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Fluids, Respiratory, Muscles > Livestock Respiratory Disease > Flashcards

Livestock Respiratory Disease Flashcards

1
Q

Why do ruminants develop SQ emphema, more easily that other species

A

1) Very few inter-alveolar pores, which normally allow for connection between alveoli and pressure equilibration.
2) Pressure can build up more easily
3) Rupture of alveoli and development of emphysematous bulla
4) Pneumomediastinum and air tract up the medaistinum to the dorsum to get SQ ephysema

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1
Q

Why do ruminants suffer from respiratory disease really rapidly

A

1) their lung is lobulated and they have a very minimal reserve capacity (unlike horses and dogs)

2) Histologically, very few inter-alveolar pores, which normally allow for connection between alveoli and pressure equilibration.
Pressure can build up more easily leading to pneumomediastinum and air tract up the medistinum to the dorsum to get SQ ephema

3) Hyper-reactive lungs - hypoxia, inflammatory, and histamine sensitive

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2
Q

What are ruminant lung hyper-reactive to

A

1) Hypoxia- pulmonary arterial constriction and subsequent pulmonary hypertension
2) Inflammatory process- macrophages and mast cells release mediators that cause disease to alveoli and interstitium
3) Histamine sensitive- significant histamine release

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3
Q

What occurs when there is degranulation of mast cells with anaphylaxis in ruminants

A

there is resulting bronchoconstriction and vasoconstriction
-resulting in pulmonary edema

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4
Q

How do chronic and acute respiratory disease in ruminants affect the rumen

A

there is decreased function of the rumen and the ability to eructate- resulting in gas bloat- distension on the rumen, pressure on diaphragm and pressure on the lungs

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5
Q

Why are the lungs smaller in ruminants

A

the rumen takes up the majority of the space
lungs are pushed cranial and smaller relative to other species

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6
Q

Ruminant lung anatomy

A

multiple lobes and within those there are lobules, which are differentiated by septal areas

Septal regions form a barrier to prevent expansion of bacterial bronchopneumonia into other areas of the lung -can have stark demarcation of disease and normal lung

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7
Q

What is significant about the ruminant lung anatomy and the distribution of bronchopneumonia

A

Septal regions form a barrier to prevent expansion of bacterial bronchopneumonia into other areas of the lung -can have stark demarcation of disease and normal lung

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8
Q

Maxillary sinuses in the ruminants

A

over the upper cheek teeth (premolars and molars)

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9
Q

What sinus connects to the cornual sinus in ruminants

A

the frontal sinus

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10
Q

What developmental condition of the upper respiratory tract is common in camelids

A

Choanal atresia

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11
Q

Choana

A

where the nasal passage opens into the nasopharynx

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12
Q

What are signs of upper respiratory disease in livestock

A

1) Nasal discharge- serous, mucopurulent
2) Sneeze
3) Cough
4) Stridor - intense musical breath sounds over upper airway, particularly the larynx, extrathroacic
5) Stertor- sonorous snoring breath sounds over the upper airway- extrathoracic
6) Decreased nasal airflow
7) Foul smelling breath
8) Facial asymmetry
9) Laryngeal swelling
10) Nasal hyperemia
11) Expanding cheeks on exhalation
11) Ocular discharge
12) Conjunctivitis
13) Respiratory distress
14) Salivation- minimally swallowing
15) Head shaking
16) Epistaxis
17) Fever
18) Quidding, dysphagia
19) Hypxemia

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13
Q

intense musical breath sounds over upper airway, particularly the larynx, extrathroacic

A

Stridor

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14
Q

sonorous snoring breath sounds over the upper airway- extrathoracic

A

Stertor

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15
Q

What are signs of lower respiratory disease in livestock

A

1) Fever
2) Cough
3) Abnormal breath sounds
4) Respiratory dyspnea- restrictive breathing pattern
5) Hemoptysis
6) SQ emphema
7) Hypoxemia
8) Bloat- inflammation of vagal nerve or enlargement of mediastinal LN putting pressure on esophagus and preventing normal eructation

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16
Q

Why do you see bloat of ruminants with lower respiratory disease

A

inflammation of vagal nerve or enlargement of mediastinal LN putting pressure on esophagus and preventing normal eructation

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17
Q

irritation and inflammation of mucous membrane inside the nose

A

rhinitis - clinical signs: sneezing, intense pruritis, nasal discharge *usually serous), stertor

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18
Q

What are common etiologies of rhinitis in cattle * know this

A

BHV-1 (IBR) *
BVDV *
PI-3 *
BRSV *
Coronavirus
MCF

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19
Q

What are clinical signs of cows with rhinitis

What about chronic*

A

sneezing, intense pruritis, nasal discharge *usually serous), stertor

chronic: lacrimation, blepharospasm, granuloma formation

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20
Q

What is Atopic rhinitis in cattle

A

allergic rhinitis
-acute, summer snuffles
-type I (IgE) allergic reaction
-older cattle
-Channel Island Breeds (Jersey, Guernsey) and Holsteins

signs: difficulty breathing, sneezing, stertor
nasal discharge (usually serous)
pruritis

chronically- develop into enzootic nasal granuloma

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21
Q

What cattle breeds do you see atopic rhinitis in?

A

Channel Island Breeds (Jersey, Guernsey) and Holsteins

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22
Q

What causes Atopic Rhinitis in cattle

A

Type I (IgE) allergic reaction

repeated exposures can lead to type IV

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23
Q

What causes acute summer snuffles in cattle

A

Atopic rhinitis- allergic rhinitis
caused by Type I (IgE) allergic reaction

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24
Q

What is the pathogenesis of Atopic Rhinitis in cattle

A

1) Antibodies (IgE) to antigen produced
2) Subsequent exposures result in type I hypersensitivity reactions
3) Repeated exposures can lead to type IV

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25
Q

What are the clinical signs of atopic rhinitis in cattle

A

difficulty breathing, sneezing, stertor
nasal discharge (usually serous)
pruritis

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26
Q

What occurs if atopic rhinitis develops into chronically

A

Enzootic Nasal Granuloma
-Chronic form
-Firm raised white granulomatous nodules

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27
Q

When do you see enzootic Nasal granuloma in cattle

A

When atopic rhinitis develops chronically
you see firm, rasied, white granulomatous nodules in the nasal passages

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28
Q

What are differential diagnosis for atopic rhinitis

A

-fungal
-foreign body
-tumor
-irritant

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29
Q

How do you diagnose atopic rhinitis

A

-Endoscopy*
-Culture (rule out)
-Biopsy
-Cytology (eosinophils)

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30
Q

How do you treat atopic rhinitis in cattle

A

-Remove allergen
-Antihistamine- often not helpful
-Corticosteroids - key treatment and useful. make sure they are not pregnant or they will abort *

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31
Q

What does fungal infection in the nasal passages of ruminants result in

A

delayed type IV hypersensitivity and nasal granuloma formation

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32
Q

Mycotic nasal granuloma in cows

A

Fungal infection leading to upper respiratory signs
-Delayed Type IV hypersensitivty forming a granuloma

Dx: endoscopy, biopsy, cytology, culute

Treatment: Surgery, Sodium Iodide, Antifungals

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33
Q

How do you treat Mycotic Nasal Granuloma in cattle

A

Surgery
Sodium iodide (IV)
Antifungals - expensive and there is a withdrawal times (contact FARAD)

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34
Q

What causes sinusitis in livestock

A

-dehorning
-tooth root infection (maxillary)
-horn injury
-respiratory disease
-nasal tumor
-actinomycosis (lumpy jaw)
-sinus cyst
-lymphosarcoma

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35
Q

What bacteria commonly cause sinusitis in livestock

A

Trueperella pyogenes
Pasteurella multocida

but any of the respiratory tract bacteria can cause it

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36
Q

What are the clinical signs of sinusitis in livestock

A

Acute: nasal discharge, fever, lethargy, anorexia, percusson

Chronic: nasal discharge, percussion, stertor, stridor, foul odor - ozena and/or halitosis, bone distortion, exopthalmos, neurological signs, unusal head carriage

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37
Q

If there is dehorning injury or broken horn, where does the sinusitis develop

A

cornual sinus that connects with the frontal sinus

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38
Q

How do you diagnose sinusitis in cattle

A

Clinical signs
Percussion
Radiograph- soft tissue density over the area of the maxillary sinus
Sinus centesis

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39
Q

How should you change your dehorning practices to prevent sinusitis

A

1) make sure you do not dehorn at later ages when the horn is communicating with the frontal sinus
2) Avoid dehorning in bad weather
3) Bandage for a prolonged time

otherwise not a lot to prevent sinusitis (esp of maxillary)

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40
Q

How do you treat sinusitis in cattle

A

Trephination- drilling a hole into the sinus and then aspirating a sample to aid in diagnosis can use for culture .Submit for aerobic and anaerobic
Aspiration
Lavage
Surgery
Antibiotics- PPG (T. pyogenes)
NSAIDs (flunixin meglumine or PO meloxicam)
Tooth extraction

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41
Q

Upon trephination of a cattle with sinusitis you get a sample to culture. What culture do you order

A

aerobic and anaerobic (although mostly aerobic)

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42
Q

How do you treat sinusitis in a ruminant caused by T. pyogenes

A

PPG - but it needs to be given twice daily and at a large volume

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43
Q

What is critical for the treatment of maxillary sinusitis

A

tooth extraction - can sometimes remove tooth orally. otherwise may need to do a maxillary surgery to remove the tooth

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44
Q

making a hole from the exterior into the infected sinus to allow for drainage and lavage. Use of Steinmann pin, drill

