Moving and Sensing Sheep and Goats 2022 PDF

Musculoskeletal Diseases and Causes of Lameness in Sheep and Goats Dr. Hollie Schramm Clinical Professor Production Management Medicine Objectives for Musculoskeletal Disease of Sheep and Goats Recognize the common problems that cause lameness in sheep and goats Understand the clinical signs of musc...

Musculoskeletal Diseases and Causes of Lameness in Sheep and Goats Dr. Hollie Schramm Clinical Professor Production Management Medicine Objectives for Musculoskeletal Disease of Sheep and Goats Recognize the common problems that cause lameness in sheep and goats Understand the clinical signs of musculoskeletal disease in small ruminants Identify what pathogens cause specific musculoskeletal diseases and the basic epidemiology of the disease Describe what diagnostics would be appropriate to diagnose specific diseases (if applicable) Develop a basic treatment plan for the common diseases of the ovine and caprine musculoskeletal system Understand how to prevent and control musculoskeletal diseases from a herd perspective Overview Management and herd health considerations for musculoskeletal disease in sheep and goats Common diseases of the ovine/caprine foot Joint diseases of the ovine/caprine Common nutritional diseases of ovine/caprine Lameness case video Foot Disorders Attributed to environmental, nutritional, management, and genetic factors Hooves grow more rapidly with increased nutritional intake Wet, muddy environmental conditions predispose to foot disease Biosecurity is essential: “The foot diseases tend to walk in on all 4 legs” Foot Health is Part of Herd Health All herds require regular foot trimming (due to overgrowth) What factors contribute to overgrowth? How often should a herd do hoof trimming (sheep and goats)? What do you see? K Foot Diseases: Interrelated, but Different Diseases Interdigital Dermatitis Benign Foot Rot or Foot Scald Pathogenesis Characterized by inflammation and necrosis of the interdigital tissue (NOT to hoof/claw) Typically only a few animals affected in a herd Location is INTERDIGITAL This can then lead to Contagious Foot Rot Treatment similar Contagious Foot Rot Contagious Foot Rot (Interdigital Necrobacillosis) One of the most economically devastating diseases in the sheep/goat industry Highly contagious! Caused by the interaction of two bacteria: Dichelobacter (Bacteroides) nodosus in the foot Fusobacterium necrophorum in soil and manure -What type of bacteria are these? Both are nonmotile, nonspore forming, anaerobic, gram-negative bacilli. Foot rot is a contagious, acute or chronic dermatitis involving the hoof and underlying tissues (Bulgin, 1986). It is the leading cause of lameness in sheep. Footscald, an interdigital dermatitis is caused primarily by D. nodosus alone. Contagious Foot Rot: Epidemiology Moisture and warmth is the perfect environment for these anaerobes D. nodosus survives in the hoof Can only survive 10-14 days outside the hoof Spread via carriers and contaminated surfaces Flock problems: Chronic carrier animals Most people BUY foot rot Contagious Foot Rot Pathogenesis of Foot Rot? Interdigital skin becomes reddened and slightly swollen Then undermining of the sole and potentially the wall Characteristic foul odor The lesion is found IN THE FOOT (sole and wall), NOT in the interdigital space Treatment/Prevention Hoof trimming (let oxygen in) Antibiotics systemically LA-200 (Oxytetracycline) Zactran (Gamithromycin) Draxxin (Tulathromycin) Excenel (Ceftiofur) PPG (Penicillin) Nuflor (Florfenicol) Consider withdrawal times Foot baths/soaks/sprays Segregate infected animals Improve environmental conditions Keep feet trimmed Contagious Foot Rot: Prevention Moving to dry area or improve areas of moisture Vaccination (will only shorten the course of the disease) Culling (genetic component, chronic carrier animals) Avoid potentially contaminated facilities Trim new additions and quarantine for 30 days Contagious (Virulent) Foot Rot Eradication Nearly impossible in endemic herds (especially if moisture present) Trim, soak, vaccine Trim, soak, vaccine, antibiotics (if foot rot present) Segregate affected animals and put on clean pasture Cull (select for genetic resistance) Foot Bathes and Topical Treatments 10-15% Zinc sulfate 5-10% Copper sulfate 5% Formalin Trim feet before using, this increases effectiveness At least 30 minutes in foot bath Weekly, 2-4 times total in high risk times for prevention Which type of foot bath do you think is preferred and why? Foot Abscess Bacteria that gain entry into the hoof via puncture injury or enter through the white line (WLD) Pocket of infection that can be small or large Foot abscesses that occur just above the hoof sometimes enter the joint of the foot, causing severe lameness Treat by opening lesion If deep infection (anti-inflammatories, antibiotics) Caprine Arthritis Encephalitis (CAE) Retrovirus- integrated into the host genome Chronic multisystemic