3. WHY SHOULD YOU CARE ABOUT THESE DISEASES?
PRODUCTION
• Death
• Premature culling
• Loss of good genetics
• Ill thrift
• Poor productivity
• Poor animal welfare
• Carcass condemnation
MARKETING
• Market access
Loss of breeding stock sales.
Higher health standards should increase
demand for breeding stock.
• Consumer demand
Increasingly consumers are demanding
products from food animals with
impeccable health.
What happens when the media says you
can get disease “x” from consuming meat
or milk from sheep/goats with disease
“x”?
4. CASEOUS LYMPHADENITIS (CL)
Boils, cheesy gland, contagious abscesses
• Infectious bacterial disease caused by
Corynebacterium pseudotuberculosis.
• Is a very common infection in sheep and
goats in the US.
• Causes significant economic loss to sheep industry.
(CL accounts for 23% of carcass condemnations.)
• Treatment is generally ineffective, as antibiotics
cannot penetrate pus-filled abscess.
• Minimal zoonotic potential:
C. pseudotuberculosis infections in people are rare.
5. TRANSMISSION OF CASEOUS LYMPHADENITIS
• Spreads from animal to animal primarily
through contact with material from subcutaneous
abscesses (pus) or objects contaminated with
abscess material.
• Organism can survive several months in
soil and environment; thus, remaining a
persistent source of infection.
• When abscesses are present in lungs, bacteria
can spread through respiratory secretions.
• Transmission via milk is rare.
• No evidence of transfer via semen.
• Once infected, an animal is infected for life.
6. SYMPTOMS OF CASEOUS LYMPHADENITIS
EXTERNAL
• Superficial (under skin) abscesses
of lymph nodes.
• Abscesses are filled with pasty,
thick yellow-green pus.
• External abscesses are responsible
for disease transmission.
• More common in goats.
INTERNAL (VISCERAL)
• Greater diagnostic challenge;
only detectable through necropsy.
• Affected animals may show weight loss and
poor productivity. They may exhibit mastitis,
respiratory distress, chronic cough or
neurologic deficits, depending upon
location of abscess.
• Associated with “thin ewe syndrome.”
• More common in sheep.
• Infected animals don’t always show signs.
• Infection leads to formation of abscesses in or near lymph
nodes (external) or in the thorax or abdomen (internal).
7. DIAGNOSING CASEOUS LYMPHADENITIS
BACTERIAL CULTURE
• Offers only definitive diagnosis.
• Submit abscess material (pus, exudate)
for culture.
• Lance and aspirate
• Have veterinarian remove whole abscess
• Should culture all abscesses regardless
of blood test results.
• Not all abscesses are CL.
• Over a 16 year period, Actionmyces
pyogenes was cultured 3x more than C.
pseudotuberculosis (1991, AVMA).
• About 50 percent of abscesses in W. MD Buck
Performance Test are C. pseudotuberculosis.
SEROLOGY (BLOOD TESTING)
• ELISA test
• Best used as a screen to find out if a herd
or flock has been infected, rather than to
diagnose an individual animal.
• Positive test does not mean an animal is
infected with C. pseudotuberculosis.
• Negative test does not rule out infection
by C. psuedotuberculosis.
• Cannot differentiate between natural
exposure and vaccination.
8. CONTROL AND MANAGEMENT OF CL
• Maintain a closed flock/herd
• Do not buy animals with abscesses.
• Isolate affected animals before
abscesses rupture.
• Test all abscesses
• Have veterinarian remove abscess.
• Lance abscess and flush with iodine
(or 10% formaldehyde).
• Treat animal with antibiotics.
• Keep animals isolated pending
culture results.
9. CONTROL AND MANAGEMENT OF CL
• Cull animals with recurrent abscesses.
• Keep infected animals separate from
clean animals.
• Practice good hygiene to prevent
spread of infection.
• Early weaning: isolate young animals
from mature animals.
• Can vaccinate to reduce incidence
of CL abscesses in flock or herd.
• Sheep vaccine (Colorado Serum Co.)
• Goat vaccine (Texas Vet Labs)
• Autogenous vaccine
10. ERADICATION OF CL
• Cull all animals with abscesses.
• Cull all animals with CL abscesses.
• Cull and necropsy all suspect
(thin, poor-doing) animals.
• Test (>6 mos. of age) and cull any animals that
test positive for C. pseudotuberculosis.
• Purchase new animals from CL-free
flocks/herds. Test 10 or more animals from
flock/herd of origin to determine disease status
or test new purchases twice 30 days apart
before introducing them into clean flock or herd.
11. OVINE PROGRESSIVE PNEUMONIA (OPP)
• Slowly progressing viral disease of adult sheep that
may affect several organ systems of the body.
• First described in 1923.
• ~25% of US sheep infected.