A

Sinusotomy (Trephination)

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45
Q

What bacteria is usually associated with frontal sinusitis in livestock

A

Trueperella pyogenes

secondary to dehorning

Tx: Penicillin

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46
Q

What is the most common isolate with frontal sinusitis NOT associated with dehorning

A

Pasteurella multocida

treat with penicillin or oxytetracycline

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47
Q

What should you treat pasteurella multocida caused frontal sinusitis in livestock

A

penicillin or oxytetracycline

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48
Q

oestrus ovis

A

nasal bots of sheep
lifecycle: spring to early fall

Signs: nasal discharge, sneezing, nose rubbing, stridor, stertor, decreased airflow (cheeks)

treatment: Ivermectin

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49
Q

What is the lifecycle of oestrus ovis

A

spring to early fall

1) Adult deposits eggs on nostrils
2) Migrate to the sinuses and go through development
3) Mature larvae migrate back down and out nostril
4) Larvae is on the ground, pupates and turn into adult fly

*Causes irration to the nasal pasages

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50
Q

How do you treat Oestrus ovis in sheep

A

Ivermectin

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51
Q

What is the nasal bot that occurs in llamas

A

Deer pharyngeal bot (Cephenemyia)

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52
Q

Deer pharyngeal bot (Cephenemyia)

A

nasal bot that occurs in llamas

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53
Q

What causes viral rhinitis in cattle ***

A

BHV-1 (IBR) *
BVDV *
PI-3 *
BRSV *
Coronavirus
MCF

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54
Q

What causes ovine nasal adenocarcinoma

A

Retrovirus

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55
Q

Ovine nasal adenocarcinoma

A

Retrovirus
Nasal signs- serous discharge, stridor/stertor, anorexia, inspiratory dyspnea, open mouth breathing, dilating/puffing out cheeks

progressive, locally invasive, not metastatic
starts unilateral but progresses to be bilateral

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56
Q

What is a primary sign of ovine nasal adenocarcinoma

A

inspiratory difficulty- some degree of open mouth breathing

livestock prefer nasal breathing but if the force mouth closed you will see them pushing their cheeks out

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57
Q

What is the treatment on ovine nasal adenocarcinoma

A

no successful treatment for it

clients may request surgery however ultimately it is locally invasive and there is no cure

Can do endoscopy and biopsy to diagnose it

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58
Q

rhinitis and atrophy of turbinates seen in young pigs <3weeks

Caused by Bordetella bronchiseptica and pasteurella multocida

Signs: nasal discharge, sneeze, nose rubbing +/- mild cough, nose asymmetry

A

Porcine Atrophic Rhinitis

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59
Q

What causes porcine atrophic rhinitis

A

Bordetella bronchiseptica and pasteurella multocida

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60
Q

What age of pigs does atrophic rhinitis affect

A

Young pigs <3weeks

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61
Q

Bordetella bronchiseptica and pasteurella multocida cause

A

rhinitis and atrophy of the turbinates of piglets < 3 weeks of age

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62
Q

How do you treat/prevent for porcine atrophic rhinitis

A

1) ID and remove carriers animals
2) Vaccination (dams immunized so there is some colostral immunity) and vaccinate piglets starting at 1-2 weeks of age.

antibiotics might not work

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63
Q

the location where embryologically as the nasal passage develops rostral to caudal and the pharynx develops caudal to rostral the two come together to meet

A

Choana

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64
Q

What species is choanal atresia common in

A

camelids - congenital condition

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65
Q

What are the clinical signs of camelids with choanal atresia

A

difficulty breathing, respiratory distress, open mouth breathing

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66
Q

What happens in crias with choanal atresia

A

crias will go to nurse and nurse vigorously and then because it is not breathing while nursing will pass out

will begin to regain consciousness

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67
Q

How can you diagnose choanatal atresia

A

1) Endoscopy
2) Radiographs with contrast- sternal. you will see pooling of contrast in the caudal aspect of the nasal passage (cannot pass through)
3) Pass a catheter

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68
Q

How do you treat choanal atresia

A

surgical options- often unsuccessful

better prognosis if just membranous choanal atresia- rather than bony

as they grow, it remains close and they need a corrective surgery

heritable so do not keep in the breeding pool

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69
Q

metastatic pneumonia in livestock

A

primary disease in other organ system (liver abscesses, jugular phlebitis, endocarditis (tricuspid valve), metritis, mastitis, foot rot

hematogenous spread to the lung

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70
Q

What can lead to metastatic pnenumonia in cattle

A

primary disease in other organ system (liver abscesses, jugular phlebitis, endocarditis (tricuspid valve), metritis, mastitis, foot rot

via hematogenous spread

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71
Q

What are typical causes of metastatic pneumonia in cattle

A

Fusobacterium necrophroum (Gram negative anaerobe)

Trueperella pyogenes (gram positive anaerobe)

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72
Q

T/F: metastatic pneumonia is frequently fatal with sporadic occurence

A

True

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73
Q

caudal vena caval thrombosis

A

septic thromboemboli originate from an abscess at the hilus of the liver

often starts in GI (rumen acidosis, rumenitis, abomasal ulcers)

showering CVC leads to septic emboli within pulmonary abscessation

Abscesses erode into bronchial wall and aneurysms can rupture into AW

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74
Q

Primary infection of the caudal venal caval thrombosis in ruminants is _________

A

often starts in GI (rumen acidosis, rumenitis, abomasal ulcers)

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75
Q

What is the clinical presentation of CVCT in ruminants

A

*Epistaxis, hemoptysis, anemia +/- dynpea
3 categories
1) Sudden death
2) Acute respiratory distress syndrome
3) Chronic bronchopneumonia

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76
Q

What are the 3 categories of clinical presentation of CVCT

A

1) Sudden death
2) Acute respiratory distress syndrome
3) Chronic bronchopneumonia

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77
Q

How do you control for CVCT

A

re-evaluate nutrition/feed management

need to prevent rumen acidosis, ruminitis, and abomasal ulcers

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78
Q

How do you treat CVCT in ruminants

A

long term penicillin, supportive care

poor prognosis

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79
Q

Hypersensitivity Pneumonitis in cattle

A

Extrinsic allergic alveolitis / Bovine Farmer’s Lung

Allergic response (Type I and IV) to dust, moldy hay, grain, plant matter
-spores: thermophilic actinomycetes (Micropolyspora faeni)

most common in dairy cows ( confined), outbreaks in winter

clinical signs: decreased milk production, appetite, weight loss, coughing, crackles on thoracic auscultation

Diagnosis: titers (exposure), identify fungi in feed

treatment: glucocorticoids, improve hay management (bailing when dry), feed hay outside, improve ventilation

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80
Q

How do you treat hypersensitivity pneumonitis in cattle

A

glucocorticoids, improve hay management (bailing when dry), feed hay outside, improve ventilation

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81
Q

How do you diagnosis hypersensitivity pneumonitis in cattle

A

Diagnosis: titers (exposure)- uncommon, identify fungi in feed

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82
Q

What causes hypersensitivity pneumonitis in cattle

A

Allergic response (Type I and IV) to dust, moldy hay, grain, plant matter
-spores: thermophilic actinomycetes (Micropolyspora faeni)

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83
Q

What is the major target organ in Type I hypersensitivity

A

the lung- shock organ

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84
Q

Clinical signs of anaphylaxis develop within

A

10-20 min

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85
Q

What are the clinical signs of anaphylaxis in cattle

A

often to vaccine, milk, drug (penicillin), insects, bee sting with signs onset of 10-20 minute

severe acute dyspnea, flaring of nostrils, extension of head and neck, open mouth breathing, urticaria (hives), pharyngeal edema

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86
Q

How do you treat anaphylaxis (Type I) in ruminants

A

1) Epinephrine (1:1000)- life saving bronchodilation (B2 agonist)

2) Corticosteroids (not in pregnant animals)- antiinflamamtion and antiedema

3) Antihistamine

4) NSAIDs- milking out/drying off (if there is a milk allergy)

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87
Q

Acute/Atypical Interstitial Pneumonia (AIP)

A

commonly non-infectious
secondary to inhalation or ingestion of toxin
usually no clinical indication of sepsis
abnormal peripheral lung sounds diffusely

*Little response to antimicrobial therapy (toxin affect)

Necropsy:
-lungs fail to collapse when thorax opened
-firm, rubbery texture with diffuse interlobular emphysema and pathcy interstitial edema
-Histo: alveolar hyaline membrane, type II pneumocyte proliferation

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88
Q

What are the necropsy findings of cattle with Acute/ Atypical Interstitial Pneumonia (AIP)

A

-lungs fail to collapse when thorax opened
-firm, rubbery texture with diffuse interlobular emphysema and pathcy interstitial edema
-Histo: alveolar hyaline membrane, type II pneumocyte proliferation

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89
Q

How do you treat Acute/ Atypical Interstitial Pneumonia (AIP)

A

Little response to antimicrobial therapy (toxin affect)

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90
Q

What is the etiology of Acute/ Atypical Interstitial Pneumonia (AIP)

A

commonly non-infectious
secondary to inhalation or ingestion of toxin
usually no clinical indication of sepsis
abnormal peripheral lung sounds diffusely

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91
Q

What is a severe clinical presentation of AIP in cattle

A

Acute Respiratory Distress Syndrome (ARDS)
sudden onset, severe dyspnea associated with gross and histological findings of AIP
Oxygenation of arterial blood to fraction of oxygen in inspired air (PaO2/FiO2) is <400
Indicates poor oxygen echange (intersitial edema)
Severe diseases fit into the AIP or ARDS category
-Acute Bovine Pulmonary edema and emphysema (fog fever)
-moldy sweet potato
-perilla mint
-feedlot AIP
-other toxic plants, gases

