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103 Cards in this Set
- Front
- Back
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pulmonary defense mechanisms
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- turbulence caused by turbinates and speed changes caused by alteration of airway diameters (>90% of particles >10u)
- mucociliary apparatus (trap particles >2u to level of terminal bronchiole) - phagocytes (especially pulmonary alveolar macrophages; few or none in healthy alveoli) - antibody production (airway IgA, alveoli IgG) |
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impairment of filtration
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damage to structure of nasal cavity
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impairment of mucociliary apparatus
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- destruction of cilia (M. hyo)
- changes in mucus viscosity (Nh3) |
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impairment of phagocytosis
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- viral destruction of macrophages (PRRSv)
- hypoxia-induced reduction in macrophage oxidative phosphorylation |
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risk factors for respiratory disease
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- introduction of new animal or semen
- physical environment in which pigs are housed - numbers of pigs per group - pig flow - number of pathogens - early weaning |
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reducing risks from introduction of new animals or semen
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- put in place biosecurity protocols to minimise risk of disease entry (stock replacement strategy including appropriate use of quarantine)
- know the health status of both the client and supplier herds (what diseases exist on each) |
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risk factors for respiratory disease in the environment
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- serves as transport medium, determines the agents survival time outside the host and the susceptibility of a new host to infection (eg NH3 effect on ciliary effect)
- pathogen survival increased at lower temperatures (higher temperatures dessicate) and at high (>80%) and low (<50%) humidity - number of pigs per group/air space and crowding increases potential for transmission |
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risk factors for respiratory diseases based on pig flow
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- pigs can be housed in "continuous flow" or "all-in/all-out"
- the number of pigs infected with and potentially shedding pathogens increases with age - a significant risk factor for respiratory disease is the comingling of pigs of different ages within the same air space: when the pig is AI-AO, the population is more likely to be age segregated and thuis more uniform health status |
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advantages of AI/AO on pig performance
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- higher average daily gain
- higher average daily feed intake - higher feed to gain ratio - shorter days to market - half the % of lung lesions |
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formula for likelihood of disease
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# of pathogens x virulence / resistance
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influences on the number of pathogens
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housing management:
- hygiene - ventilation rate - pig flow |
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influences on resisance
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environment:
- hygiene - ventilation rate - temperature flexes - draughts - dampness and respiratory system defense mechanisms |
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early weaning & respiratory disease
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early weaning can break a disease chain but makes populations more vulnerable to disease if pathogens re-enter the herd (poor resistance)
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management options for control/eradication of respiratory disease
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- pig flow: quarantine, AI/AO, multi-site production (age segregated)
- vaccination - medication - weaning age (21d minimum in EU) - depopulation (partial or total) - customised combos |
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vaccination and respiration disease
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- provides homologous protection (+/- heterologous protection)
- vaccinating sows to stabilise herd immunity and increase passive protection of piglets - vaccinating sucklers/weaners - vaccination of naive pigs prior to herd entry - vaccinate pregnant gilts 5 and 2 weeks pre-farrow and boost sow 2 weeks pre-farrow |
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side effects of vaccination
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- pathogenic potential of MLV vaccines
- vaccine combo may have adverse effects mixing M. hyo and PCV-2 may depress growth for 14d) - induce inflammatory response: may be severe enough to induce abortion or sperm defects |
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recommended vaccinations for sow
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- M. hyopneumoniae
- atrophic rhinitis - PRRS - PCV-2 |
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recommended vaccinations for sucklers/weaners
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- PRRS
- PCV-2 - M. hyo - APP - Erysipelas |
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medication options for control/eradication of respiratory disease
