Understanding Rotavirus - Dr. Kent Schwartz, Iowa State University, from the 2016 Power Of The Past, Force Of The Future Customer Appreciation event, August 16, 2016, hosted by Rensselaer Swine Services and Bethany Swine Health Services, Jasper Country Fairgrounds, IN, USA.
More presentations at http://www.swinecast.com/2016-power-of-past-force-of-future-customer-appreciation
(šVVIP ISHAAN ) Russian Call Girls Service Navi Mumbaiš9920874524šIndependent...
Ā
Dr. Kent Schwartz - Understanding Rotavirus
1. Diarrhea in Suckling Pigs
Role of Rotavirus
26th Annual Client Appreciation Day
Kent Schwartz
Iowa State University
Veterinary Diagnostic Laboratory
2. Overview
ā¢ History and changes
ā¢ Bit of science
ā¢ Causes of diarrhea in farrowing
ā¢ Role of rotavirus
ā¢ Prevention of endemic diarrhea
4. History
Housing ļ Nutrition ļ Genetics
What is ānormalā?
Normal is what you are used toā¦
Continuous improvement requires open minds
ļ ask āwhyā?
ļ willing to learn via analysis
ļ willing to implement changes
that have demonstrable benefit
5. History: Infectious Agents of diarrhea
Housing ļ Nutrition ļ Genetics
ā¢ E. coli 1900
ā¢ Salmonella 1900
ā¢ TGE 1940
ā¢ Clostridium perfringens
type C ā 1960ās
ā¢ Coccidiosis ā 1970ās
ā¢ Rotavirus A 1970ās
6. ā¢ PRRSV: 1990
ā¢ Clostridium perfringens type A:
2000
ā¢ Clostridium difficile 2005
ā¢ Rotavirus C 2010
ā¢ Rotavirus A, B 2010
ā¢ PEDV 2013
ā¢ PDCV 2013
ā¢ Seneca virus A 2015
ā¢ E. coli 1900
ā¢ Salmonella 1900
ā¢ TGE 1940
ā¢ Clostridium perfringens
type C ā 1960ās
ā¢ Coccidiosis 1970ās
ā¢ Rotavirus A 1970ās
History: Infectious Agents of diarrhea
Housing ļ Nutrition ļ Genetics
7. ā¢ PRRSV: 1990
ā¢ Clostridium perfringens A: 2000
ā¢ Clostridium difficile 2005
ā¢ Rotavirus C 2010
ā¢ Rotavirus A, B 2010
ā¢ PEDV 2013
ā¢ PDCV 2013
ā¢ Seneca virus A 2015
ā¢ Cryptosporidia
ā¢ Adenovirus
ā¢ Next Generation Sequencing
ā¢ Microbiome and ābioticsā
ā¢ Moreā¦..
ā¢ E. coli 1900
ā¢ Salmonella 1900
ā¢ TGE 1940
ā¢ Clostridium perfringens
type C ā 1960ās
ā¢ Coccidiosis 1970ās
ā¢ Rotavirus A 1970ās
Extreme and constant vigilance ļ
EXTERNAL BIOSECURITY
The rest are nearly always present
INTERNAL BIOSECURITY
MANAGEMENT
HYGIENE
HERD IMMUNITY
8. Secret to prevention of endemic diseases?
Some people try to find things in this game
that donāt exist, but football is only two
things ā blocking and tacklingā (Vince Lombardi)
One of the things young people always ask me about is
what is the secret to success. The secret is there is no
secret. Itās the basics. Blocking and tackling. (Chris Gardner)
Wins come from flawless execution of basics - the
blocking and tackling ā every day.
9. āScienceā: Sterile gut experiences āwavesā of invaders
Micro-ecology changes and variations are infinite
Ongoing from birth through adult: Metagenomics & Biomes
Birth
Types and numbers of bacteria
CHANGING
Physiology
pH
Anti-trypsin
Enzymes
Microflora
Diets
Age
Immunity
High numbers (billions) of C. perfringens, C. difficile, E. coli within hours
Logbacteriacounts
Timeļ
10. āScienceā: Completely reliant on Passive immunity
ā¢ Systemic: Absorbed from COLOSTRUM (absorbed first day)
ā Antibody (IgG) mediated immunity
ā¢ Systemic bacteria & viruses, toxins of Clostridium
ā Immunocytes (cells) that help direct immune response
ā¢ cells, cytokines, immunomodulators)
ā¢ Mucosal: Continuous via milk ingestion (every 4 hours)
ā Antibody (IgA) mediated immunity
ā¢ Mucosal pathogens
ā Rotaviruses, PEDV, E. coli, TGE
ā IgA is gone with weaning (or low milk ingestion / agalactia)
11. Science: NEONATE Risk factors: Anatomy / Physiology
Small Intestine
ā¢ Has longer villi and shorter crypts (7-20x more villus height
ā¢ More mature enterocytesļ more receptors (virus & bacteria)
ā¢ Slower to regenerate epithelium / villi (5 days)
