FA Med Exam 2

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FA Med Exam 2
2013-02-14 19:45:13
FA Medicine

FA Medicine
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  1. What are the functions of skin?
    • Protective barrier
    • Regulates temp and BP
    • Produces VitD
    • Stores nutrients
    • Innate and adaptive immunity
  2. What structures make up the epidermis?
    • Stratum corneum
    • Stratum lucidum (most animals don't have)
    • Stratum granulosum
    • Stratum spinosum
    • Stratum basale
  3. What is the function of the subcutis?
    • attaches dermis to muscle or bone
    • contains adipose tissue, collagen and elastic fibers
  4. What structures make up the adnexa?
    • hair follicles
    • sweat glands
    • sebaceous glands
    • specialized structures like hooves
  5. What are the hair growth stages?
    • anagen (active growth)
    • catagen (transition)
    • telogen (resting)
  6. What stimulates good hair growth?
    • photoperiod
    • thyroid hormone
    • growth hormone
  7. What suppresses hair growth?
    • estrogen
    • glucocorticoids
  8. What causes poor quality hair growth?
    • low protein diet
    • protein-losing diseases
  9. What types of hair follicles to cattle and horses have?
    one large follicle (simple)
  10. What kind of hair follicles to pigs have?
    simple follicle grouped in clusters
  11. What kind of hair follicles do goats have?
    compound follicles or primary and secondary follicles
  12. What kind of hair follicles do sheep have?
    • simple follicles = hair
    • compound follicles = wool
  13. When would you use a KOH prep?
    immediate dermatophyte dx
  14. When would you use a skin scraping?
    microscopic ectoparasites
  15. When would you use an acetate tape prep?
    Chorioptes dx
  16. How can dermatophilus be dx?
    • saline + crusts powdered and stained
    • look for g+ railroads tracks
  17. 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
  18. What are some pruritic mediators?
    • substance P
    • histamine
    • PGs
  19. What are some common ectoparasites of FA?
    • flying insects
    • lice
    • Sarcoptes scabiei
    • Psoroptes
    • Chorioptes
  20. What are some common causes of infectious nodules in FA?
    • Corynebacterium pseudotuberculosis
    • Hypoderma spp (warbles)
    • Sporotrichosis
    • Actinobacillosis
    • Actinomycosis
  21. What are some common causes of neoplastic nodules in FA?
    • Squamous cell carcinoma (SCC)
    • Fibroma or fibrosarcoma
    • Epidermal inclusion cyst
  22. What is the difference between an erosion and an ulcer?
    Erosion heals without a scar
  23. What are some common causes of immune-mediated erosions and ulcers in FA?
    • Adverse drug reaction
    • Contact irritant
    • Contact hypersensitivity
    • Photosensitivity
    • Vasculitis
  24. What are some common causes of infectious erosions and ulcers in FA?
    • Dermatophilus congloensis
    • Viral (IBR, Vesicular Stomatitis, Herpes Virus, FMD)
  25. What are some common causes of neoplastic erosions and ulcers in FA?
  26. 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)
  27. What can cause a bulla?
    • burn
    • viral infections
    • immune mediated diseases (bullous pemphigoid)
  28. 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)
  29. What is parakeratosis?
    Cornification with nuclear retention
  30. What is orthokeratosis?
    Cornification without nuclear retention
  31. 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
  32. 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)
  33. What are the most common causes of alopecia?
    • Dermatophytosis
    • Alopecia areata (cattle)
    • Drug reaction
    • Congenital hypotrichosis
  34. What are the most common causes of increased coat length?
    Congenital hypertrichosis
  35. How can hypopigmentation happen?
    • decreased melanin production
    • decreased dispersion of melanin granules
    • increased loss of melanin
  36. What is leukotrichia?
    acquired loss of melanin from the hair shaft, actual factors are unknown
  37. 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
  38. What is the most common cause of loss of pigmentation in FA?
    • Burns & other traumas
    • *Copper deficiency*
  39. What is the most common cause of increased pigmentation in FA?
    • Pruritus
    • Melanoma
  40. What does C. pseudotuberculosis cause?
    • Sheep & goats: caseous lymphadenitis (CLA)
    • Cattle: cutaneous granuloma
    • Horses: ulcerative lymphangitis
  41. 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
  42. What are the characteristics of C. pseudotuberculosis?
    • Facultative intracellular gram+ coccobacillus
    • Infects macrophages & monocytes
    • Soil borne, survives for months-years; even in sunlight
  43. 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
  44. 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
  45. 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)
  46. 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)
