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Ruminants > Respiratory disease > Flashcards

Respiratory disease Flashcards

1
Q

What is a normal RR in a ruminant?

A

12-24bpm

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2
Q

What are wheezes associated with? What are crackles associated with?

A

Wheezes- airway narrowing, often at the end of expiration
Crackles- airway collapse or small airway disease, often at the end of inspiration

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3
Q

What causes pleural friction rubs?

A

Underlying pleuritis

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4
Q

What is decreased bronchovesicular sounds associated with?

A

Consolidating pulmonary parenchyma, mass, or pleural effusion

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5
Q

What are hyper-resonant lung sounds associated with?

A

Pneumothorax

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6
Q

Describe stridor

A

Type of wheeze focused over extrathoracic airways, primarily heard during inspiration, often associated with laryngeal or tracheal disease

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7
Q

Describe what causes an alveolar pattern

A

Air in alveoli has been replaced with higher density material (exudate, hemorrhage, edema); seen with cranioventral pneumonia

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8
Q

Describe what causes a bronchial pattern

A

Bronchial wall is infiltrated by cells or fluid or peribronchial space is replaced by cells or fluid, causes enhanced radiographic visualization of the bronchial tree, typically seen with chronic inflammation and allergies

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9
Q

What causes a structural and non-structural interstitial pattern?

A

Structural- aggregation of cells that displace normal lung tissue (tumor, abscess, granuloma)
Non-structural- diffuse, fluid, cells, or fibrin coalescing together (cancer or edema)

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10
Q

What disease is usually seen cranioventral on radiographs? Caudo-dorsal?

A

Cranioventral- bronchopneumonia, some infectious pneumonias
Caudo-dorsal- allergies, environmental irritation, parasitic and viral diseases

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11
Q

What is the indication for nasopharyngeal swabs?

A

Detection of viral and bacterial diseases in the upper respiratory tract

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12
Q

What tests are used in conjunction with a nasopharyngeal swab?

A

PCR, antigen detection ELISA, virus identification and isolation

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13
Q

What is the indication for a transtracheal wash?

A

Identifies infectious agents of the lower respiratory tract or pleura, good for bacterial culture

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14
Q

Which airway sampling technique should be performed first?

A

Transtracheal wash- need to avoid contamination

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15
Q

What is the indication for bronchoalveolar lavage?

A

To obtain samples that aren’t appropriate for bacterial culture or identification of an infectious organism, more useful for cytology

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16
Q

What is the normal neutrophil percentage on BAL of a calf?

A

5-20%

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17
Q

What is dominant presence of neutrophils on BAL indicate? What about eosinophils?

A

Neutrophils- bacterial infection
Eosinophils- parasitic infection

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18
Q

How much of the fluid introduced on a BAL will be retrieved?

A

About 1/3 of it

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19
Q

Should you sedate an animal for BAL? Why or why not?

A

No; it will suppress their cough response making performance difficult

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20
Q

Describe normal fluid from thoracocentesis

A

Odorless, pale yellow transparent, pH ~7.2, 2.5g/dL protein, 10,000cells/uL, predominately macrophages

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21
Q

Describe abnormal fluid from thoracocentesis

A

Variable color and odor, pH <7.2, protein >2.5g/dL, nucleated cells >10,000cell/uL, variable cellular composition, high lactate and low blood glucose

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22
Q

Where do you perform thoracocentesis on a ruminant?

A

6th or 7th intercostal space at the level of the costochondral junction along the cranial aspect of the rib

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23
Q

What symptoms are consistent with upper respiratory disease?

A

Nasal discharge, sneezing, coughing, foul smelling breath

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24
Q

What symptoms are consistent with lower respiratory disease?

A

Fever, cough, abnormal auscultation, anorexia, malaise

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25
Q

Which species get Oestrus ovis?

A

Sheep > goats, rarely cattle

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26
Q

Describe the pathogenesis of O. ovis

A

Larval stage travels to ethmoid turbinates and molts, travels to sinuses and molts again, returns to nasal passage and is sneezed out

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27
Q

What clinical signs are consistent with O. ovis infection?

A

Mucoid to mucopurulent nasal discharge, sneezing, nasal rubbing, inspiratory stridor

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28
Q

What are reasonable differential diagnoses for O. ovis infection?

