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LAIM: Respiratory > Cattle - Respiratory Dz > Flashcards

Cattle - Respiratory Dz Flashcards

1
Q

Describe the epidemiology of fungal rhinitis in cattle and common fungi implicated.

A
  • Rare.
  • No age/breed/sex predisposition.
  • More common in warm, wet climates.
  • Rhinosporidium, helminthosporidium, dreschslera rostrata, aspergillus, phycomycetes, stachybotrys, bipolaris; also nocardia bacteria.
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2
Q

List the clinical signs of fungal rhinitis in cattle.

A
  • Stridor.
  • Dyspnoea.
  • Mucopurulent nasal discharge.
  • +/- epistaxis.
  • +/- open-mouth breathing.
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3
Q

How is fungal rhinitis diagnosed in cattle?

A

Histo: granulation tissue with eosinophils, mononuclear cells, sporangia, hyphae, filamentous bacteria.

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4
Q

How is fungal rhinitis treated in cattle?

A
  • Surgical debulking.

- Sodium iodide (NB overdose –> cough, scaly skin, excessive lacrimation).

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5
Q

Describe the pathophysiology of allergic rhinitis/Enzootic Nasal Granuloma of cattle and sheep.

A

Type I (IgE) hypersensitivity to pollen/fungi etc –> ongoing reaction exposure –> tissue damage by mast cell factors –> chronic epithelial, duct, goblet cell hyperplasia, mucus hypersecretion and granulomatous inflammation (type IV hypersensitivity).

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6
Q

Is there a breed or age predisposition for Enzootic Nasal Granuloma in cattle?

A
  • Channel island breeds (Guernsey, Jersey, Alderney) and Friesians.
  • 6mo to 2yo.
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7
Q

Describe the clinical signs of Enzootic Nasal Granuloma in cattle and sheep.

A
  • Sneezing.
  • Nasal pruritis.
  • Dyspnoea.
  • Stertor.
  • Profuse bilateral nasal discharge.
  • +/- facial swelling, tachypnoea, hyperpnoea, ulceration of nasal mucosa, lacrimation, chemosis.
  • Granulomas: multiple, firm, white, raised, 1-2mm.
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8
Q

How is Enzootic Nasal Granuloma in cattle and sheep diagnosed?

A
  • Endoscopy.
  • Biopsy.
  • Culture.
  • Antigen detection/serology to rule out bacterial, viral or fungal infection.
  • Inc eosinophils in nasal secretions.
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9
Q

Describe the treatment of Enzootic Nasal Granuloma in cattle and sheep.

A
  • Remove allergens.
  • Anti-histamines.
  • Meclofenamic acid.
  • Steroids.
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10
Q

List the neoplasias that have been reported to occur in the nasal passages of cattle.

A
  • Osteomas.
  • Osteosarcomas.
  • Squamous cell carcinomas.
  • Neuroblastomas.
  • Haemangiosarcomas.
  • Ethmoid adenocarcinoma: endemic pattern, 6-9yo, unilateral, viral origin? Mets in LN and lung.
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11
Q

List clinical signs of nasal neoplasia in cattle.

A
  • Inspiratory dyspnoea.
  • Stridor.
  • Nasal discharge.
  • Epistaxis.
  • Halitosis.
  • Decreased airflow through nares.
  • Open-mouth breathing.
  • Distortion of facial bones.
  • NB not typically treated.
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12
Q

Describe the lesion seen in congenital cystic nasal turbinate disease of cattle.

A

Nasal conchae lack communication with nasal cavity and fill with fluid.

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13
Q

Describe the clinical signs and diagnosis of congenital cystic nasal turbinates in cattle.

A
  • Stridor.
  • Tachypnoea.
  • Decreased air flow.
  • Exercise intolerance.
  • Open-mouth breathing.
  • Palpation.
  • Endoscopy.
  • Rads –> large, smooth, cystic ventral conchae.
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14
Q

Describe the treatment of congenital cystic nasal turbinates in cattle.

A
  • Sx: bilateral dorsal lateral nasal bone flaps.

- Sx: transnasal removal with gigli wire.

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15
Q

Describe the signalment and aetiology of sinusitis in ruminants.

A
  • Cattle > sheep or goats.
  • Usually frontal (dehorning) or maxillary (tooth).
  • Other causes: injury, extension of actinomyces or nasal neoplasia, resp viruses (MCF, IBR, PI3), sinus cysts, lymphoma, oestrus ovis.
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16
Q

Describe the clinical signs of sinusitis in cattle.

A
  • Acute or chronic.
  • Anorexia.
  • Lethargy.
  • +/- fever.
  • Dehorning site discharging pus.
  • Unilateral or bilateral nasal discharge.
  • Stridor.
  • Foul breath.
  • Head held at an angle.
  • +/- frontal bone distortion, exophthalmus, neuro signs.
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17
Q

Describe the diagnosis of sinusitis in cattle.

A
  • Clinical signs and history.
  • Percussion (dull sounds or pain).
  • Radiographs.
  • Sinus centesis (Steinmann pin).
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18
Q

Describe treatment of sinusitis in cattle.

A
  • Sinus trephination (1 or 2 sites).
  • Lavage.
  • +/- remove tooth.
  • If systemic signs: NSAIDs, ABs (penicillin for Trueperella - dehorning, oxytet for pastuerella - not dehorning).
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19
Q

Describe the aetiology of pharyngeal trauma, abscesses, cellulitis and granulomas in cattle.

A
  • Trauma: balling gun, dose syringe, specula, stomach tube, rough stemmy feeds, grass awns, brias, FBs.
  • T. pyogenes, Actinobacillus, Pastuerella, Bordatella. Fusobacterium necrophorum, Streptococcus.
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20
Q

List the clinical signs of pharyngeal trauma, abscesses, cellulitis and granulomas in cattle.

