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Horse Medicine > Equine respiratory diseases > Flashcards

Equine respiratory diseases Flashcards

1
Q

What is the LRT?

A

lungs from primary bronchi to alveoli

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2
Q

What is URT?

A 
nares
nasal passages 
pharynx
larynx
guttural pouches
trachea
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3
Q

What divides the guttural pouch into two compartments, which is the bigger compartment?

A

stylohyoid bone

medial compartment

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4
Q

Wht artery run over the guttural pouch?

A

external maxillary artery
internal carotid artery
external carotid artery

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5
Q

What nerves run over teh guttural pouch?

A

VII, IX X, XI, XII

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6
Q

What are the three main guttural puch diseases?

A

tympany
mycosis
empyema

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7
Q

What is the cause of guttural puch tympany?

A
  1. dysfunction of the nasopharyngeal orifice (1 way valve)
  2. secondary to upper airway infections/inflam
  3. congenital (not that common)
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8
Q

What are the clinical signs of guttural pouch tympany?

A
  1. non-painful elastic swelling in the retropharyngeal area!!
  2. respiratory noise
  3. cough and dysphagia
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9
Q

What is the treatment for guttural pouch tympany?

A
  1. surgery
  2. fenestration of median septum (unilateral)
  3. creation of salpinogopharyngeal fistula
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10
Q

What are the guttural pouches?

A

caudoventral diverticula of the auditory tubes

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11
Q

What is a possible function of guttural pouches?

A

cooling of arterial blood suply to brain

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12
Q

What is the capacity of each guttural pouch?

A

300mL

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13
Q

What is the lining of the guttural pouches?

A

secretory mucosa lining and thinner than in nasopharynx

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14
Q

Why can guttural pouch tympany cause resp noise?

A

enlargement of guttural pouch can bulge above the epiglottis?? because it bulges ventrally into nasopharynx?

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15
Q

What is the most common guttural pouch disease?

A

guttural pouch empyema

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16
Q

What is guttural pouch empyema secondary to?

A
  1. upper resp infections (strep equi)
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17
Q

What are the clinical signs of guttural pouch empyema?

A
  1. intermittened nasal discharge that is worse when head is lowered
  2. coughing and/or dysphagia in some cases
  3. can see white on nose due to chronic nasal discharge
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18
Q

What is treatment for guttural pouch empyema?

A

if there is only pus, daily drainage and lavage. Antibiotics?
if there are chondroids–>flush, basket retrieval, surgery

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19
Q

Why is it important to have a horse’s head down (heavy sedation) when flushing guttural pouch?

A

to prevent aspiration pneumoniae

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20
Q

What is a radiographic way to diagnose guttural pouch empyema?

A

a fluid line on radiograph

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21
Q

Why is important to flush everything out in guttural pouch empyema?

A

because won’t resolve, antibiotics won’t work

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22
Q

What does inspissated pus become?

A

chondroids

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23
Q

What is the most important cause of serious epistaxis that is not related to exercise or trauma? (important)

A

guttural pouch mycosis

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24
Q

Is there any warning that a horse will die of hemorrhage from mycosis?

A

Usually they have several bouts of hemorrhage before a fatal episode

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25
Q

What is the cause of guttural pouch mycosis?

A

aspergillus in the dorsocaudal region of the medial compartment

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26
Q

What is treatment for guttural pouch mycosis?

A
  1. horses with epistaxis the affected artery should be identified and surgically occluded
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27
Q

What can be difficult to prevent with guttural pouch mycosis?

A

aberrant vessel anatomy
thrombi
infection and persistent nerve disfunction

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28
Q

What can be the survival of a horse with guttural pouch mycosis that is treated?

A

can exceed 90%

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29
Q

What nerves run over guttural pouch?

A

VII, IX, X, XI, XII
cranial cervical ganglion
sympathetic trunk

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30
Q

What can be the signs of guttural pouch mycosis?

