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1
Q

What is the predominant clinical sign of allergic skin disease?

A

Pruritus

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2
Q

When does food allergy occur in dogs vs atopy?

A

younger dogs and older dogs, atopy starts around 1-3 years old

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3
Q

Atopy may present _ where as food allergy can present _

A

seasonally
year round

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4
Q

Distribution of CS for food allergy dermatitis vs atopy?

A

They are identical and cant be used to distinguish between the two

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5
Q
A
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6
Q

How do we diagnose atopy?

A

-ruling out other diseases

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7
Q

Signalment for flea allergy dermatitis

A

-no age predilection, usually over 6 months of age

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8
Q
A
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9
Q

What are predisposed breeds for atopy?

A

West highland terrier and English bulldog

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10
Q

Contact allergy signalment

A

No age predilection

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11
Q

Seasonality and Speed of flea allergy dermatitis

A

-seasonal or nonseasonal depending on geography
-rapid onset, often in warm weather

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12
Q

Seasonality of atopy and speed of onset of CS

A

-seasonal or nonseasonal depending what the patient is allergic to
-usually gradual onset, often starts in the summer

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13
Q

Food allergy seasonality and onset

A

-nonseasonal
usually gradual onset

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14
Q

Contact allergy seasonality and onset

A

-seasonal or non seasonal depending on what the patient is allergic to
-often rapid onset

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15
Q

Lesion distribution of flea allergy dermatitis

A

-caudal half of the body around dorsolumbosacral region, tailbase, perineum, thighs, umbilicus
-usually not ears
-itchy

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16
Q

Lesion distribution for atopy

A

-face, paws, distal extremities, ears, ventrum
-itchy

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17
Q

Food allergy lesion distribution

A

-same as atopy: face, paws, distal extremities, ears, and ventrum
-may or may not be itchy

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18
Q

Lesion distribution of contact allergy

A

Usually on hairless areas that readily come into contact with the environment - muzzle, abdomen, and ventrum of paws
-usually not ears
-primary lesions such as vesicles and erythamtaous papules
-itchy

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19
Q

What are two reaciton patterns we can see in cats?

A

miliary dermatitis and eosinophilic granuloma complex. They can be seen with all 4 types of skin allergy complexes

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20
Q

Miliary dermatitis

A

diffuse crusted papules

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21
Q

Indolent ulcer

A

most commonly observed as an ulcerative syymetrical lesion on the upper lip

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22
Q

Eosinophilic granuloma

A

found in mouth or body

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23
Q

Eosinophilic plaque

A

commonly observed as linear plaque on caudal thighs

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24
Q

Flea allergy dermatitis distribution in cats

A

caudal dorsal, symmetrical alopecia, or face and neck

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25
Q

How do we diagnose flea allergy dermatitis?

A

CS distribution, finding fleas or flea dirt or a 2-3 month treatment trial

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26
Q

How do we diagnose atopy?

A

-rule out all other differentials

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27
Q

How do we diagnose food allergy dermatitis?

A

-diet trial with either a hydrolyzed diet or novel protein
-serum tests for food allergies are not accurate

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28
Q

How do we diagnose contact allergy?

A

-patch test

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29
Q

If you are unable to make a determination about the cause of puritus, how do you proceed?

A

1_ rule out infectious disease that may cause itch such as sarcoptes, dermatophytosis, and demodex.
2. Rule out flea allergy dermatitis with at least 8 weeks of strict flea control for all animals in the house hold. The environment should also be treated
3). Rule out food allergy with 8-12 week diet trial

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30
Q

What does an alveolar pattern look like radiographically?

A

Fluid/cells within alveoli
Collapse
Soft tissue or fluid opacity
air bronchogram
-lobar sign

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31
Q

What diseases can we see with alveolar pattern

A

-Bronchopneumonia
-Edema (cardiogenic vs non cardiogenic)
-atelectasis
-hemorrhage
-mass (granulomatous, neoplasia)
-torsion

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32
Q

What is the distribution for bronchopneumia?

A

-cranio-ventral

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33
Q

Cardiogenic or non cardiogenic edema distribution

A

cardo-dorsal

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34
Q

2nd Degree AV block

A

-Non pathologic heart arrythmia in healthy horses
-Slow to normal HR
-Normal QRS complex
-p waves not followed by QRS complex
-no treatment necessary
-Just hear a break in the rhythm when you auscultate

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35
Q

Atrial fibrillation

A

-Normal to elevated HR
-Normal QRS complex
-R-R interval irregular
-No p waves, fibrillation waves
CS =none, excersise intolerance, poor performance, possible underlying condition

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36
Q

How do you treat a-fib?

A

None
-quinidine sulfate -> side effects are common which are diarrhea, colic, laminitis,

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37
Q

What is the most superifical layer of the cornea?

A

Corneal epithelium
compromised of 5-10 layers of cells

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38
Q

Corneal stroma

A

Occupies 90% of cornea thickness
Mostly collagen

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39
Q

Descemets membrane

A

The basement membrane is

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40
Q

What is an uncomplicated corneal ulcer?

A

Superficial erosions in which there is only loss of corneal epithelium
-always heal within 7 days

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41
Q

What does the fluroscenin stain adhere to?

