1. Swine Diseases

2. Sources of Information on Swine Health
Diseases of Swine, 10th ed., 2012; Straw, B., et.al.
American Association of Swine Veterinarians
Journal of Swine Health and Production
AASV.org website; disease modules
Swine Disease Manual, 4rd edition 2009; Neumann, Ramirez, Schwartz
Annual meeting proceedings,
The sources for information on swine disease are many. I have chosen to reference the 9th Edition of Diseases of Swine by Straw, et. al. for the latest on the intricacies of swine disease but I can not discount the current information that is made available via the American Association of Swine Veterinarians through their annual meeting as well as the Journal of Swine Health and Production published by the AASV.
I also do not discount some of the excellent information available through the trade publications such as Pork and National Hog Farmer magazine in both print and on the corresponding websites.

3. Definitions
Disease (from “dis” “ease”) is any abnormal state detrimental to the pig.
Infectious disease (ID) is due to microbes.
Microbes, bacteria, viruses and parasites, may or may not cause disease. If they cause disease they are often called pathogens. The normal flora of the microbes literally covers every external and internal surface of the pig’s body. The pig is exposed to many more helpful microbes than harmful ones.
Whether or not ID occurs depends on the causal agent(s), host factors, and environmental factors. These factors are variable and directly or indirectly influence the frequency or occurrence of disease.
Presence of a potential pathogen is called infection but infection does not always result in disease.

4. Disease Overview Poor Environment = Stress Temp Humidity Ammonia
Feed/Water Availability
Improved Pathogen Activity
Antibiotic Resistant
Virulence Genes
Toxin Genes
Mutation
Immunocompromised
Concurrent Disease
Stress (Fight or Flight)
Poor Nutrition/Dehydration
Population Density

5. Infectious Disease Overview
Epidemic Disease
All animals within a population are susceptible
VERY FEW pathogens are epidemic
Environment and host factors dictate disease SEVERITY
All animals will become diseased
Endemic Disease
All animals within a population are infected
MOST pathogens are endemic
Environment and host factors dictate disease PREVALENCE
Only animals with poor environment and/or immune function will become diseased
Infectious Dose vs Immunity

6. Importance of Health to Performance
Of the primary factors that affect throughput, efficiency, variation and productivity, health is the most important.
With health challenges:
genetic potential will not be expressed
the best nutrition formulation or ration will not produce top results
the best management will not shine
the perfect environment will not allow for great production
Maintaining top health is essential for maximizing throughput and optimizing productivity. When disease enters a population of pigs it can affect productivity in many negative ways. It can reduce throughput by increasing mortality and reducing average daily gain. Disease can increase variability and result in a wide range of production challenges such as an increase in undervalued pigs and reducing efficiency and thus raising the cost of production. For sow farms attempting to meet buyer specifications such as batch size or wean weight and average age, variability from week to week or within weekly batches of pigs can be devastating.

7. Health Challenges Outline
Respiratory challenges
“Suis-cide” challenges
Enteric challenges
Other health challenges
Solutions for health challenges
We can not expect to cover all swine diseases in the next hour so I have chosen to address those health issues that are currently issues in the post weaning phase of production across the Midwestern United States. This outline details how this presentation will be organized: by body system versus stage of production.

8. Respiratory Porcine Respiratory Disease Complex (PRCD) Viral agents
Porcine Respiratory and Reproductive Syndrome (PRRS virus)
Swine Influenza Virus (SIV)
Mycoplasma hyopneumoniae
Bacterial agents
Pasteurella sp.
Actinobacillus pleuropneumonia (App)
Respiratory challenges in post-weaning pigs are really caused by a combination of various agents which the end result has become known as Porcine Respiratory Disease Complex or PRDC.

