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Food Animal Respiratory 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.
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59
Q

Describe the epidemiology of PI3 infection in cattle.

A
  • Very widespread. - Often no clinical signs. - Important initiator of BRDC. - Incubation period 2d.
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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.
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61
Q

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

A
  • Rarely seen. - Experimental infection –> necropsy –> changes like mild BRSV.
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62
Q

Outline the diagnosis of PI3 infection in cattle.

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

Describe methods for prevention of PI3 infection.

A
  • Inactivated and ML vaccines. - Registered for cattle only; off-label in sheep and goats.
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64
Q

Describe the Bovine Coronavirus (BoCV).

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

List diseases caused by Bovine Coronavirus.

A
  • Calf diarrhoea. - Winter dysentary of adult cattle. - Respiratory disease (recent evidence).
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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.
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67
Q

Describe the Bovine Herpesvirus-4 Virus.

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

List the diseases caused by BHV-4.

A
  • Abortions. - Metritis. - Mammilitis. - Enteric dz. - Conflicting data whether or not causes respiratory dz.
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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.
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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?
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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.
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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.
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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.
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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.
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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.
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76
Q

Outline diagnosis of Mannheimia haemolytica infection in cattle.

A
  • Culture and cytology. - TTW, BAL, thoracocentesis or lung tissue.
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77
Q

Outline treatment of Mannheimia haemolytica infection in cattle.

A
  • Many labelled antibiotics. - NSAIDs in cattle with SIRS.
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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.
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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).
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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.
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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.
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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.
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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.
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84
Q

Outline diagnosis of Pasteurella multocida infection in cattle.

A
  • Culture and cytology. - TTW, BAL or lung tissue.
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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.
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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.
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87
Q

Describe the epidemiology of Histophilus somni infection in cattle.

A
  • Exposure common. - Dz of feedlot cattle > calves.
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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.
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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.
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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.
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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.
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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.
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93
Q

Describe the bacteria Mycoplasma bovis.

A
  • Family: mycoplasma. - Small, pleomorphic organisms w/out cell wall.
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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.
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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.
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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.
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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.
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98
Q

Outline diagnosis of Mycoplasma bovis infection in cattle.

A
  • PM: IHC or culture of organisms plus typical gross/histo lesions.
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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.
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100
Q

Does mycoplasma mycoides infection occur in cattle?

A

Exotic to North America but can cause bovine pneumonia.

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101
Q

Describe the bacteria Biberstenia trehalosi.

A
  • Family: Pasteurellaceae. - Gram negative, facultative anaerobe.
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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.
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103
Q

How can Biberstenia trehalosi infections be prevented in cattle?

A

Possible cross-protection from M. haemolytica vaccines.

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104
Q

Describe the bacteria Trueperella pyogenes.

A
  • Family: Actinomycetaceae. - Gram positive rod, facultative anaerobe.
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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.
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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.
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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).
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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.
145
Q

Group of dairy calves having outbreak of respiratory disease, otitis, CN VII deficits, septic joints. Top differential?

a. Histophilus somni
b. BHV1
c. Mycoplasma bovis
d. Pasteurella multocida

A

c. Mycoplasma bovis

146
Q

What is considered pathognomonic for Vena Caval Thrombosis and Metastatic Pneumonia in cattle?

A
  • Respiratory signs with anemia
  • Widespread wheezes
  • Hemoptysis
147
Q

By what means do bovine herpesvirus-1 spread systemically to other organs?

  1. Immune cells
  2. Red blood cells
  3. Nerve fibers
  4. Herpes-associated protein-B (HAPB)
A

A) Immune cells

Lymphocytes and macrophages, although produce little virus appear to be a means by which virus reaches extra-respiratory sites after respiratory infections.

148
Q

In BHV-1, how are the lungs in necropsy?

A

Lesions in respiratory, ocular, and reproductive mucosa, but do NOT extend to the lungs. “Boom!”

150
Q

Diagnosis of extrinsic allergic alveolitis “bovine farmer’s lung”

A

Antibody to S. rectivirgula

151
Q

Cow with lesion in lung caudodorsally

A

Bovine respiratory syncytial virus

152
Q

What is the most common isolate of Mannheimia hemolytica found in pneumonic lung due to BRD?

