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Ag Animal II > Ag Animal Dermatology > Flashcards

Ag Animal Dermatology Flashcards

1
Q

3 Basic Dermatology Tests

A
  1. Scrape
  2. Culture
  3. Biopsy
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2
Q

Which LA species gets pemphigus foliaceus?

A
  • Goats
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3
Q

Appearance of pemphigus foliaceus

A

Widespread, crusty, pruritic lesion

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4
Q

Pathophys of pemphigus foliaceus

A
  • Type II hypersensitivity
  • Autoantibodies against keratinocytes (glycocalyx)
  • Intracellular junctions breakdown, blisters and acantholysis
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5
Q

Diagnosis of pemphigus foliaceus

A
  • Biopsy
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6
Q

Treatment for pemphigus foliaceus

A

Steroids (prednisolone, dexamethasone)

  • Taper dose over time
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7
Q

Prognosis for pemphigus foliaceus

A

Unknown

  • Rare
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8
Q

What is urticaria?

A
  • Transient swelling of skin (wheals) or mucous membranes
  • Localized dermal edema
  • Transudate of fluid from capillaries and small vessels
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9
Q

Non-immune causes of urticaria

A
  • Injury, thermal, solar
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10
Q

Immune causes of urticaria

A
  • Reaction to allergens
  • e.g. penicillin, sulfas, aspirin, ingested/inhaled allergens
  • MILK at dry-off
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11
Q

Diagnosis for urticaria

A
  • Physical examination and history

- Wheals “pit” +/- pruritus

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12
Q

Treatment of urticaria

A
  • Avoid allergen
  • Corticosteroids
  • Antihistamines
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13
Q

What is angioedema?

A
  • Angioedema: same as urticaria but involves SQ and is diffuse
  • Still involves transudation of fluid from capillaries and small vessels
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14
Q

Side effect of corticosteroids in pregnant cattle

A
  • Abortion
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15
Q

What are causes of contact dermatitis?

A
  • Irritant (most common) and allergic
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16
Q

Clinical signs of contact dermatitis

A
  • Variable severity (mild itchiness to severe lesions)

- Erythema, edema, vesicles, erosion, ulcers, crusting, pigment changes

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17
Q

Causes of contact dermatitis

A

Usually iatrogenic

  • Bedding, tack, etc.
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18
Q

Diagnosis of contact dermtatitis

A
  • History is important
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19
Q

Treatment for contact dermatitis

A
  • remove source

- Symptomatic care

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20
Q

What is Dermatophilus congolensis?

A
  • Gram +, branching, filamentous, aerobic bacteria
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21
Q

Type of division of Dermatophilus congolensis

A
  • Longitudinal and transverse division
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22
Q

***Classic appearance of Dermatophilus congolensis

A

Railroad tracks (parallel rows)***

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23
Q

Other names of dermatophilosis (maybe not so important)

A
  • Mycotic dermatitis, rain scald, rain rot, lumpy wool, strawberry footrot
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24
Q

Type of infection with dermatophilosis

A
  • Superficial bacterial infection
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25
Q

Type of infection with dermatophytosis

A
  • Ringworm

- Superficial fungal infection of keratinized skin by Microsporum, Trichophyton, etc.

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26
Q

Who gets dermatophilosis?

A

-Most all domestic mammals

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27
Q

Signalment with dermatophilosis?

A
  • No predilection for age, sex, or breed
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28
Q

Where is dermatophilosis?

A
  • Worldwide
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29
Q

Seasonality of dermatophilosis

A
  • high moisture regions/conditions

- Fall/winter

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30
Q

Risk factors for dermatophilosis

A
  • Humid weather, warm or cool
  • Prolonged rainy seasons (e.g. the PNW)
  • Frequent spraying or dipping
  • Crowding
  • +/- worse in some breeds (Merino, based on the wool type)
  • High fly and tick populations
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31
Q

Which tick is associated with dermatophilois?

A
  • Amblyomma variegatum

- Immunosuppression

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32
Q

Where is Dermatophilus congolensis thought to live?