9. Porcine Respiratory Disease Complex (PRDC)
Just as the name implies…respiratory problems in growing pigs are nearly always a result of multiple bugs and insults
A “mixed” infection
Outside of the lab, rarely is respiratory disease the result of a single pathogen!
Any type of stress can be the first insult that leads to a cascade of events that can end up with disease and death
The first health challenge we will address today is PRCD. Seldom, if ever, is respiratory disease in swine a result of a single pathogen. Nearly always there are two or more pathogens affecting the pig at the same time. Often, it may stress of some kind which allows a virus or mycoplasma to gain a foothold. These organisms then act as “door openers” for the secondary bacterial invaders.

10. PRDC PRRS, SIV and Mycoplasma act as “door openers”
Secondary bacteria such as Pasteurella sp. take advantage of the lowered defense mechanisms as a result of the “door openers”
The lungs become more susceptible to the secondary invaders after becoming infected with virus or mycoplasma
Generally, one pathogen intensifies the other
Viruses such as PRRS virus and Swine Influenza Virus along with Mycoplasma hyopneumoniae, act as “door openers” for the secondary bacterial pathogens that are always around.

11. Components of PRDC Viral Bacterial PRRS, SIV, and PCV2
Mycoplasma hyopneumoniae
Pasteurella multocida
Strep. suis
Haemophilus parasuis
Actinobacillus pleuropneumoniae
Actinobacillus suis
Salmonella choleraesuis
The components of PRDC usually include (but not limited to) this list of pathogens. Some are more commonly involved such as Pasteurella sp. and H. parasuis because they are nearly always present in the population. 2

12. Clinical Signs Fever Anorexia Lethargy Coughing Gauntness
Labored breathing “Thumping”
Clinical symptoms of PRDC include all of the above but the degree or severity of the symptoms vary with factors such as age of onset, pathogenicity, duration of clinical signs, and number and type of pathogens involved in the process. This nursery pig is showing the the classic symptoms of advanced respiratory disease.

13. These are typical gross lesions of a mixed infection occurring with PRDC. One cannot identify the pathogens involved based on gross lesions alone. It is important to submit the appropriate specimens which were prepared properly to a veterinary pathology lab for confirmation of the diagnosis.

14. PRRS Virus
Remains the number one “co-factor” for swine respiratory disease complex
Research shows that PRRS virus costs swine producers hundreds of millions of dollars per year
It has been estimated that 70% of the cost of a PRRS break can be attributed to the post-weaning phase of production
PRRS virus is the most commonly mentioned co-factor for PRDC and remains the most expensive swine pathogen in history. The cost of a PRRS break in sow herds is well documented but few realize the real cost comes in the grow-finish stage.

15. PRRS Virus
Recent research has demonstrated aerosol transmission of infectious PRRS virus for nearly 3 miles
Some veterinarians believe we must control the respiratory form of PRRS in the growing pig before we hope to gain area control
Several production systems are immunizing pigs with the commercial PRRS MLV vaccine for control and reduction of virus in areas of concentrated swine production
While aerosol transmission has been dated for years, the virus has recently been collected and found to be infective up to nearly three miles from a source. Controlling the disease in the finishing phase may be the key to long term control and elimination from a region as they are often the source of large amounts of virus which then can be transmitted to neighboring sow farms. Some systems have re-thought the use of the MLV vaccine for both control of the respiratory form of the disease as well as an attempt to make the vaccine strain the dominate strain in the population. Time will tell if this approach will aid in the efforts toward regional control.

16. PRRS Virus Lung Lesions
Low Virulence
High Virulence
Lung lesions caused by PRRS virus vary with the strain of virus and therefore the virulence. The same can also be true for other pathogens. It is also important to point out that rarely are lung lesions in commercially farmed pigs due to a single pathogen so lesions represented in these pictures are a result of tightly controlled experiments in laboratory conditions.
Source: Dr. Pat Halbur, Iowa State University

17. PRRS Virus
Many boar studs and recently, some sow sites have installed air filtration equipment to prevent the introduction of aerosolized PRRS virus and other pathogens
As a result of Dr. Scott Dee’s work on aerosol transmission of PRRS virus, we are seeing more attempts at air filtration of production facilities. As would be expected, high health, PRRS naïve boar studs have been the first to adopt filtration technology but we are now seeing some sow farms attempting to filter all incoming air. The track record on the early boar studs that filtered are very encouraging.