Colon not completely functional
ā¢ Decreased ability to resorb water & salt or maintain pH balance
12. Flow: rate? Peristaltic Waves Orderly Motility?
Bacteria
ā Scienceā: Host physiology AND bacterial physiology
Piglets: high stomach pH, high metabolic rate, limited colon function,
limited regulation of body temperature & gut motility, no trypsin, moreā¦
Bacteria: Dose, maternal immunity, bacteria replication rate, toxin genes
āonā or āoffā, more ā¦
RISKS
Chilling and heat stress
Pathogen load in environment
Cross fostering
Compromised passive immunity
13. The āmathematicsā of enteric disease
Severity of disease = DOSE x virulence
Animalsā RESISTANCE
Dose can determine the outcome of infection
Subclinical infection ļļ Disease ļļ Death
DOSE can be controlled ā HYGIENE / SANITATION
Internal Biosecurity: Sanitation - Management - Commitment
14. Severity of disease = dose x VIRULENCE
animalās resistance
Virulence is difficult to influence with management/nostrums
EXTERNAL BIOSECURITY: A barrier to outside pigs/sources
Do NOT introduce ānewā pathogens to a herd
15. Severity of disease = dose x virulence
Animalsā RESISTANCE
āIMMUNITYā
PASSIVE IMMUNITY
Colostrum contains IgG and Cells ā immunomodulation
Colostrum offers systemic immunity; not much mucosal immunity
Milk (Lactogenic) immunity to provide IgA antibody for mucosal (IgA
and IgM) but not systemic immunity; GONE at Weaning
ACTIVE IMMUNITY
Vaccination or infection stimulates antibody and cellular response
What about Animal Science and RISK FACTORS?
16. Risk Factors influencing piglet resistance to disease
Temperature / chilling / drafts (these are BIG)
Nutritional status and condition of dams
Condition (too fat / too thin)
Ease of farrowing: no hypoxia
Ongoing supply of milk
Genetics, genotype, litter size, milking ability, consumption
Nutrition: quality and quantity of macro- and micro-nutrients
āHerd immunityā ā infections consistent across population
Avoid āsubpopulationsā ļ all gilts/dams exposed to all potential pathogens
Active immunity via mitigated infection or vaccinations
Good supply of colostrum ā litter size ā birth weight
Colostrum from immune dams
Acclimation & Vaccination of gilts and sows
Feed-back to gestating dams ???
Severity of disease = dose x virulence
Animalsā RESISTANCE
17. Concept: Many enteric swine āpathogensā are ENDEMIC
āPotential
Pathogensā
āimmunity, nutrition, geneticsā
āfacilities, managementā
āinfectious diseasesā
Dose x Virulence
18. Most agents of diarrhea are ENDEMIC ļ
We can find them with ātestsā
ļ Why is disease being expressed?
INSULT
Age (days)
Mortality0-4 5-8 8-wean
Agalactia x x x can be high
E. coli x x can be high
Clostridium perfringens A x x low
Clostridium perfringens C high
Clostridium. difficile x low
Rotavirus A x x low
Rotavirus B x low
Rotavirus C x x low
PEDV / TGEV x x x high
Porcine deltacoronavirus x x variable
Isospora (coccidia) x x low
PRRSV x x x variable
Salmonella x variable
19. BIAS: We can find a ābugā but often it is risk factors that allow disease expression
āfind something
infectiousā
Assign
blame
Bias AND
21. Collect Information
Diagnostic testing
DIAGNOSTIC ACCURACY
Does it āmake senseā?