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92
Q

Acute Respiratory Distress Syndrome (ARDS) in cattle

A

sudden onset, severe dyspnea associated with gross and histological findings of AIP
Oxygenation of arterial blood to fraction of oxygen in inspired air (PaO2/FiO2) is <400
Indicates poor oxygen echange (intersitial edema)
Severe diseases fit into the AIP or ARDS category
-Acute Bovine Pulmonary edema and emphysema (fog fever)
-moldy sweet potato
-perilla mint
-feedlot AIP
-other toxic plants, gases

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93
Q

What causes Acute Bovine Pulmonary Edema and Emphysema (ABPEE)

A

Fog fever- lush grass that is high in L-tryptophan
Rumen converts to 3-methyllindole (3-MI)
3-MI is absorbed and circulated (pneumotoxic)- causes AIP

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94
Q

What are the clinical signs of Fog fever *

A

Develop within 2 weeks of pasture change
-tachypnea, dyspnea, frothing at mouth

*NO coughing
mortality up to 30%

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95
Q

What produces 4-Ipomeanol

A

Fusarium solani
1) Ingestion of sweet potatoes infected with Fusarium solani (sweet potatoes are used as an energy source in beed cattle diets (palatable)
2) F. solani produces 4-ipomeanol which is a pneumotoxin
3) Develops AIP/ ARDS

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96
Q

What is the toxicity of Moldy Sweet Potato toxicity in cattle

A

Fusarium solani
1) Ingestion of sweet potatoes infected with Fusarium solani (sweet potatoes are used as an energy source in beed cattle diets (palatable)
2) F. solani produces 4-ipomeanol which is a pneumotoxin
3) Develops AIP/ ARDS

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97
Q

What are the clinical signs of Moldy Sweet potato toxicty (4-Ipomeanol)

A

Occur within 1 day of exposure
-tachypnea, dyspnea, expiratory grunt, coughing*, harshlung sounds
death 2-5 days after ingestion (high mortality)

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98
Q

T/F: Coughing is seen with 4-Ipomeanol toxicity *

A

True

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99
Q

T/F: Coughing is seen with 3-methylindole toxicity *

A

False

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100
Q

What are the causes of pharyngeal trauma and abscess in cattle

A

Causes: Trauma, Iatrogenic, Sharp Feed

Bacteria:
Trueperella pyogenes *
F. necrophorum *
Actinobacillus
Pasteurella
Strep
E Coli

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101
Q

What are the clinical signs of pharyngeal trauma and abscess in cattle

A

Stertor, stridor
respiratory distress
salivation, quidding, dysphagia
Nasal discharge, oful odor
pharyngeal swelling
+/- bloat
+/- systemic signs

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102
Q

How do you diagnose pharyngeal trauma and abscess

A

-Signs
-Oral exam under sedation (Xylazine, ket-stun)
-Endoscopy
-Radiographs
-U/S
-Needle Aspiration- if abscess submit for cytology and culture

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103
Q

How do you treat pharyngeal trauma and abscess in cattle

A

1) If there is an abscess then will want to drain and lavage - if deep make sure you dont go into jugular, carotid, or vagosympathetic trunk
*Drain with needle
2) Antibiotics- PPG
3) Anti-inflammatory agents
4) +/- tracheotomy - if severe
5) +/- rumenotomy - if rumen bloat is so severe

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104
Q

a very common disease of calves that is a necrotic inflammatory process of the larynx

A

Necrotic Laryngitis/ Laryngeal Necrobacillosis/
Calf Diphtheria

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105
Q

What is the pathogenesis of necrotic laryngitis

A

Start by different factors
1) Viral upper respiratory infection- all the viruses discussed for viral rhinitis
2) Primary bacterial- F. necrophorum and T. pyogenes are associated (also M. haemolytica, Pasteurella and other respiratory)
3) Trauma/irritation from medication admin, feed, feeding too hot of mil

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106
Q

What are the clinical signs of necrotic laryngitis

A

-Excessive salivation (wet chin)
-Moist painful cough
-Fetid odor
-Inappetance (painful to swallow)
-Stertor/ Stridor
-Respiratory distress
-Swollen larynx

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107
Q

What are differentials for necrotic laryngitis

A

Trauma
IBR
Haemophuilus
Oral abscess
Pharyngeal paralysis
Tumor

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108
Q

How do you treat Necrotic Laryngitis *

A

antimicrobials (penicillin, sulfa)
anti-inflammatory drugs (IV flunixin meglumine and then switch to oral meloxicam)
supportive care
+/- tracheotomy

use a low. stress weaning
prevention: vaccination protocol and prevent trauma

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109
Q

What antibiotics work well fornecrotic laryngitis

A

Penicillin works well for necrotic laryngitis (but the downside is that it is a large volume injected and must be given twice a day)
Sulfa antimicrobials also work well for this.
Oxytetracycline works okay and NuFlor can also be used

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110
Q

Where are laryngeal abscesses commonly located on

A

arytenoid cartilage(s)

trueperella pyogenes is most commonly

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111
Q

What is the most common bacterial cause of laryngeal abscesses in cattle

A

Trueperella pyogenes

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112
Q

What might cause a cause a lesion that looks like laryngeal abscess in cattle

A

congenital lesions of arytenoids

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113
Q

How do you treat laryngeal abscesses in cattle

A

1) Long term antibiotics
2) option for surgical therapy would be to do an arytenoidectomy or other airway surgery

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114
Q

laryngeal papillomatosis in cattle

A

Warts on the larynx due to Bovine Papilloma Virus (type 4)
Feedlot
Clinical Signs- respiratory distress, stertor, cough
Diagnosis- oral exam, endoscopy
Treatment- vaccination and surgery
Diagnosis- oral exam and endoscopy

treatment: vaccination and surgery

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115
Q

How do you treat laryngeal papillomatosis

A

generally these warts will resolve on their own, but they can cause problems for temporary period.
vaccine might help increase rate of resoliton but need two doses 3 weeks apart

Do surgery to debulk the wart

Can give NSAIDS and may consider antimicrobial if there is evidence of necrosis to reduce the risk of secondary bacterial infection

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116
Q

What causes red nose

A

Infectious Bovine Rhinotracheitis (IBR)

BHV-1

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117
Q

Infectious Bovine Rhinotracheitis

A

IBR (Rednose)
caused by BHV-1
Multiple clinical syndromes (upper respiratory, lower respiratory, reproductive, and possibly neurologic)

Diagnosis- nasal/nasopharyngeal swab (PCR or VI)

Treatment: anti-inflammatory and antimicrobial for secondary bacterial infection

Prevention: vaccination

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118
Q

How do you diagnose IBR

A

do a nasal or nasopharyngeal swab and submit it for PCR or virus isolation

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119
Q

What are the clinical signs of tracheal collapse in cattle

A

-Stridor- often loudest at the thoracic inlet (level of tracheal collapse)
-Cough
-Exercise intolerance
-Respiratory distress

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120
Q

How do cattle get tracheal collapse

A

-Commonly acquired at birth due to trauma
a) dystocia results in rib fracture (1st and 2nd) at the level of the tracheal inlet. Healing callus will put pressure on the trachea resulting in extraluminal tracheal collapse/ compression - Static collapse with both inspiratory or expiratory stridor

b) Congenital tracheal collapse but this is quite rare (more common in calves)

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121
Q

How might dystocia result in tracheal collapse in cattle

A

dystocia results in rib fracture (1st and 2nd) at the level of the tracheal inlet. Healing callus will put pressure on the trachea resulting in extraluminal tracheal collapse/ compression - Static collapse with both inspiratory or expiratory stridor

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122
Q

Dystocia results in_________ (static or dynamic) tracheal collapse

A

Static tracheal collapse

dystocia results in rib fracture (1st and 2nd) at the level of the tracheal inlet. Healing callus will put pressure on the trachea resulting in extraluminal tracheal collapse/ compression - Static collapse with both inspiratory or expiratory stridor

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123
Q

What does static tracheal collapse mean

A

it is staying collapsed regardless of inspiration/ exhalation

example: rib fracture with dystocia/ traumatic birth

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124
Q

How do you diagnose tracheal collapse in cattle

A

Radiographs- dorsoventral collapse

Endoscopy

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125
Q

How do you treat tracheal collapse in cattle

A

Surgical- prostehtic extraluminally around the trachea and suture the trachea to this device and pull the trachea open- not done very commonly, varied success with this surgical treatment

Conservative Medical Therapy- NSAIDs, rest, antibiotics

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126
Q

What is the prognosis of tracheal collapse in cattle

A

good if they can breathe well enough to allow fractures to heal and the animal to grow

go more conservative medical care

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127
Q

Tracheal Edema Syndrome (Acute Honker Syndrome)

A

Acute Honker Syndrome
Southern feedlots

inflammatory condition of the upper airways that results in edema and collapse of airways. believed to be caused by either irritants or allergens in sensitized animals

results in obstructive breathing pattern with a long, slow, and deep inhalation

Clinical signs: Sudden onset of respiratory distress
Stertor, stridor

Differentials: all other causes of partial obstruction

TreatmentL antimicrobial, steroids, +/- tracheostomy

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128
Q

Where is acute honker syndrome typically

A

southern feedlots

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129
Q

What are the clinical signs of tracheal edema (honker) syndrome in cattle

A

Sudden (acute) onset of respiratory distress
Stertor, stridor

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130
Q

inflammatory condition of the upper airways that results in edema and collapse of airways. believed to be caused by either irritants or allergens in sensitized animals
occurs in southern feedlots