18. PRRS Virus
“Rope” technology is being developed and tested for PRRS virus monitoring of populations
Another new technology that recently came to light utilizes cotton rope to collect saliva samples from pens of pigs that can be tested with PCR tests for the presence of PRRS virus. Pigs are readily attracted to the adsorbent cotton rope and after 20 minutes or so hanging in the pen, enough saliva can be wrung from the rope to easily run what is essentially a pooled sample of nearly every pig in the pen. Dr. Jeff Zimmerman of Iowa State Univeristy has pioneered this technique.

19. Swine Influenza Virus (Flu)
Flu is a common viral co-factor in PRDC
Until circa 1998, we dealt exclusively with the “classic swine flu” in pigs, a strain called H1N1
In the late 90’s, a different strain, H3N2 began infecting swine, particularly sows.
H1N1 tended to be a seasonal problem in growing pigs causing transient anorexia, fever and coughing
H3N2 has become more of an endemic virus
Swine influenza virus remains a very common co-factor or PRDC. Until the late 90’s, swine flu was well defined and a certain strain known as H1N1 was the only one found in pigs and was responsible for the classic symptoms of swine flu that was well known among pig vets and producers. In the late 90’s, a new strain called H3N2 found it’s way into pig populations in North America and along with it a new set of clinical signs. H3N2 hit sow farms with anorexia, fever, respiratory symptoms and in some cases caused abortions and increased sow mortality.

20. Swine Flu
Sow vaccination is common (either pre-farrow or twice a year to the entire herd)
Autogenous vaccine is also common in attempt to keep up with the drift and changes in the virus
SIV is an RNA virus (same type as PRRS) which means it changes frequently making it difficult to control with today’s vaccine technology
Swine flu can be zoonotic so worker vaccination is recommended
Today, vaccination of sows is very common in an attempt to improve maternal antibody in the piglets. Since SIV is an RNA virus and chances rapidly, some veterinarians have chosen to attempt to control the virus with autogenous (farm specific) vaccines. Commercial vaccines have also attempted to capture “recent” and multiple strains to produce a broader protection against multiple strains and “newer” strains. Since swine flu is known to be zoonotic (transmitted from animals to humans), it is important to urge workers and those in close contact with pigs to be vaccinated with the appropriate human vaccine.

21. Acute Swine Influenza (SIV)
High morbidity and low mortality
Fever: degrees F
Off feed and depressed
Labored abdominal breathing
Nasal discharge
Deep barking cough
Pigs may be unable to rise
Typical symptoms associated with swine flu are listed above. Should you be attempting to isolate the virus, it is very important to sample those pigs with high fever, anorexia, and those with the typical nasal discharge. Nasal swabs from these pigs will yield the virus at the diagnostic lab.

22. They don’t always cough!
Swine veterinarians and producers tend to associate a typical deep cough with the clinical signs of influenza but Dr. Marie Gramer of the University of Minnesota has remarked that in pigs experimentally inoculated with some strains of SIV do not cough! So, I tell producers that the type of cough (or the lack thereof) is not always a good diagnostic indicator of the pathogen. The experimentally infected pigs in this picture appear depressed and lethargic.
Source: Dr. Marie Gramer, University of Minnesota

23. Depends on age and immune status of the affected pigs
SIV Clinical Signs
Depends on age and immune status of the affected pigs
May vary depending on strain of SIV involved
Rapid recovery in 3-7 days if infection is uncomplicated
Of course, as with most diseases, severity of clinical symptoms has several factors that can influence it. In high health herds with few complications, recovery of the entire barn occurs in less than a week.