A

Nasal foreign body, rhinitis, nasal adenocarcinoma, trauma, sinusitis

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29
Q

How is O. ovis infection diagnosed?

A

Radiography, clinical signs, endoscopy

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30
Q

How is O. ovis treated? What treatment is approved in the US?

A

Oral ivermectin, pour on eprinomectin or injectable doramectin
No treatments approved in the US, not typically seen here

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31
Q

What are causes of sinusitis?

A

Dehorning (frontal), infected tooth (maxillary), neoplasia, trauma, actinomyces, respiratory virus

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32
Q

What are common isolates from sinusitis infected tissue?

A

Trueperella, Pasteurella

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33
Q

What clinical signs are associated with acute sinusitis?

A

Weeks to months post event (ex. dehorning), unilateral, febrile, mucopurulent discharge from horn tip, anorexic, lethargic

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34
Q

What are clinical signs associated with chronic sinusitis?

A

Unilateral or bilateral nasal discharge, foul breath, blepharospasm, holding head at an odd angle, neuro signs, fever uncommon

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35
Q

How is sinusitis diagnosed?

A

History and clinical signs + percussion (dull and painful), radiographs, and sterile collection of fluid for culture

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36
Q

How is sinusitis treated?

A

Lavage, drainage with trephination, antimicrobials (procaine penicillin G, oxytetracycline), NSAIDs, good prognosis with resolution ~10-14d

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37
Q

What are potential sequelae of pharyngeal trauma?

A

Hematoma, granuloma, cellulitis, abscess

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38
Q

What are causes of pharyngeal trauma?

A

Balling gun, dose syringe, speculum, stomach tube

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39
Q

Which bacteria are commonly involved in pharyngeal trauma and abscess?

A

Trueperella pyogenes, Actinobacillus, Pasteurella, Bordetella, Fusobacterium necrophorum

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40
Q

What clinical signs are associated with pharyngeal trauma/abscess?

A

Inspiratory dyspnea, extended head and neck, ptyalism, pain on swallowing, nasal discharge, subsequent aspiration pneumonia

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41
Q

What are reasonable differential diagnoses for pharyngeal trauma?

A

Neoplasia, LSA, rabies, botulism, necrotic laryngitis, trauma, edema

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42
Q

How is pharyngeal trauma/abscess diagnosed?

A

Examination with a mouth gag and/or endoscopy, radiographs

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43
Q

How is pharyngeal trauma or abscess treated?

A

Drain abscess, antimicrobial therapy (procaine penicillin G, oxytetracycline), NSAIDs, tracheostomy if necessary, supportive care

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44
Q

What are the causative agents of necrotic laryngitis (AKA calf diphtheria or laryngeal necrobacillosis)

A

Fusobacterium necrophorum and Trueperella pyogenes

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45
Q

What is needed for bacterial invasion (necrotic laryngitis)?

A

Laryngeal contact ulcers

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46
Q

What are sequelae of necrotic laryngitis?

A

Decreased growth rate, secondary bacterial pneumonia

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47
Q

Which animals are predisposed to necrotic laryngitis?

A

Young (3-18m) calves, crowded feedlot animals, higher incidence in fall and winter

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48
Q

What are clinical signs of necrotic laryngitis?

A

Painful, moist cough, inspiratory dyspnea, open-mouth breathing, head and neck extended, increased salivation, painful swallowing, visibly swollen larynx, cough upon stimulation, fever, anorexia, hyperemic mm, bilateral nasal discharge, foul breath

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49
Q

Describe the progression of necrotic laryngitis

A

Acute onset, most calves die within 2-7 days if untreated, recovered cases may have chronic changes

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50
Q

What are differential diagnoses for necrotic laryngitis?

A

Pharyngeal trauma, viral laryngitis, Actinobacillosis, neoplasia

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51
Q

How is necrotic laryngitis diagnosed?

A

Clinical signs, endoscopic exam, CBC with acute sepsis

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52
Q

How is necrotic laryngitis treated?

A

Antimicrobial therapy (oxytet, PPG, sulfonamides, florfenicol), NSAIDs, tracheostomy, supportive care, steroids if not immunosuppressed/septic yet

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53
Q

What is the prognosis of necrotic laryngitis?

