Chapter 15. Biology and Diseases of Ruminants Flashcards

1
Q

Sheep, cattle, goats - taxonomy

A
  • Order Artiodactyla (animals with cloven hooves)
  • Suborder Ruminatia
  • Family Bovidae - even number of toes, compartmentalized forestomach, horns; herbivores; derive all glucose from gluconeogenesis
  • Subfamily Capra = sheep & goats
  • Genus & subgenus Ovis = domestic sheep & wild Asian and European sheep
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2
Q

Domestic sheep

A

Ovis aries

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3
Q

Domestic goat

A

Capra hircus

-Originated from western Asian goats

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4
Q

Bovine taxonomy

A
  • Subfamily Bovinae & genus Bos = all domestic and wild cattle, including yak and Banteng (Bali cattle)
  • Subgenus Taurus = all today’s domestic cattle; originate from Europe
  • Bos taurus - from Europe, no hump
  • Bos indicus - Zebu cattle, have hump over withers and drooping ears
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5
Q

Sheep meat breeds

A
  • Common meat breeds in US = Dorset, Columbia, Suffolk, Hampshire
  • Smaller meat breeds = Southdown & Border Cheviot
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6
Q

Sheep wool breeds

A

-Merino, Rambouillet, Lincoln, Romney

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7
Q

Goat breeds

A

-Dairy, meat, fiber or skin types

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8
Q

Goat dairy breeds

A
  • Alpine, Nubian, Toggenburg, La Mancha (rudimentary ears), Saanen
  • All originated in Europe
  • Nubian developed from crossbreeding British & stock with Egyptian & Indian doats
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9
Q

Goat fiber breeds

A

-Angora, Cashmere

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10
Q

Goat meat breeds

A

-Boer, Kiko, Pygmy

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11
Q

Cattle dairy breeds

A

-Common in US = Holstein (Holstein-Friesian), Brown Swiss, Jersey, Ayrshire, Guernsey

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12
Q

Cattle meat breeds

A

-Common in US = Angus, Hereford, Simmental

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13
Q

Ruminant research models

A
  • Agricultural research
  • Cardiac transplantation & preclinical models for evaluation of cardiac assist or prosthetic devices (vascular stents, cardiac valves)
  • Embryo transfer, AI, control of reproductive system
  • Genetic engineering - one proposed use is for production of proteins in milk that can be isolated later
  • Sheep & goats - antibody production
  • Sheep - basic and applied fetal research; circadian rhythms; olfactory cues and behavior
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14
Q

Natural disease models in sheep

A
  • Congenital hyperbilirubinemia/hepatic organic anion EXCRETORY defect (Dubin-Johnson syndrome) = Corriedale
  • Congenital hyperbilirubinemia/hepatic organic anion UPTAKE defect (Gilbert’s syndrome) = Southdown
  • Gamma-glutamyl carboxylase deficiency = Rambouillet
  • Lysosomal storage diseases, pulmonary adenomatosis (Jaagsiekte) = several breeds
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15
Q

Induced disease models in sheep

A
  • Arteriosclerosis
  • Hemorrhagic shock
  • Copper poisoning (Wilson’s disease)
  • Metabolic toxicosis
  • Orthopedic procedures
  • Drug discovery
  • Implantation research
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16
Q

Goat research models

A
  • Immunology
  • Mastitis
  • Nutrition
  • Parasitology
  • Vascular research - large, readily accessible jugular veins
  • Inherited caprine myotonia congenita (‘fainting goats’) = model for human myotonia congenita (Thomson’s disease)
  • Nubian inbred line = beta-mannosidosis & prenatal therapeutic cell transplantation strategies
  • Osteoporosis
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17
Q

Cattle research models

A
  • Ruminal fluid research, teaching, treatment of other cattle - fistula
  • Bovine trichomoniasis (Tritrichomonas fetus) - model for human Trichomonas vaginalis
  • Holstein - inherited cardiomyopathy; leukocyte adhesion deficiency syndrome
  • Ayrshire - lipofuscinosis
  • Shorthorn & Brahman - glycogenosis
  • Saler - hemochromatosis
  • Achrondroplasia in several breeds
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18
Q

SPF sheep, goats, cattle

A
  • SPF sheep & goats housed in biosecure or closed flocks

- SPF cattle NOT typically available

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19
Q

‘Backgrounding’

A

-Preparation of cattle for research use with appropriate transition diet & vaccination schedule

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20
Q

Health screening program for sheep

A

-Q fever (Coxiella burnetti), contagious ecthyma, caseous lymphadenitis (Corynebacterium pseudotuberculosis), ovine progressive pneumonia, internal & external parasitism

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21
Q

Health screening program for goats

A

-Q fever (Coxiella burnetti), caprine arthritis & encephalomyeliis (CAE), brucellosis, TB, Johne’s disease (Mycobacterium paratuberculosis), caseous lymphadenitis, contagious ecthyma, mycoplasma

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22
Q

Minimum vaccinations for small ruminants

A
  • Tetanus toxoid

- Other clostridial diseases

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23
Q

Health screening program for cattle

A

-Johne’s disease, brucellosis, TB, persistent infx with bovine viral diarrhea virus (BVDV), respiratory diseases, internal & external parasitism, foot condition (hairy heel warts, foot rot), bovine leukosis virus (BLV)

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24
Q

Vaccination recommendations for cattle

A
  • BVDV, infectious bovine rhinotracheitis virus (IBR), bovine respiratory syncytial virus (BRSV), bovine parainfluenza-3 (PI-3), Leptospira spp.
  • Depending on herd status, endemic diseases, geographic location, may also include: veneral diseases, clostridial diseases, pathogens causing neonatal diarrhea or respiratory disease, Moraxella bovis (pink eye), Fusobacterium necrophorum (foot rot), Staphylococcus aureus (mastitis), Histophilus somni, rabies
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25
Q

Regulations regarding ruminant laboratory management and husbandry

A
  • USDA regulates use for biomedical & nonagricultural research = Code of Federal Regulations (CFR), 1985
  • Guide for the Care and Use of Agricultural Animals in Agricultural Research and Teaching (‘FASS Guide’)
  • Guide for the Care and Use of Laboratory Animals
  • Animal Welfare Act
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26
Q

Common stressors for ruminants

A
  • Standard husbandry practices: weaning, castration, dehorning, vaccinations, deworming or treatment for external parasites
  • Shipping w/ assoc feed and water deprivation
  • Introduction to new housing environments & novel personnel
  • Intercurrent disease
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27
Q

Ventilation in confinement housing

A
  • Proper ventilation is critical - ammonia buildup and other waste gases may induce respiratory problems
  • In cold weather, if the ceiling, walls or water pipes condense water vapor, th ventilation should be increased at the expense of lower temps
  • Adult goats & young cattle comfortable in colder temps if provided adequate dry dust-free bedding and draft protection
  • Sheep, because of wool, tolerant to both hot and cold extremes
  • Newborn lambs & recently shorn adults suscetible to hypothermia, hyperthermia, sunburn
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28
Q

Chain link fencing for ruminants

A

-DANGEROUS - goats & some breeds and ages of sheep like to stand on hind limbs against walls & may get forelimbs caught

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29
Q

Enrichment for ruminants

A
  • Provide for singly housed animals - including regular human contact
  • Singly housed or recently weaned calves, in particular, need play objects
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30
Q

Light intensity for ruminant housing

A

220 lux

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31
Q

Stomach anatomy of ruminants

A
  • Forestomach = rumen, reticulum, omasum

- True stomach = abomasum

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32
Q

Rumen physiology

A
  • Mature rumen functions as anaerobic fermentation chamber in which enzymes, including cellulase, of resident bacteria (10^9-10^10/mL) allow herbivorous diet
  • Digestion in rumen aided by microorganism, including protozoa (10^5-10^6/mL) and fungi
  • Produce volatile fatty acids (VFA: acetic, propionic, butyric)
  • Fermentative digestion and VFA absorption also occur in the large intestines
  • Rumen microorganisms synthesize B-complex vitamins & vitamin K & provide protein utilized by animal
  • Large amounts of fermentation gases - CO2 and methane - are naturally eructated
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33
Q

Energy sources of ruminants

A
  • Main source: VFA
  • Glucose formed from propionic acid (or from amino acids) for metabolism in the CNS, uterus, and mammary gland
  • Plasma glucose much lower & regulated differently in ruminants
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34
Q

Passive transfer in ruminant neonates

A
  • Intestinal immunoglobulin absorption is crucial for success of passive transfer
  • This transfer mechanism is functional for ~36 hr after birth
  • Neonatal ruminants are immunocompetent - advantage utilized when vaccinating calves against common neonatal juvenile diseases when the dams’ colostrum is lacking antibody against those pathogens
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35
Q

Deciduous dental formula (sheep, goats, cattle)

A

2 (Di 0/3, Dc 0, Dp 3/3) = 30

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36
Q

Permanent dental formula (sheep, goats, cattle)

A

2 (I 0/3, C 0/1, P 3/3, M 3/3) = 32

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37
Q

MHC classes in ovines

A

-3 major histocompatibility classes identified: Class I, II, III

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38
Q

Bovine immune system

A
  • Bovine lymphocyte antigen system (BoLA) - ranks after human HLA & murine H-2 systems in terms of depth of knowledge
  • Complexity of immunobiology of the bovine mammary gland is being studied b/c mastitis very prevalent
  • Several innate immune mechanisms & cellular defenses, and their variation throughout lactation, have been described
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39
Q

Bovine corneal epithelium

A

-Distinguished from other species by ability to heal without treatment, even when severely infected

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40
Q

Ruminant hematology

A
  • Generally have fewer neutrophils than lymphocytes
  • RBCs may become more fragile during rehydration = some hemolysis & hemoglobinuria
  • RBCs smaller & more fragile than most other mammals; Hct tend to be overestimated unless blood samples centrifuged for extended periods
  • Rouleaux formation: limited in sheep & goats, does NOT occur in cattle
  • Normal caprine RBCs lack central pallor b/c flat & lack biconcavity; may exhibit poikilocytosis
  • D/t high number blood groups in sheep & goats, transfusion reaction rates may be as high as 2-3% = crossmatching recommended - can give 10-20 mL/kg volumes
  • Safe blood withdrawal volume - up to 10 mL/kg
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41
Q

Ruminant serum chemistry

A
  • BUN values CANNOT be used to indicate renal function d/t metabolism of urea nitrogen by rumen microflora
  • Because of large volume or rumen water, adults can generally go several days without drinking before significant dehydration; but dehydration can occur quickly in pre-ruminant neonates, animals that are ill
  • Urine pH alkaline in adults
  • AST & LDH not liver specific
  • ALT CANNOT be used to evaluate hepatic disease in goats
  • Gamma glutamyl transferase (GGT) & ALP are assoc w/ biliary stasis; elevations in GGT assoc w/ hepatic damage
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42
Q

Sheep hemoglobin & coagulation, blood groups

A
  • Sheep have at least 6 different hemoglobins

- Coagulation similar to humans; at least seven blood groups identified in sheep (A, B, C, D, M, R, X)

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43
Q

Blood groups in goats

A

At least five (B, C, M, R-O, X)

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44
Q

Ruminant concentrate mixtures

A

Usually contain a protein source (soybean meal, for example), salt & other required macro- and microminerals, Vits A, D, and E
-Good quality pasture meets nutritional requirements for maintenance and growth of ruminants under many circumstances

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45
Q

Concerns with lush spring pastures?

A
  • Especially those containing alfalfa
  • Bloat, diarrhea, grass tetany, nitrate poisoning
  • Feed good quality hay & slowly introduce to pastures
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46
Q

Ruminant eating habits

A
  • Cattle & sheep = grazers
  • Goats = browsers; will also eat seeds, nuts, fruits, woody-stemmed plants; since goats are selective eaters, tend to consume the leafy or more nutritious parts of plants & often don’t need grain supplementation; if goats need supplementation pelleted concentrate preferred otherwise goats will pick out large particles in mixes
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47
Q

Horse feeds

A
  • May be fed to goats

- Should NOT be fed to sheep because sensitive to copper toxicity

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48
Q

Ruminant intake

A
  • Goats: 5-8% of body weight dry matter intake

- Cattle: 4% body weight intake

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49
Q

Urinary calculi in male ruminants

A
  • Assoc w/ rations that contain excessive phosphorus, low Ca:P ratio, elevated Mg
  • Forage grasses high in silicates and oxalates
  • Roughage sources should be analyzed for nutrient content
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50
Q

‘Flushing’ female ruminants

A
  • Feeding does and ewes 200-400g of concentrate per head per day for several weeks before and after initiation of breeding season
  • Thin pregnant does and ewes should receive supplemental grain & ad lib forage during last 6 weeks of gestation
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51
Q

Newborn ruminant nutrition

A
  • All newborns must receive passive immunity from colostrum
  • Colostrum contains concentrated maternal antibodies (mostly IgG1), functional leukocytes, cytokines
  • Quality of colostrum impacted by vaccination program, dam’s condition & nutrition throughout gestation & at time of parturition
  • Reliance on suckling in dairy calves has been assoc w/ failure or passive transfer - frozen or ‘banked’ colostrum may be used
  • Holstein calf should receive its first 2-1 meal of colostrum within 4 hr of birth and should consume at least 100g of IgG within first 24 hr of life - in general, this can be met with 4L of good quality colostrum
  • After 2-3 days, dairy calves can be fed milk replacer or whole milk; provide additional calories if ambient temps fall below TNZ
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52
Q

Juvenile ruminant nutrition

A
  • Can be offered good quality hay be 1 week of age
  • Rumen development in calves is enhanced by supplementation with a concentrate feed
  • Commercial ‘starter’ feeds should be fed by 2-3 weeks of age
  • Young animals should have access to fresh water at least twice daily if not continually
  • Lambs and beef calves typically fed a ‘creep’ supplement to provide additional nutrient & accustom to solid feed prior to weaning
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53
Q

Reproductive physiology - sheep

A
  • Seasonally polyestrus - estrus brought about by decreasing day length; some breeds cycle in both fall and spring
  • Induce estrus cycling by maintaining females in 8:16 hr light:dark for 8-10 wees
  • Older ewes tend to have multiple lambs; Finn & Dorset especially prolific
  • Estrus detection: mild vulvar enlargment, mucus secretion; anxious, isolate from flock; use sterile ram to mark ewes in standing heat
  • Can be ‘hand mated’ or ‘group mated’
  • Ultrasound or interrectal Doppler for pregnancy detection - work best beyond 60 days gestation
  • Commercial serums test for pregnancy specific protein B can be used beyond 30 days gestation in ewes and goat
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54
Q

Reproductive physiology- goats

A
  • Seasonally polyestrus
  • Estrus detection: uneasiness, tail switching/’flagging’, redness & swelling of vulva, clear vaginal discharge that becomes white by end of estrus, vocalization
  • Ovulate within 7-10 days after introduction of a buck
  • Most ovulate between 24-36 hr after onset of estrus - mate once signs of estrus recognized and every 12 hr until end of estrus
  • Pregnancy detection: similar to sheep
  • Dairy goats should have 6-8 week dry period for udder to fully involute & prepare for next milking period
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55
Q

Reproductive physiology - cattle

A
  • Usually have singletons; twins can occur - evaluate females of male-female twins for freemartinism
  • Estrus detection: standing heat - lasts 6-24 hr (usually 12-16 hr); clear vaginal mucous discharge; teaser animals with marking devices; blood progesterone levels, change in conductivity of cervical mucus, cange in vaginal pH, body temperature, changes in activity level via pedometry - hyperactivity, decreased feed consumption, flehmen, standing behind other cows resting their chins on their backs, licking, sniffing
  • Ovulate 12-18 hr after onset of estrus
  • Pregnancy detection: presume based on failure to return to estrus; ultrasound starting 28-32 days after insemination - fetal sex can be determined by ~55 days; rectal palpation at 30-40 days post conception; levels of pregnancy-specific protein B in serum or milk
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56
Q

Placentation in sheep, goats, cattle?

A

Epitheliochorial & cotyledonary

  • Placentomes: infolded functional units of placenta; formed as result of fusion of the villi of the fetal cotyledons projecting into the crypts of the maternal caruncles (projections of uterine mucosa)
  • Caruncles of sheep & goats = concave
  • Caruncles of cows = convex
  • Placentomes distributed between the pregnant & nonpregnant horns of the uterus; those in nongravid horn may be smaller
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57
Q

Husbandry considerations for pregnant ruminants

A
  • Proper plane of nutrition (not overnutrition)
  • Adequate exercise - confine to small pasture or sanitized maternity pen a few days to hours prior to parturition
  • Outdoor parturition = less stress & intensity of pathogens
  • Indoor maternity pens should be clean, dry, well bedded, well ventilated, well lit; water troughs/buckets elevated so offspring do not fall into them; sanitize between dams
  • Clip & clean perineal area of ewes and does
  • Check cow udder to ensure passive transfer to neonate
  • Inexperienced heifers may act indifferent or aggressive towards calves
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58
Q

Parturition space requirements for sheep, goats, cows

A
  • Doe & ewe: ~1.4-1.5 m^2 area

- Cow: 9 m^2 area

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59
Q

Parturition in sheep

A
  • Ewes isolate themselves, restless, stamp feet, blat, periodically turn & look at abdomen
  • Once contractions begin, lambs usually born quickly
  • Most cases of dystocia d/t fetal malpresentation can be corrected via vaginouterine manipulation; occasionally C-section needed
  • Cleanliness, sanitation, adequate lubrication very important for all ruminant obstectrical procedures
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60
Q

Parturition in goats

A
  • Does nearing parturition will have obviously swollen udder & red swollen vulva; pelvic ligaments at base of tail relax; restlessness; vocalization; uneasiness; pawing at bedding; mucous discharge & moist tail
  • Rectal temp drop ~24 hr prior
  • Vaginal exam indicated if labor prolonged beyond 1 hour
  • Induce parturition with prostaglandin F2alpha (PGF2α) - give 2.5-5 mg on day 144 of gestation - will deliver within 28-57 hr
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61
Q

Pseudopregnancy in goats

A
  • One of the few ungulate species that commonly exhibit ‘false pregnancy’
  • Abdominal distension; may develop hydrometra & ‘deliver’ large volumes of cloudy fluid at expected due dates
  • Subsequent pregnancies can be normal
  • Tx: prostaglandin
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62
Q

Parturition in cows

A
  • Separate from herd; lift tail & arch back when within a few hours of delivering; most are recumbent during delivery
  • Entire birthing process typically takes ~100 min - longer in primiparous animals & those carrying large calves
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63
Q

Postparturition in ruminants

A
  • Monitor for delivery of fetal membranes within 12 hr of birth; if not expelled, monitor dam temp, attitude, appetite
  • Do NOT manually remove placenta or give intrauterine boluses
  • Cows & sheep occasionally eat placenta - may subsequently obstruct rumen outflow = remove delivered membranes to prevent
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64
Q

Management of ruminant neonates

A
  • Identification: ear tag or ear notch
  • Need high-quality colostrum within first 12-24 hr of birth
  • Kids & lambs may need supplemental heat in cold weather
  • To control transmission of infectious diseases (CAE, Johne’s) may remove immediately and hand feed heat-treated colostrum
  • First feeding may be up to 125 mL colostrum (lamb, kid) or up to 4 L (calf)
  • Dehorn & castrate kids within first few days of life- CAUTION with electric or butane dehorners b/c thin calvarium & small frontal sinus
  • Calf dehorning occurs when hornbuds appear at 3-6 weeks & castration at 2-9 weeks
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65
Q

Freemartinism in cows

A

-Genetic female born as a twin to a male - results in anastomoses between blood-forming cells & germ cells - results in XX/XY chimera
-Occurs in 85-90% of phenotypic bovine femals born twin to males
-Female will often have abnormal vulva & clitoris & vagina is a blind end lacking cervix
-Singleton freemartins can occur if male fetus lost after 30 days gestation
(Twinning is common in goats - freemartinism in about 6%; intersexes seen in some goat breeds & when polled goats are mated; freemartinism rare in sheep)

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66
Q

Weaning in ruminants

A
  • Lambs: offer grain & later roughage well in advance of weaning; can wean when consuming 0.6-0.8 kg per day creep feed; 6-8 weeks old most common, sometimes as early as 4 weeks
  • Kids: offer forages within 1st week of life because naturally curious; reduced hand fed milk by 4 weeks; wean when 6-10 weeks or 18-25 lbs
  • Dairy calves: wean at 4-7 weeks
  • Avoid stressful procedures like castration, dehorning, vaccination in the week prior to & week following weaning
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67
Q

Passive immunity in ruminants

A
  • Wanes gradually until young are about 6 months old
  • Duration varies considerable in calves
  • Calves can mount B & T cell responses to vaccination even in presence of colostral antibody = can start vaccinating at 4 months of age, or as young as 1-2 months of age & continue to booster until 7 months old & passive immunity is gone
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68
Q

Artificial insemination in ruminants

A
  • More difficult in sheep than in cattles
  • Laparoscopic AI: surgical AI into uterus via small abdominal opening - as high as 70% pregnancy rate with frozen semen but technical & expensive
  • Cervical AI
  • Transcervical AI: penetration through the cervix into uterus; up to 75% success in ewes
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69
Q

Synchronization of breeding in goats

A
  • Goats in luteal phase of estrus - days 4-16 - are sensitive to PGF2α (2.5–5 mg IM) and will show estrus in 36–60 h post injection
  • Induce ovulation via introduction of a buck (pheromones) - does ovulate within 6-10 days
  • Vaginal pessaries of fluorogestone acetate left in place for 21 days in the doe followed by injection of pregnant mare serum gonadotropin (PMSG) at the time of pessary removal can be successful
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70
Q

Synchronization of breeding in cattle

A

-PGF2α or one of its analogs to induce luteolysis; vaginal suppository progestogens
-Sychronize ovulation via OvSynch: scheduled delivery
of PGF2α followed by gonadotropin-releasing hormone
-Estrus may be suppressed in beef heifers in a feedlot by feeding melengestrol acetate (synthetic progestogen)

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71
Q

Synchronization of breeding in sheep

A
  • Expose ewes to vasectomized rams prior to beginning of normal fall mating period - pheromones released by males will stimulate female cycling
  • Artificial or natural progesterones in feed, via parenteral injection, SC implant, vaginal pessaries
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72
Q

Embryo transfer in ruminants

A
  • Removal embryos from superovulated donor & transfer to synchronized recipient
  • Donor animal superovulated with gonadotropins & inseminated
  • In sheep, remove embryos surgically about 1 week after breeding
  • In cattle, nonsurgical transcervical flush
  • About 75% of expected embryos can be recovered
  • Pregnancy rates are ~70%
  • Can also freeze embryos
  • Disease screening for all animals involved important b/c several pathogens can be transmitted directly or indirectly - BVDV, bluetongue virus, infecitous bovine rhinotracheitis virus, mycoplasma
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73
Q

Castration of ruminants

A
  • Sheep & goats: elastrator in animals less than 1 week old; crushing spermatic cord with emasculatome; surgical castration; debated topic
  • Cattle: castrate no later than 3 months of age; if maximum hormone responsive muscle production important, may castrate older animals with sedation & analgesia
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74
Q

