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Advanced Clinical Management > Large Animal Respiratory Diseases > Flashcards

Large Animal Respiratory Diseases Flashcards

1
Q

What causes Allergic Rhinitis in cattle?

A

plant pollen or fungal spores which causes a localized ongoing immediate tyoe 1 hypersensitivity reaction

**mostly 6mo-2yrs

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2
Q

What season is Allergic Rhinitis most likely to occur?

A

Spring, summer or fall in cattle on pasture

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3
Q

What are the clinical signs of Allergic Rhinitis?

A

**Rhinorrhea (clear nasal d/c)
**intense nasal pruritis
-sneezing
dyspnea
Sertorous inspiration
can cause facial swelling, tachypnea and alteration of nasal mucosa
Chronic= gramuloma formation–>multiple firm white raised 1-2mm

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4
Q

How do you diagnose Allergic Rhinitis?

A
  • *Biopsy- chronic proliferative eosinophilic rhinitis
  • endoscopy to visualize granulomas in nasal passages
  • cytology, culture antigen testing
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5
Q

How do you treat Allergic Rhinitis?

A
  • remove allergen
  • block hypersensitivity reaction
  • corticosteroids (dex and pred)
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6
Q

What causes Necrotic Laryngitis?

A

infection of laryngeal mucosa and cartilage of young cattle
-typically Fusobacterium necrophorum but this will not penetrate intact mucosa–>needs previous infection or mechanical lesion

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7
Q

When do you typically see Necrotic Laryngitis?

A

fall and winter

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8
Q

What are the clinical signs that you seen for Necrotic Laryngitis?

A 
loud moist/painful cough
head/neck extended
severe inspiratory dyspnea/guttural stertor
open mouth breathing
T=102-106
ptyalism
breath smells bad
stand by water and sip frequently
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9
Q

What happens in cases of calf diphtheria (necrotic laryngitis) if it goes untreated?

A

animal will die 2-7 days from systemic effects of bacterial toxins and UAO (upper airway obstruction)

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10
Q

How do you diagnose Necrotic Laryngitis?

A
  • *laryngioscopic or endoscopic exam to confirm
  • acute bloodwork- luekopenia caused by neutropenia / left shift
  • chronic blood work- leukocytosis w/ neutrophillia, monocytosis and hyperfibrinogenemia
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11
Q

How do you treat Necrotic Laryngitis?

A 
Antibiotics
-oxytetracycline
-procain peniciillin
NSAID (flunixin) to reduce swelling/inflamm and fever
Steroids-repeated dose NOT recc.
Tracheostomy
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12
Q

How would you treat Necrotic Laryngitis in severe cases?

A

tracheostomy

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13
Q

What is the prognosis of Necrotic Laryngitis?

A

guarded, the** younger the animal the worse the prognosis**

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14
Q

What are some things that can traumatize the larynx?

A

Inappropriate roping or injury with restraint devices
Inappropriate placement of an endotracheal tube
Inappropriate use of the balling gun (bolus applicator)

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15
Q

What are the clinical signs of larynx trauma?

A

Prolongation of the inspiratory phase
Extension of the head and neck, and open mouth breathing
Stertor
Cyanosis
Inflammation of the larynx may lead to inspiratory dyspnea and aspiration pneumonia

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16
Q

How do you diagnose Larynx trauma?

A

endoscope to confirm

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17
Q

What is the treatment for larynx trauma?

A

NSAIDS

Steroids- decrease larynx edema

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18
Q

What is caudal vena cava thrombosis?

A

syndrome associated with multifocal abscessation of the lungs cause by septic thromboembolism of the pulmonary arterial system

-seen in feedlot cattle (no sex, age, breed predisposition)

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19
Q

What is CVCT (caudal vena cava thrombosis) often a sequela of?

A

liver abcesses secondary to rumenitis (can have other infectious disorders too)

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20
Q

What is the pathogenesis of CVCT?

A

rumenitis from ruminal acidosis–>proliferation of F/ necrophorum and A. pyrogens (penetrate damaged ruminal epithelium)–>trasnports to the liver in portal drainage resulting in abscess formation–>septic thrombus–>septic emboli detaches–>lungs/pulmonary arterial system–>pulmonary abscess and widespread arterial embolism–>arterial hypertension–>arteritis and endarteritis + hypertension lead to rupture of the blood vessel and massive hemoptysis

Short version:
rumenitits–>bacteria infiltrate–>abscess–>septic thrombus–>septic emboli–>lungs/pulmonary arterial embolism–>hypertension–>artreitis+hypertension–>rupture of vessels

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21
Q

What are the clinical signs of CVCT? What are some differentials?