A

Fair with early detection and aggressive therapy

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54
Q

Describe tracheal edema syndrome

A

AKA tracheal stenosis or honker syndrome; cause unknown, signs include coughing, dyspnea, and stertor, extensive edema and hemorrhage of teh dorsal wall fo the trachea

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55
Q

What are differentials for acute dyspnea?

A

Pharyngeal trauma, necrotic laryngitis, IBR, laryngeal abscess

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56
Q

Which animals are predisposed to acute dyspnea?

A

Heavy feedlot cattle, in the summer

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57
Q

Which animals are predisposed to chronic cough?

A

Smaller frame cows

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58
Q

What are differentials for chronic cough?

A

Necrotic laryngitis, pneumonia

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59
Q

How is chronic cough treated?

A

Steroids, antibiotics (especially if you can’t differentiate from pneumonia)

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60
Q

Do animals with bronchopneumonia appear sick? Do animals with interstitial pneumonia appear sick?

A

Bronchopneumonia- yes, depressed, febrile, signs of sepsis
Interstitial pneumonia- no, usually not systemically sick

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61
Q

What is the final outcome of bovine respiratory disease complex?

A

Bronchopneumonia

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62
Q

What are causative agents of bronchopneumonia?

A

Many viruses and bacteria
BRV, BHV/IBR, BRSV, BVDV, PIV-3, etc.

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63
Q

What part of the lungs are usually affected by bronchopneumonia?

A

Cranioventral lung fields

64
Q

What are risk factors for BRD?

A

Dairy calves- presence of diarrhea, failure of passive transfer, housing
Beef calves- dystocia, male sex, age of dam
Feedlot/stocker cattle- farm of origin, transit, stocker or feedlot operation

65
Q

Describe the causative agent of infectious bovine rhinotracheitis

A

Bovine herpesvirus type 1- enveloped DNA virus, an alphaherpesvirus that can cause many disease syndromes (IBR, abortion, conjunctivitis, encephalomyelitis, mastitis, vulvovaginitis, balanoposthitis)

66
Q

What are clinical signs associated with IBR?

A

Pyrexia, anorexia, decreased milk production, tachypnea, ptyalism, coughing, serous to mucopurulent nasal discharge, increased bronchovesicular sounds, hyperemia and red muzzle, conjunctivitis with corneal opacity

67
Q

Describe the pathogenesis of IBR

A

Direct contact or inhalation, requires direct injury of epithelial cells and immunosuppression

68
Q

Where does latent bovine herpesvirus 1 stay?

A

Usually trigeminal ganglion or tonsils

69
Q

Which cells are targeted by bovine herpesvirus 1?

A

Epithelial cells initially, then moves intracellularly to monocytes and lymphocytes

70
Q

What post-mortem lesions are seen from IBR?

A

Rarely fatal, may see rhinitis, laryngitis, bronchitis

71
Q

How is IBR diagnosed?

A

Virus isolation from nasal swabs or conjunctival scraping, IFA and PCR also available

72
Q

How is IBR treated?

A

NSAIDs, antimicrobials, supportive care, and vaccination

73
Q

Describe the causative agent of bovine respiratory syncytial virus (BRSV)

A

Enveloped RNA virus from Paramyxoviridae family, has cytopathic effects (forms syncytial cells)

74
Q

Which animals are typically affected by BRSV?

A

Nursing beef calves, dairy calves, adult cows and feedlot cattle, goats may serve as reservoir, can also infect sheep

75
Q

How does the morbidity rate of BRD complex change when BRSV is involved?

A

It increases

76
Q

What are the clinical signs of BRSV?

A

Pyrexia, depression, anorexia, tachypnea, ptyalism, cough, nasal discharge, increased bronchovesicular sounds (mostly middle or dorsocaudal lung fields), can have ruptured bulla leading to pneumothorax, subcutaneous emphysema

77
Q

Describe the pathogenesis of BRSV

A

Cattle infected from aerosol, incubates 3-5 days, forms fused, multinucleated syncitial cells in the airways and alveoli, dead cells slough into the lumen of the airway, develops bronchitis, bronchiolitis, alveolitis, and acute interstitial pneumonia

78
Q

How is BRSV diagnosed?

