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VDPAM 445Swine Topics

Respiratory Disease Control

Dr. Alex RamirezVeterinary Diagnostic and

Production Animal MedicineIowa State University

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General introduction

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Endemic Pneumonia • App- continual outbreaks, chronic pleuropneumonia

– Sometimes other bacteria as well• Enzootic Pneumonia

– Mycoplasma hyopneumoniae– Pasteurella multocida

• Porcine Respiratory Disease Complex– All of the above (especially M. hyo)– PRRSV– SIV– Others: PCV2, PRV, H. parasuis, S. suis,

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Diagnostics• Gross pathology: APP versus all others

– APP & A. suis vs. others• Organism identification

– Culture– FA– PCR– IHC: immunohistochemistry (with histopath)

• Fixed tissue, easy sample preservation

• Histopath– Prove disease, organism presence is insufficient

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Question: Is this mycoplasma?

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Diagnostics• Serology: serological profiling

– Timing of infection but not necessarily timing of disease

• Sampling issues– Tissue preservation in formalin

• Buffered• Multiple sites• <1cm tissue thickness

– Number of animals• Example on next slide

– Sick (necropsy) versus healthy (slaughter checks)

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Diagnostic Sampling Strategies

• Small numbers of pigs will result in missed diagnosis– PRDC case: 21 pigs submitted for necropsy–Pathology/microbiology:

– No lesions =5 Gastric ulcer = 2– PMWS = 5 PRRSV = 2– SIV? = 1 APP? = 3 (non-typeable)– P. mult. = 2 Bordetella = 2– Strep suis = 1 M. hyo = 8

– Serology: M. hyo+, SIV+, PRRSV (late +)– Slaughter check: Low average percent pneumonia,

a few pigs severe

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Diagnostic Considerations: Value of Tests

• Laboratory tests should fit with clinical observations– Pigs cough: Pursue rule-outs (M. hyo, influenza)– Pigs grow slowly without overt disease - diets/environment?

• Specific versus non-specific tests– Necropsy and slaughter exams (disease severity)– Laboratory tests (agent identification)– Record analysis (rarely identifies a specific cause)

• Documenting management activities– “Gum shoe” approach

• One revealing observation is often worth more than 100 serological tests

• SOP vs. Actual

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Mycoplasma hyopneumoniae

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Mycoplasma hyopneumoniae• Primary cause of enzootic pneumonia

– Most herds are infected except SPF herds

• Transmission is via aerosol– Air is PCR positive– Difficult to prevent between herd spread

• Disease often manifested in finishing– Organism very slow to grow (weeks)– A few get infected from sows spreads slowly through

nursery pigs– Lateral transmission from older pigs

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Mycoplasma hyopneumoniae

• Diagnosis– Clinical signs: only cough 10 days after challenge

• Severe sickness with infection of SPF herds?• Mild - minimal consequence in otherwise

disease free pigs– Macroscopic lesions

• Anterior-ventral consolidation• Not specific to M. hyo

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Mycoplasma hyopneumoniae

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Mycoplasma hyopneumoniae• Diagnosis

– Histopathology: • peribronchiolar

lymphocytic cuffing– Organism ID

• FA- need fresh tissue, approx. 50% sensitivity

• Culture - slow grow, overgrowth by M. hyorhinis

• PCR - “It’s everywhere”• IHC

– Serology: several ELISA’s available• Vaccination will also induce titers that persist for

a short time

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Mycoplasma Vaccination• Second most common vaccine used in growing pigs

– Common in population– Potentiator of other respiratory disease

• Issues– Mandatory (?) in herds with continuous flow, multiple rooms

within the same building, virulent PRRSV – One vs. two dose products

• Use one dose in “controlled” situations or if labor is a big concern

• Two doses will almost always be better• Start early (3weeks)• Product cost is usually equal• Many combine with PCV2 vaccination

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Mycoplasma Vaccination• Maternal antibody interference

– Probably will not interfere with vaccine induced protection– No real reason to vaccinate sows pre-farrow

• Only vaccinate gilts before entering herd

• PRRS eradication Mycoplasma eradication– Consider where pigs will be grown and finished– May still need to vaccinate pigs

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M. hyo Treatment plan• Antibiotics?