A 
bleeding from (external carotid, internal carotid, external maxillary)
nerve deficits
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31
Q

What is the cause of strangles?

A

streptococcus equi equi

a gram + beta hemolytic strep

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32
Q

What is strangles characterized by?

A

URT inflammation an lymph node aspiration

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33
Q

Who usually gets strangles?

A

young horses, esp in breeding farms

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34
Q

What lymph nodes are often enlarged?

A

retropharyngeal

submandibular

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35
Q

When does nasal shedding begin in strangles?

A

2-3 days after onset of fever and persists 3 wweeks in most animals but can be longer

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36
Q

Why should you isolate horses that have strangles? How do you check animals that will start shedding?

A

Because they will have nasal discharge (shedding)

check rectal temperature for fever

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37
Q

How often does carrier state occur in strangles?

A

up to 10%

don’t show clinical signs but hide infection in guttural pouch

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38
Q

How would you ID a strangles carrier?

A

sample from guttural pouch

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39
Q

What are the clinical signs of guttural pouch empyema?

A
  1. abrupt onset of fever
  2. mucopurulent nasal discharge
  3. acute swelling and abscess formation in submandibular and retropharyngeal lymph nodes
  4. severity of disease depends on immune status, challenge load and duration
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40
Q

How is strangles diagnosed?

A
  1. culture–the gold standard
    with nasal swa, nasal wash, guttural pouch wash, pus from abscesses
  2. PCR–DNA sequence of SeM (antiphagocytic M protein)
    3 times more sensitive than culture
    dead or alive organisms
  3. serology–ELISA. Detects antibodies from vaccination AND infection. serum titers peak at 5 weeks and remain high for at least 6 months
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41
Q

If a person wants to take a horse to a show after strangles, should you use culture or PCR?

A

culture, because although PCR is more sensitive, it can detect dead organisms and is not relevant for disease shedding potential

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42
Q

What is treatment for strangles if horsees have early clinical signs (fever, depressed, purulent nasal discharge)

A

antimicrobial therapy may arrest disease and control outbreak.
if horse remains exposed to infected horses, high chance of relapse if discontinue treatment

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43
Q

What is treatment for strangles if horses have lymph node abscessation?

A
  1. enhance maturation and drainage of abscesses
  2. isolation
  3. hot packs or poultice
  4. if needed lance abscess
  5. flush and drain regularly
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44
Q

What is treatment for strangles if horses have lymph node absecssation and advanced clinical signs?

A

antimicrobial therapy

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45
Q

What is treatment of horse exposured to strangles?

A

may treat with antibiotics in hopes of preventing seeding of lymph nodes

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46
Q

Why would you be worried about using antimicrobials in the face of strangles infection?

A

could cause bastard strangles

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47
Q

What are complications of strangles?

A
  1. purpura hemorrhagica
  2. metastatic spread of infection
  3. myositis
    4 .agalactia
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48
Q

What is the mechanism of purpura hemorrhagic in horses that had strangles?

A
  1. immune mediated process

2. aseptic necrotizing vasculitis

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49
Q

What is the treatment for purpura hemorrhagica?

A

corticosteroids and supportive care +/- antibiotics

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50
Q

What are the signs of purpura hemorrhagica?

A

edema?

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51
Q

When does purpura hemorrhagica occur in horses that had strangles?

A

around 2wks later?

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52
Q

IN horses that get bastard tstrangles, when does it become apparent? where does it usually occur?

A

months to years later

most commonly lung, mesentery, liver, spleen, kidney, brain

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53
Q

What is the mechanism of myositis with strangles horse?

A

immune mediated

muscle infarctions and rhabdomyolysis with progressive atrophy

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54
Q

HOw do you prevent strangles?

A
  1. after natural infection, 75% of horses not reinfected within 5 years
  2. isolate all arrivals for 2 weeks
  3. immediately isolate affect horses
  4. check rectal temp during outbreak
  5. nasal swab/washes for culture/PCR
  6. beware of water troughs
  7. vaccination
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55
Q

What is the most commonly used vaccination fo strangles?