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- in a disease outbreak, give appropriate medication, via the water supply if possible
- in-feed medication can be employed to control disease (eg. valnemulin [Econor] for control of M.hyo in grow-finish) - injection of individual pigs is time consuming but may be necessary (ceftiofur [excede], tulathromycin [draxxin]) |
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management changes to reduce bacteria to eliminate losses from PRRS
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- stop cross-fostering to save sick, "fall-behinds" or runts
- if necessary cross foster only within first 24 hours - do not move sows or piglets between rooms - minimise piglet handling (stress) - immediately euthanise very sick pigs unlikely to fully recover - do not move fall-behind or lightweight pigs backwards to younger rooms or nurse sows - stop all feedback of weak-born or aborted/stillborn fetuses - nursery pigs must be moved strictly AI/AO - nurseries may be loaded all - in by early weaning a few of the oldest, best-doing litters from the next oldest farrowing room |
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maternal protection and mucosal colonisation
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level of protection declines at different rates for different diseases, on average:
- absolute protection ~8d - clinical protection ~14d - little protection ~20d |
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using lactation length to control respiratory disease
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- sow supplies provide passive protection to piglets via colostrum and milk antibodies
- objective of early weaning is to remove the piglets from the primary source of infection (sow) while passive protection is still preventing pathogen colonisation - once weaned, move the piglets off-site |
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using depopulation to eradicate respiratory disease
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- a total depopulation followed by rigorous cleaning is very effective for disease eradication (but very expensive so last resort)
- a strategy proven effective against PRRS virus is depopulation of specific stages of production (partial depopulation: nursery, grower, finisher) - if disease is known to be cycling in the nursery then only the nursery needs to be depopulated - must result in movement of uninfected pigs into a non-infective environment - for uninfected pigs essential that sows not be shedding pathogen. For this all the sows have the same immune base - stabilizing the sow base requires that subpopulations of immunologically naive or actively infected shedding - stabilise the sow base by bringing in 4-6 months supply of replacements and closing the herd (objective is to develop a sow population of equal immune status i.e. not shedding the virus) - where a proven vaccine exists, vaccination of the entire breeding herd (including the boars) will help eliminate naive subpopulations - when sow base is stable, perform a serological profile to establish when pigs are sero-converting - use this to determine which stages to depopulate - before reopening the herd, ensure appropriate isolation/acclimatisation is established to prevent reintroduction of the disease |
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respiratory diseases of suckling pigs
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- IBR
- SIV - PRRS - bordetella |
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respiratory diseases of nursery pigs
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- SIV
- PRRS - AR |
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respiratory diseases of growers/finishers
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- M. hyo
- SIV - PRRS - APP |
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respiratory diseases of adult pigs
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- PRV
- SIV - PRRS |
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maternal protection and mucosal colonisation
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level of protection declines at different rates for different diseases, on average:
- absolute protection ~8d - clinical protection ~14d - little protection ~20d |
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using lactation length to control respiratory disease
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- sow supplies provide passive protection to piglets via colostrum and milk antibodies
- objective of early weaning is to remove the piglets from the primary source of infection (sow) while passive protection is still preventing pathogen colonisation - once weaned, move the piglets off-site |
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using depopulation to eradicate respiratory disease
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- a total depopulation followed by rigorous cleaning is very effective for disease eradication (but very expensive so last resort)
- a strategy proven effective against PRRS virus is depopulation of specific stages of production (partial depopulation: nursery, grower, finisher) - if disease is known to be cycling in the nursery then only the nursery needs to be depopulated - must result in movement of uninfected pigs into a non-infective environment - for uninfected pigs essential that sows not be shedding pathogen. For this all the sows have the same immune base - stabilizing the sow base requires that subpopulations of immunologically naive or actively infected shedding - stabilise the sow base by bringing in 4-6 months supply of replacements and closing the herd (objective is to develop a sow population of equal immune status i.e. not shedding the virus) - where a proven vaccine exists, vaccination of the entire breeding herd (including the boars) will help eliminate naive subpopulations - when sow base is stable, perform a serological profile to establish when pigs are sero-converting - use this to determine which stages to depopulate - before reopening the herd, ensure appropriate isolation/acclimatisation is established to prevent reintroduction of the disease |
