Transboundary Disease threats for Small Ruminants: What are the Risks? Tony Knight BVSc., MS. DACVIM. Colorado State University Fort Collins, Colorado

Size: px

Start display at page:

Download "Transboundary Disease threats for Small Ruminants: What are the Risks? Tony Knight BVSc., MS. DACVIM. Colorado State University Fort Collins, Colorado"

Warren Green
5 years ago
Views:

1 Transboundary Disease threats for Small Ruminants: What are the Risks? Tony Knight BVSc., MS. DACVIM. Colorado State University Fort Collins, Colorado Sheep and Goat Pox: Sheep and goat pox (SGP) are systemic pox diseases of sheep and goats characterized by fever, generalized skin papules, necrotic skin lesions, and nodular lesions in the lungs and digestive tract. Mortality is high in susceptible sheep and goats. Global Distribution: Sheep and goat pox is endemic to many areas of Asia and North Africa with outbreaks of the disease occurring with movement and importation of infected or susceptible animals. European breeds of sheep and goats if unvaccinated are particularly susceptible to the virus. Etiology: Sheep pox and goat pox are caused by closely related DNA viruses of the Capripox genus in the family Poxviridae. Most isolates are host specific, but some isolates can cause disease in both sheep and goats. Serologically the strains are indistinguishable but with genetic sequencing the 2 viruses are distinct, but recombination can occur between them. Recombinant strains usually have intermediate host specificity. Both viruses are closely related to the Lumpy Skin Disease virus (LSGV). These capripoxviruses do not infect humans. Transmission of sheep pox is by aerosol following close contact between a susceptible and infected animals. Capripox viruses can survive for long periods in scabs from lesions, hides, contaminated animal housing not exposed to sunlight. Clinical Signs: After an incubation period of 1-2 weeks, infected sheep and goats develop pyrexia and macules appear on the skin, most visible in the axilla and perineum. Macules develop into hard swellings or papules, which rarely have a fluidfilled cap. Susceptible breeds of sheep often die before the appearance of the typical clinical signs. The papules on the mucous membranes quickly ulcerate, leading to mucopurulent rhinitis, and conjunctivitis. Mastitis often develops in lactating animals. Lymphadenopathy is common and dyspnea may be prominent when the the enlarged retropharyngeal nodes compress the pharangeal area. Extensive viral damage in the lungs also cause dyspnea. Animals surviving the acute stage of the disease develop scabs on the skin lesions. Mortality and morbidity can reach 100% in susceptible sheep and goats. Post Mortem Findings: Generalized lesions on the skin, multiple necrotic foci on mucous membranes, and throughout the gastrointestinal tract. Generalized lymphadenopathy. Numerous firm lesions are present throughout the lungs. Intracytoplasmic inclusion bodies can be seen in infected cells. Diagnosis: The high mortality and typical pox lesions on the skin and internal organs are very typical. Tissue samples for transmission electron microscopy to identify the

2 capripox virions provides positive identification. An agar gel immunodiffusion test (AGID) using lymph node biopsy is also available, as is an ELISA to detect antigens of capripoxvirus. Prevention and Control Measures: In sheep and goat pox free countries there are major restrictions to importing sheep and goats and their products from countries where the capripox viruses are endemic. In endemic areas there is an effective vaccine (0240 strain) that produces lifelong immunity. Peste des Petits Ruminant (PPR) An acute contagious viral disease sheep and goats characterized by fever, conjunctivitis, erosive stomatitis, gastroenteritis, and pneumonia closely resembling rinderpest in cattle. Goats are more severely affected than sheep. Global Distribution: Asia and Africa Etiology: Peste des petits ruminants virus is a single-stranded RNA Morbillivirus in the family Paramyxoviridae. It is easily inactivated by sunlight, heat, lipid solvents, acidity, and alkalinity. Primarily a disease of goats and sheep, and can infect camelids subclinically without being able to transmit the PPRV to other small ruminants. Experimentally, the American white-tailed deer is fully susceptible. PPR virus is transmitted via all secretions and excretions. Inhalation of aerosols from clinically infected animals is typically how the virus spreads. Clinical Signs: After an incubation of 3-10days affected goats and sheep develop a high fever and are depressed and anorexia. Some may die in this acute phase. A serous-mucopurulent nasal discharge usually develops that progresses to a profuse catarrhal exudate, which crusts and occludes the nostrils. Catarrhal conjunctivitis is common. Severe diarrhea that is often profuse but not hemorrhagic resulting in dehydration, emaciation, and followed by hypothermia, and death. Bronchopneumonia is a common feature in the later stages of PPR. Pregnant animals may usually abort. Morbidity 90% mortality 100% especially in susceptible goat and sheep. Post Mortem Findings: Necrotic and inflammatory lesions (erosions) extend from the mouth throughout the gastrointestinal tract. Peyer's patches become severely necrosic and may ulcer. The large intestine is usually severely affected showing congestion around the ileocecal valve, the ceco-colic junction, and the rectum. In the terminal colon and the rectum, streaks of congestion ("zebra stripes") form on the crests of the mucosal folds. Bronchointerstial pneumonia is common. Diagnosis: The clinical signs with high morbidity/mortality are highly suggestive. Confirmation of PPR is based upon agar gel immunodiffusion, virus isolation, monoclonal antibody-based antigen capture ELISA, reverse-transcription PCR for detection of the virus; serum neutralization test and monoclonal antibody-based