Treatment, Control
Identify Opportunities
Continuous Improvement
Achieving an ACCURATE DIAGNOSIS IS A PROCESS
Think, Analyze, Research
Refine
Repeat
process
22. Case definition and epidemiology
Information to gather BEFORE making a ādiagnosisā
ā¢ OBJECTIVE:
ā Clinical signs
ā Epidemiology
ā Timeline
ā¢ SUBJECTIVE
ā Farm History
ā Area history
25. Subgross examination: Villi
Materials:
ā¢ Freshly euthanized pig
ā¢ Glass tube (red stopper blood tube)
ā¢ Water
Procedure:
ā¢ Immediately place 1 cm section of small
intestine in tube
ā¢ Add water
ā¢ Gently swirl and wait for 1 minute
ā¢ Examine directly or with magnifying glass
Interpretation:
ā¢ Length: duodenum>jejunum>ileum
ā¢ Age: villi get shorter with age
<5 days like photos
Do your own comparisons
26. 10% formalin Refrigerated Test types Agents
Cecal-colon
contents
NO 3-10 ml PCR, ELISA,
isolation
TGE, rotavirus,
Cdiff toxin
Small intestine 6-8 one-inch
segments/lesions
6ā ileum
6ā jejunum
Histo, IHC,
isolation,
impression
smear, PCR
E. coli, CptA,
CptC, Salmonella,
Isospora
Colon Cross-section of
several loops
Remainder of
colon intact
Histo, isolation C.difficile, AEEC,
Salmonella
Other affected
organs
Ā½ā slice Golf ball size Depends Multiple
BAL (lung) NO 1-5 ml (or pieces) PCR PRRSV
Specimens: Select the right pigs!!
3 Acutely Affected Pigs:
Colon Contents
Colon fresh and fixed
Ileum fresh and fixed
Jejunum fresh and fixed
Pool BALs or lung (R/O PRRSV)
27. Enterotoxigenic E coli: Diagnosis
E. coli (secretory diarrhea)
ā¢ Observations:
ā Watery diarrhea
ā Villi intact
ā Chyle in lymphatics
ā Bacterial adherence
ā¢ Frequently detected
ā¢ Frequently blamed
ā¢ Is it primary or potentiated
by risk factors?
28. E. coli Genotyping
Animal ID Gene Result
A, 107 EAST1 (toxin) Positive
LT(toxin) Positive
STa(toxin) Positive
STb(toxin) Positive
Stx1 (toxin) Negative
Stx2 (toxin) Negative
Stx2e(toxin) Negative
F18(pilus) Negative
F41(pilus) Negative
K88(pilus) Positive
K99(pilus) Negative
987P(pilus) Negative
AIDA (adhesin) Negative
EAEA (adhesin) Negative
PAA (adhesin) Positive
E. Coli will always be detected ā¦ but is it important?
Histopathology
Virulence-related disease: genotyping
29. Clostridium perfringens Type C
Disease fairly limited to defined geographical locations
Midwest USA: once common, now uncommon
Quite dramatic when it occurs
30. Coccidiosis ā Isospora suis
- ~5 days through post-weaning
Dose-related disease
Prevention is preferred!
31. Facility ā Hygiene
Internal biosecurity
0
10
20
30
40
50
60
70
80
90
Number of cases of COCCIDIOSIS in suckling piglets
ISU VDL
32. Control of Isosporosis: Example of dose and hygiene
Must eliminate āstickyā oocysts (also bacteria, viruses)
Bugs ābuild upā from previous litters ā transmit by people
Change flooring ā no concrete or wood
All-in/all-out management
SANITATION ā
ā¢ Soak, soap, degreaser
ā¢ Eliminate films
ā¢ Appropriate disinfectants
MANAGEMENT
ā¢ Mats and mat management
ā¢ Cross-fostering pigs
ā¢ Hands, boots, fomites, carts, utensils Blocking and tackling of
hygiene
management
environment
33. Clostridium difficile
Necrotizing typhlocolitis in humans, horses, piglets
Opportunist with severe consequences
in medicated humans and horses
Common (normal) flora in swine:
ā¢ MOST (>95%) of herds are colonized
ā¢ MOST piglets are colonized by 2 days
Increased frequency of ādisease diagnosisā
ā¢ Little evidence for āantibiotic inducedā
Colon important for absorbing water and
determines feces consistency
34. Clostridium perfringens type A
ā¢ Clostridium perfringens type A is common = ubiquitous
ā Environment
ā In gut from D0 (high - 108 populations by 12 hr) through adult
ā¢ CptA: There are no consistent experimental models using
biologically achievable inoculum to critically evaluate
pathogenesis, treatment and control in enteric disease
Type Alpha Beta Epsilon Iota
A + - (beta2) - -
B + + + -
C + + - -
D + - + -
E + - - +
35. PED/TGE: segmental or entire small intestine
Isospora: Lower small intestine
E. coli: mid to lower small intestine
Clostridium: upper small intestine
Rotavirus: segmental but mid to lower small intestine
C. difficile: colon
36. Swine Coronaviruses associated with diarrhea
Transmissible GastroEnteritis - TGEV
Porcine Epidemic Diarrhea - PEDV
Deltacoronavirus - PDCoV
Swine Rotaviruses
Rotaviruses Group A
Rotaviruses Group B
Rotaviruses Group C
No cross-protection between groups
37. Villi are covered with infected
epithelial cells stained brown
Crypt epithelium is spared and will
be the source of new cell growth
38. Just 36 hours post-infection in a neonatal piglet:
ā¢ Villi are gone ļ damage done / gut compromised
ā¢ Only a few brown-staining cells remain
ļ diagnosis only from ACUTELY affected)
ā¢ Millions to billions of virus particles have been shed into the environment
ā¢ Tipping point is reached ļ cows are out of the barn!!