• All breeds are susceptible, but some breeds are more
susceptible, e.g. Texel, Border Leicester, and Finn.
• Genetics affects susceptibility; sheep with two copies
of the desirable gene (TMEM154) are 3-5 times less
likely to contract the disease.
• Has infected goats experimentally.
• No known cure or vaccine.
12. TRANSMISSION OF OPP
• Primarily through the ingestion of infected
colostrum and milk.
• Contact transmission may occur in closely-
confined sheep.
• Recent research at USMARC showed that the
primary cause of OPP infection was due to
non-maternal exposure that occurs after
young ewes join the infected breeding flock.
• In utero transmission is rare.
• Transmission via semen has not been
demonstrated.
• OPP and CAE can cross infect.
13. SYMPTOMS OF OPP
• Most sheep do not show clinical signs.
• Rarely signs < 2 years; most common >4
• Loss of weight and body condition
despite normal appetite.
Associated with “thin ewe syndrome.”
• Respiratory tract
Respiratory distress, “lungers”
Secondary bacterial pneumonia
Lung infection causes sheep to waste away
• Udder involvement
Decreased milk production
Enlarged, firm udder with little or no milk
flow. Meaty udders. “Hard bag”
• Arthritis
Swelling of joints
• Central nervous system
Least frequent form
14. DIAGNOSIS OF OPP
• Because many other diseases mimic those
of OPP, diagnosis cannot be based on
clinical signs alone.
• Serological tests are the most practical
methods for detecting OPP.
• AGID
Least sensitive
Prone to false negative results
Most common test
• ELISA
Higher sensitivity
• Newer tests (PCR, cELISA ) identify
OPP viral components in blood, milk,
and other tissues.
15. ERADICATING OPP
METHOD 1
• Remove lambs from ewes at birth and
rear in isolation, especially from positive
ewes.
• Feed colostrum from negative ewes or heat-
treated colostrum.
• Artificially rear (milk replacer) or graft onto
negative ewes.
• Keep clean flock isolated from infected
sheep and goats.
• Add only sero-negative sheep to flock.
• Test annually until there are at least two
consecutive negative flock tests.
METHOD 2
• Test all sheep for OPP virus.
• Remove sero-positive ewes and their
offspring.
• Keep clean flock isolated from infected
sheep and goats.
• Add only sero-negative sheep to flock.
• Test annually until there are at least
two consecutive negative flock tests.
An alternative approach is to use
genetics to confer some immunity to OPP
and not to automatically cull lambs from
infected ewes.
16. CAPRINE ARTHRITIC ENCEPHALITIS (CAE)
• Viral disease of goats.
• First discovered in US in 1980.
• There is substantial evidence that CAE is
widespread in US goats.
• 80% of dairy goats tested at
Washington State University.
• Occurs primarily in dairy goats,
but can affect any breed of goat.
• Has infected sheep experimentally.
• No known treatment or vaccine;
supportive treatments may benefit
individual goats.
17. TRANSMISSION OF CAE
• Primarily through the ingestion of
infected colostrum and milk.
(90% of infections).
• Possibly transmitted from goat to goat
via saliva, nasal secretions, urine, feces,
and blood (via needle use).
• In utero transmission to the fetus and
infection of the kid during parturition
is unlikely.
• Infection through breeding and embryo
transfer is unlikely.
• CAE and OPP can cross-infect.
18. SYMPTOMS OF CAE
ARTHRITIS (ADULTS)
• Chronic joint disease
• Lameness
• Swollen knee joints
• Weight loss
• Paralysis
• Pneumonia
• Hard bag (viral mastitis)
• Production losses
ENCEPHALITIS (KIDS)
• Occurs rarely.
• Affects kids less than 6 months of age
• Paralysis, seizures, and death.
• Not all goats that are infected with CAE will progress to disease (~80%) , however, they may shed virus.
• Clinical signs vary and usually begin at 1-2 years of age.
19. DIAGNOSIS OF CAE
• Clinical signs and history
• Serological (blood) testing to detect
presence of antibodies
1. AGID
Better at diagnosing OPP
Improved if CAEV is used
2. cELISA
More sensitive and specific
• Blood test to detect virus genetic
material in WBCs
• PCR
More expensive
• Post-mortem exam
20. CONTROL AND ERADICATION OF CAE
• Permanent isolation of kids beginning at
birth.
• Feeding of heat-treated colostrum and
pasteurized milk.
• Serological testing of herd and segregation
of sero-negative and sero-positive goats.
• Eventual culling of sero-positive goats.
• Purchase breeding stock from CAE-free
herds; use serological testing to screen
purchases (twice at least 30 days apart).
• Semi-annual or annual testing of herd.
21. JOHNE’ DISEASE (PARATUBERCULOSIS)
• Contagious, chronic, and usually fatal disease
that affects primarily the small intestines of
ruminants.
