Respiratory diseases Flashcards
Bacterial causes of respiratory diseases
Pasteurellosis
Pleuropneumonia
Enzootic pneumonia
Glasser’s disease
Bordatella/atrophic
Viral causes of respiratory diseases
Swine influenza
PRRS
PRCV
PCMV
PCV2
Parasitic causes of respiratory diseases
Metastrongylus
Migrating ascarids
Immune defenses in the nasal chamber
Innate: physical barrier, phagocytes, anti-bacterial peptides, colostral IgA
Acquired: cell mediated (T, B cells), slgA
Progressive atrophic rhinitis
Bordatella bronchiseptica
Pasteurella multocida (toxigenic)
Catarrhal rhinitis
Influenza (H1N1)
Primary bacterial pathogens in pneumonia
Actinobacillus pleuropneumoniae
Actinobacillus suis
Bordatella bronchiseptica
Mycoplasma hyopneumoniae
Mixed/secondary bacterial pathogens in pneumonia
Glasserella parasuis
Mycoplasma hyorhinitis
Pasteurella multocida
Streptococcus suis
Trueperella pyogenes
Primary viral pathogens in pneumonia
Aujeszky’s
Influenza
PRRSV
Mixed/secondary virus pathogens in pneumonia
PCMV
PCV2
PRCV
TTV
Clinical observations in catarrhal bronchopneumonia
Dependent lobe consolidation
Pigs coughing but not ‘sick’
Possible agents causing catarrhal bronchopneumonia
Mycoplasma hyopneumoniae
Mycoplasma hyorhinitis
Streptococcal spp
Key clinical observations in Purulent bronchopneumonia - ‘Porcine respiratory disease complex’ (PRDC)
Coughing, dyspnoea
Lethargy and inappetence
Agents identified in Purulent bronchopneumonia - ‘Porcine respiratory disease complex’ (PRDC)
M. hyopneumoniae
Pasteurella multocida
Actinobacillus pleuropneumoniae
Porcine circovirus 2 -PCV2
Porcine reproductive and resp. syndrome virus - PRRSV
Key clinical observations in Acute fibrinous necrotising pleuro-pneumonia (mild case)
Severe dyspnoea
Depression, prostration, anorexia
Typical agent in Acute fibrinous necrotising pleuro-pneumonia (mild case)
Actinobacillus pleuropneumoniae
Key clinical observations in Chronic necrotising pleuropneumonia
Variable coughing, dyspnoea
Variable anorexia and fever
With sporadic acute cases
Key clinical observations of Embolic pneumonia (pyaemia)
Sporadic cases only
Rarely cough
Exercise intolerance
Evidence of primary lesion
Typical agent in embolic pneumonia (pyaemia)
Arcanobacter pyogenes
S. aureus
Key clinical observations in disseminated broncho-interstitial viral type pneumonias
Acute onset widespread coughing
Acute onset lethargy and anorexia
Typical agent in disseminated broncho-interstitial viral type pneumonias
Influenza virus
Key clinical observations in interstitial viral type pneumonias
Depends on causal agent
Agents identified in interstitial viral type pneumonias
PCV2: PMWS, dyspnoea
PRRSV: reproductive problems
Agents usually identified in pleurisy/pleuritis
M. Hyopneumoniae/ M. hyorhinis, Glaesserella parasuis, A. pleuropneumoniae, P. multocida
Underlying viral challenge (PRRSV, PCV2)
Pasteurella multocida
Commensal
Secondary invaders in many porcine respiratory diseases
Primary pathogen in pneumonic pasteurellois or pasteurella septicaemia
Incidence of pneumonic pasteurellosis
Among top 3 most frequent diagnoses
World wide distribution
Aetiology of pneumonic pasteurellosis
Pasteurella multocida
Primary infections include - influenza, mycoplasma, PRRSV
Epidemiology of pneumonic pasteurellosis
Mostly sporadic in 10-20 week old growing pigs
Clinical signs of pneumonic pasteurellosis
Finishers (10wks-finish)
Pyrexia
Anorexia
Dyspnoea
Some sudden deaths (septicaemia)
Diagnosis of pneumonic pasteurellosis
Clinical signs and isolation
Necropsy and culture
Post mortem of pneumonic pasteurellosis
acute necrotising and fibrinous bronchopneumonia
Demarcated consolidation of anteroventral lung lobes (grey-pink)
