesicles, erosions, ulcerations, crusting, skin thickening, hyperpigmentation
-
What is the distribution of contact dermatitis lesions, and why do you see them there?
- Muzzle and distal legs: Plants, environmental substances
- Face and dorsum: sprays, pour-ons, wipes
- Ventrum: bedding, filth
- Perineum and rear legs: feces, urine
- Muzzle and lips: calves fed milk replacer from pans or buckets
-
Where can you see udder cleft dermatitis?
- btw lateral aspect of udder and medial thigh
- btw udder halves
- on ventral midline (cranial to udder)
-
What are the CS of udder cleft dermatitis?
-
What is the signalment of udder cleft dermatitis?
- older cow
- concurrent udder edema
- weak fore udder attachment
- small angle between udder and abdominal wall
-
How is udder cleft dermatitis tx?
- Clean with mild soap & water;use drying agent afterwards (betadine, chlorhexidine)
- Systemic antibiotics if deep infection, maggots present or febrile
-
What is the pathophysiology of photosensitization?
- UV light (320-400 nm) absorbed by photodynamic agent in skin
- -> release of energy
- -> reactive oxygen free radicals
- -> mast cell degeneration & production of inflammatory mediators
- -> damaged cell membranes, nuclei acid, proteins
-
What are the types of photosensitization?
- Type 1: plant contains a photodynamic agent or metabolite
- Type 2: abnormal porphyrin metabolism
- Type 3: liver disease caused by a plant or toxin leads to accumulation of phylloerythrin in skin
-
What are some plant photodynamic agents?
- Helianthrone pigments: red fluorescent pigments such as hypericin (eg. St. John's wort) & fagopyrin (eg. Buckwheat)
- Furocoumarin pigments: psoralens (eg. Spring parsley, Bishop's weed), phytoalexins
-
Which drugs can be photodynamic agents?
Phenothiazines, thiazides, methylene blue, tetracyclines, sulfonamides
-
What photodynamic agents can be synthesized by the body?
uroporphyrin & coproporphyrin
-
What diseases cause type 2 photosensitization?
- Congenital erythropoietic porphyria (bred out now)
- Bovine protoporphyria
- *both have an inherited enzyme deficiency*
-
What are the characteristics of congenital erythropoietic porphyria?
- Inheritance: autosomal recessive
- Breeds: Holsteins, Shorthorns, Jamaican
- CS: pink tooth, slow growth, photosensitization & exfoliation of non-pigmented skin, ANEMIA
- Pathophysiology: deficiency of uroporphyrinogen III cosynthetase → accumulation of uroporphyrin & coproporphyrin
-
What are the characteristics of bovine protoporphyria?
- Inheritance: autosomal recessive
- Breeds: Limousin, Blond d’Aquitaine
- CS: NO anemia, NO discoloration of teeth
- Pathophysiology: defect in ferrochelatase → decreased heme synthesis → accumulation of protoporphyrin in blood & tissues
-
What is the most common form of photosensitization?
type 3 - hepatogenous
-
What are the pathophysiology of type 3 photosensitization?
- Chlorophyll -> phylloerythrin in the GI tract, impaired capacity of the liver to excrete. Phylloerythrin is a photodynamic agent
- OR
- Secondary to hepatocellular damage, inherited hepatic defects, bile duct obstruction
-
What plants can cause liver disease -> type 3 photosensitivity?
- Common Groundsel
- Ragwort
- Tarweed
- Rattleweed
-
In which animals is facial eczema seen?
sheep, goats, cattle
-
What causes facial eczema?
- Saphrophytic fungus Pithomyces chartarum
- Produces liver damaging toxin sporidesmin → phylloerythrin isn't properly metabolized → accumulation in peripheral blood → photosensitization
-
Where is Pithomyces chartarum found?
Grows commonly on perennial ryegrass in late summer & autumn
-
Where is facial eczema a problem?
New Zealand, Australia, South Africa, & Oregon
-
What are the CS of Pithomyces chartarum?
- Restless & photophobia
- Decreased growth & milk production
- Head edema & erythema → blisters, exudation, necrosis → sloughing of skin
- Droopy & swollen ears, swollen lips & eyelids
-
Which animals are more vulnerable to Pithomyces chartarum?
Newly-shorn sheep
-
How can facial eczema be tx?
- Remove animals from contaminated pasture
- Provide shade
- Reduce toxin consumption by feeding hay or grain
- Antibiotics for secondary bacterial skin infection
-
How can facial eczema be prevented?
- High levels of zinc
- Better pasture management
-
What are some type 3 photosensitizing saponins?
- Puncture Vine
- Agave
- Signalgrass
- Sacauiste / bunch Grass
- Narthecium
-
How to photosensitizing saponins cause damage?
- Contain toxic levels of steroidal sapogenins which are metabolized to glucuronide conjugates of epismilagenin -> crystallize in bile -> biliary blockage, cholangitis, secondary photosensitization
- [Sapogenin] highest in early, rapid growth
-
What are the CS of saponin photosensitization?
