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FARM ANIMAL > 3.1: Respiratory disease in cattle > Flashcards

3.1: Respiratory disease in cattle Flashcards

Taken from BRD lectures and workshop (10/10/2022)

1
Q

Bovine respiratory disease

A

general term for respiratory disease in cattle, covering various pathogens/environmental/management factors.

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2
Q

Main BRD pathogens: viruses

A
  • IBR
  • RSV
  • PI3
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3
Q

Main BRD pathogens: bacteria

A
  • Mycoplasma bovis
  • Mannheimia haemolytica
  • Pasteurella multocida
  • Mycobacterium tuberculosis
  • Histophilus somni (more common in N. America
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4
Q

Causative agent of IBR

A

Bovine herpesvirus 1 (BHV-1)
* An alpha herpesvirus of which there are several strains

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5
Q

Epidemiology of IBR

A
  • Highly infectious and contagious
  • Endemic in the UK; approx. 40% of cattle have been exposed
  • Latency is possible with recrudescence and shedding around periods of stress e.g. calving, movement, illness, corticosteroid use
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6
Q

Incubation period of IBR

A

2-20 days

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7
Q

Transmission of IBR

A
  • Highly infectious and contagious
  • Spread by aerosol - shared air space for a sustained period required
  • Spread by direct contact including nose-to-nose contact over fences
  • Present in resp tract secretions, bull semen, aborted foetuses
  • Can be transmitted by sheep and goats
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8
Q

Clinical signs of IBR

A
  • Resp signs: tracheitis, harsh URT signs
  • Nasal discharge
  • Ocular signs: epiphora, conjunctivitis
  • Pyrexia (40+)
  • Can cause abortion (up to 100 days) and genital lesions
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9
Q

IBR typically causes respiratory signs in which groups of cattle?

A
  • Typically affects cattle >6 months of age but can be younger
  • Often worse in growing age groups (6-24 months)
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10
Q

Describe signs of subacute IBR

A

Signs are vague and non-specific
* Milk drop sometimes at herd level
* Pyrexic (40=/+)
* Nasal discharge
* Hyperpnoea

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11
Q

Describe signs of acute IBR

A
  • Seen in growing cattle
  • Marked pyrexia ± secondary infection
  • Purulent nasal discharge
  • Marked conjunctivitis
  • Large submandibular LNs
  • Tracheitis (audible as rattling over the trachea)
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12
Q

True/false: IBR and IPV are caused by the same pathogen.

A

True.
Both Infectious Bovine Rhinotracheitis and Infectious Pustulo Vulvovaginitis are caused by BHV-1

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13
Q

Signs of peracute IBR

A
  • Very high fever and death in 24hrs
  • Secondary bronchopneumonia
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14
Q
A

Black tarry lining of trachea - very indicative of IBR

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15
Q

Mortality in IBR

A

Up to 10% in younger animals; rare in adults

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16
Q

Diagnosis of IBR

A

History, clinical signs, and swabs/antibody test
* History: new animals/grous into herd
* Clinical signs: in several animals
* Nasal and conjunctival swabs -> Virus on PCR
* Paired blood samples from acute cases -> rising titres on ELISA antibody test
* Bulk milk anitbody test to monitor exposure of herd

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17
Q

Control options for IBR

A
  • Do nothing - if a few mild cases expected to be self-limiting
  • Vaccination: different protocols available
  • Biosecurity: prevent nose-to-nose contact, double fence at boundaries
  • Buying in stock: avoid if you can, use CHeCS accreditation schemes, quarantine and test new animals
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18
Q

What are the different levels of CHeCS IBR accreditation?
Which level is it advisable to buy at?

A
  • Accredited free - safest
  • Vaccinated/monitored free
  • Eradication programme

You should buy at the same level as your current herd.
If good -> bring in only IBR free animals.
If not so good -> don’t want to bring in naïve animals

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19
Q

What are the different types of IBR vaccine? Which would you use in the face of an outbreak?

A
  • 2 types: live vs inactivated
  • Live vaccines are used in the face of an outbreak. Some evidence that they are more effective overall.
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20
Q

True/false: most vaccines for IBR are marker vaccines.

