Basics of Equine Respiratory Diseases Flashcards

1
Q

Guttural pouch tympany cause

A

congenital, secondary to URT, nasopharyngeal orifice

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2
Q

Guttural pouch tympany C/S

A

non-painful, elastic swelling in retrophar
resp noise
cough and dysphagia

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3
Q

Guttural pouch tympany Tx

A

surgery, fenestate median septum, salpopharyngeal fistula

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4
Q

Guttural pouch empyemia cause

A

secondary to URT infections, commonly strangles

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5
Q

Guttural pouch empyemia common etiology

A

strep equi

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6
Q

Guttural pouch empyemia C/S

A

intermittent discharge

cough, dysphagia

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7
Q

Guttural pouch empyemia tx if pus

A

daily drainge and lavage

AM

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8
Q

Guttural pouch empyemia tx if chondroids

A

flush

basket retrieval in surgery

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9
Q

Guttural pouch mycosis most important clinical sign

A

serious epistaxis with no related trauma or exercise

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10
Q

Guttural pouch mycosis cause

A

aspergillus spp. in dorsocaudal medial compart.

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11
Q

Guttural pouch mycosis tx

A

occlude artery affected

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12
Q

Guttural pouch mycosis prognosis

A

over 90% if technology o occlue

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13
Q

Strangles cause

A

strep equi equi

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14
Q

Strangles clinical signs

A

urt inflamm and discharge
abscessing lymph nodes
abrupt fever

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15
Q

Strangles who it hits most

A

young, on breeding farms

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16
Q

Strangles Dx

A

**Culture
PCR - doesnt tell if shedding
Serology - can’t tell if Vx or infection

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17
Q

Strangles Tx with early

A

just let it run unless it causes dysphagia

If it does, AM therapy but risk bastard

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18
Q

Strangles Tx with LN abscesses

A

drain, lance if needed
isolate animal
flush

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19
Q

When to AM Tx Strangles

A

lymph node abscessing

advancd clinical signs

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20
Q

What to do with horses exposed to strangles

A

AM to prevent seeding

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21
Q

Strangles common complications

A

purpura hemorrhagica
metastatic spread - bastard
myositis
agalactia

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22
Q

Strangles - treating purpura

A

corticosteroids and supportive care

maybe AM

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23
Q

Strangles - treating bastard

A

probably just AM

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24
Q

Strangles prevention

A
isolate new arrivals (2 wks)
rectal temps in outbreaks
immediate isolation if something happens
Do nasal swabs, washes
vaccinate
water trough seperation (common cause of spread)
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25
Q

Strangles re-infection rate

A

75% within 5 years of getting it.

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26
Q

Strangles culture tells if shedding or not, but what is interesting about PCR?

A

3 X more sensitive

Looking for SeM (Antiphagocytic M protein)

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27
Q

Strangles vaccination protocols

A

2-3 dose primary for killed bacterin starting at 6 months of age
boosters annually 4-6 weeks before foaling

OR

Attenuated live intranasal (pinnacle by Wyeth) under the same program but not 4-6 wks before foaling

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28
Q

Influenza presentation/ clinical signs

A

sudden onset, spreads quickly
young horses
dry, harsh cough for 1-3 weeks
pyrexia for 4-5 days (biphasic - back and forth)
reluctant to move from myalgia, myositis and limb edema
SEVERE and possible die in 48 hours

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29
Q

Influenza pathogenesis

A

N changes MC apparatus –> H moves in and binds to sugars on epithelial cells –> replication –> cell necrosis/desquamation –> inflammation –> edema, lymphocytes –> 6 weeks repaired

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30
Q

Influenza Dx

A

Viral isolation
PCR
ELISA

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31
Q

Influenza Tx

A

symptomatic

treat the secondaries if possible

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32
Q

Influenza control

A

Vx

horses will shed for 7-10 days after last sign of illness so watch for that and then it’s gone

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33
Q

Herpevirus (Rhinopneumonitis) etiology

A

EHV-1 and EHV-4

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34
Q

Herpevirus (Rhinopneumonitis) general C/S

A

URT edema, hyperemia, petech hem

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35
Q

Herpevirus (Rhinopneumonitis) 1 C/S

A

neurologic, reproductive, and respiratory signs
myeloencephalopathy
neonatal deaths, abortions, weak foals
fever, mucopur discharge