24. Swine Influenza Virus Infection Timeline
Exposure
Peak Virus
Excretion
Seroconversion
24 h
Peak
Fever
48 h
192 h
(~1 wk)
Viral Clearance
Coughing ~ 2 weeks
240 – 336 h
(10 – 14 days)
Sample Collection
This timeline of an SIV infection in pigs represents the rapid onset and resolution of influenza. Note that the best time for sample collection to isolate the virus is about 48 hours after exposure.
Dr. Mike Senn
Source: Dr. Marie Gramer, University of Minnesota

25. Swine Influenza (SIV) Typical Lung Lesions
Here again, we have a set of lungs that were experimentally infected but this time with swine influenza virus. Notice that the lesions are not significantly different than the other lesions I have shown. The take home message is that while you can identify that lungs contain pathology upon gross examination, you can not always differentiate the offending pathogens based solely on these gross lesions.

26. Maternal Antibody “Passive Immunity”
Passive antibody from the sow is generally protective
Can last up to 8-12 weeks of age
Passive immunity decay explains SIV-induced disease is most common in pigs older than 12 weeks of age
The main reason we do not see more pigs vaccinated with SIV vaccine is that the immunity passed from the sow to their piglets is very slow to decay. As long as pigs are protected by this “passive” antibody, they can not develop “active” immunity produced by their own systems. This is called maternal antibody interference and is especially prominent with SIV. Maternal antibody interference with SIV can last up to 12 weeks of age making vaccination of pigs less attractive. It also explains why SIV clinical signs is more common in growing and finishing pigs.

27. Mycoplasma
Mycoplasma hyopneumoniae is nearly ubiquitous in pig populations in the U.S.
While elimination attempts are usually successful in sow populations, re-infection of the pigs in swine-dense areas make vaccination a necessary part of most commercial herds
Mycoplasma spreads among the populations of growing pigs acting as a “door opener” for secondary bacteria

28. Mycoplasma Pathogenesis
Incubation period: days
Considerable variability in duration
Onset of disease dependent on intensity of infection (exposure rate)
Disease is not evident in most pigs until 3-6 months of age
Vaccines are effective at reducing severity of lesions, clinical signs, and affect on performance but do not prevent infection

29. Mycoplasma Clinical Signs
Described as a chronic disease with
High morbidity (high infection rate)
Low mortality (low death rate)
Chronic, non-productive cough
Fever, usually low grade
Gradual onset
Normal breathing unless severe lung damage or secondarily infected

30. Mycoplasma Lung Lesions
Lesions caused by Mycoplasma hyopneumoniae tend to be in the anterior (front) and dependent (lower) lobes of the lung. The lesions are fairly distinctive however they are rarely a result of pure mycoplasma infection. Nearly always there are secondary bacterial agents involved.

31. Secondary Bacterial Infections
Pasteurella, Actinobacillus, Haemophilus, Streptococcus, and Bordetella sps. are often resident in the population
We have been blessed with some awesome new tools for treatment of bacterial pneumonia but…
Early identification of sick pigs and treatment is the key to treatment success!

32. Pasteurella multocida, Mycoplasma and PRRS

34. “Suis-cide” Challenges
Streptococcus suis (Strep suis)
Hemophilous parasuis (Polyserositis or “Glasser’s Disease”)
Actinobacillus suis (A. suis)
These bugs are present in nearly every population
Improving management/ reducing environmental stressors are the key to control

35. “Suis-cide” Challenges
All these bugs can cause “sudden” deaths
Often mortality and morbidity are higher in “start-up” or repopulated herds.
Strep suis: CNS, arthritis, or respiratory forms
H. parasuis: polyserositis
A. suis: respiratory, skin lesions, arthritis

36. Endocarditis

37. Polyserositis/pericarditis

38. Enteric (gut) Challenges
Neonatal challenges
E.coli (K88, F18, 987P)
Clostridium perfringes type A and C. difficile
Coccidiosis
Viral (PED, PDCoV, rotavirus, TGE)
Nursery phase challenges
E.coli, Salmonella sp., ileitis, Porcine Colonic Spirochetosis, Viral
Finishing phase challenges
HBS, Ileitis, Salmonella sp., Brachyspira, PCV2
The first bullet of this slide is only to mention the main enteric issues of the nursing pig, E.coli, Clostridium perfringes, coccidiosis and sometimes viral pathogens can cause serious issues especially to the pre-weaned piglets. Unfortunately, we will only be able to address the most common of these challenges.

