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Corrine Sweeney's take on Equine Respiratory Disease!

We 
can do this any way you want. What you need to know for boards is the 
stuff you were already taught, not something new, if it was something new 
we would have already taught it (hmm?). So we can go through these 
categories:

pleuropneumonia
foal pneumonia
EIPH
COPD
strangles

COPD: 
CHRONIC OBSTRUCTIVE PULMONARY DISEASE, HEAVES

Etiology: mold, other 
allergens - release of chemical mediators in response to antigens, 
including histamines, kinins, prostaglandins, serotonin, SRSA; all 
causing reflex bronchoconstriction in smooth muscle of the small airways


pathogenesis: vagally induced bronchoconstriction, airway obstruction, 
increased work to breathe, decreased tidal volume, increased respiratory 
rate.
with chronicity, loss of elastic recoil, can't exhale passively the 
inspired volume, increased functional residual capacity and increased 
active exhalation.

necropsy findings: bronchitis, bronchiolitis, mucus 
gland infiltrate, smooth muscle hyperplasia, alveolitis. inflammation is 
the main thing you see, and mucus gland and smooth muscle 
hypertrophy/hyperplasia
emphysema - irreversible and pathological 
overdistension of alveoli, rarely present in horses!!

clinical signs, 
then: increased RR/RE, flaring nostrils, coughing - dry or productive; 
heave line - abdominal muscle hypertrophy. signs vary with severity of 
disease. horse will be afebrile, with varying exercise intolerance. 
wheezes on auscultation, maybe some crackles. think of a narrow airway 
with increased resistance, decreased compliance. usually middle aged to 
older horse, not young.

diagnostics: on clinical signs and transtracheal 
wash - increased neutrophils, nondegenerate unless secondary bacterial 
infection. usually you don't see eosinophils - you want to see them, but 
you usually don't. Kurschmann spirals (mucus plugs) may be seen. nothign 
is pathognomonic, though.

CBC nonspecific, neutrophilia if secondary 
infection present.
pulmonary function tests not yet adapted but 
resistance is increased and compliance is decreased. 
Atropine sulfate 
(parasympatholytic) test - improvement in RR/RE due to bronchodilation

blood gases - PaO2 under 90 mmHg after modest exercise

Treatment:

steroids and environmental changes and bronchodilators. environmental 
changes are really the top thing to try but on the boards, look for 
antiinflammatory drugs and bronchodilators on the list of things to 
choose. mast cell stabilizing drugs, too, but that probably won't be on 
the exam. if they suddenly ask you for an example of a corticosteroid, 
you could say dexamethasone, prednisolone. bronchodilators: clenbuterol, 
albuterol. remember there is a move to inhaled steroids now, too. 
beclomethasone can be inhaled and work well, but costs a lot to deliver 
by the special mask. or can give a systemic one.

bronchodilators - B2 
agonists and parasympatholytics
parasympatholytics: atropine (not for 
chronic use), glycopyrrolate, ipratropium bromide
B2 adrenergic agonists: 
clenbuterol, albuterol, pirbuterol, fenoterol - result in increased 
intracellular concentration of cAMP and airway smooth muscle relaxation - 
that might be worth remembering.
phosphodiesterase inhibitors: 
theophylline, aminophylline - inhibit breakdown of cAMP, promote 
bronchodilation.

skin testing and hyposensitization - not universally 
accepted so probably not on the exam. only a few schools do this so it 
isn't a likely thing to be on the test. but they do do this.

that was 
all you need for COPD, in a nutshell.

STRANGLES:

etiology: 
streptococcus equi equi (not strep equi zooepidemicus which is probably 
the most common cause of equine pneumonia), gram positive cocci. 
worldwide distribution.
disease: acute URI characterized by fever, 
lethargy, purulent rhinitis, and regional LN abscessation. very 
contagious disease!
think about equine respiratory disease in general - a 
lot of the bacterial diseases are not contagious - we put them in the 
barn, no problem. but this one would go right into isolation. this is 
contagious. good test question. 

can occur in any age group; age 1-5 
predisposed b/c immunologically naive.
older horses probably already 
exposed, therefore immune.
outbreaks seen when lots of susceptible horses 
are brought together and exposed to a horse carrying s.equi equi (may or 
may not be overtly infected). 

