Respiratory disease in cattle Flashcards
1
Q
Pneumonia definition
A
= inflammation of the lungs
2
Q
BRD
A
= bovine respiratory dz
- general term for resp dz in attle
- multifactorial (pathogens, environment, management) and varied pathogen involvement
3
Q
Shipping fever / transit fever
A
- occurs in groups of animals post weaning (usually 6m-2y) commonly following transport, mixing groups of animals from different sources or sudden diet change
- the main pathogen associated is M.haemolytic, although others may be involved
- more common in the US
- also more common in beef due to weaning age
- respiratory dz triggered by stress
4
Q
Husk
A
- cattle lungworm
- Dictyocaulus viviparus
5
Q
Impact for dairy heifers
A
- resp dz most commonly doesn’t cause death but sickness -> takes longer to wean the, stunted growth/reduced growth rates, etc, more added expenses
- cows have rubbish lungs cf horses (1/3rd size of adult horse vs adult cow), tiny airways
- damaged lunged ruins ability to oxygenate air
- oxygen really important for utilisation and getting energy out of the diet
- so efficiency and productivity drops
- don’t grow as well -> longer to get in calf and reduced milk yield
- also don’t survive on farm as long -> 6m shorter than others
6
Q
Viral causes of respiratory dz in cattle
A
- IBR (infectious bovine rhinotracheitis)
- PI3
- RSV
- BVDV
- MCF (malignant catarrhal fever
7
Q
Bacterial causes of respiratory dz in cattle
A
- Mycoplasma bovis
- Mannheimia haemolytica
- Pasteurella multocida
- TB (Mycobacteria)
- Histophilus somni (more common in North America)
- Truperella progenies (Chronic suppurative pneumonia)
- Contagious bovine pleuropneumonia (CBPP)
8
Q
Parasitic causes of respiratory dz in cattle
A
- Dictyocaulus vivparus
9
Q
Management causes of respiratory dz in cattle
A
- stocking density
- ventilation
- colostrum management
10
Q
Other causes of respiratory dz in cattle
A
- fog fever
- caudal vena caval thrombosis
- aspiration pneumonia
11
Q
IBR
A
= Infectious bovine rhinotracheitis
- Bovine Herpes Virus 1
– alphaherpes virus (several strains of BHV-1, Europe, North America, Africa)
– gammaherpesvirus (rhadinoviruses such as BHV-4, OHV-2)
- highly infectious and contagious
- endemic in the UK: approx 40% of cattle have been exposed
- carry for life, and shed
- URT dz
12
Q
Epidemiology of IBR
A
- resp infection spread by aerosol
- direct contact or shared air space for sustained period
- variable incubation period of 10-20d
- latency -> once infected (or vaccinated with live vaccine) the animal remains infected for life
- recrudescence and shedding following periods of stress (calving, movement, illness, corticosteroid use)
13
Q
Clinical syndrome of IBR (resp dz)
A
- resp disease most common form
- cattle >6m of age (but can be younger)
- often worse in growing age groups (6-24m)
- mild dz: conjunctivitis, epiphora, mild strain or immunity
- subacute dz: adult cattle - milk drop, pyrexia (40C), nasal discharge, hyperpnoea
- acute dz: growing cattle (e.g. heifers) with marked pyrexia and secondary infection, purulent nasal discharge and conjunctivitis
- worse in growing age groups
14
Q
Clinical syndromes of IBR (complications)
A
- peracute dz: very high fever and death in 24h
- secondary bronchopneumonia (due to secondary bacterial infection
- tracheitis and erosions within the trachea, so tracheal auscultation important
- mortality can be 10% in younger animals
15
Q
Clinical syndromes of IBR (repro signs)
A
- abortion (often [up to 100d] after resp signs)
- genital lesions (IPV)
- lower conception rates
- can also get bulbous lesions and ulcers on the genitalia
16
Q
Diagnosis of IBR
A