  47. 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
  48. How do you interpret the SHI test?
    • Titer interpretation
    • <1:8 not significant
    • >1:256 likely internal abscess formation
  49. 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
  50. 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
  51. 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
  52. 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
  53. What are the two types of contact dermatitis?
    • irritant
    • allergic
  54. 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
  55. 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
  56. What are the CS of contact dermatitis?
    Erythema, edema, vesicles, erosions, ulcerations, crusting, skin thickening, hyperpigmentation
  57. 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
  58. Where can you see udder cleft dermatitis?
    • btw lateral aspect of udder and medial thigh
    • btw udder halves
    • on ventral midline (cranial to udder)
  59. What are the CS of udder cleft dermatitis?
    • foul odor
    • skin necrosis
  60. What is the signalment of udder cleft dermatitis?
    • older cow
    • concurrent udder edema
    • weak fore udder attachment
    • small angle between udder and abdominal wall
  61. 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
  62. 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
  63. 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
  64. 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
  65. Which drugs can be photodynamic agents?
    Phenothiazines, thiazides, methylene blue, tetracyclines, sulfonamides
  66. What photodynamic agents can be synthesized by the body?
    uroporphyrin & coproporphyrin
  67. What diseases cause type 2 photosensitization?
    • Congenital erythropoietic porphyria (bred out now)
    • Bovine protoporphyria
    • *both have an inherited enzyme deficiency*
  68. 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
  69. 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
  70. What is the most common form of photosensitization?
    type 3 - hepatogenous
  71. 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
  72. What plants can cause liver disease -> type 3 photosensitivity?
    • Common Groundsel
    • Ragwort
    • Tarweed
    • Rattleweed
  73. In which animals is facial eczema seen?
    sheep, goats, cattle
  74. What causes facial eczema?
    • Saphrophytic fungus Pithomyces chartarum
    • Produces liver damaging toxin sporidesmin → phylloerythrin isn't properly metabolized → accumulation in peripheral blood → photosensitization
  75. Where is Pithomyces chartarum found?
    Grows commonly on perennial ryegrass in late summer & autumn
  76. Where is facial eczema a problem?
    New Zealand, Australia, South Africa, & Oregon
  77. 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
  78. Which animals are more vulnerable to Pithomyces chartarum?
    Newly-shorn sheep
  79. 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
  80. How can facial eczema be prevented?
    • High levels of zinc
    • Better pasture management
  81. What are some type 3 photosensitizing saponins?
    • Puncture Vine
    • Agave
    • Signalgrass
    • Sacauiste / bunch Grass
    • Narthecium
  82. 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
  83. What are the CS of saponin photosensitization?
    Anorexia, weight loss, icterus, hepatoencephalopathy
  84. 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
  85. In which animals are papillomas commonly seen?
    Young (< 2 years old)
  86. What kind of virus is papilloma?
    • dsDNA
    • 11 bovine strains
  87. Why are papillomas of concern in Saanen goats?
    able to transform into SCC; frequently on udder & teat
  88. 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
  89. When can papillomas be painful?
    On the teats (and predispose to environmental mastitis), penis, interdigital skin, GI tract
  90. 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)
  91. How can you make an autogenous bovine papilloma vaccine?
    • Remove warts & grind
    • Freeze-thaw 2x
    • Filter
    • Add 0.5% formalin for repeated SC injection
  92. What are the characteristics of ORF?
    • Zoonotic
    • Parapoxvirus (DNA poxvirus)
    • Epitheliotropic virus
  93. 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
  94. In which animals is ORF seen?
    Usually young animals
  95. How do animals get ORF?
    scabs from infected animals are contagious
  96. How can ORF be dx?
    • PE
    • Histopathology (eosinophilic intracytoplasmatic inclusion bodies in epithelial keratinocytes)
    • Electron-microscopy
    • PCR
    • Immunochemistry
  97. 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)
  98. What is malignant contagious ecthyma?
    Persistent ORF
  99. 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)