Management of male animals

A
  • Rams may be housed together for most of the year; bucks are penned separately
  • Ewes exhibit only a limited number of estrous cycles before becoming reproductively quiescent = critical that male can successfully breed & efficiently
  • Breeding bulls in dairy operations should be monitored for excessive weight gain, lameness due to laminitis (d/t energy dense diets); immunize for venereal diseases, campylobacteriosis, trichomoniasis
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75
Q

Tail docking in cattle

A
  • Relatively recent practice
  • Believed it will minimize bacterial contamination of the udder & therefore milk
  • Tails typically docked to ~10 inch length
  • Published research to date does NOT support tail docking in cattle to improve cow cleanliness or milk quality
  • Tail docking is common practice in sheep
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76
Q

Bruxism

A

Teeth grinding - associated with discomfort or pain

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77
Q

Ruminant behavior

A
  • All ruminants are social animals = every effort should be made to allow contact among individuals in terms of either direct contact, sound, smell, or sight
  • Cattle & sheep can hear at higher frequencies than humans and may react to sounds not perceived by handlers
  • Movement of animals is simplified by proper facility design; ruminants have wide-angle visual field; movement often disrupted by contrasts such as light and shadows
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78
Q

Ruminant flight zone

A
  • Minimum zone of comfort - will scatter when flight zone is penetrated
  • Minimal flight distance can be modified by increasing handling of the animals & by working at the edge of the flight zone
  • Always consider minimal flight distances when working with animals in chutes, pens, or other confined areas
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79
Q

Unique goat behaviors

A
  • Browsers & orally investigative
  • Inquisitive, restless, agile jumpers & climbers, mischievous
  • Strong, high fences are essential
  • Need adequate space for exercise, or boulders & rock piles for hoof maintenance and climbing
  • Goats more tolerant of isolation than sheep & cattle, but goats are still social
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80
Q

Unique cattle behaviors

A
  • Known for non-nutritive suckling, bar licking, tongue rolling
  • Non-nutritive suckling greater in hungry calves & also immediately after milk meal = provide nipples & other clean noninjurious materials for animals to suck
  • Non-nutritive suckling can transmit diseases - esp mastitis; hairball formation; behavior diminishes as animals weaned onto solid food
  • Play activity and vocalization of calves mimic adult dominance behaviors; play more common in males, can be rough, often triggered by a change in environment
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81
Q

Social hierarchies in cattle

A
  • Determined by dominance behavior, presence of horns, increasing age and body size
  • Aggression most common among intact adult males
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82
Q

Food Animal Residue Avoidance Databank (FARAD)

A
  • A food safety project of the USDA
  • Information resource to prevent drug and pesticide residues in food animals and animal products
  • Approved & off-label drug uses in ruminants, incl withholding times prior to slaughter, formularies, related information
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83
Q

Animal Medicinal Drug Use Clarification Act of 1994 (AMDUCA)

A

-Defines Extra-label drug use as: “Actual use or intended use of a drug in an animal in a manner that is not in accordance with the approved labeling. This includes, but is not limited to, use in species
not listed in the labeling, use for indications (diseases
and other conditions) not listed in the labeling, use
at dosage levels, frequencies, or routes of administration other than those stated in the labeling, and deviation from labeled withdrawal time based on these different uses”
-FDA under the provisions of AMDUCA recognizes the professional judgment of veterinarians and allows use of extra-label drugs by veterinarians within the context of a valid veterinarian-client relationship
-Extra-label use limited to circumstances when health of an animal is threatened or suffering or death may result from failure to treat
-FDA can prohibit extra-label use of a new animal drug if no sufficient analytical method exists for detection of residues and/or if drug poses a risk to human health

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84
Q

Extra-label drug use conditions

A

i. There is no approved new animal drug that is
labeled for the intended use that contains the
same active ingredient in the required dosage
form and concentration.
ii. A veterinarian has made a careful diagnosis and
evaluation of the condition.
iii. The veterinarian has established an extended
withdrawal period prior to marketing.
iv. The identity of the treated animal is assured and
maintained.
v. Ensure that no illegal drug residues occur in any
food-producing animal subjected to extra-label
treatment.
vi. The prescribed or dispensed extra-label drug must
bear labeling information which is adequate to
assure the safe and proper use of the product.

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85
Q

Extra-label use is PROHIBITED for which drugs?

A
  1. Chloramphenicol;
  2. Clenbuterol;
  3. Diethylstilbestrol (DES);
  4. Dimetridazole;
  5. Ipronidazole;
  6. Other nitroimidazoles;
  7. Furazolidone;
  8. Nitrofurazone;
  9. Sulfonamide drugs in lactating dairy cattle
    (except approved use of sulfadimethoxine,
    sulfabromomethazine, and sulfaethoxypyridazine);
  10. Fluoroquinolones;
  11. Glycopeptides;
  12. Phenylbutazone in female dairy cattle 20 months of
    age or older;
  13. Cephalosporin (excluding cephapirin) use in cattle,
    swine, chickens, and turkeys:
    Using cephalosporin drugs at unapproved
    dose levels, frequencies, durations, or routes of
    administration is prohibited;
    Using cephalosporin drugs in cattle, swine,
    chickens, or turkeys that are not approved for
    use in that species (e.g., cephalosporin drugs
    intended for humans or companion animals);
    Using cephalosporin drugs for disease
    prevention.
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86
Q

Which classes of drugs are PROHIBITED for extra-label drug use in chickens, turkeys, and ducks (because they are approved for treating or preventing influenza A in humans)?

A
  1. Adamantanes;

2. Neuraminidase inhibitors

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87
Q

Actinobacillosis (‘wooden tongue’)

A
  • Actinobacllius lignieresii: aerobic, nonmotile, nonspore forming, G(-) coccobacilli
  • Widespread in soil & manure & normal flora of respiratory and upper GI tract of ruminants
  • In sheep & cattle, causes sporadic, noncontagious, potentially chronic disease with diffuse abscess and granuloma formation in tissues of head and occasionally other body organs
  • NOT DOCUMENT IN GOATS
  • Clin signs: skin lesions - abscesses of tongue (cattle), lip lesions (sheep); soft tissue or LN swelling; draining tracts; swollen tongue protruding from mouth - difficulty prehending food, anorexia, excessive salivation
  • Transmission: organism penetrates wounds of the skin, mouth, nose, GI tract, testicles, mammary gland; rough feed material and FBs may play role in causing abrasions
  • Necropsy: purulent discharges of white-green exudate containing small white-gray granules drain from tracts
  • DDx: Contagious ecthyma, caseous lymphadenitis and Actinomyces bovis (lumpy jaw) are the primary differentials, but rabies should also be considered
  • Dx: cytology of discharge smears, biopsy
  • Tx: IV sodium iodide; oral potassium iodide; clinical response within 48 hr of IV treatment starting; systemic ceftiofur, ampicillin, or florfenicol; surgical debridement & flush with iodine
  • Prevent: Avoid poor quality, coarse feed; isolate or dispose of animals with disease
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88
Q

Actinomycosis (‘lumpy jaw’)

A
  • Actinomyces bovis - anaerobic, nonmotile, nonspore forming G(+), nonacid fast pleomorphic rods to coccobacilli; RARE IN SHEEP & GOATS
  • Clin signs: chronic, progressive, pyogranulomatous osteomyelitis of the mandible, maxillae, or other bony tissues of head; slow growing, firm, nonpainful mass on mandible - ulceration with or without draining tracts; loose teeth, painful eating, weight loss
  • Transmission: normal flora of GI tract & gain entrance through abrasions or penetrating wounds from wire or coarse hair or sticks
  • ZOONOTIC - granulomas, abscesses, skin lesions, bronchopneumonia in humans
  • Necropsy: draining lesions with sulfur-like granules (as with Actinobacillosis)
  • Ddx: Actinobacillus lignieresii and caseous lymphadenitis; tumors, trauma, dental disease, FB
  • Prevention: avoid feeds with coarse or sharp ingredients
  • Tx: IV sodium iodide - repeat several times at 7-10 day intervals; concurrent abx tx may be used- penicillin or oxytetracycline
  • Prognosis is poor if there is bone involvement; surgical excision is an option
89
Q

Trueperella associated with omphalophlebitis (Navel Ill)

A
  • Trueperella pyogenes, frequently combined with E. coli, most common organism causing omphalophlebitis
  • Clin signs: within first 3 months of age; painful enlargement of umbilicus; depression, anorexia, purulent discharge at umbilicus; if urachus involved, cystitis with dysuria, hematurial
  • Severe sequelae incl septicemia, peritonitis, septic arthritis (‘joint ill’), meningitis, patent urachus, urachal abscesses, umbilical hernias, osteomyelitis, endocarditis
  • Dx: culture & organism identification
  • Tx: debridement, drainage, antimicrobials; address any husbandry deficiencies (poor hygiene); NAVAL DIPPING
  • Research complications: omphalophlebitis is a potential source for recurrent septicemia
90
Q

Anthrax

A
  • Bacillus anthracis - ZOONOTIC, nonmotils, capsulted, spore-forming, aerobic, G(+) bacillus
  • Found in alkaline soil, contaminated feeds, water
  • Common names = woolsorter’s dosease, splenic fever, charbon, milzbrand
  • REPORTABLE
  • Clin signs: septicemia, hyperthermia, anorexia, depression, listlessness, tremors; incubation period is generally 3-7 days & ranges from peracute to chronic; hematuria, diarrhea; usually fatal within 1-3 days; death d/t shock, renal failure, anoxia
  • Peracute form = most common in cattle & sheep = sudden onset of staggering, dyspnea, trembling, collapse, convulsions leading to death
  • Dx: clinical signs alone; bacterial culture, PCR, fluorescent antibody stains; stained blood smears; Western blot, ELISA
  • Transmission: assoc. w/ drought, flooding, other types of soil disturbance; central & western US; spores remain infective in soil for many years ; anthrax organisms ingested, sporulate, replicate in local tissues
  • Cattle & sheep affected more commonly than goats d/t grazing habits
  • Necropsy: do NOT open animal as spores can contaminate environment; incomplete rigor mortis, rapid putrefaction, dark uncoagulated blood from body orifices; splenomegaly, cyanosis, lymphadenopathy, epicardial & SC hemorrhage
  • Ddx: bloat, enterotoxemia, malignant edema, blackleg, black disease
  • Control: VACCINATION available: Sterne-strain spore vaccine (virulent, nonencapsulated); vaccinate personnel working with animals
  • Tx: in early stages - penicillin & vaccination 7-10 days after conclusion of antibiotic therapy
  • Research complications: risk to personnel; B. anthracis is a select agent
91
Q

Brucellosis

A
  • Brucella abortus (B. melitensis biovar Abortus) & B. melitensis: nonmotile, nonspore forming, nonencapsulated G(-) coccobacilli
  • B. melitensis (biovar 1, 2, or 3) is the primary cause of the disease in sheep but DOES NOT OCCUR IN US
  • B. abortus is the primary cause in cattle
  • ZOONOTIC
  • B. ovis causes pyogranulomatous epididymitis and orchitis but is NOT zoonotic
  • Unlikely to encounter in the research setting
92
Q

Campylobacteriosis (vibriosis): Campylobacter fetus subsp. intestinalis; C. jejuni

A
  • C. fetus subsp, intestinalis: pleomorphic curved to coccoid, motile, nonspore forming, G(-) bacterium
  • Most important cause of ovine abortion in the US
  • Clin signs: abortion, stillbirths, weak lambs; organism inhabits the intestines and gallbladder in subclinical carriers; abortion in LAST TRIMESTER & abortion storms may occur in more susceptible animals (maiden ewes)
  • Dx: microscopic identification or isolation of organism from placenta, fetal abomasal contents, maternal vaginal discharges; GIEMSA or ZIEHL-NEELSEN stains
  • Transmission: occurs worldwide; normally inhabit ovine GI tract & shed in feces; in abortion storms considerable environmental contamination will occur; ewes may have active Campylobacter organisms in uterine discharges for several months after abortion
  • Necropsy: edematous aborted fetuses with accumulation of serosanguinous fluids within the SC and muscle tissue fascia, liver may have pale foci; placental tissues thickened and edematous & will contain serous fluids similar to fetus; placental cotyledons may appear gray
  • Ddx: Toxoplasma gondii, Chlamydophila abortus, and Listeria monocytogenes should be considered in late gestation ovine abortions
  • Control: bacterin available to prevent disease; carrier states can be cleared by treating with penicillin & oral chlortetracycline combo; immediately isolate aborting ewes; after an outbreak, ewes will develop immunity lasting 2 or 3 yrs
  • Tx: isolated infected animals & provide supportive therapy; prompt decontamination of area & disposal of aborted tissues
  • Research complications: losses from abortion may be considerable; ZOONOTIC (C. fetus spp. intestinalis may cause ‘shepherd’s scours’)
93
Q

Campylobacteriosis (Bovine Vibriosis) - Campylobacter fetus subsp. venerealis

A
  • Main cause of bovine Campylobacter abortions; does not cause disease in other ruminants
  • Clin signs: high % of cows returning to estrus after breeding & temporary infertility - virgin heifers return to estrus by day 40 after breeding; spontaneous abortions during months 5-8 of gestation - aborted fetus may be fresh or severely autolyzed; severe endometritis may lead to salpingitis and permanent infertility
  • Dx: Curved rod organism with corkscrew motility; identify by darkfield examination of abomasal contents or culture of placenta or abomasal contents; fluorescent antibody test on genital discharge from the bull or cow; PCR of semen
  • Transmission: obligate, ubiquitous organism in the genital tract; transmitted from infected bulls to heifers; bulls are carriers with no signs of disease; older cows develop effective immunity
  • Necropsy: necrotizing placentitis with hemorrhagic cotyledons, dehydration, fibrinous serositis; bronchopneumonia & hepatitis on histo
  • Ddx: trichomoniasis, brucellosis, mycoplasmosis, infectious bovine rhinotracheitis–pustular vulvovaginitis (IBR– IPV), bovine viral diarrhea (BVD), and leptospirosis
  • Control: killed bacterin vaccine, annual boosters should be given; AI to control transmission
  • Tx: cows will usually recover; intrauterine infusion with penicillin improves chance of returning to breeding condition
94
Q

Caprine staphylococcal dermatitis

A
  • Staphylococcus intermedius or S. aureus - cocci; ubiquitous skin commensals of humans and animals
  • Most common caprine bacterial skin infection
  • Clin signs: small pustular lesions around the teats and perineum; occasionally, infection on flanks, underbelly, axilla, inner thigh, neck
  • Dx: lesions & culture
  • Ddx: contagious ecthyma, fungal skin infections
  • Tx: antibiotics based on C&S; cleaning of lesions with an iodophor shampoo & spraying with an antibiotic and an astringent
95
Q

Clostridium perfringens, Type C (Enterotoxemia & Struck)

A
  • C. perfringens - anaerobic, G(+), nonmotile, sporeforming; lives in soil, contaminated feed, GI tracts of ruminants
  • Toxins produced include: alpha (hemolytic), beta (necrotizing), delta (cytotoxic & hemolytic), epsilon, iota
  • Types of C. perfringens are A, B,C, D, and E
  • Infection is common in goats, sheep, and cattle
  • Clin signs: Lethal beta toxin assoc w/ overgrowth of this bacterium results in hemorrhagic enterocolitis within first 72 hr of well-fed young ruminant’s life - found dead; anemic, dehydrated, anorexic, depressed, may display tremors or convulsions, abdominal pain; calves have acute diarrhea, dysentery, abdominal pain, convulsion, opisthotonos with death in a few hours; feces loose gray-brown to dark red and malodorous
  • Similar NONCONTAGIOUS acutely fatal enterotoxemia in yearling & adult sheep = ‘struck’ - also caused by beta toxin of C. perfringens type C; assoc w/ rapid dietary changes or shearing stress; found dead or uneasiness, depression, convulsions
  • Dx: necropsy findings; detection of beta toxin in intestinal contents
  • Transmission: ubiquitous in GI tract, environment, contaminated feeds; ingestion
  • Necropsy: milk-filled abomasum & hemorrhage in distal small and large intestinses - affected portion of intestine may be deep blue to purple in color & resemble mesenteric torsion; petechial hemorrhages of serosal surfaces of organs incl thymus, heart, GI tract; hydropericardium, hydroperitoneum, hemorrhagic mesenteric LNs; pulmonary and brain edema
  • Ddx: other Clostridial diseases such as blackleg, black disease; coccidiosis; salmonellosis; anthrax; acute poisoning
  • Control: commercial toxoid available - administer to pregnant animals during last 3rd of pregnancy; initial vaccination of young animals consists of 2 vaccinations, 1 month apart, then annually
  • Tx: difficult & usually unsuccessful; antitoxin may be useful in mild cases; antiserum may be administered immediately after birth during an outbreak
96
Q

Clostridium perfringens, Type D (pulpy kidney disease)

A
  • C. perfringens type D - releases epsilon toxin that is proteolytically activated by trypsin
  • Associated with sheep, less important in goats and cattle
  • Clin signs: peracute condition in younger animals with sudden death, preceded by neuro signs (incoordination, opisthotonus, convulsions) - death in 1-2 hrs; largest, fastest growing animals generally predisposed
  • Necropsy: extremely necrotic, soft kidneys; focal encephalomalacia, petechial hemorrhages on serosal surfaces of brain, diaphragm, GI tract, heart
  • Ddx: Tetanus, enterotoxigenic E. coli, botulism, polioencephalomalacia, grain overload, and listeriosis
  • Control: vaccination prevents disease; maternal antibodies last ~5 weeks = vaccinate young animals at about 5 weeks old; feeding regimens & feeding of concentrates to adults should be evaluated carefully
  • Tx: supportive care, antitoxin administration, oral antibiotics, diet adjustment
97
Q

Clostridium tetani (tetanus, lockjaw)

A
  • C. tetani - strictly anaerobic, motile, spore forming, G(+) rod; persists in soil, manure, and within GI tract
  • Tetanus toxemia caused by a specific neurotoxin produced by C. tetani in necrotic tissue
  • Introduced into tissue through wounds; uterus most common sire of infection in post parturient dairy cattle with retained placentas; can be assoc with banding castrations
  • Clin signs: spoardic, acute, fatal neuropathy; incubation period of 4 days-3 weeks, then animals exhibits bloat, muscular spasticity, prolapse of 3rd eyelid, rigidity, extension of the limbs leading to a stiff gait, inability to chew, hyperthermia; retracted lips, drooling, hypersensitivity to external stimuli, ‘saw-horse’ stance, convulsions; death occurs within 3-10 days & mortality nearly 100% from respiratory failure
  • Dx: clinical signs
  • Transmission: soil contaminant & often part of gut microbiome of herbivores; organism sporulates & persists in environment; may see following castration, tail docking, ear tagging, dehorning
  • Ddx: bloat, rabies, hypomagnesmic tetany, polioencephalomalacia, white muscle disease, enterotoxemia in lambs, lead poisoning
  • Necropsy: nonspecific findings except for inflammatory reaction associated with the wound
  • Tx: clean & aggressively debride the infected wound; tetanus antitoxin; vaccination with tetanus toxoid, administration of antibiotics parenterally & flushed into cleaned wound; keep animals in dark quiet environment; sedative, traquilizer, muscle relaxant; supportive fluids and glucose
  • Control: good sanitation, aseptic surgical procedures, vaccination programs; vaccinate animals 2-3 times during first year of life; does and ewes should receive booster within 2 months of parturition to ensure colostral antibodies
  • Research complications: unprotected, younger ruminants may be affected following routine flock or herd management procedures
98
Q

Clostridium novyi (bighead, black disease, bacillary hemogloinuria [red water]); Clostridium chauvoei (blackleg)

A
  • C. novyi - anaerobic, motile, spore-forming (G+) bacteria = bighead & black disease
  • C. novyi Type D (C. hemolyticum) = bacillary hemoglobinuria)
  • C. chauvoei = blackleg
  • Clin signs: bighead = dz of rams with nongaseous, nonhemorrhagic edema of the head and neck, may migrate to ventral regions such as throat, swelling of eyelids, nostrils, most animals die within 48-72 hr; black disease/necrotic hepatitis = peracute fatal disease in cattle and sheep, 2-4 yr old animals, hyperthermia, tachypnea, inability to keep up with other animals, recumbency; bacillary hemoglobinuria = acute disease in cattle with fever, anorexia, hemoglobinemia, hemoglobinuria; blackleg = necrosis & emphysema odf muscle masses (clostridial myositis), serohemorrhagic fluid accumulation around infected area, edema, more common in cattle, animals die regardless of treatment, muscles of faces, neck, perineum, thigh, back
  • Transmission: Bighead- fight wounds assoc with horn injuries on head; C. novyi Type D endemic in western US; C. chauvoei spores remain viable in soil for years - outbreaks seen with excavation or flooding, suspected organisms is ingested & travels via blood stream from GI tract to muscles; Black disease & bacillary hemoglobinuria often assoc w/ Fasciola liver disease - ingested spores develop in hepatic tissue damaged and anoxic from fluke migrations
  • Necropsy: dx of black disease usually based on post mortem lesions - SC vessels engorged with blood so dried skin has a dark appearance; carcasses putrefy quickly; hepatomegaly and endocardial hemorrhage common; hepatic damage from flukes may make dx difficult
  • DDx: Differentials include other clostridial diseases; hemolytic diseases such as babesiosis, leptospirosis, and hemobartonellosis; and photosensitization
  • Tx: For C. chauvoei & bighead = early aggressive tx with aggressive wound debridement, oxygenation, penicillin or tetracycline; treatment for black disease is not rewarding; bacillary hemoglobinuria - early tx with penicillin or tetracycline in high doses along with blood transfusion and fluids may be helpful
  • Control: vaccination with multivalent clostridial vaccines; control of fascioliasis
99
Q

Clostridium septicum (malignant edema)

A
  • Malignant edema usually caused by Clostridium septicum, but may be mixed infx with other clostridial species such as C. chauvoei, C. novyi, C. sordelli, and C. perfringens
  • Clin signs: acute & often fatal; affected area warm with gaseous accumulations & crepitation of SC tissue; overlying skin blue in color (gangrene); regional lymphadenopathy and fever, anorexia, severe depression, hyperthermia, pitting edema; death within 12 hr to 2 days
  • Transmission: ubiquitous in environment worldwide, in intestinal contents of animals, may survive in soil for years; recent wounds containing devitalized tissue are a risk factor = castration, docking, ear notching, shearing, dystocia
  • Necropsy: tissue necrosis, hemorrhagic serous fluid accumulations; spreading, crepitant lesions around wounds; gas & serosanguinous fluids with foul odors
  • Tx: large doses of penicillin, antiinflammatories, fenestration of wound; affected tissues usually slough
  • Control: aseptic technique; sanitation of environment; multivalent clostridial vaccine
100
Q