ļ Extraordinary efforts required to regain control
39. PEDV and TGEV: Donāt get them!!
EXTERNAL Biosecurityļ have and follow protocols)
ā¢ Biosecurity protocols: review, strict, tighten, update
ā People, supplies, feed, food, etc.
ā¢ Limit traffic: people and equipment
ā¢ Clean and disinfect incoming: anything
ā¢ Enforce downtime
ā¢ Disposal of dead stock
ā¢ Animal isolation, monitoring and surveillance: diagnostic tests
ā¢ Shower, clothing and boots: thorough / change
ā Truck and trailer biosecurity
ā¢ Loading and unloading procedures
ā¢ Crew and driver protocols
ā¢ Truck wash procedures
ā¢ Manure disposal biosecurity
ā¢ Swine transportation
ā¢ Verify implementation!
http://www.aasv.org/aasv%20website/Resources/Diseases/PED/PEDVBiosecurity.pdf
Vaccination???
PEDV booster of previously positive sows
Not for āprimingā ā only after exposure
40. Rotaviruses cannot be eliminated
ā¢ Non-enveloped: very resistant in environment (itās everywhere!)
ā¢ Can cause severe atrophic enteritis just like TGEV/PEDV
ā¢ 6 structural proteins (VP)
ā VP4
ā¢ 26 antigenic P genotypes with 7 P serotypes
ā¢ cleaved to VP5+VP8 for infectivity
ā VP6: most abundant
ā VP7: 15 G genotypes are antigenic with 10 G serotypes
ā¢ 6 non-structural proteins (NSP)
ā NSP4 may be hypersecretory (like E. coli)
ā¢ Structure
ā Outer layers: VP7, VP4
ā Inner layer: VP6
ā Core: VP1, VP2, VP3
ā¢ VP6 determines antigenically distinct serogroups 1-7
ā¢ Antibody to VP6, VP7, NSP2, NSP4.
ā 3 serogroups (A, B, C) and multiple serotypes
are not cross-protective
ā āinfluenza of the gutā
41. 0.00%
10.00%
20.00%
30.00%
40.00%
50.00%
60.00%
2007 2008 2009 2010 2011 2012 2013
Rotavirus Detection: IHC (group A only) prior to 2009
PCR started in 2009 ļ now usually positive for rotavirus
%B & C
%C only
%B only
%A
NOTE: IHC detects rotavirus A ļ PCR detects rotaviruses A, B and C.