  100. 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
  101. How is ulcerative dermatosis tx?
    Self limiting
  102. When does transmission of ulcerative dermatosis occur?
    during breeding season
  103. What are the CS of BHV-2?
    • Vesicular & erosive lesions on udder & teat
    • Mastitis
    • Chronic: hard milkers
  104. When do you see BHV-2 outbreaks?
    • in heifers 2 weeks after calving
    • Nov-April
  105. How is BHV-2 transmitted?
    • milking machine
    • hands
    • clothes
  106. How is BHV-2 treated?
  107. What is the tx for BHV-2?
    • mild lesions self heal in ~10 days
    • severe lesions heal in 2-3 months
    • cull
  108. How is BHV-2 dx?
    serology for 1:16 titer = exposure
  109. How can BHV-2 be prevented?
    • isolate infected cows
    • good milking hygiene: wash hands between milking, milk last
    • use iodophor disinfectant
  110. Which derm diseases are zoonotic?
    • pseudocowpox
    • bovine papular stomatitis virus
    • vesicular stomatitis virus
    • sarcoptes scabiei
    • dermatophytosis
  111. What are the characteristics of pseudocowpox?
  112. 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
  113. 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
  114. 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)
  115. 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
  116. 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)
  117. What are the characteristics of melanoma?
    • <2% of bovine tumors
    • Young Angus (pigmented), Duroc pigs
    • Are benign
  118. What are the bovine lice?
    • Linognathus vituli
    • Solenoptes capillatus
    • Haematopinus eurysternus
  119. What are the ovine lice?
    • Linognathus ovillus
    • L. stenopsis
    • L. pedalis
  120. What are the caprine lice?
    • Linognathus stenopsis
    • L. africanus
  121. What are the porcine lice?
    Haematopinus suis
  122. 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
  123. 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
  124. 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)
  125. How is pediculosis dx?
    • Hx, PE
    • Microscopy: sucking lice are blue-gray, biting lice are pale to brownish
  126. 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
  127. 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
  128. 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
  129. 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
  130. How is mange dx?
    Skin scrapings from periphery of lesions in multiple locations (deep and superficial)
  131. 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
  132. 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
  133. Where do mange mites live?
    • Sarcoptes: burrows
    • Psoroptes: on surface of epidermis
    • Chorioptes: on surface of epidermis
  134. What are the CS of Psoroptic mange?
    • Pruritus first on withers, later generalized
    • Weight loss, otitis externa, Staph. aureus secondary infx (goats)
  135. 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
  136. 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
  137. What is an important differential for pruritic sheep?
  138. 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
  139. What are the biting flies?
    • Stable flies: Stomoxys calcitrans
    • Horn flies: Haematobia irritans
    • Horse flies: Tabanus spp.
  140. What are the non-biting flies?
    Face flies: Musca autumnalis
  141. 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
  142. 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.
  143. 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
  144. 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)
  145. 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)
  146. What deramtophytes are common in FA?
    • T. mentagrophytes: cattle and goats
    • T. verrucosum: cattle and goats “club lamb fungus"
    • M. nanum: pigs and llamas
  147. What are the CS of dermatophytosis?
    • Alopecia in centrifugal pattern "ring" esp around eyes
    • Crusts, erythema, papules +/- pruritus
    • Claws and hooves weaken and split
  148. 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
  149. 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
  150. 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)
  151. How is dermatophytosis prevented?
    • Consider vaccination
    • Better hygiene
  152. 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
  153. 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
  154. What are the CS of dermatophilosis?
    • aka rain scald
    • Painful purulent crusts or ulcers on dorsum, distal legs, muzzle, claws
    • Not pruritic
  155. How is dermatophilosis tx?
    • Limit moisture
    • Topical treatments like iodines, chlorhexidine
    • Antibiotics like tetracyclines, TMS, penicillin
  156. 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
  157. What are the CS of Staph folliculitis?
    Circular alopecia, crusts, edema, pustules on ventrum, udder, lumbar region, eyes, orally
  158. 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
  159. Which Staph spp are part of Stap folliculitis?
    • Staph aureus (30% on pig farms are MRSA)
    • Staph pseudintermedius
  160. 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
  161. 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
  162. How is greasy pig disease dx?
    • CS
    • Histology and culture to differentiate
  163. What are the ddx for greasy pig disease?
    dermatophytes, zinc deficiency and swine pox
  164. How is greasy pig disease tx?
    • Isolate, better hygiene
    • Systemic abs (early in outbreak) = dramatic affect reducing mortality
    • Novobiocin (abx)