A
  • Soil
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33
Q

Main source of Dermatophilus congolensis

A

Chronic carrier animals

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34
Q

Spreading of Dermatophilus congolensis

A
  • Contact, fomites, biting and non-biting flies
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35
Q

Where does Dermatophilus congolensis persist? For how long?

A
  • Crusts (in environment)

- Up to 3.5 years

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36
Q

Pathophysiology of dermatophilosis

A
  • Moisture –> defect in stratum corneum
  • Zoospores germinate –> mycelia proliferate in the living layers of the epidermis
  • Inflammatory response (neutrophils/PMNs
  • Organisms eliminated via re-epithelialization
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37
Q

What causes the clinical signs of dermatophilus?

A
  • The inflammatory response
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38
Q

Major issues with dermatophilosis in cows

A
  • Decreased production (Moses lake case)
  • Hide damage
  • Epizootic death
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39
Q

Major issues with dermatophilosis in sheep

A
  • Decreased fleece/skin value
  • Interferes with shearing
  • Lamb deaths
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40
Q

Is dermatophilosis zoonotic?

A
  • Yes
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41
Q

Clinical signs of dermatophilosis in cattle - distribution

A
  • Neck, top line, udder, limbs, ventrum
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42
Q

Clinical signs of dermatophilosis - appearance

A
  • Thick, horn-like brown crusts (crusted paintbrush)
  • “Paintbrush” (hair stick together in variable sized lesions)
  • Moist grey/pink “granulation” tissue under crusts
  • PAINFUL*****
  • Not pruritic
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43
Q

Clinical signs of dermatophilosis in sheep - distribution

A
  • Initial lesions on wool-less areas of face, legs, scrotum

- Later wooled areas

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44
Q

Clinical signs of dermatophilosis in sheep - appearance and other issues

A
  • pyramid-shaped, thick, pigmented crusts, discolored wool
  • Heavy losses in lambs
  • Secondary fly strike
  • Fatal pneumonia
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45
Q

Clinical signs of dermatophilosis in goats - location

A
  • Starts at ears, crusts can block ear canals
  • External nares
  • Dorsal midline, medial thighs
  • Appearance same as cattle and sheep
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46
Q

Diagnosis of dermatophilosis

A
  • Scrape/impression smear***
  • Culture
  • ELISA
  • FA
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47
Q

Where to do the scrape/impression smear for dermatophilosis?

A
  • Under crusts

- He thinks that impression smears are more successful because you don’t disrupt things as much

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48
Q

What to look for with a scrape/impression smear with dermatophilosis?

A
  • Stain and railroad tracks (look at the pictures)
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49
Q

What is the most important aspect of dermatophilosis treatment?

A
  • Remove predisposing factors (SINGLE MOST IMPORTANT ASPECT OF RX)
  • Mitigate moisture**
  • Reduce external parasites
  • Optimize animal health (nutrition, stress, etc.)
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50
Q

Antibiotics for dermatophilosis - which ones? and when to administer?

A
  • Can try in some animals
  • Single, high dose (e.g. Penstrep, erythromycin, tetracycline)
  • Treat prior to shearing (8 weeks so lesions healed by shearing)
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51
Q

Topical treatments for dermatophilosis?

A
  • Chlorhexidine sprays
  • Povidine iodine spray
  • Iodine shampoo (imaging in 1000 head herd)
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52
Q

Withdrawals for topical treatments**

A
  • Still need to be considered!

- FARAD

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53
Q

Infectious agent of ovine proliferative dermatitis AKA strawberry footrot?

A
  • Dermatophilus congolensis
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54
Q

Who gets ovine proliferative dermatitis? WHen do they get it?

A
  • Lambs in summer
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55
Q

Morbidity in ovine proliferative dermatitis

A
  • High morbidity

- Primary losses are decreased weight gain

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56
Q

Where does D. congolensis come from with ovine proliferative dermatitis?

A
  • Organism or scabs in soil
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57
Q

Where are the lesions for Strawberry footrot?