- history and CS: history of new animals or groups into the herd, nose to nose contact with other farms, often CS in several animals, compared to MCF: no mouth/nasal lesions or keratitis
- individual animal testing: nasal and conjunctival swab (presence of virus on PCR)
- paired blood samples from acute cases (rising tires on ELISA antibody test)
- dairy herds: bulk milk antibody test to monitor exposure of the herd
- acute outbreak -> test for virus
- paired serology not useful for calves due to maternal antibodies
17
Q
Tx of IBR
A
- anti-inflammatories (NSAIDs)
- oral fluid if dehydrated
- most will get over it in a couple of days and milk yield will increase again
18
Q
Control and eradication of IBR
A
- do nothing
- vaccinate to control clinical signs: route herd vaccination (live vs attenuated available), conventional or marker vaccine, included in vaccines for other pathogens
- accreditation/eradication (+/- vaccination)
- intranasal vaccine -> protection within 2-4d, lasts ~60d, useful for baby calves as offers local mucosal protection
- parenteral vaccine -> protection within a few weeks, vaccinated adult herd 6-12 monthly depending on manufacturer
19
Q
IBR accreditation schemes
A
- different levels of accreditation
- accredited free: 2 qualifying tests and regular monitoring (milk/blood), requires double fencing
- vaccinated monitored free: 2 qualifying tests and regular monitoring (milk/blood), vaccinate with marker vaccine, no requirement for double fencing
- eradication programme: if no. of positive animals is low they may be removed from the herd, if this is not possible the herd can be vaccinated (marker vaccine) and enter the VMF scheme once all positive animals have left the herd
- eradication is hard
- Germany doesn’t have IBR
- benefits of these schemes: export trade, reduced disease, pedigree animals
20
Q
IBR vaccination
A
- several available
- mostly ‘marker’ vaccines: differentiate vaccinated vs naturally exposed/infected, useful where attempting to eradicate dz
- live vaccine: rapid protection, esp where given intranasally, some evidence overall more effective, baby calves or in an outbreak
- inactivated vaccine: some evidence reduce shedding in latently infected animals, e.g. in dairy herd with high bulk milk Ab
21
Q
Other control measures for IBR
A
- main risk is nose-nose contact
- good biosecurity (double fencing at boundaries)
- bought in stock: ideally avoid, don’t mix animals with others then return to herd, test & quarantine can be effective
22
Q
RSV
A
= respiratory syncytial virus
- incubation: 2-5d
- pathology: necrotising bronchiolitis and interstitial pneumonia, whilst emphysematous lesions may develop in caudodorsal lung lobes (looks like bubblewrap)
- species specific
- ubiquitous on farms
- vast majority of cases are mild and recover within 1w
- severe cases: open mouth breathing, reluctance to move
- vaccine: intranasal
- no routine surveillance
- gets worse with stress (around calving, weaning)
23
Q
PI3
A
= parainfluenza 3
- highly contagious
- more likely in stressed animals
- infects the ciliated epithelium of the resp tract, alveolar epithelium and macrophages
- signs: lethargy, pyrexia, serous nasal & ocular discharge
- coughing with secondary bacterial infection or if reaches LRT
- if only pathogen present it will be mild, but gets bad with secondary bacterial infection
- predominantly URT (rhinitis & tracheitis)
- can go on to cause bronchointerstitial pneumonia but this is not common
- diagnosis: PCR
24
Q
MCF
A
= malignant catarrhal fever
- needs to be on list of differentials for sudden death of adult cow
25
Q
MCF aetiology
A
- caused by OvHV-2 which sheep carry without showing clinical dz
- stress may increase viral shedding by sheep, e.g. at shearing or lambing
26
Q
MCF epidemiology
A
