Lower Respiratory Disease Flashcards

1
Q

describe non-productive cough

A
  1. usually loud, harsh, dry
    -can be a goose honk
    -often paroxysmal (coughing fits)
    -often inducible with cervical palpation
  2. commonly associated with:
    -upper airway disease!!
    –tracheal or bronchial collapse
    –infectious tracheobronchitis (kennel cough)
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2
Q

describe a productive cough

A
  1. expectoration of sputum: fluid, mucus, debris from the LOWER airways
  2. commonly associated with:
    -lower airway or parenchymal diseases: infectious (pneumonia) or inflammatory (bronchitis, asthma)

-edema

-if the owner thinks it’s productive, it typically is

  1. typically softer in volume, like a huff
    -may be difficult to appreciate if pet swallows sputum or owner perceives as vomiting
  2. less likely to be paroxysmal

terminal retch = NOT productive typically

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3
Q

describe coughing in cats

A
  1. RARE!! when present, pursue AGGRESSIVELY
  2. most commonly lower airway disease (asthma)
    -tracheal disease (uncommon)
    -pleural space disease (RARE cause of cough)
  3. owners often confuse with a sneeze
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4
Q

describe common first tier diagnostics for coughing (5)

A
  1. CBC
  2. thoracic rads (+/- cervical)
  3. fecal exam: float, sedimentation, Baermann
  4. heartworm testing
  5. cytology:
    -FNA: skin lesions/masses, LNs
    -nasal discharge
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5
Q

describe 2nd and 3rd tier diagnostics for coughing (7)

A
  1. chem panel
  2. urinalysis: fungal antigen titers
  3. infectious testing: respiratory PCR, TITERS
  4. cardiac testing: echocardiogram, NTproBNP
  5. advanced imaging: fluoroscopy, US, CT
  6. bronchoscopy
  7. respiratory sampling:
    -airway: TTW, ETW, BAL
    -parenchyma: lung aspirate
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6
Q

describe transtracheal/endotracheal wash

A
  1. for DIFFUSE disease diagnosis
    -bronchitis, asthma
  2. disease MUST involve AIRWAY
  3. theory:
    -push sterile fluid into airway
    -aspirate out bronchial fluid
    -analyze
  4. TTW:
    -patient awake/lightly sedated
    -shave and prep ventral neck
    -use sterile saline aliquots for instillation
    -aspirate saline, patient must cough
  5. ETW:
    -patient briefly anesthetized with sterile intubation!!
    -saline aliquot squirt down ET tube
    -suction catheter down ET tube
    -patient coupaged during aspiration to help clear mucus and secretions
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7
Q

describe BAL

A
  1. to diagnosis localized or diffuse disease
    -can sample a specific location
    -generally samples deeper in the lung
  2. sterile intubation and anesthesia
  3. catheter lodged in lower airway
    -standard: bronchoscopy guided
    -blind: without bronchoscope
  4. requires smaller aliquot volume
    -may require coupage
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8
Q

describe wash fluid diagnostics

A
  1. cytology:
    -cellular infiltrate, bacterial or fungal presence
  2. infectious testing:
    -bacterial cultures: aerobic and anaerobic
    -respiratory PCR: mycoplasma, +/- full panel
  3. reference ranges:
    -neutrophils <5%
    -eosinophils <17-20%
    -mononuclear: 70% macrophages, 5% lymphocytes
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9
Q

describe respiratory PCR

A
  1. performed on
    -oropharyngeal +/- nasal +/- conjunctival swab
    –influenza: deep nasal
    –distemper: conjunctival

-airway wash

  1. IFA for organism ID also
  2. some organisms can be isolated normally from healthy dogs (commensals)
    -presence does NOT always = cause of disease
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10
Q

describe fungal specific diagnostics

A
  1. cytology and histology
    -blastomyces dermatidis: big blue broad-based budding yeast

-histoplasma capsulatum: small narrow-based budding yeast with halo around the edge

-coccidoides immitis, posadasii:
-round double-walled structure
-may be difficult/costly to perform

  1. mira vista urine antigen EIA:
    -detects wall galactomannan antigen, which is excreted in urine
    -cannot distinguish blastomyces from histoplasma
    -used to monitor response to therapy or relapse
  2. coccidoides:
    -mira vista canine IgG antibody EIA + antibody by immunodiffusion: serum, CSF, plasma
    -antigen quantitative EIA for treatment monitoring
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11
Q

list common canine infectious respiratory disease complex (CIRDC) pathogens

A

most commonly VIRAL origin

  1. parainfluenza virus
  2. adenovirus type-2
  3. herpesvirus-1
  4. distemper virus
  5. respiratory corona virus
  6. pneumovirus
  7. influenza virus

*kennel cough is NOT synonymous with bordetella infection!!