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36
Q

Herpevirus (Rhinopneumonitis) 1 neonatal death/weak foals have…

A

IS pneum

hypoplastic thymus and spleen

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37
Q

What is not a dependable C/S of EHV 1, 4

A

coughing

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38
Q

When do they get EHV

A

around training starting, 1 year

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39
Q

Herpevirus (Rhinopneumonitis) prevention

A

Vx for 1 and 4 - mod live, divalent killed

maternal Ig for a month

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40
Q

Herpevirus (Rhinopneumonitis) Vxs don’t prevent

A

abortions or neurologic disease

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41
Q

Herpevirus (Rhinopneumonitis) abortions are tricky because

A

the serology is gone because titer is short-lived

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42
Q

Equine Viral Arteritis etiology

A

arterivirus

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43
Q

Equine Viral Arteritis outbreaks with

A

respiratory and abortions

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44
Q

Equine Viral Arteritis C/S

A
subclinical to death
pyrexia, anorexia, depression
edema in funny places (eye, scrotum, limbs)
dyspnea cough and discharge
tearing up
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45
Q

Equine Viral Arteritis C/S in neonatal foals

A

severe resp
lots die
fever
leukopeni, thrombocytpeni

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46
Q

Equine Viral Arteritis neonatal PM

A

IS pneum, lymphocytic arteritis and periarteritis

renal tubular necrosis

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47
Q

Equine Viral Arteritis differentiates from influenza with

A
lymphocytic arteritis (EVA)
lymphocytic infiltration to IS space
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48
Q

Equine Viral Arteritis abort when?

A

3-8 wks after infection, late

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49
Q

Equine Viral Arteritis can stallions transmit?

A

yes

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50
Q

Bacterial Pneumonia etiologies

A

strep zoo **
strep equi
pasteurella, ecoli, pseudo, kleb, enterbac (complicating things)
anaerobes (clost, bact)

51
Q

Bacterial Pneumonia acute C/S

A
fever
tachypnea
discharge
coughing
exercise intolerance
52
Q

Bacterial Pneumonia chronic c/S

A

acute signs
weight loss
decreased appetite

53
Q

DDx for infectious pulmonary dysfunction

A

Bacterial
viral
fungal, aspergillosis follows GI Dz
parasitic

54
Q

DDx for non-infectious pulmonary dysfunction

A

RAO
IAD
Neoplasia (LSA, Mets)

55
Q

Common mets to lungs

A

renal/gastric carcinoma

melanoma

56
Q

Dx of Bacterial Pneumonia special features (besides the PE, U/S, regular Clin path, TTW, Thor rads)

A

end ins crackles
expiratory wheezes
ascult/percuss/rads/us –> pleural effusion

57
Q

Causes of end inp crackles

A

transient atelectasis

secretions

58
Q

causes of exp wheezes

A

inflamed/narrowed airways from secretions

59
Q

Sounds to be heard with PPneum

A

rubbing sounds

nothing on the ventral thorax (line)

60
Q

What to do with pleural effusion?

A

drain it, culture it, cytology. Likely not as good as TTW

61
Q

Bacterial Pneumonia pathophysiology

A

defense gone - MC clear, PAMs, CMI/hum

inhaled something and spread from there

62
Q

Bacterial Pneumonia tx

A

do C/S first from TTW
Gr - –> aminoglycosides
GRam + –> penicillin
anaerobes –> metronidazole

Common Pen-Gent

63
Q

EMPF (Equine Multinodular Pulmonary Fibrosis) etiology

A

gamma herpes virus - same as MCF

EHV-5

64
Q

EMPF (Equine Multinodular Pulmonary Fibrosis) definitive/Histologic lesions

A

IS lung, up to 5 cm diameter fibrosis

only in alveolar parenchyma –> inflamm cells but still the right architecture

65
Q

EMPF (Equine Multinodular Pulmonary Fibrosis) Tx

A

supportive
AM, AV,
Pain control
steroids

66
Q

EMPF (Equine Multinodular Pulmonary Fibrosis) prognosis

A

76% die

67
Q

DDx for foal pneumonias

A
all the adult causes 
rhodococcus equi
actinobacillus equi (sepsis)
e coli (sepsis)
strep equi zooepidemicus ***** most common
anaerobes
68
Q

What do we know about bacterial pneumonias in foals?