A
  • Inspiratory dyspnoea with stertor.
  • Extended head and neck.
  • Ptyalism.
  • Quidding.
  • Pain or swelling.
  • Regurgitation through nostrils.
  • Mucopurulent to blood nasal discharge with fetid odour.
  • Cough.
  • Bloat.
  • Palpable swelling in the pharyngeal area.
  • If severe dz: depression, fever, anorexia, dehydration, forestomach stasis.
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21
Q

Describe the diagnosis of pharyngeal trauma, abscesses, cellulitis and granulomas in cattle.

A
  • Oral exam.
  • Endoscopy.
  • Rads.
  • CBC: neutrophilia, +/- metabolic acidosis due to saliva loss.
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22
Q

List the treatment of pharyngeal trauma, abscesses, cellulitis and granulomas in cattle.

A
  • Drain abscess into pharynx and lavage.
  • Drain externally.
  • ABs.
  • NSAIDs.
  • Tracheotomy.
  • IVFT.
  • Feed through rumenostomy.
  • Good Px.
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23
Q

Describe the epidemiology and pathophysiology of Necrotic Laryngitis (aka Calf Diphtheria).

A
  • Feedlot cattle.
  • Young (3-18mo); >30 days on feed.
  • URT infection –> laryngeal contact ulcers or H. somni infection –> damage to laryngeal mucosa –> invasion of F. necrophorum –> acute to chronic infection of laryngeal mucosa and cartilages.
  • Worldwide distribution, occur year-round but more common in Autumn and Winter.
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24
Q

Describe the clinical signs of Necrotic Laryngitis in cattle.

A
  • Acute onset moist, painful cough.
  • Severe inspiratory dyspnoea, stertor, head and neck extended.
  • Salivation/frequent swallowing or sipping water.
  • Anorexia, fever, hyperaemic MMs.
  • Bilateral fetid nasal discharge.
  • Un-treated die in 2-7d.
  • Recovered may become roarers, get aspiration pneumonia or be poor doers.
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25
Q

Describe the treatment and prognosis of Necrotic Laryngitis.

A
  • ABs: oxytetracycline, penicillin, TMPS.
  • NSAIDs (1 dose steroid if severe swelling).
  • +/- tracheotomy.
  • Nursing care.
  • Px good if dx early and aggressive tx, otherwise poor.
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26
Q

Describe lesions found at necropsy of cattle that have died from Necrotic Laryngitis.

A
  • Vocal processes and medial angles of arytenoids.
  • Acute: oedema, hyperaemia, swelling, discharge around necrotic ulcer.
  • Chronic: focus of necrotic cartilage surrounded by purulent exudate with tract to mucosal surface; arytenoid rotated into lumen or cavities.
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27
Q

Describe laryngeal papillomatosis of feedlot cattle.

A
  • Common disease.
  • Papovavirus enters via laryngeal ulcers.
  • CSx: sterterous respiration, cough.
  • Lesion: sessile to pedunculated, yellow, frond-like, 1-10mm growths on vocal processes or arytenoids.
  • Tx: usually not indicated; may remove surgically.
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28
Q

Describe the aetiology of tracheal collapse and stenosis in cattle.

A
  • Infrequently reported.

- Unknown aetiology; potential causes incl trauma (roping, dystocia), tracheostomies, congenital defects.

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29
Q

Describe the clinical signs of tracheal collapse and stenosis in cattle.

A
  • BAR –> tachypnoea, tachycardia, mucosal hyperaemia, dyspnoea exacerbated by exercise/excitement, stertor, ‘honking’ cough.
  • Lack of response to tracheostomy, NSAIDs, ABs.
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30
Q

Describe the diagnosis of tracheal collapse and stenosis in cattle.

A
  • Endoscopy.
  • Rads: dorsoventral flattening in caudal cervical or cranial thoracic trachea most common; can be lateral.
  • Necropsy: dorsally or laterally flattened trachea.
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31
Q

Describe the treatment and prognosis of tracheal collapse and stenosis in cattle.

A
  • Px poor.

- Surgery reported to enable survival to slaughter.

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32
Q

Describe the aetiology and pathogenesis of tracheal oedema syndrome (aka Honker Cattle) of feedlot cattle.

A
  • Extensive oedema and haemorrhage of dorsal wall of trachea.
  • Acute and chronic form; unknown if related.
  • Proposed aetiologies: URT viruses, bacteria e.g. P. multocida or H. somni, feedbunk trauma, fat, mycotoxins, hypersensitivity reaction.
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33
Q

Describe the clinical presentation of the acute form of tracheal oedema syndrome in cattle.

A
  • Heavy feedlot cattle in last 2/3 feeding period.
  • Summer.
  • Subclinical: sudden death.
  • Dyspnoea, guttural inspiratory sounds, open mouth breathing, extending head and neck, cyanosis, recumbency, death.
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34
Q

Describe the clinical presentation of the chronic form of tracheal oedema syndrome in cattle.

A
  • Lighter cattle (130-400kg).
  • +/- Hx of IBR/pneumonia.
  • Continuous deep, hacking cough.
  • +/- unthrifty.
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35
Q

Describe treatment and prognosis of tracheal oedema syndrome in cattle.

A
  • Acute: steroids, oxygen, decrease stress.
  • Chronic: no tx.
  • Px: poor.
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36
Q

Describe necropsy findings in cattle that have died from tracheal oedema syndrome.

A
  • Acute: dorsal oedema up to 5cm thick, caudal half of trachea; mucosal, submucosal and peritracheal oedema +/- haemorrhage.
  • Chronic: hyperaemia of mucosa in caudal third of trachea; +/- thin layer mucopurulent exudate; +/- fibre-like projections and polyps.
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37
Q

List the infectious pathogens which contribute to he Bovine Respiratory Disease Complex.