Colibacillosis

A
  • Escherichia coli = motile, aerobic, G(-) nonsporeforming coccobacillus found in environment & GI tracts of ruminants
  • 3 surface antigenic complexes: O -somatic, K -envelope, H -flagellar; used to classify serotypes
  • Clin signs: gastroenteritis and/or septicemia; Enteric colibacillosis generally develops within first 72 hr of life when newborn animals exposed to organisms; semifluid yellow to gray diarrhea with occasional blood streaking; listlessness, loss of suckling interest, abdominal pain (arched back & extension of tail), hyperthermia is rare, severe acidosis, depression, recumbency, lack of response to external stimuli - this form of disease is very acute with clinical course of 3-8 hr
  • Septicemic form affects nervous system with incoordination, head pressing, circling, appearance of blindness, opisthotonos, depression, death follow d/t endotoxemic shock; occasionally, swollen painful joints observed with septicemic form; cystitis & pyelonephritis - dysuria, pollakiuria, gross hematuria, pyuria; pyelonephritis in cows = acute depression, fever, ruminal stasis, anorexia
  • Transmission: primarily fecal-oral or through umbilicus; overcrowing, poor sanitation, failure of passive transfer are risk factors; secretory diarrhea with loss of water and electrolytes - if bacteria infiltrate the intestinal barrier, septicemic for results
  • Immunoglobulin-deficient calves far more susceptible to both enteritis and septicemia
  • Dx: clinical signs; deficiency of circulating IgG, ELISA, latex agglutination tests
  • Necropsy: swollen, yellow to gray fluid filled small and large intestines, swollen and hemorrhagic mesenteric LNs, generalized tissue dehydration; septicemic animals may have serofibrinous fluid in peritoneal, thoracic, pericardial cavities, enlarged joints containing fibrinopurulent exudates, congested & inflamed meninges
  • Ddx: enterotoxemias caused by C. perfringens A, B, or C; Campylobacter jejuni; Coccidia spp., rotavirus, coronavirus, Salmonella, Streptococcus spp., Pasteurella spp., and Cryptosporidia
  • Control: colostrum delivery, prevention of overcrowding, frequent sanitization of maternity area
  • Tx: antibiotics with efficacy against G(-): trimthoprim/sulfadiazine, enrofloxacin, cephalothin, ceftiofur - oral antibiotics NOT recommended; fluid support with dextrose & electrolytes incl bicarbonate for metabolic acidosis, NSAIDs for pain; vaccines given to dam prior to calving to boost colostral immunity
101
Q

Corynebacterium pseudotuberculosis (caseous lympadenitis)

A
  • Corynebacterium pseudotuberculosis: nonmotile, nonspore forming aerobic, short and curved, G(+) coccobacilli; caseous lymphadenitis (CLA) is very common in sheep & goats - any presentation of abscessing & draining LNs should be presumed to be CLA until proven otherwise; occurs occasionally in cattle
  • Clin signs: abscessation of superficial AND deep LNs; drain caseous, yellow-green-tan secreation; over time animal may become exercise intolerant, anorextic, debilitated; fever, increased resp rate, pneumonia
  • Dx: clinical lesions; culture or Gram stain of lymph node aspirates; ELISA serology
  • Transmission: organism can survive for 6 months of more in environment - enters via skin wounds such as shearing, castration, docking; ingestion & aerosolization also possible
  • Necropsy: disseminated superficial abscesses & lesions of mediastinal and mesenteric LNs; cut surfaces of affected LNs may appear lamellated; lungs, liver, spleen, kidneys may also be affect; cranioventral lung consolidation with hemorrhage, fibrin, edema
  • Ddx: pathogens causing lymphadenopathy and abscessation as well as injection site reactions from clostridial vaccines
  • Tx: surgical lancing and flush with iodine and/or hydrogen peroxide solutions, or remove abscess entirely; animals with draining and lanced lesions should be isolated until healed; commercial vaccines available; ANTIBIOTICS USUALLY NOT HELPFUL
  • Control: proper sanitation; segregation of affected animals; precautions to prevent injuries
  • Research complications: risk for animals undergoing routine management procedures, or invasive research procedures, due to persistence in environment, long incubation period, poor response to antibiotics
102
Q

Corynebacterium renale, C. cystitidis, and C. pilosum (Pyelonephritis, Posthitis, and Ulcerative Vulvovaginitis)

A
  • Sometimes call the ‘C. renale’ group - piliated, nonmotile G(+) rods; distinguished biochemically
  • C. renale: pyelonephritis in cattle
  • C. pilosum & C. cystitis: posthitis (pizzle rot or sheath rot) in sheep and goats
  • Bacteria ubiquitous in environment & inhabit vagina and prepuce; high protein diets, results in higher urea excretion, more basic urine, and irritation of the preputial and vaginal mucous membranes are contributing factors
  • Clin signs: acute pyelonephritis = fever, anorexia, polyuria, hematuria, pyuria, arched-back posture, weight loss, loss of production; chronic pyelonephritis = diarrhea, poluria, polydipsia, stranguria, anemia; posthitis & vulvovaginitis = ulcers, crusting, swelling, pain, distinct malodor; necrosis & scarring may be sequelae to more sever infections, fly strike may be a complication
  • Dx: clinical signs
  • Transmission: vaginitis & posthitis contribute to venereal transmission; ascending UTI; indirect transmission is possible because organisms present on wool or scabs shed from affected animals; posthitis occurs in intact AND castrated sheep and goats
  • Necropsy: pyelonephritis, multifocal kidney abscessation, dilated and thickened ureters, cystitis, purulent exudate
  • Ddx: urolithiasus, contagious echthyma although these lesions more likely to be around mouth
  • Prevention: reconsider feeding practices; clip long wool and hair; isolate affected animals
  • Tx: long term (3 weeks) penicillin or trimethoprim-suladioxine; reduce dietary protein, clip & clean skin lesions, treat & prevent fly strike, topical antibacterial treatments for posthitis/vulvovaginitis, systemic tx if severe
103
Q

Dermatophilosis (Cutaneous Streptothricosis, Lumpy Wool, Strawberry Footrot)

A
  • Dermatophilus congolensis - G(+), nonacid-fast, facultative anaerobic actinomycete; chronic bacterial skin disease with crustiness and exudates accumulating at the base of the hair or wool fibers
  • Natural habitat of organism is unknown, but has been isolated from soil
  • Clin signs: Animals are painful but NOT PRURITIC
  • 2 forms in sheep: Mycotic dermatitis (lumpy wool) - crusts & wool matting with exudates over back and sides of adults & face of lambs & Strawberry footrot - crusts and inflammation between the carpi and/or tarsi and the coronary bands, lameness
  • Goats and cattle: cutaneous streptothicosis = crusty suppurative dermatitis; in cattle is distributed over head, dorsal surfaces of neck and body; in young goats along tips of ears and under the tail
  • Most affected animals recover within 3-4 weeks and lesions have little effect on overall health; cattle with lesions over 50% of their bodies likely to become seriously ill
  • ZOONOTIC - rare human infections reported
  • Dx: clinical signs, stained skin scrapings & crusts, serology, culture, biopsy
  • Transmission: occurs worldwide, believed to be a saprophyte; direct contact with infected animals, contaminated environments, biting insects; prolonged wetness, high humidity, high temps, ectoparasites are risk factors
  • Necropsy: death unusual so necropsy rare
  • Control: Potash alum & aluminum sulfate have been used as wool dusts; minimize moist conditions; control external parasites; lesions will resolve during dry periods
  • Tx: penicillin or oxytetracycline (organism susceptible to wide range of abx); topical application of lime sulfur; control ectoparasites and biting glies; povidone iodine shampoos & chlorhexidine solutions
  • Research complications: ZOONOTIC; research personnel must be trained
104
Q

Dichelobacter (Bacteroides) nodosus and Fusobacterium necrophorum (Virulent Foot Rot;
Contagious Foot Rot of Sheep and Goats; Footscald)

A
  • Work synergistically to cause contagious foot rot in sheep and goats; both are nonmotile, nonspore forming anaerobic G(-) bacilli
  • Foot rot is contagious, acute or chronic dermatitis involving the hoof and underlying tissues
  • Leading cause of lameness in sheep
  • Footscaled is caused by Dichelobacter nodosus alone
  • Clin signs: lameness; severely affected animals show weight loss, decreased productivity, anorexia; interdigital skin and hoovers moist with necrotic odor; signs of milder disease, footscald include mild lameness, redness & swelling, little to no odor
  • Dx: smears and cultures
  • Tranmission: F. necrophorum ubiquitous in soil and manure, GI tract, and skin and hooves of domestic animals; Dichelobacter is obligate pathogen of ovine foot & rarely remains in environment for over 2 weeks; some animals chronic carriers; overcrowded warm and moist environments key to transmission
  • Ddx: Foot abscesses, selenium/vitamin E deficiencies, strawberry footrot, bluetongue virus infection (manifested with myopathy and coronitis), and trauma
  • Tx: manually trim necrotic ebris from hooves, apply topical antibiotics and foot wraps; systemic abx - penicillin, oxytetracycline, erythromycin; footbaths with 10% zinc or copper sulfate or 10% formalin (not legal in all states); separate affected animals from flock; vaccination
  • Control: quarantine incoming animals; vaccination; segregation of affected animals; regular hoof trimming; avoid muddy pens; cull animals with nonresponsive infection; D. nodosus bacterin available but cross protection between serotypes varies
  • CAUTION WITH COPPER SULFATE FOOTBATHS & SHEEP
105
Q

Fusobacterium necrophorum and Prevotella melaninogenic (Formerly Bacteroides melaninogenicus) (Footrot of Cattle, Interdigital
Necrobacillosis, Interdigital Phlegmon of Cattle, Foot
Abscesses of Sheep)

A
  • Interdigital necrobacillosis of cattle is caused by F. necrophorum & several other organisms; incidence has decreased as dairy cattle spend less time on pasture
  • F. necrophorum is assoc w/ foot abscesses or infection of the deeper structures of the foot in sheep and goats
  • Clin signs: affected foot hot, pockets of purulent material in heel or toe; mild to moderate lameness with sudden onset; hindlimbs more commonly affected; claws markedly separated with swelling in between; more severe cases may have anorexia, pyrexia, decreased milk production; lesions progress to fissures with necrosis until sloughing and healing occurs
  • Dx: odor and appearance, assessment of environmental and housing conditions; anaerobic culture
  • Transmission: cases may be sporadic or epizootics may occur; dairy cattle breeds more commonly affected
  • Ddx: hairy heel warts, laminitis, subsolar abscesses. Bluetongue virus
  • Control: keep pens and paddocks dry and well drained & free of material that may damage feet; footbaths; segregate affected animals; chronically affected animals or severely lame animals should be culled
  • Tx: cleaning feet, trimming necrotic tissue; parenteral abx - ceftiofur, oxytetracycline, procain penicillin; twice daily footbaths (10% zinc sulfate, 2.5% formalin, 5% copper sulfate); severe cases - bandaging may be needed; animals can recover without tx but will be lame for several weeks
  • Research complications: comparable to those of footrot in smaller ruminants
106
Q

Heel Warts (Bovine Digital Dermatitis, Papillomatous Digital Dermatitis [PDD], Hairy Foot Warts)

A
  • Highly contagious with morbidity of up to 90% of herd
  • Causative agent uncertain, may be more than one bacterium: Fusobacteria spp., Prevotella spp. (Bacteroides spp, Treponema), and Dichelobacter nodosus have been isolated from bovine heel lesions
  • Clin signs: lesions occur on haired digital skin, most lesion occur on the planter surface of the hind foot (near heel bulbs and/or extending into interdigital space); moist plaques being as red, granular areas - plaques enlarge, turn gray or black, and ‘hairs’ protrude from the roughened surface; lesions are very painful
  • Differentiate from foot rot = heel warts have NO SWELLING OR FEVER
  • Transmission: poorly drained loading areas, damp and dirty bedding areas, overcrowding are risk factors; interdigital lesions occur commonly in young stock and dairy facilities throughout world; introduction of new cattle into a herd not previously exposed can cause large outbreak; disease ONLY IN CATTLE
  • Ddx: foot rot, sole abscesses, laminitis, trauma
  • Control: biosecurity; sterilize equipment used for hoof trimming; clean trucks and trailers; footbaths with copper sulfate, zinc sulfate, formalin, antibiotics like tetracycline or lincomycin
  • Tx: debride or remove lesions; topical antibiotics and antiseptic regimens
  • Research complications: one of the major causes of lameness among heifers and dairy cattle
107
Q
Histophilus somni (Formerly Haemophilus somnus)
(Thromboembolic Meningoencephalitis [Teme])
A

-Histophilus somni - pleomorphic nonencapsulated, nonspore-forming, G(-) coccobacillus
-Diseases caused by this organism include thromboembolic meningoencephalitis, septicemia, arthritis, and reproductive failures due to genital tract infections in males and females
-Commensal of bovine mucous membranes; pathogenic & nonpathogenic strains found
-Nasal & urogenital secretions believed to be the source of organism & major contributor to bovine respiratory disease complex (BRDC); also assoc w/ resp dz in sheep and goats
-Clin signs: sudden death; marked dyspnea, depression, ataxia, falling, conscious proprioceptive deficits; head tilt from otitis interna-media, opisthotonus, convulsions if brainstem affected; high fever, extreme morbidity, death within 36 hr; in acute neurologic as well as chronic pneumonic infections, polyarthritis may develop; abortion, vulvovaginitis, endometritis, placentitis, infertility
-Dx: examination of tissues at necropsy; isolation of organism in CSF, brain, blood, urine, joint fluid, other internal organisms; paired serum samples recommended
-Transmission: considered part of normal flora; after inhalation, organism colonizes resp tract & gains access to bloodstream; venereal spread possible; stresses of travel and coinfection may be involved; transmission by respiratory and genital tract secretions; does not persist in environment
-Necropsy: PATHOGNOMONIC = multifocal red-brown foci of necrosis and inflammation on & within the brain and meninges; many thrombi with bacterial colonies seen on histo; ocular lesions - conjunctivitis, retinal hemorrhage, edema; resp tract lesions - bronchopneumonia, fibrinous pleuritis; focal myocardial lesion in the papillary muscle of left ventricle, fibrinous pericarditis, polyarthritis, fibrinous laryngitis; aborted fetuses, necrotizing placentitis
-Ddx: other pathogens associated with neurological
disease and respiratory disease such as M. hemolytica
and P. multocida. In smaller ruminants, C. pseudotuberculosis should be considered
-Control: susceptible to many antibiotics but use of antibiotics metaphylactically has not shown great success; late-stage polyarthritis resistant to abx; vaccination - killed whole-cell bacterins produce a humoral response; calves should be immunized prior to entering a confinement housing situation (feedlot) with 2nd vaccination upon arrival to feedlot
-Tx: rapid tx at first signs of neurologic disease important but effective treatment difficult d/t rapid disease course

108
Q

Leptospirosis

A

-Leptospira interrogans serovars pomona, icterohaemorrhagiae, grippotyphosa, interrogans,
and hardjo are recognized pathogens
-L. hardjo and L. pomona are the serovars most commonly diagnosed in cattle
-L. hardjo the major serovar in sheep
-Goats susceptible to several serovars
-Clin signs: acute and chronic infections more common in cattle than sheep & goats; cattle infections often subclinical; acute infection in calves can be severe with high fever, hemolytic anemia, hemoglobinuria, jaundice, pulmonary congestion, meningitis, death; lactating cows have severe drops in production; chronic infection in cows may cause abortion, retained placenta, weakened calves, or chronic carrier state, infertility; similar signs in sheep and goat but relatively uncommon, mortality above 50% in ewes and lambs
-Transmission: organism survives well in environment, esp moist, warm, stagnant water; wild animals are maintenance hosts but domestic livestock may also be reservoirs; organisms shed in urine, uterine discharge, milk; infection via ingestion of contaminated feed, water, placental fluids, through mucous membranes; chronically infected animals may shed organism in the urine for 60 days or longer
-Dx: identification of leptospires in fetal tissues - SILVER OR FLUORESCENT ANTIBODY STAINED sections of liver of kidney; dark-field or phase-contrast microscopy of fetal stomach contents; serology coupled with immunofluoresnce or PCR of urine
-Ddx: Because of the associated anemia, differential diagnoses should include copper toxicity and parasites in addition to other abortifacient diseases
-Control: polyvalent vaccines - immunity is serovar specific; serological titers tend to diminish rapidly (within 40-50 days in sheep) so frequent vaccination may be necessary
-Tx: antibiotics to treat ill animals and try to clear carrier state; vaccination and antibiotic therapy can be combined in an outbreak
-Research complications: ZOONOTIC - flu-like symptoms, meningitis, hepatorenal failure in humans

109
Q

Listeriosis (Circling disease, Silage disease)

A
  • Listeria monocytogenes - G(+), pleomorphic, motile, non-sporeforming, Beta-hemolytic coccobacillus; survives in soil, feeds, and other organic materials for long periods of time; found in fermented feedstuffs like spoiled silage
  • Saprophyte & psychrophile that prefers microaerophilic conditions
  • Clin signs: acute, sporadic, noncontagious disease assoc w/ neurologic signs, mastitis, abortions in 3rd trimester sheep & other ruminants
  • 3 Forms of Disease: Encephalitis, Placentitis with abortion, Septicemia with hepatitis and pneumonia; ENCEPHALITIC FORM MOST COMMON IN RUMINANTS
  • Transmission: ingestion of contaminated feed and water; can be shed by asymptomatic carriers, esp at end of pregnancy and at parturition
  • Dx: clin signs, culture (cold enrichment at 20 C improves success), impression smears of brain or reproductive tissue, tissue fluorescent antibody techniques
  • Necropsy: microabscesses of midbrain with G(+) bacilli are characteristic of encephalitis
  • Ddx: Rabies, bacterial meningitis, brain abscess, lead toxicity, PEM, and otitis media must be considered as differentials; in sheep, organisms causing abortion, pregnancy toxemia, and enterotoxemia due to C. perfringens Type D and in goats, CAE viral infection
  • Control: segregate & treat affected dams; proper storage of fermented feeds
  • Tx: early aggressive tx with penicillin or other antibiotics; fluid support, nursing care
  • Research complications: ZOONOTIC - mild to severe flu-like symptoms in humans, particular risk for pregnant women and older or immune compromised individuals; REPORTABLE
110
Q

Mastitis in sheep and goats

A
  • Sheep: Mannheimia hemolytica most common cause of acute mastitis
  • Goats: Staphylococcus epidermidis & other coagulase-negative Staphylococcus species are primary organisms
  • Dx: subclinical can be diagnosed by determining somatic cell count in milk, California Mastitis Test, culturing affected glands; indication of subclinical mastitis is thin, poorly growing offspring
  • Diffuse chronic mastitis (‘hardbag’) = d/t interstitial accumulations of lymphocytes in the udder, usually bilaterally; redness and swelling are absent; diffuse chronic mastitis may be caused by the retrovirus that causes ovine progressive pneumonia (OPP, Visna/maedi virus) in sheep & related CAE virus (CAEV) virus in goats
  • Tx: Acute: broad-spectrum abx - intramammary and systemic, supportive therapy; frequently milk out infected glands - oxytocin preceding milking will improve gland evacuation; Chronic Diffuse: currently no treatment
111
Q

Mastitis in bovines

A

-Most common bovine mastitis pathogens: Staphylococcus aureus, Streptococcus agalactiae,
Strep. spp., Corynebacterium bovis (summer mastitis of
heifers, dry cows, and beef breeds), coliform agents
(E. coli and Klebsiella pneumonia), and Mycoplasma spp. including M. bovis (California mastitis)
-Prevention/Control: many factors involved - teat and udder cleaning, pre- and post-milking dipping with disinfectants; milking equipment must be maintained to provide proper vacuum levels and pulsation rates; herd managements - vaccination programs, nutrition, isolation of incoming animals; testing newly freshened cows & periodic bulk tank sampling; at time of dry off, all cows should be treated with intramammary antibiotics - this will clear some chronic infections; milk younger disease free animals first; facility sanitation & insect control

112
Q

Moraxella bovis (Infectious Bovine Keratoconjunctivitis [IBK] or ‘Pinkeye’ in Cattle)

A
  • Moraxella bovis - G(-) coccobacillus; ONLY CATTLE
  • Clin signs: acute onset & rapid course with initial lacrimation, photophobia, blepharospasm - then conjunctival injection and chemosis within a day - then keratitis with corneal edema & ulcers; anterior uveitis may occur within a few days with a thicker mucopurulent ocular discharge; corneal vascularization begins 10 days after onset; re-epithelialization or cornea occurs by 2-3 week after onset; most ulcers will heal without loss of vision, but corneal rupture & blindness can occur
  • Dx: clin signs, culture, fluorescein stain
  • Transmission: more severe in younger cattle; bacteria shed in nasal secretions & cattle may be subclinical carriers - transmission is by fomites, flies, aerosols, direct contact; other factors contributing include UV light & trauma from dust or plant material; incidence higher in warmer weather
  • Ddx: foreign bodies, parasites, infectious bovine rhinotracheitis virus - conjunctivitis but NOT corneal ulcer
  • Control: vaccination, control insects, mow high pasture grass to minimize ocular trauma, control dust & other sources of mechanical trauma, segregate animals by age
  • Tx: cattle can recover without treatment, but younger animals should be treated - antibiotics 9topical & subconjunctival), third-eyelid flaps, temporary tarsorrhapy, eye patches
  • Research complications: carrier status of some animals, severity of disease in younger animals, treatment & labor costs; permanent visual impairment or loss and ocular disfigurement may occur
113
Q

Mycobacterium bovis (Tuberculosis)

A
  • Mycobacteria - aerobic, nonmotile, non-sporeforming, acidfast pleomorphic bacilli
  • Sheep & cattle: most cases are M. bovis
  • Goats: may be M. bovis, M. avum, M. tuberculosis
  • Clin signs: sporadic, chronic, granulomatous, contagious disease; primary sites of infx are resp system (M. bovis) & digestive system (M. avium); other tissues includ mammary & reproductive tract may be involved; resp signs: dyspnea, coughing, pneumonia; digestive signs: diarrhea, bloat, constipation
  • Dx: intradermal tuberculin test using purified protein derivatives (PPD); confirmation of diagnosis by culture or PCR
  • Transmission: M. bovis survives for months in environment, esp in cattle feces; infected from environment or from other animals via aerosols, contaminated feed and water, secretions incl milk, semen, genital discharges, urine, feces; subclinically infected animals serve as carriers
  • Necropsy: yellow primary tubercles (granulmoas) with central areas of caseous necrosis; touch impressions of lesions have acid-fast bacteria (AFB); caseous nodules assoc w/ GI organs, mesenteric LNs
  • Control: Main reservoirs of infection are humans and cattle; REPORTABLE; consult state animal health officials regarding disposal of materials & cleaning of premises following depopulation of positive animals
  • Tx: usually not allowed d/t ZOONOTIC potential, chronicity of disease, tx costs
  • Research complications: ZOONOTIC
114
Q

Paratuberculosis (M. AVIUM SUBSPECIES PARATUBERCULOSIS; JOHNE’S DISEASE)

A

-Mycobacterium avium subsp. paratuberculosis: fastidious, non-sporeforming, acid-fast, G(+) rod
-Clin signs: chronic, contagious, granulomatous disease of adult ruminants; unthriftiness, weight loss, intermittent diarrhea; long incubation period - infected cattle can appear healthy for months to years; decreased mild production; sheep & goats - chronic wasting with occasional pasty feces, diarrhea only in advanced disease
-Dx: detect organisms in feces or tissue by culture of PCR; evidence of cellular immune respone to infection by skin or interferon-gamma testing, and detection of antibody to M. paratuberculosis by ELISA or AGID; Gold Standard = post mortem culture & histopath on multiple tissues; ELISA tests most sensitive and specific ante mortem
-Transmission: prevalent in environment; to young animals via ingestion of mild or direct or indirect contact; cattle exposed as adults less likely to become infected; fecal shedding occurs BEFORE clin signs = ‘silent’ stage of infection
-Necropsy: ileum grossly thicnened in CATTLE (not sheep or goats); ileal and ileocecal LNs are best samples for histology and acid fast staining
-Ddx: Other diseases causing chronic wasting and poor body condition include chronic salmonellosis, severe parasitism, lentiviruses in
small ruminants, and pyelonephritis
-Tx: not worthwhile
-Control: prevention most effective; test and slaughter; remove calves from dam immediately & feed pasteurized colostrum & raise separately from adults until 1 year of age; prolonged survival in soil & in wildlife reservoirs (hares)
-Being investigated as a factor in the development of Crohn’s disease in humans, but currently no evidence of zoonotic potential

