Need Writing Help 11/18/2023
Law101
Module5Chapter9Slides.pptxBiosecurity & Bioterrorism: Containing and Preventing Biological Threats
Chapter 9
Recent Animal Disease Outbreaks and Lessons Learned
Learning Objectives
Discuss foot and mouth disease and its potential devastation to the beef industry.
Discuss avian influenza and its potential devastation to the poultry industry.
Discuss classic swine fever and its potential devastation to the pork industry.
Discuss bovine spongiform encephalopathy and its potential devastation to the beef industry and implications for human health.
Discuss specific case studies of animal disease outbreaks.
Key Terminology
Avian Influenza (AI)
Highly Pathogenic Avian Influenza (HPAI)
Low Pathogenic Avian Influenza (LPAI)
Bovine Spongiform Encephalopathy (BSE)
Classical Swine Fever (CSF)
Downer Cow
Foot-and-Mouth Disease (FMD)
Foreign Animal Diseases - Case Studies
Foot and Mouth Disease – UK
Highly Pathogenic Avian Influenza - Asia
Classic Swine Fever – UK
Bovine Spongiform Encephalopathy – UK & USA
4
Foot and Mouth Disease
Image courtesy of USDA
5
Foot and Mouth Disease
Picornavirus, Apthovirus
7 distinct serotypes (O, A, C, SAT1, SAT2, SAT3, ASIA1)
Not cross protective
Affects cloven-hoofed animals
Inactivated at
pH below 6.5 and above 11
Survives in milk, milk products, bone marrow, urine, lymph glands
6
| Conditions | Viability |
| Dry Feces | 14 days |
| Urine | 39 days |
| Ground – Summer | 3 days |
| Ground - Winter | 28 days |
Practical examples of FMD virus survival under temperate conditions. FMD virus can survive for long periods of time in dark, moist conditions but is rapidly inactivated by a combination of desiccation, pH and temperature.
FMD Virus Survival
Animal Transmission
Respiratory aerosols
Proper temperature and humidity
Survives 1-2 days in human respiratory tract
Direct contact
Ingestion of infected animal parts
AI, biologicals, hormones
Indirect contact via fomites
8
Clinical Signs
Incubation period: 2-12 days
Fever and vesicles
Feet, mouth, nasal passages, muzzle, teats
Progress to erosions
Abortion
Death in young animals
Recover in two weeks unless secondary infections arise
9
Clinical Signs in Cattle
Oral lesions
Vesicles on tongue, dental pad, gums, soft palate, nostrils, muzzle
Excess salivation, drooling, serous nasal discharge
Image courtesy of USDA
10
Clinical Signs in Cattle
Teat lesions
Decreased milk production
Hoof lesions
Interdigital space
Coronary band
Lameness
Reluctant to move
11
Clinical Signs in Pigs
Hoof lesions
More severe than in cattle
Coronary band, heel, interdigital space
Lameness
Snout vesicles
Oral vesicles less common
Drooling is rare
Image courtesy of USDA
12
Clinical Signs in Sheep and Goats
Mild, if any, signs
Fever
Oral lesions
Lameness
Makes diagnosis and prevention of spread difficult
Image courtesy of USDA
13
Treatment
No treatment available
Supportive care to those afflicted
U.S. outbreak could result in
Quarantine
Euthanization
Disposal
Vaccine available
Ramifications are many and discussed later
14
Morbidity/ Mortality
Morbidity 100% in susceptible animal population
Mortality less than 1%
Higher in young animals and highly virulent virus strains
Animals generally destroyed to prevent spread
15
Human Transmission
Very rarely develop mild clinical signs
Type O, C, rarely A
Act as a transmitter to animals
Harbor virus in respiratory tract for 1-2 days
Contaminated boots, clothing, vehicles
Spread to susceptible animals
Ingestion of unprocessed milk or dairy products from infected animals
16
Public Health Significance
FMD in humans is not a public health concern
40 cases since 1921 documented in humans
Europe, Africa, South America
17
Prevention
USDA APHIS: Strict import restrictions
Prohibit live ruminants, swine, and their products from FMD-affected countries
Monitor travelers and belongings at ports of entry
FADD to investigate suspicious lesions
State planning/training exercises
Biosecurity protocols for livestock facilities
18
Recommended Actions
Confirmatory diagnosis
Depopulation is likely to occur
Proper destruction of exposed cadavers, litter, animal products
19
Control and Eradication
FMD is rapidly spread, so response must be vigorous and proactive
Depopulate herd and destroy carcasses
Remove manure down to bare concrete
High pressure spray to clean equipment and surfaces
Spray with residual disinfectant
20
Disinfection
Effective solutions include
2% sodium hydroxide (lye)
4% sodium carbonate (soda ash)
5.25% sodium hypochlorite (household bleach)
0.2% citric acid
Virkon® S
Areas must be free of organic matter
21
Vaccination
U.S. has no need to vaccinate
Have not had animals affected since 1929
May be used to control an outbreak
Huge implications if we do vaccinate
Annual re-vaccination required
Costly, time consuming
Does not protect against infection, just clinical signs
Spread infection to other animals
International trade status harmed
22
History
1929: Last case in U.S.