Impact of PCR test sensitivity on āfrequency of diagnosisā
42. Age Distribution versus Serotype
29%
25%
39%
7%
Group A only (N = 479)
< 1 week
1-3 weeks
3- 6 weeks
> 6 weeks
22%
16%
31%
31%
Group B only (163)
< 1 week
1-3 weeks
3- 6 weeks
> 6 weeks
56%
10%
25%
9%
Group C only (N = 521)
< 1 week
1-3 weeks
3- 6 weeks
> 6 weeks
43. PCR Positive Cases by Month
No seasonal effect
84%
73%
85%88%
81%
89%
79%81%83%
72%72%
80%
0%
10%
20%
30%
40%
50%
60%
70%
80%
90%
100%
% Positive
% Positive
Cases tested in year 2012 (N = 1696)
44. Diagnosis: Rotavirus
ā¢ Experimentally, all serogroups cause similar disease in suckling pigs
ā¢ DX = clinical signs + detection + microscopic lesions + rule out others
ā Gross and microscopic lesions are not specific
ā Lesions segmental ļ look at multiple (>6) sections
ā PCR Ct value (lower is more virus) depend on stage of disease
ļ Sample ACUTELY affected piglets
ļ Sacrifice of 2-3 typical pigs better than simple fecal PCR
ā¢ Specific Laboratory Tests
ā IHC: Serogroup A
ā PCR: Serogroups A, B & C
ā Histopathology: compatible lesions
ā¢ No serology test available or helpful
45. Risk Factors / Noninfectious contributors
ā¢ Hygiene (ALL OUT with sanitation / disinfection) impacts DOSE
ā¢ Environment impacts RESISTANCE
ā¢ Chilling (wet, drafts, temperature, heat lamps, mats)
ā¢ Mat management; disinfection and timely removal
ā¢ Management impacts DOSE and RESISTANCE
ā Sow factors: genetics, nutrition
ā People and farm culture: teams with pride and engagement
ā Farrowing processes and procedures
ā Colostrum management
ā¢ Immunity impacts RESISTANCE
ā Proper acclimation
ā Influencing maternal immunity / dam immune status
ā Acclimation
ā Vaccination?
Vaccination???
PEDV booster of previously positive sows
Not for āprimingā ā only after exposure
Where are the data for rotaviruses?
46. Rotavirus: Controlling āFlare-upsā
Double down on basics
Blocking and tacklingļ operate in PEDV mode
Farrowing room processes and procedures / McRebel
Optimize piglet acquisition of colostrum and milk
Manage chilling, drafts, hygienic practices
Can we increase dam immunity?
Acclimation: expose incoming gilts to āprimeā their immune
system to resident viruses and bacteria
Vaccine?
Booster maybe?
Lots of effort & Lots of ātechnologyā:
Commercial, autogenous, subunit and otherwise
NO GOOD DATA (vs human vaccines)
What about āfeed-backā?
47. Evolution of concepts: Can feedback help?
ā¢ Protect the offspring from disease via IgA and/or IgG and/or CMI
ā Passive mucosal immunity ā may prevent disease
ā¢ Prototypes: TGE, PED and E. coli
ā¢ Best IgA response if boostered 10-14 days prefarrow
ā Passive systemic immunity ā may delay infections
ā¢ Systemic disease that are IgG / CMI mediated (Clostridium toxins)
ā¢ Best IgG response if boostered 4-5 weeks prefarrow
ā¢ Protect the unborn fetus during gestation
ā Active systemic immunity prevents viremia in dam
ā¢ Protect unborn fetuses
ā¢ Prototype: porcine parvovirus
ā¢ PRRSV, perhaps other āSMEDIā or unknowns
āAssumptions
ā Prototype: PRRSV ā¦ but may not be via āFeedbackā
ā Extrapolations start to get fuzzy
ā BTY: Feedback and controlled exposure are NOT the same as vaccination
48. What do we really know about
feedback to gestating dams?
Proceedings, AASV and SDC
Robbins and Byers: Field Study
1. No statistical differences in outcome over 1 year period
2. Feedback can contain agents that are unexpected
Arruda: Controlled Study
No differences measured in colostrum, sows
or piglet diarrhea after feedback of feces
containing Clostridium spp, E. coli, and rotaviruses
49. Feedback: understanding pathogenesis, mechanisms
and virulence factors
Moeser AJ, Blikslager AT: J Am Vet Med Assoc 231: 56-
ā¢ Fimbria, Pili, Adhesins: Attachment is common 1st step
F18, K88, ā¦. MANY and not just for E. coli
ā¢ Viruses and coccidia cause individual cell necrosis
ā¢ Pathogenicity islands (code for nanomachine-like proteins) for invasion
ā¢ Toxins:
Exotoxins: Clostridia, E. coli
Mediators and modulators: permeability and altered cellular machinery
ā¢ Stimulate inflammation
Helpful?
Overzealous?
What is the mechanism
for immunity for
the target agent?
51. ā¢ FEED BACK: Objectives? ļ ENHANCE HERD IMMUNITY
ā āPrimingā mode ļ First exposure to a specific strain of pathogen
ā¢ Sow Farms: assure uniform first exposure (PEDV)
ā¢ Gilt acclimation ļ PEDV, PRRSV, parvoviruses and MORE
ā āBoosteringā mode ļ rotavirus, E. coli, Clostridium sp.
ā¢ Boostering previously exposed animals requires HIGH Dose
ā¢ Can feedback spread bugs or increase persistenceļ ????