Mucopurulent exudate in airways
Differential diagnoses of pneumotic pasteurellosis
A. pleuropneumoniae, G. parasuis.
Treatment of pneumotic pasteurellosis
Antibiotic therapy
- penicillin
- streptomycin
- oxytetracycline
Anti-inflammatory
- Ketoprofen
Control of pneumotic pasteurellosis
Optimise herd management: AIAO, ventilation
Vaccination against Mycoplasma and/or PRRSV
Septicaemic pasteurellosis
consequence of uncontrolled pneumonia and a cause of ‘sudden’ death in young and growing pigs
Sudden onset of depression and some deaths
Aetiology of actinobacillus pleuropneumoniae
Actinobacillus pleuropneumoniae (APP)
kill macrophages & neutrophils lowering defences
Epidemiology of actinobacillus pleuropneumoniae
Low clinical incidence but hogh mortality
Tonsil carriage with often multiple strains present
occasionally see sudden outbreak of disease where no other pigs introduced into herd
Chiefly affects pigs from 2 - 6 months of age
Clinical signs of actinobacillus pleuropneumoniae
Sudden onset
A few sudden deaths
Other pigs severely ill, anorexic, depressed
Pyrexia
Dyspnoea with jerky breathing
May see blood stained foamy mucus coming from nose and mouth
Postmortem signs of actinobacillus pleuropneumoniae
Acute fibrinous haemorrhagic pleuropneumonia
Peracute: lung dark red and firm, lesions black/red (cannon ball haemorrhagic lesions)
Chronic: pleurisy
Differential diagnoses for actinobacillus pleauropneumoniae
Enzootic pneumonia – usually EP is a much less severe, more chronic infection
Pneumonic pasteurellosis - PM needed to differentiate as some similar signs.
Swine influenza - younger pigs worst affected, URT signs, post mortem findings.
Mortality much lower in SI. Glasser’s disease
Mulberry heart - often sudden death with abnormal heart but no pericarditis. Respiratory signs much more apparent in APP.
Treatment of actinobacillus pleuropneumoniae
parenteral antibiotic treatment for severely affected pigs - spectinomycin, tilmicosin, tulathromycin, oxytetracycline
Consider mass medication
Vaccine for actinobacillus pleuropneumoniae
Toxoid vaccine available
Aetiology of enzootic pneumonia
Mycoplasma hyopneumoniae
With frequent superimposed secondary infection (e.g. pasteurella multocida)
Epidemiology of enzootic pneumonia
attaches to epithelial lining of lower airways
spread is mostly pig to pig and also by wind/aerosol
Immunity can be short - lived
Infection of a naive herd with enzootic pneumonia
may lead to signs of pneumonia in all ages from 10 day old piglets to sows
In most chronically infected herds the growing (post weaning) pig is most often affected
Clinical signs of enzootic pneumonia
dry barking cough, non productive and worsened by exercise
may show signs of severe dyspnoea
PM of enzootic pneumonia
sharp consolidation of ventral parts of apical, cardiac and diaphragmatic lung lobes
Lymphocytic cuffing around bronchioles
Differential diagnoses for enzootic pneumonia
Actinobacillus pleuropneumoniae - more acute, highly fatal and specific pathology.
Metastrongylus apri infestation - outdoor pigs - find parasites in lungs.
Swine influenza - short course, less common, mostly URT infection.
Glasser’s disease - sudden onset of polyserositis - joints affected. Culture G parasuis.
Porcine respiratory coronavirus: widespread coughing with few other clinical signs.
Treatment of enzootic pneumonia
antibiotic therapy e.g. tylosin, tiamulin, tulathromycin (Draxxin, Pfizer)
Must treat early
Steroids/NSAIDs can help in acute cases with secondary pasteurellosis
Control of enzootic pneumonia
Vaccination (inactivated)
Eradication by partial depop repop
Aetiology of glassers disease
Glaesserella parasuis
Mostly serotypes 4 and 5 (plus 7)
Epidemiology of Glassers disease
Transfer of virulent and non-virulent strains from sow to piglet during suckling
when pigs are weaned and mixed
Clinical signs of Glassers disease
sudden onset and several pigs affected at the same time
pyrexia (41C)
anorexia
cough
dyspnoea
lameness with swollen joints
CNS signs
Septicaemia
Chronic cases: chronic arthritis, GI obstruction due to peritonitis and heart failure
Diagnosis of glassers disease
history and clinical signs. PCR on swabs or suspect culture isolates
Culture of the organism from joints and other tissues
Post mortem of glassers disease
polyserositis
polyarthritis
fibrinous meningitis
peritonitis
pleurisy
Differential diagnoses for Glassers disease
Swine erysipelas - mostly chronic lameness with epiphyseal enlargement rather than swelling of joint capsules.