Anorexia, weight loss, icterus, hepatoencephalopathy
-
What are the general txts for photosensitization?
- Remove from sunlight exposure (provide shade)
- Remove exposure to photodynamic agent or liver toxin (move to different pasture, feed hay or grain)
- Laxatives to remove material already ingested
- Supportive liver disease tx (keep animals eating)
- Antibiotics
- Cull animals with genetic defect
-
In which animals are papillomas commonly seen?
Young (< 2 years old)
-
What kind of virus is papilloma?
-
Why are papillomas of concern in Saanen goats?
able to transform into SCC; frequently on udder & teat
-
What is the txt for bovine papillomas?
- none - self cure
- Can pinch, crush, sx remove or freeze with liquid N2 to help stimulate immune response
-
When can papillomas be painful?
On the teats (and predispose to environmental mastitis), penis, interdigital skin, GI tract
-
How can bovine papillomas be prevented?
- Disinfect equipment between animals!
- -ear tag applicators, tattooers, dehorning instruments
- Isolation (impractical)
- Commercial vx (won't tx current outbreak)
-
How can you make an autogenous bovine papilloma vaccine?
- Remove warts & grind
- Freeze-thaw 2x
- Filter
- Add 0.5% formalin for repeated SC injection
-
What are the characteristics of ORF?
- Zoonotic
- Parapoxvirus (DNA poxvirus)
- Epitheliotropic virus
-
What are the CS of ORF?
- Proliferative lesions on lips, nostrils, oral mucosa, teats (reluctance to nurse, mastitis), vulva
- Early: papules, vesicles, and pustules
- Later: proliferative, coalescing, scabbed lesions
-
In which animals is ORF seen?
Usually young animals
-
How do animals get ORF?
scabs from infected animals are contagious
-
How can ORF be dx?
- PE
- Histopathology (eosinophilic intracytoplasmatic inclusion bodies in epithelial keratinocytes)
- Electron-microscopy
- PCR
- Immunochemistry
-
How can ORF be prevented?
- Isolate
- Monitor trace minerals
- Vaccinate area of scarified skin (except lactating ewes!)
- Vaccinate lambs, kids at 2-3 days of age
- Only use vaccine if you have a problem at the farm (the commercial vaccine is live, will form scabs with are contagious, so everyone on the farm gets exposed ~3weeks)
-
What is malignant contagious ecthyma?
Persistent ORF
-
What are the CS of malignant contagious ecthyma?
- Proliferative lesions esp. on distal legs & feet
- Lesions do not regres (unlike ORF)
- Not infectious (unlike ORF)
-
What are the CS of ulcerative dermatosis?
- Lesions on lip, nares, feet
- Vulvitis / balanoposthitis
- No oral mucosa involvement (...FMDV)
- Not proliferative (unlike ORF)
- Scabs bleed
-
How is ulcerative dermatosis tx?
Self limiting
-
When does transmission of ulcerative dermatosis occur?
during breeding season
-
What are the CS of BHV-2?
- Vesicular & erosive lesions on udder & teat
- Mastitis
- Chronic: hard milkers
-
When do you see BHV-2 outbreaks?
- in heifers 2 weeks after calving
- Nov-April
-
How is BHV-2 transmitted?
- milking machine
- hands
- clothes
-
How is BHV-2 treated?
self-limiting
-
What is the tx for BHV-2?
- mild lesions self heal in ~10 days
- severe lesions heal in 2-3 months
- cull
-
How is BHV-2 dx?
serology for 1:16 titer = exposure
-
How can BHV-2 be prevented?
- isolate infected cows
- good milking hygiene: wash hands between milking, milk last
- use iodophor disinfectant
-
Which derm diseases are zoonotic?
- pseudocowpox
- bovine papular stomatitis virus
- vesicular stomatitis virus
- sarcoptes scabiei
- dermatophytosis
-
What are the characteristics of pseudocowpox?
parapoxvirus
-
What are the CS of pseudopoxvirus?
- ulcers on teats, medial thigh, udder
- erythema & edema -> vesicles, small orange papules -> rupture -> crusting, falls off -> classical horseshoe lesion
-
What are the characteristics of bovine papular stomatitis?
- parapoxvirus
- see in young cattle
- CS: usually asymptomatic but can have raised papules on nose, muzzle, nose, oral mucosa (esp. hard palate) or esophagus. Won't see lesions on feet. Rat tail syndrome in feeder cattle
- Severe CS: mortality, weight loss, D
-
What are the ddx for ulcers on the teat?
- BVDV (bovine viral diarrhea)
- FMD (foot and mouth disease)
- BPSV (bovine papular stomatitis)
- VSV (vesicular stomatitis)
-
What are the characteristics of vesicular stomatitis?
