Basics of Equine Respiratory Diseases Flashcards
Guttural pouch tympany cause
congenital, secondary to URT, nasopharyngeal orifice
Guttural pouch tympany C/S
non-painful, elastic swelling in retrophar
resp noise
cough and dysphagia
Guttural pouch tympany Tx
surgery, fenestate median septum, salpopharyngeal fistula
Guttural pouch empyemia cause
secondary to URT infections, commonly strangles
Guttural pouch empyemia common etiology
strep equi
Guttural pouch empyemia C/S
intermittent discharge
cough, dysphagia
Guttural pouch empyemia tx if pus
daily drainge and lavage
AM
Guttural pouch empyemia tx if chondroids
flush
basket retrieval in surgery
Guttural pouch mycosis most important clinical sign
serious epistaxis with no related trauma or exercise
Guttural pouch mycosis cause
aspergillus spp. in dorsocaudal medial compart.
Guttural pouch mycosis tx
occlude artery affected
Guttural pouch mycosis prognosis
over 90% if technology o occlue
Strangles cause
strep equi equi
Strangles clinical signs
urt inflamm and discharge
abscessing lymph nodes
abrupt fever
Strangles who it hits most
young, on breeding farms
Strangles Dx
**Culture
PCR - doesnt tell if shedding
Serology - can’t tell if Vx or infection
Strangles Tx with early
just let it run unless it causes dysphagia
If it does, AM therapy but risk bastard
Strangles Tx with LN abscesses
drain, lance if needed
isolate animal
flush
When to AM Tx Strangles
lymph node abscessing
advancd clinical signs
What to do with horses exposed to strangles
AM to prevent seeding
Strangles common complications
purpura hemorrhagica
metastatic spread - bastard
myositis
agalactia
Strangles - treating purpura
corticosteroids and supportive care
maybe AM
Strangles - treating bastard
probably just AM
Strangles prevention
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)
Strangles re-infection rate
75% within 5 years of getting it.
Strangles culture tells if shedding or not, but what is interesting about PCR?
3 X more sensitive
Looking for SeM (Antiphagocytic M protein)
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
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
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
Influenza Dx
Viral isolation
PCR
ELISA
Influenza Tx
symptomatic
treat the secondaries if possible
Influenza control
Vx
horses will shed for 7-10 days after last sign of illness so watch for that and then it’s gone
Herpevirus (Rhinopneumonitis) etiology
EHV-1 and EHV-4
Herpevirus (Rhinopneumonitis) general C/S
URT edema, hyperemia, petech hem
Herpevirus (Rhinopneumonitis) 1 C/S
neurologic, reproductive, and respiratory signs
myeloencephalopathy
neonatal deaths, abortions, weak foals
fever, mucopur discharge
Herpevirus (Rhinopneumonitis) 1 neonatal death/weak foals have…
IS pneum
hypoplastic thymus and spleen
What is not a dependable C/S of EHV 1, 4
coughing
When do they get EHV
around training starting, 1 year
Herpevirus (Rhinopneumonitis) prevention
Vx for 1 and 4 - mod live, divalent killed
maternal Ig for a month
Herpevirus (Rhinopneumonitis) Vxs don’t prevent
abortions or neurologic disease
Herpevirus (Rhinopneumonitis) abortions are tricky because
the serology is gone because titer is short-lived
Equine Viral Arteritis etiology
arterivirus
Equine Viral Arteritis outbreaks with
respiratory and abortions
Equine Viral Arteritis C/S
subclinical to death pyrexia, anorexia, depression edema in funny places (eye, scrotum, limbs) dyspnea cough and discharge tearing up
Equine Viral Arteritis C/S in neonatal foals
severe resp
lots die
fever
leukopeni, thrombocytpeni
Equine Viral Arteritis neonatal PM
IS pneum, lymphocytic arteritis and periarteritis
renal tubular necrosis
Equine Viral Arteritis differentiates from influenza with
lymphocytic arteritis (EVA) lymphocytic infiltration to IS space
Equine Viral Arteritis abort when?
3-8 wks after infection, late
Equine Viral Arteritis can stallions transmit?
yes
Bacterial Pneumonia etiologies
strep zoo **
strep equi
pasteurella, ecoli, pseudo, kleb, enterbac (complicating things)
anaerobes (clost, bact)
Bacterial Pneumonia acute C/S
fever tachypnea discharge coughing exercise intolerance
Bacterial Pneumonia chronic c/S
acute signs
weight loss
decreased appetite
DDx for infectious pulmonary dysfunction
Bacterial
viral
fungal, aspergillosis follows GI Dz
parasitic
DDx for non-infectious pulmonary dysfunction
RAO
IAD
Neoplasia (LSA, Mets)
Common mets to lungs
renal/gastric carcinoma
melanoma
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
Causes of end inp crackles
transient atelectasis
secretions
causes of exp wheezes
inflamed/narrowed airways from secretions
Sounds to be heard with PPneum
rubbing sounds
nothing on the ventral thorax (line)
What to do with pleural effusion?
drain it, culture it, cytology. Likely not as good as TTW
Bacterial Pneumonia pathophysiology
defense gone - MC clear, PAMs, CMI/hum
inhaled something and spread from there
Bacterial Pneumonia tx
do C/S first from TTW
Gr - –> aminoglycosides
GRam + –> penicillin
anaerobes –> metronidazole
Common Pen-Gent
EMPF (Equine Multinodular Pulmonary Fibrosis) etiology
gamma herpes virus - same as MCF
EHV-5
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
EMPF (Equine Multinodular Pulmonary Fibrosis) Tx
supportive
AM, AV,
Pain control
steroids
EMPF (Equine Multinodular Pulmonary Fibrosis) prognosis
76% die
DDx for foal pneumonias
all the adult causes rhodococcus equi actinobacillus equi (sepsis) e coli (sepsis) strep equi zooepidemicus ***** most common anaerobes
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)
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,
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
How to diagnose bacterial pneumonia in the older foal?