115
Q
Navel Ill (Omphalitis, Omphalophlebitis,
Omphaloarteritis, Joint Ill)
A
  • Most commonly caused by Trueperella pyogenes; also Arcanobacterium (anaerobic, nonmotile, non-sporeforming, G(+) pleomorphic rods to coccobacilli), E. coli, Enterococcus spp, Proteus, Streptococcus spp, Staphylococcus spp
  • Clin signs: navel ill is an acute localized inflammation and infection of the external umbilicus; depression, anorexia, purulent discharge; involvement of urachus may lead to cystitis w/ dysuria, stranguria, hematuria; other common sequelae include septicemia, pneumonia, peritonitis, septic arthritis (joint ill), patent urachus, urachal abscesses, umbilical hernias, meningitis, osetomyelitis, uveitis, endocarditis, diarrhea
  • Transmission: occurs within first 3 months of cage most commonly; cleanliness of birthing & housing environment & successful passive transfer important
  • Dx: clin signs; always consider in ruminants in first week of life with fever of unknown origin & for slightly older lambs, kids, or calves that are not thriving
  • Ddx: Umbilical hernia - this should not be painful & should be reducable
  • Tx: 10-14 days of broad spectrum abx: ampicillin, ceftiofur, florfenicol, erythromycin; surgically open and flush isolated abscesses
  • Control: Clean birthing environment, adequate colostral immunity, dipping umbilicus in iodine solution
  • Research complications: disease can be costly & consequences of systemic infection may detract from research value of animals
116
Q

Pasteurellosis (Shipping Fever, Hemorrhagic

Septicemia, Enzootic Pneumonia)

A
  • Mannheimia hemolytica & Pasteruella multocida - aerobic, nonmotile, non-sporeforming, bipolar, G(-) rods
  • Clin signs: acute bacterial disease characterized by bronchopneumonia, septicemia, sudden death; invade mucosa of GI or resp tract - cause localized areas of necrosis, hemorrhage, thrombosis; lungs & liver frequent locations for formation of microabscesses; acute rhinitis, pharyngitis often preceded respiratory form; may also invade bloodstream = septicemia; nasal discharge- mucopurulent to hemorrhagic, hyperthermia, coughing, dyspnea, anorexia, depression; with resp form - dullness and consolidation on auscultation of anteroventral lobes
  • Dx: clin signs, blood cultures, blood smears showing bipolar organisms, history of predisposing stressors
  • Transmission: ubiquitous in the environment; younger ruminants between 2-12 months old are especially prone to infection when stressed - weaning, transport, dietary changes, weather changes, overcrowding; transmitted between animals by direct or indirect contact through inhalation or ingestion
  • Pneumonic form appears as a component of BRDC associated with parainfluenza-3, BRSV, and in cattle bovine herpes virus 1 or BVDV
  • Necropsy: Pneumonic form: serofibrinous exudates fill alveoli and ventral lung lobes are consolidated, congested, purple-gray; degenerate streaming leukocytes (oat cells) are PATHOGNOMONIC FOR M. HAEMOLYTICA; fibrionous pleuritis, hematogenously induced arthritis; necrosis & hemorrhage in small intestines; multifocal lesions on surface of liver
  • Pathogenesis: stress & concurrent viral infx considered key factors in pathogenesis of infection; macrophages and neutrophils are lysed by bacterial leukocidin as they arrive at the lung, and enzymes released by phagocytes cause additional damage to lung tissue
  • Ddx: Mycoplasma bovis pneumonia
  • Tx: antibiotics, anti-inflammatories; in outbreaks, cultures from fresh necropsies for C&S
  • Control: minimize stress; vaccinate for viral respiratory pathogens; M. haemolytica-P. multocida bacterinas labeled for cattle, sheep, and goats available; passive immunity important; maintain good ventilation
117
Q

Salmonellosis

A

-Salmonella enterica - motile, aerobic to facultatively anaerobic, non-sporeforming, G(-) bacillus; common inhabitant of GI tract of ruminants
-Genus Salmonella contains 2 species: S. bongori - mainly infects poikilotherms & S. enterica - includes ~2500 serovars
-Most common serovars in animals: S. Typhimurium, S. Newport, S. Agona, S. Heidelberg
-S. Dublin and S. Abortusovis - implicated in bovine and ovine abortions
-Clin signs: acute gastroenteritis, dysentery, septicemia; feces may contain mucus or blood& have distinctive odor; anorexia, hyperthermia, depression, weakness, weight loss, dehydration; morbidity & mortality highest in neonates; septicemia may result in meningitis, polyarthritis, pneumonia; chronically infected animals may have intermittent diarrhea; may cause abortions in sheep, goats, and cattle throughout gestation - hemorrhage, placental necrosis, edema; metritis and placental retention may occur
-Dx: clinical signs; culture of feces or at necropsy; shedding is intermittent so may need repeated cultures; leukopenia & degenerative left shift
-Transmission: stresses assoc w/ shipping, overcrowding, inclement weather; bird and rodents may be natural reservoirs ; transmission is fecal-oral; animals that survive may become chronic carriers and shedders
-Necropsy: perineal staining; ileum, cecum, colon contain mucoid feces +/- hemorrhages; petechial hemorrhages and areas of necrosis on surface of liver, heart, mesenteric LNs; wall of intestines, gall bladder, mesenteric LNs edematous; psuedodiphtheric membrane lining distal small intestines & colon in cattle & sheep; splenomegaly; necrosuppurative inflammation of Peter’s patches; FIBRINOUS CHOLECYSTITIS = PATHOGNOMONIC
-Pathogenesis: after ingestion, organism proliferates in intestine - bacteria selectively taken up by M cells of Peyer’s patches and GALT; damage to intestines and diarrhea d/t bacterial production of cytotoxin and endotoxin; Salmonella organisms survives and multiply further in phagocytic cells
-Ddx: young animals = E. coli, rotavirus, coronavirus, clostridial infections, cryptosporidiosis,
and coccidiosis; adults = bovine viral diarrhea and winter dysentery in cattle,
and parasitemia and enterotoxemia in all ruminants
-Control: isolate affected animals; samples herdmates, water, feed, recently arrived livestock, area wildlife for culture; cull carrier animals; pest control; intensive cleaning and disinfection of facilities
-Tx: supportive care; antibiotics may be useful for septicemia, but use controversial as may create carrier animals
-Research complications: ZOONOTIC

118
Q

Tularemia

A
  • Francisella tularensis - nonmotile, non-sporeforming, aerobic, G(-) rod
  • Clin signs: sheep most commonly affect; hyperthermia, muscular stiffness, lymphadenopathy; anemia; diarrhea; infected LNs may enlarge and ulcerate
  • Dx: culture of organism from LNs, spleen, liver where granulomatous lesion form; serology
  • Transmission: ticks & biting flies; wood tick - Dermacenter andersoni - is an important vector in transmission western states; wild rodents & rabbits are natural reservoirs; can also transmit orally through contaminated water
  • Necropsy findings: suppurative necrotic LNs; lungs congested & edematous; necrosuppurative splenitis
  • Tx: oxytetracycline, aminoglycosides, cephalosporins
  • Ddx: When tick infestations are heavy, F. tularensis should be suspected. Mannheimia hemolytica (sheep), Histophilus somni (cattle), and Mycoplasma mycoides (goats), and anthrax (all ruminant
    species) should be considered as differentials
  • Control: eliminate tick vectors and deer flies
  • Research complications: ZOONOTIC, REPORTABLE
119
Q

MYCOPLASMA BOVIGENITALIUM, MYCOPLASMA

BOVIS

A
  • Associated with sporadic bovine infertility & abortions; M. bovis is a significant respiratory pathogen - also reported in sheep & goats
  • Clin signs: M. bovigenitalium = granular vulvovaginitis - raised papules on the mucous membranes & mucopurulent exuudate; M. bovis = abortions and mastitis, calves born may be weak
  • Transmission: mycoplasmal species are considered ubiquitous, carried in genital tracts r males and females; transmitted during natural breeding or through contaminated insemination materials, by aerosol, by passage through birth canal, by direct contact, & by contamination from urine and infected animals; feeding unpasteurized mild to dairy calves is a major risk factor
  • Tx: fluroquinolone, oxytetracycline, tilmicosin, tulathromycin; prevention far more rewarding than treatment
120
Q

Mycoplasma ovipneumoniae (Ovine Mycoplasmal Pneumonia)

A
  • Acute or chronic pneumonia in lambs
  • Clin signs: acute and chronic pneumonia, conjunctivitis, genitourinary disease; may be coincidental with pasteurellosis; resp distress, coughing, nasal discharge
  • Dx: Bronchoalveolar lavage followed by culture - Mycoplasmas are fastidious organisms that require special handling techniques
  • Isolated from genitourinary tract of sheep; vulvovaginitis & reproductive problems are associated conditions
  • Tx: tylosin, quinolones, oxytetracycline, gentamicin
121
Q

M. MYCOIDES BIOTYPE F38 (CONTAGIOUS CAPRINE PLEUROPNEUMONIA,
CAPRINE PNEUMONIA, PLEURITIS, AND
PLEUROPNEUMONIA)

A

-Mycoplasma mycoides biotype F38 is found worldwide
-In the US, caprine pneumonia is also caused by M. ovipneumoniae, M. mycoides subspecies
capri, and M. mycoides subspecies mycoides (Large Colony Type)
-Clin signs: severe dyspnea, nasal discharge, cough, fever
-Transmission: highly contagious with high morbidity and mortality; transmission is by aerosols
-M. mycoides subspecies mucoides has become a serious cause of morbidity and mortality of goat kids in US
-Necropsy: large amounts pale straw-colored fluid & fibrinous pneumonia and pleurisy; some lung consolidation; meningitis, fibrinous percarditis, fibrinopurulent arthritis
-Dx: culture of lungs and other internal organs
-Ddx: caprine arthritis & encephalitis (CAE)
-Tx: tylosin & oxytetracyline; some infections are slow to resolve
-Control: vaccination; quarantine infected herds & new goats
-Research complications: chronic subclinical infection can result in anesthetic complications in sheep

122
Q

Mycoplasma conjunctivae (Mycoplasmal Keratoconjunctivitis)

A

-Infectious conjunctivitis or pinkeye in sheep & goats
-Clin signs: lacrimation, hyperemia, edema, conjunctival vessel injection, keratitis, neovascularization, corneal lesions, uveitis; presenttion usually unilateral; recurring infections common
-Transmission: between animals by direct contact; animals can become reinfected and carrier animals may be a factor in outbreaks
-Necropsy: unlikely that animals would undergo necropsy for this
-Ddx: primary differential in
sheep and goats is Chlamydophila, as well as Branhamella, Rickettsia (Colesiota) conjunctivae, and IBR in goats only
-Tx: recovery spontaneously within ~10 weeks; tetracycline ointments and powders; third eyelid flaps if corneal ulceration develops
-Control: quarantine new animals

123
Q

Mycoplasma mastitis

A
  • Can spread from cow to cow via aerosol, milking equipment
  • Bacteria spread in the milk in large numbers before clinical signs appear & very few organisms are required to infect a quarter
  • Infected cows may have normal somatic cell counts (SCCs) = a cow may be asymptomatic with a normal SCC and serve as a source of infection for other cows
  • Clin signs: swollen quarter sensitive to touch, decreased milk production; abnormal milk generally develops 1-3 days later - milk first has visible particles, then pus, then becomes watery; affected cows do not appear sick & maintain good appetites; cows that have recovered from the clinical presentation generally always have a subclinical infx
  • Necropsy: does not generally result in death
  • Dx: suspect if increase in number of clinical cases of mastitis; culture organism from milk - request Mycoplasma culture
  • Tx: no effective treatment for Mycoplasma mastitis - if cow has good immune status, will eventually eliminate; treat any other organisms cultured in milk
  • Control: screen new animals before they enter the milking herd; 3-5 negative individual cow or bulk tank cultures is highly recommended
124
Q

Q Fever (Coxiella burnetti)

A

-Coxiella burnetti: small, G(-), obligate intracellular organism - etiologic agent of Q Fever/Query Fever/Queensland Fever, Nine-mile agent; major cause of late abortion in sheep; thought to be more closely related to Legionella & Francisella than to Rickettsia
-Clin signs: usually asymptomatic; in other mammals has resulted in transient hyperthermia, mild respiratory disease, mastitis; abortions, stillbirths, and births of weak lambs also seen
-Transmission: extremely resistant to environmental changes as well as disinfectants - can persist in environment for a year or longer; associated with either a free-living or arthropod-borne cycle; especially concentrated in placental tissues &reproductive fluids; also shed in milk, urine, feces, oronasal secretions
-Necropsy: no specific lesion in aborted or stillborn fetuses; necrotizing placentitis with white chalky plaques & red-brown exudate; INTRACYTOPLASMIC ORGANISMS WITHIN TROPHOBLASTS - stain red with MODIFIED ZIEHL-NEELSEN & MACCHIAVELLO stains & purple with GIEMSA stain
-Dx: based on detection of antibodies; 2-3 weeks after infection, IgM & IgG antiphase II antibodies against C. burnetti are detected; IgG antiphase I C. burnetti antibodies at titers of ≥1:800 by microimmunofluorescence is
indicative of chronic Q fever; PCR of genital swabs, mild, feces; culture NOT recommended d/t risk of lab acquired infx
-Tx: oxytetracyclines; vaccination
-Control: segregate aborting animals & treat other pregnant animals prophylactically with tetracycline; serologic screening of ruminant sources; barrier housing; Q fever can occur in many mammalian species including cats
-Research complications: C. burnetti free animals are particularly important in studies involving fetuses and placentation; ZOONOTIC - greatest concern for immunocompromised, pregnant women, other animals; SELECT AGENT

125
Q

Bluetongue (Reoviridae)

A

-RNA virus in genus Orbivirus, family Reoviridae; 26 serotypes have been identified, 15 from US
-Bluetongue is an acute arthoropod-borne viral disease of ruminants characterized by stomatitis, depression, coronary band lesions, congenital abnormalities; mostly found in western states
-Clin signs: sheep most likely to show clinical signs; early in infection - animals will spike a fever, develop hyperemia, congestion of tissues of mouth, lips, ears, cyanotic membranes - fever may subside but tissue lesions erode causing ulcers; increased salivary discharges, anorexia, ulcers of dental pad, lips, gums, tongue, salivation and lacrimation may precede ulceration; chorioretinitis & conjunctivitis also common signs in cattle and sheep; lameness, skin lesions - drying and cracking of the nose, mammary gland, alopecia; secondary bacterial pneumonia; severe diarrhea; sudden deaths d/t cardiomyopathy at any time during the disease; leukopenia; course of disease is about 2 weeks, mortality may reach 80%
-Virus crosses placenta & causes CNS lesions; abortions at any stage gestation in cattle; prolonged gestation, cerebellar hypoplasia, lack of normal sequence to induce parturition; hydrocephalus, cataracts, gingival hyperplasia, arthrogryposis
Dx: clin signs, virus isolation from blood collected during febrile stage or brain tissue from aborted fetuses; fluorescent antibody tests, ELISA, virus neutralization tests, PCR, Agar gel immunodiffusion (AGID) to confirm diagnosis
-Most common in outdoor-housed animals in western US
-Transmission: primarily by biting Culicoides midges; Charolais & Merino sheep breeds more susceptible; direct contact, virus-contaminated semen, other animal products, transplacental transfer possible but less common
-Necropsy: erosive lesions at mouth, tongue, palate, esophagus, pillars of the rumen; ulceration or hyperemia of the coronary bands; many internal organs will contain surface petechial & ecchymotic hemorrhages; SUBINTIMAL HEMORRHAGES OF THE LARGE PULMONARY ARTERIES ARE NEARLY PATHOGNOMONIC
-Pathogenesis: incubation period is 6-14 days; prolonged viremia; virus migrates to and attacks the vascular endothelium - resulting vasculitis accounts for the lesions of the skin, mouth, tongue, esophagus, rumen & edema
-Ddx: infectious vesicular diseases such as foot-and-mouth disease, contagious ecthyma, bovine virus diarrhea, mucosal disease, infectious bovine rhinotracheitis virus,
bovine papular stomatitis, and malignant catarrhal fever
-Control: modified live vaccines - should not be used in pregnant animals - congenital defects are more common from vaccine use than naturally occurring infx; minimizing exposure in endemic areas
-Tx: supportive & nursing care, easily accessed water & shaded resting places; NSAIDs
-Research complications: REPORTABLE because clinical signs resemble foot and mouth disease & other exotic vesicular diseases

126
Q

Enzootic bovine lymphoma (Bovine Leukemia Virus; Bovine Leukosis)

A
  • ‘Bovine lymphosarcoma’ may refer to either sporadic lymphproliferative disease affecting young cattle (juvenile, thymic, cutaneous) as well as diseases of older cattle assoc w/ bovine leukemia virus
  • BLV is a B lymphocyte-associated, genus Deltaretrovirus - integrates into host target cell DNA by means of the reverse transcriptase enzyme, creating a proenzyme
  • Clin signs: only the adult or enzootic form of bovine lymphoma is assoc w/ BLV infx; majority of animals will not develop any malignancies or clinical signs of infection & will simply remain permanently infected; ~30% will have an elevated peripheral lymphocyte count and subtle immune defects (persistent lymphocytosis), less than 5% of infected animals develop B cell lymphoma - loss of condition, drop in production of dairy cattle, anorexia, ataxia, melena d/t bleeding abomasal ulcer, paresis, other signs dependent on the location of neoplastic lesions; tumors will be assoc w/ lymphoid tissues - common sites include abomasum, extradural spinal canal, uterus; cardiac tumors develop at the right atrial or left ventricular myocardium & assoc beat and rate abnormalities may be ausculted; common ocular manifestation of the disease is exophthalmus d/t retrobulbar masses
  • Dx: based on animal’s age, clin signs, serology, aspirates or biopsies of masses, necropsy findings; kits for AGID for which the BLV antigens gp-51 and gp-24 are used; antibodies may be detected within weeks after expsoure & may also help in predicting disease in clinically normal cattle; serology most reliable method for diagnosis; most countries recognize AGID as the official import/export test; ELISA most common test for routine diagnostic use; serology unreliable in calves that have ingested colostrum from BLV (+) cows
  • Transmission: inhalation of BLV in secretions, in utero or by colostrum, horizontally by contaminated equipment, by rectum during rectal exams
  • Necropsy: tumors may be local or widely distributed; definitive diagnosis = neoplastic tissue by histology
  • Control: maintain BLV-free herd or control infection within herd; single-use needles, disinfecting equipment; feed calves colostrum from seronegative cows - however, protective effect of colostral antibody outweighs the risk of infections
  • Tx: corticosteroids, chemotherapy for short-term improvement
  • Research complications: Many US states, Australia, NZ, and some European countries have official programs for eradication of enzootic bovine leukosis; BLV is closely related to human T-lymphotropic virus type I (HTLV-1) - research model
127
Q

BOVINE HERPES MAMMILLITIS (BOVINE HERPES 2 VIRUS, BOVINE ULCERATIVE MAMMILLITIS)

A
  • Bovine herpesvirus 2 - acute ulcerative test & udder lesions + oral & skin lesions
  • Clin signs: lesions begin with teat swelling, tenderness, edema; vesicles progress to ulcers; may take 10 weeks to heal; secondary mastitis b/c cows resist milking
  • Dx: clin signs, histopath, virus isolation
  • Transmission: occurrence often seasonal; biting insects may be vectors; successful infection requires deep penetration of skin; also transmission by contaminated milking equipment, other fomites
  • Ddx: other diseases that cause teat lesions: pseudocowpox, papillomatosis, vesicular stomatitis and foot-and-mouth disease virus (FMDV)
  • Control: milking hygiene, milker handwashing; separate affected animals
  • Tx: no treatment; lesion can be cleaned and treated with topical antibacterials
128
Q

Bovine Virus Diarrhea & Mucosal Disease Complex

A

-BVDV: pestivirus of family Flaviviridate; cattle & other ungulates (pigs, sheep, goat) susceptible; one of the most economically impt diseases of cattle
-Strains are cytopathic (CP) & noncytopathic (NCP) based on cell culture growth
-Virus also categorized as Type 1 & Type 2 isolates w/ subtypes 1a, 1b, etc.; heterogenous strains may confound vaccination programs
-Clin signs: abortions, congenital abnormalities, reduced fertility, immune suppression, acute & fatal disease; presence of antibodies, from passive transfer or immunization, does NOT guarantee protection
-Acute form = Type 2 BVDV; 5-7 days incubation; fever, anorexia, oculonasal discharge, oral erosions, diarrhea; disease course may be shorted with hemorrhagic syndrome
-Calves: severe enteritis and pneumonia
-In utero infection: 50-100 days gestation = abortion, stillbirth; 90-170 days gestation = congenital defects - thymic atrophy, cerebellar hypoplasia, ocular defects, alopecia, hypothrichosis, hydrocephalus
-Cerebellar dysfunction in calves = wide-based stance, weakness, opisthotonus, hyperreflexia, hypermetria, nystagmus, strabismus
-Fetuses infected in utero can be persistently infected (PI) & immunotolerant at birth - many PI animals do not survive to maturity d/t weakened immune systems; PI animals shed virus throughout life = impt source of infx; PI animals may develop mucosal disease (MD) caused by CP BVDV strain
-Mucosal Disease: fever, anorexia, profuse diarrhea +/- blood, fibrin casts; oral & pharyngeal erosions; interdigital space erosion on teats and vulva; anemia, thrombocytopenia, leukpenia, hemorrhage, dehydration
-Dx: hed health history, clin signs, virus culturing, PCR, serology; identify PI calves = IHC of skin biopsies (ear notch) or blood
-Transmission: direct contact, feed contaminated by secretions, feces, aborted fetuses & placentas; fomites; semen; PI females transmit to fetuses
-Necropsy: cerebellar hypoplasia in in utero affected calves; older animals - intestinal necrosis, erosions in oral cavity & GI tract, resp tract lesions with secondary bacterial pneumonia; hemorrhagic syndrome - petechiation & mucosal bleeding
-Ddx: enteritis
of calves include viral infections, Cryptosporidia,
E. coli, Salmonella, and Coccidia; adults - Salmonella, winter dysentery, Johne’s disease, intestinal parasites, and malignant catarrhal fever (MCF); respiratory pathogens - BRSV, Mannheimia, Pasteurella, Histophilus, and Mycoplasma; oral lesions: MCF, FMDV, vesicular stomatitis, bluetongue and papular stomatitis; abortions: Infectious bovine herpesvirus 1,
leptospirosis, brucellosis, trichomoniasis, and mycosis
-Control: MLV or inactivated vaccines; MLV vaccines induce rapid immunity with longer duration, but not recommended in pregnant cattle, may induce mucosal disease, may be immunosuppressive; inactivated vaccines require booster & do not produce cell-mediated immunity; passive immunity protects calves up to 6-8 mths old; annual boosters recommended
-Virus persists in environment for 2 weeks; susceptible to chlorhexidine, hypochlorite, iodophors, aldehydes
-Tx: supportive care; antibiotics for secondary infection