– Now– Earlier– Routes

• Water• Feed• Injectable

• Control other diseases• Vaccination

– Other groups– Timing – watch for PRRS seroconversion

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Actinobacillus pleuropneumoniae(APP)

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Actinobacillus pleuropneumoniae (APP)

• Cause of contagious pleuropneumonia• Transmission by close contact and short

distance aerosols• Many pigs harbor organism in upper airways

– Clinical disease occurs with environmental stress in many cases• Malfunctioning curtain controller temperature

fluctuation organism gains entrance to lung severe (bad), rapidly developing necrotizing and hemorrhagic pneumonia with pleuritis

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Actinobacillus pleuropneumoniae (APP)

• Clinical signs–Sudden death–Sudden onset of rapid, deep breathing–Minimal cough (not an airway irritant)–Fever initially or if mild-to-moderate;

subnormal in severely affected pigs–Hemoptosis and blood from nostrils in agonal

phase (euthanize if possible)–Mortality can reach 10% of barn in one day–Pigs quit eating AND DRINKING

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Actinobacillus pleuropneumoniae (APP)

• Post-mortem lesions–Necrotizing, hemorrhagic, usually multi-focal

pneumonia–Pleuritis will be present if pig survives for at

least 18 hours after challenge–Similar lesions can be seen with

Actinobacillus suis– If APP mass treatment via injection often

indicated; other types of pneumonia treated less aggressively; can’t wait for test results to start therapy

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Actinobacillus pleuropneumoniae (APP)

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Actinobacillus pleuropneumoniae (APP)

• Diagnosis– Initially: clinical signs and gross pathology– Culture: isolation followed by capsular serotyping

• Some relationship between capsular serotype and virulence: Type 1’s are worst; followed by 5’s

• USA: 1, 5, 7 and 3 are most common (odd numbers)• Europe: 2 and 6 are most common

– Serology• Complement fixation: recent infection• ELISA’s: capsule, endotoxin, cross-reactivity problems• Hemolysin neutralization: cross-reactions with A. suis

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APP Vaccination• Most commercial vaccines are bacterins

– Administer 2X at 2-4 week interval prior to finishing – Capsular serotypes must be matched

• Use autogenous vaccines if:–Commercial vaccines don’t contain the

correct serotype–May have within serotype heterogeneity

– Marginally effective: lack ApX toxins which are the main virulence factors for causing disease

– Side effect potential:• Injection site reactions• Fever, off-feed, reduced daily gain

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APP Vaccination• Newer vaccines

– Capsular deficient mutant (MLV): BINOBL• Given IM• Frozen product: order, shipped on dry ice,

use immediately• Limited replication at injection site• Sufficient production of ApX toxins to induce a

protective immune response–Riboflavin deficient mutant

• Not commercially available• Knock out riboflavin synthetase• Add riboflavin to organism and inject IM

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APP Treatment Plan

• Antibiotics– YES!! ASAP

• INJECTABLE• Water• Feed

– Duration of treatment

• Ventilation• Vaccination ?• Different source of pigs

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Actinobacillus suis

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Actinobacillus suis• Will behave like APP but less severe and

short term• Problem with “healthier” herds• Generalized septicemia like H. parasuis,

erysipelas• Produces Type I hemolysin• No commercial vaccines available• Autogenous vaccines used in

refractory cases

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A. suis Treatment Plan

• Antibiotics– APP vs A. suis need immediate action– Sources

• Injectable• Water• Feed ???

• Correct diagnosis is critical• Vaccination with autogenous??