A

Virus isolation, seroconversion, can use IF, IHC, and PCR
Virus is difficult to grow so identification is not necessary for diagnosis

79
Q

How is BRSV treated and prevented?

A

Supportive care, NSAIDs, antimicrobials, vaccination

80
Q

Describe the causative agent of bovine viral diarrhea virus (BVD)

A

Enveloped RNA virus of Pestivirus genus and Flaviviridae family that causes a wide spectrum of diseases (mild pneumonia, diarrhea, immunosuppression, abortion, fetal mummification, congenital defects)

81
Q

How does infection with BVD change response to BRD pathogens?

A

Immunosuppresses, impairs immune response to vaccines and infects lymphocytes and macrophages causing impaired function

82
Q

What are clinical signs of BVD?

A

Fever, tachypnea, increased bronchovesicular sounds

83
Q

How is BVD diagnosed?

A

Skin biopsy with PCR, IHC, or ELISA, or blood PCR

84
Q

Describe the causative agent of bovine parainfluenza virus (PI3)

A

Enveloped RNA virus of paramyxoviridae family, commonly causes subclinical infections but can initiate respiratory disease

85
Q

What are clinical signs of PI3?

A

Usually mild, fever, cough, nasal/ocular discharge, tachypnea, increased bronchovesicular sounds, severity increases with secondary bacterial pneumonia

86
Q

Describe the pathogenesis of PI3

A

Aerosol transmission, incubates ~2 days, damages the mucociliary apparatus and decreases macrophage function

87
Q

How is PI3 diagnosed?

A

Virus isolation along nasal passages, trachea, or bronchiolar epithelium, PCR

88
Q

What kind of bacteria is Mannheimia haemolytica?

A

Gram negative aerobic bacteria, commensal agent of nasopharynx

89
Q

Where is M. haemolytica commonly isolated from?

A

Feedlot cattle that have died of fibrinous pleuropneumonia

90
Q

What are the clinical signs of M. haemolytica infection?

A

Dull and depressed, anorexia, fever, tachypnea, coughing (if virus co-infection), thoracic pain, increased bronchovesicular sounds

91
Q

What part of M. haemolytica causes endotoxemia?

A

LPS

92
Q

What are the signs of endotoxemia?

A

Fever, tachypnea, tachycardia, pale or brown mucous membranes, cool extremities

93
Q

Briefly describe the virulence factors of M. haemolytica

A

Leukotoxin- causes cytolysis of platelets, lymphocytes, macrophages, and neutrophils
LPS- causes endotoxemia, inflammation, complement and coagulation cascade

94
Q

Describe the pathogenesis of M. haemolytica

A

Not a normal pathogen of the lung, animals get infected at a young age and carry as part of the nasal flora, when in lungs it creates endotoxins and destroys cells

95
Q

What necropsy findings are typical of M. haemolytica?

A

Fibrinopurulent bronchopneumonia or pleuropneumonia, usually cranioventral, dark purple to red (maybe gray or brown) heavy lungs, gelatinous material within bronchial lumen, covered in yellow fibrin

96
Q

How is M. haemolytica diagnosed?

A

Bacterial culture (TTW), septic purulent inflammation (BAL), seroconversion

97
Q

How is M. haemolytica treated?

A

Antimicrobials, vaccination (questionable)

98
Q

What kind of bacteria is Pasteurella multocida?

A

Gram negative aerobic bacteria, commensal agent of nasopharynx

99
Q

What are the clinical signs of P. multocida?

A

Depression, anorexia, pyrexia, tachypnea, coughing, mucoid to mucopurulent nasal discharge, harsh bronchovesicular sounds over cranioventral lung field with crackles, +/- endotoxemia

100
Q

Briefly describe the pathogenesis of P. multocida

A

Needs an insult/weakening of the lower respiratory tract, uses virulence factors (LPS, capsule, iron regulated proteins) to attack

101
Q

What post-mortem lesions are typical of P. multocida?

A

Purulent bronchopneumonia in calves, cranioventral consolidation with purulent exudate

102
Q

What kind of bacteria is Histophilus somni?

A

Gram negative aerobic bacterial, commensal agent of genital and respiratory tract

103
Q

List the diseases associated with H. somni

A

Sepsis, thrombotic meningoencephalitis, reproductive disease, myocarditis, polyarthritis

104
Q

Which animals is H. somni common in?