A
  • Lower leg

- Coronet to stifle

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58
Q

Clinical signs of strawberry footrot

A
  • Small, coalescing scabs
  • Scabs grow, wart like, hair loss
  • Under scabs is a bloody, fleshy mass (strawberry-like)
  • Not painful unless inter-digital, but he thinks it’s painful
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59
Q

Treatment for strawberry footrot

A
  • Same

- Bath would be appropriate here - walk them through a footbath

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60
Q

Control of strawberry footrot

A
  • Quarantine

- Rest paddocks can help, but if they stay moist, the organism can live for years

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61
Q

Folliculitis

A
  • Inflammation of hair follicles

- AKA superficial pyoderma

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62
Q

Furunculosis

A
  • Severe inflammation of follicles
  • Ruptured follicles, “boils”
  • Inflammation of adjacent dermis and SQ
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63
Q

Impetigo

A
  • Infection causing subcorneal pustules, but not follicles

- Pustules that aren’t in the follicles

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64
Q

Who gets folliculitis/furunculosis/impetigo?

A
  • Goats and cattle
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65
Q

Signs of folliculitis/furunculosis/impetigo? - distribution

A
  • Udder, abdomen, perineum
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66
Q

Pain/pruritus in folliculitis/furunculosis/impetigo?

A
  • Painful but not pruritic
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67
Q

Which bacterium are most common with folliculitis/furunculosis/impetigo? ?

A
  • Coagulase positive Staph spp (especially S. aureus, S. pseudintermedius)
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68
Q

Diagnosis for folliculitis/furunculosis/impetigo?

A

Culture, biopsy

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69
Q

Treatment for folliculitis/furunculosis/impetigo?

A

Antibiotics (parenteral)

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70
Q

Appearance of folliculitis/furunculosis/impetigo?

A
  • look at the pictures
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71
Q

What is hairy heel warts?

A
  • Infectious contagious dermatitis of digital skin

- Important cause of lameness

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72
Q

WHo gets hairy heel warts?

A
  • Mostly dairy cattle

- 1st and 2nd lactation, near parturition or freshening

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73
Q

Where do hairy heel warts usually manifest?

A
  • Hind feet*** (80% of the time on the hind, plantar aspect)
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74
Q

Clinical signs of hairy heel warts

A
  • Hind feet
  • Raised, oval, demarcated, +/- filiform, red/brown/grey
  • Tends to be in the interdigital area
  • Foul odor!
  • EXTREMELY painful
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75
Q

How contagious is hairy heel warts?

A
  • Spreads rapidly
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76
Q

Risk factors for hairy heel warts

A
  • Muddy, wet conditions

- Introduction of new animals (carriers?)

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77
Q

What causes hairy heel warts?

A
  • Associated with numerous obligate anaerobes
  • Treponema spp. often found
  • Mode of transmission unknown
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78
Q

Treatment for hairy heel warts

A
  • Topical antibiotics such as tetracycline powder (extralabel drug use!; unless cow isn’t lactating)
  • Parenteral antibiotics (PPG, ampicillin, Ceftiofur?)
  • Footbaths
  • Improve hygiene (stalls, bedding, alleys, etc.)
  • Reduce stocking rate
  • Disinfect trimming equipment
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79
Q

What is the label for ceftiofur?

A
  • BRD, metritis, “footrot” (F. necrophorum/B. melaniogenicus)
80
Q

Etiology of papillomatosis

A
  • Bovine papilloma virus
  • At least 6 strains (BPV 1, 2)
  • Single viral type associated with lesions
  • > 1 type can infect an animal
81
Q

What determines the distribution and appearance of papillomatosis?

A
  • Distribution and appearance related to strain
82
Q

Papillomatosis in horses, goats, and sheep

A
  • 1 strain recognized in each species thus far

- BPV genome found in equine sarcoids

83
Q

Are the different strains of BPV cross-protective?

A
  • No
84
Q

When are animals most susceptible to papillomatosis?