A

pinnacle live intranasal vaccine

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56
Q

Why should you not use vaccination in animals with high titers?

A

can cause vasculitis?

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57
Q

The influenza virus is in what group?

A

orthomyxovirus group

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58
Q

What are the types of influenza in horses?

A

H7N7

H3N8

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59
Q

What is the incubation time of influenza?

A

1-3d

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60
Q

What animals get influenza?

A

outbreaks in young horses 1-3years, often at race tracks

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61
Q

What is the pathogenesis of influenza?

A
  1. neruaminidase alters efficiency of mucociliary apparatus
  2. virus attach via hemagglutinin antigens to sugar goups on surface of resp tract epithelial cells
  3. viral replication followed by cell necrosis and desquamation
  4. inflammation leads to massive edema and lymphocyte infiltration
  5. recovery of normal epithelal architecture can take more than 6 weeks
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62
Q

Why should horses be rested after influenza infection?

A

because recovery of normal epithelial architecutre can take more than 6 weeks

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63
Q

What are the clinical signs of influenza?

A
  1. dry harsh cough 1-3 weeks
  2. biphasic pyrexia for 4-5 days
  3. in some horses: myalgia, myositis, limb edema and thus reluctant to move–immune mediated
  4. in young foals influenza is SEVERE–viral pneumonia, possible death in 48hr
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64
Q

How is influenza diagnosed?

A

detection of virus–nasopharyngeal swabs
(viral isolation, PCR, ELISA–nucleoprotein antigen)
seroconversion

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65
Q

What is treatment for influenza?

A

symptomatic

secondary bacterial pneumonia and pleuropneumonia are potential complications

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66
Q

How is influenza controlled?

A
  1. vaccination (not that effective). there are different types. Recombitek e.g.
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67
Q

What herpes viruses (rhinopneumonitis) cause resp form of dz?

A

EHV-1, EHV-4

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68
Q

What is the incubation period of herpesvirus?

A

3-7 days but has latent state!!

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69
Q

What are the signs of herpes virus infection?

A

URT edema, hyperemia, petechial hemorrhaeg

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70
Q

What does EHV-1 cause that EHV-4 does not?

A
  1. neonatal death or weak foals with interstitial pneumonia, hypoplasia of thymus and spleen
  2. abortions–infection several months before–serology not useful (imp!)
  3. myeloencephalopathy (neural)
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71
Q

What are the respiratory signs of herpesvirus EHV-1, 4

A
  1. cannot distinguish EHV-1, 4
  2. first year of life, usually soon after entry into training
    sudden onset of fever, (often biphasic)
  3. serous to mucopurulent nasal discharge
  4. coughing NOT dependable!
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72
Q

What are signs on farm of an EHV infection?

A

abortions
young horses with nasal discharge?
maybe neuro case
over a period of time

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73
Q

When do animals usually get the resp form of EHV?

A

first year of life
usually mild disease
nasal discharge, fever

74
Q

does vaccination prevent the neurologic form of EHV?

A

NO

75
Q

DOes vaccination prevent abortion caused by EHV-4?

A

debated

76
Q

Can horses vaccinated against EHV still become infected/shed virus?

A

yes. but may reduce clinical signs

77
Q

What EHV virus besides 1 and 4 can cause resp disease in foals?

A

EHV-2

and may play a role in R. equi pneumoniae

78
Q

What is the half life of maternal antibodies for EHV?

A

1 month

79
Q

Is the titer for EHV vaccination long lived or short lived?

A

short lived

80
Q

What is the equine viral arteritis vvirus?

A

enveloped RNA virus of arterivirus

81
Q

Are most infections of equine viral arteritis clinical or subclinical?

A

usually inapparent or subclinical (IMPORTANT)

82
Q

What does infection of equine viral arteritis cause?