disease In USA, seroprevalence from 38-81% Small Ruminant Lentivirus (SRLV) SRLV’s (include OPP, Maedi-Visna, and CAE) CAE: Epidemiology Transmission thru infected macrophages in fluids Vertical: Most common is from ingestion of colostrum or milk Horizontal: Physical contact, milking equipment, semen, surgical equipment Infects monocytes and macrophages and induces a persistent lifelong infection Not all infected animals will develop disease - - - - Caprine Arthritis Encephalitis (CAE) Four clinical syndromes & D 1. Arthritis (most common) 25% of seropositive animals > 6 months of age 2. Leukoencephalomyelitis in kids 3. Mastitis, interstitial pneumonia 4. Old goat encephalitis Pictures taken by Dr. John King, Cornell Lymphocyte proliferation is the hallmark pathologic lesion Lung Mammary gland Serological Testing - Diagnosis ELISA- more sensitive then AGID, great specificity (100%, 99.6%) AGID- fair sensitivity, good specificity (85-90%, 100%) Often used for herd screening Included in biosecurity panel (CAE, CL, Johne’s, Q fever) What is the best prevention if you have a seropositive doe that you don't want to cull??? CAE Prevention Caprine Arthritis Encephalitis: Prevention Feed CAE free milk and colostrum Separate infected from non-infected Milk non-infected does first Use seronegative bucks Disinfect equipment between animals Cull positive animals Septic Arthritis: Prevalent in all Food Animal Species Bacterial infection of the joint(s) What age of animal is commonly affected? Where does the infection come from? Bacteria isolated (lambs) [ I Escheria coli, Streptococcus, Truperella pyogenes, Erysipelothrix rhusiopathiae and insidiosa, Mannhemia hemolytica, Corynebacterium pseudotuberculosis, and Fusobacterium necrophorum Septic Arthritis Pathogenesis Septicemia→ Hematogenous seeding of joint(s)→ Synovitis→ Joint pain, heat, swelling, synovial effusion→ Damage to articular cartilage and subchondral bone→ As bacteria proliferate, inflammatory cells produce hydrolytic enzymes These enzymes destroy the bacteria but also the normal cartilage (erosion) If untreated, chronic changes occur Thickening of synovial tissue and fibrosis of the joint capsule Degenerative Joint Disease and Osteomyelitis Clinical Signs Lameness (how lame?) Warm swelling of the joints Possibly febrile and anorexia Look for other signs of septicemia What are these? Carpus, tarsus and stifle most common (but it can be any joint) Diagnosis and Treatment Sterile aspirate of synovial fluid Look at consistency and color May be thin or thick Clear, cloudy, or purulent material Pleocytosis and neutrophilia Radiographs and Ultrasound Utilized to determine degree of degenerative change (prognosis) Can be used to assess soft tissue and also for treatment Treatment/Prevention Antibiotics systemically and/or intra-articularly Lavage of the joint (need to sedate) Flush daily with sterile isotonic fluids (for 3 days) Take sample prior to flushing and potentially put antibiotics into the joint after flushing Arthotomy or arthroscopy Regional limb perfusion Adequate colostrum intake/dipping navels/clean environment at birth Mycoplasma Polyarthritis: Goats Same as respiratory agents Mycoplasma mycoides subspecies capri (most common) M. capricolum, M. agalactaie, and M. putrefaciens Can occur as outbreaks (epizootic) Typically infected by colostrum and milk Mycoplasma Polyarthritis: Goats Clinical Presentation 3 - 8 week old kids (highly fatal) high fever, lameness painful joints +/- swelling meningitis, conjunctivitis, pneumonia mastitis (in adult does) Treatment Florfenicol, Tylosin Prevention pasteurize milk/colostrum and feed to kids culture does and bulk tank Chlamydial Polyarthritis: Sheep Agent: Chlamydophila pecorum Clinical signs 1 - 8 month old lambs, feedlot (outbreaks, high morbidity) High fever, lameness, joints are enlarged, conjunctivitis Treatment Florfenicol, tetracycline Nigerian Goat Kid: 1 day of age, with muscle weakness White Muscle Disease aka Nutritional Muscular Dystrophy (NMD) Deficiency of Selenium or Vitamin E Skeletal form Cardiac form These forms can occur concurrently May result in death Selenium deficient diets Often during gestation Occurs in Se deficient regions Selenium deficient regions White Muscle Disease aka Nutritional Muscular Dystrophy (NMD) Clinical Signs Young, rapidly growing animals Cardiac form Labored breathing, tachypnea, tachycardia, frothy nasal discharge, heart murmur Skeletal form Stiff gait, tremble while standing, recumbent, weakness and unable to nurse White Muscle Disease or NMD Diagnosis CK and AST levels elevated Whole blood levels of Se and plasma levels of vit E Necropsy - whitish streaks in muscle fibers Treatment Vit E and Se injections Vit E may not be bioavailable in some injectable forms of Se/Vit E combos Prevention Mineral salts (continuously available) Vit E and Se injections are often given shortly after birth to calves/lambs/kids Practice: Where is she lame? Diagnosis?