  1. A1
  2. A2
  3. A7
  4. A9
A

A. A1

  • A2 in sheep and goats
153
Q
  1. How does the immune response to vaccination cause worsening of disease with bovine syncytial virus?
    a. Increased IL 8 production –> overwhelming neutrophil chemotaxis –> lung tissue destruction
    b. Increased IgG production from vaccine –> purpura-like vasculitis–> systemic illness
    c. Increased IgE from vaccine/natural exposure –> degranulation of mast cells–> severe lower airway pathology
    d. Increased adhesion of neutrophils to pathogen –> secondary neutropenia + immune suppresion
A

c. Increased IgE from vaccine/natural exposure –> degranulation of mast cells–> severe lower airway pathology

154
Q

“Calf pneumonia” is usually referred to which infectious agent?

A

P. multocida

  • Chronic or ongoing pneumonia
156
Q

This clinical presentation corresponds most likely to which condition?

A

Ovine Pulmonary Adenocarcinoma

  • Frothy fluid in the respiratory tract
  • Evident with the wheelbarrow test
157
Q

Which is the most common virus isolated from lungs of calves euthanized for pneumonia

A

Bovine parainflueza 3

158
Q

Main characteristic of M. hemolytica lung lesions

A

CV, fibrinous pleuritis **Necrotizing fibrinous pleuropneumonia**

160
Q

Lesions of Haemophilus in cattle

A

Pleuritis, myocarditis, fibrinopurulent pneumonia

162
Q

Important source of infection of M. mycoides LCT

A

Does that recover from mastitis become chronic carriers

164
Q

What is the function of the surface glycoproteins in BHV-1 infection?

A

Surface glycoproteins gC, gD, gB interact with heparan sulfate proteoglycans for cell attachment and entry

165
Q

What are the six different components of Mannheimia hemolytica that causes pathogenicity ?

A
  1. Exotoxin (leukotoxin) - binds to cells via CD18 - contact increases expression of LFA-1 on ruminant leukocytes (increases sensitivity to injury). Low concentration: leukocyte death via apoptosis. Higher concentration: cell lysis.
  2. LPS - Excessive inflammation. Potentiates effects of Leukotoxin. IL-8 expression is especially important because it is a major inducer of neutrophil chemotaxis.
  3. Polysaccharide capsule - aids in attachment and prevents phagocytosis by neutrophils
  4. IROMP (Iron regulated outer membrane proteins)- bind transferrin - alters function of neutrophils
  5. Adhesions - mediate attachment to host cells
  6. Neuraminidase - aid in host colonization - decrease viscosity of respiratory mucus and decrease repellant negative charge on host cells by cleaving sialic acid residues.
166
Q

Lung lesions for M. bovis

A
  • Caseonecrotic lesions
  • Foci of coagulation necrosis
167
Q

Pathophysiology of OPP

A

Ingestion of milk/colostrum → monocytes or macrophages → spread to tissues

168
Q

Cow in feedlot with fever, cough, red nose. Main differential?

169
Q

With respect to BRSV and vaccination of calves before 1 month old

A

vaccination of calves before 1 month old is not effective.

170
Q
  1. Which best describes the pathophys of interstitial pneumonia/fog fever?
    a. eat lush grass with tryptophan –> forms perilla ketones –> directly kills clara cells/type 1 pneumocytes in lungs
    b. eat lush grass with tryptophan –> forms 3 methyl-indole in rumen –> directly kills clara cells/type 1 pneumocytes in lungs
    c. eat lush grass with tryptophan –> forms perilla ketones –> metabolized by clara cells/type 1 pneumocytes in lungs into toxic byproducts
    d. eat lush grass with tryptophan –> forms 3 methyl-indole in rumen –> metabolized by clara cells/type 1 pneumocytes in lungs into toxic byproducts
A

d. eat lush grass with tryptophan –> forms 3 methyl-indole in rumen –> metabolized by clara cells/type 1 pneumocytes in lungs into toxic byproducts