129
Q

CAE virus

A
  • Genus Lentivirus, Family Retroviridae
  • Most important viral disease of goats; causes chronic arthritis & mastitis in adults, encephalitis in young; same genus as OPPV
  • Clin signs: insidious progressive arthritis in animals 6 months or older - stiff, difficulty getting up, lameness, swollen carpal joints - walk on ‘knees’; decreased mild production, firm udders; neurologic signs in kids 2-6 months old - unilateral weakness in a rear limb - progress to hemiplegia, tetraplegia; lower motor neuron deficits but spinal reflexes intact; head tilt, blindness, ataxia, facial nerve paralysis; older animals - interstitial pneumonia or chronic arthritis, weight loss
  • Dx: clin signs, post mortem lesions, serology; AGID test identifies antibodies; kids acquire anti-CAEV in colostrum; antibody does NOT prevent viral transmission
  • Transmission: most commonly oral - to kids in colostrum or milk; contact among adult goats, rare intrauterine transmission
  • Necropsy: synovial hyperplasia with infiltrates of lymphocytes, macrophages, plasma cells; demyelination in brain and spinal cord with invasion of lymphocytes, macrophages, plasma cells; lung pathology; mastitis with lymphoid tissue in udder
  • Ddx: Neuro form = copper deficiency, enzootic pneumonia, white muscle disease, rabies, listeriosis, thiamine deficiency, and spinal cord disease or injury; Arthritis/Pneumonia form = Chlamydophila and Mycoplasma
  • Control: screen herds serologically by AGID, ELISA, immunoprecipitation, PCR; highly prevalent in US; seronegative animals can shed in milk; retest annually; test & cull; prevent milk transmission - feed kids heat-treated colostrum (56 C for 1 hr); isolate affected animals
  • Tx: there is no treatment
130
Q

INFECTIOUS BOVINE RHINOTRACHEITIS VIRUS (IBRV) (INFECTIOUS PUSTULAR VULVOVAGINITIS (IBR-IPV), BOVINE HERPESVIRUS I)

A

-Contributes to several bovine respiratory and reproductive syndromes
-One of the primary pathogens of bovine respiratory disease complex
-Clin signs: conjunctivitis, rhinotracheitis, pustular
vulvovaginitis, balanoposthitis, abortion, encephalomyelitis, and mastitis; Respiratory Form = ‘red nose’/IBR -fever, anorexia, restlessness, hyperemia of muzzle & nares, gray pustules on the muzzle (later plaques), nasal discharge, hyperpnea, coughing, salivation, conjunctivitis w/ epiphora, decreased milk production - generally recover in 4-5 days if no secondary bacterial pneumonia; neonates may have resp as well as systemic disease; Encephalitic Form = young calves most susceptible; dull attitude, head pressing, vocalization, nystagmus, head tilt, blindness, convulsions, coma; usually fatal within 5 days; abortion in second half of pregnancy or early embryonic death; infectious pustular vulvovaginitis (IPV) - fever, depression, anorexia, vulvar labia swelling, vulvar discharge, reddened vaginal mucosa - lasts about 4-5 days & lesions heal in 2 weeks; younger bulls - balanoposthitis with edema, swelling, pain
-Dx: clin signs, virus isolation, paired serum samples; virus isolation or fluorescent antibody staining of aborted fetal tissues
-Transmission: widely distributed throughout world; adult animals are reservoirs of infection; transmission mainly through nasal secretions
-Necropsy: FIBRINONECROTIC RHINOTRACHEITIS PATHOGNOMONIC; if secondary bacteria, congested tracheal mucosa, bronchopneumonia, petechial & ecchymotic hemorrhages; Encephalitic Form = lymphocytic meningoencephalitis through gray matter (neuronal degeneration, perivascular cuffing) & white matter (myelitis, demyelination); young animals - ulders in nose, esophagus, forestomachs; white foci in liver, kidney, spleen, LNs; pale necrotic lesions in all tissues, esp liver, of aborted fetus
-Ddx: conjunctivitis of IBR
may initially be mistaken for that of a Moraxella bovis
(Pinkeye) infection; the IBR will be peripheral and there
will not be corneal ulceration
-Control: vaccination = inactivated, attenuated, modified live, and genetically altered temperature-sensitive intranasal (IN) and parenteral preparations; IN MLV good for inducing mucosal immunity in calves; some newer vaccines with gene deletion allow serologic differentiation btwn antibody responses to infx vs vaccine; immunize when 6-8 months old, prior to breeding, & annually
-Tx: supportive care; antibiotics for secondary bacteria; treatment for encephalitis unrewarding

131
Q

Parainfluenza-3 (PI-3)

A
  • Bovine parainfluenza 3 (BPI 3) - RNA virus, family Paramyxoviridae; mild resp disease when sole pathogen; serotypes in smaller ruminants distinct from cattle
  • Clin signs: asymptomatic to mild URI signs, abortions; signs more severe when additional pathogens - BVDV, M. haemolytica, etc. are involved
  • Dx: virus isolation, direct IFA from nasal swabs, paired serum samples
  • Transmission: ubiquitous in cattle, common in sheep; assumed to be widespread in goats
  • Necropsy: infection with PI-3 only: findings negligible; - some congestion of respiratory mucosa, swelling of resp tract assoc LNs, mild pneumonitis
  • Ddx: IBRV, BVDV, and BRSV
  • Control: vaccination, management, nutrition; MLV IN vaccine = immunity within 3 days, stimulates production of interferon; booster vaccines recommended after 2-6 months; no approved PI-3 vaccines for sheep & goats - cattle formulation has been used
  • Tx: uncomplicated disease not treated
132
Q

Respiratory Syncytial Viruses of Ruminants (RSV)

A

-Genus Pneumovirus, family Paramyxoviridae; 2 serotypes of BRSV described in cattle - may be similar or identical to virus seen in sheep & goats
-Clin signs: subclinical to severe illness; high fever, hypernea, spontaneous or easily induced cough, nasal discharge, conjunctivitis; interstitial pneumonia usually develops w/ harsh resp sounds; open mouth breathing in later stages; EMPHYSEMA OF DORSAL SC FROM RUPTURED BULLAE = characteristic, poor prognosis; secondary bacterial pneumonia, esp with M. haemolytica; abortion
-Dx: virus isolation - nasal swabs should be taken when animals have fevers, serology (acute, convalescent)
-Transmission: aerosols; considered ubiquitous in cattle
-Necropsy: consolidation of anteroventral lung lobs, edema & emphysema; SYNCYTIA - may have small eosinophilic intracytoplasmic & rarely intranuclear inclusions - form in areas of lungs infected with virus; necrotizing bronchiolitis, bronchiolitis obliterans, hyaline membrane formation
-Ddx: other ruminant respiratory tract viruses such as
BPI3, BVDV and bovine herpesvirus 1
-Control: vaccination; passive immunity does not prevent infx but reduces severity; virus easily inactivated in environment
-Tx: supportive care; antibiotics for secondary bacterial pneumonia; antihistamines, corticosteroids

133
Q

Border Disease (Hairy Shaker Disease)

A
  • Caused by virus closely related to BVDV - Pestivirus in Togaviridae family; disease of sheep & goats
  • Clin signs: early embryonic death, abortion of macerated or mummified fetuses, birth of lambs with developmental abnormalities; lambs infected in utero may be born weak & have congenital defects - tremor, hirsutism (darkly pigmented over shoulders, head), hypothyroidism, joint abnormalities (arthrogryposis), CNS defects; hisutism NOT seen in goats
  • Dx: clin signs, serology, virus isolation, ELISA, PCR
  • Transmission: present worldwide; persistently infected animals shed virus in urine, feces, saliva
  • Necropsy: placentitis, joint & haircoat changes in the fetus
  • Control: euthanize congenitally affected animals; screen new animals via serology; cattle housed near sheep should be routinely vaccinated for BVDV; BVDV is antigenically distinct from border disease, so sheep CANNOT be vaccinated with cattle BVD vaccine
  • Tx: supportive care
134
Q

Orf Virus Disease (Contagious Ecthyma, Contagious Pustular Dermatitis, Sore Mouth)

A
  • Parapoxvirus; occurs worldwide; ZOONOTIC
  • Clin signs: papules, vesicles, pustules & scabs on skin of face, genitals, coronary bands; lesions develop most frequently at mucocutaneous junctions - most common at commissures of mouth; usually identified in animals less than 1 yr old; lambs have difficulty nursing & become weak; course of disease may last up to 6 weeks
  • Dx: characteristic lesions, clin signs
  • Transmission: all ages of sheep & goats susceptible; seasonal occurrences after lambing & move to feedlot b/c stress; virus extremely resistant to environment
  • Necropsy: except for debilitated lambs, usually does not result in necropsy
  • Ddx: ulcerative dermatosis, blutongue - sheep & goats; Staph dermatitis - goats
  • Control: PPE, separate equipment between sheep/disinfect equipment; vaccination of lambs & kids; vaccinate animals arriving to infected environment, but don’t vaccinate flocks free of disease; vaccine may introduce orf to animal handlers
  • Tx: isolate affected animals & provide supportive care
  • Research complications: carrier animals may be a factor in outbreaks; ZOONOTIC - human lesions extremely painful & may last as long as 6 weeks
135
Q

Foot and Mouth Disease (AFTOSA, FMDV)

A

-Picornavirus, Genus Aphthovirus; North & Central America have been free of disease since 1950s; cattle most susceptible species; swine are important host; usually subclinical in goats
-Clin signs: vesicle formation around & in mouth, hooves, teats; fever, anorexia, salivation
-Dx: MUST be based on ELISA, virus neutralization, fluorescent antibody tests, complement fixation - send samples of vesicular fluid or epithelium to national laboratory
-Transmission; highly infectious; hosts include domestic & wild ruminants, swine, rats, bears, llamas; transmission is inhaled aerosols (can be carried over 70 miles) & fomites
-Necropsy: vesicles, erosions, ulcers in oral cavity, rumen pillars, mammary alveolar epithelium
-Ddx: vesicular stomatitis (VS), contagious ecthyma (orf), bluetongue, malignant
catarrhal fever, bovine papular stomatitis, bovine
herpes mammillitis, and IBR virus infection
-Control: movement of animals & animal products from endemic areas is regulated; vaccination, quarantine, slaughter
-Tx: any suspicion of FMD = notify regulatory authorities; destroy infected animals in FMDV-free countries
-Research complications: importation into US of animals or animal products from endemic areas is prohibited

136
Q

Malignant Catarrhal Fever

A
  • Bovine herpesvirus 6 - subfamily Gammaherpesvirinae, genus Macavirus
  • Sheep form = ovine herpesvirus-2 (OvHV-2)
  • Clin signs: subclinical to recrudescing infections to lethal disease in susceptible species like cattle; 3 forms: Alimentary, Encephalitis, Skin; CORNEAL EDEMA STARTING AT LIMBUS & PROGRESSING CENTRIPETALLY - NEARLY PATHOGNOMONIC; photophobia, keratoconjunctivitis, prolonged fever, oral mucosal erosions, salivation, lacrimation, ropey catarrhal nasal discharge, encephalitis, lymphadenopathy, severe diarrhea; recovery usually prolonged & permanent debilitation possible
  • Dx: history of exposure, clin signs, lesions; serology, PCR, viral isolation, cell culture
  • Transmission: most ruminant species susceptible; sheep = asymptomatic & cattle are dead-end hosts = DON’T MIX CATTLE & SHEEP; goats may harbor virus; transmission is aerosol, direct contact, fomites - water troughs, placental tissues, birds, caretakers; incubation period up to 3 mths
  • Necropsy: lesions can be found in any organ b/c systemic; necrotic & ulcerated nasal & oral mucosa; thickened edematous ulcerated & hemorrhagic areas in intestinal tract; swollen friable hemorrhagic LNs & other lymphatic tissues; erosion of mucosal surfaces
  • Ddx: BVDV/mucosal disease, IBR, bluetongue vesicular stomatitis, FMD
  • Control: in North America, sheep & cattle that have been exposed or have survived disease are reservoirs for outbreaks in other cattle; virus very fragile outside of host cells - will not survive in environment more than a few hours
  • Tx: prognosis grave; supportive treatment
137
Q

Ovine Progressive Pneumonia (OPP; Visna/Maedi)

A
  • RNA virus - genus Lentivirus, family Retroviridae
  • ‘Maedi’ = progressive pneumonia
  • ‘Visna’ = CNS disease - predominantly reported in Iceland
  • Genetic susceptibility has been implicated
  • Clin signs: weakness, unthriftiness, weight loss, pneumonia in adult sheep; progressive pulmonary disease w/ extremely long incubation period up to 2 YEARS; resp rate & dyspena gradually increase; mastitis; consolidation of ventral lung lobes; anemia, leukocytosis; neuro signs are rare - flexion of fetlock & pastern joints, facial muscle tremors, progressive paresis & paralysis, depression, prostration; death occurs in weeks to months; secondary bacterial pneumonia
  • Dx: AGID, virus isolation, serum neutralization, complement fixation, ELISA, PCR
  • Transmission: prevalance in some US states 60-80%; transmitted horizontally - inhaled aerosolized virus & vertically from dam to fetus, through milk/colostrum
  • Necropsy: lesions in lungs, mammary glands, joints, brain; pulmonary adhesions, ventral lung consolidation, bronchial LN enlargement, mastitis, degenerative arthritis; meningeal edema, thickening of choroid plexus & foci of leukoencephalomalacia in CNS
  • DDx: pulmonary adenomatosis, mycoplasmosis
  • Control: isolating or removing infecting animals can prevent disease; disinfect facilities; some states have control programs
  • Tx: treatment unsuccessful
138
Q

Ovine Viral Dermatosis

A
  • Parapoxvirus
  • Veneral disease
  • Lesion painful but resolve within 2 weeks & resemble C. renale posthitis/vulvovaginitis
  • Tx: supportive care; NO vaccine
  • Do not use animals for breeding when clin signs present
139
Q

Proliferative Stomatitis (Bovine Papular Stomatitis)

A
  • Parapoxvirus - closely related to contagious echthyma & pseudocowpox
  • ZOONOTIC: handlers develop lesions on hands at sites of contact with lesions
  • May see high morbidity in outbreaks
  • Lesions comparable to vesicular stomatitis, BVDV, FMD
  • Clin signs: raised red papules/erosions/shallow ulcers on muzzle, nose, oral mucosa (incl hard palate), esophagus, rumen of cattle 1 mth-2 year old; may also be asymptomatic
  • Dx: clin signs, virus isolation
140
Q

Pseudocowpox (Milker’s nodes, Paravaccinia)

A
  • Parapoxvirus - related to bovine papular stomatitis & orf
  • Lesions confined to teats
  • ZOONOTIC - nodular lesions in humans
  • Clin signs: lesions start as small red papules & proceed quickly to small vescile/pustules & scabs; DISTINCTIVE RING OR HORSESHOE SHAPE OF SCABS; some lesions may persist for months; may predispose cows to mastitis d/t resistance to milking
  • Ddx: bovine herpes mammillitis, papillomatosis
  • Control: virus spread on contaminated hands & equipment - disinfection/hygiene
  • Tx: symptomatic treatment of lesion; milk affected animals last
  • Research complications: ZOONOTIC
141
Q

Pulmonary adenomatosis (Jaagsiekte Sheep Retrovirus)

A
  • Rare but progressive wasting disease of sheep; worldwide distribution
  • Retrovirus in genus Betaretrovirus
  • Related to Mason-Pfizer monkey virus
  • REPORTABLE in ome states
  • Clin signs: progressive respiratory signs - dyspnea, rapid respiration, wasting
  • Dx: chronic clin signs, viral antigen RNA, IHC, immunoblot, PCR
  • Research impact: is a common model for research of retrovirus development, pulmonary neoplasia, transmissible pulmonary neoplastic diseases
142
Q

Papillomatosis (Warts, Verrucae)

A
  • Very common in cattle; much less common in sheep & goat
  • Papilloma virus - DNA virus, family Papillomaviridae
  • Viruses are host specific & often body-site specific; in cattle, site specificity of strains is around head & neck
  • Clin signs: papillomas may last for up to 12 months; seen more frequently in younger animals; wart-like appearance, single or multiple; small (1 mm) to very large (500 mm); generally benign but if severe weight loss may occur; secondary mastitis possible if warts on teats; prognosis poor only when papillomatosis covers >20% of body
  • In sheep & goat, warts are verrucous type - disease is of little consequence unless warts cause discomfort - between digits, lips, over joints; warts on goat udders tend to be persistent
  • Dx: typical proliferative lesions
  • Transmission: direct contact, fomites; enters surface wounds & sites like tattoos; DNA from papillomavirus has been found in blood, milk, urine, & other fluids; incubation period = 1-6 mths; disease generally self-limiting
  • Control: vaccination; autogenous vaccines generally more effective than commercial; virucidal products for disinfection of contaminated environments; minimize cutaneous injuries & sanitize equipment
  • Tx: warts will often spontaneously resolve as immunity develops; can amputate warts with scissors & autogenous vaccines made to help prevent spread; cryosurgery with liquid nitrogen or dry ice
143
Q

Pseudorabies (Mad Itch, Aujeszky’s Disease)

A

-Suid herpesvirus 1 -neurotropic member of subfamily Alphaherpesvirinae; 1 serotype but strain differences exist; has been eradicated from domestic livestock in US but prevalent in feral swine; worldwide distribution; primarily seen in swine & cattle, less often sheep & goats
-Clin signs: site of virus inocluation: abrasions, swelling, intense pruritis, alopecia; hyperthermia, frantic vocalization; hoof stamping, kicking at pruritic area, salivation, tongue chewing, head pressing, circling, nystagmus, strabismus, paresthesia, hyperesthesia, ataxia, conscious proprioceptive deficits, fearful, depressed, aggressive; recumbency, coma
-Rapid disease progression; usually fatal
-Dx: virus isolation, fluorescent antibody testing from nasal of pharyngeal secreations or post mortem tissues, histology
-Transmission: swine are primary hosts but are usually asymptomatic & serve as reservoirs; other animals dead end hosts; unprotected virus only survives a few weeks in environment but viable in meat (carcasses) for weeks to months; transmission = direct contact, fomites, fecal-oral, aerosol, inadvertent exposure of ruminants to MLV vaccines used for swine; pets & wildlife can carry organism between farms but only live 2-3 days after becoming infected
-Necropsy: severe, focal nonsuppurative encephalitis, myelitis
-Ddx: rabies, polioencephalomalacia, salt poisoning, meningitis, lead
poisoning, hypomagnesemia, and enterotoxemia
-Control: REPORTABLE in US; nationwide eradication program
-Tx: no treament; most affected animals die
-Research complications: any suspicion of pseudorabies should be reported to animal health authorities

144
Q

Rabies (Hydrophobia)

A

-Neurotropic RNA virus os genus Lyssavirus, family Rhabdoviridae; sheep, goats, cattle susceptible
-ZOONOTIC, REPORTABLE in North America
-Clin signs: acute behavioral changes, unexplained progressive paralysis; 3 phases: Prodromal, Excitatory, Paralytic; clinical course usually 1-4 days
-Prodromal = hyperthermic, apprehensive
-Excitatory = refuse to eat and drink, active, aggressive; repeated vocalizations, tenesmus, sexual excitement, salivation
-Paralytic = recumbency & death over several hours to days
-Dx: clin signs; confirmation is fluorescent antibody technique on brain tissue
-Transmission: via bite wound; common disease vectors in North America = cats, dogs, raccoons, skunks, foxes, wild canids, bats
-Necropsy: NEGRI BODIES PATHOGNOMONIC - in cytoplasm of neurons of hippocampus & in Purkinje cells
-Ddx: herpesvirus encephalitis, thromboembolic
meningoencephalitis, nervous ketosis, grass tetany, and nervous cocciodiosis
-Control: inactivated vaccines approved for sheep & cattle; no approved vaccine for goats; exclude wildlife from facilities
-Research Complications: PPE when handling animals with neuro disease signs = gloves, face mask, eye shield

145
Q

Schmallenberg Virus

A
  • Orthobunyavirus named for German city where discovered in 2011; sheep, goats, cattle susceptible; only in Europe currently
  • Clin signs: fever, diarrhea, decreased milk production; stillbirths, congenital malformations - no illness in dams; congenital malformations incl scoliosis, hydrocephalus, arthrogryposis, cerebellar hypoplasia
  • Dx: RT-PCR of blood, brain, spleen
  • DDx: several other pathogens described in this chapter
  • Control: transmitted by midges = seen mostly in warm weather months; affected herds have tendency toward acquired immunity; currently import bans from areas where diagnosed
146
Q

Bovine Spongiform Encephalopathy (BSE, ‘Mad Cow Disease’)

A
  • Following outbreak in Great Britain in 1980s, USDA restricted importation of live cattle & certain ruminant products from countries affected with BSE
  • USDA has ongoing BSE surveillance program
  • Probably of encountering in research setting is very low; be aware of measures taken by suppliers of biological reagents to mitigate risk of contamination with BSE
147
Q

Scrapie

A
  • Transmissible spongiform encephalopathy of sheep & goats; REPORTABLE; much more common in sheep
  • Clin signs: early stage - excitable, hard to control animals, tremors of head and neck muscles, uncoordinated movements, ‘bunny hopping’ gait, lip smacking, severe pruritis & self-mutilation rubbing on fences, trees, etc., blindess, abortion; most animals die within 4-6 weeks but some may survive to 6 months
  • Goats - pruritis less severe; listlessness, stiffness or restlessness, behavioral changes- irritability, hunched posture, twitching, erect tail & ears; progresses to anorexia, debilitation, death
  • Dx: clin signs, histopath,; newer diagnostic test = biopsy of 3rd eyelid by regulatory veterinarians; blood tests of genetic susceptibility
  • Transmission: horizontally to neonates or juveniles by direct or indirect contact; nasal secretions or placenta;; transplacental transmission UNLIKELY
  • Long incubation period of 2-5 years = only adult animals show clin signs
  • State and federal eradicaiton programs exist
  • Necropsy: no gross lesions; histo = neuronal cytoplasmic vacuolization, astrogliosis, spongiform degeneration in brainstem, spinal cord & esp thalamus
  • Ddx: ectoparasites, pseudorabies, photosensitization
  • Control: if diagnosed in a flock, quarantine, slaughter & disinfection required; genetic selection for shipping, breeding, purchasing then used to eradicate; Scrapie-free flocks given identification tags
  • Tx: no treatment or vaccine available
  • Research complications: REPORTABLE; stringent regulations in US regarding import of small ruminants from scrapie-infected countries
148
Q

Genetic susceptibility for Scrapie

A
  • Suffolk particularly susceptible
  • 3 polymorphisms in PRP gene govern susceptibility, at codons 136, 154, 171
  • VRQ/VRQ animals most susceptible
  • ARR/ARR animals resistant
149
Q

Vesicular stomatitis (VS)