A

True
This allows differentiation between vaccinated and naturally exposed/infected animals.
Useful when attempting to eradicate disease.
Both live and inactivated vaccines can be marker vaccines

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21
Q

Which IBR vaccine type is most appropriate for a herd where disease is endemic?

A

Inactivated - it is better at reducing shedding than a live vaccine.

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22
Q

True/false: some IBR vaccine protocols combine live and inactivated forms of the vaccine.

A

True
Many start with the live vaccine, then move on to the inactivated form.

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23
Q

Provide some examples of IBR vaccines (trade names)

A
  • Bovilis IBR (MSD)
  • Rispoval IBR (Zoetis)
  • Hiprabovis (Hipra)
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24
Q

What is the causative agent of Malignant Catarrhal Fever?

A
  • OvHV-2
  • This is carried by sheep without causing them to show clinical signs
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25
Q

Describe the epidemiology of MCF in cattle

A
  • Disease is usually sporadic, affecting a small number of animals rather than an entire herd
  • Outbreaks have been recorded but are rare
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26
Q

Transmission of MCF

A
  • Methods of transmission: by aerosol, direct contact, contaminated feed/water/bedding
  • Cattle cannot pass MCF to other cattle. They have to get it from a sheep
  • Stress may increase shedding by sheep e.g. shearing, lambing
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27
Q

What important piece of information from the history can tell you if cattle may be at risk for MCF?

A

Any history of exposure to sheep

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28
Q

True/false: deer and bison can carry MCF asymptomatically

A

False
MCF kills deer and bison and is a major problem for these industries.

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29
Q

Clinical signs of MCF

A
  • Pyrexia
  • Enlarged LNs
  • Mucopurulent nasal and ocular discharge
  • Corneal opacity
  • Sloughing of oral and nasal mucosa
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30
Q

Treatment and control of MCF

A
  • Testing is available: antibodies/virus PCR
  • Almost always fatal: no licensed treatment or vaccines
  • Euthanasia is usually best option
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31
Q
A

Malignant catarrhal fever (MCF)
* Can see corneal opacity and mucopurulent nasal discharge

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32
Q
A

Malignant catarrhal fever (MCF)
* Image shows severe sloughing of nasal mucosa

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33
Q
A

Malignant catarrhal fever (MCF)

34
Q

What is the incubation period for Respiratory Synctial Virus?

A
  • Incubation: 2-5 days
35
Q

What is the incubation period for Respiratory Syncytial Virus?

A

Incubation: 2-5 days

36
Q

Describe the pathology caused by RSV

A
  • Necrotising bronchiolitis
  • Diffuse interstitial pneumonia
  • Severe bullous emphysema
  • Emphysematous lesions typically in the caudo-dorsal lung lobes
37
Q

Clinical signs of BRSV

A

BRSV = RSV (there is a human version which is different)
* Pyrexia
* Depression
* Decreased feed intake
* Increased RR
* Cough
* Nasal and lacrimal discharge
* Dyspnoea and potentially open-mouthed breathing in later stages

38
Q

Diagnosis of RSV

A
  • Hard to isolate - may manage to get PCR
  • Paired serology demonstrating a rising titre
39
Q

Treatment of RSV

A
  • Centres on antimicrobial therapy to control secondary bacterial infections
  • No specific treatment for viral interstitial pneumonia: supportive therapy
40
Q

Which animals are typically affected by RSV?

A
  • Young naïve animals
  • Can affect cattle, sheep and goats
41
Q

True/false: this calf is happy :)

A

False!!!
* Outstretched neck, open-mouthed breathing and froth around mouth = severe respiratory distress
* This calf had RSV

42
Q
A

Severe bullous emphysema from a calf with RSV
* There is oedema in the cranial lobes, bullae in the right caudal lung lobe, and interlobular emphysema

43
Q

Describe the clinical features of PI3

A

Parainfluenza 3
* RNA virus
* Virus has similar features to influenza in humans
* Highly contagious
* More likely in stressed animals
* Key role as an initial that leads to the development of secondary bacterial pneumonia