A
  • Young most susceptible
85
Q

Transmission of papillomatosis

A
  • Contact
  • Usually need abrasions (wire, thorns, etc.)
  • Perianal via rectal exams, etc.
  • Single viral type associated with lesions
86
Q

Significance of papillomatosis

A
  • Aesthetic
  • Milking (teats)
  • Breeding (perineum)
  • Sale/transfer (health certificates)
87
Q

Clinical signs of papillomatosis in cattle

A
  • Teats: may obstruct milking
  • Perianal: breeding difficulties
  • Oral: eating difficulties
  • Reticular: chronic bloat
  • Penile: paraphimosis, phimosis, etc.
88
Q

Treatment of penile warts

A
  • Debride it and get rid of it
  • They will clean it up, and put a a ring block
  • Lidocaine and cut off the wart
  • Have to avoid the dorsal nerve of the penis (would not be able to ejaculate)
  • Ventral side is the urethra

They use a hyfercator, which is a thermal instrument that will burn it off

89
Q

Clinical signs of papillomatosis in goats

A
  • Common on udder, un-pigmented skin
90
Q

Clinical signs of papillomatosis in sheep

A
  • Rare

- Face and legs

91
Q

Papillomatosis and fomites**

A
  • Be cognizant of transmission
  • We can be the fomite

When you’re vaccinating animals, have some hygiene between animals

92
Q

Treatment for papillomatosis

A
  • Often none
  • Remove if a show animal
  • Surgical removal (cryotherapy, hyphrication or heat)
  • Many “farmer” treatments that are ineffective
  • Vaccinate with commercial or autogenous vaccine
93
Q

Who gets ringworm AKA dermatophytosis?

A
  • All species (cattle and horses especially)
94
Q

Most common species for ringworm and who gets it

A
  • T. verucosum

- bovine, ovine, caprine

95
Q

Risk factors for ringworm

A
  • Contact (group housing)
  • Infected housing
  • High humidity
  • Young animals
  • Carriers
  • Fomites (grooming, interchangeable equipment, etc.)
96
Q

Clinical signs of ringworm in cattle

A
  • Thick, grey, rounded, coalescing crusts
  • Moist (initial) –> dry
  • Alopecia, dandruff
  • Mostly head, neck, perineum (general distribution)
97
Q

Clinical signs of ringworm in sheep

A
  • Lesiosn on head, non-wooled areas
  • Round hairless lesions with grey crust
  • Regress spontaneously at 4-5 weeks but persists in a herd
98
Q

Clinical signs of ringworm in goat

A
  • Lesions, similar to sheep, but cover more body
99
Q

Ringworm in people

A
  • Superficial fungal infection
  • Tinea corporis (any area, all ages)
  • Tinea cruris (inguinal area)
  • Tinea pedis (“athletes foot”)
100
Q

Diagnosis of ringworm

A
  • Skin scraping
  • Smear see spores, hyphae
  • Culture on DTM and color change
  • Some infected hairs fluoresce with Wood’s lamp (both false positives and false negatives)
101
Q

Treatment for ringworm

A
  • Spontaneous recovery common

- Individual vs group treatment

102
Q

Individual treatment for ringworm

A
  • Not common
  • Brush off scabs
  • Apply iodine solutions or lime sulfur rinse, bleach rinse, enilconazole rinse (Canada, Europe)
103
Q

Treatment for groups of animals

A
  • Captan (orchard fungicide)
  • 1:300 sprayed twice 1-2 weeks apart
  • 1:150 sprayed on facilities (barn, feeders, wood, etc.)
  • Bleach solutions
  • Captan you must be careful with withdrawals
  • SYstemic sodium iodide or griseofulvin (but griseofulvin is expensive and a teratogen)
104
Q

Control of ringworm

A
  • Isolate and treat affected
  • Disinfect housing
  • Destroy bedding
  • Vaccines may have success in Europe but not available in US
105
Q

Host specificity of lice

A
  • They are typically host specific
106
Q

Biting lice vs sucking lice names

A
  • Mallophaga (biting or chewing lice)

- Anoplura (sucking lice)

107
Q

Specific mallophaga lice in cattle

A
  • Damalinia
108
Q

Specific anoplura lice in cattle

A
  • Haematopinus, linognathus
109
Q

When do you see lice?