TTW, thor rads, and thor U/S
Who does undiff. RTD hit
80-90% 4-5 mo foals
Undiff RTD etiologies
strep zoo***
staph epidermidis
r. equi
maybe viruses
Undiff RTD clinical signs
crackles, wheezes, mucopur discharge, cough, tachypnea
Undiff RTD rads will show
bronchoIS pattern
Undiff RTD BAL will show
neutrophils and possible cocci.
Undiff RTD Tx
ampicillin, penicillin, or TMS all BID
Undiff RTD prognosis
30% relapse, but hard to know
Rhodococcus equi pneumonia for sure clinical signs
fever
crackles,
wheezes
tachypnea
Rhodococcus equi pneumonia variable signs
mucopur nasal discharge
cough
respiratory distress
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.
Rhodococcus equi pneumonia Dx (Need)
Clinical signs
PCR - especially the presence of the VAP-A gene
Cytology from TTW
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)
Rhodococcus equi pneumonia Dx (help with it)
rads - alveolar, and abscesses
serology showing exposure
US showing abscesses
CBC and Fibrinogen
What is the source of contamination and route of infection?
foals feces, and inhaling dust and virulent r. equi
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
Rhodococcus equi gram, behaviour, and site of replication/habitat
grm pos,
facultative IC pathogen
replicates in pulmonary macrophages
Rhodococcus equi pneumonia most important epidemiological point
Overcrowding, dusty conditions predispose, especially with related weather changes
Rhodococcus equi comes from?
the soil - lives there a long time
Acute respiratory Distress Syndrome is also
Bronchointerstitial pneumonia (this pattern will be on rads too)
Acute respiratory Distress Syndrome hits who
1-7 months of age
Acute respiratory Distress Syndrome clinical signs
tachypnea, increased resp effort, cyanosis
hypoxemia, hypercapnia –> respiratory acidosis
Acute respiratory Distress Syndrome Tx
NOT AM because will not respond
GIve O2, bronchodilators and steroids
Acute respiratory Distress Syndrome prognosis
guarded, especially for athletics
tend to die in 1-2 days
Acute respiratory Distress Syndrome cause
we don’t know (looks like r equi and pneumocystis carinii)
IAD important characteristics
mucoid/mucopur exudate in nasopharynx, trachea, and bronchial bifur
AND
non-septic inflammation
IAD is mainl yin
young, performance horses
How many coughing horses have IAD
85%
IAD cause?
related to RAO?
unknown
dust, molds, pollutants
possibly low grade persistent infections
IAD clinical signs
mostly subclinical, but poor performance coughing NOT febrile MAYBE EIPH evidence
IAD Dx
endoscope for exudate in the airways
and R/O other causes
BAL
IAD BAL will be significant when…
Mast cells >2%
PMNs cells >5%
or eosinophils > 1%
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
RAO (not COPD) hits
middle-aged horeses
RAO (not COPD) is associated with
stabling
hay, straqw and molds
rarely summer pastures
Hypersensitivity? not really.
RAO (not COPD) etiologies
organic dust hypersensiticvity to poorly cured hay aspergillus fuigatus faenia rectivirgula some pollensv --> SPAOPD
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)
RAO (not COPD) pathogenesis if a chronic bronchiolitis
mucopur in airways –> bronchospasm –> peribronchiolar infiltration –> goblet cell hyperplasia and viscous mucus
RAO (not COPD) pathogenesis if a non-specific hyper-responsiveness
cold air, Nh3, exercise
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
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
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
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)
What are normal levels of neutrophils on BAL
RAO (not COPD) treatment
Environmental management Corticosteroids Bronchodilators Mast cell stab (disdoium cromoglycate again) mucolytics and kinetics maybe AM
Because of the possibility of hypersensitivity causing RAO (not COPD), Dx may include
Intradermal skin testing and
serum allergen testingf
What are the mucolytics and kinetcs?
dembrexine hydroCl (sputolysin) acetylcysteine
EIPH is characterized by
strenuous exercise associated with extravasation of RBCs from pulmonary vasc into the IS space and alveolie and airways
EIPH shows in which part of the lung
caudal dorsal
EIPH only consistent finding is
a direct consequence of intense exercise
EIPH potential causes/pathogenesis
increase cap pressure–> decrease IPleural pressure
abdominal contents hit the dorsocaudal lobe
pulmonary hypertension to being with
EIPH clinical signs
excessive swalloing
10% actually bleed
decreased performance
some coughing and labored breathing
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
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