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Pasteurella multocida

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Pasteurella multocida Pneumonia

• Not a primary cause of pneumonia– Experimental infection only with active M. hyo

infection present– “Fuzzy thinking”: not important because

secondary pathogen but primary causes are nearly always present!!• Medication of pigs with non-App pneumonia

is mostly directed at P. multocida–Acute swine influenza outbreaks–Enzootic pneumonia or PRDC–Environmental mishaps

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Pasteurella multocida Pneumonia

• Little known about pathogenesis– Studies just beginning– Generally Type A, non-AR toxin producing– Normal inhabitant of upper airways

• Can cause pleuritis• Diagnosis

– Culture and sensitivity– Sort out primary causes

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P. multocida Treatment Plan

• Antibiotics– Injectable– Water– Feed

• Environment – Ventilation• Address other diseases

– PRRS– Mycoplasma– Etc.

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Atrophic Rhinitis(AR)

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Atrophic Rhinitis• Bordetella bronchiseptica

– Causes atrophic rhinitis– Enables P. multocida to colonize nasal epithelium

• Pasteurella multocida– Causes progressive atrophic rhinitis– Produces AR toxin (dermatonecrotoxin)

• Highly potent: inject small quantity turbinate atrophy

– Mainly capsular Type D but also Type A

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Atrophic Rhinitis• Clinical signs

– Deviated snout: side ways or pushed up– Tear staining at medial canthus– Sneezing– Bleeding from nostrils

• Lesions– Turbinate atrophy: primarily ventral scroll of

ventral turbinate– Septal deviation

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Atrophic Rhinitis

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Atrophic Rhinitis• Severity influenced by:

– Air quality and environment; especially in nurseries– Genetics

• Yorkshires more susceptible to developing severe lesions

–Age of sow herd: immunity of dams• Colostral antibody levels• Level of shedding vertical transmission• Age at infection

–Weaning age: <14 days eliminates vertical transmission

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Atrophic Rhinitis• Stepwise approach

– Sow vaccination pre-farrowing• Gilts pre-breeding is always recommended

– LA200 (200 mg/ml oxytetracycline) to piglets• 15 mg/# dose• 1, 7, 14, 21 days or 1, 7-10, weaning

– Naxcel (2 mg/# dose) instead of LA200• No benefit against Bordetella bronchiseptica

– Vaccinate pigs• Two doses: 7 days and weaning• One dose: weaning

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AR Treatment Plan

• Antibiotics– Water– Feed– Injectable

• Prevention– Antibiotics– Vaccination

• Environment

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Psuedorabies(Aujesky’s or PRV)

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Pseudorabies Virus• Eradicated from the USA commercial herds

in late 2003 to early 2004• Respiratory disease in any age pigs in

addition to CNS signs in neonates and reproductive disease in sows

• Occasional necrotic rhinitis crusty nose and nasal discharge

• Important rule-out (along with SIV and PRRS) for sow herd off-feed– Will have fever

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PRV Vaccination• Vaccines were highly effective• Regulatory based vaccination in Stage II areas

– Vaccinated sow herd 4 times per year- IM– Vaccinated pigs once IM by 12 weeks of age

• In herds with active infections– Vaccinated pigs at birth intra-nasally

• Used vaccines that were approved for IN use, must replicate in the nasal epithelium to be effective

– Vaccinated pigs twice IM• Vaccine reduced shedding in individual pigs

– Can stop shedding on a population basis

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PRV Eradication

• Blanket vaccination to reduce/eliminate shedding and transmission

• Improve internal biosecurity– AIAO production– People, equipment movement

• Improve external biosecurity– Hog truck sanitation

• Monitor closely via serology to determine where failure (active infection) is occurring

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Other Viruses

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Other Viruses• PRCV

– Mild respiratory disease in young pigs– Natural deletion mutant of TGE virus

• Can’t attach to intestinal epithelium– Significance ?????