A
  • Winter (typically)
110
Q

What’s the medical term for lice?

A
  • Pediculosis
111
Q

Diagnosis of pediculosis

A
  • Pruritus
  • See lice
  • Dry, scaly skin, alopecia
  • Phytobezoars weight loss
112
Q

Treatment for pediculosis

A
  • Topical (coumaphos, malathion, pyrethrins, lindane, methoxychlor)
  • They try to avoid OPs in lactating animals so stick with pyrethrins
  • Ivermectin
113
Q

What’s the medical term for mite infestation?

A
  • Acariasis
114
Q

Psoroptic mange - who gets?

A
  • Cattle and goats
115
Q

Appearance of psoroptic mange

A
  • Crusty papular lesions, on head and neck
116
Q

Diagnosis of psoroptic mange

A
  • Pruritus, scrape, biopsy
117
Q

Treatment of psoroptic mange

A
  • Ivermectin

- Reportable in cattle in US

118
Q

Chorioptic mange distirubtion

A
  • Alopecia, crusts, scales

- - Hind limbs, tail, perineum

119
Q

Dx of chorioptic mange

A

Pruritus, scrape, biopsy

120
Q

Tx of chorioptic mange

A
  • Ivermectin
121
Q

Reportability of mites

A
  • Report all of them basically if you see one
122
Q

Sarcoptic mange - what’s unique?

A
  • Zoonotic

- Mites can live off the host***

123
Q

Appearance of sarcoptic mange

A
  • Scaling, crusts, alopecia, self trauma

- Head and neck (or generalized)

124
Q

Dx of sarcoptic

A
  • Pruritus, scrape, biopsy
125
Q

Tx of sarcoptic mange

A
  • Ivermectin
126
Q

Demodectic mange - who gets?

A
  • Goats and cattle
127
Q

Demodectic mange - where are the lesions?

A
  • Nodular lesions (zits) on head and neck
128
Q

Dx of demodectic mange

A
  • Pruritus
  • Scrape
  • Biopsy
129
Q

Treatment of demodectic mange

A
  • Amitraz, ivermectin (tought to treat, may regress spontaneously)
130
Q

Stephanofilariasis - what is it?

A
  • Filarial dermatitis via female horn fly
131
Q

Where does stephanofilariasis end up?

A
  • Ventral midline
132
Q

Appearance of stephanofilariasis?

A
  • Alopecia, crusting, nodules, ulcers
  • Ventral midlien
  • Mild pruritus
133
Q

Treatment of stephanofilariasis

A
  • Typically not

- Ivermectin? Not approved

134
Q

Three types of photosensitization

A
  1. Primary
  2. Secondary
  3. Congenital
135
Q

Primary photosensitization

A
  • Criculating photodynamic agents - activated by UV light
  • Emits energy and damages tissues
  • This is something they ingest
  • e.g. St. John’s wort
136
Q

Secondary photosensitization

A
  • Toxins, bacteria, viruses, neoplasia –> damages liver –> phylloerythrin (degraded chlorophyll) not conjugated –> acts as a photodynamic agent
  • Carbon tetrachloride is the poster child for secondary
137
Q

Which photosensitization carries a better prognosis: primary or secondary?

A
  • Primary
138
Q

Congenital photosensitization

A
  • Aberrant pigment synthesis
  • Porphyria
  • Rare
139
Q

Which plants cause primary photosensitization?

A
  • St. John’s wort (hypericum perforatum)**
  • Possible Lady’s thumb
  • Buckwheat (Fagopyrum)
  • Wild carrot
  • Perennial rye grass
  • Burr trefoil
140
Q

Drugs that cause primary photosensitization

A
  • Sulfonamides, tetracyclines, phenothiazine, thiazides, etc.
141
Q

Where do you often see lesions for primary hypersensitization?