39. Coronaviruses Alphacoronavirus (Cats – Feline Infectious Peritonitis):
TGEV
PEDV
Betacoronoavirus (Humans – SARS, MERS)
Deltacoronavirus:
PDCoV
Gammacoronavirus (Avian – infectious bronchitis)

40. Porcine Epidemic Diarrhea
May 17, 2013 first confirmed case in USA
PEDv is a coronavirus related to transmissible gastroenteritis virus -- similar lesions – little cross protection
Europe 1971 – Asia 1982
Young >>>>Old
100% mortality for 3-4 weeks

43. Ileitis Lawsonia intracellularis Confirmed in 1993
Replicates within cytoplasm of epithelial cells of the ileum
Lawsonia intracellularis was identified as the cause of ileitis in pigs in As it’s name implies, it is an intracellular organism.

44. Ileitis Lawsonia intracellularis Porcine Enteritis
Porcine Proliferative Enteritis
Porcine Enteropathy
Porcine Proliferative Enteropathy
Proliferative hemorrhagic enteropathy
Intestinal Adenomatosis
Necrotic enteritis
“Garden-hose Gut”

45. Ileitis Clinical Signs
Clinical signs of acute ileitis can vary from a mild, non-hemorrhagic diarrhea to severe, hemorrhagic, watery diarrhea with rapid onset
Pigs chronically affected display looseness sometimes tinged with blood along with loss of body condition and fail to thrive
Subclinical form of ileitis has also been identified which affects growth performance

46. The type of diarrhea caused by ileitis varies with the stage of production where it occurs as well as the duration of the disease.

47. Lesions of ileitis are variable
Confirmation of a case of ileitis in a group of pigs requires submission of tissues to a veterinary diagnostic laboratory . Thickening of the intestinal mucosa along with varying degree of frank blood or proliferative psuedo-membrane lining are gross lesions that are indicative of ileitis.
Source: Dr. Connie Gebhart, University of Minnesota

48. Where is the ileum ?
It is important to have a basic understanding of swine anatomy especially in the event of attempting to make a tentative diagnosis of ileitis. The ileum is the last portion of the small intestine and there are some unique landmarks that make it easy to locate and evaluate the ileum. First, locate parts of the large intestine that look like a blind pouch which is called the cecum and the spiral colon which looks disturbingly like a “honey bun”. The ileum joins these two portions of the large intestine and is attached to the cecum (blind pouch) by a thin, translucent ligament. The ileum is the final 18 to 24 inches of the small intestine.

49. Solutions for Ileitis
We have several effective antimicrobials approved for ileitis and when pulse-dosed at critical periods are very effective in control of ileitis
We also have an approved and effective avirulent live vaccine that can be used to orally vaccinate for ileitis
Timing and implementation are paramount regardless of the approach you take

50. Porcine Circovirus Associated Disease (PCVAD)
First identified and diagnosed in Canada in mid 1990’s as PMWS (Post-weaning Multi-systemic Wasting Syndrome).
Became a serious health problem with high mortalities in nursery pigs in UK and Europe in 2001 and beyond. Called PCVD in Europe
Emerged in the US in
Substantial losses across U.S. industry
Initially called PMWS and associated with PDNS
Porcine Circovirus Associated Disease (PCVAD) has been one of the most devastating health challenges of recent years while also being an overwhelming success story. As cases of this serious disease swept across the U.S., a race for a cure ensued with three companies crossing the finishing line at nearly the same time with vaccines that were safe and very effective. Unfortunately, there were substantial losses incurred before the vaccines made it to the market.