A

Hydrophilic stroma

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42
Q

What are causes of superficial corneal ulcers?

A

Traumatic -> exogenous (foreign body) or endogenous (eyelid abnormality)
Decreased corneal protection -> KCS or decreased tear quality (exposure keratitis or pigmentary keratitis)
Decreased blink reflex (CN 5 or 7 deficit)

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43
Q

What is the primary goal for uncomplicated ulcers?

A

1) find and remove the cause if possible
2) use a broad spectrum topical antibiotic
3) cytoplegia, using a topical anticholinergic such as Atropine (decreases secondary anterior uveitis)
4) Self trauma -> use an e-collar to prevent trauma
5) NEVER use a topical steroid

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44
Q

What is the prognosis superifical ulcers?

A

-Excellent
-should always heal within 5-7 days
-if ulcer does not heal within this time, dont change therapy plan change your diagnosis

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45
Q

What is the uvea composed?

A

-iris, ciliary body, and choroid
-when all three structures are inflammed its called panuveitis

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46
Q

What can owners present with a cat that has panuveitis?

A

1) photophobia
2) red eye consistent with conjunctival hyperemia
3) epiphora or seromucoid discharge
4) blephrospasm
5) third eyelid elevation

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47
Q

On optho exam, what can we see with panuveitis?

A

aqueous flare
miosis
corneal edema
intaoccular inflammatory cells
hypophon
ocular hypotension
synechiae
cataract
iridal thickening or hyperpigmentation

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48
Q

What is aqeuous flare due to?

A

breakdown of the aqueous blood barrier and release of protein and cells into the anterior chamber from iridal and ciliary vessels

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49
Q

What are causes for panuveitis?

A

Idiopathic (50-70)%
Intraocular (Cataract, Intraocular tumor)
Infectious (4Fs and T, B)
Neoplastic (lymphoma)

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50
Q

What are the 4F’s of panuveitis?

A

FELv
FIV
FIP
Fungal (cryptococcus is the most common)
T= toxoplasma gondii
B= bartonella hensalae

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51
Q

How do we figure out if a cat has panuveitis?

A

1) complete history and physical
2) CBC, chem, UA
3) serology for infectious causes
4) thoracic radiographs
5) abdoominal ultrasound

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52
Q

How do we treat panuveitis?

A

-Treat underlying cause if found
Nonspecific therapy
-topical steroid
Topical mydriatic (make sure IOP is low or normal)
-Oral steroid (only if negative or infectious disease)

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53
Q

What is the prognosis of panuveitis?

A

-depends on underlying cause or chroniciity
-idiopathic may cause recurrence despite therapy
Sequela include: secondary gluacoma, synechia, cataract, retinal detachment, blindness

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54
Q

Feline Asthma

A

Airway inflammation and mucous accumulation resulting in labored breathing and wheezing

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55
Q

How do we diagnose feline asthma?

A

Diagnosis of exclusion, made by ruling out other causes of dyspnea, wheezing, coughing in an otherwise healthy cat

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56
Q

What are the CS of feline asthma?

A

Expiratory dyspnea (expiratory push), wheezing and coughing
Often acute onset at first but then gradual
Radiograph bronchial pattern
Treated with oral or inhaled steroids and bronchodilators

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57
Q

What are the 3 presentations of feline asthma?

A

-cats with intermittent signs
-cats with consistent signs
acute emergency presentation

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58
Q

What should we rule out?

A

-heart diseae
-pneumonia
-penumothorax and pleural effusion
-pulmonary neoplasia
-inhaled foreign body
-respiratory parasites

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59
Q

What are the diagnostic tests of choice for feline asthma?

A

-CBC
-thoracic radiographs

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60
Q

Prognosis for feline asthma?

A

-The disease is not curable but can be managed through appropriate therapy

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61
Q

What are predisposing factors that cause gastric ulcers?

A

-Catecholamine release
-decreased mucosal blood flow (less PGE due to NSAIDS, shock)
-sepsis
-increase gastrin or histamine release

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62
Q

What are the four clinical syndromes of Abomasomal ulcers?

A

1) Non perforating but painful, little bleeding
2) Non perforating but significant bleeding
3) slowly perforate and adhere to parietal peritoneum simultaneously, demonstrates cranial abdominal pain similar to TRP
4) rapid perforation and massive peritonitis, shock, death

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63
Q

With bleeding ulcers, what CS can we see?

A

melena
pale mm
rapid poudning heart
weakness
death if enough blood is lost

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64
Q

Prognosis with perforating ulcer?

A

-poor prognosis
-requires immediate surgery and flushing abdomen
-requires agressive antibiotic treatment, NSAIDS and IV fluids
-long recovery from peritonitis
-This type also occurs in foals and people

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65
Q

How can we minimize gastric or abosomal secretion?

A

TYpe 2 antihistamines such as cimetidine, raniditine, famotidine, to decrease acid secretion
-omeprozle decrease acid secretion

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66
Q

How do we treat abomasomal ulcers?

A

-H2 agonists
discontinue NSAIDs
-bland fiber diet (hay)
-Blood transfusion if bleeding
-if perforated with localized adhesions and peritonitis, discontinue NSAIDS and treat with antibiotics

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67
Q

What is placentitis?