A
  • Bovine Herpesvirus-1 (BHV-1).
  • Bovine Respiratory Syncytial Virus (BRSV).
  • Bovine Viral Diarrhoea Virus (BVDV).
  • Bovine Parainfluenza 3 Virus (PI3).
  • Bovine Coronavirus (BCoV).
  • Adenovirus.
  • Viruses of unknown clinical sig: Bovine Rhinitis Virus, Bovine Reovirus, Calicivirus, Influenza.
  • Mannheimia haemolytica.
  • Pastuerella multicodia.
  • Histophilus somni.
  • Mycoplasma bovis.
  • Biberstenia trehalosi.
  • Trueperella pyogenes.
  • Bacteria w unknown clinical sig: Chlamydial organisms.
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38
Q

Describe the Bovine Herpesvirus-1 (BHV-1).

A
  • Family: Herpesviridae.
  • Subfamily: alpha.
  • Enveloped DNA virus.
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39
Q

List the diseases caused by BHV-1.

A
  • Infectious Bovine Rhinotracheitis (IBR).
  • Conjunctivitis.
  • Infectious pustular vulvovaginitis.
  • Balanoposthitis.
  • Encephalomyelitis.
  • Mastitis.
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40
Q

List the clinical signs of IBR in cattle.

A
  • Can be mild to severe (influence of type-1 interferon genotype??)
  • ‘Red nose’: hyperaemic muzzle.
  • Pustules on nasal mucosa –> diphtheritic membranes.
  • Conjunctivitis +/- corneal opacity.
  • Pyrexia.
  • Anorexia.
  • Dec milk prod.
  • Tachypnoea.
  • Ptyalism.
  • Cough.
  • Nasal discharge (serous to mucopurulent).
  • Harsh bronchovesicular sounds; referred tracheal noise.
  • +/- secondary bacterial pneumonia.
  • +/- abortion.
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41
Q

Describe the pathophysiology of IBR.

A
  • Transmitted via aerosol and direct contact.
  • BHV-1 surface glycoproteins interact w heparin sulfate proteoglycans and other host cell proteins –> enter resp epi cells and neighbouring epi cells via intracellular bridges.
  • Invade lymphocytes and monocytes –> extra-respiratory infections.
  • Latency in trigeminal ganglia and tonsils mediated by latency-related transcript (prevents apoptosis, re-activates shedding).
  • Disease mechanisms:
    i) Direct injury of infected URT/bronchial epi cells –> inflammation and susceptibility to secondary infection.
    ii) Immunosuppression: dysfunction of neuts, lymphs, macro incl dec neut chemotaxis, dec mitogen-induced blastogenesis of lymphocytes, dec expression of MHC-1 molecules, inc apoptosis of lymphs, mono.
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42
Q

Describe the epidemiology of IBR.

A
  • Widespread.
  • Adult cattle are reservoir.
  • Increased attack rate and fatality in feedlot cattle.
  • Historically first few weeks after entry, now seeing late outbreaks (mutation not covered by current vacc?).
  • Not important in epizootic pneumonia of calves.
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43
Q

Describe necropsy findings in animals that have died from IBR.

A
  • Rhinitis, laryngitis, tracheobronchitis.
  • Mucosa congested or haemorrhagic.
  • Pustular lesions –> plaques on resp. ocular, repro mucosa.
  • +/- oesophageal lesions.
  • Neonates: systemic dz w necrotic foci in all organs.
  • NB intranuclear inclusion bodies NOT common feature of BHV-1 infections.
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44
Q

How is IBR diagnosed in cattle?

A
  • Virus isolation, IFA, PCR from nasal and conj swabs.

- Paired serology (Ab titre).

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45
Q

Describe treatment and prevention of IBR in cattle.

A
  • Decrease stress.
  • Ensure access to food and water.
  • +/- NSAIDs.
  • +/- ABs (if evidence of secondary infection).
  • +/- vaccination (outbreak).
  • IN/IM vaccines are widely available; protect from infection in challenge studies but few field trials; inactivated for preg cows and neonates, MLV others –> immunity in 2-3d therefore must induce CMI.
  • Management essential in prevention e.g. dec co-mingling, dec stress.
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46
Q

Describe the Bovine Respiratory Syncytial Virus (BRSV).

A
  • Family: Paramyxoviridae.
  • Subfamily: Pneumovirina.
  • Enveloped RNA virus.
  • Recent change in BRSV G glycoprotein reported in Europe, likely secondary to antigenic pressure from vaccination.
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47
Q

List the clinical signs of BRSV infection in cattle.

A
  • Inapparent to severe; CSx limited to resp tract.
  • Fever, depression, inappetence.
  • Tachypnoea.
  • Ptyalism.
  • Cough.
  • Nasal/lacrimal discharge.
  • Inc bronchovesicular sounds +/- wheezes/crackles in mid- to dorsocaudal lungfields.
  • +/- absent dorsal BV sounds (ruptured bullae).
  • Late infection: pronounced dyspnoea, inc expr effort, open-mouth breathing, +/- s/c emphysema.
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48
Q

Describe the epidemiology of BRSV infection in cattle.

A
  • 60-80% US cattle have Abs assoc w seroconversion.
  • High morbidity, low mortality (0-20%).
  • Adult cattle believed to be reservoir.
  • Tranmission: aerosol, direct contact, fomites.
  • Incubation period: 3-5 days.
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49
Q

Describe the pathogenesis of BRSV infection in cattle.

A
  • Infects cells of nasal, tracheal, bronchial epi +/- alveolar and circulating macrophages.
  • Epi cells fuse –> multinucleated cells (syncytia) –> slough into lumen –> phagocytosed by neut/alv macro.
  • Bronchitis, bronchiolitis, alveolitis +/- AIP.
  • Infected macro have dec function, dec phagocytosis, dec prod chemotactic factors.
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50
Q

Describe the role of the immune response in BRSV infection in cattle.

A
  • Severity of dz is related to humoral and CM immunity.
  • CSx most notable mast cell degran –> bronchoconstriction, pulmonary oedema.
  • Vaccine-enhanced dz is rare but is reported w inactivated and MLV vaccines (vacc is still recommended as rare).
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51
Q

Describe necropsy findings in cattle that have died from BRSV infection.