A

most frequently in under 1 month

most commonly a manifestation of septicemia (so when sepsis, worry about pneumonia)

69
Q

How is the diagnostic approach different for neonatal foals with pneumonia than older foals and adults? So what are our mainstays?

A

there will be tachypnea and increased respiratory effort but that may be all
NO lung sounds or mucous necessarily.

Our mainstays are the PE, thor rads, blood gas and cultures,

70
Q

what are some special cellular/immunity characteristics in neonatal foals that may contribute to bacterial pneumonia

A
less cells (Macrophages) in the BAL by 3-6 weeks
mostly macrophages there
maternal ig are waning, and the amount they had in the first place is important
71
Q

How to diagnose bacterial pneumonia in the older foal?

A

TTW, thor rads, and thor U/S

72
Q

Who does undiff. RTD hit

A

80-90% 4-5 mo foals

73
Q

Undiff RTD etiologies

A

strep zoo***
staph epidermidis
r. equi
maybe viruses

74
Q

Undiff RTD clinical signs

A

crackles, wheezes, mucopur discharge, cough, tachypnea

75
Q

Undiff RTD rads will show

A

bronchoIS pattern

76
Q

Undiff RTD BAL will show

A

neutrophils and possible cocci.

77
Q

Undiff RTD Tx

A

ampicillin, penicillin, or TMS all BID

78
Q

Undiff RTD prognosis

A

30% relapse, but hard to know

79
Q

Rhodococcus equi pneumonia for sure clinical signs

A

fever
crackles,
wheezes
tachypnea

80
Q

Rhodococcus equi pneumonia variable signs

A

mucopur nasal discharge
cough
respiratory distress

81
Q

What is the clinical manifestion (PM would find for ex) of Rhodococcus equi pneumonia

A

chronic suppurative bronchopneumonia with extensive abscessation . They are remarkably able to deal with it considering how mild the signs are.

82
Q

Rhodococcus equi pneumonia Dx (Need)

A

Clinical signs
PCR - especially the presence of the VAP-A gene
Cytology from TTW

83
Q

Rhodococcus equi pneumonia Txs. Which is better?

A

6-8 wk minimum Erythromycin and rifampin
OR
azithromycin and clarithromycin (better concentriaons in the BAL cells and pulmonary epithelial lining)

84
Q

Rhodococcus equi pneumonia Dx (help with it)

A

rads - alveolar, and abscesses
serology showing exposure
US showing abscesses
CBC and Fibrinogen

85
Q

What is the source of contamination and route of infection?

A

foals feces, and inhaling dust and virulent r. equi

86
Q

When does Rhodococcus equi pneumonia hits these guys?

A

2-5 months old. It is the most devastating of dz from 3wk to 5 month foals

87
Q

Rhodococcus equi gram, behaviour, and site of replication/habitat

A

grm pos,
facultative IC pathogen
replicates in pulmonary macrophages

88
Q

Rhodococcus equi pneumonia most important epidemiological point

A

Overcrowding, dusty conditions predispose, especially with related weather changes

89
Q

Rhodococcus equi comes from?

A

the soil - lives there a long time

90
Q

Acute respiratory Distress Syndrome is also

A

Bronchointerstitial pneumonia (this pattern will be on rads too)

91
Q

Acute respiratory Distress Syndrome hits who

A

1-7 months of age

92
Q

Acute respiratory Distress Syndrome clinical signs

A

tachypnea, increased resp effort, cyanosis

hypoxemia, hypercapnia –> respiratory acidosis

93
Q

Acute respiratory Distress Syndrome Tx

A

NOT AM because will not respond

GIve O2, bronchodilators and steroids

94
Q

Acute respiratory Distress Syndrome prognosis

A

guarded, especially for athletics

tend to die in 1-2 days

95
Q

Acute respiratory Distress Syndrome cause

A

we don’t know (looks like r equi and pneumocystis carinii)

96
Q

IAD important characteristics

A

mucoid/mucopur exudate in nasopharynx, trachea, and bronchial bifur
AND
non-septic inflammation

97
Q

IAD is mainl yin

A

young, performance horses

98
Q

How many coughing horses have IAD

A

85%

99
Q

IAD cause?