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respiratory diseases of suckling pigs
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- IBR
- SIV - PRRS - bordetella |
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respiratory diseases of nursery pigs
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- SIV
- PRRS - AR |
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respiratory diseases of growers/finishers
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- M. hyo
- SIV - PRRS - APP |
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respiratory diseases of adult pigs
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- PRV
- SIV - PRRS |
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etiology: mycoplasmal pneumonia
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mycoplasma hyopneumonia
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chars mycoplasmal pneumonia
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- contagious disease
- very common: her prevalence ~99% - primary pathogen - carrier sows transmit to piglets - sow also provides antibody to piglet - antibody begins to decline in the nursery at 4-10 wks of age - slow insiduous development of disease |
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CS mycoplasmal pneumonia
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- chronic dry/barking non-productive cough
- group infected over 3-14 wks - fever is unusual - slow, progressive size variation (same age so should be same size) - dyspnea if secondary infection: usually with non-toxigenic P. multocida, but also M. hyorhinis, or H. parasuis) which causes enzootic pneumonia (will see productive cough, fever and weight loss) |
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lesions/pathogenesis mycoplasmal pneumonia
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- paralysis and loss of tracheal and bronchial cilia
- loss of mucociliary clearance mechanism - gravitation distribution of lesions: anterio-ventral, firm, tan plum-colored areas |
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Dx mycoplasmal pneumonia
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- culture is difficult (3-30 days)
- histopath: peribronchial lymphoreticular hyperplasia - fluorescent antibody, PCR or immunoperoxidase of lung section - serology: CF and ELISA |
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mycoplasmal pneumonia Tx/control
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- injectable: Lincomysin, Tylosin, Draxxin
- in feed: lincomycin in nursery, valnemulin - age segregated all in/all out pig flow - vaccine: inject pigs at 3 and 5 weeks (careful of PRRS seroconversion) - eradication by medicated early weaning or total or partial depopulation (all animals except breeding stock which are medicated) |
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chars actinobacillus pleuropneumoniae (APP)
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- G- rod
- prevalence 60-80% of herds (~40% of swine) - 12 serovars (1, 5 and 7 most common in US, 1, 5, 9, 10 and 11 most pathogenic) - carrier sow source of infection (Ab upto 14 weeks) - low survival in environment - sensitive to drying (transport with medium and swabs) - no long distance transmission |
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CS actinobacillus pleuropneumoniae (APP)
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- grower pigs
- fever - severe dyspnea - cyanosis of extremities - sudden death - 30-50% case mortality within 36 hours of onset of CS - in sub-acute form pigs anorexic, dyspnea and coughing with variable mortality |
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APP lesions/pathogenesis
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- dorso-caudal (diaphragmatic lobe) necro-hemorrhagic lesion
- via direct cntact and aerosol, bacteria clonise the tonsils and also enter the lung - lesion is the result of toxin production (Apx I and III) evident by 3h in challenge model: macrophage death within 30-60 min, reduced neutrophil function - lungs congested and edematous (3-12h) - by 12-24 h, fibrinous exudate on pleural surface over pneumonic areas - by 48h, hemorrhagic/necrotic lesions observed especially in caudal lobe |
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APP toxins
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- Apx I and III highly toxic to leukocytes
- Apx moderately toxic alone, but effects are more severe if combined with other toxins - effect of serotype can vary (in US serotype 2 produces only Apx II and has low virulence, in Europe produces II and III and is highly pathogenic) |
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APP Dx
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- acute, fatal respiratory disease with fibrous pleurisy and firm lung infarcs, confirmed by serology and culture of the organism
- main differential is A. suis which is further differentiated on basis of toxin production (A. suis doesn't produce Apx III) - serology: CF (highly specific, low sensitivity), ELISA (low spec, high sens, x-reacts with A. suis) |
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APP Tx/control
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- injectable: ceftiofur (Excede), Penicillin, Tetracycline -> walk each pen, treat affected pigs or treat whole and adjacent pens if several affected
- in feed:pulmatil (Tilmicosin) 5d before expected outbreak - in water: prevents new cases - eradication: total depopulation or partial depopulation with vaccination/medication of sow herd and then weaning at <21 d - vaccine |