A
  • Neutrophilic to mononuclear bronchitis, broncheolitis, alveolitis +/- syncytial cells.
  • AIP –> dorsocaudal lungs heavy, rubbery, emphysema.
  • Histo: alveolar epi hyperplasia, hyaline membranes, interstitial inflamm cells, haemorrhage, oedema.
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52
Q

Outline diagnosis of BRSV in cattle.

A
  • Virus does not survive well, therefore not virus iso.
  • PCR, IHC, IFA of nasal swabs, TTW or BALF, lung tissue; less likely to be found 10-15d post-infection.
  • Seroconversion: ELISA or VN Abs.
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53
Q

Describe treatment and prevention of BRSV infection in cattle.

A
  • Goal: decrease resp inflamm and prevent secondary bacterial infection.
  • NSAIDs; steroids if severe resp distress/AIP.
  • Antibiotics.
  • InO2, furosemide if required.
  • IN/IM vaccines available.
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54
Q

Describe the Bovine Viral Diarrhoea Virus (BVDV).

A
  • Family: Flaviviridae.
  • Genus: Pestivirus.
  • Enveloped RNA virus.
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55
Q

Describe the respiratory disease causes by BVDV infection in cattle.

A
  • Some strains cause mild pneumonia.

- Importance is as a co-infector in BRDC e.g. w M. haemolytica, M. bovis, BHV-1, BRSV.

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56
Q

Describe the pathogenesis of BVDV in BRDC infections.

A
  • Suppresses immune resp to co-infecting agents.
  • Suppresses immune resp to vacc against other BRDC pathogens.
  • Infects the resp tract and enhances pathogenicity of co-infectors.
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57
Q

Describe the Bovine Parainfluenza-3 Virus (PI3).

A
  • Family: Paramyxoviridae.
  • Subfamily: Paramyxovirinae.
  • Enveloped RNA virus.
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58
Q

List the clinical signs of PI3 infection in cattle.

A
  • Range from subclinical to mild.
  • Fever.
  • Cough.
  • Nasal and ocular discharge.
  • Tachypnoea.
  • Inc bronchovesicular sounds, wheezes.
59
Q

Describe the epidemiology of PI3 infection in cattle.

A
  • Very widespread.
  • Often no clinical signs.
  • Important initiator of BRDC.
  • Incubation period 2d.
60
Q

Describe the pathophysiology of PI3 infection in cattle.

A
  • CSx of URT and LRT infection.
  • Virus found in nasal, tracheal, broncheolar, alveolar epi cells.
  • Damages mucociliary apparatus, dec alveolar macro function (Fc receptor expression, phagocytosis, microbicidal action) –> predisposes to secondary infection.
61
Q

Describe necropsy findings in cattle that have died from PI3 infection.

A
  • Rarely seen.

- Experimental infection –> necropsy –> changes like mild BRSV.

62
Q

Outline the diagnosis of PI3 infection in cattle.

A
  • Virus isolation.
  • PCR of nasal swabs.
  • Paired serology to demonstrate rising titre.
63
Q

Describe methods for prevention of PI3 infection.

A
  • Inactivated and ML vaccines.

- Registered for cattle only; off-label in sheep and goats.

64
Q

Describe the Bovine Coronavirus (BoCV).

A
  • Family: Coronaviridae.
  • Group 2 Coronavirus.
  • Enveloped, single-stranded RNA virus.
65
Q

List diseases caused by Bovine Coronavirus.

A
  • Calf diarrhoea.
  • Winter dysentary of adult cattle.
  • Respiratory disease (recent evidence).
66
Q

Describe the contribute of BoCV to BRDC in cattle.

A
  • Important role identified in two Shipping Fever outbreaks.
  • Evidence vaccination –> less resp dz in feedlot cattle.
  • Other evidence suggests no role in BRDC.
67
Q

Describe the Bovine Herpesvirus-4 Virus.

A
  • Family: Herpesviridae.
  • Subfamily: Gamma herpesviridae.
  • Enveloped DNA virus.
68
Q

List the diseases caused by BHV-4.

A
  • Abortions.
  • Metritis.
  • Mammilitis.
  • Enteric dz.
  • Conflicting data whether or not causes respiratory dz.
69
Q

Describe adenoviruses of ruminants.

A
  • Family: Adenoviridae.
  • Serotypes: Cattle - at least 10, sheep - at least 6, goats - 2.
  • Non-enveloped, double-stranded DNA viruses.
70
Q

Describe presentation of Bovine Adenovirus infections.

A
  • Widespread.
  • Frequently subclinical, often assoc w other pathogens.
  • Assoc w pneumonia, enteritis, keratoconjunctivitis; weak calf syndrome?
71
Q

Describe the bacteria Mannheimia haemolytica.

A
  • Family: Pasteurellaceae.
  • Gram negative aerobe, small rod.
  • At least 12 serotypes.
  • Cattle: A1, A6 most common pneumonic lungs, A2 normal flora in nasopharynx.
  • Sheep and goats: A2 most common pneumonic lungs; A7, A9 pathogenic.
72
Q

Describe the epidemiology of Mannheimia haemolytica infection in cattle.

A
  • Most common bacterial isolate from feedlot cattle w fatal fibrinous pleuropneumonia.
  • Not commonly associated with outbreaks of pneumonia in dairy calves.
73
Q

Describe the pathophysiology of Mannheimia haemolytica infection in cattle.

A
  • Infected v early in life -> n commensal org in nasopharynx.
  • Numbers inc w transport/URT viral infection –> opportunistic pathogen of LRT –> multiply in lungs –> severe, necrotising, fibrinous pleuropneumonia.
  • Virulence factors:
    • Leukotoxin: binds to cells via CD18, beta subunit of beta 2 integrins –> inc expression of LFA-1 by leukocytes –> apoptosis/cell lysis of platelets, lympho, macro, neut.
    • LPS: works synergistically w leukotoxin; v rapid resp –> initiation of complement and coag cascades, activation of endo cells, recruitments of neuts, activation of neuts and macro –> inc pro-inflam cytokines (IL-1b, IL-8, TNF-a); death of massive influx of neuts –> elastase, collagenase, reactive O2 –> necrosis/fibrinous exudation.
    • Polysaccharide capsule: aids attachment, prevents phagocytosis by neutrophils.
    • Iron-regulated outer membrane proteins: bind transferrin, alter neutrophil function.
    • Adhesins: mediate attachment to host cells.
    • Neuraminidase: dec viscosity of mucus, dec repellant negative charge on host cells.
74
Q

List clinical signs of Mannheimia haemolytica infection in cattle.