171
Q

Test for carriers of Mycoplasma mycoides-large colony type

A

PCR of auricular swabs

“hot swollen joints”

172
Q

3 important features of ABPEE

A
  1. Absence of coughing
  2. No signs of sepsis
  3. No adventitious lung sounds
173
Q

Main features in the pathogenesis of H. somni

A

Binds to Fc in antibody –> preventing opsonization

Vasculitis and vascular thrombi Induce IgE

174
Q

Thin ewe syndrome

A

Ovine progressive pneumonia - Maedi visna

  • Aseptic indurative lymphocytic mastitis
176
Q

ATBs to be used in prophylaxis for M. hemolytica

A

Tilmicosin, florfenicol

177
Q

Vaccine with highest efficacy to decrease BRDC?

A

Killed: BVDV MLV: BHV-1, BRSV, PI3

178
Q
  • Most common lung worm in small ruminants
  • where is the adult parasite located?
A

Muellerius capillaris

  • Goat: subpleural tissue
  • Sheep: nodules

*Resistant to levamisole

179
Q

Why is Mycoplasma bovis resistant to b-lactams?

A

Bacteria lacks cell wall

  • Chronic pneumonia and polyarthritis
180
Q

Virulence factor of M. bovis

A

Variable surface proteins (VSPs)

Lack of cell wall –> resistant to b-lactams

182
Q

Contagious disease in small ruminant. Clinical signs include respiratory distress, nasal discharge, skull deformations and sometimes exophtalmia. What is the disease? What is the reason for the skull deformation?

A

Enzootic nasal adenocarcinoma (retrovirus) Skull deformation ocurrs secondary to development of a tumor. The neoplasia is presumplty origined at the nasal glands (respiratory and olfactory mucosal glands)

183
Q

Cattle with cough, harsh dorso-caudal lung sounds, subcutaneous edema

184
Q

Diagnostic method for verminous pneumonia

185
Q

Sheep with cough, weight loss, hard udder

A

Ovine progressive pneumonia (OPP)

186
Q

Cow in feedlot with fever, cough, red nose

187
Q

Diagnosis for Cryptococcus neoformans

A

Latex agglutination

188
Q

Cow with lesion in lung caudodorsally

A

Bovine respiratory syncytial virus

189
Q

Adult cow with respiratory signs, mild, fever, tachypnea:

A

BHV-1, BRSV?

190
Q

Acute interstitial pneumonia in cattle, associated with?

A

Hyperplasia of pneumocytes type 2

191
Q

Most common lung worm in small ruminants

A

Muellerius capillaris

192
Q

Muellerius capillaris: where is the adult parasite located?

A

Goat: subpleural tissue Sheep: nodules

193
Q

Thin ewe syndrome

A

Ovine progressive pneumonia - Maedi visna

194
Q

Clinical pathology in cases of OPP

A
  • Lymphocytosis
  • Hypochromic anemia
  • Hypergammaglobulinemia in advance cases
195
Q

Pathophysiology of OPP

A

Ingestion of milk/colostrum → monocytes or macrophages → spread to tissues

196
Q

Explain the “test and cull” for the control of OPP

A

if (+) → isolate or cull adult and lamb < 1 year age

197
Q

Diagnosis of bovine tuberculosis

A

TB test → injection of M. bovis purified protein derivate

  • At ≠ sites → ↑ specificity

Culture is gold standard (8 weeks incubation)

198
Q

Tretment for Oestrus ovis infestation

A
  • Ivermectin -> treat after the first hard freeze
  • Oral moxidectin is not effective
199
Q

Texel-cross lamb with prolonged inspiration and a honking cough

A

Inherited chondrodysplasia causing tracheal collapse

  • Autosomal recessive
200
Q

Honker cattle

A

Tracheal Edema Syndrome of Feedlot Cattle

201
Q

Death cattle, bloody nose, hematuria

A

C. haemolyticum

202
Q

Virulence factor for Trueperella pyogenes

203
Q

Mycoplasma other than M. bovis causative of BRD? ©

A

M. dispar

(can be normal upper respiratory flora)

204
Q

Best treatment for BRD in dairy cattle ©

205
Q

List neoplasias that have been reported to occur in the nasal passages of sheep and goats.