A

A common cause of abortion in the horse and is commonly caused by Streptococcal species and E.coli
-Treatment =the use of antimicrobials, anti-inflammatory drugs, and drugs to maintaine uterine quiescence

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68
Q

What is the most common viral cause of abortion in the horse?

A

Equine herpesvirus 1, which typically causes abortion in the latter part of gestation
-vaccine is administered at 5,7,9 months of gestation

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69
Q

What is the most common cause of abortion in the horse that is non infectious

A

Twin fetuses

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70
Q

What is the most common route in which bacteria are introduced to the uroplacental unit?

A

Ascending infections, which result in inflammation and palcental detachment at the cervical star region

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71
Q

How do we treat placentitis?

A

a) antimicrobial therapy
b)Non-steroidal anti-inflammatory drugs (Flunixine meglumine) to suppress inflammation
c) Altrenogest (progesterone) to promote uterine quinescence
d) clenbuterole to suppress uterine motility

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72
Q

What other viruses other than equine herpes virus can cause abortion?

A

EHV-4 and equine viral arteritis

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73
Q

How do we diagnose abortion in the horse due to EHV1?

A

small necrotic foci on the liver, necrotizing bronchiolitis, and intranuclear inclusion bodies on histologic examination
-some fetuses may be alive and cause cause neonatal herpes virus -> mahy of these foals dont survive for more than a few hours or days and may demonstrate signs of respiratory distress, icterus, fever and lethargyHow

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74
Q

How do we treat EHV 1 infections?

A

-There is no direct treatment in the mare of infected neonatal foal, although antiviral medications such as acyclovir and valacylocvir may be of benefit

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75
Q

Umbilical torsion

A

-relatively uncommon cause of abortion in the mare
-fetus is able to rotate within the amniotic sac and can result in excessive twisting of the umbilical cord
-this results in abnormal constriction of the normal flow through the umbilical cord along with edema, hemorrahge and thrombosis

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76
Q

What is Pituitary pars Intermedia Dysfunction?

A

Decreased dopaminergic innervation of pars intermedia results in hypertrophy or hyperplasia of pars intermedia

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77
Q

Equine cushings typcially occurs in what signalment?

A

Older horses (15-20 years)

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78
Q

What are the CS of equine cushings?

A

-hirsutism
-polydipsia
-polyuria
hyperglycemia
laminitis (chronic)
muscle wasting

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79
Q

How do we daignose equine cushings?

A

-CS
-dexamethasone suppression test
ACTH

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80
Q

How do we treat equine curshings?

A

pergolide (dopamine agonist)
cyproheptadine (serotonin antagonist)
-supportive care (clip hair, regular deworming)

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81
Q

What virus causes blue tongue?

A

Orbivirus

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82
Q

What is bluetongue closely related to?

A

-epizootic hemorragic disease virus of deer and to african horse sickness virus

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83
Q

How is blue tongue transmitted?

A

Culicoides spp midges
-Midges feed on viremic sheep and become infectious a week later. Also transmitted via infected semen

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84
Q

What animals can be infected by bluetongue?

A

-sheep, cattle, deer, antelope, goats, and camels can be affected usually with inapparent infection

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85
Q

What does blue tongue look like?

A

-Foot and mouth disease
-incubation usually 5-10 days
-normally endemic disease with less dramatic effects

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86
Q

What are the CS of blue tongue in sheep?

A

-fever
-vasculitis results in edema, oral lesions, and mucopurulent nasal discharge
-pulmonary edema makes breathing labored and stimulates pneumonia
-hemorrhages and necrosis in muscles can cause lameness and heart failure

-coronits, sore feet, and hoof can slough
-abortion or tetrogenic effects

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87
Q

What are other differentials if you are thinking about blue tongue?

A

-FMD, orf, peste de petitis ruminants, sheep pox, epizootic hemorrahgic disease of deer, several other exotic diseases

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88
Q

When do we typcally see diseaes outbreak with foot and mouth disease?

A

-summer and fall

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89
Q

What reproductive signs can we see with blue tongue?

A

-abortions
-stillbirths
-weak dummy lambs
-in bovine fetus , it can cause cataracts

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90
Q

How do we diagnose blue tongue?

A

-lab tests include ELISA, AGID, PCR
-CS
-Post mortem: widespread vasculitis and petechia
-oral lesions
-pulmonary congestion and SQ edema
-enlarged lymph nodes and spleen
-fluid in thorax and pericardium

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91
Q

How do we prevent blue tongue?

A

-control of vector
-quaratine and restricted animal movement may help control
-both killed and live attenuated vaccines exist
-Pregnant ewes should be vaccinate

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92
Q

How old are neonate pigs?

A

0-3 weeks

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93
Q

How old are isowean pigs?

A

3 weeks

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94
Q

How old are feeder pigs (nursery)

A

3-10 weeks

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95
Q

How old are grower/finisher pigs?

A

10-26 weeks

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96
Q

How old are market weight pigs?