A
  • Fever.
  • Tachypnoea.
  • Depression.
  • Dec appetite.
  • NB no cough during early disease.
  • +/- thoracic pain.
  • +/- endotoxaemia.
  • Harsh BV sounds over cranioventral lungs.
  • +/- death/chronic infection.
  • Usually secondary to viral dz.
75
Q

Describe necropsy findings in cattle infected with Mannheimia haemolytica.

A
  • Fibrinopurulent bronchopneumonia or pleuropneumonia OR pulmonary consolidation w/out fibrin (dairy calves, sheep, goats).
  • Cranioventral lobes to whole lung.
  • May see infarcts, coagulative necrosis, swollen red LNs.
76
Q

Outline diagnosis of Mannheimia haemolytica infection in cattle.

A
  • Culture and cytology.

- TTW, BAL, thoracocentesis or lung tissue.

77
Q

Outline treatment of Mannheimia haemolytica infection in cattle.

A
  • Many labelled antibiotics.

- NSAIDs in cattle with SIRS.

78
Q

Outline methods for prevention of Mannheimia haemolytica infection in cattle.

A
  • Antibiotic metaphylaxis e.g. tilmicosin, florfenicol just pre- or post-shipping.
  • Ensure no FPT.
  • Vaccination.
  • Minimise stressors: viral infection, co-mingling, long distance shipping, pre-conditioning.
79
Q

Describe the bacteria Pasteurella multocida.

A
  • Family: Pasteurellaceae.
  • Gram negative aerobe.
  • 5 serogroups: A - most common resp infection, B+E - haemorrhagic septicaemia (Asia and Africa), D+F - resp infection in some regions (esp in sheep).
80
Q

Describe the epidemiology of Pasteurella multocida infection in cattle.

A
  • Normal URT commensal in cattle, sheep and goats.

- Debate if primary or only secondary lung pathogen.

81
Q

Describe the pathophysiology of Pasteurella multocida infection in cattle.

A
  • Little known.
  • LPS.
  • Capsule: resists phagocytosis.
  • Iron-regulated outer membrane proteins: inc ability to proliferate in host.
  • Damage to resp epi (viruses, poor ventilation etc) –> chronic inhalation of small numbers of bacteria –> bronchopneumonia.
  • Possible cause of enzootic pneumonia of calves.
82
Q

List clinical signs of Pasteurella multocida infection in cattle.

A
  • Fever.
  • Tachypnoea.
  • Depression.
  • Coughing.
  • Mucoid to mucopurulent nasal discharge.
  • Harsh BV sounds cranioventrally; crackles (fluid in large airways).
  • +/- endotoxaemia.
  • Generally milder CSx than M. haemolytica.
  • Calves > feedlot cattle.
83
Q

Describe necropsy findings in cattle infected with Pasteurella multocida.

A
  • Purulent bronchopneumonia w plum-coloured CV consolidation and purulent exudate on cut section.
  • Fibrin possible.
84
Q

Outline diagnosis of Pasteurella multocida infection in cattle.

A
  • Culture and cytology.

- TTW, BAL or lung tissue.

85
Q

Outline methods for treatment and prevention of Pasteurella multocida infection in cattle.

A
  • Many labelled antibiotics; as infections usually chronic may require 3-5d at labelled dose.
  • Dec exposure to viruses and environmental contributors.
  • Vaccines available but questionable efficacy.
86
Q

Describe the bacteria Histophilus somni.

A
  • Family: Pasteurellaceae.
  • Gram negative aerobe.
  • NF of URT and genital mucosa of cattle, goats, sheep.
  • Different strains have different virulence.
87
Q

Describe the epidemiology of Histophilus somni infection in cattle.

A
  • Exposure common.

- Dz of feedlot cattle > calves.

88
Q

Describe the pathophysiology of Histophilus somni infection in cattle.

A
  • Primary viral dz –> secondary bacterial infect of resp tr.
  • Virulence factors:
    • Outer membrane proteins: bind Fc region of Ab –> escape opsonisation, resist killing following phagocytosis.
    • Lipooligosaccharide: like LPS; interacts w P2X7 receptor on endo cells –> apoptosis –> vasculitis and thrombosis; induces IgE prod –> hypersens post-vacc/more severe dz.
89
Q

List clinical signs of Histophilus somni respiratory infection in cattle.

A
  • Causes dz in multiple body systems: septicaemia, TEME, endometritis, abortion, infertility, pneumonia, pleuritis, laryngitis, otitis, conjunctivitis, myocarditis, mastitis, polyarthritis.
  • Mild to severe respiratory infections.
  • Fever.
  • Tachypnoea.
  • Cough.
  • Nasal discharge.
  • Depression.
  • Harsh BV sounds cranioventrally.
  • Pain (pleuritis).
  • +/- SIRS.
90
Q

Describe necropsy findings in cattle infected with Histophilus somni.

A
  • Plum and brown consolidation CV lungs.
  • +/- abscesses.
  • Purulent material on cut section of lung tissue.
  • +/- fibrinous pleuritis.
  • +/- haemorrhage.
91
Q

Outline diagnosis of Histophilus somni infection in cattle.

A
  • Culture: TTW, BAL, pleurocentesis, lung tissue; NB hard to grow in culture therefore trans immediately, pre-tx samples.
  • IHC lung tissue.
  • Paired titres.
92
Q

Outline methods for treatment and prevention of Histophilus somni infection in cattle.