ā Is that a good thing or bad thing?
ā¢ Clostridium perfringens type C or type A or C. difficile?
ā¢ Rotaviruses, PRRSV and PCV2
ā¢ Erysipelas, Brachyspira, Salmonella, Lawsonia, toxigenic E. coli
ā¢ Parasites: Isospora, nematodes
52. What are some obstacles to
āboostering immunityā via re-infection?
ā¢ āHypo-responsiveā to feed matrix / microbiome / diet antigens
ā¢ Physiologic: Stomach pH, digestion
ā¢ Epithelium
ā¢ Innate resistance mechanisms, including
ā Mucus flux
ā Tight Junctions
ā Antimicrobial peptides (kill zone)
ā Inflammatory response
ā¢ Adaptive immunity ā antibody and CMI
ā Systemic
ā Mucosal
Slight perturbations may not āboosterā immunity
ā Happens locally
ā No need to call in all the āreinforcementsā
53. WHAT and WHEN to feed back?
ā¢ For Rotavirus ( enteric viruses, bacteria, piglet scours)
ā Feces from acute piglets, 10-14 days prior to farrowing
ā Source?
ā¢ Feces, wipes, processing carts, anything with poop
ā¢ Macerated gut tissue from dead pigs
ā¢ Feces/content from intentionally infected pigs??
ā Colostrum deprived and sow milk deprived
ā Harvest feces and intestines from 1-2 day old pigs
ā Easily 1000x more virus particles/unit (Ct 25ļ 15)
ā¢ Disclaimer: no published, peer-reviewed research!!
ā¢ To protect unborn piglets (congenital tremors, PPV, SMEDI)
ā Entrails (guts/viscera/mummies) given prior to breeding
ā Eviscerate and macerate (garbage disposal or meat grinder)
54. IF doing feedback, suggestions are:
1. What is your stated objective? ļ booster IgA to control rotavirus
2. DOSE is important
ā High dose better than multiple doses for āboosterā
ā One dose done right probably better than multiple doses
(Antigenic mass / agent replication sufficient to induce response)
3. TIMING is probably important
ā 10-14 days for IgA booster (to control scours)
ā 5 weeks for IgG booster (to increase antibody for systemic
diseases or toxins of Clostridium, influenza, IAV, erysipelas)
4. Define and refine the process and procedures
ā What are the risks?
ā What material to use? Feces/intestines?
ā Dilute with cold saline and use immediately or refrigerate < 3 days
ā Can retain for future use (for a while) by freezing
5. Be tidy ā spend time cleaning
55. Controlling endemic scour flare-ups
If itās not TGE or PED, fall back to basics
Go into āPED elimination modeā in farrowing rooms
Develop a checklist / McRebel
ļ¼ Gilt acclimation (truly acclimated)
ļ¼ Sow condition, colostrum management, attended farrowings
ļ¼ Sow farrowing processes and procedures
ļ¼ Farrowing hygiene between groups and throughout suckling phase
ļ¼ Stop cross-fostering
ļ¼ Stop transmitting feces (boots, hands, fomites, carts, etc.)
ļ¼ Scrupulous hygiene ļ It is an OB ward!!!
Attempt to develop good herd immunity
ļ¼ Gilt acclimation, controlled exposure, vaccination, feedback
ļ¼ Feedback to gestating dams
ļ¼ Assess risk factors
ļ¼ Establish a process
ļ¼ Reinforce basic concepts
ļ¼ One big dose more important than lots of little doses
60. ADDED COMMENTS
Does diagnosis matter?
Endemic flareupsā¦
specific interventions?
We can control some level of disease just by management
Hygiene, sanitation, not spreading it, etc
All interventions work better if
Sows are healthy and well fed
Facilities are clean
People are not spreading infectious agents between litters/rooms
People not tranfering disease by moveing pigs or holding them back to
Infect younger pigs
Sometimes it is useful to know the specific agent, particularly if
There are specific interventions!!!
Editor's Notes
You have seen this before
Epidemic
Endemic
Objective: observations, check list, numbers, dates, timeline, parities
Subjective: lots of biasesā¦.prior history, neighboring farms, what others are talking about
WHAT DOES GENOTYPING TELL YOU????
ANTIBIOTIC SENSITIVITY is NOT PREDICTIVE OF PATHOGENIC POTENTIAL
Other than a few months in here (Feb, Oct, Nov), most of the months have a higher percentage of positive cases (in the mid 80s), compared to the previous years.