• Caused by the bacterium Mycobacterium avium
sub paratuberculosis (MAP)
• Cattle [C] and Sheep [S] strain
• Prevalence in sheep and goats is not known;
however, the infection has been confirmed in
many US flocks and herds.
• There is no cure and no vaccine.
• The zoonotic potential of Johne’s is debated.
Does MAP cause Crohn’s disease?
22. TRANSMISSION OF JOHNE’S DISEASE
• MAP organism is most commonly passed in the manure.
• Johne’s disease typically enters a flock or herd when an
infected, but healthy-looking animal is purchased.
• The infected animal sheds the organism onto the
premises.
• Other animals get infected when they swallow the
organism via water, milk, or feed that has been
contaminated by the manure from infected animals.
• Young animals are most susceptible to infection.
• Can be transmitted between species: cows to goats, goats
to sheep, etc.
23. SYMPTOMS OF JOHNE’S DISEASE
• Infected animals may remain free from
clinical disease for months or years.
• In affected animals, intestines become
thick and less efficient at absorbing
nutrients.
• There is rapid weight loss despite
a normal appetite
• Diarrhea is a less common symptom in
sheep and goats than cattle
• Symptoms can be similar to other
diseases: parasitism, dental disease,
CL, CAE, and OPP.
• Stage 1
No signs of disease
• Stage 2
Subclinical disease
May be shedding organism
• Stage 3
Clinical disease
Eat well, but losing weight
Blood test can detect some infected animals.
• Stage 4
Advanced clinical disease
Weak and emaciated
Shedding large numbers of organism in feces
Death is eminent
24. DIAGNOSIS OF JOHNE’S (MAP)
Diagnostic testing
• Organism based
• Culture
Isolate living organism from manure,
tissue, soil, water, or grass
• PCR $$
Assay that looks for MAP’s genetic
material in a manure sample
• Antibody (blood or milk) test
• AGID (test of choice)
• ELISA – cross-infectivity with CL
• Necropsy
• Difficult to diagnose
• Testing less reliable in small ruminants
25. CONTROL AND ERADICATION OF JOHNE’S
• Maintain a closed flock/herd. Don’t buy Johne’s disease.
• Manure management
Reduce exposure of lambs/kids to adult manure
• Milk and colostrum management
Feed pasteurized colostrum and milk.
• Do not feed on the ground.
• Cull more recent born offspring from infected dams.
• Separate test-positive animals.
• Test and cull.
• If your flock or herd has numerous cases of Johne’s,
consider depopulation.
26. SCRAPIE
• Always fatal, degenerative disease affecting the
central nervous system of sheep and goats.
• Among family of diseases classified as transmissible
spongiform encephalopathies (TSEs): BSE, CJD,
nvCJD, FSE, and CWD.
• First US case of scrapie was diagnosed in 1947.
• Affects mostly black and mottled-faced sheep;
low incidence in goats.
• Low prevalence in US (0.0146%):
85% reduction since 2001.
• No known human health risk.
• No treatment or vaccine.
27. TRANSMISSION OF SCRAPIE
• Scrapie agent is spread most commonly from
infected female to her offspring at birth (via
placenta and placental fluids), or to other
animals exposed to birth environment.
• The risk of transmitting scrapie via embryos
and semen is negligible.
• The scrapie agent has been experimentally
transmitted through the milk.
• The scrapie agent persists in soil.
• Only sheep with certain genotypes will develop
scrapie if they are exposed to the infective agent.
• Resistant genotypes haven’t been identified
in goats yet.
28. SYMPTOMS OF SCRAPIE
• Signs of scrapie vary widely among
individuals and develop very slowly.
• Subtle changes in behavior
or temperament.
Scratching and rubbing against objects
Lip smacking
Biting of feet and limbs.
Loss of coordination
Weight loss
Gait abnormalities, high stepping
Hopping like a rabbit
Swaying of back end
Excitable
• Differential diagnosis: OPP, listeriosis,
rabies, external parasites, pregnancy
toxemia and toxins.
29. DIAGNOSIS OF SCRAPIE
• Initial diagnosis is on the basis of
clinical signs and animal history.
• Diagnostic tests for scrapie
• Pre-clinical (live animal)
Third eyelid test
Rectal biopsy
• Clinical (post-mortem)
Microscopic examination of
brain tissue
30. NATIONAL SCRAPIE ERADICATION PROGRAM
• Scrapie is a reportable disease.
• Report any scrapie-suspect animal to animal
health authorities.
• Submit heads of mature sheep/goats
(> 18 months) that are found dead on farm for
scrapie testing, especially if you don’t market
culls through traditional marketing channels.
• Comply with mandatory animal identification
requirements. 1-866-USDA-TAG
• Use resistant genotypes for breeding.
• Consider enrolling in the Voluntary Scrapie
Flock Certification program.