A
  • Several antibiotics.
  • Prophylaxis w oxytet does not result in improvement.
  • Killed whole bacterins –> IgE prod –> risk of anaphylaxis on subsequenc vacc therefore only vacc high risk cattle.
  • Enviro/stress management, dec viral infections.
93
Q

Describe the bacteria Mycoplasma bovis.

A
  • Family: mycoplasma.

- Small, pleomorphic organisms w/out cell wall.

94
Q

Describe the epidemiology of Mycoplasma bovis infection in cattle.

A
  • Cattle; rare in sheep and goats.
  • Found in healthy and diseased cattle.
  • Spread by aerosol, direct contact, in milk.
  • Spreads rapidly in feedlots.
  • Found in dairy calves and feedlot cattle, partic w chronic resp dz.
95
Q

Describe the pathophysiology of Mycoplasma bovis infection in cattle.

A
  • Little known.
  • General mycoplasma characteristics:
    • Variable surface proteins allow attachment to host cells.
    • Invasion of tissues e.g. can move b/w resp epi cells.
    • Evade host IR, impair neut activity, kill lymphocytes, induce inflammatory response.
96
Q

List clinical signs of Mycoplasma bovis infection in cattle.

A
  • Fever.
  • Tachypnoea.
  • Inappetence.
  • +/- resp distress.
  • +/- cough.
  • +/- nasal discharge.
  • Outbreaks: some –> otitis (young calves), arthritis or polysynovitis (calves or weanlings).
  • Lack of response to therapy, chronic infections.
  • Ill-thrift.
  • Usually secondary but can cause primary resp dz.
  • Other dz: mastitis, otitis, arthritis, polysynovitis, sinusitis, myocarditis, pericarditis, reproductive failure.
97
Q

Describe necropsy findings in cattle infected with Mycoplasma bovis.

A
  • Dark red, firm, consolidated CV lungs.
  • +/- raised white-yellow firm nodules = foci of caseous necrosis (eosinophilic coagulative necrosis).
  • +/- arthritis, tenosynovitis, otitis.
98
Q

Outline diagnosis of Mycoplasma bovis infection in cattle.

A
  • PM: IHC or culture of organisms plus typical gross/histo lesions.
99
Q

Outline methods for treatment and prevention of Mycoplasma bovis infection in cattle.

A
  • Poor response to ABs in many cases.
  • ABs labelled for M. bovis incl tulathromycin, florfenicol, enrofloxacin, gamithromycin; tx 7-10d+.
  • Success suggested to be based on early tx.
  • Vaccines: field trials lacking.
  • Predisposing factors unknown.
100
Q

Does mycoplasma mycoides infection occur in cattle?

A

Exotic to North America but can cause bovine pneumonia.

101
Q

Describe the bacteria Biberstenia trehalosi.

A
  • Family: Pasteurellaceae.

- Gram negative, facultative anaerobe.

102
Q

List clinical signs of Biberstenia trehalosi infection in ruminants.

A
  • Cattle/calves: severe acute/peracute bronchopneumonia –> death.
  • Sheep: pneumonia or systemic dz w multi-organ infection.
103
Q

How can Biberstenia trehalosi infections be prevented in cattle?

A

Possible cross-protection from M. haemolytica vaccines.

104
Q

Describe the bacteria Trueperella pyogenes.

A
  • Family: Actinomycetaceae.

- Gram positive rod, facultative anaerobe.

105
Q

What is the significance of Trueperella pyogenes in respiratory disease of cattle.

A
  • Secondary or tertiary invader in pneumonia –> lung abscesses.
  • Virulence factors incl pyolysin: cytolytic toxin; molecules that aid in adherence to host cells.
  • Tx primary dz to prevent chronic pneumonia and involvement of T. pyogenes.
106
Q

Define the clinical presentation and list the necropsy findings in Acute Respiratory Distress Syndrome of cattle.

A
  • Acute onset (usually severe) dyspnoea and AIP.
  • Gross findings: lungs fail to collapse, heavy, firm, rubbery texture; usually interlobular or bullous emphysema; +/- oedema; +/- ‘patchwork’ appearance.
  • Histo: alveolar hyaline membranes, alveolar fibrin, interstitial oedema, type II pneumocyte proliferation; +/- haemorrhage, emphysema, inflam infiltrates.
107
Q

Describe the definition and aetiology of Acute Bovine Pulmonary Oedema and Emphysema.

A
  • Definition: ARDs w change to lush green pastures in cattle >2yo; aka ‘Fog Fever’.
  • Aetiology: L-tryptophan in lush pasture –> rumen –> 3-methylindole (pneumotoxin).
108
Q

Describe the epidemiology of Acute Bovine Pulmonary Oedema and Emphysema.

A
  • Seen in adult cattle; nursing calves not affected.
  • Autumn.
  • May be indv but usually outbreaks.
  • ~50% morbidity, 30% mortality.
109
Q

Describe the pathophysiology of Acute Bovine Pulmonary Oedema and Emphysema.

A

L-tryptophan (lush forage) ingested –> ruminal micro-org convert to indole acetic acid –> 3-methylindole –> bloodstream –> metab by P-450 in Clara cells and type I pneumocytes –> reactive intermediates bind w intracellular proteins/macromolecules –> degen/necrosis/exfoliation of Clara cells and type I pneumocytes + oedema –> hyaline membrane formation, adenomatosis (type II pneumocyte prolif) and Clara cell proliferation.

110
Q

List the clinical signs of Acute Bovine Pulmonary Oedema and Emphysema.

A
  • CSx dev w/in 2wk of change to lush pasture.
  • Severe dyspnoea w expr grunt, tachypnoea, frothing at mouth, open-mouthed breathing, head/neck extended, nostril flaring.
  • +/- fever, tachycardia.
  • Lung sounds quiet +/- crackles.
  • Severe exercise intolerance.
  • Up to 30% mortality OR improve after 3d –> tachypnoea, harsh BV sounds, crackles, wheezes (esp caudal), +/- s/c emphysema.
  • Rpt episodes can –> pulmonary fibrosis and alveolitis.
  • NB no cough, sepsis, adventitious lung sounds.
111
Q

Outline diagnosis of Acute Bovine Pulmonary Oedema and Emphysema.