- Two types: New Jersey (most virulent, most common) and Indiana
- Cattle, horse & donkeys most susceptible
- Calves more resistant
- Incubates in 24 hours
- CS: oral vesicles -> ulceration -> large eroded areas -> tongue, gums, teat, coronary band -> salivation, off feed, fever
- Transmission: cow to cow, milking machine, hands, insects
-
How is vesicular stomatitis virus dx and tx?
- Diagnosis: CF test, fluorescent antibody test, EM for bullet shaped virus
- Treatment: supportive care (soft feed, abx)
-
What are the characteristics of melanoma?
- <2% of bovine tumors
- Young Angus (pigmented), Duroc pigs
- Are benign
-
What are the bovine lice?
- Linognathus vituli
- Solenoptes capillatus
- Haematopinus eurysternus
-
What are the ovine lice?
- Linognathus ovillus
- L. stenopsis
- L. pedalis
-
What are the caprine lice?
- Linognathus stenopsis
- L. africanus
-
What are the porcine lice?
Haematopinus suis
-
What are the characteristics of biting lice?
- Large mouthparts, broad head
- Feeds on dead skin cells, hair & oil secretions
- Survival off host up to 2 wks
- Mainly females, lay <1 egg/day
- 7-10 days until hatching
- Temperature sensitive, so see in winter more
-
What are the characteristics of sucking lice?
- Narrow head, pointy mouth
- Obligate blood feeders
- Survival off host limited
- Females lay 2-6 eggs/day
- 8-11 days until hatching
- Feeds on dead skin cells, hair & oil secretions
- Survival off host up to 2 wks
- Mainly females, lay <1 egg/day
- Temperature sensitive, so see in winter more
-
What are the CS of pediculosis?
- Wintertime pruritus -> alopecia esp. neck & tail (sucking) or dorsal surface & flank (biting)
- Stamping & biting = sheep with foot lice
- Hairballs from excessive licking
- Anemia (sucking lice)
-
How is pediculosis dx?
- Hx, PE
- Microscopy: sucking lice are blue-gray, biting lice are pale to brownish
-
What is the tx for pediculosis?
- Topical insecticide: kills hatching eggs (e.g. Ivermectin injection or pour on kills sucking lice)
- Environmental clean up: blankets, brushes
-
What is the pathophysiology of Stephanofilariasis?
- Stephanofilaria stilesi ingested by horn flies (Haematobia irritans)
- Larva develop in fly, get deposited in skin wounds
- Microfilaria in surrounding dermis/lymphatics
- Adults live around hair shafts of ventral abdomen
-
What are the characteristics of Stephanofilariasis?
- Alopecia & hyperkeratosis of ventral abdomen
- Crusting, small ulcers & color changes in the skin leads to ventral midline dermatitis
- Lesion is of little economic significance, so optional txt is ivermectin or topical OPs
-
What are the types of mange?
- Sarcoptic mange (aka barn itch), reportable
- Psoroptic mange (eradicated from US), reportable
- Chorioptic mange, reportable
- Demodectic mange
- Follicular mange
- Hallmark of disease is pruritus
-
How is mange dx?
Skin scrapings from periphery of lesions in multiple locations (deep and superficial)
-
How is mange tx?
- Ivermectin (Psoroptes, Chorioptes, Sarcoptes), doramectin (P, C, S), moxidectin (P, C), eprinomectin (C, S)
- Treat all in contact animals
- Treat the environment
-
What are the CS of Sarcoptic mange?
- Pruritus around head, ears initially, later generalized
- Entire body can be affected within 6 weeks
- Loss of hair, scabs
- Only mange which occurs in pigs
-
Where do mange mites live?
- Sarcoptes: burrows
- Psoroptes: on surface of epidermis
- Chorioptes: on surface of epidermis
-
What are the CS of Psoroptic mange?
- Pruritus first on withers, later generalized
- Weight loss, otitis externa, Staph. aureus secondary infx (goats)
-
What are the CS of Chorioptic mange?
- Relatively host specific
- Less severe / variable pruritus
- Cattle: perineum, back of udder, severe cases are legs & rump
- Sheep: wool-less area, hind legs, scrotum causes infertility
-
What are the CS of demodectic mange?
- Small nodules & pustules -> larger abscesses on face, neck, shoulder
- No pruritus or hair loss
- Can be very severe in goats -> death
-
What is an important differential for pruritic sheep?
scrapie
-
What are the CS of scrapie?
- Nervous, restless
- PRURITUS of increasing intensity
- Rubbing & scratching with horn & hooves
- Bite & lick excessively
- Head, withers, flank, back, rump
- Secondary wool loss, dermatitis, excoriations
- Scratch or nibble reflex
- Bruxism, ptyalism
- Tremors, ataxia
-
What are the biting flies?
- Stable flies: Stomoxys calcitrans
- Horn flies: Haematobia irritans
- Horse flies: Tabanus spp.