S.equi equi is inhaled or ingested after 
direct contact with mucopurulent d/c from infected horse or contaminated 
equipment. so you need direct contact, not like with viruses where you 
can spread it across the room. shared water buckets, sharing pasture and 
socializing, etc. 

the bacteria adhere to the epi cells of buccal and 
nasal pneumonia, spread to regional LNs - submandibular, submaxillary, 
retropharyngeal.

M protein is the adherence factor and protects the bug 
from being phagocytosed by PMNs. also a hyaluronic acid capsule is 
present and is a virulence factor and is in the vaccine.

signs: 
depression, anorexia, fever, nasal d/c, cough, large submand. LNs, 
sometimes dyspnea. severity varies. mucopurulent nasal d/c. the 
lymphadenopathy can be profound, the LNs can open and drain. sometimes 
respiratory obstruction can occur. nodes in thoracic inlet can also be 
involved. 

dx: clinical signs, esp with abscess and rupture of nodes; 
also culture of s.e.e. from nose or LNs. this is not normal flora! If it 
looks like strangles, treat it like strangles. any positive culture is 
significant. 

this isn't probably a test thing but as with any disease, 
there are plenty of false negatives, but there aren't false positives 
with this disease. 

transmission: horses get it from other horses. it 
doesn't stay in environment - unless protected by moist discharge it dies 
quickly. rhodococcus stays forever but s.equi equi only lives 7-9 weeks 
under perfect conditions. you get it from infected horses or contaminated 
fomites like buckets, utensils. 

recovered horses- may shed for a while, 
most shed for under a month. up to 20% do shed after clinical signs end, 
though. 

location of persistent infection/shedders/carrier - think 
guttural pouch. that's where the bacteria may hang out. probably too new 
to be on the test but you never know.

lab findings: neutrophilic 
leukocytosis, hyperfibrinogenemia, possibly anemia of chronic disease. 
positive culture. 

treatment: to treat a horse with strangles - you can 
do nothing, and let it run its course. if the horse is really really 
sick, you can treat with penicillin. they will (not?) probably try to 
trick you. you should do nothing if he's not that sick. if he is really 
sick, you want to give antibiotics. this is a gram positive organism. the 
classic anti-gram-positive drugs are beta-lactams, penicillins. you can 
also use TMS, ceftiofur. keep in mind that it is gram positive. if there 
is no antibiotic on the list of choices, you could do tracheostomy if the 
horse is dyspneic, you could hotpack the LNs; you could give 
antiinflammatories aka flunixin, you could lance/drain the LNs, that 
would be reasonable. 
abx - depends on situation
antipyretics
trach if 
needed
encouraging or establishing drainage
also isolate the affected 
horse!

Prevention: vaccination is possible. there is a MLV-intranasal, 
relatively new vaccine. also there are killed bacterins and killed M 
protein vaccines. vaccine efficacy is questionable - IM one is not that 
effective, IN one is suppsed to be better but in any case it is not 100%, 
objective is to decrease incidence and decrease severity of the disease. 
regarding vaccination in the face of an outbreak. why not to do that: 
vaccine takes some time to work, so the horse will probably get it before 
you finish your vaccine series. and this is probably not on the test but 
if your horse was already exposed and you boost with a vaccine and 
hyperimmunize him, you might cause complications like purpura. 

most 
horses with strangles get better uneventfully
some have complications:

purpura - immune complex disease - signs include peripheral pitting 
edema, lid edema, fever, vasculitis, warm limbs, pain, ag/ab complexes in 
capillaries. tx steroids.
bastard strangles - disseminated, or metastatic 
strangles. it affects other LNs - mesenteric, etc - also brain, testes - 
you can get abscesses anywhere. 
most other complications are related to 
bastard strangles. also seen in lung, liver, spleen, kidney. 
Respiratory 
tract obstruction may occur
Laryngeal hemiplegia may occur due to 
involvement of recurrent laryngeal nerve
Guttural pouch empyema may occur

suppurative bronchopneumonia may occur
myocarditis
etc.

expected course 
and prognosis - good. usually horses get better and do fine.  probably 
will see a couple questions about this on the test.

