Basics of Equine Respiratory Diseases Flashcards
1
Q
Guttural pouch tympany cause
A
congenital, secondary to URT, nasopharyngeal orifice
2
Q
Guttural pouch tympany C/S
A
non-painful, elastic swelling in retrophar
resp noise
cough and dysphagia
3
Q
Guttural pouch tympany Tx
A
surgery, fenestate median septum, salpopharyngeal fistula
4
Q
Guttural pouch empyemia cause
A
secondary to URT infections, commonly strangles
5
Q
Guttural pouch empyemia common etiology
A
strep equi
6
Q
Guttural pouch empyemia C/S
A
intermittent discharge
cough, dysphagia
7
Q
Guttural pouch empyemia tx if pus
A
daily drainge and lavage
AM
8
Q
Guttural pouch empyemia tx if chondroids
A
flush
basket retrieval in surgery
9
Q
Guttural pouch mycosis most important clinical sign
A
serious epistaxis with no related trauma or exercise
10
Q
Guttural pouch mycosis cause
A
aspergillus spp. in dorsocaudal medial compart.
11
Q
Guttural pouch mycosis tx
A
occlude artery affected
12
Q
Guttural pouch mycosis prognosis
A
over 90% if technology o occlue
13
Q
Strangles cause
A
strep equi equi
14
Q
Strangles clinical signs
A
urt inflamm and discharge
abscessing lymph nodes
abrupt fever
15
Q
Strangles who it hits most
A
young, on breeding farms
16
Q
Strangles Dx
A
**Culture
PCR - doesnt tell if shedding
Serology - can’t tell if Vx or infection
17
Q
Strangles Tx with early
A
just let it run unless it causes dysphagia
If it does, AM therapy but risk bastard
18
Q
Strangles Tx with LN abscesses
A
drain, lance if needed
isolate animal
flush
19
Q
When to AM Tx Strangles
A
lymph node abscessing
advancd clinical signs
20
Q
What to do with horses exposed to strangles
A
AM to prevent seeding
21
Q
Strangles common complications
A
purpura hemorrhagica
metastatic spread - bastard
myositis
agalactia
22
Q
Strangles - treating purpura
A
corticosteroids and supportive care
maybe AM
23
Q
Strangles - treating bastard
A
probably just AM
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)
25
Strangles re-infection rate
75% within 5 years of getting it.
26
Strangles culture tells if shedding or not, but what is interesting about PCR?
3 X more sensitive
| Looking for SeM (Antiphagocytic M protein)
27
Strangles vaccination protocols
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
28
Influenza presentation/ clinical signs
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
29
Influenza pathogenesis
N changes MC apparatus --> H moves in and binds to sugars on epithelial cells --> replication --> cell necrosis/desquamation --> inflammation --> edema, lymphocytes --> 6 weeks repaired
30
Influenza Dx
Viral isolation
PCR
ELISA
31
Influenza Tx
symptomatic
| treat the secondaries if possible
32
Influenza control
Vx
| horses will shed for 7-10 days after last sign of illness so watch for that and then it's gone
33
Herpevirus (Rhinopneumonitis) etiology
EHV-1 and EHV-4
34
Herpevirus (Rhinopneumonitis) general C/S
URT edema, hyperemia, petech hem
35
Herpevirus (Rhinopneumonitis) 1 C/S
neurologic, reproductive, and respiratory signs
myeloencephalopathy
neonatal deaths, abortions, weak foals
fever, mucopur discharge
36
Herpevirus (Rhinopneumonitis) 1 neonatal death/weak foals have...
IS pneum
| hypoplastic thymus and spleen
37
What is not a dependable C/S of EHV 1, 4
coughing
38
When do they get EHV
around training starting, 1 year
39
Herpevirus (Rhinopneumonitis) prevention
Vx for 1 and 4 - mod live, divalent killed
| maternal Ig for a month
40
Herpevirus (Rhinopneumonitis) Vxs don't prevent
abortions or neurologic disease
41
Herpevirus (Rhinopneumonitis) abortions are tricky because
the serology is gone because titer is short-lived
42
Equine Viral Arteritis etiology
arterivirus
43
Equine Viral Arteritis outbreaks with
respiratory and abortions
44
Equine Viral Arteritis C/S
```
subclinical to death
pyrexia, anorexia, depression
edema in funny places (eye, scrotum, limbs)
dyspnea cough and discharge
tearing up
```
45
Equine Viral Arteritis C/S in neonatal foals
severe resp
lots die
fever
leukopeni, thrombocytpeni
46
Equine Viral Arteritis neonatal PM
IS pneum, lymphocytic arteritis and periarteritis
| renal tubular necrosis
47
Equine Viral Arteritis differentiates from influenza with
```
lymphocytic arteritis (EVA)
lymphocytic infiltration to IS space
```
48
Equine Viral Arteritis abort when?