A
  • White areas
142
Q

Treatment of photosensitization

A
  • Eliminate source of photo agent
  • Avoid sunlight
  • Antibiotics (secondary pyoderma)
  • Wound management/debridement
  • SYmptomatic for liver disease
143
Q

Photosensitization diagnosis

A
  • Diagnostic is if you take them out in the sunlight for a few minutes and they get very frantic
  • Get them back in the shade, and they calm down
144
Q

Prognosis for primary, secondary, and congenital photosensitization (i.e. porphyria)

A
  1. Primary = favorable
  2. Secondary (hepatogenous) = poor
  3. Porphyria = poor
145
Q

What’s the biggest problem with lice?**

A
  • Itching and irritation
  • The animals are constantly grooming themselves and licking themselves, so you also end up with other issues (like phytobezoars, etc.)
146
Q

Contagious ecthyma common name

A

Orf

147
Q

Contagious ecthyma - what’s one of the big concerns for this

A
  • Zoonotic

- You do need an abrasion, but it’s pretty bad

148
Q

Contagious ecthyma - what type of virus? What is the significance?

A
  • Poxvirus

- Can last for a long time in the environment

149
Q

Who gets orf?

A
  • Sheep and goats mostly

- Also camelids, wild sheep and goats, musk ox, etc.

150
Q

Morbidity and mortality of orf in adults vs lambs

A

High morbidity, low mortality in adults

  • Mortality can be high in lambs (they can starve if the lesion is around the mouth)
151
Q

Risk factors for orf

A
  • Dry seasons
  • Access to wild ruminants
  • Surgical procedures (any sort of procedure)
  • FPT (malignant form)
152
Q

Transmission of contagious ecthyma

A
  • Contact (animals, inanimate objects)
  • Stable in the environment (it’s a poxvirus!!!)
  • Lives in crusts up to 12 years
  • Farms that have it will have it for awhile
153
Q

Significance of contagious ecthyma

A
  • Can’t nurse
  • Fly strike
  • secondary bacterial infections
154
Q

Clinical signs of contagious ecthyma (typical)

A
  • Ulcers and scabs at mucocutaneous junction!
  • eyelids, lips, nostril, coronet, gingiva, teats, etc
  • EXTREMELY PAINFUL!***
  • Progressive
155
Q

Malignant form signs of contagious ecthyma

A
  • Spreads to trachea, lungs, esophagus, etc.

- Happens with FPT

156
Q

Recovery from contagious ecthyma

A
  • Spontaneous recovery in 2-3 weeks

- Unless there’s a secondary issue going on

157
Q

Progression of contagious ecthyma***

A
  • Papular –> vesicular –> pustular –> proliferative, coalescing, scabbed lesion
158
Q

Signs of contagious ecthyma in lambs

A
  • Reluctance to nurse, walk, be nursed
159
Q

Diagnosis of contagious ecthyma

A
  • History and clinical signs (progressive, painful, mucocutaneous lesion that has a high morbidity)
  • SErology
  • Viral ID (EM, culture)
160
Q

Differentials for orf

A
  • Sheep pox and goat pox
  • Blue tongue
  • Ulcerative dermatosis
161
Q

How to differentiate Blue tongue from orf**

A
  • Blue tongue mostly around the mouth

- **Blue tongue is in the fall; orf is in the spring

162
Q

How to differentiate Sheep and goat pox from Orf?

A
  • Sheep and goat pox are more virulent
  • Also have pyrexia
  • Also have rhinitis
163
Q

How to differentiate ulcerative dermatosis from Orf?

A
  • Leg and lip ulcer
164
Q

Treatment for Orf****

A
  • DO NOT DEBRIDE*** (Delays healing)
  • Support (tube feed young)
  • Soft palatable feeds
  • Prevent secondary bacterial infections
  • Cryosurgery (not as much)
  • Intralesional steroids, chemotherapeutics (not universal)
165
Q

Is Orf reportable?