A

6-10 months

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97
Q

What is the basic flow unit of how pigs move

A

Sow unit -> isowean or weaner pigs (8-15 lbs) -> nursery where they are feeder pigs -> finisher 1 (fat hogs) or finisher 2 (finisher markets

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98
Q

Pig temperament

A

-pigs are temperature sensitive (neonates hate the cold)
-lactating sows hate the heat
normal rectal temperatures are 101-103

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99
Q

What mycotoxin do we use to treat aspergillus flavus

A

alfatoxin

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100
Q

What do we use to treat fusaverium graminerarum

A

Vomitoxin

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101
Q

Describe a basic vaccination program for pigs?

A

Pre-breeding- Protect Pregnancy (4 and 2 weeks prior) (parvo, lepto, ersipylas)
Pre farrowing - protect newborns (5 and 3 weeks prior) (E.coli, C.perfringens, Rotavirus
-Piglets (-3 weeks of age) (none)
-At weaning or early nursery (3-5 weeks of age) (PCV2, mycoplasmahypopneumonia. E.coli, Haemophilus parasuis)
-End of nursery or early grower (10-12 weeks of age) (Erysipelas, swin flue, samonella, ileitis

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102
Q

When calves are first born, when do they suckle?

A

2-20 minutes

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103
Q

When should calves stand by?

A

1-3 hours

104
Q

When should calves nurse by?

A

1-4 hours

105
Q

When does most nonspecific diarrhea occur in calves?

A

7-15 days of age

106
Q

If a cow has calf losses, what should we consider?

A

-Birthing area, assistance, and sanitation
-colostrum managment
-housing and handeling
-feeding and cleaning utensils
-treatment protocols
-diagnosis of specific pathogen
-vaccines

107
Q

Describe the process of handeling calves and giving colostrum

A

-Remove calf from cow as soon as possible

-in cold weather dry the calf and put in a warm dry clean place. In hot weather provide shade. Poor thermoregulation
-Dip navel in 2% tincture of iodine or other disinfectant
-milk out cow cleanly and feed 4 liters of first milking colostrum by esophageal feeder within 2 hrs of birth
-do not pool colostrum. handle to prevent bacterial growth

108
Q

How much colostrum do we want to give calves?

A

4 liters colostrum

109
Q

What are calves with low immunoglobulins suscpetible to?

A

sepsis and bacteremia

110
Q

How can we differentiate between waste milk and milk replacer?

A

-Milk replacer advtanges are consistent product, ease of storage, disease control, good calf performance and economics

111
Q

What pathogens are transmitted through milk?

A

M avium sp paratuberculosis (Johnes disease)
Salmonella
Mycoplasma
Listeria
Campylobacter
M bovis
Ecoli
Staph and Strep

112
Q

What are other names for cervical veretbral malformation?

A

cervical stenotic myelopathy and wobblers

113
Q

What is cervical vertebral malformation?

A

CVM causes compression of the spinal cord resulting in associated clinical signs

114
Q

What signalment do we see wobblers with?

A

1-2 rapidly growing male horses
-thoroughbreed and quarterhorses are more commonly affected

115
Q

What are the main takeaways with wobblers syndrome?

A

-young horses (less than 4-5 years of age)
-narrowing of the vertebral canal
-symmetrical clinical signs
-treatment is limited and often unrewarding

116
Q

What are the CS of wobblers?

A

-symmetric ataxia,paraesis and spasicity
-usually worse in the hindlimbs
-wide based stance may be observed at rest as well as proprioceptive deficits
-stumbling, toe dragging and circumduction of the hind limbs can be observed

117
Q

How do we diagnose wobblers?

A

-signalment and CS
-supported by survey radiographs with or without myelography

118
Q

How do we treat wobblers?

A

-treatment is fairly limited
-vertebral stabalizeation and decompression have been shown to have positive results

119
Q

Prognosis of wobblers

A

Prognosis tends to be poor

120
Q

Describe a horses estrous cycle and what kind of breeders they are

A

-long day breeders
-seasonally polyesterous (april-october)
-spring transition period of follicular growth and recession

-cycle is 21 days

121
Q

Describe estrus in the horse

A

-period mare will stand for the stallion
-estrogen levels increasing
-duration is 5-7 days
-ovulate 1-2 days prior to estrus

122
Q

What breeding options do we have for mares?

A

-every other day beginning on the second day of estrus until mare goes out of heat
or
within 24-48 hours prior to ovulation

123
Q

How long is diestrus in the horse?

A

14-16 days

124
Q

How can estrus synchronization be done in the mare?

A

PGF2a ->works on the CL >5 days of age and diestrus
-mare CL is more sensitive than cow CL
-side effects can be sweating, abdominal cramps, increased HR, muscle weakness and balance problem
-all side effects begin about10 minutes after injection and last an hour long

125
Q

When you do estrus synchronization, when does the mare ovulate?

A

8-9 days later

126
Q

When do we do the mare estrus synchronization program?

A

-sychronize estrus/ovulation for aritifical insemination or embryo transfer
-prolonged diestrus (failure of CL to regress)

127
Q

What can we do to syncrhonize mares?

A

Progestins (regumate)
-this is oral progestin

-treatment -> feed daily for 12-14 days, on last day give PGF2a, Will be in heat in 3-4 days but ovulation will not happen until day 8 of treatmetn

128
Q

What can we use regumate for in mares?