A

-Vesicular stomatitis virus - family Rhabdoviridae; REPORTABLE; ZOONOTIC New Jersey & Indiana strains cause sporadic disease in cattle in US
-Clin signs: adult cattle most likely to develop; fever, vesicles on oral mucous membranes, lesions on teats & interdigital spaces; vesicles quickly progress to ulcers & erosions; tongue may be severely involved; anorexia, salivation, weight loss, decreased milk production; morbidity high, mortality low
-SImilar to FMD = regulatory agencies should be involved in work-up
-Dx: analysis of fluid, serum, or membranes assoc w/ vesicles - virus isolation, ELISA, CELISA, CF, serum neutralization, RT-PCR
-Transmission: occurs in swine, horses, wild ruminants; survives well in different environmental conditions including soil & extremes of pH & low temps; transmission from contaminated water, feed, insects; incubation period is 2-8 days; believed that carrier animals do NOT occur
-Necropsy: rare for animals to be necropsied
-Ddx: LESIONS IDENTICAL TO FMDV LESIONS; bovine viral diarrhea, malignant catarrhal fever, contagious
ecthyma, photosensitization, trauma, and caustic
agents
-Control: quarantine & restriction of shipping of infected animals or animals from same premises; vaccination for use in outbreaks; phenolics, quaternaries, halogens effective for inactivating & disinfecting facilities
-Tx: segregate affected animals; provide separate water and softened feed; topical or systemic antibiotics control secondary bacterial infections
-Research complications: animals with vesicular lesion must be reported promptly to eliminate possibility of FMDV; ZOONOTIC - flu-like illness in humans

150
Q

Rotavirus

A
  • Family Reoviridae
  • Acute, transient diarrhea in calves & lambs within FIRST FEW WEEKS OF LIFE
  • Clin signs: yellow semifluid to watery malabsorptive diarrhea occurring 1-4 days after infx; dehydration, anorexia, weight loss, depression, acidosis, death
  • Transmission: fecal-oral; virus may remain in environment for several months
  • Dx: virus isolation, electron microscopy of feces, fecal fluorescent antibody, fecal ELISA (generally detect group A rotavirus), fecal latex agglutination tests
  • Tx: supportive care
  • Control: vaccine available for cattle; cross-species immunity = oral administration of high-quality bovine colostrum to at risk lambs may be helpful
151
Q

Coronavirus

A
  • Family Coronaviridae
  • MORE SEVERE, LONG-LASTING DISEASE VS. ROTAVIRUS
  • Incubation periods tends to be shorter (20-36 hr); mild resp disease; may be complicated by parasites (Cryptosporidia, Eimeria) or bacterial (E. coli, Salmonella) infxs
  • Tx: supportive
  • Control: strict hygiene & effective passive tranfer; bovine vaccines avilable both for prepartum dams & neonates
152
Q

Diarrheal diseases in goats

A
  • Rotaviruses, coronavirus, adenovirus all affect neonatal goats; however, litter has been documented on pathology & significant of these agents
  • Unlike calves, appears that bacteria play a more important role in neonatal kid
153
Q

Additional diarrheal agents in calves

A

Parvovirus and BVDV may also cause diarrhea in neonatal calves

154
Q

Winter Dysentery

A
  • Acute, epizootic diarrheal disease in housed adult cattle in winter months (reporte din as young as 4 mth old calves)
  • Etiology unknown; but coronavirus-like viral particles have been silated from cattle feces
  • Outbreaks typically last a few weeks - first lactation or younger cattle are affected first w/ waves of illness for only a few days
  • Incubation period is ~2-8 days
  • Clin signs: explosive diarrhea, anorexia, depression, profound decrease in production; diarrhea has distinct musty, sweet odor, light brown & bubbly w/ some blood streaks or clots; dehydration occurs quickly but animals are thirsty; nasolacrimal discharge, coughing may occur; mortality rare
  • Dx: eliminate diarrheas caused by coccidia & other parasites, Salmonella, M. paratuberculosi, viruses like BVDV
  • Pathology: present in colonic mucosa & necrosis present in crypts
155
Q

Enzootic Abortion of Ewes (EAE; Chlamydophilal Abortion)

A
  • Chlamydophila abortus (C. psittaci serotype 1) - nonmotile, obligate, intracytoplasmic G(-) bacteria
  • Clin signs: enzootic abortion in sheep & goats with hyperthermia, LATE ABORTION or birth of stillborn or weak lambs or kids; serosanguineous vulvar discharge may be only sign; arthritis, pneumonia
  • Infx prior to 120 days of gestation = abortion, stillbirths, birth of weak lambs/kids
  • Infx after 120 days of gestation = potentially normal births, but dam or offspring may remain latently infected
  • Ewes/does generally abort only once; recovered animals immune to future infx
  • Transmission: direct contact with infectious secretions - placental, fetal, & uterine fluids; indirect contact with contaminated feed, water
  • Necropsy: intercotyledonary plaques & necrosis, cotyledonary hemorrhages; histo: leukocytic infiltration, edema, necrosis throughout placentome; fetal lesions include giant cell accumulation in mesenteric LNs & lymphohistiocytic proliferations around blood vessels in liver
  • Dx: clin signs, immunofluorescence, ELISA, cell culture isolation, RT-PCR; impression smears of placental tissue stained with GIEMSA, GIMENEZ, MODIFIED ZIEHL-NEELSEN
  • Ddx: other causes of late abortions: Q fever, Campylobacter, Toxoplasma
  • Tx: oxytetracycline; vaccination will prevent abortions but not eliminate infections - vaccinate before breeding & annually to at least young females entering breeding herd or flock
  • Research complications: pregnant women should not handle aborted tissues
156
Q

Chlamydophilal Polyarthritis of Sheep

A

-Chlamydophila pecorum - nonmotile, obligate intracellular G(-) bacterium; causes acute polyarthritis & conjunctivitis in growing and nursing lambs
-Clin signs: lameness, esp of major joints - scapulohumeral, humeroradioulnar, coxofemoral, femorotibial,
and tibiotarsal; anorexia, febrile, conjunctivits; usually resolves in ~4 weeks; joint inflammation usually resolves without chronic articular changes
-Transmission: direct contact, contaminated feed or water; organisms penetrates GI tract and migrates to joints & synovial membranes & conjunctiva
-Necropsy: lesions in joints, tendon sheaths, conjunctiva, lungs; edematous & hyperemia sites with fibrinous exudates, but without articular changes, mononuclear cell infiltrate; lung lesions include atelectasis and alveolar inspissation
-Dx: clin signs; synovial taps & smears
-Tx: oxytetracycline (parenteral)

157
Q

Chlamydophilal Conjunctivitis (Infectious Keratoconjunctivitis; ‘Pinkeye’)

A

-Chlamydophila psittaci & Chlamydophila pecorum = most common causes of infecitous keratoconjunctivits in sheep
-Chlamydophila & Mycoplasma most common causes of infectious keratoconjunctivitis in goats
-Clin signs: early stage photophobia, conjunctival hyperemia, epiphora, edema; later stages ulceration & opacity; perforation may results from ulceration; in less severe cases, corneal healing assoc w/ fibrosis & neovascularization occurs in 3-4 days; associated lymphoid tissue enlargement may prolapse eyelids; morbidity 80-90%; bilateral & symmetrical infections in most outbreaks; relapses may occur; other concurrent systemic signs incl polyarthritis, abortion in sheep; polyarthritis, mastitis, uterine infx in goats
-Transmission: direct contact; mechanical vectors like flies
-Necropsy: usually does not result in mortality
-Ddx: Mycoplasma conjunctiva,
Mycoplasma agalactiae in goats, Moraxella (Branhamella,
Neisseria) ovis, and Colesiota conjunctivae (a rickettsialike
organism); eyeworms, trauma, foreign bodies (pollen, dust, poor-quality hay)
-Control: minimize sources of mechanical irritation; provide shade; quarantine new animals & treat before introduction into flock or herd
-Tx: infections self-limiting in 2-3 weeks; topical tetracycline ophthalmic ointments; systemic or oral oxytetracycline may be used with ophthalmic treatment; atropine added when uveitis present

158
Q

Anaplasma

A
  • Anaplasma marginale - cattle
  • Anaplasma ovis - sheep & goats
  • Relatively rare transmissible hemolytic disease
  • Clin signs: Developmental stage = acute anemia, weakness, pallor, lethargy, dehydration, anorexia; incubation may be as long as 3-8 weeks; most clin signs occur during 4-9 day developmental stage - death most likely to occur during this stage or beginning of convalescent stage; death may also occur d/t anoxia b/c animal unable to handle stress or exertion; Convalescent stage = reticulocytosis; morbidity high, mortality low
  • Carrier stage = time in the convalescent stage when animal host becomes reservoir of the disease & parasitemia is not discernable
  • Dx: clin signs, necropsy; serology - complement fixation, rapid card tests - become positive after incubation phase; stain thin blood smears with WRIGHT’S or GIEMSA = basophilic spherical A. marginale bodies near RBC peripheries
  • Transmission: common in cattle in southern & western US & other tropical/subtropical areas; mechanical transmission - passed on mouth parts of seasonal biting flies, mosquitos, instruments like dehorners; biological transmission by Dermacentor andersoni & Dermacentor occidentalis ticks; recovered animals are disease reservoirs
  • Necropsy: pale tissues, watery thin blood; splenomegaly, hepatomegaly, gall bladder distension
  • Ddx: babesiosis
  • Control: offspring of immune carriers resist infx up to 6 months of age; vector control & hygiene; vaccination - not entirely effective - can still be infected & become carriers; do NOT VACCINATE PREGNANT cows = neonatal isoerythrolysis; no A. ovis vaccine; identify carriers via serology; interstate movement of infected animals is regulated
  • Tx: single dose of long-acting tetracycline reduces severity of infx during developmental stage; other tetracycling treatment programs for carriers
159
Q

Babesiosis (Red Water, Texas Cattle Fever, Cattle Tick Fever)

A

-Babesia bovis & Babesia bigeminia - intraRBC protozoans; one of the most impt arthropod-borne diseases of cattle; prevalent in tropical/subtropical areas worldwide; not seen in smaller ruminants in US
-Clin signs: liver & kidney failure d/t hemolysis with icterus, hemoglobinuria, fever; acute encephalitis with fever, ataxia, depression, conscious proprioceptive deficits, mania, convulsions, coma - Encephalitic form = poor prognosis; sudden death
-Dx: GIEMSA stain blood smear = Babesia trophozoites; complement fixation, immunofluorescent antibody, ELISA
-Transmission: ticks of Boophilus genus; some wild ruminants - white-tailed deer, American buffalo - are susceptible; Bos indicus are resistant; stress can cause disease development
-Necropsy: acute hemolytic crisis = hepatomegaly, splenomegaly, dark & distended gallbladder, pale tissues, thin blood, scattered hemorrhages, petechiation; animals dying after longer course of dz will be emaciated, icteric w/ thin blood, pale kidneys, enlarged liver
-Ddx: anaplasmosis, leptospirosis, copper toxicity and bacillary hemoglobinuria are differentials for the hemolytic form; encephalitic presentation include rabies, nervous system coccidiosis, polioencephalomalacia, lead poisoning, IBR,
and salt poisoning
-Control: control ticks, clean equipment; vaccination in South America & Australia, not available in US
-Tx: supportive care - transfusions; most common medications include diminazene diaceturate, diisethionate, and imidocarb dipropionte
-Research complications: REPORTABLE in US

160
Q

Coccidiosis in ruminants

A

-Phylum Apocomplexa = obligate intracellular parasites
-Complex life cycle with sexual & asexual reproduction in GI enterocytes; sheep, goats, & cattle affected by several species of Eimeria - species are host-specific & host-cell specific
-Clin signs: hemorrhagic diarrhea, esp in young ruminants; diarrhea develops 10 days to 3 weeks after infection; tenesmus, rectal prolapse, anorexia, weight loss, dehydration, anemia, fever (infrequent), depression weakness; intestinal hemorrhage - anemia, hypoproteinemia
-Dx: clin signs, history, fecal float (salt or sugar solution); prepatent period is 2-3 weeks
-Transmission: subclinically infected adults are reservoir; young animals ingest sporulated oocysts - severity of disease correlated with # ingested; remain viable for long periods in moist, shady conditions; isolated outbreaks may occur in adults related to stress
-Necropsy: ileitis, typhlitis, colitis w/ necrosis, hemorrhage; mucosal scrapings show oocysts
-Ddx: acute diarrhea in young ruminants: cryptosporidiosis, colibacillosis, salmonellosis,
enterotoxemia, viral diarrheas, and other intestinal parasites such as helminths
Control: sanitation of maternity & young stock housing; supportive care; coccidiostats preferred to coccidiocidals b/c allow immunity to develop - sulfonamies, amprolium may aid tx in addition to decoquinate, lasalocid, monensin

161
Q

Cryptosporidiosis

A
  • Cryptosporidium - very common cause of diarrhea in young ruminants; at least 16 species, more than 40 genotypes; multiple host species; ZOONOTIC
  • Clin signs: protracted malabsorptive diarrhea - may last only 6-10 days or be persistent & fatal; tenesmus, anorexia, weight loss, dehydration, depression; morbidity high, mortality variable
  • Dx: mucosal scrapings, fixed tissue histo, oocysts on fecal float, iodine-stained feces, PAS or methenamine silver stained tissues; STAINS RED W/ KINYOUN OR ZIEHL-NEELSEN stain; fecal IFA
  • Transmission: usually affected btwn 5-10 days of age for lambs & kids, less than 30 days old for calves; shed sporulated oocysts immediately infective; diarrhea & oocyst shedding occur within 2-7 days of exposure; oocysts extremely resistant to desiccation in environment - may survive in soil for months; autoinfection within lumen of intestines may occur & cause persistent infx; cattle frequently subclinical or asymptomatic carriers = all cattle should be assumed Cryptosporidium positive
  • Necropsy: emaciation; enteritis, hyperplasia of crypt epithelial cells with villous atrophy, villous fusion - primarily of lower small intestines; organim at APICAL MARGIN OF ENTEROCYTES = INTRACELLULAR EXTRACYTOPASMIC PARASITOPHOROUS VACUOLE
  • Ddx: disinfection with bleach or 5% ammonia; don’t powerwash b/c will spread oocysts; clinical cryptosporidiosis often assoc w. failure of passive transfer
  • Tx: halofuginone lactate approved in Europe; nitazoxanide & paromomycin approved in humans but not veterinary spp; supportive care
  • Research complications: ZOONOTIC; easily spread from calves to humans
162
Q

Giardiasis

A
  • Giardia lamblia (G. intestinalis, G. duodenalis) - flagellate protozoal worldwide diarrhea in mammals & some birds
  • Clin signs: diarrhea continuous or intermittent; pasty or watery, yellow, may contain blood; fever, dehydration, depression; chronic cases - ‘poor doer’, weight loss, unthrifty
  • Dx: motile trophozoites in fecal mounts; oval cysts floated wth zinc sulfate (33%) solution - standard solutions tend to be too hyperosmotic and distory cysts; ELISA, IFA
  • Transmission: young animals more susceptible; prevalent in beef & dairy calves in North America; calves typically do not develop diarrhea until after 4 weeks of age; fecal-oral transmission; wild animals may serve as reservoirs
  • Necropsy: generally doesn’t result in necropsy
  • Control: intensive housing & warm environments minimized; cysts can survive in environment long periods but susceptible to desiccation; effective disinfectants = bleach (1:16 or 1:32), quaternary ammonium, steam, boiling water
  • Tx: oral metronidazole; benzimidazole anthelmintics effective but not approved for use in animals for this purpose
  • Research complications: ZOONOTIC
163
Q

Neosporosis

A

-Neospora caninum - common, worldwide protozoa; neonatal disease in lambs, kids, calves; abortions in sheep, goats, cattle
-Clin signs: abortion only sign in adult cattle - sporadically, endemically, or as abortion storms btwn 3-7th month gestation; decreased milk production in congenitally infected cows; calve born aymptomatic, rare clin signs of weakness that resolves, exophthalmus or asymmetric eyes, weight loss, ataxia, hyperflexion or hyperextension of all limbs, decreased patellar reflexes, conscious proprioception deficits, opisthotonus, seizures
-Dx: IHC & histopath of fetal tissues; serology - IFA,ELISA; titers of dams elevated at time of abortion; fetal serology influenced by stage of gestation and course of infection; no tests predictive of disease
-Transmission: widespread in dairy and beef herds; common cause of abortion in cattle; definitive host is dog -infective oocysts shed in canine feces; placental/abortive tissues sources of infection & may play minor role in transmission to intermediate hosts, including ruminants, deer, horses; transplacental transmission causes perpetuated latent lifelong infx; seropositive immunity NOT protective from future abortions; many seropositive animals never abort or have clin signs
-Necropsy: autolyzed aborted fetuses - tissue cysts most common in brain; cysts & tachyzoites cannot be distinguished from T. gondii = requires ultrastructural microscopy or IHC, PCR, etc.
-Ddx: Abortion: leptospirosis,
BVDV, IBRV, salmonellosis, and campylobacteriosis; BVDV esp for abortion storms; Weak calves: BVDV, perinatal hypoxia following dystocia,
bluetongue virus, Toxoplasma, exposure to teratogens, or
congenital defects
-Control: eliminate contact with contaminated dog feces; recent vaccine but efficacy not well-established
-Tx: no known tx

164
Q

Sarcocystosis

A

Sarcocystis - cyst-forming sporozoan; separate species infect sheep, goats, cattle; definitive hosts are carnivores, all ruminants are intermediate hosts

  • Clin signs: parasite encysts in soft tissues; usually asymptomatic; fever, ataxia, symmetric lameness, tremors, tail switch hair-loss (‘rat tail’), excessive salivation, diarrhea, weight loss; abortions in 2nd trimester in cattle; small ruminants abort ~28 days after ingestion of sporulated oocysts; encephalomyelitis in sheep, wool loss
  • Dx: merozoites & meronts in fetal neural tissue lesions = definitive dx
  • Transmission: infection rates very high in US cattle; ingestion of feed or water contaminated by feces from dogs (species infecting smaller ruminants) or cats, dogs, primates (species infecting cattle)
  • Necropsy: autolyzed aborted fetuses; lesions in neural tissues - meningoencephalomyelitis, focal malacia, perivascular cuffing, neuronal degeneration, gliosis most marked in cerebellum & midbrain; sarcocysts (grains of rice) in skeletal or cardiac muscle
  • Pathogenesis: ingestion of muscle flesh from infected ruminant results in intestinal infx & sarcocystic shedding in feces as sporocysts by definitive hosts - sporocysts eaten by ruminant -several stages of development occur in endothelial cell arteries, culminating in merozoites that enter soft tissue & encyst
  • Control: protect feed supplies from fecal contamination; prevent carnivores from accessing carcasses
  • Tx: monensin fed during incubation is prophylactic but efficacy in clinically affected cattle unknown; amprolium fed prophylactically in cattle & sheep reduces illness
165
Q

Toxoplasmosis

A

-Toxoplasma gondii - obligate intracellular protozoan; cats are only definitive host & several warm blooded animals, including ruminants, are intermediate hosts
-Major cause of abortion sheep & goats; less common in cattle
-Clin signs: placentitis, abortion, stillbirths, weak young; pneumonia, nonsuppurative encephalitis; infx of ewe during 1st trimester = abortion, infx of ewe during 3rd trimester = weak or normal lambs w/ subsequent high perinatal mortality; congenitally infx lambs = circling, incoordination, muscular paresis, prostration; adult goats may die, adult sheep no systemic illness
-Dx: serology - fetal thoracic fluid best sample; IHA, IFA, latex agglutination, ELISA; crescent shape tachyzoites in impression smear of post mortem tissue
-Transmission: ubquitous; ruminants ingest cat feces; cats ingest tissue cysts from intermediate hosts
-Necropsy: placental cotyledons contain multiple small white areas of necrosis, edema, calcification; fetal brain coagulative necrosis, nonsuppurative encephalomyelitis, pneumonia, myocarditis, hepatitis; GIEMSA STAIN impression smears of retina, myocardium, liver, kidney, brain = rapid dx; organism in tissue sections (brain, heart)
-Pathogenesis: felids ingest cyst stage in mammalian tissues, oocysts in feces, or transplacental transfer; infected cats shed oocysts in feces for few weeks; ruminants ingest sporulated oocyst contaminated feed/water; ingested sporozoite invades bloodstream & migrates to brain, liver, muscle, placenta; placental infx develops 14 days after ingestion of oocysts
-Ddx: Neospora caninum, Campylobacter, Chlamydophila,
and Query Fever
-Control: control feline populations on farms; sporulated oocysts can survive in soil & other places for long periods, resistant to desiccation and freezing; vaccines for abortion prevention available in NZ & Europe for sheep
-Tx: tx ineffective, but feeding monensin during pregnancy may be helpful; monensin NOT APPROVED IN US
-Research complications: ZOONOTIC

166
Q

Trichomoniasis

A
  • Tritrichomonas (Trichomonas) fetus - large, pear shaped flagellated protozoan; obligate parasite of bovine repro tract; in US primarily seen in western beef herds
  • Clin signs: infertility - low pregnancy rates, periodic pyometras, abortions in first half of gestation; abortion rate from 5-30%; causes no systemic signs; affected cows clear infection over a span of months & maintain immunity for about 6 mths but bulls may become chronic carriers
  • Dx: infertility & pyometra; trichomonads may be identified or cultured in preputial smegma, cervicovaginal mucus, uterine exudates, placental fluids, abomasal contents of aborted fetuses; culturing requires SPECIFIC MEDIA - DIAMOND’S OR MODIFIED PASTRIDGE
  • Transmission: venereal exposure from breeding bulls or cows; contaminated breeding equipment
  • Necropsy: pyogranulomatous bronchopneumonia of fetuses & placentitis, may be seen in aborted material; fetal lung and placenta most useful for culturing
  • Ddx: campylobacteriosis
  • Control: bacterin vaccine available; AI reduces but does not eliminate disease; use of younger vaccinated bulls is recommended in all circustances; cull chronically infected bulls
  • Tx: imidazole compounds effective, but their use not permitted in food animals in US; therapeutic immunizations
  • Research complications: should be considered whenever natural service is used & fertility problems occur
167
Q

Gastrointestinal nematodiasis

A

-Major helminths may result in gastroenteritis assoc w/ intestinal hemorrhage, malnutrition
-Disease associated with grazing exposure to infective larvae
-Generally older animals develop resistance to some of the species; animals btwn 2 months and 2 years of age are most susceptible
-Infection in younger animals is a major contributor to a cycle of poor nutrition & digestion, compromised immune responses, impaired growth & development
-Dx: fecal flotation, but many appear similar so may need to hatch eggs and identify larvae; prepatent period for most nematodes ins 2-3 weeks
-Nematodes with highest potential for pathogenicity: Sheep & Goats = Haemonchus contortus (Barber-pole worm), Teladorsagia (formerly Ostertagia) circumcincta (Medium stomach
worm), Cooperia (Small intestinal worms), Trichostrongylus spp. (Hair worms), Oesophagostomum columbianum (Nodule worm disease, pimply gut), Cooperia curticei, and Strongyloides pappilosus
Cattle = Haemonchu placei, Ostertagia ostertagi, Trichostrongylus axei, Cooperia spp., Strongyloides
spp., and Oesophagostomum spp
-Trichostrongyles such as Ostertagia, Haemonchus, Trichostrongylus, Cooperia,
Dictyocaulus, and Oesophagostomum may undergo seasonal
hypobiosis or arrested development of the lifecycle
-In northern hemisphere, larvae arrest & accumulate inside grazing animals in the fall, allowing the parasite to overwinter in the animal protected from winter pasture conditions
-Rotation of anthelmintics d/t inherent resistance development & appropriate pasture management are key principles in parasite control