- in cattle, dz is usually sporadic (outbreaks have been recorded but these are rare)
- tranmission is by aerosol, direct contact, or contaminated feed/water/bedding
- cattle can’t pass MCF to other catle
- major problem for deer and bison industry worldwide
27
Q
Clinical signs of MCF
A
- pyrexia
- enlarged LN
- mucopurulent nasal and ocular discharge
- corneal opacity (blindness)
- sloughing of oral and nasal mucosa
- mouth lesions - also think FMD
28
Q
MCF tx/control
A
- almost always fatal
- no currently licensed tx or vaccines
- symptomatic tx
- get lots of euthanasia on welfare grounds
29
Q
MCF PM
A
- inflammation and necrosis of the resp system, GIT, CNS, urinary system
- causes huge vasculitis around the body
30
Q
bTB
A
- bovine tuberculosis
31
Q
bTB epidemiology
A
- reservoirs of infection: badgers, deer, ferrets able to spread dz from developed lesions, infected cattle
- killed by sunlight: able to survive desiccation, acids, alkalis, can survive for 6-8w on pasture
- routes of infection: ingestion (outside or when wildlife reservoir involved) or inhalation (when housed)
- excreted in: urine, sputum, faeces, milk (baby calves), exhaled air, vaginal and uterine discharge
32
Q
New infections of bTB
A
- from infected cattle: cattle-cattle spread is mainly via inhalation in buildings (low aerosol infectious dose), occasionally via infected milk to calves, false negatives during testing using skin test
- from infected badgers: M. Bovis is present in badgers in areas of high bTB, same spoligotypes in both cattle and badgers in the same area, spread both ways
- from other wildlife and contaminated slurry
33
Q
Clinical signs in cattle of bTB
A
- usually testing regimes are such that clinical dz is rarely seen
- soft, productive cough, worse if exercised or pharynx palpated
- weight loss, LN enlargement? can also have mastitis with udder induration, alimentary and generalised forms unusual
- but should always be a differential for chronic resp dz even though rare
34
Q
Testing for bTB
A
- SICCT: 2 injections (avian & bovine TB), clear inconclusive reaction, spec: 99.98%, sens: 50-80%
- IFN gamma testing: spec: 96.5%, sens 90%
- Antibody test: occasionally used as a 3rd line test, spec 98%, sens 65%
- PM inspection: all cattle are inspected, but reactors/cattle from restricted herds have more detailed inspection, approx 60% of skin test reactors have no visible lesions at PM - due to insensitivity of this as a diagnostic technique
35
Q
Vaccination for bTB:
A
- vaccinating cattle: BCG vaccine has protective effect in cattle but it causes them to react to the TB test, international trade requires cattle to be TB test, a DIVA test is required to allow both vaccination and testing (test developed and going through authorisation process)
- vaccinating badgers: 2010 BCG licensed for use in badgers, reduces lesion development and shedding, but won’t cure an infected badger, requires trapping of sufficient animals for a social group to have ‘herd immunity’, oral vaccine in development
36
Q
CBPP
A
- contagious bovine pleuropnomonia
37
Q
CBPP aetiology
A
- caused by bacterium Mycoplasma mycoides
- widespread in Africa, eradicated from the UK
38
Q
CBPP epidemiology
A
- transmission is mainly via aerosol
- survival of the organism in the environment is poor
- recovered animals may become carriers which creates challenges for control programmes
39
Q
CBPP clinical signs
A
- pyrexia
- increased respiratory rate and effort
- weight loss
- polyarthritis may be seen in affected calves
- causes diffuse pneumonia with some oedema in the lungs -> get thrombosis of pulmonary vessels, so fluid leaks out
- marvelling of the lungs on PM
40
Q
CBPP diagnosis
A
- PCR on PM
41
Q
CBPP control
A
