Lecture 20: Equine Respiratory Diseases (MacKay) Flashcards

1
Q

Dx/Txof guttural pouch mycosis

A

Dx: endoscopy, culture (Emericella, Aspergillus, etc.)
Tx: sx occlusion of affected artery or systemic and/or topical antifungal if less severe

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2
Q

guttural pouch tympany

A

distension of one or both guttural pouches with air. Occurs in horses <1yo

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3
Q

CS/Dx/Tx of guttural pouch tympany

A

-external swelling in parotid area
-dyspnea if severe
-rarely dysphagia
Dx based on CS
Tx: surgical

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4
Q

Primary sinusitis and Tx

A

-maxillary sinus most commonly affected
-S. equi zooepidemicus commonly involved
Tx: systemic Abx, sinus flush

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5
Q

2ary sinusitis and Tx

A

causes tooth root abscess

Tx: systemic abx, tooth extraction, tooth repulsion through maxillary sinus flap

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6
Q

CS of sinusitis

A
  • unilateral nasal discharge**
  • ozena
  • ocular discharge
  • facial sensitivity/deformity
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7
Q

Dx of sinusitis

A
  • percussion
  • rads
  • endoscopy
  • oral exam
  • CT
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8
Q

2 main viral resp. diseases

A
influenza
herpes virus (rhinopneumonitis)
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9
Q

Viral resp. diseases general CS

A

fever, cough, nasal d/c

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10
Q

Dx of viral resp. diseases

A
  • virus isolation
  • PCR amplification***
  • Serology (paired samples 10-14 days apart)
  • Ag detection
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11
Q

most common cause of severe epidemics of upper respiratory disease in horses**

A

Equine Influenza. Comprises 40-60% of cases

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12
Q

What type of virus is equine influenza?

A

orthomyxovirus with an RNA genome

-only influenza type A to affect horses

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13
Q

How is level of virulence determined in equine influenza?

A

By some combination of Hemagglutinin (HA) and Neuaminidase (NA) immunodominant antigens which are used to penetrate the cells

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14
Q

What combos of HA and NA have been id’d in horses?

A

H7N7

H3N8 <—major subtype***

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15
Q

What is unique about H3N8 strain of equine flu?

A

subject to antigenic drift, in which HA or NA mutate so that virus can escape neutralization by antibody made to earlier strains. It likes to accumulate mutations over time

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16
Q

incubation period of equine flu

A

1-3 days

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17
Q

equine flu affects which pop. of horses the most?

A

1-3 year old horses in training

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18
Q

pathogenesis of equine flu

A

1) aerosol infection
2) adhesion to resp. ep.
3) desquamation of ciliated cells
4) decreased mucociliary clearance

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19
Q

morbidity/mortality of equine flu?

A

high morbidity (100%), low mortality

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20
Q

CS of equine flu

A
  • acute onset fever
  • anorexia, depression
  • dry cough
  • serous nasal discharge
  • submandibular lymph node enlargement
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21
Q

Dxof equine flu

A
  • viral isolation (difficult)
  • RT-PCR***
  • serology (retrospective only)
  • influenza A Ag detection Kit: rapid
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22
Q

Possible complications of equine flu

A
  • bacterial pneumonia/pleuropneumonia
  • myositis
  • myocarditis
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23
Q

how long does it take tracheal ep. to restore after equine flu?

A

1 month, but horses appear healthy after 1 week

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24
Q

Tx of equine flu

A

3 wks rest
NSAIDs for fever
Abx for 2ary bacteria pneumonia
Antiviral usually NOT warranted

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25
Q

How long does immunity last following natural equine flu infection?

A

1 yr

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26
Q

Types of vax for equine flu

A

1) killed IM
- effective for 3-4 mo
- provides transient systemic IgG response
- not effective in presence of maternally-derived Ab
- does not prevent infection/shedding
2) MLV IN
- protect 6-12mo
- does not provide systemic response
3) Canary Pox Vector Vax
- use in foals of vaccinated dams
- provides robust immune response

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27
Q

Effects of Equine Herpesvirus-1 (EHV-1)***

A
  • abortion
  • perinatal dz and death
  • neuro
  • resp. dz
  • viremia (virus in blood) is common**
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28
Q

EHV-2 effects

A
  • mild resp. signs
  • immunosuppression?
  • keratoconjunctivitis
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29
Q

EHV-3 effects

A

equine coital exanthema (genital horsepox)