168
Q

Dictyocaulosis (Lungworms)

A
  • Sheep = Dictyocaulus filaria, Protostrongylus rufescens, and Muellerius capillaris
  • Goats = Dictyocaulus
  • Cattle = Dictyocaulus viviparus is only lungworm found in cattle
  • Infections in US tend to be assoc w/ cool, moist climates
  • Lungworms induce a severe parasitic bronchitis (‘husk’, verminous pneumonia) in sheep ~2-18 months old
  • Sheep & cattle display coughing, dyspnea, nasal discharge, weight loss, unthriftiness, occasionally fever
  • Dx: clin signs, identifying larvae in feces - Baermann technique - or adults in lung tissue
  • Dictyocaulus has direct life cycle = adult worms reside in large bronchi, produce embryonated eggs that are coughed up & swallowed - eggs then hatch in the intestines & larvae are expelled in the feces; expelled larvae infectious in ~7-10 days; after ingestion, penetrate intestinal mucosa & move through lymphatics & blood into lungs - develop into adults in about 5 weeks
  • Protostrongylus & Muellerius require snail or slug intermediate host
  • Necropsy: bronchiolitis, bronchitis, atelectasis, hyperplasia of peribronchiolar lymphoid tissue
  • Control: appropriate pasture management to minimize exposure of young, susceptible animals; elimination of intermediate hosts impt for sheep & goat pastures; infected animals can be treated with invermectins, milbemycins, levamisole; effective irradiated larval vaccine in UK & Western Europe
169
Q

Parelaphostrongylus tenuis (Meningeal Worm, Brain Worm)

A
  • Paraelaphostrongylus tenuis - nematode parasite common to white tailed deer
  • Sheep, goats, camelids, elk, caribou, moose may be aberrant hosts
  • Adult worms in meningeal tissue lay eggs that develop into first stage larvae - migrate through bloodstream into lungs - larvae coughed up, swallowed, expelled in feces where ingested by snails & slugs - develop into 2nd and 3rd stage larvae - large animals ingest gastropods & larvae migrate to brain
  • Clin signs: rare in white tailed deer; can be severe in aberrant hosts - paraplegia; goats can develop vertically oriented pruritic skin lesions on neck, shoulders, back
170
Q

Moniezia expansa, Thysanosoma actinoides

A
  • Tapeworms - rarely of clinical or economic importance
  • Young animals with heavy infx: pot bellies, constipation, mild diarrhea, poor growth, rough coat, anemia
  • Moniezia expansa, less commonly Moniezia benedini, inhabit small intestines of grazing ruminants
  • Thysanosoma actinoides (fringed tapeworm) - lives in duodenum, bile duct, pancreatic duct of sheep & cattle raised primarily west of Mississippi River
  • All have indirect life cycles
  • No clinical signs usually seen
  • Thysanosoma infx may result in liver condemnation at slaughter
  • Dx: segments of worms in feces or triangular-shaped eggs on fecal float
  • Tx: albendazole
171
Q

Abdominal or Visceral Cysticercosis & Echinococcosis (Hydatid Cyst Disease)

A
  • Tapeworme eggs from primary host contain an oncosphere - hatches & penetrates intestinal wall when ingested by intermediate host
  • 2nd stage larvae develops in intermediate host - called metacestode = space occupying cystic structure
  • Metacestode forms are tapeworm specific & include the cysticercoid (microscopic & in small intermediate hosts like mites); cysticercus (small blister to ping pong ball sized); coenurus (usually intracranial in host); hydatid cysts (usually intraabdominal in host)
  • Coenurus & hydatic cyst can be quite large
  • When metacestode form ingested by primary host, the larval brood capsules containing protoscolices evaginate to form the tapeworm head (scolex)
  • Abdominal or visceral cysticercosis is occasionally found at ruminant slaughter
  • ‘Bladder worms’ typically affect liver, peritoneal cavity & are caused by larval form (metacestode) of Taenia hydatigena - common tapeworm of dogs
  • Larval intermediate of Echinococcus granulosus may form hydatid cysts in liver or lungs
  • Ruminants are intermediate hosts; infected by feed or water contaminated with gravid segments or ova
  • Clin signs: anorexia, hyperthermia, weight loss d/t larval migration; usually asymptomatic
  • Dx: usually seen at necropsy or slaughter; may lead to condemnation of carcass
  • Control: minimized exposure to canine feces-contaminated feed & water
172
Q

Coenurosis (Gid)

A
  • Coenurus cerebralis - larval form of Taenia multiceps dog tapeworm
  • Rare condition called Gid; occurs in ruminants and other mammals
  • Larval parasite, ingested from feces contaminated food/water, invades brain and spinal cord & develops as a bladderworm that causes pressure necrosis in nervous tissues
  • Clin signs: hyperesthesia, meningitis, paresis, paralysis, ataxia, convulsions
  • Dx: usually made at necropsy
  • Control: eliminating transfer from canid hosts
173
Q

Fascioliasis (Liver Fluke Disease)

A
  • Important cause of acute and chronic dz in grazing sheep & cattle
  • Fasciola hepatica in southern & western US; Fascioloides magna in Texa, Gulf coast, Great Lakes, northwestern states where ruminants share pasture with deer, elk, moose
  • Dicrocoelium dendriticum in eastern US, Atlantic Canada, occasionally Europe, Asia
  • Liver fluke eggs based in bile & feces - hatch in 2-3 weeks to form free-swimmin miracidia - each fluke egg represents sources of potentially thousands of cercariae & metacercariae - miracidia penetrate body of intermediate host (snails) - develop through sporocysts & rediae stages to cercariae - cercariae leave intermediate hosts, swim to grassy vegetation & become dormant cyst-like metacercariae on grass for 6 mths or longer - ingested by ruminants, penetrate small intestinal wall, migrate through abdominal cavity to liver where they locate in a bile duct, mature & remain for up to 4 years
  • Clin signs: Acute disease: migration of liver flukes leads to liver inflammation, hemorrhage, necrosis, fibrosis; F. magna can be fatal in sheep & goats from just one larva tunneling in liver; in cattle often asymptomatic; liver fluke damage may predispose to Clostridium species (C. novyi) invasion = Black Disease, hemoglobinuria; Chronic disease: cholangiohepatitis, blood loss in bile & anemia, hypoproteinemia; increased gamma glutamyl transferase (GGT), persistent eosinophilia; anorexia, weight loss, unthriftiness, edema, ascites
  • Necropsy: pale, friable livers, may have distinct migration tunnels along serosal surfaces; enlarged bile ducts with areas of fibrosis
  • Dx: clin signs, necropsy; blood chemistry suggestive of liver dz & eosinophilia
  • Tx: reduce intermediate host population, treat affected animals
  • Tx: albendazole or clorsulon
174
Q

Mange

A
  • Genera Sarcoptes, Psoroptes, Chorioptes, Demodex
  • Clin signs: flaking, itching, pruritis, skin damage, self-mutilation; papules, crusts, alopecia, secondary dermatitis; more severe cases - anemia, disruption of reproductive cycles, increased susceptibility to other diseases
  • In US, Sarcoptes & Psoregates = REPORTABLE; these mites cause severe signs in cattle, sheep, goats
  • Dx: skin scraping, clin signs, response to therapy
  • Chorioptic Mange = ‘barn ithc’, ‘leg mange’; common in ruminants in winter months; Chorioptes bovis, C. ovis, C. caprae relatively specific to hosts & do not invade epidermal tissue - feed off dead skin; lower limbs, tail, perineum, scrotum most often affected; variable pruritis, papules, crustiness, alopecia
  • Tx: insecticides like coumaphos, diazinon, lime sulfer traditionally; now macrocyclic lactone anthelmintics - injection or topical
  • Demodectic Mange = relatively uncommon in cattle, sheep, goats; nodualr lesions around face, head, shoulders; no effective treatment
  • Ddx: pediculosis
  • Psoroptes cuniculi: Psoroptic Mite - common in goat ear canals & causes head shaking and scratching
175
Q

Pediculosis (Lice)

A
  • Order Mallophaga, Genus Damalina = biting or chewing lice
  • Order Anoplura, Genus Linognathus = sucking lice
  • Wingless insect; seasonal (winter to spring) chronic dermatitis; generally species specific
  • Clin signs: pruritis, alopecia, excoriation; hairballs from overgrooming in cattle; anemia, weight loss, damaged wool in severe cases in sheep; damaged pelts; young animals with severe cases - anemia, death; pregnant animals with severe cases - abortion; foot louse - lameness
  • Transmission: direct contact, attachment to flies or fomites
  • Biting or chewing lice inhabit host’s face, lower legs, flanks & feeding on epidermal debris & sebaceous secretions
  • Sucking lice inhabit host’s neck, back & feed on blood
  • 3 nymphal stages (instars) between egg and adult; cannot survive for more than few days off host
  • Ddx: mites
  • Tx: insecticides - coumaphos, dichlorvos, crotoxyphos, avermectin, pyrethroids; only products approved for lactating or dry dairy should be used on female dairy animals >20 mths old; must repeat treatment at least twice at intervals appropriate for nit hatches (~every 16 days); fall treatment useful in managing infection; systemic treatment contraindicated in cattle when there may be concurrent larvae of cattle grubs (Hypoderma lineatum, Hypoderma bovis); back rubbers with insecticides for self-treatment; sustained release insecticide-containing ear tags
176
Q

Ticks (Arachnids)

A
  • Ruminants susceptible to many species of Ixodidae (hard shell ticks) & Argasidae (soft-shell ticks)
  • Can transmit anaplasmosis, babesiosis, Q fever
  • Clin signs: decreased productivity, loss of blood & blood protein, transmission of diseases, debilitation, death; Tick Paralysis - ascending paralysis that may lead to death if tick no removed before paralysis reaches respiratory muscles
  • Dx: identification of species
  • Transmission: ticks are not as host specific as lice; classified as one-host, two-host, or three-host ticks - based on whether they drop off the host between larval & nymphal stages to molt
  • Tx: systemic or topical insecticides
177
Q

New World Screwworm

A
  • Cochliomyia hominivorax - parasitic fly whose larvae eat living tissue of warm-blooded animals
  • Eradicated in US; present in New World topics, Mexico, Central America
  • REPORTABLE to state veterinarian
178
Q

Nasal Bots (Nasal Myiasis, Head Grubs)

A
  • Oestrus ovis: botfly, larval forms cause chronic rhinitis, sinusitis
  • Botfly deposits eggs around nostrils of sheep - ova hatch & larvae migrate throughout the nasal cavity & sinus, feeding on mucus and debris; in 2-10 months, larvae complete growing phase, migrate back to nasal cavity, sneezed out - mature larvae penetrate soil, pupate for 1-1.5 mths & emerge and botflies
  • Clin signs: stamping, snorting, sneezing, rubbing nose; hypersensitivity to larvae can occur; mucopurulent nasal discharge
  • Necropsy: larvae in nasal cavity or sinuses; mild inflammatory rxn, mucosal thickening and exudates
  • Dx: observing behaviors or identifying organisms
  • Up to 80% of flock potentially infected
  • Tx: invermectins, other insecticides - treat in early fall when larvae are small; fly repellents may prevent additional infectiong
179
Q

Sheep Keds (‘Sheep Tick’)

A
  • Melophagus ovinus - flat, brown blood-sucking wingless fly; adult fly lives entirely on skin of sheep
  • Female flies mate & produce 10-15 larvae after gestation of 10-12 days - larvae attach to wool - pupate for about 3 weeks; adult female feeds on blood & lives 5-6 weeks
  • Infx highest in fall & winter
  • Clin signs: pruritis around neck, sides, abdomen, rump; anemia
  • Keds can transmit Bluetongue virus
  • Dx: gross or microscopic identification
  • Tx: ivermectin, other insecticides
180
Q

Dermatophytes (Ringworm)

A
  • Genuses Trichophyton & Microspoum
  • Sheep = T. mentagrophytes, T. verrucosum
  • Goats = T. metagrophytes, M. canis, M. gypseum, T. verrucosum
  • Cattle = T. verrucosum
  • Clin signs: multiple gray, crusty circumscribed hyperkeratotic lesions around head, neck, ears; in goats & cattle, lesions will extend down neck; in cattle lesions develop particularly around eyes & on thorax; hair shafts become brittle and break; intense pruritis
  • Dx: microscopic identification of hyphae & conidia on hairs following skin scraping & 20% potassium hydroxide digestion; Dermatophyte Test Medium (DTM) culture most reliable dx method - use broken hairs or periphery of lesion
  • Transmission: younger animals more susceptible; risk factors = crowding, indoor housing, warm & humid conditions, poor nutrition; direct contact or fomites
  • Tx: spontaneous recovery occurs in 1-4 months; immune mechanisms not well understood & immunity may not be long duration; recovery enhanced by sunlight, correcting nutritional deficits, improve housing and ventilation; topical tx = 2-5% lime sulfur, 3% Captan, iodophores, thiabendazole, 0.5% sodium hypochlorite; severe case - systemic griseofulvin
  • Control: reassess living situation, particularly crowding, sanitation, nutrition; clean & disinfect pens
  • Research Complications: ZOONOTIC
181
Q

Entropion

A
  • Inverted eyelids
  • Common inherited disorder in lambs & kids of most breeds
  • Generally lower eyelid is affected - turns inward = tearing, blepharospams, photophobia initially; progress to corneal ulcers, perforating ulcers, uveitis, blindness
  • Tx: suture or staple in lower eyelid & cheek to anchor lid in everted position
182
Q

Beta Mannosidosis of Goats

A
  • Autosomal recessive lysosomal storage disease
  • Affects kids of Nubian breeds
  • Clin signs: intention tremors, difficulty or inability of newborns to stand; characteristic flexion of carpal joint & hyperextension of pastern joint; born deaf; domed skull, small narrow muzzle, enophthalmus, depressed nasal bridge
  • Carrier adults can be identified by plasma measurement of beta mannosidase activity
183
Q

Congenital Myotonia of Goats

A
  • ‘Fainting’ goats
  • Inherited autosomal dominant disease - affects voluntary striated skeletal muscles
  • Fainting is actually transient spasms of skeletal musculature brought about by visual, tactile, or auditory stimuli; contractions sustained for up to 1 min
  • Kids exhibit condition by 6 weeks of age
  • Males have more severe clinical signs than females
184
Q

Polled Intersex Goats

A
  • Western European goat breeds: Saanen, Alpine, Toggenburg
  • Genetic relationship between polled (hornless) phenotype & intersex (hermaphrodite) characteristics
  • Gene deletion on chromosome 1 = affects regulation of horn bud & fetal ovarian development, resulting in genetically female animals with masculine characteristics = enlarged clitoris, decreased anogenital distance, muscular neck development
  • Animals are infertile
  • Testosterone production often results in characteristic male odor & aggressive behavior
185
Q

Congenital Erthyropoietic Porphyria (CEP)

A
  • Rare autsomal recessive disease of cattle - primarily in Holsteins, Herefords, Shorthorns
  • Homozygous recessive animals: reddish-brown discoloration of teeth and bones, discolored urine, general weakness, failure to thrive, photosensitization, photophobia
  • Porphyrins are excreted in varying amounts in the urine - discoloration fluoresces under Woods lamp
  • Bones are fragile; regenerative anemia d/t shortened lifespan of RBCs d/t accumulation of porphyrins
  • Associated with low activity of an essential enzyme - uroporphyrinogen III synthase, in the porphyrin-heme synthesis pathway in erythrocytic tissues
  • Heterozygotes may have milder clin signs
186
Q

Other inherited conditions of cattle

A
  • Leukocyte adhesion deficienct, citrullinemia of Holstein cattle = models of genetic disease
  • Syndactyly, complex vetebral malformation in Holstein & other breeds, arthrogryposis multiplex in Angus, lysosomal storage diseases (alpha-mannosidosis) in beef breeds; progressive degenerative myeloencephalopathy (‘weaver’) in Brown Swiss
  • Inherited periodic spasticity (‘crampy syndrome’) - relatively common in dairy breed, esp Holsteins; develop muscle spasms in hip & upper leg btwn 3-8 yrs of age; during spasm, animal will typically extend or flex one rear leg & shake the leg for 15-30 sec - disease is progressive over course of 1-2 years, thought to be transmitted by a single recessive gene
187
Q

Congenital Dyshormonogenetic Goiter of Sheep

A
  • Defect in synthesis of thyroid hormone in Merino sheep
  • Autosomal recessive disease in Corriedale, Dorset Horn, Merino, Romney sheep & Saanen dwarf goats
  • Clin signs: lambs & kids born with defect have enlargement of thyroid gland, silky appearance to wool, high mortality; edema, bowing of legs, facial abnormalities; immaturity of lungs at birth causes neonatal respiratory distress & results in dyspnea & respiratory failure
188
Q

Spider Lamb Syndrome (Hereditary Chondrodysplasia)

A
  • Inherited, often lethal, musculoskeletal disorder primarily occurring in Suffolk & Hampshire breeds
  • Severely affected lambs die shortly after birth
  • Animals that survive perinatal period develop angular limb deformities, scoliosis, facial deformities
  • Dx: clin signs (similar to Marfan syndrome in children)
  • Long term survival rare; tx unsuccessful
189
Q

Other inherited conditions of sheep

A
  • Gangliosidosis (β-galactosidase deficiency): Suffolk & Coopworth-Romney sheep
  • Gamma-glutamyl carboxylase deficiency: Rambouillet
  • Globoid cell leukodystrophy (Krabbe’s disease, galactocerebroside beta-galactosidae deficiency): polled Dorset
  • Ceroid lipofuscinosis: South Hampshire, Swedish Landrace, Rambouillet
  • Neuraxonal dystrophy: Suffolk
  • Primary cerebellar degeneration: Merino, Charollais
190
Q

Abomasal, Duodenal Ulcers

A
  • More frequently in preweaned beef calves & adult dairy cattle than in sheep or goats
  • Assoc w/ abrupt dietary changes, stress d/t crowding, transport, parturition
  • Concurrent dz: Salmonella, Bluetongue, C. perfringens abomasitis or overuse of NSAIDs, in older cattle abomasal lymphoma
  • Ulcers classified as perforating or nonperforating; nonperforating then classified as bleeding or nonbleeding
  • Cin signs: Non-Perforating: reduced feed intake, decreased milk production, chronic hemorrhage leading to anemia; dark feces, melena, abdominal pain, arched back, restlessness, kicking at abdomen, bruxism, anorexia; Perforated: peritonitis more common than hemorrhage; may be asymptomatic in calves
  • Dx: fecal occult blood test; marked elevation in BUN with normal serum creatinine indicates bleeding ulcer
  • Tx: GI protectants, antihistamines; iron injections & anabolic steroids for anemia
  • Prevention: minimize stress to calves, strive for BLV free herd
191
Q

Abomasal Empyting Defect

A
  • Sporadic syndrome of sheep; Suffolf tend to be predisposed, also seen in Hampshires, Columbia, Corriedales
  • Mechanism of disease unknown; may be d/t defect in autonomic nervous system, dyautonomia, possible neurotoxicosis
  • Clin signs: abomasal distension -ventral abdominal distension, weight loss with normal appetite & normal feces
  • Dx: history, clinical signs; elevations in rumen chloride (>15 mEq/L); radiography or US may show distended abomasum
  • Eventually fatal
  • Tx: metoclopramide, mineral oil may be helpful in early disease
192
Q

Abomasal Displacement

A

-Sporadic disorder usually assoc w/ dairy cows in early lactation
-Left displacemnt (LDA) more common (90%); RDA may be further complicated by right abomasal volvulus (RAV), a surgical condition
-DA occurs b/c of gas accumulation in abomasum, often assoc w/ periparturient hypocalcemia, allowing abomasum to migrate up from its normal ventral location
-Clin signs: anorexia, lack of cud chewing, decreased ruminations, shallow respirations, increased heart rate, abdominal pain, decreased milk production
Dx: tympanic resonance during auscultation-percussion of lateral to ventro-lateral abdomen, ruminal displacement, clin signs; hypoglycemia, ketonuria, mod to severe electrolye & acid-base abnormalities
-Risk factors: parity (multiparous cows have higher incidence), twinning, breed, season (higher incidence in winter), ‘lead feeding’ concentrate feeds, hypocalcemia, retained placenta, metritis, mastitis, body size, conformation, possible genetic predisposition
-Tx: surgical & nonsurgical correction - former has better change of permanent correction
-Prevention: reduce stress in periparturient period, greater care in feeding concentrates, reduce incidence of predisposing diseases

193
Q

Bloat (Rumen Tympany)

A
  • Frequently occurs in animals recently fed abundant quantities of succulent forages or grains
  • Two categories = Frothy Bloat vs. Free-Gas Bloat
  • Frothy Bloat assoc w/ ingestion of feeds that produce a stable froth not easily expelled from rumen; fermentation gases - CO2, methane - incorporate into froth eventually compromising respiration by limiting diaphragm movement; caused by fresh or dried legumes (alfalfa, clover) or cereal grains (corn, barely)
  • Free-Gas Bloat: more often related to rumen atony or physical problems with gas eructation -esophageal obstructions, positional, tumors, abscesses, enlarged cevical or thoracic LNs, vagal nerve paralysis or injury, traumatic reticulitis, hypocalcemia, CNS conditions
  • Clin signs: rumen distension in Left paralumbar fossa; colic-like abdominal pain, dyspnea
  • Tx: stomach tube for manual removal of gas - in frothy bloat foam may block tube - add mineral oil, surfactants, antifermentative compounds via the stomach tube to break down surface tension; in severe cases, can place trocar or surgical rumenotomy via left paralumbar fossa
  • Prevention: feeding management; feed poloxalene to decrease incidence of legume bloat; ionophors like monensin or lasalocid can reduce incidence of frothy bloat
194
Q

Lactic Acidosis -Acute or Subacute

A

-Acute: sudden engorgement on grains or other highly fermentable carbohydrates or by rapid diet change to one with high proportion of grain; common cereal grains, sugar beets, molasses, potatoes predispose to acidosis; proliferation of G(+) bacteria leading to rapid fermentation with increase in lactic acid production & decrease in rumen pH = G(-) bacteria die in large numbers and release endotoxin; high osmolarity of rumen contents results in accumulation of fluid & low pH and perturbed rumen microflora cause rumen mucosal inflammation
-Sequelae: rumenitis, abomasal ulcers, liver abscesses, lung abscesses leading to episodes of
epistaxis, laminitis from absorbed toxins, and polioencephalomalacia
from the inability of the altered rumen bacterial populations to produce sufficient B-complex
vitamins
-Clin signs: anorexia, depressed, weak; incoordination, ataxia, dehydration, hemocontration (hypovolemia & endotoxic shock); rapid pulse & respiration, diarrhea, abdominal pain, lamness, rumen bloat
-Rumen pH normally ~6.0 - may drop to <5.0; severe cases as low as 3.8; urine pH also becomes acidic, blood pH drops below 7.4
-Subacute ruminal acidosis (SARA syndrome): more subtle; intermittent anorexia, diarrhea, depressed milk fat percentage, sporadic epistaxis, increased incidence of laminitis; dx via rumenocentesis
-Necropsy: Acute = inflammation, swelling, necrosis of rumen papillae, abomasal hemorrhage & ulcers; Chronic or Subacute = parakeratosis of rumen papillae - blunt, thickened, rough; papillae dark in color, clump together; abscesses in lung & liver, stellate ruminal scars = previous episodes of acute acidosis
-Tx: severe carb engorgement = rumenotomy & evacuation of contents; mineral oil & antifermentatives; hypertonic saline is hypovolemic shock; bicarbonate, magnesism carbonate, mabnesium oxide antacids; oral tetracycline or penicillin to decrease G(+) bacteria; Subacute = correct ration formulation, give more fiber, incorporate sodium bicarbonate or sodium sesquicarbonate buffers into rations