Mycoplasma hyosynoviae - milder disease.
Streptococcal infections - often lead to meningitis and occasionally polyserositis
Treatment of Glassers disease
Parenteral antibiotics
- penicillin/streptomycin
- oxytetracycline
- trimethoprim sulpha
Aetiology of atrophic rhinitis
Toxigenic strains of Bordetella bronchiseptica (zoonotic) and Pasteurella multocida type D
here are progressive (PAR) and non – progressive (NPAR) forms
Epidemiology of atrophic rhinitis
Disease in neonates and newly weaned pig
spread by direct or droplet contact
Bordetella bronchiseptica is a common inhabitant of the pig’s nasal cavity
toxigenic strains of Pasteurella multocida produces a osteolytic toxin which has a predilection for the turbinate bones
Clinical signs of atrophic rhinitis
first seen at 3 - 9 weeks
sneeze and have a clear or purulent nasal discharge
Occasional nasal haemorrhage seen and piglets may rub their blocked noses on the floor
later evidence of facial deformity and lacrimal staining
Dianosis of atrophic rhinitis
Nasal swabs for bacteriology - PCR or ELISA
Post mortem of atrophic rhinitis
a degree of destruction of the turbinates
Differential diagnoses of atrophic rhinitis
Bordetella bronchiseptica infection by itself – rhinitis (NPAR), tear staining and sometimes pneumonia in pigs > 1 week - usually no signs of snout deviation in older pigs.
Inclusion body rhinitis - milder disease usually only transient effect and no turbinate damage (swine herpesvirus).
Swine influenza - severe disease - usually affecting older pigs with acute respiratory signs and no turbinate damage.
Necrotic rhinitis - uncommon but may accompany atrophic rhinitis or follow from other trauma. Caused by Fusobacterium necrophorum causing rhinitis and facial swellings - ‘bull nose’. Lesions in mouth and on skin as well as nose. High mortality.
Inherited prognathia - individual piglets have excessively long lower jaws.
Treatment of atrophic rhinitis
Helps in early stages but doesn’t reverse facial deformity
Tylosin or trimethoprim - sulpha
Vaccinate sows and gilts
Aetiology of swine influenza
Acute, zoonotic respiratory infection
Influenza A virus - Orthomyxovirus
H1N1, H1N2, H3N2
Epidemiology of swine flu
High jmorbidity but low mortality
Direct pig-pig transmission via infected droplets
Young pigs most frequently affected
Clinical signs of swine flu
T41.5C,
anorexia,
jerky breathing,
sneezing,
painful (sometimes paroxysmal) cough,
Ocular conjunctivae inflamed
Muscles painful and stiff
Severe weight loss
Usually sudden recovery in 4 - 6 days.
Sows may abort following infection and surviving piglets may be born with deformed or infected lungs.
Diagnosis of swine flu
Antibody ELISA on serum and haemagglutination inhibition test
Post mortem of swine flu
severe congestion of URT,
cervical and mediastinal LN’s enlarged.
Thick exudate in bronchi.
Localised red - purple areas of lung collapse
Emphysema may surround collapsed areas.
Some lung necrosis.
Differential diagnoses of swine flu
Enzootic pneumonia - more chronic and insidious.
Classical Swine Fever - other systems involved.
Atrophic rhinitis - bony changes. APP – cases more sporadic but higher mortality.
Inclusion body rhinitis - can look very similar in young pigs.
Treatment of swine flu
Oral or parenteral antibiotics for secondary infection
Nursing care
Aetiology of porcine reproductive and respiratory syndrome (PRRS)
Virus belongs to Arteriviridae family - two genogroups
Epidemiology of PRRS
virus present in semen and in faeces.
Windborne spread is possible Fomites
Virus may take 5 months to spread through herd causing abortion etc.
Viraemia can persist for up to 70 days and shedding in semen for up to 40 days.
Respiratory disease (with PRRS underlying secondary pathogens) may persist in herd for years.
Multiple infections with different strains of PRRS may occur in the same herd in series or in parallel – heterologous immune protection is weak .