A

resp signs and abortion

83
Q

What is the seroprevalance of equine viral arteritis in standardbreds?

A

as high as 80%

84
Q

What are the clinical signs of equine viral arteritis

A

often subclinical but can be severe disease, death
pyrexia, anorexia, depression
edema scrotum, ventrum, limbs, periocular
serous nasal discharge, dyspnea and cough
conjunctivitis and lacrimation

85
Q

WHat is the mechanism of edema with equine viral arteritis

A

arteritis

86
Q

What are the signs of equine viral arteritis in foals.?

A

severe resp signs
high mortality
fever, leukopenia, thrombocytopenia

87
Q

What are the signs equine viral arteritis on necropsy in neonatal foals?

A
  1. interstitial pneumonia

2. lymphocytic arteritis and periarteritis and renal tubular necrosis

88
Q

When do mares abort with equine viral arteritis?

A

abort LATE in gestation, 3-8 weeks after infection

89
Q

Why are stallions important in equine viral arteritis transmission

A

because can transmit infection venereally AND in semen (even frozen semen!!)
often these stallions have no signs

90
Q

What is the EVA cycle?

A
  1. horses infected by resp route may show signs in 3-4 days
  2. infected mare may transmit to stallion (or recover)
  3. infected stallions shed virus for 1-3 weeks (may recover)
  4. 30% of stallions recover and shed long term in semen alone
  5. shedding stallion infects mare
  6. mare may show clinical signs, shed from nose and mouth and may abort 10-17d later
91
Q

What is the most common cause of bacterial pneumonia?

A

streptococcus zooepidemicus

92
Q

Where is strep zooepidemicus found in normal horses?

A

in pharynx

93
Q

What is a less common cause of bacterial pneumonia?

A

strep equi

94
Q

What bacteria can complicate strep pneumonia?

A

gram negative bacteria

  1. PASTEURELLA
  2. e coli
  3. enterobactrer
  4. klebsiella
  5. pseudomonas
95
Q

What anaerobes can complicate arobic bacterial pneumonia?

A
  1. bacteroides

2. clostridium

96
Q

Why do you start with bnroad spectum antibiotics with bacterial pneumonia?

A

because often mixed infection of gram +, gram - and anaerobes

97
Q

What are the clinical signs of acute bacterial pneumonia?

A
  1. fever, may be intermittent
  2. tachypnea
  3. nasal discharge
  4. coughing
  5. exercise intolerance
98
Q

What are the clinical signs of chronic bacterial pneumonia?

A
  1. fever, tachypnea, nasal discharge, coughing, exercise intolerance
  2. weight loss
  3. +/- decreased appetite
99
Q

When clinical signs indicate pulmonary dysfunction, you must differentiate between infectious and non-infectious! What tests must be performed?

A

transtracheal wash and culture

100
Q

What are causes of infectious pulmonary dysfunction?

A
  1. BACTERIAL
  2. viral *usually URT
  3. fungal
  4. aspergillosis (oft follows GI dz)
  5. parasitic–parascaris equrum, dictyocaulus
101
Q

What are causes of non-infectious pulmonary dysfunction

A
  1. recurrent airway obstruction
  2. small airway inflammatory disease
  3. neoplasia (lymphosare coma, metastatic–renal/gastric carcinoma, melanoma)
102
Q

What is the diagnstic approach for pulmonary dysunction LRT dz

A
  1. physical examination
  2. auscultation
  3. clinical pathology
  4. tracheobronchial aspirate
  5. thoracic radiographs
  6. ultasonography
103
Q

When expiratory sounds are louder than inspiratory sounds what should you think of?

A

lower airway disease

104
Q

What can be heard with ascultation with lower airway disease?