A

-synchronize estrus

-suppress estrus in performance mares

129
Q

How can we induce ovulation in anestrus mares?

A

-increase light exposure
-if they are post partum (breed at foal heat, provide adequate nutriton and dont see lactational anestrus

130
Q

What are prohibited drugs in food animals?

A

Diethylstilbestrol
chlormaphenicol
nitromidazoles
sulfas in dairy cattle greater than 20 months
clenbuterol
dipyrone
FQ
glycopeptides (vancomycin)
nitrofurans
phenylbutazone in cattle greater than 20 months
DMSO
inophores in lactation rings

131
Q

What is woody tongue caused by?

A

actionbacillus linguieseri
-common in animals eaten hard and dry feeds that can damage mucosa
mainly soft tissues involved
-releatively easy to treat with sodium iodide

132
Q

Lumpy jaw

A

Actinomyces bovis
-not as common as woody tongue
-develops slowly, involves bone
-often leads to tooth problems
-diffuicult to resolve
-avoid surgery -> too bloody

133
Q

Classical swine fever/ hog cholera

A

a) pestivirus - splenic infarction is pathopneumonic

134
Q

African swine fever

A

Asfivurs -> hemorrhage

135
Q

CN I

A

Olfactory Nerve
-mediates the sense of smell
-observing patient sniff around the

136
Q

CN2

A

Optic Nerve
-to test do cotton ball test, menace response, pupillary light resopnse

137
Q

CN 3

A

Oculomotor Nerve
-provides motor to most of the extraocular muscles and for pupil constriction
Examine by:
-observing for phsyiologic nystagmus when turning head
-observing pupillary constriction in PLR

138
Q

CN 4

A

Trochlear Nerve
-provides motor function to the dorsal oblique extraocular muscle and rolls globe medially
-observe by looking for dorsomedial rotation of the pupil

139
Q

CN 5

A

Trigeminal Nerve (Maxillary, Mandibular, Opthalmic Branches)
-Provides motor to muscles of mastication and sensory to eyelids, cornea, tongue, nasal mucosa, and mouth
Examine by:
-palpate masseter and temporal muscles for symmetry atrophy and pain
Check jaw tone
Touch medial septum of nose and look for retraction
Touching the globe and observing for retraction
-Palpebral response
-Pinching the lip and observing for snarl

140
Q

CN 6

A

Abducens Nerve
-Provides motor function to the lateral rectus extraocular and retractor bulbi
Examine by:
-touching the globe and observing for retraction
-observing for medial strabismus

-observing for physiologic nystagmus when turning head

141
Q

Cn 7

A

Facial Nerve
-provides motor to muscles of facial expression and sensory to medial pinnae. Also taste to rostral tongue and parasympathetic innervation to lacrimal glands and some salivary glands
Examine by:
-Menace response
Palpebral response
Observe for facial paralysis, deviation of nose to one side, or droopy lips
-schirmer tear test
-ear flick in repsonsee to stimulation of medial pinnae

142
Q

Cn 8

A

Vestibulochoclear Nerve
-sensory input for hearing and head position
Examine by:
-hearing assesment, deaf animals may startle easily
-Observe for head tilt, abnormal nystagmus and presence of normal physiologic nystagmus

143
Q

Cn 9

A

Glossopharyngeal Nerve
-provides motor and sensory innervation to pharynx for swallowing. Also innervates some salivary glands and provies taste innervation to caudal tongue
Examine by:
-eliciting a gag reflex and observing for dysphagia

144
Q

CN 10

A

Vagus nerve
-Innervates the larynx, esophagus, and pharynx, . Also provides paraysmpathetic innervation to the heart and viscera
Examine by:
-elicit a gag reflex
-observe for laryngeal paralysis
-assess for megaesophagus and regurgitation

145
Q

CN 11

A

Spinal Accessory Nerve
Innervates cranial cervical muscles
-rarely assess and rarely a clinical problem

146
Q

CN 12

A

Hypoglossal Nerve
-provides motor to the tongue

147
Q

Idiopathic Trigeminal Neuritis

A

-A syndrome seen with dogs with peracute onset of a dropped jaw and inability to close the mouth
-No other sensory deficits or other cranial deficits present

-dogs are normally alert and responsive without difficulty swallowing food that is placed on back of tongue
-Other ddx:
-mandibular fracture
-rabies
-neoplasia of mandibular nerve
-masticatory of muscle myositis
-treated with supporitive fluids and hand feeding of soft food is excellent prognosis, with most dogs regaining function within 1-2 weeks

148
Q

Idiopathic Facial Nerve Paralysis

A

-Acute onset of several signs
a) inability to blink
b) drooping lip and ear
c) drooling from one side of the mouth
d) dry eye
-Facial sensation is normal

149
Q

When should a newborn foal nurse?

A

Within a few hours of birth to absorb maternal antibodies

150
Q

How can we evaluate to make sure they have enough maternal antibodies from mom?

A

Check igG in blood stream/seru

151
Q

How can we measure FPT?