- notifiable in england
- vaccination may be attempted in countries where cattle movements cannot be restricted
- treatment may be used in endemic areas
- quality issues around supply of vaccine currently, as well as can’t due to exports
42
Q
Mycoplasma bovis
A
- sole pathogen, or more commonly in combination with other pathogenic respiratory bacteria, viruses or parasites
- ~13 different types of mycoplasma, not all pathogenic
- dz of LRT, also found in URT
- haematogenous spread within the animal
- intracellular pathogen
- biofilm production contributes to bacterial survival in the environment and its persistence inside the host
- often herds with mastitis with mycoplasma, culling is the solution
- shed in respiratory surface secretions and can be transmitted by aerosols through coughing, there is initial colonisation of the tonsils
- infected cows shed M.bovis in their milk -> pass into calves
- asymptomatic carrier animals
- seen commonly on robotic feeders for calves as they share the teat
43
Q
Mycoplasma bovis pathology
A
- caseonecrotic pneumonia is recognised commonly in dairy calves
- otitis media -> head tilt
- yellowy thick fluid on joint tap -> polyarthritis
- initially colonises the tonsils
- can cause abortions, but not high up on differentials list for abortions
- lots of fibrin will attach to the lung lobes and pleural cavity in the thorax
44
Q
Mycoplasma bovis diagnosis
A
- BAL -> risks putting bacteria into the lungs, false positives, only testing 1 small part of the lung (i.e. 1 lobe on 1 side)
- PCR -> very sensitive, only need a small bit, doesn’t need to be live to test positive
- PCR & ELISA -> for bulk milk from adult cows, or for polyarthritis
45
Q
Mannheimia haemolytica cf. P.multocida
A
- most commonly confirmed aerogenous infection in suckler cows and often associated with ‘feedlot’ cattle
- can be primary cause or secondary invader
- diseases tends to be more severe than P.multocida
46
Q
Pasteurella multocida cf M. haemolytica
A
- more commonly isolated from calves, less commonly from feedlot cattle
- more likely to be secondary invader
- disease tends to be less severe
47
Q
M. haemolytica & P. multocida
A
- Gram negative, aerobic bacteria
- commensals of URT and several serotypes
- may be involved in sporadic cases or outbreaks
- systemic vaccines available, unable to use for baby calves
- routinely test at 8m
- reduction: reduce stress, mixing, transport
48
Q
Fog fever
A
- acute bovine pulmonary oedema and emphysema
- more commonly diagnosed in sucklers, associated with grazing
- typically causes disease when cattle move from spares to lush, high protein pasture
- ‘fog’ pastures are lush regrowth pastures following cutting for hay or silage, cattle typically moved onto these in the autumn
- L-tryptophan is ingested and converted into 3-methylindole which is pneumotoxic
- high mortality rate (up to 30%) and often animals are found dead (acute onset)
- young stock in 1st 6m of life are picky eaters and so don’t eat much of it
- not very common in the UK
49
Q
Clinical signs of fog fever
A
- severe respiratory distress (air hunger, open mouth breathing) without coughing or pyrexia (as not infectious)
- main differentials: lungworm and RSV
50
Q
Fog fever prevention
A
- introducing cattle to lush pasture slowly/grazing pasture before it gets lush
- feeding palatable hay/silage prior to turnout (gradual diet change)
- grazing young stock rather than adults on lush pasture
51
Q
BRD diagnosis
A
- no gold standard
- pathogen detection
- lung pathology detection
- clinical signs based
- epidemiology based
52
Q
Pathogen detection - antigen testing
A
- who? acutely unwell animals before secondary bacterial infections have become established
- what samples?