A

increased harshness/intensity of expiratory sounds

  1. when expiratory sounds loudher than inspiratory sounds
  2. end inspiratory crackles (transient atelectasis, increased secretion)
  3. expiratory wheezes–inflamed airways, narrowed by thick secretions
  4. if pleuropneumonia then rubbing sounds, quiet ventral thorax (sub-pleural abscessation, pleural effusion–horizontal line demonstrated by ausculatation, percusion)
105
Q

What is seen on CBC and biochemistry with lung dysfunction?

A

leukocytosis (neutrophilia +/- bands)
hyperfibrinogenemia
increased total plasma proteins in chronic cases due to chronic antigenic stimulation

106
Q

What is seen on tracheal wash with bacterial infection?

A
  1. degenrated neutrophils
  2. precipitation
  3. necrotic material
  4. damaged epithelial cells
107
Q

What should be performed on tracheobronchial apsirate?

A
  1. cytology
  2. culture
  3. gram stains
108
Q

What is seen on thoracic radiographs with pulmonary dz bacterial pneumonia

A
  1. opacity in anteriovental thorax
  2. horiztonal line across ventral thorax if pleural effusion
  3. large cavitary lesions with horizontal line
  4. abscesses-anaerobic gas forming organisms
109
Q

What is the most sensitive tool to evaluate the pleural space?

A

ultrasonography

110
Q

How do you detect pleural effusion?

A
  1. detect by
    a. auscultation
    b. percussion
    c. radiography
    d. ultasounography
  2. can be aspirated and drained
111
Q

Why should you preferntially culture tracheal aspirate over pleural aspirate?

A

because tracheal aspirate often yields pathoenic organisms while pleural aspirate may not

112
Q

What is the pathophysiology of bacterial pneumonia?

A
  1. compromize of pulmonary defense mechanisms (mucociliary clearance, phagocytic cells, cellular and humoral immune systems)
  2. inhalation, aspiration (adults), hematogenous spread (neonates common) of bacteria
113
Q

What is the treatment for bacterial pneumonia?

A
  • based on culture/sensitivity*
    1. penicillin
    2. ampicillin
    3. aminoglycosides
    4. second and third gen cephalosporins
    5. TMS
    6. fluoroquinolones
    7. metronidazole
    8. rifampin
114
Q

What anaerobe does penicillin no tget?

A

bacteroides?

115
Q

What is the most common combination of antimicrobials for bacterial pneumonia?

A

penicillin and aminoglycosides may had metronizdazole if suspect anaerobes?

116
Q

Why is TMS not very good for bacterial pneumonia?

A

at the site of infection there is high PABA etc

117
Q

What is equine multinodular pulmonary fibrosis?

A

interstitial lung disease and fibrosis
caused by gama herpesvirus EHV-5
numerous coalescing nodules of fibrosis
Lesions confined to alveolar parenchyma (mixed inflam, preserved alveolar like architecture

118
Q

What the cause of equine multinodular pulmonary fibrosis

A

gamma herpesvirus EHV-5

119
Q

How is equine multinodular pulmonary fibosis treated?

A
  1. supportive (antibiotics, antivirals NSADs)

2. corticosteroids to reduce inflammation causing fibrosis!!

120
Q

What is the prognosis for equine multinodular pulmonary fibrosis?

A

poor. 76% die or euthanized

121
Q

What are immunological considerations in foal pneumonia?

A
  1. failure of passive transfer
  2. maternal antibodies
  3. immunologic system maturation
122
Q

What is the most common agent of peumonia in adult and foal pneumonia?

A

strep equi zooepidemicus

123
Q

What are causes of septicemia/pneumonia?

A

actinobacillus equuli

e. coli

124
Q

If you see a foal with pneumonia, diarrhea, what should you think unless proven otherwise?

A

septicemia

125
Q

Are anaerobe common or rare in foals?

A

rare

126
Q

In nenonatal foals, bacterial pneumonia is a frequent manifestation of what?

A

NEONATAL SEPTICEMIA

127
Q

What is the greatest cause of mrobidity and mortality in foals less than 1 month of age?