-
What are the non-biting flies?
Face flies: Musca autumnalis
-
What are the characteristics of the stable fly?
- Head upwards position
- Intermittent blood feeders - painful bites
- Feed esp. on horses, cattle
- Complete life cycle: 3-4 wks
- Eggs laid in high moisture area
- Mechanical vector for anthrax
-
What are the characteristics of horn flies?
- Most serious pests of cattle
- Up to 20 - 40 meals/day -> loss of 0.3- 0.5 lbs/day BW, ↓milk production
- Stay mostly on host, 100 flies/half beef = economic threshold
- Eggs in fresh cattle manure
- Vector for Stephanofilaria spp.
-
What are the characteristics of horse flies?
- Only female sucks, legs & ventral abdomen
- Eggs on leaves on plants close to standing water
- Life cycle 4-5 months
- Vector for bovine leukosis, vesicular stomatitis, anthrax
-
What are the characteristics of face flies?
- Face of cattle, feeding on nasal & lacrimal secretions & saliva
- Eggs in fresh manure
- Vector for pink eye (Moraxella bovis)
-
What are the aspects of good fly control?
- Face & horn flies can develop resistance
- Insecticide impregnated ear-tags, bt offer little protection against horse flies
- Three main types: OPs (diazinon, fenthion), pyrethroids (fenvalerate, permethrin), combined OP & SP (lambda-cyalothrin, pirimofos methyl)
-
What deramtophytes are common in FA?
- T. mentagrophytes: cattle and goats
- T. verrucosum: cattle and goats “club lamb fungus"
- M. nanum: pigs and llamas
-
What are the CS of dermatophytosis?
- Alopecia in centrifugal pattern "ring" esp around eyes
- Crusts, erythema, papules +/- pruritus
- Claws and hooves weaken and split
-
How is dermatophytosis dx?
- Wood’s lamp (rare in food animals)
- Microscopic examination of hairs is difficult and takes practice
- Biopsy is quick, use special stains (dx 70% of the time)
- Fungal culture dx 90% of the time, Trichophyton harder to culture
-
What is a positive dermatophyte on culture?
- white / buff colony, cotton-like growth
- within 24-48 hours of growth media turns red
- color change + media change in first 3 weeks
- if contaminated likely to be saprophyte
-
How is dermatophytosis tx?
- Lime sulfur 5%
- Bleach 1:10 solution (not in black show animals!).
- Chlorhexidine 2.5%
- Shampoo 1% miconazole or ketaconazole if small area affected
- Systemic e.g. griseofulvin (teratogen) or NaI (abortion)
-
How is dermatophytosis prevented?
- Consider vaccination
- Better hygiene
-
What are the characteristics of dermatophilosis?
- Dermatophilus congolensis
- Gram+ actinomycete
- Most economically important bacterial skin disease of food animals due to hide damage
- More prevalent in humid climates, and cattle and sheep
-
What does dermatophilosis need infect?
- Source of infection (carrier animal crusts are infectious)
- Moisture to release zoospores
- Damage to the skin e.g. trauma, insect bites
-
What are the CS of dermatophilosis?
- aka rain scald
- Painful purulent crusts or ulcers on dorsum, distal legs, muzzle, claws
- Not pruritic
-
How is dermatophilosis tx?
- Limit moisture
- Topical treatments like iodines, chlorhexidine
- Antibiotics like tetracyclines, TMS, penicillin
-
How is deramtophilosis dx?
- CS + Hx of painful purulent scabs after rain
- Microscopic exam of stained crusts w/ sterile water on a slide
- Thick bundles of coccoid forms aka "railroad tracks"
- Occasionally use culture or biopsy
-
What are the CS of Staph folliculitis?
Circular alopecia, crusts, edema, pustules on ventrum, udder, lumbar region, eyes, orally
-
How is Staph folliculitis tx?
- TMS for 2-6 weeks
- Topicals include localized (mupirocin 2% or silver sulfadiazine) or shampoos (chlorhexidine or ethyl lactate)
- Betadine is a good abx but delays re-epithelialization
-
Which Staph spp are part of Stap folliculitis?
- Staph aureus (30% on pig farms are MRSA)
- Staph pseudintermedius
-
What are the characteristics of greasy pig disease?
- Agent: Staphylococcus hyicus releases exfoliative toxins Exh A-D which destroys desmoglein-1
- Suckling pigs (1-4 weeks): most common and severe
- Older pigs (6-10 weeks): get chronic form with thicker crusts, more morbidity
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What are the CS of greasy pig disease?
- Lethargy, anorexia, thirst then skin signs
- No fever, pain, or pruritus
- Scaling progresses to red-brown macules + pustules -> eventually greasy (sebum, sweat and serum)
- Coronary band erosions; conjunctivitis; constipation
- 3-5 days after first CS piglets begin to die
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How is greasy pig disease dx?
