Resp disease in Pigs Flashcards
1
Q
Implications of respiratory disease in pigs?
A
- Animal welfare
- Performance & production
- Mortality
- Meat quality
2
Q
How does respiratory disease impact production in pigs?
A
- Morbidity and mortality
- Treatment/veterinary costs/need for vaccination
- Reduced growth rates/increased days to slaughter
- Reduced FCE – feed conversion efficiency (energy into immune system)
- Variation in supply – growth rates, back fat
- Penalties at abattoir – slow line, increased trimming
- Assurance schemes/market (multiplier)
- Having to treat more pigs.
- Environmental impact- more food, slurry, antibiotics
3
Q
Cause of respiratory disease in pigs?
A
- Like other species, they can be broken up by causative agent. Virus often comes in and starts damage, bacteria often secondary.
- Virtually all resp. dz in pigs are multifactorial, rare for it to just be one.
- Bacterial/mycoplasmal
- Viral
- Parasitic
- Secondary bacterial infection of lung tissue already compromised by primary pathogens frequently occurs
- Often more than one agent involved
- Often highly contagious
- Spread by direct or aerosol contact
- Or indirect via birds and vehicles
4
Q
What defence mechanisms do pigs have against respiratory infections?
A
- Nasal chambers
- Turbinates create turbulence
- Changing airway diameters alter speed
- Mucociliary apparatus
- Cough reflex
- Pulmonary alveolar macrophages
- Neutrophil invasion
- Antibody production (airway IgA, alveolar IgG)
5
Q
Clinical signs of resp disease in pigs?
A
- Coughing (often 1stthing noticed)
- Dyspnoea +/- hyperpnoea
- Snuffling sounds (nasal obstruction)
- Heart failure and cor pulmonale (severe/chronic)
- Pleurisy
- Anorexia
- Ocular discharge
- Sudden death
- Why PMs are so important.
6
Q
Diagnosis of resp disease in pigs?
A
- History and CE/observation may provide tentative diagnosis
- Clinical examination often limited and challenging
- Brief auscultation may be possible and increased lung sounds may be evident:
- Wheezing – narrowed airways
- Bubbling sounds – blocking of bronchioles
- Squeaking sounds – pleuritic
- Harsh rubbing sounds – pleurisy
- This must be confirmed with lab tests/PME
- Abattoir surveillance data may indicate current diseases
- Remember mixed infections!
- Dealing with more than one pathogen, but not always clinically relevant.
7
Q
Resp disease in pre-weaned pigs
A
- However, last three are the most common.
- Progressive atrophic rhinitis
- Bordetella bronchisepticum
- Inclusion body rhinitis (pig CMV)
- PRRSv (reproductive and respiratory syndrome virus).
- Hugely important
- Endemic
- Enzootic pneumonia (Mycoplasmasp)
- Glassers disease (Haemophilus parasuis).
- Quite prevalent.
8
Q
Resp disease in weaners, growers and fatteners
A
- Bordetella bronchiseptica
- Glassers disease
- Most common
- Actinobacillus pleuropneumonia
- Most common
- Pasteurella multocida
- Most common
- Mycoplasma hyopneumonia(EP) / hyorrhinis
- PRRSV
- Most common
- Porcine respiratory coronavirus (PRCV)
- Influenza
- Most common
- PMWS?/PCVAD
- (Aujeszky’s disease (pig herpesvirus 1))
9
Q
Significant resp disease in non-immune adult pigs
A
- Glassers disease
- Actinobacillus pleuropneumoniae
- Pasteurellosis
- Enzootic pneumonia
- PRRSV
- Influenza
10
Q
Progressive atrophic rhinitis
A
- Worldwide distribution, mainly intensive units
- Used to be a huge problem, but now larely controlled in UL.
- Less of a problem in recent years – better management
- Caused by Toxigenic Pasteurella multocidain association with Bordetella bronchiseptica
- Bordetella comes in, creates a cytotoxin and then Pasteurella comes in and causes the damage.
