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.
2
Q
List the clinical signs of fungal rhinitis in cattle.
A
- Stridor.
- Dyspnoea.
- Mucopurulent nasal discharge.
- +/- epistaxis.
- +/- open-mouth breathing.
3
Q
How is fungal rhinitis diagnosed in cattle?
A
Histo: granulation tissue with eosinophils, mononuclear cells, sporangia, hyphae, filamentous bacteria.
4
Q
How is fungal rhinitis treated in cattle?
A
- Surgical debulking.
- Sodium iodide (NB overdose –> cough, scaly skin, excessive lacrimation).
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).
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.
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.
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.
9
Q
Describe the treatment of Enzootic Nasal Granuloma in cattle and sheep.
A
- Remove allergens.
- Anti-histamines.
- Meclofenamic acid.
- Steroids.
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.
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.
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.
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.
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.
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.
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.
17
Q
Describe the diagnosis of sinusitis in cattle.
A
- Clinical signs and history.
- Percussion (dull sounds or pain).
- Radiographs.
- Sinus centesis (Steinmann pin).
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).
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.
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.
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.
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.
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.
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.
25
Describe the treatment and prognosis of Necrotic Laryngitis.
- ABs: oxytetracycline, penicillin, TMPS.
- NSAIDs (1 dose steroid if severe swelling).
- +/- tracheotomy.
- Nursing care.
- Px good if dx early and aggressive tx, otherwise poor.
26
Describe lesions found at necropsy of cattle that have died from Necrotic Laryngitis.
- 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.
27
Describe laryngeal papillomatosis of feedlot cattle.
- 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.
28
Describe the aetiology of tracheal collapse and stenosis in cattle.
- Infrequently reported.
| - Unknown aetiology; potential causes incl trauma (roping, dystocia), tracheostomies, congenital defects.
29
Describe the clinical signs of tracheal collapse and stenosis in cattle.
- BAR --> tachypnoea, tachycardia, mucosal hyperaemia, dyspnoea exacerbated by exercise/excitement, stertor, 'honking' cough.
- Lack of response to tracheostomy, NSAIDs, ABs.
30
Describe the diagnosis of tracheal collapse and stenosis in cattle.
- Endoscopy.
- Rads: dorsoventral flattening in caudal cervical or cranial thoracic trachea most common; can be lateral.
- Necropsy: dorsally or laterally flattened trachea.
31
Describe the treatment and prognosis of tracheal collapse and stenosis in cattle.
- Px poor.
| - Surgery reported to enable survival to slaughter.
32
Describe the aetiology and pathogenesis of tracheal oedema syndrome (aka Honker Cattle) of feedlot cattle.
- 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.
33
Describe the clinical presentation of the acute form of tracheal oedema syndrome in cattle.
- 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.
34
Describe the clinical presentation of the chronic form of tracheal oedema syndrome in cattle.
- Lighter cattle (130-400kg).
- +/- Hx of IBR/pneumonia.
- Continuous deep, hacking cough.
- +/- unthrifty.
35
Describe treatment and prognosis of tracheal oedema syndrome in cattle.
- Acute: steroids, oxygen, decrease stress.
- Chronic: no tx.
- Px: poor.
36
Describe necropsy findings in cattle that have died from tracheal oedema syndrome.
- 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.
37
List the infectious pathogens which contribute to he Bovine Respiratory Disease Complex.
- 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.
38
Describe the Bovine Herpesvirus-1 (BHV-1).
- Family: Herpesviridae.
- Subfamily: alpha.
- Enveloped DNA virus.
39
List the diseases caused by BHV-1.
- Infectious Bovine Rhinotracheitis (IBR).
- Conjunctivitis.
- Infectious pustular vulvovaginitis.
- Balanoposthitis.
- Encephalomyelitis.
- Mastitis.
40
List the clinical signs of IBR in cattle.
- 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.
41
Describe the pathophysiology of IBR.
- 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.
42
Describe the epidemiology of IBR.
- 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.
43
Describe necropsy findings in animals that have died from IBR.
- 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.
44
How is IBR diagnosed in cattle?
- Virus isolation, IFA, PCR from nasal and conj swabs.
| - Paired serology (Ab titre).
45
Describe treatment and prevention of IBR in cattle.
- 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.
46
Describe the Bovine Respiratory Syncytial Virus (BRSV).
- Family: Paramyxoviridae.
- Subfamily: Pneumovirina.
- Enveloped RNA virus.
- Recent change in BRSV G glycoprotein reported in Europe, likely secondary to antigenic pressure from vaccination.