A

related to RAO?
unknown
dust, molds, pollutants
possibly low grade persistent infections

100
Q

IAD clinical signs

A
mostly subclinical, but
poor performance
coughing
NOT febrile
MAYBE EIPH evidence
101
Q

IAD Dx

A

endoscope for exudate in the airways
and R/O other causes
BAL

102
Q

IAD BAL will be significant when…

A

Mast cells >2%
PMNs cells >5%
or eosinophils > 1%

103
Q

IAD Tx

A

Envirnomental stuff: turn out to pasture, rest them, decrease all exposure

Steroids - but we need to know there is not an underlying problem first

Bronchodilators
Sodium cromoglycate (if mast cells are the problem –> inhibit them)
Decrease EIPH

104
Q

RAO (not COPD) hits

A

middle-aged horeses

105
Q

RAO (not COPD) is associated with

A

stabling
hay, straqw and molds
rarely summer pastures
Hypersensitivity? not really.

106
Q

RAO (not COPD) etiologies

A
organic dust
hypersensiticvity to poorly cured hay
aspergillus fuigatus
faenia rectivirgula
some pollensv --> SPAOPD
107
Q

RAO (not COPD) pathogenesis if a hypersensitivity

A

exposure to allergens –> asymp to clinical in 4-6 hours –> neutrophil influx –> clinical signs (mucopurulent nasal discharge, exp effort, heave line, incr. RR, Advent lung sounds, etc)

108
Q

RAO (not COPD) pathogenesis if a chronic bronchiolitis

A

mucopur in airways –> bronchospasm –> peribronchiolar infiltration –> goblet cell hyperplasia and viscous mucus

109
Q

RAO (not COPD) pathogenesis if a non-specific hyper-responsiveness

A

cold air, Nh3, exercise

110
Q

RAO (not COPD), basically what happens

A

neutrophil accum –> changes walls or airways –> then mucous accum. –> bronchospasm –> les lung compliance —> lung resistance –> increase work of breathing –> arterial hypoxemia w/o hypercapnia

111
Q

RAO (not COPD) pathogenesis changes acutely and chronically how?

A

acute- edema in airway causes mucous accumulation
Chronically - airway remodelling causing mucous metaplasia, smooth muscle hypertrophy, peribronchial fibrosis and inflammation

112
Q

RAO (not COPD) Clinical signs

A
chronic spont. cough
mucopur nasal discharge
expi effortt
heave line (hypertrophy of abdom oblique and rectus abdominus
higher RR
advent lung sounds
doesn't like exercise
weight loss
NOT A FEVER
113
Q

RAO (not COPD) Dx

A
History and C/S
Wheezes and crackles on exp
Expanded lung field
bronchointerstitial pattern
Endoscope 
TTW - neutrophils/copious mucous
BAL - for increase neutrophils, nondegen, non-septic inflammation
Atropine/Glycopyrrolate test (GP is LA and 2X potency)
114
Q

What are normal levels of neutrophils on BAL

A
115
Q

RAO (not COPD) treatment

A
Environmental management
Corticosteroids
Bronchodilators
Mast cell stab (disdoium cromoglycate again)
mucolytics and kinetics
maybe AM
116
Q

Because of the possibility of hypersensitivity causing RAO (not COPD), Dx may include

A

Intradermal skin testing and

serum allergen testingf

117
Q

What are the mucolytics and kinetcs?

A
dembrexine hydroCl (sputolysin)
acetylcysteine
118
Q

EIPH is characterized by

A

strenuous exercise associated with extravasation of RBCs from pulmonary vasc into the IS space and alveolie and airways

119
Q

EIPH shows in which part of the lung

A

caudal dorsal

120
Q

EIPH only consistent finding is

A

a direct consequence of intense exercise

121
Q

EIPH potential causes/pathogenesis

A

increase cap pressure–> decrease IPleural pressure
abdominal contents hit the dorsocaudal lobe
pulmonary hypertension to being with

122
Q

EIPH clinical signs

A

excessive swalloing
10% actually bleed
decreased performance
some coughing and labored breathing

123
Q

EIPH Dx and what to see with the tests

A

Hx and PE
Endoscope WITHIN 90 MINUTES OF EXERCISE to see blood in the trachea
BAL - hemosiderophages, RBCs, neutrophils (degen and not degen), maybe bacteria
Rads for IS pattern

124
Q

EIPH Tx (there are a lot of them but the main ones are..)

A

Furosemide
Nasal strips (seem to bring down 30-40%)
post-race anti-inflammatories/corticosteroids/bronchodilators–to prvent IAD
AM because blood is a good agar for bacteria