A

a Tracheal Edema Syndrome -
Acute Honker Syndrome

treat with antimicrobials, steroids, +/- tracheostomy

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131
Q

What happens when a cow with tracheal edema syndrome (acute honker syndrome) attempts to inhale

A

the tracheal tissue is pulled further into the lumen and the trachea collapses down

these animals have an obstructive breathing pattern with a long, slow, deep inhalation

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132
Q

How do you treat tracheal edema syndrome (Acute Honker) in cattle

A

Generally NSAIDs dont really work well

Treat with corticosteroids, often start with injectable dexamethasone and then oral prednisolone

if there is an inflammatory component to it or suspicions of bacterial infection, then use antimicrobials

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133
Q

What is Chronic Polupoid Tracheitis

A

A tracheal edema syndrome that occurs at Western Feedlots

Clinical signs are continuous dry, hacking nonproductive cough

Differentials: pneumonia

Diagnosis: history, clinical signs, endoscopy

Treatment: none

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134
Q

Where is chronic polypoid tracheitis

A

Western Feedlots

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135
Q

What are the two tracheal edema syndromes of cattle

A

1) Acute Honker Syndrome- Southern feedlots and present with sudden onset of respiratory distress, stertor, stridor Treat with Corticosteroids (dexamethasone and then pred)

2) Chronic Polypoid Tracheitis- Western Feedlots, rpesent with continuous dry hacking nonproductive cough and have no treatment

136
Q

What is the treatment for Chronic Polypoid tracheitis in cattle

A

there is not a lot to do for these cases

137
Q

How does colonization resistance occur

A

1) Direct microbe-microbe inhibition
2) Indirect stimulated host immunity

Host epithelium also maintains mucociliary apparatus

138
Q

What is the pathogenesis of BRD

A

Multifactorial

1) Central dogma: immunocompromised host risk factors -> virus causes directi njury to mucociliary apparatus, tracheal epithelium, immunosuppression where the upper respiratory tract commensal overgrow leading in nasopharyngeal bacteria to invade lower airways

2) Expanded to have immunocompromised host, environment, risk factors and viral infection leads to a dysbiosis between URT and LRT

Pathobionts dominate the niche leading to pathogenic behavior expression of virulence factors: leuktoxin, endotoxin

139
Q

pathobionts

A

commensal / mutualistic behavior colonization resistance
where there is dysbiosis of URT and LRT leading to pathogenic behavior

140
Q

What are the risk factors for BRD

A

*Complex
-Reduce host immunity (FPI and stress)
-Genetics, sex
-Viral infection
-Group housing
-Poor airquality
-Dehydration
-Weaning
-Weather
-Transport
-Cominging
-Nutritional deficiencies
-Surgical procedures

141
Q

What is the BRD epidemiology in the dairy industry

A

Preweaned calves (<56 days of age) endemic (up to 30% in most herds)
differentiate between aspiration vs BRD

Weaned calves (most common 2-5 months)
enzootic calf pneumonia
viral exposure, stress (mixing groups)

Replacement heifers and cows: more commonly sporadic, metastatic

142
Q

What is enzootic calf pneumonia

A

BRD in calfs after being weaned (most common 2-5 months)
due to viral exposure, stress (mixing of groups)

143
Q

What is the BRD epidemiology of beef cattle

A

1) Cow-calf: up to 10% pre=weaned calves (3-5 months)
nadir of IgG, short calving interval leads to herd immunity low

2) Weaned Calves (shipping fever) transport from farm of origin to stocker/feedlot. Highest morbidity during 1st 21 days after arrival

3) Finishers (Feedlot) Cows: Sporadic outbreaks, interstitial pneumonia
route out high altitidue pulmonary hypertension

144
Q

When is the highest morbidity of BRD in weaned calves

A

during the 1st 21 days after arrival

“Shipping fever”

145
Q

BRD in older animals (finishers in beef and replacement heifers/cows in dairy) is often

A

sporadic outbreaks

146
Q

What is the epidemiology of cow-calf beef BRD

A

up to 10% pre-weaned calves (3-5 months)
nadir of IgG
short calving interval leading to low herd immunity

147
Q

What does the pathophysiology of BRD in the lungs depend on

A

dominant pathobiont and/or infectious agent and passive transfer status (IgG)

innate immune system is stimulated through pattern recognition receptors (PRRs)- toll like receptors, neutrohphils, and alveolar macrophages

pro-inflammatory cascade- increases oxidative host damage

secondary invaders, opportunists- consolidation of airways, pulmonary abscess, pleuropneumonia

148
Q

Mannheimia hemolytica

A

Gram -, Aerobic Rod
Normal nasopharyngeal inhabitant
Dysbiosis allows for niche takeover by pathogenic serovars (A1, A6) and viral co-infection increases severity

Virulence factors: leukotoxin: cytolysis of ruminant leukocytes
endotoxin/LPS: pro-inflammatory (neutrophil chemostaxis)

causes lobar pneumonia leading to necrotizing fibrinous pleuropneumonia

peracute rapidly consolidating syndrome

emerging antibiotic resistance of field strains

149
Q

What are the virulence factors of Mannheimia hemolytica

A

Virulence factors:

1) leukotoxin: cytolysis of ruminant leukocytes

2) endotoxin/LPS: pro-inflammatory (neutrophil chemostaxis)- generates oxidative damage

150
Q

What organism is commonly associated with shipping fever

A

Mannheimia hemolytica

151
Q

What are the pathogenic serovars of Mannheimia

A

A1 and A6

152
Q

Mannheimia hemolytica causes ______________

A

necrotizing lobar fibrinous pleuropneumona

153
Q

Pasteurella multocida (cattle)

A

Gram -, aerobic coccobacilli. Normal nasopharyngeal inhabitant (A 3 most commonly pathogenic)
Opportunistic
virulence factors:
1) Endotoxin (can lead to systemic endotoxemia/bacteremia)

Pathology: purulent lobar bronchopneumonia, less likely fibrin and necrosis
often dark red cranioventral lung consildation

154
Q

T/F: unless there is a co-infection Pasteurella is not as severe in cattle as Mannheimia

A

True

155
Q

What pathology does Pasteurella cause in cattle

A

purulent lobar bronchopneumonia, less likely fibrin and necrosis
often dark red cranioventral lung consildation

156
Q

What bug is associated with endemic disease in groups of housed calves “enzootic pneumonia”

A

Pasteurella multocida

157
Q

Bibersteinia trehalosi (cattle)

A

Gram - aerobe
Normal nasopharyngeal inhabitant (pathobiont)
occasional opportunist in the lungs
Similar to Mannheimia hemolytica as it causes sporadic outbreaks in feedlots

Presentation: outbreaks with high mirtality, may lack clinical signs and lead to sudden death

158
Q

Histophilus somni (cattle)

A

Gram -, aerobic rod or coccobaccilus
normal nasopharyngeal inhabitant that is and opportunisit in the lung and extrapulmonary sites*

Virulence Factors (dictate systemic severity)
1) LOS: induce inflammatory cascade causing apoptosis of endothelial cells (vasculitis/ thrombosis) and induce IgE, histamine (hypersensitivity leading to increased permeability of bronchial epithelium)
2) Evasion of opsonization (outer membrane protein)

159
Q

**Know this: Histophilus somni is an opportunist. of the lung and ___________

A

extrapulmonary sites

160
Q

What are the virulence factors of Histophilus somni

A

opportunisit in the lung and extrapulmonary sites*

Virulence Factors (dictate systemic severity)
1) LOS: induce inflammatory cascade causing apoptosis of endothelial cells (vasculitis/ thrombosis) and induce IgE, histamine (hypersensitivity leading to increased permeability of bronchial epithelium)
2) Evasion of opsonization (outer membrane protein)

161
Q

What are the extrapulmonary signs of Histophilus somni **

A

1) sepsis
2) thrombotic meningoencephalitis
3) Otitis
4) Mastitis
5) Polyarthritis
6) Myocarditis
7) Abortion
8) Endometritis
*important pathology includes vascultis and thrombi

162
Q

What pathology does Histophilus cause *

A

Bronchopneumonia (common in feedlots_

Extrapulmonary sites:
1) sepsis
2) thrombotic meningoencephalitis
3) Otitis
4) Mastitis
5) Polyarthritis
6) Myocarditis
7) Abortion
8) Endometritis
*important pathology includes vascultis and thrombi

163
Q

What BRD bacteria has extrapulmonary sites

A

Histophilus somni

164
Q

What is the significance of treating BRD infections with Mycoplasma bovis *

A

It is a facultative anaerobe with no cell wall. Will not respond to antibiotics that target cell wall

165
Q

Mycoplasma bovis/ dispar (cattle)

A

No cell wall, facultative anerobe (wont respond to antibiotics that target the cell wall)
Primary pathogen or opportunist at pulmonary and extrapulmonary sites

Virulence factors
1) Vsp A, B, C for immune evasion
2) Adhesins associated with virulence - to adhere to synovium or inner ear to persist longer times

Pathology: fibrinosuppurative or caseonecrotic pneumonia, peribronchial lymphoid hyperplasia
-cranioventral nodules that contain abscesses of coagulation necrosis
-“cuffing pneumonia: lymphoid hyperplasia around the airways