A

**tachycardia, tachypnea, dyspnea, coughing, heart murmurs, pale MM (anemia), widespread wheezes, epistaxis, hemoptysis (spitting up of blood)

other: fever, thoracic pain, hepatomegly, SQ emphysema, froth at muzzle, melena

Differentials:

  • anaphylaxis
  • hypersensitivity pneumonitis
  • lungworms
  • acute bronchopnemonia
  • ARDS
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22
Q

How do you diagnose CVCT?

A

hematology: anemia and nuetrophillic leukocytosis w/ regenerative shift
blood chem: hyperglobulinemia, elevated liver enzymes

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23
Q

What is the treatment of CVCT? Is there any way to prevent it?

A

antibiotic therapy: penicillin, oxytetracyclin, florfenicol
supportive care: furosemide and flunixin
corticosteroids
**prognosis is grave–>treatment rarely indicated

prevention of rumenitis and liver abscessation (monensin to animals to promote more stable rumen + high energy rations and feeding of antibiotics to reduce incidence of liver)

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24
Q

What is Fog fever caused by?

A 
aka ABPEE (**acute bovine pulmonary edema and emphysema
-triggered by sudden change from dry sparse forages to lush green pastures

***caused by conversion of L-tryptophan–>pnemotoxin 3-methylindole whcih leads to pulmonary edema, alveolar epithelial hyperplasia, hyaline membranes and emphysema

***affects parenchyma of lungs

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25
Q

What are the clinical signs of Fog fever?

A 
begin within **2 weeks of access to new forage
-dypsnea
exercise intolerance
tachypnea
frothing at mouth
abnormal lung sounds: wheezing, crackles in caudal area
SQ emphysema
coughing rare
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26
Q

What is the prognosis of Fog fever?

A

30% death possible usually in first 2 days
if the survive dramatic improvement after 3 days

-repeated bouts may develop chronic diffuse pulmonary fibrosis w/ alveolitis

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27
Q

How do you diagnose Fog Fever?

A

history
clinical signs
gross path/histopath in fatal cases
**TTW or BAL cytology reveal non-septic mixed inflammatory cell response

nothing unique on bloodwork/biochem can show stress leukogram

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28
Q

What do you find following a necropsy on a cow with Fog fever?

A

petechial hemorrhage throughout respiratory tract
**frothy fluid in all airways
congestion (edema and emphysema in lungs w/ large bullae)

histopath: eosinophillic hyaline membranes and proliferation of type 2 cells and clara cells

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29
Q

How do you treat Fog fever?

A

removing them from pasture does not necessarily prevent additional cases, some say could cause more deaths

can five furosemide, flunixin and steroids–>use cautiously

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30
Q

How can you prevent Fog fever?

A
  • ***modification of management and the use of prophylactic drugs
  • gradually decrease the amount of hay fed and increase the time on pasture over a period of 10-12 days
  • delay the use of lush pastures (until after hard frost)
  • use the pasture for young stock (<15 mo of age)
  • use of pasture before it becomes particularly lush

can so prophylactic medication: monensin

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31
Q

What is the common parasite found in Lungworms?

A

Dictyocaulus viviparus**

others: Toxicara vitulorum and Ascaris suum

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32
Q

What is the lifecycle of Dictyocaulus viviparus?

A

Direct
L3 consumed at pasture–>becomes L4 in host intestine–>migrates to lung for final maturation

L4 enter alveoli an encite eosinophilic exudate that blocks bronchi and brononchioles

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33
Q

As these larvae mature and migrate up the airways these lesions ___A___ but the adult worms produce an ____B___ _____C______ in the larger airways

A

A. resolve
B. inflammatory
C. response

34
Q

What are the clinical signs of lung worms?

A
  • marked coughing
  • tachypnea
  • dypsnea
  • anorexia
  • weight los
  • wide spread crackles and wheezes
35
Q

What affects the severity in Lungworm infections?