- CS
- Histology and culture to differentiate
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What are the ddx for greasy pig disease?
dermatophytes, zinc deficiency and swine pox
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How is greasy pig disease tx?
- Isolate, better hygiene
- Systemic abs (early in outbreak) = dramatic affect reducing mortality
- Novobiocin (abx)
- Topical antibacterial washes
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What is the pathophysiology of Zn responsive dermatosis in cattle?
Hereditary autosomal recessive defect in GI Zn absorption, aka lethal trait 46
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What are the CS of Zn responsive dermatosis in cattle?
- Diarrhea, skin lesions, poliosis & decreased suckle reflex
- Inflammation & crusts around eyes, base of ears, coronary bands, and muzzle; may progress to become generalized
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How is Zn responsive dermatosis dx, including expected CS?
- Cattle: plasma [Zn] of calves are normal at birth; histology of skin lesions shows parakeratosis (need Zn metalloenzyme to remove nuclei)
- Sheep: Crusts, alopecia, abnormal hoof growth, slow wool growth, depression, wool eating, flexed knees, stiff gait; histology shows hyperkeratosis + parakeratosis
- Goats: Crusts, bilateral symmetrical alopecia, rough hair coat, abnormal hoof growth, weight loss, unthriftiness, stunted growth, kyphotic gait, anorexia; histology of skin shows parakeratosis + hyperkeratosis
- Llamas: "munge" crusty hyperkeratotic nose or periocular
- Swine: Poor growth, thickened -> encrusted -> fissured skin
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How is Zn responsive dermatosis tx?
Give elemental Zn supplement
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What is the pathophysiology of Zn responsive dermatosis in sheep?
- Fed diet with <4 mg Zn/kg BW, so see in young sheep and lambs
- Or fed high Ca diet (e.g. alfalfa)
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What is the pathophysiology of Zn responsive dermatosis in sheep?
- Fed high Ca diet (e.g. alfalfa)
- Over-liming & excessive application of superphosphate = soil Zn deficiency
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What are the characteristics of Pityriasis rosea?
- Affects 1-5month old piglets, common in white breeds (ie, Landrace)
- May rapidly spread through herd, esp with stress
- Circular, brown crusts w/ erythema, initially ventral abdomen & medial thighs
- Systemic signs uncommon, precede skin lesions, are appetite loss, V, D
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What is the tx fr Pityriasis rosea?
self-limiting in 3-10 weeks
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What are the normal HR for each spp?
- Adult cattle: 60 – 80
- Adult sheep, goat: 70 – 90
- Adult pig: 60 – 90
- <6 month old: 90 -120
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What is the PMI on cow when ausculting?
- Triscupid: right side 3rd ICS (far forward between shoulder & elbow)
- Pulmonic: left side 3rd ICS at level between shoulder & elbow
- Aortic: left side 4th ICS at shoulder level
- Mitral: left side 5th ICS just above elbow
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What makes the heart sounds?
- S1: “lub” at closure of AV valves = onset of ventricular ejection, same time as QRS
- S2: “dup” at closure of semilunar valves = early diastolic sound after T wave
- S3: mid diastole, near end of rapid ventricular filling, after T wave
- S4: end diastole + atrial contraction, acceleration of blood into ventricles, heard after P wave
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What do split sounds tell you?
- split S1: mitral and tricuspid not closing at same time
- split S2: pulmonic and aortic not closing at same time
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What causes split heart sounds?
- Pulmonary hypertension
- Right sided heart failure
- Bundle branch block
- Endocarditis
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What does it mean if S3 or S4 are louder than S1 or S2?
- = gallop rhythm
- Proto-diastolic: (exaggerated S3) thickened ventricular walls bouncing & vibrating after systole
- Pre-systolic: (exaggerated S4) pushing blood into a stiff ventricle “LUB-DUB---BUP”
- Summated: (exaggerated S3 & S4, cannot differentiate between sounds) usually a sign of diffuse heart failure with high HR
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What are some reasons heart sounds can be decreased?
- Obesity
- Long hair coat
- High muscle development
- Hydrothorax
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What are some reasons heart sounds can be increased?
- Excitement
- Exercise
- Anemia
- Heart insufficiency
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What are the reasons for heart murmurs?
- Alteration of morphology any of the heart valves (stenosis or insufficiency)
- Abnormal communication between the two sides of the heart or great vessels (ie.VSD, ASD)
- Increased blood flow velocity through normal or abnormal valves
- Decreased viscosity
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What are the causes of displaced heart sounds?
- Mediastinal mass (leftward & caudal shift)
- Pleural fluid (sound over entire thorax
- Vagal indigestion (no heart anomaly, heart sounds in rumen)
- Apex not discernable and muffled heart sounds (cardiac tamponade usually from TRP)
- Ectopia cordis (abnormal location of heart usually neck)
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When is a systolic murmur, and what are some examples?