-co-infections are common with multiple viruses or virus + bacteria (bordetella bronchiseptica, mycoplasma spp., strep equi or zooepidemicus)

-co-infections increase disease severity!!

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12
Q

describe parainfluenza virus (cPiV)

A
  1. enveloped ssRNA virus
  2. paramyxoviridae (distemper and pneumovirus)
  3. replicate in upper airway
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13
Q

describe adenovirus type-2 (CAV-2)

A
  1. non-enveloped dsDNA virus
  2. replicates in upper and lower airways
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14
Q

describe bordetella bronchiseptica

A
  1. aerobic, gram negative coccobacillus
  2. highly contagious
    -dogs to cats to dogs to sick people!!
  3. replicates on ciliated epithelium
  4. virulence factors/toxins:
    -paralyzes cilia
    -impairs phagocytosis
    -invades intracellularly to avoid immune detection
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15
Q

describe mycoplasma spp.

A
  1. fastidious bacteria that lack a cell wall= very difficult to culture/isolate
  2. colonized ciliated and non-ciliated epithelium
    -lower > upper resp tract
    -likes to cause purulent bronchitis
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16
Q

describe canine influenza virus

A
  1. strains:
    -H3N8: minor continued circulation in NE US
    -H3N2: reportable in some states!!
  2. often mimic kennel cough:
    -majority develop mild signs of illness
    -signs:
    –non-productive cough (+/- productive if secondary bacterial infection)
    –nasal/ocular discharge: serous to mucopurulent
    –systemic signs: fever, lethargy, anorexia
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17
Q

describe CIRDC pathogenesis

A
  1. source of infection:
    -respiratory secretions
    -environmental contamination
  2. transmission:
    -close or direct contact
    -aerosolization
    - +/- fomites
    -HIGHLY contagious: high morbidity, low mortality
  3. incubation period: approx 7 days post infection
  4. pathogen shedding:
    -most <2 weeks
    -exceptions (weeks to months): bordetella, mycoplasma, distemper virus, strep and herpes

-shedding can start PRIOR to showing clinical signs: as early as 24 hours post infection and can continue after recovery!!

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18
Q

describe CIRDC diagnosis

A
  1. signalment and history:
    -young, immunocompromised, recent exposure, vaccinated
  2. clinical signs:
    -harsh, DRY cough: often non productive, typically inducible, paroxysmal
    -usually otherwise healthy
  3. canine respiratory PCR
19
Q

describe CIRDC management

A
  1. most cases are:
    -mild, uncomplicated, AND self-limiting (resolve within 7 days)
  2. manage as outpatient if possible
  3. isolation and supportive care if canine influenza!!
  4. THINK before antibiotic use!
    -rarely shown to help! just bc bacteria are found does NOT mean they are a problem
  5. ideally treat when:
    -persistent (>7 days) non-productive cough
    -complicated/progressive disease
    -juveniles (6-8weeks old)
    -anytime you feel quality of life is negatively impacted by cough
20
Q

what should you treat CIRDC with?

A
  1. persistent (>7d) NON PRODUCTIVE cough:
    -step 1: anti-inflammatory +/- antitussive
    -step 2: doxycycline or minocycline
  2. severe, progressive, or complicated disease
    -doxycycline or minocycline
  3. juvelines (6-8wks):
    -clavamox
    -doxycycline: DONT give to pregnant/nursing bitches!
21
Q

describe CIRDC prevention

A
  1. DHPP vx
    D = distemper
    H = infectious hepatitis (adenovirus type-1); CAV-2 is usually in vaccine so cross-protective
    P = parainfluenza virus
  2. +/- influenza vx if at risk population
  3. will reduce disease incidence, severity, and shedding
22
Q

describe bordetella bronchoiseptica vaccination

A
  1. ML intranasal:
    - +/- viral pathogens
    -faster immunity: approx 72 hours, occurs with maternal abx
    -can initiate younger (approx 3 weeks of age)
    -reduces shedding
    -accidental injection associated with: severe injection site reaction, hepatic necrosis, death!!!!
  2. parenteral:
    -B. bronchioseptica Ag only
    -immunity requires booster 1-2 weeks after 2nd injection
    -initiate at 6 weeks
23
Q

when is cough suppression CONTRAINDICATED?

A
  1. productive cough
  2. infectious disease

coughing is a protective mechanism!