166
Q

What pathology is seen with Mycoplasma bovis

A

fibrinosuppurative or caseonecrotic pneumonia, peribronchial lymphoid hyperplasia
-cranioventral nodules that contain abscesses of coagulation necrosis
-cuffing pneumonia: lymphoid hyperplasia around the airways

167
Q

What are the virulence factors of Mycoplasma bovis

A

1) Vsp A, B, C for immune evasion
2) Adhesins associated with virulence - to adhere to synovium or inner ear to persist longer times

168
Q

What pathogen should be high on your differential list if you cut through the bovine lung and see a lot of abscesses/ foci of coagulation necrosis

A

Mycoplasma bovis

169
Q

What are the clinical signs of Mycoplasma bovis

A

Pneumonia
Otitis (preweaned calves)
Arthritis
Tenosynovitis (weaned calves)

other signs: mastitis, conjunctivits, myocarditis, pericarditis, abortion

Important transmission route: milk and colostrum

170
Q

What is an important transmission route of Mycoplasma bovis? *

A

Milk and colostrum

171
Q

Trueperella pyogenes

A

gram + anaerobic coccobacillus
opportunistic pathogen
secondary or tertiary invader (co-infection is common)

Indicator of chronicity is pulmonary abscess

Virulence factor: Pyolysin: cytolytic toxin that aids in adherence

172
Q

What bacteria of BRD is gram +

A

Trueperella pyogenes

173
Q

T/F: Trueperella causes acute cases of BRD

A

False- it is often a secodnary or tertiary invader (co-infection is common)

174
Q

What bacteria are associated with the BRD complex

A

1) Mannheimia hemolytica
2) Bibersteinia trehalosi
3) Pasteurella multocida
4) Trueperella pyogenes
5) Histophilus somni
6) Mycoplasma bovis

175
Q

What is the pathogenesis of BHV-1 causing bronchopneumonia

A

1) Direct contact/ aerosol
2) Surface glycoproteins allow for host attachment and cause direct injury to epithelial cells and immunosuppresion (decrease MHC 1 expression)
3) facilitates binidng of leukotoxin (Mannheimia hemolytica)
4) Latency related transcript allows for survival of infected cells beyond message of apoptosis and latency is important for spread (recurdescence from ganglia)

176
Q

BHV-1 causes direct immunosuppression by __________ which allows ____________

A

decrease MHC class 1 expression

facilitates binding of leukotoxin (Mannheimia hemolytica)

177
Q

What bacteria is associated with viral infection of BHV-1

A

Mannheimia hemolytica

178
Q

What is the prognosis of BHV-1 primary respiratory disease

A

HIgh morbidity- common in feedlots of weaned steers

low mortality unless co-infection (Mannheimia hemolytica)

179
Q

What is the pathogenesis of Bovine Respiratory Syncytial Virus (BRSV)

A

1) Direct contact, aerosl
2) G glycoprotein induces attachment
3) Epithelial cells fuse forming multinucleated cells, syncytia
4) Suppress function of macrophages
5) Develop atypical interstitial pneumonia (emphysema, bullae)

180
Q

What does BRSV cause

A

it causes epithelial cells to fuse (multinucleated cells, synctia)

causes an atypical interstitial pneumonia

181
Q

What is the virulence associated with BRSV *

A

BRSV-specific IgE (mast cell degranulation and eosinophil influx) - vaccine induced disease?

Lymph node infection (tracheobronchial, mediastinal) may allow for persistance

182
Q

Why might a herd with BRSV have reaction to vaccination

A

BRSV-specific IgE (mast cell degranulation and eosinophil influx) - vaccine induced disease?

183
Q

BRSV most commonly infects

A

Calves <6months of age

presentation often acute and confined to respiratory tract

184
Q

How do cows with BRSV typically present

A

Calves <6months of age
presentation often acute and confined to respiratory tract
Peracute presentation (severe dyspnea)
-Hypersensitivity (immune mediated)
-Pneumothorax (ruptured bullae)

185
Q

What is the pathogenesis of Parainfluenza Virus Type 3 (PI-3) in cattle

A

1) direct ocntact, aerosol
2) Direct injury to ciliated epithelial cells, mucus layer, mucociliary apparatus
3) Infection of alveolar macrophages (decreased finction)

Causes immunosupression that predisposes to secondary invader

186
Q

PI-3 in cattle causes

A

immunosupression that predisposes to secondary invader

via infecting epithelial cells, mucus layer and mucociliary apparatus
infect the alveolar macrophage and decrease function

*Disease is often mild/subclinical unless secondary bacterial infection

187
Q

How does BVDV affect the respiratory tract

A

impairs host immunity and associated with outbreaks of BRD
coinfections with Mannheum, Mycoplasma bocis, and BRSV

188
Q

What a viruses that are associated with BRD

A

1) BHV-1 *
2) BRSB *
3) PI-3 *
4) BVDV
5) Bovine coronavirus
6) Influenza D
7) Bovine Reovirus
8) Bovine Rhinovirus
9) Adenovirus

189
Q

How do you prevent BRD

A

1) Colostrum management (quality and quantity) *
2) Ventilation (group housing), shelter (weather protection)
3) Nutrition (volume and quality)
4) Transport management (water access)
5) Reduce stress and reduce mixing in vulnerable age groups **
6) Herd surveillance, Treatment approach *
7) Vaccination, Herd immunity

190
Q

What is important regarding the vaccination timing of cattle for BRD prevention

A

MLV vaccine may have lower evidence

-Stress is immunosuppressive and leads to poor vaccianre response
-Maternal inference is no no
-Preconditioning: administration of vaccine prior to weaning
-Any vacine given at arrival period leads to a suboptimal response

191
Q

What are the two major risk factors in dairy and beef that contribute to BRD

A

1) Inadequate colostrum
2) Host immunity are major factors

192
Q

What MLV vaccine has the most evidence for reducing BRD i nweaned beef cattle *

A

BVDB- superior to killed vaccines

193
Q

What signalment and history best describes cattle at high risk for BRD?

A) 8 month Angus steer on a feedlot that arrived 6 weeks ago
B) 21 day old Holstein Heifer calf housed indoors within group pens
C) 2yo Holstein first lactation heifer that freshened 10 days ago
D) 6month old Hereford steer that was weaned 5 days ago
E) both B and D
F) Both A and D
G) All of the above

A

Both B and D

A) Feedlot is a risk but 6 weeks is beyond the time where BRD is typically developed (within the first 3 weeks of arriving)

B) is correct because 3 weeks is within the early pre-weaned range and also in a group pen which increases

C) Stress from first lactation but outside the common range- would have been more

D) Is correct because of weaning

194
Q

A gram positve associated with BRD, commonly a secondary or tertiary invader
has pyolysin *

A

Trueperella pyogenes

195
Q

A gram negative associated with BRD
has leukotoxin* and endotoxin
associated with viral co-infections
and causes shipping fever

A

Mannheimia hemolytica (A1 and A6)

196
Q

A gram negative associated with BRD, has endotoxin and causes enzootic calf pneumonia

A

Pasterella multocida (A3)

197
Q

What strain of Pasteurella is pathogenic in cattle

A

A3

198
Q

A gram negative associated with sporadic feedlot outbreaks

A

Bibersteinia trehalosi

199
Q

A gram negative that is associated with BRD
has LOS, IgE and causes apoptosis of endothelial cells leading to vasculitis and extrapulmonary disease

A

Histophilus somni

200
Q

What are challenges with diagnosing BRS

A

-Imprecise case definitions- interpreting sequencing data requires an accurate phenotype
-thoracic auscultation may be sensitize
-Anatomic localization (URT and LRT)
-Clinical vs subclinical- does subclinical warrant treatment (judicious use of antimicrobials)

201
Q

What is DART

A

A herd surveillance technique used in cattle for BRD
-Depression
-Appetite Loss
-Respiratroy character change
-Temperature elevation

Low sensitivity (higher risk of false negative)
High specificity

202
Q

How do you detect pathogens associated with BRD

A

-Nasal swabs (least ideal for bacteria)

Deep nasopharyngeal swabs - are better for bacteria but still challenging to interpret because it is polymicrobial

-Transtracheal wash/ aspirate - not as practical for cattle

-Bronchoalveolar lavage fluid (non-endoscopic is typically used or endoscopic)

203
Q

Deep Nasopharyngeal Swabs used for BRD

A

captures respiratory and associated lymphoid epithelium of nasopharynx

High risk for contamination- double guarded and cleaned nares to reduce this

Aerobic culute: often polymicrobial and challenging to determine antibioitc plan

Mycoplasma is good at getting a single positive for culture

young calves and small ruminants, placement in ventral nasal meatus is challenging

204
Q

When is lower airway sampling (Transtracheal wash and BALF) contraindicated in livestock *

A

If the animals a dyspneic

205
Q

What are potential complications of doing transtracheal wash or BALF in livestock

A

Subcutaneous emphysema
Wound infection
Tracheal tear
Dyspnea (inadequate fluid return)

206
Q

What is important when doing sample analysis of BRD pertaining to Mycoplasma bovis

A

It needs to be cultured in very specific condition

PCR is more sensitive

207
Q

A 3 week old pre-weaned dairy calf with a cough reduced milk consumption and a head tilit. On lung ultrasound you find lobar consolidation. The producer is concerned about BRD in their calves and would like you to definitively diagnose a pathogen to determine an optimal treatment protocol

A) Nasal swab: submit for Mycoplasma culture and mutiplex viral PCR
B) Deep nasopharyngeal swab: submit for Mycoplasma PCR
C) Bronchoalveolar lavage fluidL submit for aerobic culture and anaerobic culture
D) Deep nasopharyngeal swab: submit for aerobic culture, anaerobic culture and multiplex viral PCR