- Between S1 and S2
- Mitral or tricuspid insufficiency
- Aortic or pulmonic stenosis
- Interventricular septal defect
- Interatrial septal defect
- Tetralogy of Fallot
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What is a diastolic murmur, and what are some examples?
- Between S2 and S1
- Classified as early, mid, late
- Aortic or pulmonic insufficiency
- Mitral or tricuspid stenosis
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What is a continuous murmur, and what are some examples?
- S1 through S2 into part or all of diastole
- Patent ductus arteriosus
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S1 through S2 into part or all of diastole
Patent ductus arteriosus
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How are cardiac murmurs graded?
- I: barely audible
- II: audible after few seconds
- III: immediately audible
- IV: loud without thrill
- V: loud with thrill
- VI: very loud, thrill heard with stethoscope off chest
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What do splashing heart sounds mean?
- Pericarditis if gas & fluid are in pericardial sac
- Almost always accompanied by muffled heart sounds & tachycardia
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What does friction rub heart sound mean?
- Pericardial friction sounds
- Diagnostic for fibrinous pericardits
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What are the two classes of arrhythmias?
- Abnormality in impulse formation
- Abnormality in impulse propagation
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What is a sinus arrhythmia, and in which animals is it seen?
- Increasing heart rate during inspiration
- Common in pigs
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What does a wide tachycardia tell you vs. a narrow one?
- Narrow: origin at or above AV node
- Wide: origin within ventricular walls
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What is the most common cause of a heart block or arrhythmia?
IV Ca - causes bradycardia
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What is the txt for FA arrhythmias?
- Tx the underlying disease and arrhythmia will correct itself
- Except in atrial fib or plant toxicity
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What are the CS of R-CHF?
- True jugular pulse
- Pulsing, distended mammary veins
- Abnormal heart sounds
- Gallop rhythm
- Split heart sounds
- Murmur
- Splashing
- Brisket edema
- Bottle jaw
- Hepatomegaly
- Tachycardia
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What are the CS of L-CHF?
- Coughing
- Tachypnea
- Frothy nasal or oral exudates
- Tracheal rales
- Pulmonary wheezes & crackles
- Tachycardia
- Arrhythmia
- Heartblocks
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Where are the ECG leads placed?
- Right shoulder (white), left heart (black), neck over right jugular (red)
- OR
- Right jugular (white), left jugular (black), heart (red)
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What is the most common irregularly irregular arrhythmia?
atrial fib
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What is the gold standard for diagnosis of myocardial injury?
cTnI in myocardium sarcomere
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What agents are responsible for hematogenous pericarditis?
- Cattle: M. hemolytica, blackleg (if survives 24hrs), H. somni, sporadic bovine encephalomyelitis (Chlamidophila pecorum)
- Sheep & goats: Pasteurellosis, Staph aureus, Mycoplasma spp
- Pigs: Glasser's disease (Haemophilus spp), Strep, Salmonellosis, Mycoplasma spp
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What are the CS of pericarditis?
- Abducted elbows, neck & head stretched out
- +/- positive scootch test
- Signs of right heart failure
- Sudden death!
- Reluctance to move, arched back, stiff
- Shallow, abdominal respiration, grunting
- Pericardial friction rub; elevation of percussable cranioventral lung border
- Absent lung sounds cranioventrally
- Increased body temperature (103- 106F)
- Muffling of heart sounds (effusion),
- Decreased peripheral pulse
- Splashing sound if gas is present
- Tachycardia, fever & toxemia
- Diarrhea
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How you dx cranial abd pain?
- Wither’s pinch response test -> grunt and failure to go down if painful = positive
- Bar test
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When do you commonly see hardware disease, and what are the CS?
- Often late pregnancy or couple weeks after calving
- Acute anorexia & drop in milk production
- +/- Fever
- Abducted elbows, arched back
- If penetration of L ventricle: Embolization of pus, dissemination of infection to joints, meninges, spleen, eyes -> sudden death
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How do you perform a pericardiocentesis, and what are the expected results?
- L 5th ICS, 2.5- 10 cm dorsal to olecranon, above lateral thoracic vein
- +/- ultrasound guided
- Cytology & culture
- See increased protein (>3.5 g/dl), elevated WBC (>2500/ul), slightly blood tinged, foul odor
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What is the txt for pericarditis?
Poor prognosis
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How is pericarditis prevented?
- Give magnet at ~500lbs = ~ 1 year old
- Use magnets on feed trucks
- Laparotomy & rumenotomy to remove hardware
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What are the CS of idiopathic pericarditis?
- Usually hemorrhagic pericardial effusion
- No abd pain or cardiac murmurs
- No signs of infection (in CBC, pericardial fluid)
- Good prognosis
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Which valve is most often affected by endocarditis, and what agents are present?