47
List the clinical signs of BRSV infection in cattle.
- 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.
48
Describe the epidemiology of BRSV infection in cattle.
- 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.
49
Describe the pathogenesis of BRSV infection in cattle.
- 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.
50
Describe the role of the immune response in BRSV infection in cattle.
- 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).
51
Describe necropsy findings in cattle that have died from BRSV infection.
- 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.
52
Outline diagnosis of BRSV in cattle.
- 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.
53
Describe treatment and prevention of BRSV infection in cattle.
- 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.
54
Describe the Bovine Viral Diarrhoea Virus (BVDV).
- Family: Flaviviridae.
- Genus: Pestivirus.
- Enveloped RNA virus.
55
Describe the respiratory disease causes by BVDV infection in cattle.
- Some strains cause mild pneumonia.
| - Importance is as a co-infector in BRDC e.g. w M. haemolytica, M. bovis, BHV-1, BRSV.
56
Describe the pathogenesis of BVDV in BRDC infections.
- 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.
57
Describe the Bovine Parainfluenza-3 Virus (PI3).
- Family: Paramyxoviridae.
- Subfamily: Paramyxovirinae.
- Enveloped RNA virus.
58
List the clinical signs of PI3 infection in cattle.
- Range from subclinical to mild.
- Fever.
- Cough.
- Nasal and ocular discharge.
- Tachypnoea.
- Inc bronchovesicular sounds, wheezes.
59
Describe the epidemiology of PI3 infection in cattle.
- Very widespread.
- Often no clinical signs.
- Important initiator of BRDC.
- Incubation period 2d.
60
Describe the pathophysiology of PI3 infection in cattle.
- 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
Describe necropsy findings in cattle that have died from PI3 infection.
- Rarely seen.
| - Experimental infection --> necropsy --> changes like mild BRSV.
62
Outline the diagnosis of PI3 infection in cattle.
- Virus isolation.
- PCR of nasal swabs.
- Paired serology to demonstrate rising titre.
63
Describe methods for prevention of PI3 infection.
- Inactivated and ML vaccines.
| - Registered for cattle only; off-label in sheep and goats.
64
Describe the Bovine Coronavirus (BoCV).
- Family: Coronaviridae.
- Group 2 Coronavirus.
- Enveloped, single-stranded RNA virus.
65
List diseases caused by Bovine Coronavirus.
- Calf diarrhoea.
- Winter dysentary of adult cattle.
- Respiratory disease (recent evidence).
66
Describe the contribute of BoCV to BRDC in cattle.
- Important role identified in two Shipping Fever outbreaks.
- Evidence vaccination --> less resp dz in feedlot cattle.
- Other evidence suggests no role in BRDC.
67
Describe the Bovine Herpesvirus-4 Virus.
- Family: Herpesviridae.
- Subfamily: Gamma herpesviridae.
- Enveloped DNA virus.
68
List the diseases caused by BHV-4.
- Abortions.
- Metritis.
- Mammilitis.
- Enteric dz.
- Conflicting data whether or not causes respiratory dz.
69
Describe adenoviruses of ruminants.
- Family: Adenoviridae.
- Serotypes: Cattle - at least 10, sheep - at least 6, goats - 2.
- Non-enveloped, double-stranded DNA viruses.
70
Describe presentation of Bovine Adenovirus infections.
- Widespread.
- Frequently subclinical, often assoc w other pathogens.
- Assoc w pneumonia, enteritis, keratoconjunctivitis; weak calf syndrome?
71
Describe the bacteria Mannheimia haemolytica.
- 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
Describe the epidemiology of Mannheimia haemolytica infection in cattle.
- Most common bacterial isolate from feedlot cattle w fatal fibrinous pleuropneumonia.
- Not commonly associated with outbreaks of pneumonia in dairy calves.
73
Describe the pathophysiology of Mannheimia haemolytica infection in cattle.
- 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
List clinical signs of Mannheimia haemolytica infection in cattle.
- 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
Describe necropsy findings in cattle infected with Mannheimia haemolytica.
- 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
Outline diagnosis of Mannheimia haemolytica infection in cattle.
- Culture and cytology.
| - TTW, BAL, thoracocentesis or lung tissue.
77
Outline treatment of Mannheimia haemolytica infection in cattle.
- Many labelled antibiotics.
| - NSAIDs in cattle with SIRS.
78
Outline methods for prevention of Mannheimia haemolytica infection in cattle.
- 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
Describe the bacteria Pasteurella multocida.