A

bacterial pneumonia

128
Q

What are the reasons that neonatal foals get bacterial pneumonias?

A
  1. decreased cells in BAL (until 3-6wk)
  2. macrophage predominant cell (in adult is same)
  3. transfer of maternal antibodies
  4. waning of maternal antibodies
  5. different immune response compared to adults
129
Q

What is seen on BAL with undifferentiated bacterial pneumonia?

A

neutrophils +/- cocci

130
Q

What is the diangostic approach for neonatal foals?

A
  1. clinical signs may be few but tachypnea and increased resp effort
  2. thoracic radiographs
  3. arteiral blood gas analysisi
  4. blood cultures
131
Q

Why must you be careful with tracheobronchial aspirates and BAL in septic foal?

A

can be dangerous in compromized septic foal

132
Q

What is the diagnostic method for older foals?

A
  1. tracheobronchial aspirates
  2. thoracic radiographs
  3. thoracic ultasonography
133
Q

Who gets undifferentiated resp tract dz?

A

foals 4-5 months old

134
Q

What is the morbiditiy in undifferentiated resp tract dz foals?

A

up to 80-90%

135
Q

what are the causes of undifferentiated resp tract dz of foals?

A
  1. strep zooepidemicus most prominent
  2. staph epidermidis
  3. r. equi
  4. viruses?
136
Q

What are the clinical signs of undifferentated resp tract dz?

A
  1. crackles
  2. wheezes
  3. mucopurulent nasal discharge
  4. cough and tachypnea
137
Q

what is seen on radiograph with undifferentiated resp tract dz?

A

mild bronchointerstitial pattern

138
Q

What is seen on BAL with unidfferentiated resp tract dz of foals?

A

increased neutrophils +/- intracellular cocci

139
Q

What is treatment for undifferentiated resp tract dz of foals?

A

strep zoo senisitive to beta lactams (penicillin, ampiciling, TMS)

140
Q

What is the prognosis of undifferentiated resp tract dz of foals?

A

30% relapse rate

long term prognosis hard to assess

141
Q

What is the mean age of rhodococcus equi pneumonia?

A

2 months (1-6 months)

142
Q

What are the clinical signs of rhodococcus equi pneumonia?

A
  1. fever, crackles, wheezes, tachypnea
  2. +/- mucopurulent nasal discharge
  3. +/- cough
  4. +/- resp distress
143
Q

What is the most devastating cause of pneumonia in foals between 3wk to 5 months?

A

R. equi pneumonia

144
Q

What can predispose to R. equi pneumonia?

A

overcrowding and dusty conditions

145
Q

What is the major source of contamination of soil with R. equi

A

FOAL FECES (question he may ask)

146
Q

What is the major route of infection for R. equi?

A

inhalation of dust and virulent R. equi

147
Q

When are foals infected with R. equi? when do they show signs?

A

they are infected at a very early age but signs usually evident 2-5 months old

148
Q

What are the features of R> equi?

A
  1. gram +
  2. facultative intracellular
  3. lives and multiplies inside alveolar macrophages
  4. pathogenic R. equi contains plasmids encoding for specific virulence associated proteins (VAP-A)
149
Q

What gene is required for virulene of R. equi?

A

VAP-A

150
Q

What are the clinical manifestations of R. equi?

A

chronic suppurative bronchopneumonia with extensive abscessation

151
Q

Why is early clinical diagnosis of R. equi difficult?

A

slow spread of lung infection

foals can compensate for loss of lung parenchyma!!

152
Q

What are the early signs of R. equi pneumonia?

A

often only mild fever or slight increase in resp rate

153
Q

What is the subacute form of R. equi? is it common?

A

acute resp distress and high fever. Not common

154
Q

What are extrapulmonary manifestations of R. equi?

A
  1. intestinal lesions
  2. polysynovitis
  3. uveitis, anemia, thrombocytopenia
155
Q

What are intestinal lesions caused by R. equi?