FUNGAL PNEUMONIA


don't expect much on this. but for some reason, when talking about fungal 
pneumonia in horses and if they don't say you are in california and it is 
a weird case, the most common fungus will be Aspergillus. This is 
*uncommon* in the horse but is the most common fungal pneumonia in the 
horse. immunosuppressed horses are susceptible. a certain population of 
horses with salmonella enterocolitis and compromised bowel may develop 
aspergillosis. A. fumigatus is most common species. it's ubiquitous in 
environment. GI tract is main portal of entry, or it can be inhaled and 
infect an immunosuppressed animal. pathogenic mechanism postulated to be 
profound neutropenia associated with colitis. don't worry about most of 
this. risk factors are acute colitis or immunosuppression or possibly 
prolonged steroid use. that's probably all you need to know, risk factors 
or most common organism.

in California, coccidiomycosis (not crypto) is 
also out there. that's more a regional thing and it wouldn't be likely to 
be on national boards. 

treatment is difficult for aspergillus. systemic 
antifungals cost a lot. fluconazole, itraconazole, or amphoteracin b are 
options. 

prognosis is grave despite treatment.

FOAL PNEUMONIA:


Bacterial Foal Pneumonia
signs: fever, depressed, weight loss, etc etc.

etiology: strep equi zooepidemicus is most common cause of bacterial 
pneumonia in all ages of horses. found on mms of normal horses. an 
opportunist in the lungs. rapid secondary invader when resp epi is 
damaged - eg, postviral.
pasteurella, klebsiella also important
in foals, 
but not adults, rhodococcus equi is important. 

foals may just have 
pneumonia.
foals can also get pneumonia from being septic. 

e.coli, 
actinobacillus, salmonella - these are more associated with generalized 
septicemia. anaerobes are rarely cultured from uncomplicated pneumonia. 
septic presentation more in neonates under 1 month old.

neonates often 
have FPT and generalized sepsis along with pneumonia.

tx: many 
antibiotics, depends on the bugs. bronchodilators theoretically useful 
but really not that helpful. expectorants may be used for dry cough or 
tenacious expectoration. these things are used in foals, though, more 
than in adults. antipyretics too.

RHODOCOCCUS EQUI often on the test...

an important cause of pneumonia in foals under 6 mos. this bug can also 
cause diarrhea, joint sepsis, intraabdominal abscesses, and multifocal 
abscesses. epiphysitis, septic physitis.

remember it is gram positive, 
pleomorphic rod shaped bacterium. is facultative intracellular 
opportunistic pathogen that lives in phagocytes. remember this! it's a 
saprophytic opportunist from the soil, can be aerosolized from soil via 
dust. prospers in manure of herbivores. used to be called corynebacterium 
equi. 

pathogenesis of r.equi: INHALED is big one. can be ingested from 
soil too. 
inhaled --> primary pneumonia, may spread to intestine

INGESTED -->intestinal infection, metastatic pneumonia can occur.

pathogenesis:
almost all foals are exposed, most get an immune response 
and are protected; there is an overwhelming dose in a period of low 
passive immunity -->disease. 
remember it is intracellular, and inhibits 
phagosome-lysosome fusion. this makes it harder to kill.

it causes 
insidious chronic pneumonia. not like acute pleuropneumonia. often 
characterized by pulmonary abscesses of varying sizes. signs are not 
pathognomonic. depression, anorexia, dyspnea, tachypnea, nasal d/c, 
fever, crackes/wheezes. joint swellings may occur due to septic joints OR 
due to immune mediated synovitis. joint fluid rarely cultures positive 
for R.equi but it can. be careful of question on joint effusion!
labwork: 
leukocytosis with mature neutrophilia - some of the highest white counts 
and fibrinogens of any foals. high fibrinogen, high TP. 
AGID for 
detection of antibody is used for diagnosis, also ELISA for detection of 
antibody.
cytology reveals gram positive pleomorphic intracellular rods 
"chinese characters"; abscesses can be seen on rads, ultrasound of chest, 
abdomen. 
tx: erythromycin and rifampin
complications of these drugs in 
foals: fatal mare colitis; diarrhea in foal

prevention: don't crowd 
paddocks, avoid dusty areas, good colostrum management, take daily 
temperatures or monitor fibrinogens for early detection; possibly use 
hyperimmunized plasma to prevent it, during the first month of life on 
endemic farms. the plasma is given IV, so it's a big deal. some people 
try to hyperimmunize the mares, too, to increase colostral antibody. this 
(the plasma thing) is somewhat used worldwide for endemic problem farms. 
NO VACCINE YET in this country. 