- Colonisation of nasal mucosa by B.bwith production of cytotoxin – allowing P.mto invade
- PM damages osteoblasts with osteolytic toxin and enhances osteoclast activity
- CS usually seen at 3-9 wks age – sneezing, nasal discharge/h+, facial deformity - later
- Reduced growth rates and increased risk of pneumonia
11
Q
Diagnosis, treatment and control of progressive atrophic rhinitis
A
- Diagnosis – Causal organisms can be cultured from nasal swabs, serology for B. bronchiseptica.
- PME – Section snout at level of 2ndpremolar – damage to turbinates assessed on 0 (no damage) -5 (severe) scale
- Tx: antibiotics may help if early
- Vacc: sows 2-6wks before farrowing
- Control: Depop-repop with AR-free stock, strategic medication if CS, screening herds with ELISA for B. bronchiseptica
12
Q
Bordetella bronchisepticum in pigs
A
- Found in most pig populations
- Generally mild, self-limiting rhinitis (non-progressing)
- Therefore, clinically and economically of little importance
- Only a problem when in combination with toxigenic Pasteurella multocida.
13
Q
Inclusion body rhinitis
A
- Porcine Cytomegalovirus (herpesvirus)
- >90% UK herds affected
- Transmission pig-pig or aerosol
- Mostly young pigs but outbreak in naive herd may affect all ages
- CS: sneezing, serous nasal discharge and brown ocular discharge, high morbidity, low mortality
- Diagnosis: ELISA, inclusion bodies from nasal swabs
- Control: Maintain closed herd, protect suckling pigs from exposure
14
Q
PRRS
A
- Very important disease – can cause immunosuppression and hence, has a lot of clinical manifestations.
- See repro notes for more details
- PRRS virus – Arterivirus
- Virus replicates in and destroys macrophages and endothelial cells →vasculitis
- Leads to impact on immune function and vasculitis as a result.
- Mixed infections with other resp pathogens very common
- Clinical signs – weaned pigs, mild coughing, sneezing, tachypnoea, innapetence, increased mortality
- Tx: in-feed/water antibiotics to cover period at risk – to reduce 2obacterial infections (usually 6-8 wks)
- Control: early weaning off-site to break cycle, review pig flow, consider partial dep-pop of 1stand 2ndstage housing, vaccination @ weaning and breeding stock
15
Q
PRRS control
A
- Vaccination:
- Modified live (avoid in pregnant)
- Killed (breeders)
- Use in breeders and growers.
- Stabilise infection:
- Expose gilts / vaccinate prior to breeding.
- Stream grower pigs in separate airspaces.
- Eradication:
- Stabilise sow/gilt infection and then depopulate all exc sows. Wean off-site to rest buildings for period.
- Depop-repop:
- Infection transmits up to 3km
- Purchase uninfected stock and quarantine / test at isolation.
- Purchase uninfected semen.
16
Q
Enzootic pneumonia in pigs
A
- Common syndrome, very prevalent in the UK.
- Great economic importance
- Clinical disease, food conversion, weight gain
- 30-80% pigs have lesions at slaughter
- Mostly caused by Mycoplasma hyopneumoniaewith frequent superimposed infection (secondary infection), esp. Pasteurella multocida
- Spread pig-pig mostly, also aerosol and wind (2 miles)
- Multifactorial– housing, temperature, humidity, mixing different ages/sources, overcrowding, continuous throughput systems
- Immunity short-lived, no colostral transfer, so not much protection.
17
Q
M. hyopneumoniae in pigs
A
- Weaned pigs
- ↑coughing – non-productive, worsened by exercise
- Primary clinical sign.
- Walk around pen of infected pigs, you will really notice this.