24
Q

describe how bacterial pneumonia occurs

A

doesn’t just happen! need to consider WHY host defenses impaired

  1. congenital defect: ciliary dyskinesia
  2. immune compromise: iatrogenic or comorbidity
  3. prolonged recumbency: sedation, anesthesia, critical illness
  4. disease-induced: bronchitis/asthma, viral, laryngeal paralysis, regurgitation
25
Q

describe bacterial pneumonia routes of infection

A

respiratory tract is UNsterile to the level of the carina!!

routes:

  1. aspiration
  2. community-acquired
    -bordetella bronchiseptica most common CAP in dogs!
    -esp important in dogs <1 year (CAP avg age approx 5 months)
  3. hematogenous:
    -cat > dog
  4. traumatic: penetrating injury, open wound
26
Q

describe aspiration pneumonia

A
  1. MOST COMMON cause of pneumonia in ADULT dogs
  2. healthy stomach/upper GI is POORLY colonized by bacteria
    -initial problem is airway irritation and caustic injury (pneumonitis is NOT pneumonia)
    -things that increase number of gastric bacteria: use of antacids, oral disease, intestinal ileus, enteral feeding
  3. many dogs with aspiration pneumonia have a history of vomiting or recent anesthesia
  4. common co-morbidities:
    -regurgitation
    -megaesophagus
    -laryngeal paralysis
    -myasthenia gravis
  5. most commonly isolated oganisms: (aerobes > anaerobes)
    -E. COLI!!!!!!!!!
    -klebsiella
    -strep, staph
    -enterobacter
    -enterococcus
    -mysoplasma
    -pasteurella
    -pseudomona
    -proteus
27
Q

describe common clinical findings of bacterial pneumonia

A
  1. lethargy/ADR
  2. reduced appetite
  3. exercise intolerance
  4. TACHYPNEA/dyspnea
    -most common in cats
  5. fever
  6. cough: productive, huffing
  7. +/- nasal discharge
  8. +/- crackles

HISTORY is important!! need to gather known medical conditions and recent pathogen exposure

28
Q

describe bacterial pneumonia diagnosis

A
  1. CBC: inflammatory leukogram, maybe with a left shift or toxic changes
  2. thoracic radiographs: 3-view
    -RIGHT MIDDLE LUNG LOBE!!!
    -right cranial love
    -caudal subsegment of left cranial lobe
  3. pulse ox with blood gas
  4. airway wash: C&S
  5. other testing as indicated looking for causative or contributory disease: HW, FeLV/FIV
29
Q

describe bacterial pneumonia empiric treatment

A
  1. uncomplicated/mild disease:
    -narrow spectrum/single therapy
    -amoxicillin/clav
    -cephalexin
    -TMS: remember side effects of KCS, thyroid suppression, hepatopathy, immune reactions
    -doxycycline (bordetella, mycoplasma)
    -azithromycin (cats)
    -for 7-14d (NOT radiographic resolution)
  2. complicated/severe disease:
    -broad spectrum/combination therapy; ideally wash and C&S
    -amoxi calv/amoxi sulbactam
    -clindamycin
    PLUS
    -2nd or 3rd gen cephalosporin
    OR
    -fluroquinolone (floxacin)
    PR
    -metronidazole (aspiration)
    OR
    -amikacin (severe or drug-resistant infections)
    -for 2-4 weeks

the more lung lobes involved, the worse the prognosis, developing resistance to antibiotics :(

30
Q

list 4 causative agents of fungal pneumonia

A
  1. blastomyces dematitidis
  2. histoplasma capsulatum
  3. coccidioides immitis: southwest US (esp arizona)
  4. cryptococcus neoformans
    -feline nasal granuloma pathogen
31
Q

describe clinical findings of fungal pneumonia

A
  1. respiratory signs NOT commonly present
    -60% have no resp signs at time of dx
  2. 75% have OTHER systemic signs
    -fever, lethargy, anorexia, weight loss
  3. other possible findings
    -chorioretinitis/uveitis
    -lameness, bone pain
    -lymphadenopathy
    -cutaneous or dermal lesions/nodules
32
Q

describe fungal pneumonia workup

A
  1. CBC and chem
    -nonregen anemia
    -inflammation
  2. cytology:
    -airway wash
    -FNA: LNs, skin lesions/nodules, lungs
  3. thoracic rads:
    -miliary or nodular pattern
    -solitary mass/granuloma
  4. urine antigen testing
33
Q

describe pulmonary mycoses treatment

A
  1. itraconazole: hepatotoxicity, blood dyscrasias
  2. fluconazole: hepatotoxicity
  3. amphotericin B (liposomal): nephrotoxicity

for a minimum of 3-6 months!!