A
  • Adenopapillomas. - Adenomas. - Adenocarcinomas. - Squamous cell carcinomas. - Ovine/caprine adenocarcinoma virus.
206
Q

Describe the type of virus, clinical signs and prognosis for small ruminants infected with the Ovine/Caprine Adenocarcinoma Virus.

A
  • Retrovirus. - Infected secretory epithelial cells of the nasal turbinates. - No breed/sex predilection. - Typically affects young adults. - Benign, locally invasive; eventually causes weight loss, asphyxia, secondary infection, death. - Dx: endoscopy, rads, PCR (serology not useful). - Surgical tx has been attempted but poor Px.
207
Q

Describe the lifecycle of oestrus ovis.

A
  • Infects sheep more frequently than goats; occ infects other animals –> conjunctivitis in people. - Adult female fly lays 1st instar larvae near the nose of sheep, migrates to nasal and ethmoid turbinates. - 2nd instar larvae develops and migrates to sinus. - 3rd instar larvae migrates to nasal passages. - Sneezed onto ground –> pupate –> adult flies (active in warm months and climates).
208
Q

Describe the clinical signs of oestrus ovis infection in sheep and goats.

A
  • Larvae irritate nasal passages/sinuses. - Mucoid-mucopurulent-blood-tinged nasal discharge. - Sneezing. - Nose rubbing. - Inspiratory stridor. - Adult flies annoy sheep, decrease productivity, predispose to secondary bacterial rhinitis, sinusitis, pneumonia.
209
Q

Describe treatment and prevention of oestrus ovis infection.

A
  • Ivermectin after a frost (when adults are dead). - Outside US: inj moxidectin and doramectin, pour on epinomectin.
210
Q

Are there breed and sex predilections for development of laryngeal abscesses in sheep?

A
  • Rams > ewes. - Texel and Southdown.
211
Q

Describe the aetiology of laryngeal abscesses in ruminants.

A

FB, trauma or congenital cavitation in cartilage –> infection with T. pyogenes.

212
Q

Describe the clinical signs and diagnosis of laryngeal abscesses in ruminants.

A
  • Alert, afebrile, eating well until terminal dyspnoea. - Tachypnoea. - Extension of head and neck. - Progressive dyspnoea. - Cyanosis. - Stertor.
213
Q

Describe the treatment and prognosis of laryngeal abscesses in ruminants.

A
  • Tracheostomy. - PPG. - NSAID. - Px: guarded.
214
Q

Ingestion of what plant by ewes can cause congenital tracheal stenosis in lambs?

A

Veratrum californicum at 31-33 days gestation –> rapid death of lambs after birth.

215
Q

Do herpesviruses cause respiratory disease in small ruminants?

A

Importance of ovine and caprine herpesviruses in respiratory disease is unknown.

216
Q

Do respiratory syncytial viruses cause respiratory disease in small ruminants?

A

Yes, there is an ovine respiratory syncytial virus and a caprine respiratory syncytial virus. No vacc available. CSx similar to cattle with BRSV.

217
Q

Describe presentation of Ovine Adenovirus infections.

A

Causes mild respiratory and enteric disease in lambs.

218
Q

What are the clinical signs of Mycoplasma mycoides ss mycoides (large colon type) infection in goats?

A
  • Adults: polyarthritis, mastitis, AIP +/- death. - Kids (2-8wks): high mortality: i) High fever, death in 12-24h. ii) CNS syndrome w opisthotonus and death in 24-72h. iii) Fever, swollen/painful joints, pneumonia, recumbency.
219
Q

Describe necropsy findings in goats that have died of Mycoplasma mycoides ss mycoides (large colon type) infection.

A
  • Fibrinopurulent polyarthritis. - Pneumonia: patchy to diffuse red consolidation, bronchointerstitial pneumonia +/- fibrinous exudate +/- pleural effusion. - +/- pericarditis, peritonitis, enlarged liver/spleen/kidneys.
220
Q

Describe diagnosis of Mycoplasma mycoides ss mycoides (large colon type) infection in goats.