A

Feedlot cattle

105
Q

What are the clinical signs of H. somni infection?

A

Fever, tachypnea, cough, nasal discharge, depression, increased bronchovesicular sounds, thoracic pain, may have clinical signs from other body systems infected

106
Q

Describe the pathogenesis of H. somni

A

Predisposed by viral infection, has virulence factors (LPS and outer membrane proteins), causes vasculitis and vascular thrombi, resists attack from neutrophils and macrophages

107
Q

What are the post-mortem findings indicative of H. somni?

A

Similar to P. multocida (purulent bronchopneumonia, cranioventral consolidation, purulent exudate), rarely a fibrinous pleuropneumonia

108
Q

How is H. somni diagnosed?

A

Bacterial culture, septic purulent inflammation, seroconversion

109
Q

How is H. somni treated?

A

NSAIDs, antimicrobials, vaccination

110
Q

What kind of bacteria is Mycoplasma bovis?

A

Small, pleomorphic bacteria with no cell wall, commensal agent of nasopharynx

111
Q

How is M. bovis spread?

A

Direct contact, inhalation, ingestion of contaminated milk

112
Q

Describe the clinical signs of M. bovis

A

Fever, tachypnea, anorexia, coughing/nasal discharge
In young calves- otitis, facial nerve and vestibulocochlear nerve involvement
Can cause mastitis, arthritis, tenoxynovitis, conjunctivitis, otitis, sinusitis, myocarditis, and pericarditis

113
Q

What is the proposed pathogenesis of M. bovis?

A

Impairs neutrophils (suspected)

114
Q

What post-mortem lesions are indicative of M. bovis?

A

Dark red consolidated lobules of cranioventral lungs, may have white to yellow firm nodules that cluster in the cranioventral lung field with caseous material

115
Q

How is M. bovis diagnosed?

A

Bacterial culture, IHC

116
Q

How is M. bovis treated?

A

Vaccination, poor response to antimicrobials (resistant to beta-lactams)

117
Q

Which antimicrobials are approved for BRD control (metaphylaxis)?

A

Ceftiofur, Enrofloxacin, Florfenicol (higher dose), Gamithromycin, Tilmicosin, Tildipirosin, Tulathromycin

118
Q

Which antimicrobials are approved for sheep and goats?

A

Ceftiofur, erythromycin for sheep, procaine penicillin G for sheep

119
Q

What types of vaccines are available for preventing respiratory disease?

A

MLV and killed vaccines, cover multiple viral pathogens
Vaccines for Mannheimia and Pasteurella are available as well

120
Q

What is preconditioning?

A

Attempts to eliminate certain risk factors, ex. wean well before shipping, train to eat from bunks, process prior to shipping, vaccinate

121
Q

What is backgrounding?

A

Processing weaned calves from various origins and housing and vaccinating them together

122
Q

What is metaphylaxis?

A

Antimicrobial therapy at the early stage of disease or in those at high risk for disease

123
Q

What causes acute bovine pulmonary edema and emphysema (ABPEE)?

A

Change from a dry sparse field to a lush green pasture, L-tryptophan is causative agent

124
Q

What clinical signs are associated with ABPEE?

A

Severe dyspnea with loud expiratory grunt, frothing and open mouth breathing

125
Q

What is the colloquial term for ABPEE?

A

Fog fever

126
Q

Describe the pathogenesis of ABPEE

A

L-tryptophan is converted in the rumen, absorbed by blood cells, metabolized by P-450 in type I pneumocytes. This process is reactive and causes interstitial inflammation and cell bridging, resulting in cell death, degeneration, necrosis, and exfoliation. There is then a proliferation of type II pneumocytes- called adenomatosis.

127
Q

What does the typical ABPEE event look like?

A

Within 2 weeks of pasture change, animals experience acute onset of severe dyspnea, loud expiratory grunt, frothing, mouth breathing, and tachypnea. Many die within 2 days, but those who survive have dramatic improvement in clinical signs.

128
Q

How is ABPEE treated?

A

There is no treatment, removal from pasture is too stressful, if they make it past 48 hours they’ll probably live

129
Q

What is the toxin in moldy sweet potatoes?