51. When PCVAD hit producers in the U. S
When PCVAD hit producers in the U.S. in , the losses in some groups of pigs reached 50% mortality!
Dr. Mattew Turner

52. PCVAD
“Race for a cure” yielded three commercially available and efficacious vaccines
Vaccine has proven itself beyond doubt!
Subclinical cases are now the focus as it has been found that vaccine in the absence of typical clinical PCVAD, has led to improved ADG and reduction in the number of light pigs at market time.
To the surprise of some, researchers have shown that the vaccine substantially reduces viremia levels in groups of non-clinical pigs which seems to allow the pigs to better express their genetic potential. Some have shown increases in ADG of 0.1 pounds. While there have no significant differences in mortality on these sub-clinical studies, they show a statistically significant decrease in light pigs at normal market time.

53. This pigs shows the typical look of an individual case of PCVAD.

54. PCVAD can be subclinical or include one or more of the following clinical manifestations:
Multi-systemic disease with weight loss (formerly known as PMWS)
High mortality: Doubling of historical mortality rate without introduction of a new known additional pathogen
Respiratory signs including pneumonia
Porcine Dermatitis and Nephropathy Syndrome (PDNS)
Enteric signs including diarrhea and weight loss
PCVAD can result in a wide array of clinical signs in pigs. It has been incriminated in all the items listed. The enteric signs are easily confused with ileitis.

55. Brown-red-black diarrhea
PCV2 associated diarrhea is often seen in the group prior to PCV2-associated PMWS
Brown-red-black diarrhea
PCVAD

56. Enlarged mesenteric lymph nodes
Thickened small intestinal mucosa in a case of PCV2-associated enteritis
Thickening in PCV2 associated diarrhea is from inflammation below the mucosal surface of the gut.
Goblet cells that produce mucus (clear circles above) are present in high numbers in PCV2 infections, but are few or none in Lawsonia infections.
Enlarged mesenteric lymph nodes
PCV2 antigen in the intestine
(abundant goblet cells: red arrow)

57. Severe mesenteric edema of the spiral colon was one of the more unusual lesions found in severe cases of PCVAD.
Dr. Matt Turner

58. Interstitial pneumonia – wet heavy, edematous lungs was another typical gross lesions with severe PCVAD
Dr. Matt Turner

59. Dr. John Waddell Dr. Matt Turner
Colitis – mesocolitis – wish we would have taken a picture of the mucosa (thickened and hemorrhagic)
Dr. Matt Turner

61. Non-Infectious Challenges
Hemorrhagic Bowel Syndrome (HBS)
Gastric Ulcers
Cannibalism
Hernias
Kyphosis/Lordosis (hump-back)

62. HBS / Torsion Cause is unknown Risk Factors Feed interruption
Rapid ingestion of large amounts of feed / water
“Binge” eating
Overcrowding
Limited feeder space
Genetic susceptibility
Hemorrhagic Bowel Syndrome has been a recognized as a leading cause of sudden death of late finisher pigs for some time but there has been an ongoing debate as to the cause. Veterinarians have looked for an infectious agent for some time but most now agree that this syndrome is likely due to an intestinal accident. Some now believe that any feed interruption event, involuntary or voluntary (binge eating) leads to type of intestinal bloating which distends the large bowel and causes it to turn on its axis cutting off the circulation. Eliminating all out of feed events and evaluating genetic lines based on eating patterns.

63. Gastric Ulcers Risk Factors Stress Intermittent Feeding Crowding
Fasting
Mixing
Ventilation
Finely ground feed
Intermittent Feeding
Delivery / ordering
Disease
Gastric ulcers are generally a sequel to a feed interruption event. When pigs go without feed the acids produced by the glandular portion of the stomach act on the non-glandular portion of the stomach creating erosions which can eventually lead to ruptured blood vessels. A pig that does not eat for any reason is more susceptible.
ANY INTERUPTION IN FEED INTAKE !!!!

64. Cannibalism Primarily “tail biting”
“Vices” such as tail and ear biting are generally a result of stressors which make the pigs uncomfortable and restless
Uniform tail length and pig comfort are essential in addressing these problems
The most important thing you can do with tail biting is to treat every case as an emergency!