1953: Last cases in Canada and Mexico
1993: Italy
1997: Taiwan
2001: United Kingdom
Other outbreaks in 1967-68 and 1981
2007: United Kingdom – an outbreak associated with a vaccine production facility – a breakdown in biosecurity/biosafety!
23
2001 UK Economic Impact
Direct costs
Economic losses to farmers and producers
Eradication costs
Millions to billions of dollars lost from domestic sales
Indirect costs
Exports shut down
$3.1 billion in beef
$1.3 billion in pork
$14 billion in lost farm income
$6.6 billion in livestock exports
Consumer fear
Lapse in tourism
24
2001 UK FMD Tally
No. premises where animals destroyed: 9,996
Animals killed in control measures: 4,080,001
Killed in Animal Welfare Disposal Schemes: 2,573,317
Piglets, calves, lambs killed (estimated): 2,000,000
Total of animals killed: 8,653,318
Source: DEFRA Report, 2002
Avian Influenza
Fowl plague
Image courtesy of USDA
26
Influenza Virus
Family Orthomyxoviridae
Three main types
Type A
Multiple species – to include poultry, wild birds, humans and swine
Type B
Mostly humans
Type C
Humans and swine
Image courtesy of CDC PHIL
27
Influenza A
Multiple species
Humans
Cause of Avian Influenza
Most virulent group
Classification by surface antigens into subtypes
Hemagglutinin (H or HA)
Neuraminidase (N or NA)
Image courtesy of CDC PHIL
28
Surface Antigens and Subtypes
18 HA and 11 NA for influenza A
All known subtypes of influenza A viruses can infect birds, except subtypes H17N10 and H18N11, which have only been found in bats
Hemagglutinin (HA)
Function: Sites for attachment to infect host cells
Neuraminidase (NA)
Function: Remove neuraminic acid from mucin and release from cell
29
Influenza A Viruses
Mutate frequently
Antigenic drift
Point mutations accumulated during virus replication
Antigenic shift
Hybrid virus emerges when cell infected with two different influenza viruses
Human, avian, swine, equine
Transfer of influenza virus to a different species
30
Influenza A Viruses.
Human influenza vaccines
Antigenic drift
Requires new strains to be used in vaccines each year
Antigenic shift
Believed to be the cause of pandemics in 1918, 1957, 1968
Current human influenza vaccines have no efficacy against avian influenza
31
Avian Influenza.
Pathogenicity based on genetic features and/or severity of disease in poultry
Low pathogenic AI (LPAI)
H1 to H16 subtypes
Highly pathogenic AI (HPAI)
Some H5 or H7 subtypes
LPAI H5 or H7 subtypes can mutate into HPAI
32
Geographic Distribution
Worldwide distribution
Reservoir
Free flying aquatic birds: ducks, geese, shorebirds, gulls, terns, auks
Recent outbreaks
Netherlands, Australia, UK, SE Asia, Eurasia
Similarity to Newcastle Disease makes actual distribution difficult to define
Altered avian ecosystems have created new niche for AI viruses
33
Morbidity/Mortality
Approaches 100% in commercial poultry flocks
Deaths within 2 to 12 days after first signs of illness
Survivors in poor condition
Image courtesy of USDA
34
Animal Transmission.
Initial source of infection
Other poultry, migratory waterfowl, pet birds
Spread by aerosol, shared drinking water, fomites
Virus in respiratory secretions and feces
Virus present in eggs but eggs unlikely to survive and hatch
35
Human Transmission.
Previously considered non-pathogenic for humans
1997, Hong Kong
18 humans infected, 6 died
H5N1 virus linked to outbreak in live bird market and area farms
2003, the Netherlands
83 confirmed cases in humans, 1 death
H7N7 strain
36
Human Transmission.