A

B) Deep nasopharyngeal swab: submit for Mycoplasma PCR

nasal swab is not good

multiplex viral PCR wont tell you

given dairy signalment likely mycoplasma is playing a role.
needs to be specific culture or PCR

some evidence BRD but some extrapulmonary disease evidence

208
Q

What should you treat Mycoplasma bovis with **

A

Macrolides, florfenicol, tetracyclines labeled

-NO cell wall (beta lactams are ineffective)

209
Q

What increases the clinical severity of BRD

A

Co-infection of viral and bacterial agents
ie. BHV-1 and Mannheimia hemolyticum

210
Q

What best approximates lung bacterial overgrowth in cattle

A

Nasopharyngeal and lower airway sampling

211
Q

What is important transmssion route of Mycoplasma bovis *

A

milk and colostrum

clinical signs: pneumonia, otitis (preweaned calves), arthritis, tenosynovitis

212
Q

When do outbreaks of bronchopneumonia occur in small ruminants

A

SPring: lambs 2 weeks to 2 months of age- severe weather

Fall outbreaks- lambs, 5-7 months with the arrival at feedlots

213
Q

What is the pathogenesis of bronchopneumonia in small ruminants

A

Stress diminishes lung’s natural defense mechanism leading to enhances in viral infections, dysbiosis of respiratory microbiome\

common stressors: FPI, transport, overcrowding, parasitism, social changes, poor nutrition, weather, diet change, dust and mold exposure

214
Q

Clinical signs of small ruminants with bronchopneumonia

A

-Separation from herd
-lethargy
-exericse intolerance
-inappetance
-Increased respiratory rate or effort
-cough
-poor body condition

physical exam findings: acute respiratory disease- fever, tacypnea, nasal +/- ocular discharge
chronic or progressive: weight loss, cough, tachypnea

215
Q

What are the most common respiratory bacterial pathogens in small ruminants

A

1) Mannheimia hemolytica (A2) - different strain from cattle, coinfections (bacterial, viral)

2) Pasteurella (D,F): pneumonia, sepsis, arthritis, otitis, mastitis, with coifnections (bacterial, viral)

3) Bubersteinia trehalosi - more common in sheep

4) Corynebacterium pseudotuberculosis- caseous lymphadenitis (chronic abscess)- internal/ visceral and external form

5) Mycoplasma spp
M. ovipneumonia (sheep) causes enzootic/atypical pneumonia
M mycoides and capricolum (high morbidity, low mortality, coinfections inccreases mortality, extrapulmonary disease (arthritis, mastitis, septicemia)

216
Q

How do you treat sheep and goat bronchopneumonia

A

Antimicrobial
-Ceftiofur sodium* or others
-NSAID
-Nursing care

Contro: vaccination- sheep and goats up to 6 months of age, improves management practices, limit stress, provide high quality diet, quarantine new arrivals, isolate isck animals

217
Q

What is the only FDA approved drug for treating pneumonia in goat

A

Ceftiofur sodium

218
Q

What causes pigeon fever in horses

A

Corynebacterium pseudotuberculosis

219
Q

chronic disease of sheep and goats (rarely in camelids)- no cure
pyogranulomatous abscesses in lymph nodes and internal organs
highly contagious
resistant in environment
zoonotic- consuming infected, unpasteurized milk, contaminated equipment, infected pus in abdrasions

A

Caseous lmyphadentis
(Corynebacterium pseudotuberculosis)

220
Q

What are common sites for caseous lymphadenitis

A

Lymph nodes:
mandibular
parotid
prescapular
preforma

221
Q

What species does caseous lymphadenitis infect

A

sheep and goats (rarely in cameids)

222
Q

How do you diagnose caseous lymphadenitis

A

Culture

223
Q

How do you control for caseous lymphadenitis in small ruminants

A

biosecurity is key- purchase animals from known negative herds and flocks, prevent spread on fomites like shearing equipement

testi incoming animals- know limitx of test and possibility of negative SHI test

Vaccination: may help reduce incidence in herd and # abscesses per animals

Treatment: surgical removal of infected LNs, lance and drain, cull known + animals

224
Q

What are the treatments for caseous lymphadenitis

A

surgical removal of infected LNs, lance and drain, cull known + animals

225
Q

what are causes of viral pneumonia in small ruminants

A

Secondary Risk factor
Parainfleunza Type 3
Adenovirus
Respiratoy Syncytila Virus
Herpes virus

Major viral pathogens: lentiviurses
-Ovine progressive pneumonia (OPP)/ Maedi-Visna
-Ovine Pulmonary adenocarcinoma/ jaagsiekte
-Caprine Arthritis Encephalitis Virus (CAEV)

226
Q

What are major viral pathogens causing direct pulmonary disease in small ruminants

A

Lentiviruses
1) Ovine progressive pneumonia (OPP)/ Maedi-Visna
2) Ovine Pulmonary adenocarcinoma/ jaagsiekte
3) Caprine Arthritis Encephalitis Virus (CAEV)

*Lentiviruses so they have persistent infections

227
Q

infects goats and sheep
progressive, debilitating disease with no treatment
horizontal and perinatal spread (colostrum and milk)
World wide distribution
High seroprevalence within the US

A

Caprine Arthritis Encephalitis Virus (CAEV)

228
Q

Caprine Arthritis Encephalitis Virus (CAEV) causes

A

-Leukoencephalomyelitis (neonates)
-Arthritis (carpal joints)
-Mastitis
-Chronic pneumonia: interstitial pathogenesis (type II pneumocyte proliferation)
-Chronic encephalomyeltiis

229
Q

How do you diagnose CAEV

A

-Screening: lung ultrasound/ CXR
-ELISA: blood and milk
-PCR: BALF/Lung, blood, synovial fluid/ tissue, brain

230
Q

T/F: caseous lymphadenitis is highly contagious and zoonotic

A

True

Zoonotic- consuming infected, unpasteurized milk, contaminated equipment, infected pus in abrasions

231
Q

External form of caseous lymphadenitis

A

more common in goats
external lymph nodes commonly on neck and throat

Signs: swelling associated with lymph nodes

Diagnosis: Culture

Be careful as the pus is loaded with bacteria and highly contagious

232
Q

What is the visceral or internal form of caseous lymphadenitis

A

-More common in sheep
mediastinal and mesenteric lymph nodes, lungs, liver, kidney, CNS

Clinical signs: progressie weight loss, exercise intolerance, tachypnea, dyspnea, chronic cough

233
Q

What form of caseous lymphadenitis is more common in sheep

A

Visceral or internal form

mediastinal and mesenteric lymph nodes, lungs, liver, kidney, CNS

Clinical signs: progressie weight loss, exercise intolerance, tachypnea, dyspnea, chronic cough

234
Q

What form of caseous lymphadenitis is more common in goats

A

External form

external lymph nodes commonly on neck and throat

Signs: swelling associated with lymph nodes

Diagnosis: Culture

Be careful as the pus is loaded with bacteria and highly contagious

*Culture pus

235
Q

How do you do diagnostics for CL

A

External form: Culture pus

Visceral form: Radiograph thorax for abscess + cultue/PCR TTW fluid- failure to isolate CL from TTA fluid does NOT rule out CL

Asymptomatic animals: Do a synergistic hemolysis inhibition (SHI test)
False negatives are possible, a low titer does NOT rule out disease
theoretically, lower tier = exposure vs higher titer= infection

236
Q

When do you perform Syngeristic hemolysis inhibition (SHI test)

A

Asymptomatic animals with CL

False negatives are possible, a low titer does NOT rule out disease
theoretically, lower tier = exposure vs higher titer= infection

237
Q

What are the downsides to doing Syngeristic hemolysis inhibition (SHI test) for CL

A

False negatives are possible, a low titer does NOT rule out disease
theoretically, lower tier = exposure vs higher titer= infection

238
Q

How do you control for CAEV

A

1) Prevent infection in neonates
-Separate newborns from dams
-Feed only virus free colostrum and milk

2) Prevent horizontal spread- test regularly and cull positive animaals

3) Prevent introduction to the herd
-Isolate and test all newly purchased animal
-SR lentivirus or SR biosecurity panel

239
Q

How is CAEV spread?

