1. VDPAM 445 Swine Topics Respiratory Disease Control
Dr. Alex Ramirez
Veterinary Diagnostic and Production Animal Medicine
Iowa State University

2. General introduction

3. 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,

4. 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

5. Question: Is this mycoplasma?

6. Diagnostics Serology: serological profiling Sampling issues
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)

7. 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

8. 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

9. Mycoplasma hyopneumoniae

10. 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

11. 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

12. Mycoplasma hyopneumoniae

13. 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

14. 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

15. 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

16. M. hyo Treatment plan Antibiotics? Control other diseases Vaccination
Now
Earlier
Routes
Water
Feed
Injectable
Control other diseases
Vaccination
Other groups
Timing – watch for PRRS seroconversion

17. Actinobacillus pleuropneumoniae (APP)

18. 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

19. 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

20. 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

21. Actinobacillus pleuropneumoniae (APP)

22. 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

23. 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

24. APP Vaccination Riboflavin deficient mutant 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

25. APP Treatment Plan Antibiotics Ventilation Vaccination ?
YES!! ASAP
INJECTABLE
Water
Feed
Duration of treatment
Ventilation
Vaccination ?
Different source of pigs

26. Actinobacillus suis

27. 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

28. A. suis Treatment Plan Antibiotics Correct diagnosis is critical
APP vs A. suis need immediate action
Sources
Injectable
Water
Feed ???
Correct diagnosis is critical
Vaccination with autogenous??

29. Pasteurella multocida

30. 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

31. 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

32. P. multocida Treatment Plan
Antibiotics
Injectable
Water
Feed
Environment – Ventilation
Address other diseases
PRRS
Mycoplasma
Etc.

33. Atrophic Rhinitis (AR)

34. Atrophic Rhinitis Bordetella bronchiseptica Pasteurella multocida
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

35. Atrophic Rhinitis Clinical signs Lesions
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

36. Atrophic Rhinitis

37. 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

38. 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

39. AR Treatment Plan Antibiotics Prevention Environment Water Feed
Injectable
Prevention
Vaccination
Environment

40. Psuedorabies (Aujesky’s or PRV)

41. 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

42. 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

43. 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

44. Other Viruses

45. Other Viruses PRCV Inclusion body rhinitis
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

46. Other bacteria

47. Other bacteria Will be discussed in other sections
Salmonella cholerasuis
Interstitial pneumonia – Wet lung
Septicemia – purple pigs
+/- diarrhea
Steptococcus suis
Cranioventral consolidation
Haemophilus parasuis

48. Agents Discussed in future

49. Swine Influenza (SIV)

50. 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

51. 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

52. Answer: SIV

53. 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

54. Porcine Reproductive and Respiratory Syndrome Virus (PRRS)
Discussed in another lecture

55. Circovirus (PCV2 & PCVAD)
See Dr. Baker’s Lecture

56. 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

57. PCV2 Small DNA virus none-enveloped Present in most pigs
Hard to disinfect
Present in most pigs
Exposure is VERY common
Negative herds ???
Concern with present case definition (PMWS/PCVAD)
Wasting
Lymphoid depletion
PCV2
Excellent web site 

58. 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!

59. PCV Vaccines

60. PCVAD is usually seen in 4-10 week old pigs in Canada and Europe
PCVAD is typically seen in the week old pigs in the US
-Morbidity 2-25%
-Mortality 1-10%
Courtesy Dr. J. Harding

61. Markedly enlarged inguinal lymph nodes are commonly observed in pigs with PCVAD

62. Porcine Dermatitis and Nephropathy Syndrome (PDNS)
Etiology unknown
PRRS
PCV2
PRRSV + PCV2
P. multocida
Streptococcus sp.

63. PCV2 coinfections in 484 U.S. field cases: ISU-VDL9
164 10 77 13 3 92 68 37 11 20 40 60 80
100
120
140
160
180
PCV2 Alone
PCV2+PRRSV
PCV2+PRRSV+SIV
PCV2+PRRSV +M.hyo.
PCV2+SIV
PCV2+SIV +M.hyo.
PCV2+M. hyo.
PCV2+Bacterial septicemia
PCV2+Bacterial pneumonia
PCV2+ Others
Number of Cases
Rarely see PCV2 singular infection

64. PCV2 Treatment Plan Vaccination Work on co-infections!
Earlier the better
Work on co-infections!

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

66. Questions ?