44
Q

Clinical signs of PI3 infection

A
  • Pyrexia
  • Cough
  • Serous nasal and lacrimal discharge
  • Increased RR
  • Increased breath sounds
  • Severity of signs worsen with the onset of secondary bacterial pneumonia
45
Q

Treatment and control of PI3

A
  • Antimicrobial therapy for any secondary bacterial pneumonia
  • NSAIDs and supportive care
  • Vaccines available: often combined in IBR vaccine
46
Q

Describe the epidemiology of bTB

A
  • 25 year eradication strategy with 3 management zones (High, edge, low risk)
  • Reservoirs of infection: badgers, deer, ferrets, infected cattle
  • Infection is often latent for a variable time period
  • Mycobacteria can be killed by sunlight but otherwise quite resilient to desiccation, acids and alkalis.
  • Can survive for 6-8 weeks on pasture
47
Q

Routes of infection for bTB

A
  • Ingestion (e.g. on pasture where wildlife reservoir present)
  • Inhalation (when housed)
  • Excreted in urine, sputum, faeces, milk, exhaled air, vaginal and uterine discharge
48
Q

Major routes of transmission for bTB

A
  • Cattle to cattle spread: mainly through inhalation when housed (aerosol infectious dose = low). Sometimes to calves through infected milk. False -ves at SICCT allow infected cattle to slip through.
  • From infected badgers: e.g. through mineral licks. Can use genetic fingerprinting (spoligotypes) to identify if badgers and cattle infected with same strain.
49
Q

Clinical signs of bTB

A
  • Testing is such that clinical disease hardly ever seen; disruption of testing (FMD) may lead to this
  • Soft, product cough -> worse at exercise/if pharynx palpated
  • Weight loss
  • (sometimes) LN enlargement
  • Sometimes mastitis with udder induration
  • Some forms are generalised/affect GIT specifically
50
Q

Pathology of bTB

A

Rarely seen in UK
* Emaciation
* Chronic cough
* Dyspnoea
* Swelling of submaxillary, retropharyngeal, prescapular, supramammary, mastitis

51
Q

True/false: bTB is zoonotic and notifiable.

A

True.

52
Q
A

Acute bronchointerstitial pneumonia in a calf infected with PI3

53
Q
A

Granulomatous inflammation associated with bTB

54
Q

Methods of testing for bTB

A
  • SICCT
  • Blood testing: antibody, IFN gamma
  • PM inspection
55
Q

When might an IFN gamma test be commissioned?

A
  • When a herd is having continuous TB breakdowns on SICCT
  • SICCT may be missing positive animals -> never quite get on top of it
  • IFN gamma is more sensitive than SICCT -> can cause false positives, but hopefully allows proper clearout of missed cases
56
Q

Treatment and control measures for bTB

A
  • BCG vaccine currently licensed for use in badgers; won’t cure, but will reduce shedding
  • BCG cattle vaccine and DIVA test currently undergoing UK market authorisation
  • Biosecurity: wildlife proof fencing, secure feed storage, raised feed troughs and mineral licks
  • Store slurry for long periods before use and at least 2 months before grazing; do not spread anyone else’s slurry/share equipment
  • Risk based trading: pre and post movement testing
57
Q

Causative agent of Contagious Bovine Pleuropneumonia

A

Mycoplasma mycoides

58
Q

True/false: Contagious Bovine Pleuropneumonia (CPBB) is endemic in the UK.

A

False.
It has been eradicated from the UK and is notifiable.
It is theoretically on the ddx list if you see pyrexia and respiratory dz.

59
Q

True/false: Mycoplasma bovis is commonly seen as a sole pathogen in a cow with pneumonia.

A

False
* Mycoplasma bovis can be a sole pathogen but is more commonly seen in combination with other pathogenic respiratory bacteria, viruses or parasites

60
Q

Describe the pathology seen in Mycoplasma bovis infection

A
  • Caseonecrotic pneumonia (see image)
  • Classic sign in calves: otitis media producing a head tilt
  • Polyarthritis
  • Contagious mastitis that is very hard to get rid of
61
Q

How does Mycoplasma bovis spread through and persist in the animal?