A
  • Ear canal PCR identifies chronic carriers. - Culture of milk, joint fluid, blood, urine or tissue.
221
Q

Describe treatment and prevention of Mycoplasma mycoides ss mycoides (large colon type) infection in goats.

A
  • ABs almost always unsuccessful (tylosin, tetracycline). - Kids that survive –> arthritis; does –> carriers. - Prevention: maintain MmmLC free herd; purchase does w no hx of kid deaths from pneumonia or arthritis and neg bulk tank +/- indv milk cultures. - Control in an outbreak: feed pasteurised goat or cow colostrum, pasteurised milk to 1mo, pasteurised milk/replace till weaning; cull kids w swollen joints.
222
Q

What disease syndromes are associated with BVDV infection in camelids?

A
  • Diarrhoea. - Ill thrift. - Reproductive losses or congenital infection –> PI crias. - Disseminated disease.
223
Q

What is the period of susceptibility of camelid foetuses for induction of BVDV PIs?

A

Unknown, as the gestation period of camelids is much longer than cattle.

224
Q

What methods can be used to diagnose BVDV infection in camelids?

A
  • Virus isolation from LNs, blood, foetal tissues, placenta. - PCR from whole blood. - IHC on formalin fixed tissues. - NB antigen-capture ELISA used in cattle can give false positive results. - PI-specific assays used in cattle e.g. BVD viral antigen ELISAs on ear notches or serum have not been validated in camelids.
225
Q

Is there a BVDV vaccine licensed for use in camelids?

A

No. Use of cattle vaccines is not recommended as this is not a widespread problem in camelids.

226
Q

Adenovirus-associated pneumonia has been reported in four camelids. What type of virus is this? What clinical signs and necropsy findings were reported?

A
  • Double-stranded DNA virus. - Bronchopneumonia, fibrinous pleuritis and peritonitis, chronic wasting, nasal discharge and lethargy. - Inclusion bodies in liver and virus detected by fluorescent antibody testing in lungs.
227
Q

What virus has been implicated (but not proven) to be the cause of acute respiratory syndrome in alpacas?

A
  • A group 1 coronavirus. - Mild to severe respiratory signs; interstitial pneumonia with lymphocytic infiltrates on post mortem exam.
228
Q

Virulence factor of Manheimia hemolytica?

A

Leukotoxin

229
Q

What is the efficacy of BRSV vaccination of calves before 1 month old?

A

vaccination of calves before 1 month old is not effective.

230
Q

Lesions of Haemophilus in cattle

A

Pleuritis, myocarditis, fibrinopurulent pneumonia

231
Q

BRSV and vaccination of neonatal calves

A

Non protective

232
Q

Vaccine with highest efficacy to decrease BRDC?

A

Killed: BVDV MLV: BHV-1, BRSV, PI3

233
Q

Requisite for M. haemolytica vaccine

A

Leukotoxin

234
Q

In BHV-1, how are the lungs in necropsy?

A

Lesions in respiratory, ocular, and reproductive mucosa, but do NOT extend to the lungs. “Boom!”

235
Q

Effects on vaccine for BRSV

A

Th2 response After intranasal vaccine –> IgA

236
Q

Which is the most common virus isolated from lungs of calves euthanized for pneumonia

A

Bovine parainflueza 3

237
Q

Serotypes causing pneumonia in Manheimmia hemolytica

A

A1 –> Cattle A2 –> Sheep and goats

238
Q

Main characteristic of M. hemolytica lung lesions

A

CV, fibrinous pleuritis **Necrotizing fibrinous pleuropneumonia**

239
Q

Virulence factor for M. hemolytica

A

Leukotoxin –> CD18 receptor Also: PS capsule, IROM P

240
Q

ATBs to be used in prophylaxis for M. hemolytica

A

Tilmicosin, florfenicol

241
Q

Most time of infection for H. somni

A

First 2 months or 2 weeks of the feeding period

242
Q

Why is Mycoplasma bovis resistant to b-lactams?