A

Horizontal and perinatal spread (colostrum and milk)

240
Q

What causes ovine progressive pneumonia (OPP)

A

Maedi-Visna Virus

241
Q

How is OPP spread

A

Horizontal and perinatal spread (colostrum and milk)

242
Q

Ovine Progressive Pneumonia (OPP)

A

Maedi-Visna Virus
Infects sheep primarily horizontal and perinatal spread- colostrum and milk
Cross species transmission to goats is possible via infected milk and colostrum

25-30% of infected animals will exhibit clinical signs (4-5 years)

Clinical signs: interstitial pneumonia, wasting, mastitis, arthritis, neurological signs

243
Q

T/F: Transmission of ovine progressive pneumonia can be spread to goats

A

True-
Cross species transmission to goats is possible via infected milk and colostrum

244
Q

What are the clinical signs of Ovine Progressive Pneumonia

A

Rapid progression over 1 year

interstitial pneumonia, wasting, mastitis, arthritis, neurological signs

245
Q

How do you diagnose OPP

A

Screening: Lung ultrasound/ CXR

ELISA: Seroconversion may take weeks to 1 year, maternal antibodies may interfere, low-cost screening on milk

PCR: Milk, BALF, lymph node

246
Q

HOw do you treat/ control OPP

A

no treatment
-most animals die within 1 year of signs

No vaccine available

difficult to eradicate once in herd- test and cull is expensive and impractical

prevention is best- strict biosecurity: isolation and testing, dont share rams, segregate animals at shows, purchase animals from known OPP-free flocks

247
Q

What causes OVine Pulmonary Adenocarcinoma

A

Jaagsiekte Sheep Retrovirus (JSRV) or Pulmonary Adenomatosis Virus

248
Q

How is Ovine Pulmonary Adenocarcinoma Spread *

A

Via respiratory ecretions (ie Nasal secretion)

also shed in milk and colostrum but vertical transmission is unlikely

249
Q

How do you treat ovine pulmonary adenocarcinoma

A

no effective diagnostic for subclinical
no vaccination
no treatment

*May cause fatal neoplasia (1-5%)

250
Q

What animals are suscpetible to JSRV

A

young lambs

tumors develop over months to years

and cause progressive emaciation, respiratory compromise when lead is lowered (Wheelbarrow test)

251
Q

pleuritis and pleural effusions in camelids can be secondary to

A

Overhydration

252
Q

What might cause pleuritis and pleural effusion in livestock

A

1) Bronchopneumonia (Histophilus, Manheimia) *
2) Traumatic reticulopleuritis
3) Camelid Strep zoo. (Alpaca fever)
4) Neoplasia
5) Pulmonary hypertension *
6) Overhydration in camelids

253
Q

T/F: pleuritis and pleural effusions is painful

A

True

254
Q

What are clinical signs of pleuritis and pleural effusions in cattle

A

-Signs of pneumonia
-Thoracic pain: reluctance to move, abducted elbows, grunting, groaning, bruxism, decreased chest excursion, abdominal breathing
-Decreased ventral breath sounds- fluid line
-Ventral dullness on thoracic percussion
-Friction rubs

255
Q

What test hsould you do to confirm a cow is painful do to pleural effusion and pleuritis

A

Withers test

256
Q

How do you diagnose pleuritis and pleural effusions in cattle *

A

Ultrasound- pleural effusion +/- lung consolidation

Radiographs

Thoracocentesis with cytology +/- culture

CBC/CP: left shift with hypergammaglobulinemia

257
Q

How do you diagnose JSRV

A

PCR on blood, nasal secretions, BALF

258
Q

What do you see with JSRV

A

young lambs - spread with nasal secretions

tumors develop over months to years

and cause progressive emaciation, respiratory compromise when lead is lowered (Wheelbarrow test)

diagnosis: PCR ob blood, nasal secretions, BALF

259
Q

How do you treat pleuritis and pleural effusions in cattle

A

-Appropriate antimicrobials
-Anti-inflammatory
-+/- Drainage -caution because endotoxemia

260
Q

Why should you be careful draining pleural effusion in cattle

A

As you are draining it out, likely to leak out around needle
endotoxemia

If it is clear fluid, you can possibly just drain it

261
Q

What might cause pneumothorax in cattle

A

1) Rupture of emphysematous bullae
-BRSV
-AIP, 3-Methyl Indole
-Lungworm
-Metastatic pneumonia

2) Rib fracture and puncture of lung - dystocia

3) Laryngeal/ pharyngeal trauma - balling gun

4) other trauma

*Usually unilateral (complete mediastinum)

262
Q

Why is pneumothorax typically unilateral in ruminants

A

because ruminants have a complete mediastinum *

263
Q

How do you diagnose pneumothorax in cattle

A

-Thoracic auscultation
-Thoracic percussion
-Ultrasoun (Gap between visceral and parietal pleura with no glide signs)
-Radiographs

264
Q

How do you treat pneumothorax in cattle

A

-Thoracocentesis and suction
-Closure of opening, if applicable
-Maintenance of negative intrathoracic pressure

265
Q

Pneumothorax causes *

A

Inspiratory effort dyspnea

266
Q

Pulmonary edema in cattle is most commonly secondary to ___________ *

A

*Hypoproteinemia
-Protein loss from kidney or GI tract
-Cachexia, cardiac
-Fluid overload

267
Q

What are clinical signs of pulmonary edema in cattle

A

Dyspnea with crackles
head extension
tachypnea
obtundation
abscence of fever
+.- recumbency

268
Q

Causes of pulmonary edema in cattle

A

1) Hypoproteinemia: Protein loss from kidney or GI tract
2) Cachexia, cardiac
3) Fluid overload
4) Pneumonia
5) Toxic gases
6) Ehrlichia ruminantum

269
Q

How do you treat pulmonary edema in cattle

A

-Reduce or stop fluids
-Diuretics (furosemide)
-Administer colloids if hypoproteinemic
-Intranasal oxygen
-Limit handing asm uch as possible
-Dexamethasone may be beneficial

270
Q

What bacteria may be associated with left ventricular failure and pulmonary edema in cattle

A

Histophilus somni

or

Ionophore toxicity

271
Q

How might cattle get diaphragmatic hernia ****

A

1) Congenital
2) Acquired (most common) via dystocia associated with backwards or breech presentation
or others (truma, hadware disease- reticulum)

272
Q

How can dystocia lead to a diaphragmatic hernia in cattle **

A

Backwards or breech presentation- sternum gets pulled and tearing of the diaphragm

273
Q

What is the most common cause of diaphragmatic hernia in cattle

A

Dystocia associated with backwards or breech presentation

274
Q

How do you diagnose diaphragmatic hernias in cattle

A

Radiographs* +/- barium
Ultrasound

275
Q

Calves with diaphragmatic hernia are often treated for

A

Septicemia but it is unresponsive

only treatment is surgical closure (valuable animals only)

276
Q

What are the clinical signs of diaphragmatic hernia in calves

A

vague signs most commonly related to GI signs not repsiratory

many falsely get treated for GI diseases but diaphragmatic hernia should always be on your list for a dystocia calf

277
Q

What might be occurring if it appears that a ruminant is “vomiting”

A

Megaesophagus - can lead to aspiration pneumonia

can be secondary to Vitamin E deficiency

278
Q

What might cause megaesophagus in ruminants

A

Vitamin E deficiency can lead to megesophagus

279
Q

thymoma (livestock)

A

Occur in sheep and goats

-often asymptomatic, dynpnea, nuffled lung sounds, +/- congestive heart failure, +/- rumen tympany, +/- megaesophagus

Dx: Radiographs, Ultrasounds

280
Q

Cutaneous Paraneoplastic Syndrome *

A

Adenocarcinoma of the Thymus leading to chronic skin disease, weight loss and pruritus

281
Q

How might an animal have chronic skin disease from neoplasia *

A

Adenocarcinoma of the thymus

Cutaneous paraneoplastic syndrome

need to take the chest film

282
Q

What cancers may cause cutaenous paraneoplastic syndrome *

A

Adenocarcinoma of the thymus *

other differentials: adenocarcinoma, chemodectoma, thymoma

283
Q

What should you recommend for an animal with extensive dermatological workups that is idiopathic*

A

take a radiograph

could be cutaneous paraneoplastic syndrome

284
Q

What might cause thymomas in cattle

A

Iodine deficiencies

285
Q

Where does bovine cardiac lymphoma typically occur

A

right atrium

286
Q

What are common sites of Bovine Leukemia Virus

A

Heart
Uterus
Lymph node
Abomasum

are the most common sites for enzootic lymphoma in cattle

287
Q

How do you diagnose Bovine Cardiac Lymphoma

A

ultrasound to detect pericardial effusion and possible right atrial mass

pericardiocentesis with fluid analysis -> lymphocytes

BLV serology test

288
Q

What is one of the most common areas affected by bovine leukosis

A

the spinal cord

289
Q

What might cause diaphragmatic paralysis in camelids

A

Suspected degeneration or trauma to the phrenic nerve

Etiologies: Vitamin E deficiency, aberrant parasite migration, trauma to cervical spinal cord or thorax, nearby abscess or tumor

290
Q

How do you diagnose Diaphragmatic paralysis

A

Radiographs or Fluroscopy

*a must to diagnose the problem

291
Q

What is the pathogenesis of caudal vena caval thrombosis (CVCT)

A

1) Septic thromboemboli orginate from an abscess at the hilus of the liver - primary infection often starts in GI from rumen acidosis or rumenitis)
2) Showering CVC leads to septic emboli within the pulmonary circulation
3) Abscesses erode into bronchial wall and aneurysm can rupture into AW

292
Q

How do you treat CVCT in cattle

A

long term penicillin, supportive care

293
Q

What are the most common clinical presentation of CVCT

A

*Epistaxis, hemoptysis, anemia +/- dyspnea/tachypnea

294
Q

Hypersensitivity pneumonitis in cattle is a type ______ reaction to dust, moldy hay, grain, and plant matter associated to the spores of __________

A

Type I and IV

Thermophilic actinomycetes (Micropolyspora faeni)

295
Q

Spores of what is associated to allergic response, causing Hypersensitivity Pneumonitis in cattle *

A

Thermophilic actinomycetes (Micropolyspora faeni)

296
Q

Hypersensitivity Pneumonitis is most common in what kind of cow

A

Dairy cows (confined)

signs: decreased milk production, appetite, weight loss, coughing, crackles on thoracic auscultation

297
Q

How do you diagnose hypersensitivity pneumonitis in cattle

A

Titers for exposure, identify fungi in feed
-Thermophilic actinomycetes (Micropolyspora faeni)