A
  • Usually presumptive.
  • Can perform rads –> interstitial pneumonia.
  • Research: measure 3-MI in blood and urine.
112
Q

Outline treatment of Acute Bovine Pulmonary Oedema and Emphysema.

A
  • Controversial; stress of handling/moving off pasture more dangerous than not tx?
  • Potential meds: furosemide, flunixin, dexamethasone.
113
Q

Outline methods for prevention of Acute Bovine Pulmonary Oedema and Emphysema.

A
  • Limit access to lush pasture e.g. feed hay –> put out for 2h –> inc to 24h over 10d, put sheep/young cattle on lush pastures, strip-grazing, use after hard frost, mow.
  • Monensin, lasolacid: feed 1-6d prior to, and first 10d on, pasture.
114
Q

Describe aetiology of Feedlot Acute Interstitial Pneumonia.

A
  • Unknown.
  • Proposed mechanisms: feed assoc pneumotoxins or factors related to protein metab, chronic bacterial pneumonia, gender/hormonal influences, chronic small airway injury, BRSV, heat or dust exposure, hypersensitivity reactions –> multifactorial?
115
Q

Describe the epidemiology of Feedlot Acute Interstitial Pneumonia.

A
  • Second leading cause of death of feedlot cattle behind bronchopneumonia.
  • Most often cattle on feed >60d (vs 45d peak for Shipping Fever).
  • Inc risk in Summer and in heifers.
116
Q

List the clinical signs of Feedlot Acute Interstitial Pneumonia.

A
  • Found dead.
  • Rapid onset expr dyspnoea +/- tachypnoea, open-mouth breathing, head and neck extended.
  • +/- froth from mouth.
  • +/- fever.
  • +/- cyanosis, tachycardia, s/c emphysema.
  • Ausc –> dull areas throughout lungs w some crackles.
117
Q

Describe necropsy findings in cattle that die from Feedlot Acute Interstitial Pneumonia.

A
  • Petechial/eccymotic haemorrhages in larynx, trachea, bronchi; frothy fluid in airways.
  • Lungs fail to collapse, heavy, firm, rubbery texture; usually interlobular or bullous emphysema; +/- oedema; +/- ‘patchwork’ appearance.
  • Histo: alveolar hyaline membranes, alveolar fibrin, interstitial oedema, type II pneumocyte proliferation; +/- haemorrhage, emphysema, inflam infiltrates.
  • +/- changes related to chronic resp dz e.g. fibrin on pleura, peribronchiolar lymphoid cuffing or vascular fibrosis.
118
Q

Outline treatment and prevention of Feedlot Acute Interstitial Pneumonia.

A
  • Furosemide, flunixin, dexamethasone, ABs (often concurrent bronchopneumonia).
  • Px guarded therefore consider slaughter.
  • No specific methods of prevention, dec infections and dust, monensin not effective.
119
Q

Describe aetiology of Mouldy Sweet Potato Toxicity.

A

Ingestion of toxin produced by sweet potatoes (Ipomoea batatas) infected with Fusobacterium solani.

120
Q

Describe the epidemiology of Mouldy Sweet Potato Toxicity in cattle.

A
  • Outbreaks when cattle fed mouldy sweet potatoes.
  • High morbidity and mortality.
  • Nursing calves not affected.
121
Q

Describe the pathophysiology of Mouldy Sweet Potato Toxicity in cattle.

A
  • F. solani infects sweet potato –> sweet potato produces 4-hydroxymyoporone (hepatotoxic) –> fungus converts to pneumotoxins; most abundant is 4-ipomeanol.
  • 4-ipomeanol ingested –> bloodstream –> lungs –> metab by P-450 mixed oxidase system in Clara cells and type I pneumocytes –> reactive intermediates bind w intracellular proteins/macromolecules –> degen/necrosis/exfoliation of Clara cells and type I pneumocytes + oedema –> hyaline membrane formation, adenomatosis (type II pneumocyte prolif) and Clara cell proliferation.
122
Q

List the clinical signs of Mouldy Sweet Potato Toxicity in cattle.

A
  • Acute onset tachypnoea, tachycardia, hyperpnoea, dyspnoea w expr grunt, extension of head/neck, flaring nostrils, frequent deep cough.
  • Ausc: crackles, harsh BV sounds.
  • CSx dev in 24h, death in 2-5d.
123
Q

Describe necropsy findings in cattle with Mouldy Sweet Potato Toxicity.

A
  • Lungs wet, firm large, fail to collapse, haemorrhagic, gelatinous oedema fluid, emphysematous w bullae.
  • Histo: alveolar hyaline membranes, alveolar fibrin, interstitial oedema, type II pneumocyte proliferation; +/- haemorrhage, emphysema, inflam infiltrates.
124
Q

Outline treatment and prevention of Mouldy Sweet Potato Toxicity in cattle.

A
  • Furosemide, flunixin, dexamethasone.

- Do not feed mouldy sweet potatoes.

125
Q

Describe aetiology of Perilla Ketone Toxicity.

A
  • Perilla/purple mint (Perilla frutescens) leaves and seeds contain a pneumotoxin.
  • Common weed in SE USA.
  • 2m high, square stem, serrated leaves, small white-purple flowers.
126
Q

Describe the epidemiology of Perilla Ketone Toxicity in cattle.

A
  • Cattle, sheep and goats susceptible.
  • Adult cattle avoid plant, calves may prefer it.
  • Most toxic seed-flower stage (Aug-Oct).
  • Toxic in hay.
127
Q

Describe the pathophysiology of Perilla Ketone Toxicity in cattle.