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30
Q

EHV-4 effects***

A

respiratory disease (rhinopneumonitis)

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31
Q

EHV-5 effects

A

Equine Multinodular Pulmonary Fibrosis (eventually fatal)

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32
Q

What percent of horses carry EHV-1 or 4 in a latent state?***

A

85% (in lymph nodes, trigeminal ganglia)

33
Q

path. of EHV-1 and 4

A
  • young horses
  • responsible for 15-20% of outbreaks of URT dz!
  • up to 85% of horses are carriers!!**
  • acquired via inhalation or recrudescence of a latent infection
  • incubation period 2-10 days
  • viremia common in EHV-1 infections
34
Q

Dx of EHV-1 and 4

A
  • virus isolation or PCR amplification <–**

- serology (not important)

35
Q

vax. for EHV-1 and 4

A

inactivated or modified live vaccines available for EHV-1, 4, or both
-labeled to prevent abortion

36
Q

foal pneumonia***

A
  • leading cause of morbidity and mortality!!
  • inhalation of aerosolized or dust-borne pathogens
  • causes bacteremia and hematogenous spread of bacteria to the lungs in neonates (1-10 mo.)
37
Q

CS of foal pneumonia

A
  • cough
  • bilateral nasal d/c
  • fever
  • inc. resp. rate
  • resp. distress
38
Q

Dx of foal pneumonia

A
  • abnormal lung sounds
  • hematology: neutrophilic leukocytosis, hyperfibrinogenemia
  • rads and ultrasonography
  • tracheobronchial aspiration: mainly degenerate neutrophils +/- bacteriaon cytology
39
Q

most common cause of foal pneumonia***

A

streptococcus equi subs. zooepidemicus

40
Q

agents of foal pneumonia

A

strep equi zooepidemicus***
Rhodococcus equi
others: Pasteurella, E. coli, Klebsiella, Actinobacillus,etc.

41
Q

tx of foal pneumonia

A
Abx:
-Ceftiofur (broad spec)
-Penicillin (for S. zooepidemicus)
-Trimethoprim-sulfa (oral, mostly useless now)
-Penicillin-aminoglycoside
O2 therapy
42
Q

Duration of therapy for foal pneumonia based on:

A

-resolution of CS
-normal WBC count and fibrinogen concentrations
-imaging techniques (rads, ultrasound)
Only stop tx when everything is normal!

43
Q

prognosis of foal pneumonia

A

usually complete recovery if dx/tx early

44
Q

rhodococcus equi pneumonia path.

A
  • Gram + facultative intracellular pathogen (NOT obligate!)
  • can survive and replicate in macs
  • normal inhabitant of soil
  • infection by inhalation
  • can be devastating dz
  • usually affects foals 1-6 mo.
45
Q

CS of rhodococcus equi pneumonia

A
-bronchopneumonia
Extra-pulmonary disorders:
-intestinal manifestations --> weight loss
-non septic immune-mediated polysynovitis
-septic arthritis and osteomyelitis
-uveitis
-ulcerative lymphangitis, cellulitis
-abscesses
46
Q

Dx of rhodococcus equi pneumonia

A
  • hematology: neutrophilic leukocytosis, hyperfibrinogenemia
  • rads/ultrasound
  • tracheobronchial aspiration: degenerate neuts, Gram + coccobacillus on gram stain, culture, PCR***
47
Q

only way to make definitive dx of rhodococcus***

A

tracheobronchial aspiration

48
Q

Tx of rhodococcus equi pneumonia

A

long-term therapy of macrolide and rifampin abx (able to penetrate caseous material and cells)

49
Q

side effect of macrolides

A

suppress sweating –> hyperthermia

50
Q

prog. of rhodococcus equi pneumonia

A

survival rates b/w 60-80%

affected foals less likely to race, but perform as well

51
Q

prevention of rhodococcus pneumonia

A
  • decrease size of infective challenge (i.e. prevent grass degradation)
  • earlier recognition/close monitoring
  • hyperimmmune plasma
52
Q

pneumonia

A

infection involving the lung parenchyma

53
Q

pleuropneumonia

A

pneumonia or lung abscess that extends to and involves the visceral pleura

54
Q

most common cause of pleuropneumonia

A

bacteria

55
Q

causes of pleural effusion

A
  • pneumonia
  • pleuropneumonia
  • hemothorax
  • chest wound
  • neoplasia
  • hypoproteinemia
  • CHF
56
Q

Path. of pneumonia/pleuropneumonia

A

viral infection/toxic gases/stress/malnutrition/general anesthesia –> decreased # and bactericidal activity of alveolar macs –> pneumonia/pleuropneumonia

57
Q

CS of pneumonia/pleuro.