    • Topical antibacterial washes
  165. What is the pathophysiology of Zn responsive dermatosis in cattle?
    Hereditary autosomal recessive defect in GI Zn absorption, aka lethal trait 46
  166. 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
  167. 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
  168. How is Zn responsive dermatosis tx?
    Give elemental Zn supplement
  169. 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)
  170. 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
  171. 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
  172. What is the tx fr Pityriasis rosea?
    self-limiting in 3-10 weeks
  173. 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
  174. 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
  175. 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
  176. 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
  177. What causes split heart sounds?
    • Pulmonary hypertension
    • Right sided heart failure
    • Bundle branch block
    • Endocarditis
  178. 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
  179. What are some reasons heart sounds can be decreased?
    • Obesity
    • Long hair coat
    • High muscle development
    • Hydrothorax
  180. What are some reasons heart sounds can be increased?
    • Excitement
    • Exercise
    • Anemia
    • Heart insufficiency
  181. 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
  182. 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)
  183. 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
  184. 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
  185. What is a continuous murmur, and what are some examples?
    • S1 through S2 into part or all of diastole
    • Patent ductus arteriosus
  186. S1 through S2 into part or all of diastole
    Patent ductus arteriosus
  187. 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
  188. What do splashing heart sounds mean?
    • Pericarditis if gas & fluid are in pericardial sac
    • Almost always accompanied by muffled heart sounds & tachycardia
  189. What does friction rub heart sound mean?
    • Pericardial friction sounds
    • Diagnostic for fibrinous pericardits
  190. What are the two classes of arrhythmias?
    • Abnormality in impulse formation
    • Abnormality in impulse propagation
  191. What is a sinus arrhythmia, and in which animals is it seen?
    • Increasing heart rate during inspiration
    • Common in pigs
  192. What does a wide tachycardia tell you vs. a narrow one?
    • Narrow: origin at or above AV node
    • Wide: origin within ventricular walls
  193. What is the most common cause of a heart block or arrhythmia?
    IV Ca - causes bradycardia
  194. What is the txt for FA arrhythmias?
    • Tx the underlying disease and arrhythmia will correct itself
    • Except in atrial fib or plant toxicity
  195. 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
  196. What are the CS of L-CHF?
    • Coughing
    • Tachypnea
    • Frothy nasal or oral exudates
    • Tracheal rales
    • Pulmonary wheezes & crackles
    • Tachycardia
    • Arrhythmia
    • Heartblocks
  197. 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)
  198. What is the most common irregularly irregular arrhythmia?
    atrial fib
  199. What is the gold standard for diagnosis of myocardial injury?
    cTnI in myocardium sarcomere
  200. 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
  201. 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
  202. How you dx cranial abd pain?
    • Wither’s pinch response test -> grunt and failure to go down if painful = positive
    • Bar test
  203. 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
  204. 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
  205. What is the txt for pericarditis?
    Poor prognosis
  206. How is pericarditis prevented?
    • Give magnet at ~500lbs = ~ 1 year old
    • Use magnets on feed trucks
    • Laparotomy & rumenotomy to remove hardware
  207. 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
  208. 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
  209. 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)
  210. 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)
  211. What is brisket disease?
    • Right sided heart failure from pulmonary hypertension (cor pulmonale)
    • Mainly calves
  212. 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
  213. 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
  214. 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
  215. What are some ddx for R-CHF?
    • hardware disease
    • endocarditis
    • lymphoma
    • emoblic pneumonia
    • viral / bacterial
  216. 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
  217. How can brisket disease be prevented?
    PAP testing - must be performed at high altitudes
  218. 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
  219. 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
  220. 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
  221. What are the primary and secondary cardiomyopathies?
    • Primary: hypertrophic (pigs), congestive, restrictive
    • Secondary: heritable, nutritional, toxic, infection, neoplastic
  222. 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
  223. In which animals is cardiomyopathy esp seen?
    • feeder steers
    • pneumonia can be a pre-disposing factor like brisket disease
  224. 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
  225. 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
  226. 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
  227. 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
  228. Which animals are most sensitive to ionophore toxicity?
    • Monensin: horse > sheep > cattle
    • Lasalocid: horse > cattle > sheep
    • Salinomycin
    • see decrease in ventricular contraction
  229. 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
  230. 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
  231. Where is lymphoma seen?
    R atrium
  232. 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)
  233. What are the characteristics of FMDV?
    • Picornavirus (Aphtovirus)
    • Reportable!!!
    • Morbidity high, mortality low
    • Except: calves which have high mortality
  234. 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
  235. 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:
  236. 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
  237. 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
  238. 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
  239. What is the Tetralogy of Fallot?
    • Overriding aorta
    • VSD
    • Right ventricular hypertrophy
    • Pulmonary stenosis
    • ...with ASD = Pentalogy of Fallot
  240. 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!