- Tricuspid (right AV valve)
- T. pyogenes (cattle); Ersipelo. insidiosa, Strep. suis, Stephanurus edentatus (swine)
- Long-standing Tetralogy of Fallot (jet lesion), VSD, or ASD
- Common history of chronic infections
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What are the CS of endocarditis?
- +/- Fever, anorexia, depression, exercise intolerance, weight loss
- R sided holosystolic heart murmur with gallop rhythm
- Tachycardia
- R-CHF
- Jugular distension & pulse
- Diarrhea
- Hepatomegaly
- (Shifting) lameness
- Water-hammer pulse (abnormal tricuspid valve)
- Panopthalmitis, hypema, photophobia
- Meningits
- Reddened skin (swine)
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What is the txt for endocarditis?
- Cull
- Long term abx (up to 3 months) with penicillin, florfenicol
- Aspirin & low dose heparin
- Treat CHF with furosemide and digoxin (improves contractility)
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What is brisket disease?
- Right sided heart failure from pulmonary hypertension (cor pulmonale)
- Mainly calves
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What is the pathophysiology of brisket disease?
Alveolar hypoxia -> pulmonary arteriolar vasoconstriction -> increased resistance in the pulmonary alveoli -> pulmonary remodeling -> pulmonary hypertension -> right ventricle hypertrophy -> right ventricle dilation -> right sided congestive heart failure
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What are some primary and predisposing factors of brisket disease?
- Primary: high altitude, resp disease (viral, bacterial, non-fatal cases of atypical pneumonia, lung worms)
- Predisposing: Genetics (exaggerated pulmonary vasoconstrictor response), or ingestion of Locoweed (Oxytropis or Astragalus spp) -> periarterial fibrosis -> reduce compliance of pulmonary arterioles
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What are the CS of brisket disease?
- Bulging eyes
- Brisket edema
- Ventral thorax edema
- Jugular distension/ pulsation
- +/- split S2 during inspiration
- No pleural or pericardial effusion
- Dyspnea & tachypnea
- +/- gallop rhythm
- +/- Murmur
- Tachycardia
- Lethargy
- Weakness
- Collapse
- Diarrhea
- Death
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What are some ddx for R-CHF?
- hardware disease
- endocarditis
- lymphoma
- emoblic pneumonia
- viral / bacterial
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How can pericarditis be dx?
- Hx: Recent change in location or elevation, lineage, plant exposure (locoweed)
- Rads: pulmonary disease, bronchopneumonia, interstitial pneumonia, chronic bronchitis
- Fecal sedimentation: lungworm infection
- Blood work: increased AST & SDH, +/- azotemia, CBC normal
- ECG: Right ventricular hypertrophy & dilation, increased septal thickness, abnormal septal motion, dilation of the pulmonary artery
- Necropsy: edema, enlarged liver (nutmeg appearance), excessive pleural, pericardial & peritoneal fluid; heart enlarged
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How can brisket disease be prevented?
PAP testing - must be performed at high altitudes
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How do you interpret PAP scores?
- 30-35mmHg: excellent, highly reliable
- 36-39mmHg: excellent if >12 months old
- 39-41mmHg: good if yearling
- 41-45mmHg: acceptable if >16 months old
- 45-48mmHg: acceptable if >16 months old and acclimated to higher elevations
- >49mmHg: high risk for them and their offspring to develop brisket disease
- Testing should be done in cattle >12 months old and elevation >6500ft
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How can you interpret PAP scores not done in ideal locations or ages?
- <5000 feet is for screening only or Sitz Angus
- There is a 1–1.5 mmHg increase per 1000 feet elevation rise
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What is the txt for brisket disease?
- Remove from high altitude (potentially reversible)
- Antibiotics
- Oxygen (not practical or available)
- Furosemide, digoxin, cull (pedigree)
- Control measures for CAE or OPP
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What are the primary and secondary cardiomyopathies?
- Primary: hypertrophic (pigs), congestive, restrictive
- Secondary: heritable, nutritional, toxic, infection, neoplastic
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What are the CS of cardiopmyopathy?
- Tachy- or bradyarrhythmia
- Pulmonary edema
- R-CHF
- Dead/down
- Myoglobinuria (esp from what?)
- Cold extremities
- Pallor, cyanosis
- Weak pulses
- Hyper- or hypothermia
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In which animals is cardiomyopathy esp seen?
- feeder steers
- pneumonia can be a pre-disposing factor like brisket disease
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What are the characteristics of Cassia occidentalis (“coffee weed” or “sickle pod cassia”) toxicity?
- Severe muscle degeneration
- Coffee brown urine (myoglobinuria) → kidney failure
- Chronic → cardiomyopathy
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What are the characteristics of Persea americana (Avocado) toxicity?
- Direct toxic effect on myocardium → heart failure
- Brisket & neck edema, pulmonary edema
- Acute death can occur
- Cattle, goats have died from avocado poisoning
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What are the characteristics of Phalaris arundinacea (reed canary grass) toxicity?