— conjunctival swab submitted for an immunoflourescent antibody test (IFAT) or PCR can be used for IBR diagnosis
— nasopharyngeal swab and BAL: usually not used as 1st course of action, result of tx failure or to allow more specific directed tx, unlike NP swab, BAL ensures samples are obtained from the LRT and hence reduces chances of isolating commensal bacteria - can be very expensive
- unlikely to change tx/prevention/control
- definitely use to look for IBR: won’t impact tx for resp dz but does for fertility
53
Q
Lung pathology detection - PME
A
- any dead or moribund animals should be sent for PM
- tx, widespread mucosal destruction and secondary bacterial infections may reduce the likelihood of identifying the causative agent(s)
- if full PME not possible, examine the abdomen, lungs and trachea on farm
- note distribution and severity of lesions
- cranioventral lung lobes typically worst affected
- take samples that include the margin between normal and affected tissue, send fresh tissue for C&ST and fixed tissue for histopathology
54
Q
Pathogen detection - exposure
A
- serology can be useful, esp in older calves, however a rising antibody titre between 2 samples taken 2w apart is required before any conclusions can be drawn
- serology is likely to cost in excess of £500 and take at least 3w to yield results
55
Q
Secondary problems - immunosuppression
A
- FPT: sample 10 calves less than 7d and send for serum total protein or zinc sulphate turbidity testing to assess FPT (in younger calves only)
- BVD testing: herd status is super important
- it may be appropriate to consider taking samples for other causes of immunosuppression including selenium deficiency, liver fluke and parasitic gastroenteritis
- BVD is immunosuppressive -> leukopenia
56
Q
Advantages of detection of antigen in clinical samples (including nasal/nasopharyngeal swabs, TTW, BAL)
A
- rapid test results
- multiple animals can be sampled including cases and controls
- identification of viral pathogens can be highly significant depending on the nature of the herd
57
Q
Disadvantages of detection of antigen in clinical samples (including nasal/nasopharyngeal swabs, TTW, BAL)
A
- viral infections are transient
- identification is impaired by rising antibody titres
- bacterial isolates from some samples are of dubious significance due to may of them being commensals
58
Q
Advantages of serology to detect rising antibody titres
A
- high sensitivity as most resp pathogens induce a strong antibody response
- less time dependent as it can be effective in the relatively late stage of the dz
- multiple animals tested makes the result relevant to the herd problem
59
Q
Disadvantages of serology to detect rising antibody titres
A
- requires convalescent serum so results aren’t available for >3w
- testing multiple samples can be expensive
- correlation of seroconversion with clinical dz may be impossible in situations when viral infections are accepted to be common
60
Q
Advantages of PM examination with subsequent lab testing
A
- gross and histopathologic examination usually suggests a cause and may be pathognomonic
- comprehensive and robust investigation
- easy to sample the lung and trachea and are ideal sites for sampling further tests
61
Q
Disadvantages of PM examination with subsequent lab testing
A
- diagnosis may be based on a few animals
- animals that diet might not be representative of the herd problem
- death may occur in the subacute phase of the infection when viruses are no longer present
- cases are often treated prior to PM which can be misleading in terms of pathogen identification
62
Q
Most important clinical signs for farmers to notice
A
- calves: not eating, isolation
- adults: eating less of ration, pyrexia
- hard to detect - hence hard to treat early on
63
Q
US uses
A
- looking for: B lines, oedema, nodular areas
- increasing the reliability of BRD diagnosis, esp in cases where there are few other clinical signs
- assessing recovery post tx
- assessing the diagnostic ability of farm staff
- detecting calves in the early stages of disease
- ruling out chronic BRD in cases of poor growth rates and ill thrift
- hard to implement and o properly on famr
64
Q
Measuring BRD: incidence vs prevalence
A
- treatment records: relies on farmers picking up on clinical signs
- recurrence: is the farmer following the protocol? are the animals chronically damaged (not getting tx early)
- seasonality: see more in the winter -> warm and wet, then cold = great for resp dz to spread
- for seasonality go look at housing – see what makes it okay in the summer but not in the winter e.g. ventilation, shelter, humidity
65
Q
Tx of BRD
A
- NSAIDs: meloxicam, kerogen, carprofen
- antibiotics: because mixed dz of viral and bacterial antibiotic tx is justified
- electrolytes?
- TLC
- calves: give anti-inflammatories, if 2d not resolved then justified use of antibiotics
- antibiotics to use: broad spec, cat D = amoxicillin, oxytet, TMPS
- oxytet: resistant to pus, broad spec, good lung penetration
- cat C AB: not wrong to use but need C&ST (proof oxytet won’t work)
66
Q
isolation of sick calves
A
- if treating don’t bother isolating as too late, it’s already circulating in the group
- no point in isolating sick calves with resp dz
67
Q
Ventilation: 8 functions
A
- supply fresh air
- humidity control
- eliminating air borne pathogens
- eliminating endotoxins
- temperature control
- eliminating noxious gases
- eliminating drafts
- decreasing dust
