Lower Respiratory Disease Flashcards

(44 cards)

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
describe bacterial pneumonia routes of infection
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
describe aspiration pneumonia
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
describe common clinical findings of bacterial pneumonia
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
describe bacterial pneumonia diagnosis
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
describe bacterial pneumonia empiric treatment
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
list 4 causative agents of fungal pneumonia
1. blastomyces dematitidis 2. histoplasma capsulatum 3. coccidioides immitis: southwest US (esp arizona) 4. cryptococcus neoformans -feline nasal granuloma pathogen
31
describe clinical findings of fungal pneumonia
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
describe fungal pneumonia workup
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
describe pulmonary mycoses treatment
1. itraconazole: hepatotoxicity, blood dyscrasias 2. fluconazole: hepatotoxicity 3. amphotericin B (liposomal): nephrotoxicity for a minimum of 3-6 months!! 4. will often get worse before improving -may require intensive supportive care, O2 support
34
what are two common inflammatory airway disease?
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
describe pathology and clinical signs of inflammatory airway diseases
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 2. tachypnea at rest 3. expiratory dyspnea: prolonged expiration, expiratory push 4. 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
what is the big issue with inflammatory airway diseases?
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 2. these changes impede air movement through airways via -inflammation, secretions, and smooth muscle contraction
37
compare airway reactivity between chronic bronchitis and feline asthma
chronic bronchitis: -little to no spontaneous bronchoconstriction -static narrowing feline asthma: -reversible! spontaneous bronchoconstriction -dynamic narrowing
38
describe the workup for inflammatory airway disease
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
describe classic asthma radiographs
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
describe end-stage inflammatory airway disease radiographs
1. pulmonary fibrosis 2. airway remodeling: -bronchomalacia -bronchiectasis 3. pulmonary hypertension
41
describe treatment of inflammatory airway disease
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
describe bronchodilators
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
describe treatment goals of inflammatory airway disease
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
describe eosinophilic bronchoopneumonopathy
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