3 competitive ELISA for antibody detection. Prevention & Control: PPR control in non-endemic areas is by restriction of importation of sheep and goats. In non-endemic areas PPR would be controlled using quarantine, slaughter with proper disposal of carcasses and fomites, and decontamination of premises. Vaccination is a method of choice for PPR control in endemic areas. Rift Valley Fever Rift Valley fever (RVF) is an arthropod-borne viral disease characterized by hepatitis of ruminants. The disease is most severe in sheep, goats, and cattle, causing high mortality rates in neonates and abortion in pregnant animals. Camels may abort after subclinical disease. It is a zoonotic disease transmitted by hematophagous insect. It is a zoonotic disease affecting humans bitten by RVF virus infected mosquito species or through exposure to tissues of infected animals. Global Distribution: Africa and occasionally in some Middle Eastern countries. Etiology: RVF is an RNA Phlebovirus virus of the Bunyaviridae family. All RVF virus strains belong to 1 serotype, and are classified into 3 distinct lineages: Egyptian, West African, and Central-East African. The usual vectors for the virus are various mosquito species, and in one species of Aedes mosquito transovarian transmission has been demonstrated. It can also be mechanically transmitted by other biting insects including Culicoides spp., black flies, sand flies etc. The virus is inactivated by lipid solvents, detergents and low ph. Sheep, goats, cattle and camels are all susceptible hosts for RVF virus. Lambs and kids are especially susceptible, while the adults of these species are less severely affected. Clinical signs: After an incubation period of 1-3 days, newborn lambs and kids develop a high fever which declines shortly before death. Lambs rarely survive more than hours after the onset of clinical signs. Lamb and kids older than 2 weeks are pyrexic, anorexic, weak, listless, with an increased respiratory rate. Some animals may develop melena or fetid diarrhea, regurgitation and a blood-tinged, mucopurulent nasal discharge. Older animals living longer develop icterus. Infected pregnant sheep, goats, cattle, and camels may abort at any stage of gestation, with the aborted fetuses being autolyzed. Abortion storms often occur in ewes. Mortality can be 100% in newborn lambs and kids. Older lambs and kids, and adult sheep and goats, are less susceptible with mortality in the range 10-70%. Post Mortem Findings: Hepatic necrosis is the most common lesion of RVF. The most severe lesions occur in newborn lambs and aborted fetuses of sheep. Lesions include an enlarged, friable, soft, and red to yellow-brown liver. Petechial to ecchymotic hemorrhages on most organs, patchy congestion, and small gray-white foci 1-2 mm in diameters are scattered throughout the liver.

4 Histologically hepatic necrosis is the major finding with eosinophilic oval or rod-shaped intranuclear inclusion bodies in up to 50% of the hepatocytes Diagnosis: RVF should always be considered in sheep and goats where abortion storms are occurring, or when there is high mortality in neonates. Blood and tissues from animals can be tested for RVF virus using virus isolation, RT- PCR, ELISA methods. Prevention and Control Measures: In endemic areas, RVF control is managed through vaccination especially prior to the rainy season, and insect control. In the USA, where RVF has never been recorded, prevention through restriction of importation of animals from RVF endemic areas. Foot and Mouth Disease Foot-and-Mouth Disease (FMD) is a highly contagious viral disease, primarily of domestic cloven-hoofed animals and many wild animals. FMD is characterized by fever, vesicular lesions, and subsequent erosions of the epithelium of the mouth, tongue, nares, muzzle, feet, or teats. Global Distribution: FMD is endemic in Africa and parts of Asia and Russia, and sporadically in South America. FMD last occurred in the USA in 1929, Canada 1952, and Mexico Etiology: FMD virus is a small RNA Aphthovirus of the Picornaviridae.There are 7 immunologically distinct types: A, O, C, SAT-1, SAT-2, SAT-3 (South African Territories), and Asia 1. The FMD virus is readily inactivated by low or high ph. All cloven-hoofed animals including wildlife species are susceptible to FMDV infection, but sheep and goats generally show very mild, self-limiting infections, and usually require infected cattle and pigs to perpetuate the disease. Once FMD is eliminated from the cattle, FMD disappears from sheep and goats. FMD does affect camels but South American camelids (llamas, alpacas, and vicuñas) have low susceptibility. There is considerable variability of FMD in wildlife, and recent evidence indicates that once FMD is removed from domestic animals, it disappears from wildlife Clinical signs: Unlike cattle and pigs, FMD in sheep and goats is very mild and often unapparent clinically. A few small vesicles or erosions may be seen on the dental pad, lips, gums or tongue, and vesicles may appear on the coronary band causing lameness that can be mistaken for foot rot. Agalactia in lactating sheep and goats is common. Post Mortem Findings: Very mild vesicles or ulcers may be present in the mouth and on the coronary band. Lambs and kids that die may have grayish or yellowish streaking in the heart due to myocardial necrosis ("tiger heart").

5 Diagnosis: Samples of vesicular fluid or epithelium are best for detection of the FMD virus using virus isolation, RT-PCR, or for detecting FMD antibodies (AGID, ELISA) Prevention and Control Measures: Prohibiting the importation of animals or their products from FMD endemic areas is the primary means of prevention in the USA. In the face of an FMD outbreak, if it is not immediately diagnosed and contained/eliminated, massive ring-vaccination, quarantine and surveillance will be implemented. Resources: Infectious Diseases of Livestock. 2 nd Edition. Editors J.A.W. Coetzer & R.C. Tustin. Volumes 1,2,3. Oxford University Press Foreign Animal Diseases. USAHA. 7 th Edition United States Animal Health Association. Foreign Animal Diseases World Organization for Animal Health (OIE)

Lumpy skin disease and bluetongue training of trainers in FYR of Macedonia Skopje, September 2017

Lumpy skin disease and bluetongue training of trainers in FYR of Macedonia Skopje, September 2017 1 Bluetongue Agent and hosts Epidemiology: Spreading routes and transmission Clinical diagnosis: Clinical sings, Differential diagnosis, post-mortem lesions and findings Tsviatko Alexandrov DVM, PhD, FAO