A
  • fever*
  • anorexia, depression*
  • tachypnea, resp. distress
  • soft cautious cough
  • pain in thorax
  • bilateral nasal d/c
  • fetid breath
  • ventral edema
  • colic-like signs
  • weight loss if chronic
  • won’t lay in lat. recumb.
58
Q

infectious agents of pneumonia/pleuro.

A
  • S. equi zooepidemicus
  • Gram - bacteria (Pastuerella, E. coli, Klebsiella, Pseudomonas, Enterobacter)
  • Anaerobes (Bacteroides, Peptostrep., Eubacterium)
59
Q

Dx of Pneumonia/Pleuro.**

A
  • auscultation: decreased lung sounds ventrally and presence of pain
  • percussion: horizontal line
  • pleurodynia (pleural pain)
  • hematology: leukopenia followed by leukocytosis, hyperfibrinogenemia
  • ultrasonography, rads
  • tracheobronchial aspiration***
    • cytology: degenerate neuts +/- bact.
    • culture: more likely to yield + culture than pleural fluid
  • thoracocentesis
60
Q

Tx of pnuemonia/pleuro:

A

1) Abx
- initially broad-spec, then based on culture/sensitivity
- long-term usually required
2) Pleural drainage
- removal of exudate
- re-expansion of lungs
* Go all out on Day 1!!*
3) Supportive care
- fluids
- prevention of endotoxemia
- analgesia
4) thoracotomy and rib resection
- chronic cases
- manual removal

61
Q

Complications of pneumonia/pleuro.

A
  • endotoxemia
  • thrombophlebitis (vein swelling)
  • laminitis
  • pleural and/or pulmonary abscess form.
  • pneumothorax
  • pericarditis (rare)
62
Q

Prog. of pneum/pleuro.

A

38-75% survival depending on how quickly tx is started

40-60% of survivors race

63
Q

Exercise-Induced Pulmonary Hemorrhage (EIPH)

A

presence of blood in the airways after intense exercise/pulmonary hemorrhage (usually caudodorsal lung fields)

64
Q

Incidence of EIPH

A

5% of race horses have epistaxis

Up to 90% of race horses have EIPH!

65
Q

EIPH effect on performance**

A

unlikely; rule out all other causes!

66
Q

Dx of EIPH

A
  • endoscopy
  • cytology (TBA or BAL): hemosiderin-laden macs
  • rads: opacities in caudodorsal lung fields
67
Q

path. of EIPH

A

failure of pulmonary capillaries during exercise when pressure exceeds 70 mmHg

68
Q

Tx of EIPH

A

furosemide (loop diuretic)
-decreases pulmonary capillary pressure
nasal strips

69
Q

Heaves aka

A

RAO (recurrent airway obstruction)

COPD

70
Q

heaves affects young/mature horses?

A

mature >3 yo

71
Q

Path. of Heaves

A

fungi/molds/endotoxins/allergens –> hypersensitivity/non-specific inflammation –> bronchiolitis, neutrophilic airway infiltration, excess mucus, bronchoconstriction
genetic disposition also possible

72
Q

Path.of hypersensitivity reactions in Heaves

A

1) Type I –> IgE, mast cell degranulation

2) Type III –> IgG or IgM, immune complexes

73
Q

CS of mild heaves

A

intermittent cough
exercise intolerance
abnormal lung sounds
mild increase in resp. rate

74
Q

CS of severe heaves

A

resp. distress
abd effort during expiration (heavy line)
weight loss

75
Q

When is fever present in Heaves?***

A

ONLY when there is a 2ary bacterial infection

76
Q

Dx of heaves***

A
History/PE:
-increased expiratory effort
-crackles/EXPIRATORY wheezes
-lack of fever**
-normal WBC count and fibrinogen
Bronchoalveolar lavage:
-well-preserved neuts**
Response to bronchodilators
77
Q

Tx of Heaves

A

NOT a cureable disease
Env. management: reduce dust**/allergen exposure
Corticosteroids: most effective
Bronchodilators (supportive)

78
Q

most effective therapy for heaves

A

corticosteroids

79
Q

Which aerosol therapy drugs get down to distal airways best?

A

AeroHippus, Torpex