Clinical signs of PRRS
Very variable
Reproductive failure - late abortion, stillbirth, weak piglets may persist for many months.
Respiratory disease - pyrexia, anorexia, cough, dyspnoea, skin discolouration and ill - thrift.
Diagnosis of PRRS
herd history of breeding losses and respiratory disease
A number of serological tests are available – best is the IDEXX ELISA.
Herd serological profiles
oral fluid (OF) can be tested as an alternative to serum.
PCR is available for use on blood, lung and semen.
Immunostain available for lung tissue.
Necropsy – heavy rubbery lungs due to interstitial pneumonia in growing pigs.
Virus also detectable in tissues using fluorescent antibody. Increased pleural fluid.
Enlarged LNN
Histopathology:
* Reduced alveolar macrophages
* Increased Type 2 pneumocytes
* Insterstitial pneumonia
* IHC for PRRSV.
Differential diagnoses of PRRS
Reproductive
e.g. parvovirus,
leptospirosis, brucellosi
Respiratory
e.g. enzootic
pneumonia (M hyopneumoniae), Pasteurella multocida, Strep. suis, Actinobacillus pleuropneumoniae & Glaesserella parasuis (Glasser’s disease
Treatment and control of PRRS
vaccination of all breeding females and replacement gilts.
may be economic to vaccinate growing pigs as well as breeding stock.
Vaccine: Modified live freeze dried vaccine for use in growing pigs from 6 weeks upwards and in breeding pigs. May cause abortion in pregnant sows if they are naive.
Aetiology of Procine respiratory coronoavirus (PRCV)
coronavirus very similar to the TGE virus
Maternal antibody persists until 5-6 months
Broncho-interstitial pneumonia.
Clinical signs of PRCV
signs of broncho-interstitial pneumonia, pyrexia, coughing, anorexia and delayed growth.
Clinically difficult to differentiate from enzootic pneumonia.
No gastro - intestinal signs seen.
Diagnosis of PRCV
ELISA serology, virus isolation
PM: low grade broncho-interstitial pneumonia
Control of PRCV
once endemic then usually little indication to control. No vaccines available.
Aetiology of pig cytomegalovirus/inclusion body rhinitis
Porcine cytomegalovirus (beta herpesvirus)
common cause of rhinitis in suckling pigs
Epidemiology of inclusion body rhinitis
transmission by direct pig - pig contact or aerosol.
Transplacental / perinatal infection after reactivation of latent infection in pregnant sow possible.
Mostly affects young pigs pre/per-weaning
Clinical signs of inclusion body rhinitis
mostly in pigs < 3 weeks of age.
Sneezing,serous nasal discharge (occasionally bloody) and brown ocular discharge.
High morbidity and low mortality
In naive herds - symptoms much more severe.
Piglets may have generalised disease with diarrhoea followed by anaemia, rhinitis, pulmonary oedema, pneumonia and death.
Adult pigs may show respiratory signs and may see stillbirth and abortion in sows.
Diagnosis of inclusion body rhinitis
ELISA for serum antibodies.
Inclusion bodies from nasal swabs and tissues including nasal discharge from sacrificed piglets.
PCR to detect nucleic acid.
Differential diagnoses of inclusion body rhinitis
atrophic rhinitis - herd history, bony changes,
necrotic rhinitis - necrotic tissues and facial swelling,
swine influenza - sudden onset and affects older pigs too.
Treatment of inclusion body rhinitis
Antibiotic therapy to control secondary infection
Usually self limiting
Aujeszkys disease (pseudorabies)
Respiratory disease (pneumonia) is a feature of infection by some strains in weaner, grower and finisher pigs.
Necropsy reveals anteroventral dark red consolidation with evidence of extensive necrotizing bronchointerstitial pneumonia.
not present in the UK
notifiable disease.
Swine herpesvirus type 1 (SHV1)
Clinical presentation is age 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,
PCV2 pneumonia (porcine circovirus associated disease)
Interstitial pneumonia
Heavy, grey, rubbery lung
part of Porcine respiratory disease complex (PRDC)
Post-weaning multisystemic wasting syndrome
May see pulmonary oedema alone (cardiac failure)
Metastrongylosis
Metastrongylus apri & Metastrongylus edentatus
coughing and dyspnoea in piglets or growing pigs.
adult worms 45 mm long found in the bronchi / bronchioles of the diaphragmatic lobes of the lungs.
Ivomec injection