2004-2005, SE Asia
118 cases, 61 deaths
Indonesia, Viet Nam, Thailand, Cambodia
H5N1 strain
Within the vicinity of poultry outbreaks
Limited clustering of some cases
Role of swine
Proposed “mixing vessel”
Image courtesy of CDC PHIL
37
Clinical Signs
Incubation period: 3-14 days
Birds found dead
Drop in egg production
Neurological signs
Depression, anorexia, ruffled feathers
Combs swollen, cyanotic
Conjunctivitis and respiratory signs
Image courtesy of USDA
38
Treatment
No specific treatment
Supportive care and antibiotics for secondary infections
Antivirals (amantadine) effective in reducing mortality
Not approved in food animals
Results in resistant viruses
39
Clinical Signs in Humans
1997: Hong Kong (H5N1)
Fever, respiratory, vomiting, diarrhea, pain
Fatal cases: severe bilateral pneumonia, liver dysfunction, renal failure, septic shock
1979: MP AI in harbor seals (H7N7)
Conjunctivitis in humans in contact
40
Clinical Signs in Humans.
2003: Netherlands (H7N7)
Conjunctivitis
Mild influenza or respiratory symptoms
Fatal case: acute respiratory distress syndrome
2004-2005: S.E. Asia, EurAsia
41
Public Health Significance
Risk is normally low
Strains vary in ability to infect humans
High occupational exposure may increase risk
2003: 83 cases
Human infections from non-compliance with personal biosafety measures
Evidence of human-to-human transmission
42
Economic Impact
Direct losses:
High morbidity and mortality
Movement Control
Quarantine
Surveillance
Depopulation
Carcass Disposal
Disinfection
Indemnities – have to pay owners fair market value for their losses
43
Recommended Actions.
Confirmatory diagnosis
In HPAI outbreaks, depopulation will occur!
Infected premises
Contact-exposed premises
Contiguous premises
Image courtesy of USDA
44
Control and Eradication.
Depopulate flock and destroy carcasses
Remove manure down to bare concrete
High pressure spray to clean equipment and surfaces
Spray with residual disinfectant
EPA maintains list of approved disinfectants
Virkon® S proven to be effective
Image courtesy of USDA
45
Prevention.
Import restrictions
Surveillance
Appropriate biosecurity
Control human traffic
Introduction of new birds into flock
Avoid open range rearing in waterfowl prevalent areas
Education of the poultry industry
Prompt response to outbreaks
Image courtesy of USDA
46
Avian Influenza Vaccine
Traditional killed vaccines are effective
Vaccines will protect only against other avian influenza viruses with the same hemagglutinin (H) type.
47
Vaccination.
Drawbacks to vaccination
Expensive
No cross protection between 18 H subtypes
Possible creation of reassortant virus
Inactivated H5 and recombinant vaccine licensed in the U.S. for emergency in HPAI outbreaks
48
History.
1878: First identified case in Italy
1924-25: First U.S. cases
Low pathogenic avian influenza first identified mid-twentieth century
1970’s: Migratory waterfowl carriers
1997-present: H5N1 “bird flu”
Image courtesy of USDA
49
Significant Outbreaks
1983: U.S. outbreak (H5N2)
$65 million in losses
Destruction of 17 million birds
30% increase in egg prices
1999-2000: Italy outbreak (H7N1)
$100 million in compensation to farmers
18 million birds destroyed
Indirect losses of $500 million
50
Significant Outbreaks (continued)
1997: Hong Kong outbreak (H5N1)
$13 million for depopulation and indemnities
1.4 million birds
2001: Hong Kong outbreak (H5N1)
1.2 million birds
$3.8 million
51
Significant Outbreaks (continued).
2003: European outbreak (H7N7)
Over 33 million birds destroyed
¼ of Netherlands’ poultry stock
2003-2004: SE Asia (H5N1)
8 countries
>100 million birds destroyed
2004-2005: SE Asia and Eurasia
Spread to Eurasia by migratory birds
At present, more than 200 million birds have been destroyed due to H5N1 outbreak worldwide
52
Classic Swine Fever
Hog cholera
Image courtesy of USDA
53
Classical Swine Fever Virus
Family Flaviviridae
Genus Pestivirus
Lipid-enveloped RNA virus
Range of virulence
Acute, subacute, chronic, persistent
Stable, survives in adverse conditions
Natural hosts
Pig and wild boar
54
Geographic Distribution.
Distributed worldwide
Higher prevalence
East and Southeast Asia, India, China, South and Central America
Eradicated in:
U.S.
Australia
New Zealand
Canada
Parts of Europe
Image courtesy of USDA
55
Morbidity/Mortality.
High morbidity in acute infections
Mortality
Acute cases: up to 90%
Chronic cases: most are fatal
Mild cases: low mortality
Some cases asymptomatic
56
Animal Transmission
Highly contagious
Feeding of contaminated garbage
Contact with infected pigs
Oral or aerosol spread
Infected pigs are the only reservoir
Virus in secretions and tissues
Humans are not susceptible
57
Clinical Signs.