A
  • # of larvae ingested
  • rate of ingestion
  • proportion of larvae reaching the lungs
36
Q

How do you diagnose Lungworms?

A

larvae in TTW (detected by Baermann test) or in feces (only nematode parasite routinely producing larvae found in feces)

37
Q

What are the common findings for cattle infected with Lungworms when doing a necropsy?

A

***bilaterally symmetric red consolidation od the ventral caudal ling lobes

38
Q

How do you treat Lungworm infections?

A
  • pasture management

- anthelmintic (ivermectin)

39
Q

What is the most common metastatic Neoplasia in the lungs of cattle?

A

***Lymphosarcoma most freq. neoplasm to become metastatic to the lung

tumors are most likely to be detected antemortem by radiographic exam

40
Q

What is the shock organ of the Cow? Horse?

A 
cow= lung
horse= gi tract
41
Q

What is the recommended treatment of anaphylaxis in cattle?

A

epinephrine administration 4-8 mg diluted (IV/SQ)

42
Q

What are some other names of Extrinsic allergic alveolitis?

A

farmers lung

hypersensitivity pneumonitis

43
Q

What causes Extrinsic allergic alveolitis?

A

response to airborne antigens from dusty or moldy hay that causes progressive inflammatory changes in alveoli and bronchioles

micropolyspora faeni and thermophilus vulgaris most common allergens

  • *Exclusively housed cattle
  • *signs can dec in summer
44
Q

What are the clinical signs associated with extrinsic allergic alveolitis? (Acute vs chronic)

A

Acute: reduced milk, poor appetite/dullness, tachypnea, abnormal lung sounds
chronic: similar signs + **weight loss

more common in Northern US (incr humidity)

45
Q

How do you diagnose alveolar allergic alveolitis?

A

hx and clinical signs

serology–>antibody NOT useful since expose animals will test positive

46
Q

How do you treat Extrinsic allergic alveolitis? Prognosis?

A

removing triggering agent from barn/reduce exposure (make silage instead of hay–>ensure proper drying before baling/feeding)
corticosteroids (dexmethasone)

prognosis = good if you remove agent quickly

47
Q

What causes Tuberculosis?

A

mycobacterium bovis- most often in cattle

-sporadic cases from wildlife/imported cattle

48
Q

How is TB transmitted?

A

direct contact w/ exhaled droplets, saliva, feces, milk, urine, vaginal d/c, semen or exudate from Tb lesion
indirect–>contaminated feed/water, building, feeding/cleaning equipment

***source of infection can be infectious secretions from other cattle or caretakers

49
Q

What are the clinical signs of TB?

A

no clinical signs until late in course of disease
milk respiratory signs (soft moist cough most noticeable in cold weather or after exercise)
advanced stages = dyspnea, emaciation, respiratory distress

enlarged lymph nodes may rupture and drain

enlarge internal lymph nodes–>can lead to GI/repro abnormalities

50
Q

What is the official Tb test (antemortem) for cattle?

A
  • *Caudal fold tuberculin test (CFT)
  • comparative cervical tuberculin test (CCT)
  • cervical tuberculin test
  • bovine interferon gamma assay

**CFT as a presumtative diagnosis–>after can be evaluated further w/ CCT, gamma interferon or sent to slaughter under permit

51
Q

If an animal shows positive response for the CFT test its ____A_____ to ___B____ hours and peaks about ____C____ hours after injection.

A

A. 8
B. 12
C. 72

52
Q

What do you do after a positive CFT diagnosis?

A

contact APHIS and district office and state animal health officials

53
Q

What do you find on necropsy for TB?

A

most affected are internal lymph nodes, pleural and peritoneal serosa

  • presence of firm encapsulated nodules containing thick, white yellow creamy to caseous purulent material commonly found
  • histopath = granuloma lesion w. caseous necrosis surrounded by macrophages multinucleated giant cells and lymphocytes
54
Q

What is the gold standard test for TB?

A 
mycobacterial culture (incubation for 8 weeks-->growth after 3-6 weeks)
PCR determination
55
Q

How can you treat/prevent TB?

A

generally NOT treated in domestic animals
-test not sensitive so depopulation is often used for tx
vx are rarely used to control bovine TB–>can interfere w/ antemortem testing

56
Q

What are some other names used for BRD?