- Tryptamine alkaloid toxin has effect on cholinegic receptors
- 2 clinical forms
- Acute death: from cardiovascular collapse is 12 -72 hrs after placement on toxic pasture. CS include acute dyspnea, cyanosis, pounding heart sounds, irregular heart rate with alternating periods of extreme tachycardia & then bradycardia
- Chronic: nervous form
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What are the characteristics of bovine dilated cardiomyopathy (BDCMP)?
- Autosomal recessive mutation in optic atrophy 3 gene
- Usually ~2–4 years old
- Systolic dysfunction → right sided heart failure
- Hallmark: cardiomegaly with ventricular and atrial dilatation & hypertrophy
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Which animals are most sensitive to ionophore toxicity?
- Monensin: horse > sheep > cattle
- Lasalocid: horse > cattle > sheep
- Salinomycin
- see decrease in ventricular contraction
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What are the characteristics of copper deficiency?
- Primary: in milk fed animals or copper deficient pasture
- Secondary: mineral imbalances (dietary Mo excess), most prominent signs in young growing animals
- See fibrosis of the heart muscle
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What are the characteristics of gossypol toxicity?
- 0.1–0.2% of total ration can be tolerated (cattle)
- No more than 0.01% of total gossypol (swine)
- If stressed lower tolerance, effects are cumulative
- Acute toxicosis: large amounts of proteinaceous fluids in all body cavities causes myocardial degeneration & necrosis, and liver necrosis
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Where is lymphoma seen?
R atrium
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What can cause myocarditis?
- Viral: FMDV
- Bacterial: H. somni, Clostridium chauvoei (blackleg)
- Protozoan: Toxoplasma, Sarcocystis
- Parasitic: Cysticercus (T. solium pig), (T. saginata cattle), (T. ovis sheep)
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What are the characteristics of FMDV?
- Picornavirus (Aphtovirus)
- Reportable!!!
- Morbidity high, mortality low
- Except: calves which have high mortality
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What are some diagnostics for DCM / myocarditis?
- History: plant exposure, feed additives, toxins, infectious disease
- Clinical signs
- ECG: dilated ventricles, systolic dysfunction
- Clinical pathology: VitE / Se (blood/liver), high cTnI, BLV test (interpret with caution), toxin analysis
- Necropsy
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What is the txt for DCM / myocarditis?
- Supportive care: abx e.g. H. somni
- Remove toxic agents: remove plants, AC, rumenotomy (cattle) / flush stomach (pig)
- VitE/Se: ALL affected young animals
- Diuretic: furosemide (for CHF)
- Digoxin:
- Oxygen:
-
What are the characteristics of VSD?
- Most common congenital defect, usually in membranous septum
- Subpulmonic location common in calves
- Heritable in Limousine & possibly in Herford cattle
- Loud, harsh pansystolic murmur
- PMI in the tricuspid valve area (right side)
- Softer murmur on the left (loudest on pulmonic valve area)
- Small defect: only murmur
- Large defect: poor growth, lethargy, dyspnea, signs of CHF
- Blood shunts from left to right
- Can increase in pulmonary resistance because of concurrent pulmonary dz or left-sided heart failure from chronic volume overload
- Right ventricle gets chronic pressure overload, which may be sufficient to reverse the direction of the shunt→ Eisenmenger’s complex
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What are the characteristics of ASD?
- Hereditary (pigs), possibly in Jersey
- Tobacco ingestion by dam
- Hypovitaminosis A in dam
- Often asymptomatic
- Up to 2-4 month of age
- CS: Stunting, exercise intolerance, weakness, cold extremities when heart fails, other signs of right sided heart failure
- Holosystolic, cresendo-decresendo murmur at the left heart base
- Shunts from left to right
- Both atria & right ventricle enlarged
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What are the characteristics of PDA?
- Persistent patency of pulmonary artery to aorta
- Rare (usually seen as part of complex defect)
- Ruminants close ductus at birth
- Piglets may be patent up to 24hrs (some up to 7 days)
- Continuous, high pitched murmur aka “machinery murmur”
- Loudest on the left
- Large PDA has no murmur
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What is the Tetralogy of Fallot?
- Overriding aorta
- VSD
- Right ventricular hypertrophy
- Pulmonary stenosis
- ...with ASD = Pentalogy of Fallot
-
What are the CS of Tetralogy of Fallot?
- Cyanosis
- Exercise intolerance
- Pansystolic murmur: (loudest left) with palpable thrill, either cresendo-decrescendo murmur of a pulmonic stenosis
- Or a harsh, plateau-shaped murmur of a VSD
- Shunting form right to left!!!
- ClinPath shows increased PCV, increased RBC, increased hemoglobin concentration, POLYCYTHEMIA
- Secondary bacterial endocarditis -> septic embolization into aorta, septic arthritis, meningitis, nephritis, panophthalmitis, petechial hemorrhages, fever, anorexia, depression -> death!
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