A

> 800 is adequate
400-800 -> partial failure of passive transfer
<400 -> complete failure of passive transfer

152
Q

What is the systemic inflammatory repsonse syndrome?

A

a) tachycardia
b) tachypnea
c) hypo or hyperthermia
d) leukocytosis or leukopenia
e) presence of immature neutrophils

153
Q

Septicemia is common in what age of horses?
What are predisposing factors/

A

foals
a) FPT
b) contaminated environment
c) endemic infectious diseases
d) overcrowding

154
Q

What are the most common isolated organisms isolated from foals that cause septicemia?

A

-E,coli, Klebsiella, Enterobacter, Salmonella
-Strep, Enterococcus, Actinerobacter

155
Q

What are CS of septicemia?

A

weakness, lethargy, inappetence
hypovolemia
tachycardia
tachypnea
hypothermia/hyperthermia
diarrhea

156
Q

How do we treat septicemia?

A

Supportive care (fluid therapy, plasma)
Antimicrobials (Beta lactama + aminoglycoside)
Nutritional Support

157
Q

How do we diagnose Crypto, salmonella, EEC, Rotavirus?

A

Feces

158
Q

What diagnosis is likely to yield the greatest amount of info with diarrhea in a calf?

A

Post mortem on euthanized calf with typical signs

159
Q

Salmonella cultured from where is more signifcant?

A

Tissues

160
Q

Which can cause more severe colonic lesions?

A

Corona more than rota

161
Q

What will decrease the need for IV fluid therapy and improve survival in calves?

A

Early application of good oral fluids
-once calf is ill , use a fluid which treats hypovolemia, acidosis, hypoglycemia, and hypokalemia

162
Q

How can we estimate fluid deficit in calves?

A

Body weight in kg x percentage dehydrated
8-10% moderate
10-12% severe
More than 15% is usually fatal

163
Q

Younger calves, less than _ days are floppy sooner

A

8 days

164
Q

What are sources of lactic acid?

A

Gut bacteria (Produce both D and L isomers, only the L form metabolized by mammals)
Anaerobic glycolysis in tissues. Metabolizing glucose to pyruvate and lactate

165
Q

What are maintenace fluids in a calf?

A

40-80 ml/kg/day

166
Q

When do we use oral fluids vs IV fluids in calves?

A

Use oral fluids when dehydrated not yet severe, and to supplement IV fluids when it is
-Use IV fluids when gut motility is compromised or obstructed
-Use IV fluids when animal is seriously dehydrated or hypovoemic or floppy due to metabolic acidosis

167
Q

What fluids do we use to treat dehydrated calves?

A

Should be hypotonic or isotonic
feed some small amounts of milk, because lactase and other enymes are induced by having lactose in the lumen

168
Q

What alkanizing agents can we use for fluids in calves?

A

Bicarbonate, lactabe, citrate, acetate

169
Q

What do bicarbonate and citrate interfere with?

A

milk clot in the abomasum
bicarb raises the pH, citrate binds calcium
lactate pathway is backed up, because the calf has lactic acidosis
Best agent is thus acetate

170
Q

How do we know how much alkalizing agent to give to a calf?

A

Mutliple calf weightx 0.60 x base deficit

171
Q

How do we give IV fluids to calves?

A

-Need good catheter -> suture or glue in place
-Need good lines that will not tangle or pull out. Use rubber bands, hang over center of small pen
-Keep calf warm and dry
-offer fresh whole milk within shortest possible time, multiple small feedings ideal

172
Q

How fast do we give IV fluids to calves?

A

5-10 ml/kg/hr okay
10-20 ml/kg/hr for shock
-slow or stop if animal becomes restless, dyspneic, or shows any CNS signs

173
Q

What are the most common dermatologic diseases in pigs?

A

-mange
-greasy pig disease
-swine pox
-erysipelas
-pitryasis rosea
-porcine dermatitis and nephropathy syndrome

174
Q

What causes mange in pigs?

A

Sarcoptes scabeii var suis

175
Q

What kind of pigs do we see mange in?
CS?

A

Young nursery or grower pigs
Intense puritius, thickened skin
poor production
susceptible to other diseasesH

176
Q

How do we diagnose mange in pigs?

A

See them present behind the ears and ear canals

177
Q

How do we treat manage in pigs?

A

Avermectin and control

178
Q

What is greasy pig disease?
How do we diagnose and treat?

A

Exudative dermatitis
Staphylococcus hiyucs
Affects late pre-weaning pigs (large number of gilts farrowing)
CS are Exfolation of skin excess sebaceous secretion
Puritus not a feature unless complicated by magne
Treatment =Injectible penicllin, ceftiofur
Chlorohexidine or clorox dips
Control -> sanitation, control external parasites, good nutrition

179
Q

Swine pox is cuased by what?
How old are the pigs that are usually affected?
CS?
dIAGNOSIS?
Treatment?

A

Swine pox virus
Less than 4 months old
CS -> papules 1-6 mm in diameter, pusutles and crusts, clear spontaneously
Diagnosis : intracytoplasic inclusion bodies
Treatment: get rid of lice or other blood sucking lice

180
Q

Erysipelas

A

Erysipelothrix rhusiopathiae
Diamound skin disease
Pigs less than 3 months of age
CS: widespread ecchymotic hemorrahges due to microthrombi
arthritis, endocarditis,

181
Q

How do we diagnose and treat erysipelas?