298
Q
A
299
Q

Anaphylaxis in cattle is a Type _______ hypersenitivity reaction to ________

A

Type I

vaccine, milk, drug (penicillin), insects, bee sting

300
Q

Milk allergy in cattle

A

auto-allergy
Type I hypersensitivity
common in Jersey, Guernsey, Shorthorn

Risk factor: change in milking routine

Urticaria, tachypnea, tachycardia, watery diarrhea, dyspnea

301
Q

What breeds of cattle have an autoallergy to milk

A

Jersey, Guernsey, Shorthorn

302
Q

T/F: Acute/Atypical intersitital Pneumonia (AIP) in cattle is treated with antimicrobials

A

false- little respopnse to antimicrobials

this is commony non-infectious, secondary to inhalation or ingestion of toxin

303
Q

What causes Acute/Atypical intersitital Pneumonia (AIP) in cattle

A

this is commonly non-infectious, secondary to inhalation or ingestion of toxin

304
Q

What causes Acute/Atypical Interstitial Pneumonia (AIP) and Acute Respiratory Distress Syndrome (ARDS) in cattle characterized by severely acute interstitial edema and poor oxygenation

A

1) Acute Bovine Pulmonary Edema and Emphysema (fog fever)

2) Mold sweet potatio (R-ipomeanol) toxicity

3) Perilla mint toxicity

4) Feedlot AIP

Other toxic plants and gases

305
Q

Cattle in ARDS have a PaO2/FiO2 of _______

A

<400

306
Q

What is the pathogenesis of ARDS associated with lush pasture

A

1) Adult cattle >2 years old eat lush pasture that is high in L-tryptophan
2) Rumen converts to 3-methylindole (3-MI)
3) 3-MI is absorbed and circulated and causes AIP as it is pneumotoxic
4) Clinical signs seen within 2 weeks of pasture change: tachypnea, dyspnea, frothing at mouth, no coughing*

307
Q

How do you treat/ prevent fog fever

A

move pasture, suportive care (NSAID/steroid)
furosemide for intersitital edema
gradual pasture introduction
feed ionophores (monensin)

308
Q

Are clinical signs of 3-methylindole or 4-ipomeanol seen sooner?

A

4-IP: seen within 1 day of exposure while 3-MI is within 2 weeks of the pasture change

309
Q

Perilla frutescens toxicity

A

associated with perilla mint, purple mint, wild coleus, beefsteak plant
-oils contain pneumotoxin similar to 4-IP
Common in the southeast (Aug-Oct- seed and flower stage)

Pathogenesis is similar to fog fever and moldy sweet potato toxicity

Clinical signs: sudden death, ARDS

310
Q

What is Feedlot Acute/ Atypical Interstitial pneumonia

A

Cause is unknown but possible feed assocated pnemotoxin- BRSV?

cattle on feed more than 60 days following arrival a feedlot
-summer and fall
-more common in heifers
-high mortality

Clinical presentation
-rapid onset of dypsnea
-tachypnea
-cyanosis
-subcutaneous emphysema

*Inophores (monensin) ineffective

311
Q

Feedlot Acute/ Atypical Interstitial pneumonia affects cattle that *

A

are on feed more than 60 days following arrival at feedlot

312
Q

What causes Feedlot Acute/ Atypical Interstitial pneumonia

A

Cause is unknown but possible feed assocated pnemotoxin- BRSV?

313
Q

T/F: Ionophores (monensin) is effective in treating/preventing Feedlot Acute/ Atypical Interstitial pneumonia

A

False

314
Q

T/F: Inophore (monensin) is effective in treating/preventing Fog Fever

A

True

315
Q

What are toxic gases that affect cattle

A

-Nitrogen dioxide in silo gas
-Zinc oxide (welding)
-Manure gas (hydrogen sulfide, ammonia, CO2, CO, methane
-Smoke inhalation
-Chlorine

Clinical signs consistent with ARDs

Treatment: move to a ventilated area, supportive care (furosemide, anti-inflammatories/ steroids)

316
Q

What is the lifecycle of lungworms that cause parasitic bronchitis and pneumonia in cattle *

A

1) Eggs from L5 mature worms are coughed up from lungs and swallowed
2) Hatch within the GIT
3) Shed as L1 in feces
4) L1 molts 2x to become ineffective L3
5) L3 penetrates GIT and enters lymph nodes (molts to L4)
6) L4 travels to lungs in lymph/blood and incite eosinophilic exudate that blocks airways
7) L5 move to larger airways (tracheitis)

clinical signs: graudal progressive cough with possible complications of pulmonary edema, emphysema, secondary bacterial infection

317
Q

What age of cows do lungworms affect

A

young non-immune yearlings/adults

temperate areas with high rainfall

318
Q

How long does it take from ingestion of L3 lungworms intil they are in the respiratory tract

A

28 days

319
Q

What stage of lung worms incite eosinophilic exudate that blocks airways

A

L4- creates inflammation

320
Q

What are the clinical signs of lungworms

A

clinical signs: gradual progressive cough with possible complications of pulmonary edema, emphysema, secondary bacterial infection

321
Q

How do you diagnose lungworms in cattle

A

1) Baermann on fresh feces to detect the L1 stage
-feces suspended in water
-larvae actively move into the water
-sink for collection

2) TTW or BAL- larvae or eosinophils

322
Q

What stage of lungworm does Baermann detect

A

L1 larvae

-feces suspended in water
-larvae actively move into the water
-sink for collection

323
Q

How do you treat lungworms in cattle

A

Anthelminthics
1) Levamisole - nicotinic acetylcholine receptor agonist
2) Benzimidazoles (-azoles)- bind tubulin and disrupt tubulin microtuble equilibrium
3) Macrocylic lactones (-mectins) : bind glutamate gated chloride channels

others: anti-inflammatories (NSAID/steroid) +/- antibiotics (secondary infection)

324
Q

What is the mechanism of macrocyclic lactones like ivermectin and eprinomectin in the treatment of lungworms in cattle

A

bind glutamate gated chloride channels

325
Q

What is the mechanism of Benzimidazoles like Fenbendazole and Albendazole in the treatment of lungworms in cattle

A

bind tubulin and disrupt tubulin microtubule equilibrium

326
Q

What is the mechanism of Levamisole (imidazothiazole) in the treatment of lungworms in cattle

A

nicotinic acetylcholine receptor agonist

327
Q

What causes bovine lungworm

A

1) Dictyocaulus viviparus
2) Ascaris suum- if exposed to high egg exposure in pigs, 10d post ingestion, causes rumen stasis interstial pneumonia via aberrant migration

328
Q

Ascaris suum

A

a bovine lungworm if exposed to pigs (high egg exposure)
-Aberrant migration
-10days post ingestions
-Interstitial pneumonia
-Fever
-Rumen stasis
-Depression

329
Q

What are different small ruminant lungworms

A

1) Dictyocalus filaria- 4 weeks post ingestion
2) Muellerius Capillaris- goats are more severe (interstitial) with an indirect lifecycle (snal and 6 weeks prepatent), resistant to levamisole

330
Q

Muellerius capilalris is resistant to

A

Levamisole

331
Q

Muellerius Capillaris infection are most common small ruminant lungworm and they cause severe disease in

A

goats- interstitial

332
Q

What lifecycle does Muelleris capillaris have

A

indirect life cycle
snail (intermediate host)
6 weeks prepatent

333
Q

You are called out to look at a pen of Angus heifers
that have had respiratory signs over the last 2 days .
The producer reports that he found 4 dead this
morning. As you get out to the dry lot pen you notice
that most of the heifers are coughing and tachypneic,
and some are dyspneic. Based on this information,
what is the most likely diagnosis and best intervention
strategy?

A. AIP/ARDS secondary to L-tryptophan ingestion; move to pasture and feed
monensin to the group
B. AIP/ARDS secondary to pneumotoxin 4-IP ingestion; investigate feed bunk
for potatoes and remove
C. AIP/ARDS secondary to aspiration of lungworm larvae; treat group of heifers
with levamisole
D. AIP/ARDS secondary to liver abscesses and pulmonary thrombi; treat group
with penicillin

A

B. AIP/ARDS secondary to pneumotoxin 4-IP ingestion; investigate feed bunk
for potatoes and remove

334
Q

What parasite is resistant to Levamisole

A

Muellerius Capillaris

335
Q

A second lactation Jersey cow 180 DIM was let out to
graze fresh pasture during the summer. The herd
manager decided to keep her with the dry cows and
forego milking her that afternoon. At the evening check,
the herd manager notices her standing with her head and
neck extended, tachypneic and open-mouth breathing.
Thankfully, you are already at the farm finishing up with a
dystocia (you saved the calf!)

What is the BEST next step for treating this cow?
A. You administer dexamethasone and tell the herd manager she
needs to be moved off the pasture immediately.
B. You tell the herd manager she likely has ARDS, which as a poor
prognosis, and humane euthanasia is recommended.
C. You prepare to take a deep nasopharyngeal swab that you will
submit for culture and sensitivity and treat her with flunixin
meglumine and florfenicol.
D. You administer epinephrine and flunixin meglumine and move her
to the parlor for milking immediately.

A

D. You administer epinephrine and flunixin meglumine and move her
to the parlor for milking immediately

336
Q

Mestastic pneumonia in cattle manifest as ___________ *

A

epistaxis with varying degrees of respiratory distress
Rumen is primary origin of the disease

337
Q

What makes you suspicious for anaphlaxis in cattle *

A

Respiratory distress is accompanied by pharyngeal edema and urticaria

*Give Epinephrine, glucocorticoid (if not pregnant)

338
Q
A

Fluids, Respiratory, Muscles (7 decks)

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