A
  • Haematogenous spread within the animal -> it does not just stay in the respiratory tract
  • It is an intracellular pathogen so immune system/drugs may struggle to reach it
  • The bacterium produces a biofilm which aids survival in the environment and within the host
62
Q

What type of bacteria is Mycoplasma bovis?

A

Gram positive with no cell wall

63
Q

How is Mycoplasma bovis transmitted?

A
  • Direct contact: it is shed in respiratory tract secretions
  • Close contact via a fomite e.g. teat feeders
  • Aerosols
  • Can be shed in milk, possibly transmitted in utero
64
Q

Clinical signs of Mycoplasma bovis infection

A
  • Chronic pneumonia (may also present acutely) with a hacking cough
  • Conjunctivitis
  • Head tilt
  • Ear droop
  • Head shake
  • Arthritis
  • Mastitis
  • Abortion
65
Q

Diagnosis of Mycoplasma bovis infection

A
  • Serology from joint tap/milk
  • PM
66
Q

Treatment and prevention of Mycoplasma bovis infection

A
  • Emerging resistance to tetracyclines and macrolides (remember - no cell wall so amoxicillins ineffective)
  • No commercially available vaccine in the UK
67
Q

These images show clinical signs associated with…

A

Mycoplasma bovis infection

68
Q

What type of bacteria are Mannheimia haemolytica and Pasteurella multocida? Are they pathogenic/commensal?

A
  • Gram negative aerobic bacteria
  • Both can be commensals of the URT
69
Q

True/false: Pasteurella multocida is more likely to be a secondary invader than a primary cause of disease.

A

True
It is most likely to be a secondary invader.

70
Q

True/false: disease caused by Mannheimia haemolytica tends to be more severe than that caused by Pasteurella multocida

A

True.

71
Q

True/false: in any cattle farming operation, identifying the primary cause of respiratory disease is highly important and must be prioritised.

A

False
Sometimes finding the primary causative agent is desired, BUT:
* Pathogen hunts are not guaranteed to provide results or be the best use of money and time
* Respiratory disease often involves multi-pathogen infections
* Many treatment and control measures will be similar across different pathogens
* Consider management/environmental factors that need addressing

72
Q

True/false: Mannheimia haemolytica can be a primary cause of respiratory disease or a secondary invader.

A

True.

73
Q

Fog fever

A

Acute bovine pulmonary oedema and emphysema

74
Q

Pathogenesis of fog fever

A
  • Fog fever = nutritional resp disease caused by ingestion of L-tryptophan
  • (L-tryptophan is found in lush grass/mouldy sweet potatoes)
  • L-tryptophan is ingested and metabolised to 3-methylindole by rumen bacteria
  • 3-methylindole is pneumotoxic, damaging Type 1 ciliated cells and Clara cells
  • There is pulmonary oedema and epithelial hyperplasia
75
Q

Clinical signs of fog fever

A
  • High mortality rate (up to 30%)
  • Animals often found dead
  • Severe respiratory distress without coughing or pyrexia
76
Q

Differential diagnoses that might also be on your list if you suspect fog fever

A
  • Lungworm
  • RSV
77
Q

Diagnosis of fog fever

A
  • Based on history of movement of cattle from dry, sparse pasture to lush pasture
  • Definitive diagnosis on pathology
78
Q

Treatment and prognosis for fog fever

A
  • No specific treatment
  • Palliative therapy, minimise stress
  • Prognosis is guarded with up to 30% mortality
79
Q

Prevention of fog fever

A
  • Introduce cattle to lush pastures slowly
  • Feed palatable hay/silage prior to turnout to allow gradual diet change
  • Graze youngstock rather than adults on lush pastures as they seem to less susceptible
80
Q

Post mortem findings: fog fever

A
  • Pulmonary oedema, alveolar epithelial hyperplasia, emphysema
  • Ecchymotic/petechial haemorrhage in larynx, trachea, bronchi
  • Frothy fluid in airways
  • Congestion/oedema in the lungs: lungs appear wet/shiny due to oedema, and fail to collapse when the thorax is opened

FARM ANIMAL (56 decks)

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