- ↓FCE - <14%
- Variance in growth - 17% reduction in DLWG
- 2º infection
18
Q
M. hyopneumoniae- diagnosis
A
- Herd history
- Clinical signs
- Lung lesions at slaughter/PME
- Culture (difficult) /PCR
- Quite fastidious
- Histology
- Serology
19
Q
M.hyo-Treatment
A
- Acute cases may respond to antibiotics but only if early
- Strategic dosing of growing pigs may be necessary on some farms
20
Q
M. hyo -Control
A
- Improve environment & management
- Ventilation, groupings, husbandry
- All-in, all-out management of growers
- De-pop, re-pop infected herd
- Partial de-pop and tx – original breeding stock retained and treated (10d), all other pigs removed
- Medicated early weaning (removed at 5d)
- Vaccination (1 and 3wks)
21
Q
Glasser’s disease
A
- A lot of pigs carrier it, not usually associated with clinical disease – it is usually a secondary invader.
- Haemophilus parasuis – found in the nasal cavity of many pigs
- Usually a 2oinvader but can also be a primary pathogen
- Associated with polyserositis, arthritis and meningitis. Resp. signs usually in weaners - 4 months of age as piglets have colostral immunity
- CS: acute onset pyrexia, cough, dyspnoea, lameness, swollen joints, CNS signs
- Diagnosis: history, clinical signs, or confirm in lab - PCR, ELISA, PME
- Tx: Antibiotic injections to sick pigs, in-feed/water Abs to contacts. Early tx essential
- Control: Avoid stress, strategic medication at times of high risk, Vaccination <10 wks of age
22
Q
Actinobacilus pleuropneumoniae (APP) disease in pigs
A
- Prevalent disease, different serotypes – produces a toxin that kills macrophages and neutrophils.
- 12 capsular subtypes but cross reactions occur
- Produces toxins that kill macrophages and neutrophils
- Explosive outbreaks of pneumonia with high morbidity and mortality – to - seroconversion with few clinical signs
- CS: sudden onset, sudden deaths, pyrexia, dyspnoea (jerky), coughing, blood-stained foamy mucus from mouth and nose.
- Dx: ELISA, culture from nasal swabs/lung tissue, PCR, PME- fibrinous pleuritis and firm lung infarcts
- Tx: Parenteral Abs, Isolation, NSAIDs
- Control: Closed herd, eradicate with de-pop, re-pop, wean piglets at 10d and move to separate unit
23
Q
Pasteurellosis in pigs
A
- Pasteurella multocida –important as secondary invaders – EP, AR, APP
- Can also act as a primary pathogen – resulting in pneumonic pasteurellosis or pasteurella septicaemia
- CS: mostly sporadic dz of 10-20wk old growers, pyrexia, dyspnoea, open-mouth breathing, coughing, sudden death
- Tx: Parenteral Abs
- Control: improve management, segregated early weaning to prevent infection of piglets.
24
Q
Aujeszky’s disease pseudorabies in pigs
A
- Swine herpesvirus type 1 (SHV1)
- Notifiable and not present in UK (present in NI until 2012).
- Can cause resp signs, repro and neuro signs. Notifiable disease, but not been in UK for a while.
- Clinical presentation is age and strain specific:
- <4 wks: neurological, mortality <100%.
- 4 wks – 5 months: neurological + pneumonia, mortality <15%
- Adult: few clinical signs
- Abortion and mummification
- URT coughing
- Rare neurological signs
- Slaughter policy in UK, targeted vaccination in NI, Ireland, Spain.
25
Swine Influenza in pigs
* Influenza A virus, orthomyxovirus
* Direct pig-pig transmission, also airborne
* Mostly young pigs but rapid involvement of up to 100% pigs
* CS: Pyrexia, lethargic, prostrate, skin erythema, anorexia, severe cough sneezing, dyspnoea, conjunctivitis, pregnant sows may abort
* Recovery equally rapid (5 days)
* Dx: ELISA, PCR, PME – severe congestion of upper resp. tract, enlarged LNs, necrotising bronchiolitis
* Tx: Abs to prevent 2obacterial infection
* Control: Closed herd
26
Porcine respiratory coronavirus (PRCV) and clinical signs
* Coronavirus closely related to TGE
* May be subclinical, usually mild disease.
* PME: Interstitial pneumonia, hyperplasia of bronchial epithelium, virus in macrophages
* The exact role of the virus is unknown but it is thought to predispose to other respiratory diseases
* Clinical signs:
* Coughing:
* In growers and finishers (endemic).