A
  • Volatile oils of P. frutescens contain furans.
  • Perilla ketone predominates in late growing season –> ingested –> absorbed from rumen into bloodstream –> lungs –> metab by P-450 mixed oxidase system in Clara cells and type I pneumocytes –> reactive intermediates bind w intracellular proteins/macromolecules –> degen/ necrosis/exfoliation of Clara cells and type I pneumocytes + oedema –> hyaline membrane formation, adenomatosis (type II pneumocyte prolif) and Clara cell prolif.
128
Q

List the clinical signs of Perilla Ketone Toxicity.

A
  • Animals often found dead.
  • Sudden onset moderate to severe dyspnoea, wheezing, frothing at mouth, expr grunt.
  • Worse with exertion.
  • Death in 3-7 days.
129
Q

Describe necropsy findings in cattle with Perilla Ketone Toxicity.

A
  • Lungs distended, fail to collapse, moist, heavy, oedematous, emphysematous.
  • Often bullae, pleural effusions, froth.
  • Histo: oedema, alveolar epi hyperplasia, emphysema, congestion.
130
Q

Outline treatment and prevention of Perilla Ketone Toxicity in cattle.

A
  • Furosemide, flunixin, dexamethasone.

- Eliminate perilla mint from pasture/take cattle off hay.

131
Q

Describe the presentation of pulmonary disease in animals with pyrrolizidine alkaloid toxicity.

A
  • Animals w chronic liver dz from PA tox can also develop lung lesions.
  • PA toxin activated by P-450 mixed oxidase system in lungs –> oedema, congestion, haemorrhage, prolideration of bronchiolar and alveolar epi cells with megalocytosis, interstitial fibrosis and inflammatory infiltrates.
132
Q

Describe the pathophysiology of toxic gas-induced lung injury in cattle.

A
  • Enviro gases/fumes/smoke.
  • Chronic low level exposure –> dec dz resistance, dec growth rate.
  • Exposure to higher levels –> lethargy, mild dyspnoea, anorexia, dec growth rate, excessive lacrimation or salivation.
  • Low incidence sudden death/stillbirths.
  • Acute, severe outbreaks of ARDs possible.
133
Q

List sources of toxic gas exposure in ruminants.

A
  • Silos: nitrogen dioxide.
  • Cutting/welding galvanised pipes: zinc oxide.
  • Machinery exhausts/heaters: carbon monoxide.
  • Ag chemical spills: chlorine, formaldehyde, insecticides.
  • Manure: hydrogen sulphide, ammonia, methane, CO, CO2.
134
Q

Describe the aetiology of Hypersensitivity Pneumonitis in cattle.

A

Exposure to dusk from mouldy hay/grain/plant matter containing actinomycete spores.

135
Q

Describe clinical signs of Hypersensitivity Pneumonitis in cattle.

A
  • Similar to RAO in horses; coughing, inc expr effort/wheezes.
  • Dz of confined cattle (Winter).
  • Acute and chronic forms.
136
Q

Describe necropsy findings in cattle with Hypersensitivity Pneumonitis.

A
  • Acute: lungs superficially normal but see small grey spots which represent interstitial and peribronchiolar acumm of lympho, in others see red centres of atelectasis surrounded by pink, inflated lung.
  • Chronic: similar findings plus intra-alveolar fibrosis and epithelial hyperplasia.
137
Q

Describe treatment of cattle with Hypersensitivity Pneumonitis.

A
  • Environmental management key i.e. remove mouldy hay/grain/straw etc. from environment, improve ventilation, turnout if possible.
  • Steroids +/- bronchodilators.
138
Q

Describe Dictyocaulus viviparus.

A

Trichostrongylid nematode that lives in the bovine trachea and bronchi; 8cm white worms.

139
Q

Describe the lifecycle of Dictyocaulus viviparus.

A
  • Survives in temperate climates.
  • Adult worm in lungs lay eggs, mature to larvae –> coughed up and swallowed –> faeces –> L3 –> ingested –> migrated through intestines to mesenteric LNs –> L4 –> migrate through blood and lymph to lungs –> adult.
140
Q

Describe clinical signs of Dictyocaulus viviparus infection in cattle.

A
  • CSx in eosinophilic exudate in small airways –> gradual cough and tachypnoea; if very severe infection may see death.
    ii) Patent phase (25-55d): adults, eggs, larvae in airway –> tracheitis, bronchitis, pneumonia w consolidation in caudodorsal lungs; cough, tachypnoea, dyspnoea, anorexia, wt loss, fever if secondary bacterial inf, harsh BV sounds, wheezes and crackles; may –> death.
    iii) Late patent phase (55-90d): CSx grad resolve, adults expelled, may –> worsening CSx/death with secondary infection/re-infection.
141
Q

Outline diagnosis of Dictyocaulus viviparus infection in cattle.

A
  • Larvae ID from faeces or TTW via Baerman test: 390-450um, pointed end, dark granules in intestines.
  • CBC: eosinophilia.
  • Abs ID via ELISA of serum or milk.
142
Q

Describe necropsy findings in cattle that died of Dictyocaulus viviparus infection.

A
  • Atelectic lung lobules –> consolidation in caudoventral lungs.
  • Larvae and worms in airways.
  • If re-infection occurred: pulmonary lymphoid nodules under pleura with eosinophilic parasitic debris, macrophages, multi-nucleated giant cells, hyperplastic bronchiolar epithelium, eosinophils, plasma cells.
143
Q

Describe treatment and prevention of Dictyocaulus viviparus infection in cattle.

A
  • Azoles and mectins.
  • Only cough –> good Px, additional CSx –> guarded.
  • Rotational deworming and pasture management.
144
Q

What parasitic organism can cause acute interstitial pneumonia in cattle co-grazing pastures with pigs?

A
  • Ascaris suum.
  • CSx: depression, anorexia, fever, tachycardia, tachypnoea, dyspnoea, coughing, ruminal stasis, bloat, inc BV sounds.
  • Dx: necropsy and demonstration of larvae.

LAIM: Respiratory (5 decks)

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