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chars APP vaccine
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- serotype specific: 1, 5, 7
- titer of 1:64 (CF) is protective - takes 3-4 weeks to develop - reduces mortality by 50% (no effect on ADG) - oil adjuvant causes abscess |
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etiology actinobacillosis
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Actinobacillus suis
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pathogenesis actinobacillosis
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- likely via direct contact and aerosol
- bacteria colonise the tonsils and become systemic - systemic emboli adhere or are trapped in vessel walls (especially in lung), form micro-colonies surrounded by areas of toxin-induced haemorrhage and necrosis |
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CS actinobacillosis
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- sudden death in 2d to 4wk old piglets in one of more litters
- in high health herds, wweaners and older pigs (including young adults), may have a persistent cough and signs of pneumonia as well as red blotches on the skin (not raised like Erysipelas) |
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pathology actinobacillosis
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haemorrhagic-necrotising pneumonia that is more randomly distributed than that seen with APP
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Dx actinobacillosis
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- acute, fatal respiratory disease with firm lung infarcts
- due to its ability to mimic other pathogens and serological cross-reaction with APP, diagnosis requires culture of the organism |
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Tx and control A suis
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- sensitive to most commonly used antibiotics (e.g penicillins, tetracyclines)
- older pigs in-feed medication is usually effective - anectotally, autogenous vaccines have been successful in herds with repeated outbreaks |
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etiology atrophic rhinitis
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combination of bordetella bronchiseptica and pasteurella multocida (type D and sometimes A)
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chars bordetella bronchiseptica (atrophic rhinitis)
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- fimbria for attachment
- primary but weak pathogen - toxin causes local defective osteogenesis - affects pigs <6 wks |
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chars pasteurella multocida (atrophic rhinitis)
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- requires initial insult (i.e. inflammation) to colonise
- produces potent dermonecrotoxin - toxin causes destruction of osteoblasts and upregulates osteoclasts resulting in destruction of nasal turbinates |
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pathogenesis atrophic rhinitis
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- source in herd is infected sow: infects piglets soon after birth
- antibody not protective against infection but may provide anti-toxin - other animals can also be source - spread in nursey |
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CS atrophic rhinitis
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- sneezing in young pigs
- conjunctivitis - purulent/serous nasal discharge - epistaxis - bilateral shortening of snout - bending of snout |
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Dx atrophic rhinitis
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- CS
- nasal swab: Calgiswab - PCR for organism - evaluate severity in the herd at slaughter: section at 2nd upper premolar, measure space, symmetry, septal deviation and consider season |
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control of atrophic rhinitis
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- vaccination (pre-farrow and/or 7 and 21d of age)
- medication of litters - water medication in nursery - in-feed sulfa in nursery - all in-all out pig flow - for acute pre-weaning disease, parenteral or oral TMP-sulfa, ampicillin, tetracyclines, ceftiofur - prophylaxis by medication at 3, 10 and 21 days - water/feed medication from weaning - vaccination of sows (P. multocida toxoid and killed B. bronchiseptica) to boost piglet passive immunity. can vaccinate piglets at 7 and 21d - eradication by total depopulation - if <20% sows infected, testing/tx of sows on entry to clean farrowing house and culling if not resolved (small farm) |
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vaccination for atrophic rhinitis
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- toxoid for sows and piglets
- variable success - abscess former |
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atrophic rhinitis antibiotics
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- LA 200
- inject piglets at 0, 7 and 21d - usually in conjunction with vaccine |
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etiology bordetellosis
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B. bronchiseptica
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pathogenesis of bordetellosis
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- colonisation and destruction of cilia in nasal cavity
- may colonise lung causing bronchopenumonia |
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CS bordetellosis
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- sneezing in pigs >1 wk of age (may be paroxysmal with epistaxis) and mucopurulent nasal discharge progressing to a cough when lung involved
- may see mild (reversible) turbinate atrophy (regressive atrophic rhinitis) |