3-8 wks after infection, late
49
Equine Viral Arteritis can stallions transmit?
yes
50
Bacterial Pneumonia etiologies
strep zoo ****
strep equi
pasteurella, ecoli, pseudo, kleb, enterbac (complicating things)
anaerobes (clost, bact)
51
Bacterial Pneumonia acute C/S
```
fever
tachypnea
discharge
coughing
exercise intolerance
```
52
Bacterial Pneumonia chronic c/S
acute signs
weight loss
decreased appetite
53
DDx for infectious pulmonary dysfunction
Bacterial
viral
fungal, aspergillosis follows GI Dz
parasitic
54
DDx for non-infectious pulmonary dysfunction
RAO
IAD
Neoplasia (LSA, Mets)
55
Common mets to lungs
renal/gastric carcinoma
| melanoma
56
Dx of Bacterial Pneumonia special features (besides the PE, U/S, regular Clin path, TTW, Thor rads)
end ins crackles
expiratory wheezes
ascult/percuss/rads/us --> pleural effusion
57
Causes of end inp crackles
transient atelectasis
| secretions
58
causes of exp wheezes
inflamed/narrowed airways from secretions
59
Sounds to be heard with PPneum
rubbing sounds
| nothing on the ventral thorax (line)
60
What to do with pleural effusion?
drain it, culture it, cytology. Likely not as good as TTW
61
Bacterial Pneumonia pathophysiology
defense gone - MC clear, PAMs, CMI/hum
| inhaled something and spread from there
62
Bacterial Pneumonia tx
do C/S first from TTW
Gr - --> aminoglycosides
GRam + --> penicillin
anaerobes --> metronidazole
Common Pen-Gent
63
EMPF (Equine Multinodular Pulmonary Fibrosis) etiology
gamma herpes virus - same as MCF
| EHV-5
64
EMPF (Equine Multinodular Pulmonary Fibrosis) definitive/Histologic lesions
IS lung, up to 5 cm diameter fibrosis
| only in alveolar parenchyma --> inflamm cells but still the right architecture
65
EMPF (Equine Multinodular Pulmonary Fibrosis) Tx
supportive
AM, AV,
Pain control
steroids
66
EMPF (Equine Multinodular Pulmonary Fibrosis) prognosis
76% die
67
DDx for foal pneumonias
```
all the adult causes
rhodococcus equi
actinobacillus equi (sepsis)
e coli (sepsis)
strep equi zooepidemicus ***** most common
anaerobes
```
68
What do we know about bacterial pneumonias in foals?
most frequently in under 1 month
| most commonly a manifestation of septicemia (so when sepsis, worry about pneumonia)
69
How is the diagnostic approach different for neonatal foals with pneumonia than older foals and adults? So what are our mainstays?
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
what are some special cellular/immunity characteristics in neonatal foals that may contribute to bacterial pneumonia
```
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
How to diagnose bacterial pneumonia in the older foal?
TTW, thor rads, and thor U/S
72
Who does undiff. RTD hit
80-90% 4-5 mo foals
73
Undiff RTD etiologies
strep zoo***
staph epidermidis
r. equi
maybe viruses
74
Undiff RTD clinical signs
crackles, wheezes, mucopur discharge, cough, tachypnea
75
Undiff RTD rads will show
bronchoIS pattern
76
Undiff RTD BAL will show
neutrophils and possible cocci.
77
Undiff RTD Tx
ampicillin, penicillin, or TMS all BID
78
Undiff RTD prognosis
30% relapse, but hard to know
79
Rhodococcus equi pneumonia for sure clinical signs
fever
crackles,
wheezes
tachypnea
80
Rhodococcus equi pneumonia variable signs
mucopur nasal discharge
cough
respiratory distress
81
What is the clinical manifestion (PM would find for ex) of Rhodococcus equi pneumonia
chronic suppurative bronchopneumonia with extensive abscessation . They are remarkably able to deal with it considering how mild the signs are.
82
Rhodococcus equi pneumonia Dx (Need)
Clinical signs
PCR - especially the presence of the VAP-A gene
Cytology from TTW
83
Rhodococcus equi pneumonia Txs. Which is better?