A

Furapoterpernoid, caused by Fusarium solani

130
Q

Describe the pathogenesis and progression of moldy sweet potato toxicity

A

High mortality rates with hepatotoxicity, toxin is carried to lungs via blood, there is no treatment, take food away

131
Q

What is metastatic pneumonia?

A

Pneumonia from a septic embolism from a foci in the body

132
Q

Describe vena caval thrombosis

A

Multifocal abscessation of the lungs from septic thromboembolism of the pulmonary arterial system, a type of metastatic pneumonia

133
Q

What are potential causes of vena caval thrombosis?

A

Jugular phlebitis, mastitis, metritis, foot rot, liver abscess, any septic condition

134
Q

What clinical signs are associated with vena caval thrombosis?

A

Tachycardia, tachypnea, dyspnea, coughing, epistaxis, wheezes, depression, anorexia, decreased milk production, right sided heart failure, death

135
Q

What are differential diagnoses for vena caval thrombosis?

A

Anaphylaxis, parasitic pneumonia, acute bronchopneumonia

136
Q

What is the cause of death in vena caval thrombosis?

A

Sudden acute episode of severe intrapulmonary hemorrhage or hemoptysis

137
Q

Describe the typical pathogenesis of vena caval thrombosis

A

Rumenitis from highly fermentable diet -> F. necrophorum and T. pyogenes enter portal circulation -> hepatic abscessation impinging on caudal vena cava -> septic emboli travels to thoracic cavity -> arteritis and pulmonary abscessation -> pulmonary hypertension -> aneurysm -> death

138
Q

How is vena caval syndrome treated?

A

There is no treatment

139
Q

What are parasites that cause parasitic pneumonia in cattle? Small ruminants?

A

Cattle- Dictyocaulus viviparus
SR- Dictyocaulus filaria, Meullerius capillaris, Protostrongylus rufescens

140
Q

Describe the life cycle of parasites that cause parasitic pneumonia

A

Eggs laid in lungs -> larvae travel up respiratory tree -> coughed up and swallowed, passed in feces -> become infective 3rd stage in pasture -> ingested -> migrate through SI to mesenteric LN -> molt into 4th stage -> enter lungs via blood and lymph -> enter alveoli, mate, mature

141
Q

What population of animals are more likely to develop parasitic pneumonia?

A

Young, naive livestock

142
Q

What clinical signs are associated with parasitic pneumonia?

A

Coughing and tachypnea, consolidation of lung lobes, tracheitis, bronchitis, increased bronchovesicular sounds (crackles and wheezes)

143
Q

How is parasitic pneumonia diagnosed?

A

Baermann test on feces, ELISA on milk or serum, peripheral eosinophilia is supportive

144
Q

How is parasitic pneumonia treated?

A

Levamisole, Fenbendazole, Ivermectin, Albendazole, Moxidectin

145
Q

What is the other term for ovine progressive pneumonia?

A

Maedi-Visna

146
Q

What virus causes ovine progressive pneumonia?

A

RNA lentivirus containing reverse transcriptase

147
Q

What kind of disease does ovine progressive pneumonia cause?

A

Pneumonia, mastitis, arthritis, and neurologic disease in adult sheep
Disease is chronic, progressive, and debilitating

148
Q

What clinical signs are associated with ovine progressive pneumonia?

A

Progressive pneumonia and septic arthritis in animals around 4-5 years of age, emaciation with good appetite, tachypnea

149
Q

What are differentials for ovine progressive pneumonia?

A

M. haemolytica, parasitic pneumonia, caseous lymphadenitis

150
Q

How is ovine progressive pneumonia diagnosed?

A

Serologic testing (ELISA/western blot), virus isolation (culture, PCR)

151
Q

How is ovine progressive pneumonia treated?

A

There is no treatment

152
Q

What are the four clinical syndromes caused by caprine arthritis encephalitis?

A

Leukoencephalomyelitis, polysynovitis, mastitis, interstitial pneumonia

153
Q

What kind of virus is caprine arthritis encephalitis?

A

RNA lentivirus

154
Q

What is the causative agent of caseous lymphadenitis?

A

Corynebacterium pseudotuberculosis

155
Q

Describe caseous lymphadenitis

A

Chronic disease of pyogranulomatous abscesses in lymph nodes and internal organs
External LN in goats, internal LN in sheep

Ruminants (10 decks)

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