A

Bacteria lacks cell wall

243
Q

Syndrome caused by Mycoplasma bovis

A

Chronic pneumonia and polyarthritis

Resistant to ATB

244
Q

Virulence factor of M. bovis

A

Variable surface proteins (VSPs)

Lack of cell wall –> resistant to b-lactams

245
Q

Sources of infection for M. bovis

A

Contact Aerosol Infected milk

246
Q

Lung lesions for M. bovis

A

Caseonecrotic lesions Foci of coagulation necrosis

247
Q

Test for carriers of Mycoplasma mycoides-large colony type

A

PCR of auricular swabs

248
Q

Important source of infection of M. mycoides LCT

A

Does that recover from mastitis become chronic carriers

249
Q

What is the function of the surface glycoproteins in BHV-1 infection?

A

Surface glycoproteins gC, gD, gB interact with heparan sulfate proteoglycans for cell attachment and entry

250
Q

Effect of bovine PI3 in RBCs

A

Hemagglutinates and hemadsorbs

251
Q

Serogroup causing pneumonia in P. multocida

252
Q

“Calf pneumonia” is usually referred to which infectious agent?

A

P. multocida

253
Q

What is a main feature of the clinical presentation of P. multocida pneumonia

A

Chronic or ongoing pneumonia

254
Q

Main features in the pathogenesis of H. somni

A

Binds to Fc in antibody –> preventing opsonization Vasculitis and vascular thrombi Induce IgE

255
Q

M. mycoides-large colony type

A

*hot swollen joints*

256
Q

Prevention of m. mycoides LCT

A

Feed heat treated colostrum, or cow colostrum at birth, then pasteurized milk or replacer from 1 month to weaning

257
Q

“Fog fever”

A

Acute Bovine Pulmonary Edema and Emphysema

258
Q

If suspected of M. haemolytica, P. multocida or H. somni, what is the best way to collect a sample that is clinically significant?

A

Distal to the nasopharynx –> TTW, BAL

If not possible, at least deep NPS

259
Q

Neutrophils in BAL of llama ©

A

11% –> higher than horses

260
Q

Diagnosis of extrinsic allergic alveolitis “bovine farmer’s lung”

A

Antibody to S. rectivirgula

261
Q

Which conditon is related to this image and why?

A

Ovine progressive pneumonia

Aseptic indurative lymphocytic mastitis

262
Q

This clinical presentation corresponds most likely to which condition?

A

Ovine Pulmonary Adenocarcinoma

  • Frothy fluid in the respiratory tract
  • Evident with the wheelbarrow test
265
Q

What is considered pathognomonic for Vena Caval Thrombosis and Metastatic Pneumonia in cattle

A
  • Respiratory signs with anemia
  • Widespread wheezes
  • Hemoptysis
266
Q

Most common bacteria implicated in pleuritis and pleuropneumonia in cattle

A
  • M. haemolytica
  • H. somni
267
Q

Most common bacteria in cases of sinusitis in cattle

A
  • Dehorning → T. pyogenes
  • Not dehorning → Pasteurella multocida
268
Q

Possible initial cause of laryngeal necrobacillosis

A

Laryngeal contact ulcers

Histophilus somni?

269
Q

Bacteria implicated in laryngeal necrobacillosis

A

Fusobacterium necrophorum

  • Needs portal of entry
270
Q

Which is an effective way to protect calves against infection with B. trehalosi?

A

Administration of a multivalent MLV vaccine containing M. haemolytica toxoid

271
Q

Which is the best drug for treatment and prevention of BRD? ©

A

Oxytetracycline

272
Q

Best treatment for dyspnea in alpaca ©

273
Q

Cause of ABPEE

A

L-tryptophane from lush pastures –> 3-Methylindole

274
Q

3 important features of ABPEE

A
  1. Absence of coughing 2. No signs of sepsis 3. No adventitious lung sounds
275
Q

Target cells is ABPEE

A

Type I pneumocytes and Clara cells

276
Q

Moldy Sweet Potato

A

4 - Ipomeanol toxicity –> interstitial pneumonia

277
Q

Most common bacteria in pneumonia due to transportation

A

Actinobacillus

Pasteurella

Streptococcus

Respiratory LA (5 decks)

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