• Test cross reacts with TGE

• Inclusion body rhinitis– Porcine cytomegalovirus– Common disease in early nursery pigs– High pitched sneezing– Minimal clinical impact if no other problems– Severely affected will develop necrotic rhinitis

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Other bacteria

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Other bacteria

• Will be discussed in other sections• Salmonella cholerasuis

– Interstitial pneumonia – Wet lung– Septicemia – purple pigs– +/- diarrhea

• Steptococcus suis– Cranioventral consolidation

• Haemophilus parasuis

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Agents Discussed in future

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Swine Influenza(SIV)

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Swine Influenza Virus (SIV)• Type A influenza virus• H1N1: traditional strain in US• H3N2: new strain in US 1998

– Present in Europe for many years– Some evidence for presence in US before– Spread throughout country in 2-3 years

• H1N2: Detected in Indiana 1999– Combination of H1N1 and H3N2

• Others: Exposure to water fowl outbreak limited to a one or a few herds

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Swine Influenza Virus (SIV)

• Clinical signs– Short term disease: <4-7 days– Fever: variable– Respiratory signs: 1-2 days after challenge

• Increased rate• “Thumps”: abdominal breathing• “Wet Cough”: minimal with pure infection

• Gross lesions–Look like M. hyo

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Answer: SIV

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SIV Vaccination• Strains: H1N1 (traditional), H3N2 (new)• Sow herd vaccination: common, concerns?• Pig vaccination

– Two doses recommended, often one dose given– Relatively high cost – Multivalent vaccines and/or autogenous– Role of maternal antibody interference

• Vaccinate sows pre-farrowing protective titers until 12 weeks of age

• MDA’s may interfere until 8-10 weeks of age small time frame to vaccinate

– Original antigenic sin

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Porcine Reproductive and Respiratory Syndrome Virus

(PRRS)

Discussed in another lecture

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Circovirus(PCV2 & PCVAD)

See Dr. Baker’s Lecture

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Porcine Circovirus Type II• Type I: cause of infectious congenital tremors?;

porcine cell line contaminant• Type II: Cause of PCVAD (Porcine Circovirus

Associated Disease); old name = PMWS (post-weaning multi-systemic wasting syndrome) – Depletion of germinal centers in lymph nodes and

Peyer’s patches are characteristic lesions• Much virus located in these tissues• Virus also present in normal pigs and tissues• Lesions like PRRS

– Disease in US: PRRS associated, mild, older pigs

– Disease in Europe: devastating, younger animals

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PCV2

• Small DNA virus none-enveloped– Hard to disinfect

• Present in most pigs– Exposure is VERY common– Negative herds ???

• Concern with present case definition (PMWS/PCVAD)1. Wasting2. Lymphoid depletion3. PCV2

• Excellent web site www.pcv2.org

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Vaccines

• Just on the market in 2006• In Europe have had a vaccine from Merial

but for sows only!• ISU involved in development of

one vaccine (chimeric with Fort Dodge)• Results?

– So far looking VERY PROMISSING!

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PCV Vaccines

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PCVAD is typically seen in the 10-20 week old pigs in the US

-Morbidity 2-25%-Mortality 1-10%

PCVAD is usually seen in 4-10 week old pigs in Canada and Europe

Courtesy Dr. J. Harding

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Markedly enlarged inguinal lymph nodes

are commonly observed in pigs with

PCVAD

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Porcine Dermatitis and Nephropathy Syndrome

(PDNS)

Etiology unknownPRRSPCV2PRRSV + PCV2P. multocidaStreptococcus sp.

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PCV2 coinfections in 484 U.S. field cases: ISU-VDL

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Rarely see PCV2 singular infection

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PCV2 Treatment Plan

• Vaccination– Earlier the better

• Work on co-infections!

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Acknowledgements

• I would like to recognize others for their significant contributions to this presentation:– Dr. Brad Thacker– Dr. Locke Karriker– Dr. Pat Halbur

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Questions ?