A
  • Yes in WA (within 24 hours)
166
Q

Control of Orf

A
  • Isolate early cases

- Vaccination

167
Q

Vaccination of Orf

A
  • Ineffective if incidence already high
  • Local, autogenous most effective (in the axilla)
  • Once you start, you have to continue from then on out
  • Annual of 6-8 weeks lambs (pre-lambing ewe vaccination ineffective)
168
Q

Fly strike - what’s the problem?

A
  • Serious loss to sheep in terms of life and wool
169
Q

Which species of fly cause fly strike?

A
  • Green bottle fly
  • Black blow fly
  • 2° screw worm (Cochliomyia macellaria)
170
Q

Pathophys of Fly Strike

A
  • Female flies attracted to decaying matter (wounds, feces, etc.)
  • Screwworm larvae can feed on live tissue!
  • Larvae feed on necrotic tissue
171
Q

Treatment of fly strike

A
  • Management (“crutching”)
  • Shearing
  • Wound management
172
Q

Crutching

A

Shearing the perineal area and back of the udder so that it’s clean when they lamb

173
Q

Which genus is the screwworms?

A
  • Cochliomyia hominivorax
174
Q

Appearance of Cochliomyia?

A
  • 3x the size of the house fly (green/blue)

- Previously in Southern USA and Mexico (eradicated)

175
Q

What’s the main problem with screwworms?

A
  • Larvae are aggressive, feed on living tissue

- Cavernous lesions, liquefaction, necrosis, death!

176
Q

Treatment with screwworms (historical vs contemporary)

A

Historic: OPs

Contemporary: Fipronil and doramectin

177
Q

Florida Keys Outbreak

A
  • Key deer
  • Irradiated pupae
  • Male sterile but active
178
Q

Fipronil and yellow jackets

A

If you have yellow jacket problems

Put fipronil in the spam and the yellow jackets take it back to the next

Day one you’ll lose 90%

Day 3 is 98%

179
Q

What’s the main problem with hypoderma?

A
  • Loss to cattle industry (millions of $)

- Loss of hide (holes in the hide)

180
Q

Two species of hypoderma?

A
  • H. bovis

- H. lineatum

181
Q

Where is H. bovis?

A
  • N and S USA
182
Q

Where is H. lineatum

A
  • Prefers warmer climates
183
Q

Appearance of cows being attacked by hypoderma?

A
  • They’re literally running away
184
Q

When are hypoderma active and laying eggs?

A
  • Spring and summer
185
Q

Where do the hypoderma lay their eggs?

A
  • Rear limbs (Heel flies)
186
Q

Where do hypoderma lineatum and hypoderma bovis over-winter?

A
  • H. lineatum (esophagus)

- H. bovis (spinal canal) - RULE out for an acutely down animal

187
Q

At what time of the year do L1 larvae hibernate in the animal? When do they migrate toward the dorsum

A
  • L1 larvae stay through fall/winter

- Late winter - migrate toward dorsum

188
Q

What drugs for treatment of Hypoderma?

A
  • OPs

- Macrocyclic lactones (doramectin, ivermectin, moxidectin)

189
Q

When should you NOT treat Hypoderma?

A
  • Between Oct 1st and March 1st
190
Q

Crowpeck

A
  • Birds often land on the backs of animals
191
Q

Miscellaneous

A

look at the images

192
Q

Eliophora

A
  • Crusting lesions

- Filarial worm of white tailed deer that can cause crusting lesions in the wrong host

193
Q

Frostbite - where in Cattle?

A
  • often on the feet
  • Can be ears, tails, etc.
  • Calves when they lay down will have one back leg exposed, which is why one back leg is usually frostbitten
194
Q

Treatment for frostbite

A
  • Aloe vera (thromboxane inhibitor)

- NSAID

195
Q

Treatment for wounds

A
  • Debridement
  • Systemic antibiotics
  • Kept it clean
  • Dress with sugar and betadine mixture

Ag Animal II (13 decks)

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