Incubation period: 2-14 days
Variable
Acute to asymptomatic
Strain of virus
Susceptibility of pigs
Clinically indistinguishable from African swine fever
58
Clinical Signs.
Huddling
Fever, dullness
Anorexia
Staggering, weakness
Erythema
Cyanosis
Convulsions
Image courtesy of USDA
59
Sampling
Before collecting or sending any samples, the proper authorities should be contacted
Samples should only be sent under secure conditions and to authorized laboratories to prevent the spread of the disease
60
Treatment.
No treatment should be attempted
Slaughter
Confirmed cases
In-contact animals
Possibly complete herd slaughter
Area restrictions on pig movements
Vaccination?
61
Quarantine
Suspicion or diagnosis
Confirmed cases, contact animals slaughtered
Strict quarantine imposed
Prevents spread of disease
62
Disinfection
Detergents
Sodium hypochlorite
Phenolic compounds
Sensitivity
Drying
Ultraviolet light
pH of less than 3
63
Vaccination.
Available in endemic countries
Protects from disease
Does not eliminate infections
Helpful in outbreak control
We all need to do our part
Keep our pigs healthy and free of disease
64
Economic Impact
Control through
Quarantine
Slaughter
Eradication
Loss of import and export markets
Pigs
Pig products
65
History
1864: first confirmed in UK
1989
CSF recognized in 36 countries
Suspected in two other countries
Eradication
Successful
Australia, Canada, the U.S., New Zealand
Underway
Eastern European states
66
United KINGDOM, 2000
A serious outbreak affecting 16 farms in the UK occurred in August, 2000
A total of 74,793 pigs including those on contact farms were slaughtered to eradicate the disease
The cause of this outbreak was never firmly established but was most likely due to pigs consuming contaminated imported pork products
Bovine Spongiform Encephalopathy (BSE)
Mad Cow Disease
Image courtesy of USDA
68
Prion
Smaller than smallest known virus
Not yet completely characterized
Most widely accepted theory
Prion = Proteinaceous infectious particle
Normal Protein
PrPC (C for cellular)
Glycoprotein normally found at cell surface inserted in plasma membrane
69
Normal protein
Secondary structure dominated by alpha helices
Easily soluble
Easily digested by proteases
Encoded by PRNP gene (in humans)
Located on human chromosome 20
70
Abnormal Protein
PrPSc (Sc for scrapie)
Same amino acid sequence and primary structure as normal protein
Secondary structure dominated by beta conformation
When PrPSc contacts PrPC
Converts it to the abnormal form
71
Abnormal Protein
Insoluble in all but strongest solvents
Highly resistant to digestion by proteases
Survives in tissues post-mortem
Extremely resistant
Heat, normal sterilization processes, sunlight
No detectable immune response
72
Animal Transmission
Reasons for emergence under debate
Feed contaminated with scrapie or unknown BSE
Spontaneous
Changes in feed processing
Maternal transmission
Possible, low risk
Retrospective offspring culling
Current thought
Spread via ingestion of BSE contaminated feed
73
Human Transmission
Humans consuming cattle products infected with BSE can develop vCJD
Brain and spinal tissue
Dose required not known
Genetic susceptibility
All human cases have been homozygous for methionine at codon 129 of PrPC
74
Human Transmission
Possible modes
Transmission from surgical instruments used on tonsils, appendix, or brain tissue
Growth hormone injections
Vaccines
75
Clinical Signs
Incubation: 2-8 years
Initial neurological signs
Apprehension, fear, easily startled, depressed
Final stages
Excitable, hyperreflexia, hypermetria, ataxia, muscle fasciculation, tremors
76
Clinical Signs .
Terminal state
Decreased rumination
Loss of body weight and condition, despite good appetite
There is no treatment for BSE
Affected herds
2% morbidity
100% mortality
77
Rapid Diagnostic Tests
At least 5 rapid tests are licensed for use in the US
Experimentally all have very good sensitivity and specificity
100% accurate when 1000 negative samples and 300 positive samples were tested experimentally
Unknown sensitivity and specificity when used on thousands of field samples
78
Recommended Actions .
Notify authorities immediately of any suspicious cases
Submit brain, medulla
Incinerate the carcass
Quarantine the premises
Confirmatory diagnosis
Depopulation and trace backs
Proper disposal of suspect animals
79
Image courtesy of FDA
Cow parts
80
Disinfection
Porous load autoclaving
134-138 oC for 18 minutes
Not always effective
Sodium hypochlorite
With 2% available chlorine
2-N sodium hydroxide
Both on surfaces 1 hour, equipment 8 hours
Rendering at high temperature and pressure
Resistant in tissues, dried organic material, high titer
81
Public Health Significance.
