Published on February 27, 2014
2014 WINTER WEBINAR SERIES SHEEP & GOAT HEALTH PART V: DISEASE MANAGEMENT SUSAN SCHOENIAN & JEFF SEMLER – UNIVERSITY OF MARYLAND EXTENSION
CHRONIC WASTING DISEASES OF SHEEP AND GOATS 1. Caseous lymphadentitis (CL) 2. Ovine progressive pneumonia (OPP) 3. Caprine arthritic encephalitis (CAE) 4. Johne’s disease (JD) 5. Scrapie
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”?
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.
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.
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).
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.
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.
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
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.
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.
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.
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
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.
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.
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.
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.
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.
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
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.
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?
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.
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
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
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.
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.
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.
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.
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
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.
THANK YOU FOR PARTICIPATING IN THE 2014 WEBINAR SERIES www.sheepandgoat.com/recordings.html
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