A

Diagnosis: diamound skin lesions pathopnomnic, culture of blood, lungs and joint fluid
Treatment: penicllin is the drug of choice
Control: general sanitation
Vaccination: pre-breeding, maternal interference, middle of end of nursery

182
Q

Pityriasis Rosea

A

Juvenile pustular psiorariform dermaitits
-pseudoringworm
spontanoues regression

183
Q

Porcine Dermatitis and Nephropathy Syndrome

A

Condition associated with systemic PCV-2 virus infection
Type 3 hypersensitivity reaction: causing vasculitis, dermal and cutaneous infarction, large red sloughing lesions usually over rear and legs
-commonly have bilaterally enlarged kidneys

184
Q

If we see disease affecting the cerebral cortex, what CS do we see?

A

Change in mentation, blindness, circling

185
Q

What CS can we see with disease affecting the brainstem?

A

Cranial nerve deficits, circling, head tilts

186
Q

What CS can we see with disease affecting the cerebellum?

A

Intention tremors, hypermetria, incoordination

187
Q

What CS can we see with disease affecting the spinal cord?

A

Ataxia, spinal reflexes, paralysis

188
Q

What CS can we see with disease affecting the peripheral nerves?

A

muscle tone/ atrophy, paralysis

189
Q

What are ddx for brainstem diseases in bovine?

A

-Listeriosis
-Otitis media/interna (Mycoplasma bovis, Pasteurella multocida, Haemophilus somni, Corynebacterium pseudotuberculosis)
-TEME
-Brain /pituitary abscess
-Meningeal worm

190
Q

Describe Listeriosis in bovine

A

Listera monocytogenes
-poorly fermented silage
-cranial nerve deficits
-microabscess in brain stem

191
Q

What are the CS of listeria in cows?

A

-signs of commonly assymetrical
-dull, depressed
-assymetrical cranial nerve deficits

192
Q

How do we diagnose Listeria?

A

-Primarily mononuclear pleocytosis
-bacteria is difficult to grow in CSF
-zoonotic through milk and meat products

193
Q

Prognosis for listeria?

A

Good if caught early enough

194
Q

How do we treat listera?

A

-amoxicillin
-procaine penicillin G
-oxytetracycline
-correct acid base derangements

195
Q

What are ddx for cerebral disease in bovine

A

-Cerebrocortical necrosis
-TEME
-nervous ketosis
hypomagnesium
BSE
Rabies
Vitamin E deficiency
Nervous coccidiosis

196
Q

Differentials for cerebellar disease in boine?

A

Cerebellar hypoplasia

197
Q

What are ddx for spinal cord disease in bovine?

A

-tetanus
-lymphosarcoma

198
Q

Polioencephelomalacia

A

Softening of the gray matter in the brain
Histologic diagnosis
-altered thiamine deficency

199
Q

What are causes of CCN or polioencephelomalacia

A

-lead poisoning
-lactic acidosis (grain overload)
salt intoxication/water deprivation
bracken fern poisoning
sulfur intoxication
amprolium intoxication

200
Q

What would a CSF tap look like with polioencephelomalacia?

A

-Increased protein
-increased monocytes

201
Q

What are complicated corneal ulcers?

A

-Involve the corneal stroma and or have some depth to them and or persist longer than a week, are infected, and are melting

202
Q

Where does the fluroscein stain dye?

A

Binds to the hydrophilic stroma and NOT the hydrophilic epithelium

203
Q

What are causes of complicated corneal ulcers?

A

a) failure to find, diagnose and or treat the underlying cuase of the previously uncomplicated ulcer
-there is a secondary bacterial infection with or without secondary malacia
-the secondary ulcer has now become indolent

204
Q

What is the goal of treating complicated ulcers?

A

-prevent progression and promote healing

205
Q

How do we treat complicated ulcers?

A

-agressive topical antibiotic
-cycloplegia (atropine once or twice daily)
-stop corneal melting
-prevent self trauma
-anti-inflammatory therapy (oral only)

206
Q

How can complicated ulcers progress?

A

-may result in desmetocele or corneal perforation
-requires emergency structural support

207
Q

Treatment with structural support for corneal ulcers include?

A

Conjunctival graft -> a piece of conjunctiva is placed over the defect
Corneal conjunctival Transportation -> a piece of adjacent cornea is slid over the defect and sutured in place

208
Q

What is the prognosis of complicated ulcers?

A

-fair: healing may take several weeks
-may result in significant scarring that may affect long term vision

209
Q

What are the 4 main anti-puritic drugs?

A

Apoquel, cytopoint, cyclosporine (atopica), and steroids (prednisone)

210
Q

What is the mediator for pruitus?

A

IL-31

211
Q

How do apoquel and cytopoint work?

A

They both work in the same pathway, but cytopoint acts higher in the pathway

212
Q

What is apoquel?

A

A JAK inhibitor, targeting JAK 1

213
Q

Cytopoint?

A

A monoclonal antibody that binds to IL-31 which prevents it from binding and activating the JAK/STAT pathway

214
Q

How is apoquel given?