1996-2004
154 cases of vCJD worldwide
146 from UK
No cases of indigenous vCJD in U.S.
Unknown incubation period and consumption
Possibly more cases of vCJD in future
82
Economic Impact
United Kingdom
£3.7 billion total by end of 2001-02
In 1996-97
£850 million for compensation
Prior to 1996
£288 million on research, surveillance, compensation
Very costly, far reaching disease
83
Economic Impact
Single Canadian case
4 month ban
Mid-May to mid-September
$2.5 billion
Trade losses alone at $1.5 billion
Direct costs
Feed, lower prices, reduced sales,
disposal of surplus animals
Harvest/packaging plants
84
Geographic Distribution
95% of all BSE cases in U.K.
Outside U.K. due to importation or contaminated feed
No cases reported from
Australia, New Zealand, Central America, South America
2003
Canada and US reported single cow
2005
Additional Canadian cases
85
History.
1986
First confirmed case in United Kingdom
1988
UK bans meat and bone meal from ruminants in cattle feed
1989
USDA bans importation of ruminants from countries with BSE
86
History .
1993
Peak of BSE in UK
1,000 new cases reported weekly
1997
US and Canada ban feeding of ruminant products to ruminants
US importation ban extended to all of Europe
2001 in European Union
Mandatory testing on cattle older than 30 months destined for slaughter
87
History: Canada
Alberta
May 2003
6 yr old Angus beef cow
Over 2,500 slaughtered, all negative
Dec 2003
6½ yr old Holstein living in U.S.
Jan 2005
8 yr old Holstein
135 slaughtered, all negative
6 yr old beef cow
41 slaughtered, all negative
Prior case in 1993
Cow imported from UK
88
History: U.S.
December 2003
Washington State
Dairy cow
6½ years old
Imported from Canada
Confirmed by DNA tests
Complications following calving
Sent to slaughter
Brain tissue sent to NVSL–per FSIS protocol
Presumptive positive
Definitively positive by UK lab
89
U.S. Response to Its First Case
Dec 30, 2003: Additional safeguards
All downer cattle banned from human food chain
Suspect cattle carcass held until BSE test results received
Specified Risk Material (SRM) prohibited from human food chain
Cattle over 30 months of age
Skull, brain, trigeminal ganglia, eyes, vertebral column, spinal cord, dorsal root ganglia
All cattle: distal ileum and tonsils
90
U.S. Response to Its First Case
Additional process control for AMR (advanced meat recovery) system
Prohibition of spinal cord tissue, dorsal root ganglia, and skull
Routine testing by FSIS
Prohibition of air-injection stunning of cattle at slaughter
Immediate implementation of national animal identification plan
91
Texas, 2004/5
On June 24, 2005, the U.S. Department of Agriculture announced receipt of final results from The Veterinary Laboratories Agency in Weybridge, England, confirming BSE in a cow that had conflicting test results in 2004. This cow was from Texas and represented the first endemic case of BSE in the United States
Alabama, 2006
On March 13, 2006, the U.S. Department of Agriculture (USDA) announced the confirmation of bovine spongiform encephalopathy (BSE) in a cow in Alabama. The newly confirmed case was identified in a non-ambulatory (downer) cow on a farm in Alabama. The animal was euthanized by a local veterinarian and buried on the farm. The age of the cow was estimated by examination of the dentition as 10-years-old. It had no ear tags or distinctive marks; the herd of origin could not be identified despite an intense investigation
Image courtesy CDC
BSE Cases
94
Chapter Discussion Questions
Why is it likely that future human civilizations will become ever more dependent on inexpensively produced animal protein?
Compare and contrast the four Foreign Animal Diseases discussed in this chapter with relation to:
What agent caused each outbreak?
How quickly did the problem spread?
How might the concept RAIN apply to these outbreaks? Construct a table similar to the one in Chapter 7.
What were the implications for human health in each of the outbreak situations?
What would be the affects to the economy should an outbreak like one of these occur locally? Also, determine the role of local responders.
95
Chapter Summary
FMD presents a nightmare scenario for the livestock industry
HPAI is a serious problem with major implications for human health
Classic Swine Fever has great potential to devastate the pork industry
BSE has been a major problem in the UK and was introduced into Canada and the US
Containment measures for all of these FAD have to be aggressive and proactive
Lessons learned from outbreaks studied here need to be applied in biosecurity programs and FAD response plans and training
96