- 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
Describe the epidemiology of Pasteurella multocida infection in cattle.
- Normal URT commensal in cattle, sheep and goats.
| - Debate if primary or only secondary lung pathogen.
81
Describe the pathophysiology of Pasteurella multocida infection in cattle.
- 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
List clinical signs of Pasteurella multocida infection in cattle.
- 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
Describe necropsy findings in cattle infected with Pasteurella multocida.
- Purulent bronchopneumonia w plum-coloured CV consolidation and purulent exudate on cut section.
- Fibrin possible.
84
Outline diagnosis of Pasteurella multocida infection in cattle.
- Culture and cytology.
| - TTW, BAL or lung tissue.
85
Outline methods for treatment and prevention of Pasteurella multocida infection in cattle.
- 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
Describe the bacteria Histophilus somni.
- Family: Pasteurellaceae.
- Gram negative aerobe.
- NF of URT and genital mucosa of cattle, goats, sheep.
- Different strains have different virulence.
87
Describe the epidemiology of Histophilus somni infection in cattle.
- Exposure common.
| - Dz of feedlot cattle > calves.
88
Describe the pathophysiology of Histophilus somni infection in cattle.
- 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
List clinical signs of Histophilus somni respiratory infection in cattle.
- 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
Describe necropsy findings in cattle infected with Histophilus somni.
- Plum and brown consolidation CV lungs.
- +/- abscesses.
- Purulent material on cut section of lung tissue.
- +/- fibrinous pleuritis.
- +/- haemorrhage.
91
Outline diagnosis of Histophilus somni infection in cattle.
- Culture: TTW, BAL, pleurocentesis, lung tissue; NB hard to grow in culture therefore trans immediately, pre-tx samples.
- IHC lung tissue.
- Paired titres.
92
Outline methods for treatment and prevention of Histophilus somni infection in cattle.
- 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
Describe the bacteria Mycoplasma bovis.
- Family: mycoplasma.
| - Small, pleomorphic organisms w/out cell wall.
94
Describe the epidemiology of Mycoplasma bovis infection in cattle.
- 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
Describe the pathophysiology of Mycoplasma bovis infection in cattle.
- 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
List clinical signs of Mycoplasma bovis infection in cattle.
- 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
Describe necropsy findings in cattle infected with Mycoplasma bovis.
- Dark red, firm, consolidated CV lungs.
- +/- raised white-yellow firm nodules = foci of caseous necrosis (eosinophilic coagulative necrosis).
- +/- arthritis, tenosynovitis, otitis.
98
Outline diagnosis of Mycoplasma bovis infection in cattle.
- PM: IHC or culture of organisms plus typical gross/histo lesions.
99
Outline methods for treatment and prevention of Mycoplasma bovis infection in cattle.
- 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
Does mycoplasma mycoides infection occur in cattle?
Exotic to North America but can cause bovine pneumonia.
101
Describe the bacteria Biberstenia trehalosi.
- Family: Pasteurellaceae.
| - Gram negative, facultative anaerobe.
102
List clinical signs of Biberstenia trehalosi infection in ruminants.
- Cattle/calves: severe acute/peracute bronchopneumonia --> death.
- Sheep: pneumonia or systemic dz w multi-organ infection.
103
How can Biberstenia trehalosi infections be prevented in cattle?
Possible cross-protection from M. haemolytica vaccines.
104
Describe the bacteria Trueperella pyogenes.
- Family: Actinomycetaceae.
| - Gram positive rod, facultative anaerobe.
105
What is the significance of Trueperella pyogenes in respiratory disease of cattle.
- 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
Define the clinical presentation and list the necropsy findings in Acute Respiratory Distress Syndrome of cattle.
- 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
Describe the definition and aetiology of Acute Bovine Pulmonary Oedema and Emphysema.
- 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
Describe the epidemiology of Acute Bovine Pulmonary Oedema and Emphysema.
- Seen in adult cattle; nursing calves not affected.
- Autumn.
- May be indv but usually outbreaks.
- ~50% morbidity, 30% mortality.
109
Describe the pathophysiology of Acute Bovine Pulmonary Oedema and Emphysema.
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
List the clinical signs of Acute Bovine Pulmonary Oedema and Emphysema.
- 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
Outline diagnosis of Acute Bovine Pulmonary Oedema and Emphysema.
- Usually presumptive.
- Can perform rads --> interstitial pneumonia.
- Research: measure 3-MI in blood and urine.
112
Outline treatment of Acute Bovine Pulmonary Oedema and Emphysema.