6-8 wk minimum Erythromycin and rifampin
OR
azithromycin and clarithromycin (better concentriaons in the BAL cells and pulmonary epithelial lining)
84
Rhodococcus equi pneumonia Dx (help with it)
rads - alveolar, and abscesses
serology showing exposure
US showing abscesses
CBC and Fibrinogen
85
What is the source of contamination and route of infection?
foals feces, and inhaling dust and virulent r. equi
86
When does Rhodococcus equi pneumonia hits these guys?
2-5 months old. It is the most devastating of dz from 3wk to 5 month foals
87
Rhodococcus equi gram, behaviour, and site of replication/habitat
grm pos,
facultative IC pathogen
replicates in pulmonary macrophages
88
Rhodococcus equi pneumonia most important epidemiological point
Overcrowding, dusty conditions predispose, especially with related weather changes
89
Rhodococcus equi comes from?
the soil - lives there a long time
90
Acute respiratory Distress Syndrome is also
Bronchointerstitial pneumonia (this pattern will be on rads too)
91
Acute respiratory Distress Syndrome hits who
1-7 months of age
92
Acute respiratory Distress Syndrome clinical signs
tachypnea, increased resp effort, cyanosis
| hypoxemia, hypercapnia --> respiratory acidosis
93
Acute respiratory Distress Syndrome Tx
NOT AM because will not respond
| GIve O2, bronchodilators and steroids
94
Acute respiratory Distress Syndrome prognosis
guarded, especially for athletics
| tend to die in 1-2 days
95
Acute respiratory Distress Syndrome cause
we don't know (looks like r equi and pneumocystis carinii)
96
IAD important characteristics
mucoid/mucopur exudate in nasopharynx, trachea, and bronchial bifur
AND
non-septic inflammation
97
IAD is mainl yin
young, performance horses
98
How many coughing horses have IAD
85%
99
IAD cause?
related to RAO?
unknown
dust, molds, pollutants
possibly low grade persistent infections
100
IAD clinical signs
```
mostly subclinical, but
poor performance
coughing
NOT febrile
MAYBE EIPH evidence
```
101
IAD Dx
endoscope for exudate in the airways
and R/O other causes
BAL
102
IAD BAL will be significant when...
Mast cells >2%
PMNs cells >5%
or eosinophils > 1%
103
IAD Tx
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
RAO (not COPD) hits
middle-aged horeses
105
RAO (not COPD) is associated with
stabling
hay, straqw and molds
rarely summer pastures
Hypersensitivity? not really.
106
RAO (not COPD) etiologies
```
organic dust
hypersensiticvity to poorly cured hay
aspergillus fuigatus
faenia rectivirgula
some pollensv --> SPAOPD
```
107
RAO (not COPD) pathogenesis if a hypersensitivity
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
RAO (not COPD) pathogenesis if a chronic bronchiolitis
mucopur in airways --> bronchospasm --> peribronchiolar infiltration --> goblet cell hyperplasia and viscous mucus
109
RAO (not COPD) pathogenesis if a non-specific hyper-responsiveness
cold air, Nh3, exercise
110
RAO (not COPD), basically what happens
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
RAO (not COPD) pathogenesis changes acutely and chronically how?
acute- edema in airway causes mucous accumulation
Chronically - airway remodelling causing mucous metaplasia, smooth muscle hypertrophy, peribronchial fibrosis and inflammation
112
RAO (not COPD) Clinical signs
```
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
RAO (not COPD) Dx
```
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
What are normal levels of neutrophils on BAL
115
RAO (not COPD) treatment
```
Environmental management
Corticosteroids
Bronchodilators
Mast cell stab (disdoium cromoglycate again)
mucolytics and kinetics
maybe AM
```
116
Because of the possibility of hypersensitivity causing RAO (not COPD), Dx may include
Intradermal skin testing and
| serum allergen testingf
117
What are the mucolytics and kinetcs?
```
dembrexine hydroCl (sputolysin)
acetylcysteine
```
118
EIPH is characterized by
strenuous exercise associated with extravasation of RBCs from pulmonary vasc into the IS space and alveolie and airways
119
EIPH shows in which part of the lung
caudal dorsal
120
EIPH only consistent finding is
a direct consequence of intense exercise
121
EIPH potential causes/pathogenesis
increase cap pressure--> decrease IPleural pressure
abdominal contents hit the dorsocaudal lobe
pulmonary hypertension to being with
122
EIPH clinical signs
excessive swalloing
10% actually bleed
decreased performance
some coughing and labored breathing
123
EIPH Dx and what to see with the tests
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
EIPH Tx (there are a lot of them but the main ones are..)
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