ADULT BACTERIAL PNEUMONIA

associated 
with viral infections, stress, anesthesia, endotoxemia, 
immunosuppression, or aspiration. stress includes racing, transportation. 


etiology: most often strep equi zooepidemicus. not contagious! or B 
hemolytic strep found in skin of normal horses.  gram negatives can 
complicate it. e.coli, pasteurella is most common, enterobacter, 
klebsiella. anaerobes are not usually primary isolates, but may be seen. 


if there's any question about tracheal aspirates, is there anything you 
can imagine that you dn't know about it? you know how to do it, a couple 
of ways, you know why you might do it, you know when it is indicated - to 
look for something to culture or to characterize something like COPD, 
right. those are the key things. what about BAL? you just need to know 
the difference b/w that and the TTW like where you sample from with the 
BAL. (trachea vs bronchus). also ultrasound - good for finding pleural 
effusions, cranial mediastinal masses, peripheral stuff, ruling out 
diaphragmatic hernias. 
chest rads - you just get laterals. can see 
fluid, abscess. 

therapy - KPen/Gent, Metronidazole...TMS, ceftiofur...

for anaerobic infections you add in the metronidazole, or you can put in 
KPen!

PLEUROPNEUMONIA

disease process whereby pleural 
effusion/pleuritis  or pleurisy occurs secondary to pneumonia or 
pulmonary abscessation. note that sometimes pleuritis is used to mean 
pleuropneumonia even though that is technically wrong.

severe forms 
often involve anaerobic bacteria on top of whatever was originally there.


1st stage - exudative
2nd stage - fibrinopurulent
3rd stage - 
organization - limits lung expansion, lots of fibrin, "pleural peel" 
encasing the lung.adhesions form. 

any age/breed/sex 
stress, transport, 
exercise can precede pleuropneumonia. sometimes it is called transport 
pneumonia.
racehorses may have higher risk due to transport, housing with 
transient populations of horses, heavy exercise, poorly ventilated barns, 
EIPH, and aspiration of dirt. 

signs: fever, lethargy, anorexia, 
etc...sternal or pectoral edema (specific for thoracic disease, not 
necessarily pleuropneumonia), pleurodynia - pawing, stiff gait, abducted 
elbows, guarded/shallow breathing. cough. relucctance to move.

pleurodynia can be detected by painful response to digital palpation of 
chest wall. also bad breath is associated with anaerobic infections. resp 
distress is related to the volume of pleural fluid. mm color, scleral 
injection reflect toxemia.  remember about auscultation - harsh, 
crackles, dull in area of pleural fluid, pleural rubs, etc. 

percussion, 
chest taps, ultrasonography - adhesions, abscesses, etc. 

airway and 
pleural fluid specimesn - submit for cytology, aerobic and anaerobic 
culture. gram stain the stuff. 

noraml equine pleural fluid is clear to 
light yellow, sterile, odorless, and has a protein concentration under 
2.5 g/dl and ncc under 10000/ul
parapneumonic pleural fluid is yellow to 
red, high protein and high cell count

pathogens:aerobes: strep, 
pasteurella, ecoli, enterobacter
anaerobe- bacteroides is big one, also 
clostridia, fusobacterium et al
tx: antibiotics, drainage with chest 
tube, teat cannula, etc. 
frequent ultrasounds are good to assess 
progression. 
complications include: endotoxemia, laminitis, 
thrombophlebitis, pneumothorax d/t lung necrosis, cranial mediastinal 
abscesses.

prognosis varies greatly.