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pathology bordetellosis
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catarrhal rhinitis, conjunctivitis and possible bronchopneumonia (particularly cranial and middle lobes)
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Dx bordetellosis
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CS confirmed by culture of nasal swab
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Tx and control of bordetellosis
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- severely affected pigs, use parenteral followed by oral administration of TMP-sulfa, tetracyclines
- for disease control, use in-feed medication of above or sulfa-tylosin mix (Tylasul, Elanco) - vaccinate sows pre-farrowing and pigs at 7 and 28 days - eradication required medicated early weaning (<10d) |
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chars Salmonella choleraesuis
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- Salmonella enterica, serovar choleraesuis
- resides in macrophages = protected from immune system, protected from antibiotics - stress-related |
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CS salmonella choleraesuis
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- any age but most frequently 3-4 mo old pigs
- fever, shallow moist cough, huddling, rough hair coat, cyanosis of extremities, sudden death |
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S. choleraesuis lesions
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- interlobular edema and hemorrhage in lung
- splenomegaly - hepatomegaly - DDx S. typhimurium which is largely enteric |
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treatment S. choleraesuis
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individual parenteral antibiotics (eg. tetracycline, ceftiofur, ampicillin, enrofloxacin) for acutely ill animals, then population treatment in-water (eg tetracycline or ampicillin) for 5d
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control S. choleraesuis
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hygiene and all-in all-out pig flow, feed medication and vaccination (live vaccine SC 54), reduce stress
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chars swine influenza
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- influenza type A virus (orthomyxovirus, RNA)
- 2 structural proteins: hemagglutin (15): drives immune response, neuraminidase (9) - four main subtypes in swine: H1N1, H1N2, H3N2, H1N7 - fairly stable comparable to human |
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swine influenza transmission
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- primarily pig-to-pig
- also humans and waterfowl - virus shed for 30 days |
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CS swine influenza
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- classic diz: fall-winter, all pigs affected, extreme prostration, open-mouth labored respiration, sneezing, barking cough, red eyes, conjunctival discharge, but rarely fatal
- sows may abort - enzootic form: constant circulation, usually one of several pathogens, nursery or finisher |
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swine influenza pathogenesis
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- virus replicates in bronchial epithelium within 2h and by 24h most cells are infected, as are alveolar septae and ducts
- small bronchi become blocked by neutrophil-rich exudate, and alveolar necrosis/bronchial epithelial hyperplasia - widespread interstitial pneumonia with enlarged "patchy" hemorrhagic lymph nodes (bronchial, mediastinal) |
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Dx swine influenza
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- classic diz = CS
- enzootic form = virus isolation, histopathology, paired serology, antigen detection IHC |
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Tx swine influenza
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- clean, dry, draft-free
- minimise stress - antibiotics for 2ndary infection |
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control swine influenza
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- strain specific vaccine
- ventilation to reduce re-circulation of air and thus virus exposure |
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chars porcine reproductive and respiratory syndrome (PRRS)
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- primary pathogen (RNA arterivirus)
- lysis of alveolar macrophages with loss of phagocytic and antigen presenting capability - infected porcine lungs have "rubbery feel" |
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prevalence and transmission of PRRS
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- 60-80% of herds, many strains of virus
- pig-to-pig transmission but also aerosol across a region - constant recycling within a farm |
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CS PRRS
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- usually in weaned pigs, will observe tachypnea and a "thumping" respiration
- may see eyelid oedeme and conjunctivitis |
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Dx PRRS
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- virus isolation from sick pigs: viremia for 4-7 wks post-infection, isolate from tonsils and/or lungs
- histopath, IHC - targeted serology |
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serology for PRRS
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- maternal immunity usually persists 6-8 weeks, but occasionally as long as 16 weeks
- vaccine titer not distinguishable from field virus titer - rising titer indicates recent infection |
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PRRS pneumonia in the nursery (enzootic herd)