- Controversial; stress of handling/moving off pasture more dangerous than not tx?
- Potential meds: furosemide, flunixin, dexamethasone.
113
Outline methods for prevention of Acute Bovine Pulmonary Oedema and Emphysema.
- 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
Describe aetiology of Feedlot Acute Interstitial Pneumonia.
- 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
Describe the epidemiology of Feedlot Acute Interstitial Pneumonia.
- 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
List the clinical signs of Feedlot Acute Interstitial Pneumonia.
- 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
Describe necropsy findings in cattle that die from Feedlot Acute Interstitial Pneumonia.
- 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
Outline treatment and prevention of Feedlot Acute Interstitial Pneumonia.
- 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
Describe aetiology of Mouldy Sweet Potato Toxicity.
Ingestion of toxin produced by sweet potatoes (Ipomoea batatas) infected with Fusobacterium solani.
120
Describe the epidemiology of Mouldy Sweet Potato Toxicity in cattle.
- Outbreaks when cattle fed mouldy sweet potatoes.
- High morbidity and mortality.
- Nursing calves not affected.
121
Describe the pathophysiology of Mouldy Sweet Potato Toxicity in cattle.
- 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
List the clinical signs of Mouldy Sweet Potato Toxicity in cattle.
- 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
Describe necropsy findings in cattle with Mouldy Sweet Potato Toxicity.
- 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
Outline treatment and prevention of Mouldy Sweet Potato Toxicity in cattle.
- Furosemide, flunixin, dexamethasone.
| - Do not feed mouldy sweet potatoes.
125
Describe aetiology of Perilla Ketone Toxicity.
- 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
Describe the epidemiology of Perilla Ketone Toxicity in cattle.
- Cattle, sheep and goats susceptible.
- Adult cattle avoid plant, calves may prefer it.
- Most toxic seed-flower stage (Aug-Oct).
- Toxic in hay.
127
Describe the pathophysiology of Perilla Ketone Toxicity in cattle.
- 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
List the clinical signs of Perilla Ketone Toxicity.
- 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
Describe necropsy findings in cattle with Perilla Ketone Toxicity.
- Lungs distended, fail to collapse, moist, heavy, oedematous, emphysematous.
- Often bullae, pleural effusions, froth.
- Histo: oedema, alveolar epi hyperplasia, emphysema, congestion.
130
Outline treatment and prevention of Perilla Ketone Toxicity in cattle.
- Furosemide, flunixin, dexamethasone.
| - Eliminate perilla mint from pasture/take cattle off hay.
131
Describe the presentation of pulmonary disease in animals with pyrrolizidine alkaloid toxicity.
- 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
Describe the pathophysiology of toxic gas-induced lung injury in cattle.
- 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
List sources of toxic gas exposure in ruminants.
- 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
Describe the aetiology of Hypersensitivity Pneumonitis in cattle.
Exposure to dusk from mouldy hay/grain/plant matter containing actinomycete spores.
135
Describe clinical signs of Hypersensitivity Pneumonitis in cattle.
- Similar to RAO in horses; coughing, inc expr effort/wheezes.
- Dz of confined cattle (Winter).
- Acute and chronic forms.
136
Describe necropsy findings in cattle with Hypersensitivity Pneumonitis.
- 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
Describe treatment of cattle with Hypersensitivity Pneumonitis.
- Environmental management key i.e. remove mouldy hay/grain/straw etc. from environment, improve ventilation, turnout if possible.
- Steroids +/- bronchodilators.
138
Describe Dictyocaulus viviparus.
Trichostrongylid nematode that lives in the bovine trachea and bronchi; 8cm white worms.
139
Describe the lifecycle of Dictyocaulus viviparus.
- 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
Describe clinical signs of Dictyocaulus viviparus infection in cattle.
- 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
Outline diagnosis of Dictyocaulus viviparus infection in cattle.
- 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
Describe necropsy findings in cattle that died of Dictyocaulus viviparus infection.
- 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
Describe treatment and prevention of Dictyocaulus viviparus infection in cattle.
- Azoles and mectins.
- Only cough --> good Px, additional CSx --> guarded.
- Rotational deworming and pasture management.
144
What parasitic organism can cause acute interstitial pneumonia in cattle co-grazing pastures with pigs?
- Ascaris suum.
- CSx: depression, anorexia, fever, tachycardia, tachypnoea, dyspnoea, coughing, ruminal stasis, bloat, inc BV sounds.
- Dx: necropsy and demonstration of larvae.