A

BRD
shipping fever
enzootic pneumonia of calves
BRDC (bovine respiratory disease complex)

57
Q

What are some common vaccines of cattle prevent? (what viruses does it cover)

A
  • BHV-1
  • BRSV
  • BVD
  • PI-3
58
Q

What is another name for BHV-1?

A

Infectious bovine rhinotracheitis

59
Q

How is BHV-1 spread?

A

SUPER CONTAGIOUS

spread via oral and nasal d/c

60
Q

What is the most common form of BVH-1? Second?

A

1st- Respiratory form-hangs out in trigeminal nerve
2nd- Conjunctival
3rd infectious pustular vulvuvaginitis/blanoposthitis

61
Q

What are the clinical signs of BHV-1/IBR?

A

high pyrexia (105-108)
-incr. RR
-nasal/ocular d/c–>increasing mucopurolent as illness progresses
-plaques on mucosa of the nasal septum, muzzle or palpebral conjunctiva
-possible ulceration of muzzle and oral mucosa (red nose from erythema)
-diptheritic membranes (dead/necrotic) in the larynx and trachea
PAINFUL

62
Q

BHV one has a __A___ mortality and __B___ morbidity. (fill in the blank)

A

A & B is high

63
Q

What are BHV-1 affects on other pathogens?

A

upregulates genes which activate Mannhemia hemolytica leukotoxin (causes incr tissue damage)
acts synergistically w/ BVD and BRSV

64
Q

BHV-1 affects the URT. (T/F)

A

False- it affects the Lower respiratory tract by affecting the mucociliary transport and mucus layer which prevent the cilia from pushing mucus/bacteria up
-alters alveolar macrophages

PAINFUL

65
Q

What are some other names for bovine respiratory syncytial virus?

A

-atypical interstitial pneumonia (AIP)

Highly contagious NOT related to stress***

66
Q

BRSV has a __A___ morbidity and ___B__ mortality. (fill in the blank)

A

A. high

b. low

67
Q

BRSV does NOT affect the alveolar macrophages. (T/F)

A

True- BRSD affects LRT and mucocilliary transport and mucus layer and activates the complement immune response

68
Q

Does BRSV affect other pathogens?

A

no directly but there can be secondary bacterial infections

69
Q

What are the BRSV clinical signs?

A

High pyrexia (105-108)**
depression
salivation and mucoid nasal d/c
variability of RR and dyspnea
SQ emphysema on dorsum (behind withers & feels like bubble wrap)
can have lung sounds/bronchial tones/crepitation/rales

70
Q

How does BVDV work?

A

loves to destroy immune cells and can cause secondary respiratory infections

71
Q

What are some ways that BVD can affect cattle?

A

can cause:

  • abortions
  • congenital defects
  • persistently infected
  • mucosal disease
72
Q

How does BVD spread?

A
  • persistently infected animal shedding
  • recent infected animal shedding
  • fomites
73
Q

What are BVD’s clinical signs?

A
  • high pyrexia
  • mild clinical signs (mild elevated RR)
  • can have interstitial pneumonia in Type 2 infections of naive cattle
  • mucosal disease
  • abortions
  • congenital birth defects
74
Q

How does BVD cause disease? (where)

A

affects LRT and suppresses immune system for 7-14 days which can lead to secondary bacterial infections

75
Q

What system is affected by Parainfluenza-3? (PI 3)

A

LRT, damages to ciliary epithelial/mucus transport system, causes infection of alveolar macrophages–>can lead to secondary bacterial infections

76
Q

What are the clinical signs of PI 3?

A

high pyrexia

-little distinguishing clinical signs (depression. Anorexia)

77
Q

How does mycoplasma pneumonia work?

A

damage to cilary epithelial/mucus transport system

  • causes humoral; and cell-mediated immunosupression
  • peribronchiolar and peribronchial lymphoid hyperplasia
78
Q

Is mycoplasm pnemonia primary of secondary?

A

primary- high morbidity and low mortality by itself

79
Q

What are the clinical signs of mycoplasm pneumonia?

A

hard to distinguish

  • can also have:
  • otitis media
  • mastitis
  • arthritis
80
Q

How does mycoplasm pnemonia cause infection?

A

air quality
milk
**opportunistic and chronic

Advanced Clinical Management (12 decks)

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