A
  1. multifocal ulcerative enterocolitis and typhlitis
  2. in 50% of foals with pneumonia
  3. most don’t show GI signs!!!!!
  4. weight loss, colic, diarrhea
156
Q

Do most foals with R. equi show GI signs?

A

no, most don’t, but 50% of those with pneumonia have lesions.

157
Q

How common is polysynovitis in foals with R. equi pneumonia?

A

1/3

158
Q

Are foals with polysynovitis due to R. equi infection lame?

A

no! can allow to differentiate from bacterial synovitis

159
Q

What is the mechanism of polysynovitis in foals with R. equi?

A

immune complex deposition

NON-septic (mononuclear)

160
Q

What are the most common joints affected by polysynovitis in foals with R. equi?

A

tibiotarsal and stifle

161
Q

How do you differentiate polysynovitis due to R. equi and bacterial joint infection in foals?

A

with bacterial infection they are painful, with r. equi polysynovitis they are not

162
Q

How is R. equi diagnosed?

A
  1. culture, PCR (VAP-A) + cytology of trachchial aspirate
  2. CBC
  3. serology
  4. radiography
  5. ultrasonography
163
Q

Why is isolation of R equi alone from a tracheobronchial wash not sufficient for diagnosis of R equi pneumonia?

A

because R. equi can be prevalent on farms and some foals may have without being sick

164
Q

What is seen on CBC and fibrinogen with R. equi?

A
  1. neutrophilic leukocytosis

2. hyperfibrinogenemia

165
Q

What is seen on radiographs with R. equi pneumonia?

A
  1. prominent alveolar pattern, regional consolidation

+/- hilar lesions (abscesses)

166
Q

What do you see with ultrasonography with R. equi pneumonia?

A

abscess at periphery of the lungs

167
Q

How do you differentiate R. equi pneumonia vs baterial pneumonia?

A

big abcesses with R. equi vs cranioventral consolidation with bacterial pneumonia?

168
Q

Why is serology not very useful for R. equi pneumonia diagnosis?

A

widespread exposure

169
Q

How is R. equi pneumonia diagnosed?

A
  1. antimicrobials 6-8wks
  2. erythromycin + rifampin
  3. azithromycin and clarithromycin
170
Q

Why do we now use more azithromycin and clarithromycin instead of erythromycin and rifampin for treatment of R. equi?

A

E + R can cause diarrhea, hyperthermia, tachypnea, increased liver enzymes and clostriidum difficile enterocolitis in dams

171
Q

What are benefits of using azithromycina nd clarithromycin in R. equi pneumonia?

A
  1. enhanced oral bioabilability
  2. prolonged half lives
  3. high concentratrions in bronchoalveolar cells and pulmonary epithelial lining fluid
172
Q

What is the pattern of pneumonia with acute resp distress syndrome?

A

bronchointerstitial pneumonia

173
Q

What is acute resp distress syndrome characterized by?

A

severe resp distress

174
Q

What is the causative organisms of acute resp distress snydrome?

A

unknown

175
Q

What animals are affected by acute resp distress syndrome?

A

foals 1-7 months

176
Q

What are clinical signs of acute resp distress syndrome?

A

tachypnea, increased resp effort, cyanosis

hypoxemia, hypercapnia, resp acidosis

177
Q

What is seen on radiography with foals with acute resp distress syndrome?

A

interstitial for bronchointerstitial pattern

178
Q

What is treatment for acute resp distress syndrome? why can this be an issue?

A

They do NOT respond to antibiotics
use oxygen therapy, bronchodilators, and CORTICOSTEROIDS
but corticosteroids suppress immune system! so if you are wrong then could kill foal faster?

179
Q

What is the prognosis for acute resp distress syndrome?

A

guarded for life and future athletic activity

180
Q

What kills foals with acute resp distress syndrome?

A

overwhelming inflammatory response

Horse Medicine (14 decks)

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