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1st scenario: sows stable, low titers and not actively shedding virus. Wean naive, negative piglets that become infected in the nursery
- Scenario 2: sow herd not stable due to frequent susceptible additions (up to 80% positive) -> sows actively shedding virus to piglets - differentiate serologically |
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- PRRS pneumonia in enzootic herd
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- 1st scenario: sows stable with low level of titers 5-20%, not actively shedding virus and weans naive, negative piglets that are infected in the nursery -> depopulate nursery and leave empty for 2 weeks
- 2nd scenario: sow herd not stable due to frequent susceptible additions (upto 80% +), actively shedding virus to piglets -> close sow herd to new additions for 6 months |
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PRRS control
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- limied cross fostering: none after 24 hours
- do not move pigs between rooms: strict all-in/all-out - multi-site production - remove very sick pigs from the system: limit risk of "typhoid Mary" |
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PRRS sow vaccination
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- killed vaccine; safe but relatively ineffective
- modified live virus vaccine: possible reversion to virulence; lack of similarity to field strain; infectious, contagious, pathogenic -> 3rd trimester abortion, weak pigs; confuses interpretation of serology |
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PRRS pig vaccination
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- original label use
- can be very effective in controlling clinical disease and mortality |
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serum therapy (PRRS)
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- consider only if other methods have failed
- injection of serum from viremic pigs: variation of autogenous vaccine - inject sows and 4-6mo of replacements, close herd) - risks = infection of wild type virus will cause clinical problems - benefits = decreases number of breeding groups with abortions and in utero infections - ultimately stops PRRS-affected production sooner |
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etiology: porcine circovirus 2
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- a "new" porcine circovirus disease (PCV 2) that has been associated with several disease states
- new designation is PCVAD |
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CS porcine circovirus 2
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- usually in weaned pigs (5-6 wks), may observe icterus or dyspnea and will observe wasting
- PRRS and PCVAD lung will look the same = "rubbery feel" - jaundice - nephritis - purple skin discoloration over body |
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pathology porcine circovirus 2
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- moderate to severe interstitial pneumonia
- enlarged lymph nodes - many other "suggestive" lesions - |
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Dx porcine circovirus 2
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- CS
- confirmed by serology and demonstration of cytoplasmic inclusion bodies in lymphoid tissue (eg. Peyer's patches) |
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Tx and control of PCVAD
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- ensure all piglets receive colostrum: dose manually with 10 ml any pig <1kg or any born >2.5 hours after start of farrowing
- minimise stress - follow PRRS protocol re: x-fostering, mixing, etc. - vaccine available but in short supply |
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etiology inclusion body rhinitis
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porcine cytomegalovirus
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CS inclusion body rhinitis
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- sneezing in pigs <3 wks of age
- nasal discharge - epiphora - may lead to otitis media if chronic |
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pathology: inclusion body rhinitis
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rhinitis and conjunctivitis
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Dx inclusion body rhinitis
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- turbinates plugged with mucus/debris
- basophilic intranuclear inclusion bodies in nasal mucosa - if herd is naive any age can be affected and 25% mortality in affected litters may be seen |
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chars roundworm migration
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- naive pigs with access to new soil
- larval migration damages liver and lungs: petechial hemorrhage in lung, "milk spots" in liver (resolve in 4 wks) - adults shed 2 to 9x10^5 - Tx: pyrantel, fenbendazole, dichlorvos, ivermectin |
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life cycle of Ascaris suum
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cycle takes 5 to 6 weeks
- excretion of eggs with faeces - in the faeces, embryonated eggs pass from non-infective, non-embryonated to infective, embryonated and become very resistant - swallowing of eggs - L3 travels to digestive mucosa and moves to the liver via the circulation of the veins - L3 migrates to the periphery of the liver causing white spot lesions - L3 changes into L4 in the alveolus - L4 goes through the bronchi and the trachea and is swallowed at the level of the pharynx - L4 changes to L5 in the small intestine |
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Dx Ascaris suum
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petechial hemorrhages evident all over lung
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