65. Kyphosis/Lordosis Straw, et. al. 2008
Hump-backed or “camel-back” pigs are actually a curvature of the spine. There are varying degrees of this curvature and mild cases may not affect performance. Severe cases however affect structure to a point of impinging on internal organs such as the lungs which leads to severely stunted growth. Recently, researchers at the U.S. Meat Animal Research Center at Clay Center, Nebraska were able to demonstrate the genetic origin of this defect. Also, Dr. Barb Straw of Michigan State University studied the effect on growth and survivability. Her work showed that less than 50% of these pigs reach market weight.
Straw, et. al. 2008

66. Senecavirus A (SVA)
SVA, Seneca Valley Virus, resembles Foreign Animal Disease (FAD) clinical signs which we are required by federal law to report to the state veterinarian.
While SVA is not a FAD we cannot tell the difference by clinical signs. Early identification of FAD will minimize disease transmission and economic fallout to the U.S. swine industry.
If SVA is spread throughout a system animal movements will stop until all FAD are ruled out.

67. What To Look For: Sows and Gilts
Blisters (vesicles) intact or ruptured on the snout or mouth (Photo 1 & 2)
Sudden lameness with ulcers like lesions on or around hoof wall (Photo 3)
Sows not eating all feed or off feed
Some fevers up to 105

68. What to Look For: Piglets
Sudden increase in PWM less than 7 days of age
Affected piglets will be observed shortly after birth
Can be confused with PED or TGE
Short lived clinical signs - Production can resume to normal in 4 to 7 days

69. What to Look For: Growing Pigs Sudden and severe lameness
Signs include redness and ulcers around the top of hooves and the skin between hooves
Blisters (vesicles) intact or ruptured on the snout or mouth (Photo 1 & 2)

71. Novel Pathogens Microbe identification tools continue to improve
Remember Koch’s Postulates
The microorganism or other pathogen must be present in all cases of the disease
The pathogen can be isolated from the diseased host and grown in pure culture
The pathogen from the pure culture must cause the disease when inoculated into a healthy, susceptible laboratory animal
The pathogen must be reisolated from the new host and shown to be the same as the originally inoculated pathogen

74. Solutions for Health Challenges
Prevention
Treatment
Elimination
Once a health challenge is identified in a population, the approach to solutions can placed in one three categories: treat, prevent or eliminate it. In most cases, the long term approach will require the use of all three categories.

75. First, Know Thy Enemy!
Diagnose! Find out what pathogens are in the population!
Attempt to sort the wheat from the chaff!
Which pathogens are primary? Secondary? Incidental?
What stressors could be allowing expression?
Upon identifying a problem or a clinical issue in the herd it is imperative that a proper diagnosis is obtained. Before a treatment or preventative measure can be determined, you must know the cause of the clinical symptoms. Without this step, the potential for failure increases exponentially.

76. Diagnose! Clinical signs History Morbidity/Mortality
Respiratory, enteric, lameness, CNS, ADR?
History
Morbidity/Mortality
Response to therapy?
Fever?
Laboratory confirmation

77. After the diagnosis Estimate the prevalence of the disease.
Estimate the cost of the disease in mortality, performance and profit
Determine if there is an effective treatment or immunization tool available
Calculate a cost:benefit ratio
Implement the tool
Assess response

78. Treat
One the diagnosis has been reached and the decision to treat is made:
Use the right tool at the right animal at right time, in the right dose in the right route and in the right frequency
Choosing the correct therapeutic tool is only a fraction of the process
Implementation of the treatment plan is critical!

79. Prevent Choices abound for preventative options:
Feedback
Planned exposure
Avirulent live, attenuated vaccines
Bacterins or killed virus vaccines
Autogenous vaccines
Prophylactic use of therapeutics
As with other tools, proper implementation is essential to success

80. If you can’t live with it…
Eliminate it!
Multiple options exist
Depopulation/repopulation
Age segregated rearing
Medicated early weaning
Test and remove
Mass vaccination and unidirectional pig flow
Load/immunize/close

81. In the end… It is always best to keep disease out!
Biosecurity should be first on the list
We now have the knowledge to implement herd biosecurity that really works

82. The days of the snake oil salesman are over!