* Across all age groups (epizootic)
* Absence of other causes:
* Occasional pasteurellosis.
* Not usually a significant problem but:
* Contributes to multifactorial pneumonia.
* Indicates biosecurity issue on high health herd.
27
PCV-2 (PMWS) in pigs
* Highly prevalent virus in the UK.
* Immunosuppressive syndrome, so implicated in lots of different things.
* PCV-2 associated disease – respiratory component is very important
* Immunosuppressive
* 90% UK pigs seropositive
* Involved in many disease syndromes
* Can cause respiratory signs in growers
* Impact on growth is particularly prominent.
28
Parasites in pigs?
* Not too common in commercial herds, but maybe outdoor organic units.
* Metastrongylus
* Relatively uncommon
* earth worm as intermediate host
* Most likely in outdoor units
* Worms found in lungs 20-24d after the pig consumes the egg containing L1
* Coughing and dyspnoea in piglets or growers
* Ascaris suum
* Milk spot liver most common symptom but coughing may be observed due to migrating larvae 1 wk after infestation
29
Porcine Respiratory Disease Complex (PRDC)
* Clinically, this is often when you get presented with: coughing pig with lots of pathogens involved.
* PRDC results from a combination of infectious agents and environmental stressors
* Results in reduced performance, increased medication costs and increased mortality
* Typically 30-70% of pigs will be affected, with a mortality rate of 4-6 %
* Usually seen in pigs 14-20wks old (growing pigs)
* CS: Lethargy, anorexia, fever, nasal discharge, ocular discharge, coughing, laboured breathing, purple discolouration of skin, especially of ear-tips – variable CS, depending on pathogens involved and baseline level of immunity
* Viral agents often involved include:
* PRRS\*
* Coronavirus
* Swine Influenza virus
* Circovirus (PCV2)\*
* The bacterial agents often involved, which may act alone or together, are primarily:
* Mycoplasma hyopneumoniae\*
* Haemophilus parasuis
* Streptococcus suis
* Bordetella bronchiseptica
* Actinobacillus suis
* Actinobacillus pleuropneumoniae
* \*Considered most important
30
Epidemiology of PRDC
* Piglets get infected, often when they move to weaning – get colostral immunity as they are born, this declines and they get exposed and fall down to clinical disease or become a carrier, depending on challenges in the environment.
* A new-born pig receives colostral protection from its mother – dependent upon her immunity
* This immunity will decline over time, with young pigs becoming susceptible to challenge
* As they become exposed, infection follows the usual pattern of colonisation, replication, excretion and immune development
* Disease may occur following replication and excretion phases and duration will depend upon the level of replication and the agents involved.
* In the typical continual production system of, say, weekly farrowings, older pigs are a source of infection for younger pigs, maintaining a cycle of infection
* However, it should also be realised that this source of infection is also relevant to the breeding herd. A trickle of challenge to immune sows will maintain their immunity and help maximise colostral protection
* Conversely excessive challenge may override their immunity, rendering them a source of infection for their own and other litters.
31
Diagnosis of PRDC
* detailed clinical history, including age of onset, morbidity and mortality estimates, response to treatment, and the most current vaccination status of the sows and pigs.
* On-farm/laboratory post-mortem examination of affected pigs with appropriate diagnostic sampling
* cross-sectional blood sampling of the herd to establish epidemiological pictures of suspected pathogens
* use of abattoir data for slaughter pigs to indicate levels of lung consolidation and pleurisy and the involvement of other pathogens (e.g. Actinobacillus pleuropneumonieae- Acpp) (BPHS)
32
Control of PRDC
* Medication and vaccination are fundamental to the long-term control of PRDC but are no substitute for sound management principles
* Even the best and most extensive programmes will not overcome extreme disease where pig-flow and management have not been corrected
* Vaccines should only be used with full diagnostic knowledge, including targeting the timing of vaccination. Vaccines against Mycoplasma and PCV2 are probably the most widely used vaccines in young piglets, but strategies are also needed to identify additional pathogens for which vaccine can be introduced
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