A

Orally, given twice daily for 2 weeks then once daily for

215
Q

How do you give cytopoint?

A

Sub q. Give one injection every 4-8 weeks

216
Q

How do we adminster prednisone for itchiness?

A

Oral. Dose and taper schedule depends on severity of disease

217
Q

How do we adminster cyclosporine for itchiiness?

A

Oral. Given twice daily. can be tapered for maintenace

218
Q

What is the onset of activity for Prednisone, cytopoint, and apoquel?

A

Usually within 24 hours

219
Q

How long does it take cyclosporine to work?

A

-Takes about 4 weeks to reduce puritius in dogs and 2-3 weeks in cats

220
Q

Side effects of apoquel?

A

-May increase susceptibility to demodex and other infections. Also may exacerbate neoplasia. GI effects have been observed. Do not adminster to patients less than 1 year of age

221
Q

Side effects of cytopoint?

A

Gi upset was similiar to placebo group.

222
Q

Cyclosporin side effects

A

The main side effect is GI upset
Increased hair growth, papillomas, gingivial hyperplasia but these resolve after cessation of use.

223
Q

Prednisone side effects

A

PU/PD, polyphagia, behavioral changes, GI ulceration, hepatoapthy, diabets. With skin can see delayed healing,. Can get secondary infections

224
Q

Do not use prednisone with?

A

NSAIDS

225
Q

What drugs do we use for itchiness in cats?

A

Cyclosporine

226
Q

What virus is caprine arthritis encephalitis caused by?
How is it transmitted?

A

-Retrovirus (lentivirus)
-Primary vertical transmission from dam to kid
-horizontal transmission does not occur with any secretion that contains monnuclear cells

227
Q

What are the clinical signs of CAE in adult goats vs kids?

A

-large swollen knees with degenerative joint changes
-symmetrical swelling of mammary gland

-inability to maintainweight
-loss of production ability

-encephalitis in kids is rare

228
Q

How do we survey for CAE in a herd?

A

-annual testing of every animal in the herd
-all clincially affected seropostive animals should either be culled or maintained in completely seperate housing with no contact with negative animals
-all kids of positive animals should be raised on preventative programs

229
Q

How do we test for CAE?

A

Most available tests are AGID and the cELISA

229
Q

What signalment do we see CCL ruptures?

A

-usually middle aged dogs but can be younger
-can be seen in larger breeds mostly but not exclusively

230
Q

What is the number one orthopedic disease in dogs?

A

CCL rupture

231
Q

What woud you expect the history to be for CCL rupture?

A

-chronic intermittent lamenss which progresses to acute lameness
-owners may only appreciate acute lameness

232
Q

What breeds are genetically predisposed to CCL tear?

A

Newfoundlands

233
Q

What does the CCL do?

A

-prevent tibial thrust, prevent cranial drawer, prevent excessive internal rotation, prevent excessive hypertension

234
Q

How do we diagnose CCL rupture?

A

-cranial drawer, tibial thrust, pain on extension, stifle effusion, lamness, medial butress

235
Q

What can we see radiographically with CCL tear?

A

stifle effusion
degenerative joint disease
radiographically apparent tibial thrust

236
Q

What is the seasonality of pigs estrous cycle?

A

Non seasonal
Polyestrous
21 day cycle

237
Q

Pigs puberty depends on what?

A

-depends on maturation rate

238
Q

When do pigs reach puberty?

A

5.5-7 months
210-240 pounds

239
Q

When do pigs first breed?

A

7-8 months
2nd or 3rd estrus

240
Q

What is important to increase the onset of puberty in sows?

A

Keep the boars in contact with them

241
Q

How long are pigs in proestrus for?

A

4-5 days
-follicular phase

242
Q

How long is esturs?

A

2-2 days
-ovulation occurs 24-48 hours after estrus

243
Q

How do we know a pig is in estrus?

A

-restlessness, swollen vulva, decreases appetite

244
Q

When is the optimal breeding time in sows?

A

12-30 hours after onset of estrous
-conception rates max out if mating occurs 12 hours before ovulation

245
Q

What tends to creat seasonal anestrous in sows?

A

Heat stress

246
Q

How long are sows in diestrus for?

A

14 days
CL not responsive to PGF until after day 12 of cycle

247
Q

Describe the post partum period in pigs?

A

Anestrus while lactating

248
Q

When does estrus occur in pigs after weaning?

A

3-9 days

249
Q

How is goat secreted in goats unlike sheep and cattle?

A

Apocrine fashion
-results in cytoplasmic plugs that cna be confused for SCC

250
Q

What tends to be higher in goats than cattle milk?

A

SCC
-made predominantly of neutrophils

251
Q

Higher degree of subclincial intrammary infections in dairy goats
What are the culprits?

A

-Coagulase negative staph
-staph aeureus
-environmental streps, corynbacterium and gram negatives

252
Q

What is the most common cuase of clinical mastitis?

A

-staph auerus or pasteruella species
-often associated with gangrenous mastitis

253
Q

How do we treat mastitis in dairy goats?

A

-intrammary antibiotics
-treat systemically and use IV fluids

254
Q
A

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