EIPH: exercise induced pulmonary 
pneumonia

occurs in racehorses, other high performance athletes
no sex 
predilection, no real age predilection, no breed predilection
definition: 
bleeding originating from lung, associated with exercise.
"Bleeder" is a 
synonym. NB: epistaxis == blood from the nose. doesn't specifically mean 
EIPH. 

incidence: worldwide prior to endoscopy 1%, since endoscopy up to 
86% - probably all horses bleed if exercising enough - it's a factor of 
how hard you look for the blood. faster or longer exercise is more likely 
to cause it.

diagnosis is via endoscopy, trach wash, clinical signs - 
blood at one or both nostrils during or post-exercise. you should examine 
the horse 60-90 minutes post exercise. do an endoscopic exam and look for 
blood flowing up the trachea. it takes time for blood to come up the 
mucociliary elevator. ttw will show hemosiderophages - very sensitive but 
not very specific, just indicates pulmonary hemorrhage. test is positive 
weeks to month after a bout of EIPH. 
The blood is found in the 
dorsocaudal lung areas.
there are no pathognomonic clinical signs of 
EIPH. 
dyspnea is very rare
exercise intolerance?? stopping at end of 
race?? no one really talks about it but sometimes trainers say it. 

etiology is not known with certainty. that doesn't mean there isn't a lot 
known. we know it isn't a coagulopathy or vitamin deficiency. we know it 
isn't a bacterial pneumonia or cardiac arrhythmia. not due to hormonal 
deficiency. we think it is probably due to mechanical failure/stress 
failure of the walls of the capillaries in the lungs when the pressure 
inside them gets very high. pulmonary vascular pressure of galloping 
horses is very very high. 

"EIPH is an inevitable consequence of the 
extremely high cardiac output required by these elite athletes" is one 
interesting phrase.

repeated bouts of hemorrhage in lungs is responsible 
for changes such as bronchiolitis.

effective treatment - lasix? it's 
used but doesn't stop most horses from bleeding.

---sorry, I got paged, 
had to leave. but I am back now.
I was only gone for a couple of minutes.


THORACIC NEOPLASIA:

most common is lymphosarcoma. 
most common in 
abdomen is also lymphosarcoma
in eye is squamous cell carcinoma

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there is one protozoal disease which is sometimes seen in foals, 
sometimes in rhodococcus foals...pneumocystis carnii! 

--

how do you 
keep track of the viral diseases of the lung? 

VIRAL DISEASES:

two big 
ones - herpes and influenza. EHV-4 is the respiratory herpes. there are 
some adenoviruses, a rhinovirus, a rheovirus. there is another one that 
is almost asymptomatic although it is respiratory....probably better 
known as a virus that might cause a vasculitis - EVA!

pathogenesis - 
attachment, multiplication, ulceration, invasion, etc....tx is 
symptomatic, rest is important, prevent with vaccines. 

INFLUENZA 

highly contagious
most important equine respiratory disease in many 
countries. 
remember -antigenic drift is important with flu, no lasting 
immunity
spread via inhalation, droplets. endemic in europe and USA

animals 1-3 yrs old are most susceptible
sudden onset dz with short 
incubation period, rapid spread, high morbidity, low mortality. foals 
without maternal antibody thoguh may die of severe viral pneumonia. this 
is rare. 
fever, cough, serous nasal d/c
sometimes secondary myocarditis 
with arrhythmia
a vaccination exists, short lived protection
expected 
good prognosis, good return to function

HERPES EHV4 aka rhinopneumonitis

don't get confused b/w 1 and 4. Four is the one that is localized to 
respiratory tract. 1 can also cause respiratory disease and then go on to 
cause CNS or repro problems. both 1 and 4 may cause respiratory disease; 
1 can cause more than respiratory disease. ok?EHV1 infects WBCs, that is 
how it spreads around.  tx is symptomatic and supportive. 

remember 
about equine herpes myelitis, that's EHV1
virus can be isolated from 
nasopharyngeal swabs

don't confuse this with rhinovirus. that's a 
different virus. rhinopneumonitis is equine herpesvirus 1. (?)(4?)
most 
horses recover
vaccine not protective against neurologic form of herpes. 

vaccination q three months is good for respiratory protection for those 
at risk. that means if they are in the right age group, if they ship a 
lot, etc. hey, it's a pretty cheap vaccine and often given with tetanus 
so it is used a lot. 



necropsy - 
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