Specific pathogen prevention program for the tough diseases of sheep and goats (Proceedings)


Specific pathogen prevention program for the tough diseases of sheep and goats (Proceedings)

Nov 01, 2009

Several insidious diseases cause significant economic loss to sheep and goat producers through decreased longevity, growth rate, milk production and animal sales, and they are often purchased through inapparent carriers. Direct contact can transmit these diseases between adults over time, but they can be transferred quickly from the adults to the young through colostrum, milk and direct contact. There is no effective treatment for any of these diseases, and a specific pathogen prevention program has been developed to decrease their incidence. Infected herds remove the newborns from the adult population at birth, feed heat-treated colostrum and pasteurized milk or milk replacer, and permanently separate the new clean replacements from the infected adult population. These insidious diseases include, but are not limited to, Johnes disease, caprine arthritis-encephalitis, ovine progressive pneumonia, mycoplasma, caseous lymphadenitis, and scrapie.

Johne's disease

Johne's disease or paratuberculosis affects both wild and domestic ruminants. Mycobacterium avium subspecies paratuberculosis (MAP) can survive for extended periods in contaminated environments or in manure spread on pasture for over one year. Contaminated soil and bacteria-laden feces coat the teats and udder of the dam and are nursed by the newborn, while infected animals shed mycobacteria in both milk and colostrum. In utero transmission of MAP has been documented in both sheep and cattle, but the percentage of goats born with infection has not been determined. The incubation period is very long and clinical symptoms are more common in animals between 2 and 4 years of age. The severe stress associated with pregnancy, parasitism, or environmental change may trigger clinical disease. The most common presentation of Johne's disease in sheep and goats is severe, progressive weight loss leading to emaciation in spite of good nutrition. Affected animals exhibit lethargy, anemia, rough haircoat, flaky skin and occasionally bottle jaw or pendulant edema. Diarrhea is uncommon in small ruminants with Johnes disease but may appear terminally. Fecal culture and AGID or ELISA testing of blood samples may be used for antemortem diagnosis, but most cases are confirmed with histopathology at necropsy.

Caprine arthritis-encephalitis

Caprine arthritis-encephalitis (CAE) is caused by a retrovirus that lives in macrophages, and the virus is shed by inapparent carriers and clinically ill animals in colostrum, milk, lochia, aerosol droplets and other body secretions. Any method that moves white blood cells from one goat to another can transmit CAE: colostrum, milk, close contact, shared housing, feeding equipment and water sources, injection needles and equipment. The virus does not survive long outside the host, so environmental contamination has minimal importance in transmission or maintenance of the infection in a herd. The percentage of infected animals that demonstrate clinical disease is low, but stress and poor management increase the appearance of clinical symptoms. Chronic progressive arthritis affecting multiple joints, chronic progressive interstitial pneumonia, and weight loss associated with chronic disease are the most common presentations. The least common expression of CAE is an ascending paralysis in otherwise healthy afebrile kids. An unusual form of udder edema that is non-responsive to diuretic therapy may be associated with CAE. There is no difference in prevalence between breeds or sex, but the incidence of infection increases with age in herds with virus-positive animals. Both tests for antibody (AGID and ELISA) and virus (PCR) are commercially available. CAE does not kill goats but decreases productivity, life span and quality of life.

Ovine progressive pneumonia

The virus that causes ovine progressive pneumonia (OPP) or maedi-visna (MV) is a retrovirus affecting sheep that is closely related to the caprine arthritis-encephalitis virus. These viruses are similar enough that either virus may cause disease in the other specie and both diseases can be passed back and forth between the two species through prolonged direct contact. OPPV persists within macrophages similar to CAEV and can be transmitted through direct contact, milk or colostrum. The rate at which OPP spreads through a flock may be markedly influenced by whether the sheep are on extensive pasture or closely confined, and the incidence of seropositive animals increases with age in infected flocks. The onset of clinical disease may follow stress, exertion, severe weather, or change of environment and is insidious in nature. The most common presentation would be chronic progressive interstitial pneumonia leading to open mouth breathing, flaring of the nostrils, expiratory dyspnea, and coughing with chronic weight loss. Affected females exhibit "hardbag" or a large firm udder due to macrophage infiltration of the mammary tissue, and their lambs have slower growth rates due to decreased milk production. Chronic arthritis and ascending paresis are occasionally observed. Affected animals eventually die due to wasting or chronic pneumonia or are culled for low production. Serologic tests using AGID, ELISA or PCR are available but most cases are confirmed at necropsy.