  1. will often get worse before improving
    -may require intensive supportive care, O2 support
34
Q

what are two common inflammatory airway disease?

A
  1. feline asthma and bronchitis
    -prevalence 1-5%, possible siamese overrepresentation
    -eosinophilic inflammation
  2. canine chronic bronchitis
    -exact prevalence unknown; moderately common, co-morbid diseases OFTEN present
    -neutrophilic inflammation

often diagnosed in middle age (4-8 yrs)

35
Q

describe pathology and clinical signs of inflammatory airway diseases

A

pathology: likely multifactorial
-why sending inflam cells to lungs?
-prior single resp insult, chronic irritant exposure or repeated injury, culmination of many small insults over time

clinical signs:
1. chronic cough: starts as non-productive

  1. tachypnea at rest
  2. expiratory dyspnea: prolonged expiration, expiratory push
  3. exercise intolerance

issues with cats:
-signs may only be intermittent and may not seem severe so
-acute respiratory distress emergent presentation much more common in cats than dogs!!

36
Q

what is the big issue with inflammatory airway diseases?

A
  1. if chronically untreated, leads to permanent airway remodeling:

-smooth muscle hypertrophy and reactivity

-mucosal infiltration and edema

-goblet cell hypertrophy and increased mucus production

-epithelial cell hypertrophy and metaplasia

  1. these changes impede air movement through airways via
    -inflammation, secretions, and smooth muscle contraction
37
Q

compare airway reactivity between chronic bronchitis and feline asthma

A

chronic bronchitis:
-little to no spontaneous bronchoconstriction
-static narrowing

feline asthma:
-reversible! spontaneous bronchoconstriction
-dynamic narrowing

38
Q

describe the workup for inflammatory airway disease

A

a diagnosis of exclusion!

  1. physical exam: wheezes
    -airflow limitation + positive intra-thoracic pressure on expiration causes air trapping = wheezes
  2. CBC: evidence of inflammation or eosinophilia
  3. thoracic rads
    -bronchial pattern: donuts and tram lines
  4. infectious screening:
    -heartworm Ag +/- Ab
    -fecal float/sedimentation
    -fecal baermann
    -respiratory PCR panel

5 airway wash + cytology!!

39
Q

describe classic asthma radiographs

A

can be normal in 25% of cases!!

  1. broncho-interstital pattern
  2. pulmonary hyperinflation: increased lucency, flattened/caudally displaced diaphragm
  3. right middle lung lobe atelectasis: mucus plugging
  4. +/- rib fractures
40
Q

describe end-stage inflammatory airway disease radiographs

A
  1. pulmonary fibrosis
  2. airway remodeling:
    -bronchomalacia
    -bronchiectasis
  3. pulmonary hypertension
41
Q

describe treatment of inflammatory airway disease

A

bronchitis:
1. glucocorticoids: oral/inhaled
2. +/- bronchodilators
3. +/- antiitussives: use only if needed, may mask response, but could break inflammatory cycle

asthma:
1. glucocorticoids: oral/inhaled
2. bronchodilators: maintenance vs. rescue

empiric deworming: fenbendazole for 14 days

-aeroKat/aeroDawg: training of owner and patient required!! patient must acclimate and owner must practice!!

-other considerations:
–weight loss, harness vs collar, environmental trigger avoidance

42
Q

describe bronchodilators

A
  1. reverse spontaneous bronchoconstriction as seen in asthma
  2. other benefits:
    -anti-inflammatory synergism with steroids
    -stimulate mucociliary clearance
    -reduce respiratory effort: prevent respiratory fatigue via methylxanthines
    -improve pulmonary perfusion
    -improve expiratory airflow
43
Q

describe treatment goals of inflammatory airway disease

A
  1. resolve clinical signs
    -resolved cough does NOT mean resolved inflammation
  2. prevent remodeling:
    -bronchiectasis
    -pulmonary fibrosis
    -pulmonary hypertension
    -cor pulmonale
  3. monitoring and treatment decisions are ideally based on repeated airway washes and cytology
44
Q

describe eosinophilic bronchoopneumonopathy

A
  1. typically idiopathic
    -eosinophilic inflammation fo pulmonar interstitium
    –eosinophilic infiltrate on airway wash
    -overrepresented breeds: rottweiler, husky, malamute
  2. radiographic findings variable
  3. ddx: neoplasia, fungal
  4. treatment:
    -oral steroids
    -less responsive to inhaled therapy to control
    -can often taper to lower dose or eventually stop
    -can maintain control with inhaler if needed