195
Q

Traumatic Reticulitis-Reticuloperitonitis (Hardwarde Disease)

A

-Rarely seen in small ruminants; due to indiscriminate eating of cattle
-Clin signs: asymptomatic to severe, depending on penetration and damage by foreign object; early signs attributable to pain & rumen stasis - anorexia, listlessness, arched back, grunting when forced to move, painful response to pressure on xyphoid or pinching of withers, fever, decreased production, decreased ruminations, bloat, regurgitation, tachypnea, tachycardia; sudden death
-Prognosis poor when peritonitis becomes diffuse
-Necropsy: inflammation throughout cranial abdomen, malodorous peritoneal fluid accumulations, lesions at reticular sites of migration of foreign objects, pericarditis and/or cardiac puncture
-Consumed objects settle in rumen but are desposited in reticulum during digestive process - puncture reticular wall - localized inflammation or more generalized peritonitis
-Dx: clin signs, signs of chronic infection on hemogram; US, abdominocentesis
-Ddx: abomasal
ulcers, hepatic ulcers, neoplasia (such as lymphoma in
older animals or intestinal carcinoma), and cor pulmonale; systemic leptospirosis, internal parasitism; diseases causing sudden death
-Control: eliminated sharp objects in cattle feed or environments; adequately size magnets placed in feed-handling equipment; forestomach magnets placed at 6-8 months of age - only every place one magnet per animal - can use compass near xiphoid to check for presence of magnet
-Tx: forestomach magnet, confinement & nursing care, antibiotics; rumenotomy if severe

196
Q

Hypocalcemia (Parturient Paresis, Milk Fever)

A
  • High-producing multiparous dairy cows most susceptible - Jersey breed in particular; cows that have survived one episode are prone to recurrence
  • In sheep, occurs primarily in overweight ewes during last 6 weeks of pregnancy or first few weeks of lactation
  • Now as common in dairy goat; not common in beef cattle unless poor nutrition
  • Clin signs: Sheep = last 6 wks of pregnancy, muscle tetany, incoordination - esp hind limbs, paralysis, coma; Goats = bloat, weak, unsteady, eventually recumbent; Cows = 24-48 hr before or after parturition; weak, muscle tremors, muscle weakness predisposes to traumatic injuries; tachycardia, dilated pupils, anorexia, hypothermia, depression, ruminal stasis, bloat, uterine inertia, loss of anal tone, coma, death; high heart rates but pulse may not be detectable
  • Dx: pregnancy stage of female, clin signs; low serum Ca; sheep = drop from 8-12 mg/dl to 3-6; cows = drop below 7.5 mg/dl
  • Necropsy: muscle damage d/t crush syndrome if recumbent for more than 12 hours
  • Control: in sheep, maintain appropriate body condition during last trimester; in cows, limit sodium & potassium (high in legume & grass forage dry cow diets) to just meeting maintenance levels; dietary chlorides may help; oral calcium supplements
  • Tx: 20% Ca borogluconate solution IV; relapses common; measure HR during calcium adminstration - irregular or rapid HR, slow or D/C calcium
197
Q

Hypomagnesemia Tetany (Grass Tetany, Grass Staggers)

A
  • Unlike calcium, magnesium is not under hormonal control & Mg stores in bone not readily mobilized; adequate blood levels rely on presence of adequate levels in diet
  • Occurs most frequently in early lactation beef cows grazing lush pastures; dairy cattle, calves, ewes, and goats can also develop
  • Clin signs: twitching of muscles, apprehension, excitability; muscular spasms become more frequent until animal becomes ataxic and falls; clonic convulsions, bruxism, hypersalivation; Hr & RR very elecated, hyperthermia due to muscle activity; blood Mg <1.1 mg/dl = clinical signs
  • Epizootiology: low magnesium concentrations in rapidly growing forages; higher concentrations of potassium in these forages interferes with Mg absorption; hypocalcemia often accompanies hypomagnesemia as lack of Mg impairs PTH secreation
  • Tx: IV Mg; many solutions for hypocalcemia in dairy cattle also contain Mg; to prevent relapse, oral drenching with Mg salts; to prevent add Mg supplement to diet
198
Q

Ketosis (Acetonemia), Fat Cow Syndrome, Hepatic Lipidosis, Pregnancy Toxemia, Protein Energy Malnutrition

A

-Ketosis & hepatic lipidosis = high-producing dairy cows
-Pregnancy toxemia = ewes & does in advance pregnancy
-Protein energy malnutrition (PEM) = beef heifers
-All related to negative energy balance
-Clin signs: anorexia, wekaness, lethargy; Dairy = ketosis in first 6 weeks of actation - weight loss, thin, hypoglycemia, ketonemia, ketonurina, fruity ketone smell on breath; severe ketosis = neuro signs - circling, head pressing, apparent blindness; Sheep & Goats = last 6 weeks gestation w/ multiple fetuses - wander aimlessly, move away from flock, incoordination, muscle tremors, teeth grinding, convulsions, coma, if fetal death occurs - acute toxemia & death; PEM in beef cattle - late gestation or early lactation, higher incidence in cows with twins, marginal diet & poor quality forage may play role
-Pathogenesis: negative energy balance + increasing nutrient demands of growing fetus and colostrogenesis/mobilization of adipose stores for demands of milk production - when adipose reserves mobilized, ketone bodies (acetone, acetoacetate, and betahydroxybutyrate) produced in liver + increased mobilization of stored triglyerides in adipose - increased blood nonesterified fatty acids (NEFAs); inadequate supply of glucose for maternal & fetal needs; oxidation of fatty acids results in formation of ketone bodies & ketoacidosis
-Dx: clin signs; Dairy Cattle: blood glucose <40 mg/dl, blood ketones >30 mg/dl, milk ketones >10 mg/dl; Small Ruminants: blood glucose <25 mg/dl; prepartum & lactating cows: NEFA >1000 uEq/L & 325-400 uEq/L abnormal
-Tx: IV 50% glucose than oral propylene glycol; glucocorticoids or long-acting insulin may be used; sheep & goats - can reduce glucose dmaned by inducing abortion or surgical removal of offspring; treating individual ewe often unsuccessful
-Necropsy: enlarge, yellow, greasy, friable liver with fatty degeneration - if severe, livers float in formalin or water; beef heifers will be very thin; small ruminants with multiple fetuses - fetuses may have died & decomposed
-Ddx: hypocalcemia, toxemia d/t mastitis, enterotoxemia, peritonitis; Johne’s, lymphoma, parasitism, abomasal disease,
vagal indigestion, and chronic respiratory diseases
-Prevention: provide adequate nutrition, manage body weight gain in late lactation; reduce stress & maintain feed intake in prepartum cows; provide monensin or rumen-protected choline in prepartum diet may reduce fatty infiltration of liver; sheep & goats, dietary energy & protein should be increased 1.5-2x the maintenance level in late pregnancy
-Reserach complications: consider in animals on studies of late gestation likely to bear twins or be transported or stressed during this period of gestation

199
Q

Urinary Calculi (Obstructive Urolithiasis, Water Belly)

A

-Metabolic disease of intact & castrated male sheep, goats & cattle
-Male sheep & goats have a urethral process & cattle have a narrowing of the urethra at the sigmoid flexure = calculi can get stuck
-Removal of testosterone by early castration may also result in hypoplasia of the urethra and penis
-Clin signs: vocalization, treading, straining postures, arched backs, raised tails, squatting while attempting to urinate, male cattle swelling in ventral perineal areas; crystal deposits attached to preputial hairs; In smaller ruminants, vermiform urethral appendage may become dark purple to black in color; pulsing pelvic urethra, bladder distension; abdominal distension as bladder enlarges and may rupture; uremia, hyperkalemia eventually lead to death
-Dx: clin signs, abdominocenttesis may yield urine; creatinine contration in abdominal fluid 1.5-2x greater than serum creatinine = uroperitoneum;
-Calculi are usually calcium phosphate or ammonium phosphate
-Necropsy: severe hemorrhage & inflammation of bladder wall; urine in abdomen with bladder or urethral rupture; calculi or struvite crystal sediment in bladder and urethra
-Ddx: Grain engorgement, colic,
gastrointestinal blockage, and causes of tenemus, such
as enteritis or trauma are differentials; trauma to urethral process
-Prevention: one case often indicates a problem in the group; urolithiasis can be minimized by maintaing Ca:P ratio in diet at 2-.25:1 with P no more than 0.6% of diet dry matter; increase amount of dietary roughage to balance minderal intake & increase amount of P excreted via feces rather than urine; increase amount of salt in diet (2-4% NaCl), add ammonium chloride (10 g/head/day or 2% of ration) to acidify diet; ensure palatable and accessible water
-Tx: primarily surgical; lumbosacral epidural to allow examination of penis; amputation of vermiform urethral appendage may alleviate disease in small ruminants; perineal urethrostomy
-Research complications: young, castrated and intact male ruminants in the lab setting will be susceptible to this

200
Q

Copper Deficiency (Enzootic Ataxia, Swayback)

A
  • Chronic copper deficiency in pregnant ewes & does may produce metabolic disorder in offspring
  • Lams & Kids - called enzootic ataxia; also called ‘swayback’ in goat fetuses
  • Rare in North America as most diets have adequate copper
  • Clin signs: progressive hind limb ataxia, apparent blindness in lambs up to about 3 months of age; ewes may appear unthrifty, anemia, poor quality depigmented wool with a decrease in wool crimp; kids born weak, tremble, concavity to spin cord (‘swayback’); cattle - chronic diarrhea, weight loss, unthriftiness, changes in coat color; pathologic fractures
  • Dx: low copper levels in feed & in tissues at necropsy
201
Q

Copper Toxicosis

A

-Acute or chronic copper ingestion or liver injury often causes severe acute hemolytic anemia in weanling to adult sheep, calves and adult dairy cattle
-Growing lambs most susceptible
-Rare in goats
-Clin signs: intravascular hemolysis, anemia, hemoglobinuria, icterus; copper release from overloaded liver; irritation of GI tract mucosa - weakness, vomiting, abdominal apin, bruxism, diarrhea; respiratory difficulty, circulatory collapse, recumbency death
Dx: hepatic biopsy = BEST METHOD; serum or plasma levels of copper & AST and GGT elevations
-A single toxic dose for sheep is in the range of 20–100 mg/kg, and for
cattle is 220–880 mg/kg
-Copper-containing pesticides, soil additives, therapeutics, improperly formulated feeds, feeding of poultry litter or forages fertilized with poultry or swine manure; copper sulfate footbaths
-Cattle feed & mineral blocks contain more copper than sheep need
-Pregnant dairy cattle & Jersey cattle may be more susceptible
-Necropsy: icterus; soft, dark, friable enlarged spleen; enlarge, yelow-brown friable liver, ‘GUN BARREL’ BLACK KIDNEYS, hemoglobin stained urine visible in bladder; copper accumulations in liver reaching 1000-3000 ppm are toxic
-Ddx: Other causes of hemolytic disease include babesiosis, trypanosomiasis, anaplasmosis, and plant poisonings such as kale; Arsenic ingestion,
organophosphate toxicity, cyanide and nitrate poisoning
should also be considered as a cause of poisoning.
Urethral obstruction and gastrointestinal emergencies
should be considered for the abdominal pain
-Prevention: carefully monitor copper access in sheep & copper supplementation in cows; do not feed cattle feedstuffs to sheep or goats & do not use dairy calf milk replacer for lambs
-Tx: sodium molydenate (and sodium thiosulfate) orally for 3 weeks to aid in excretion of copper; oral D-penicillamine daily for days (50 mg/kg) to increase copper excretion in sheep
-Research complications: Breeds of sheep, such as
the Merino and Merino crosses as well as British breeds, may be more susceptible to copper toxicosis caused by
phytogenous sources

202
Q

Selenium/Vitamin E Deficiency (Nutritional Muscular Dystrophy or NMD Nutritional Myodegeneration White Muscle Disease)

A

-‘Stiff lamb disease’; seen in young ruminants
-Selenium & Vitamin E function together as antioxidants that protect cell membranes from oxidative damage; selenium is a cofactor for glutathione peroxidase - converts hydrogen peroxide to water & other nontoxic compounds; lack of one of both nutrients = loss of membrane integrity
-Clin signs: 2 Forms = Cardiac & Skeletal; Cardiac: most common in neonates, rapid onset, respiratory difficulty, damage to cardiac, diaphtagmatic, intercostal muscles, in older animals locomotor disturbances and/or circulatory failure, paresis, stiffness, inability to stand, rapid but weak pulse, acute death, paresis + acute death in neonates with assoc pathologic signs = diagnostic; Skeletal: stiff, reluctant to move, painful muscles, young reluctant to get up, difficulty nursing (dysphagia), subtle immune defects
-Dx: whole blood levels of Se (>0.07 ppm Se is normal) and plasma levels of vitamin E (<1.1 ppm).
Glutathione peroxidase levels in red blood cells can be measured as an indirect test
-Se-deficient soils are common in many areas of
the United States (including the Northeast, Northwest,
and Great Lakes regions) and throughout the world - diets based on feeds grown in these areas need Se supplementation (limited to 0.3 ppm; no more than 0.7 mg/day for adult sheep & 3 mg/day for adult cattle - this level INSUFFICIENT in soil deficient areas = add injectable sources)
-Necropsy: petechial hemorrhages, muscle edema; PALE-WHITE STREAKING OF AFFECTED SKELETAL & CARDIAC MUSCLE, DIAPHRAGM, TONGUE
-Ddx: neonatal ruminants
presenting with respiratory and cardiac dysfunction,
differentials include congenital cardiac anomalies and pneumonia
-Control: awareness of regional selenium deficiencies; Vit E & Selenium supplementation
-Tx: Vit E & Selenium injections

203
Q

Selenium Toxicity

A
  • Feed manufacturing errors, ingestion of Se-containing plants, excessive dosing to prevent/corret Se deficiency
  • Ruminants on arid alkaline soils (primarily in Western states) may be subject to Se toxicity
  • Clin signs: weakness, dyspnea, bloating, diarrhea; shock, paresis, death
  • Initial signs of excessive selenium intake = cracked hoof walls & subsequent infection and irregular hoof growth
204
Q

Thiamine Deficiency/Polioencephalomalacia (PEM)

A

-PEM caused by inadequate ruminal thiamine production or bacterial thiaminase production in cattle & sheep consuming diets high in fermentable carbohydrates
-Risks: exposure to toxic plants (bracken fern, equisetum), moldy feed containing thiaminases, feed or water high in sulfates
-Occurs in cattle, sheep, goats, deer, camelids
-Clin signs: anorexia, ataxia +/- hypermetria, bruxism, hypersalivation, hyperesthesia, muscle tremors; cortical blindness, head-pressing, head tilt, opisthotonus, nystagmus, dorsalmedial strabismus, seizures, death; hyperthermia from muscle activity; high morbidity & mortality in young animals
-Dx: clin signs, response to parental thiamine hydrochloride
-Necropsy: cerebral lesions - softening and discoloration of gray matter - neruonal edema, chromatolysis, shrinkage
-Ddx: lead poisoning, hypomagnesemia,
listeriosis, rabies, pregnancy toxemia, infectious thromboembolic meningoencephalitis, and type D
clostridial enterotoxemia
-Control: monitor diet & provide adequate roughage necessary to support ruminal production of B vitamins; excess sulfates are the primary factor - immediately remove source
-Tx: early aggressive tx essential; frequent parenteral adminstration of thiamine hydrochloride; dexamethasone, B vitamins, diazepam
-Research complications: risk of feeding concentrates or moldy feed

205
Q

Salt Toxicity

A
  • Risks: Feeding high-salt supplements to restrict intake, consuming water high in sodium, mistakes in formulation/preparation of feed or electrolyte solutions, restriction of water
  • Clin signs: colic, diarrhea, blindness or ‘star gazing’, hyperexcitability, head-pressing, ataxia, incessant chewing, nystagmus, seizures progressing to coma and death
  • Dx: elevated serum & CSF sodium
  • Animals allowed to rehydrate rapidly may develop intravascular hemolysis, hemoglobinuria
  • Necropsy: cerebral edema
  • Treatment: IV normal or hypertonic saline followed by oral fluid replacemnt; mannitol; prognosis is poor for animals with severe neuro signs
  • Control: avoid water restriction if high-sodium feeds used; oral electrolyte solutions for young ruminants must always be prepared according to manufacturer; provide adequate fresh water with <7000 ppm sodium
206
Q

Failure of Passive Transfer

A

-Because of epitheliochorial placentation, neonatal ruminants born without immunoglobulins & must receive colostrum ASAP after birth
-Failure of passive
transfer is defined by serum concentration of less than
10 mg/ml IgG1 at 48 h after birth
-Dx: single radial immunodiffusion (quantitates
immunogloblin classes), ELISA test kits (available
commercially), zinc sulfate turbidity (semiquantitative),
sodium sulfite precipitation (semiquantitative), glutaraldehyde
coagulation (coagulates above specific level),
and serum gamma-glutamyltransferase activity (assays enzyme in high concentration in colostrum and absorbed simultaneously with colostrum)
-Total serum protein of greater than 5 g/dl measured by refractometer has been assoc w/ adequate immunoglobulin concentrations in hydrated animals

207
Q

Laminitis (Subsolar Abscesses, White Line Disease)

A
  • Common in ruminants, particularly dairy cattle
  • Risks: secondary to rumen acidosis, sudden changes in diet, excessive carbohydrate (starch & sugar) intake, inadequate fiber; concrete flooring or inadequate resting areas
  • Alterations in vascular endothelium result in chronic inflamm of the sensitive laminae of the hoof, separation of corium and hoof wall, rotation of the third phalanx
  • Rotation of 3rd phalanx often leads to subsolar abscesses - occur in toe or heel region of sole d/t pressure on solar corium, may progress to full-thickness defects - severe lameness, reluctant to move, lose weight and production
  • Dx: reluctant to get up or walk, shift weight frequently, bruxism, walk on carpi; chronically, hoof takes on ‘slipper’ apperance
  • Tx: correct underlying cause; regular foot trimming; bandaging for sole abscesses; can glue wooden block or slipper onto the healthy claw to remove weight from claw with abscess
  • Control: proper diet formulation, preparation, delivery
208
Q

Hemorrhagiv Bowel Syndrome (Jejunal Hemorrhage Syndrome)

A
  • Acute enteric disease, primarily affecting dairy cows in first 3-4 months of lactation
  • Appears to be increasing in prevalence since first reported in 1990s
  • Clin signs: hemorrhage into a region of the small intestine, resulting in a blood clot which produces a functional obstruction
  • Clin signs: depending on rate and volume of hemorrhage - hypovolemic shock, elevated HR, weak pulse, pale mucous membranes, cold extremities; cases with slower progression - abdominal distension, anorexia, fluid splashing sounds or pings in lower right abdomen; fees may be normal or tarry-colored or contain clotted blood; most develop fatal septic shock within 24-48 hr d/t necrosis of intestinal wall; fatality is 80-100%
  • Etiology not well-understood, likely multiple factors - C. perfringens Type A? Aspergillus fumigatus?
  • Assoc w/ larger & higher-producing dairy herds w/ energy dense diets, low fiber
  • Necropsy: purple or red discolored segments of small intestine; intestinal contents may be mixed with unclotted blood, or firm blood clots tightly adhered to mucosa
  • Tx: usually unsuccessful; fluids, laxatives, anti-inflammatories, antibiotics typically just prolong course of disease
209
Q

Nutritional Diarrhea

A
  • Calves with ad libitum access to milk may consume up to 20% body weight daily without developing diarrhea
  • Poor-quality milk replacers may exacerbate diarrhea d/t enteric pathogens
210
Q

Photosensitization (Bighead)

A
  • Animals with lack of pigment more susceptible
  • Photosensitive chemicals usually ingested - interact with sunlight leading to acute dermatitis
  • 3 Types: Primary, Secondary - Hepatogenous, Aberrant
  • Primary = related to plant pigments or drugs such as phenothiazine, sulfonamides, or tetracyclines
  • Secondary = more common in large animals; related to plant pigment PHYLLOERYTHRIN = porphyrin compound, degradation product of chlorophyll released in ruman microbial digestion - liver disease or injury prevents normal conjugation of phylloerythrin & excretion through bile = predisposes to photosensitization
  • Aberrant = congenital porphyria in cattle
  • Pathology: photosensitive chemical is deposited in the skin & activated by absorbed sunlight - activated pigments convert local amino acids & proteins to vasoactive substances that increased permeability of capillaries leading to fluid and plasma protein losses and eventually local tissue necrosis
  • Photosensitization can occur within hours to days after sun exposure - produces lesions of the face, vulva, coronary bands; lesions most common on white-haired or thinly haired areas
  • Clin signs: facial edema, nostril constriction, swollen lips, potentially difficulty breathing; secondary = icterus; necrosis, gangrene
  • Dx: lesions, exposure to photosensitive chemicals and sunlight
  • Tx: symptomatic
211
Q

Reproductive (Vaginal, Uterine) Prolapses

A
  • Ewes & cattle, less commonly in does
  • Vaginal prolapses usually occur during late gestation related to relaxation of pelvic ligaments in response to hormone levels; In sheep, most common in overconditioned ewes carrying twins/triplets; May also result from excessive straining assoc w/ dysuria from pressure of fetuses on bladder; may have a hereditary basis in ewes and cows & may recur in following year - these animals should be culled; occur in nonpregnant animals grazing estrogenic plants
  • Uterine prolapses occur sporadically in postpartum ewes & cattle; cause is unknown - maybe excessive traction to correct dystocia? Overconditioning & lack of exercise? Uterine atony, hypocalcemia?
  • Clin signs: increased HR & RR, straining, restlessness, anorexia
  • Tx: reduction & repair if discovered early - Buhner suture or bearing retainer (‘truss’); passively infusing several gallons of warm fluid into the uterus following reduction will aid in completely inverting uterus; supportive therapy including tetanus prophylaxis; oxytocin to induce uterine involution
  • Prevention: regular exercise for breeding animals, prevention of hypocalcamia and management of body condition in cows and ewes
212
Q

Rectal Prolapse

A
  • Common in growing, weaned lambs and cattle from 6 mth-2 yrs old
  • May occur secondary to GI infection or inflammation - coccidiosis, Salmonella, intestinal parasites; urolithiasis, cystitis, urethritis, vaginal irritation, vaginal prolapse, some forms of hepatic disease, tail docking too short, coughing during respiratory infx, abdominal enlargement during late pregnancy, excessive rumen filling or bloat - may all lead to rectal prolapse
  • Dx: clin signs; early prolapses may be corrected with purse-string suture around anus; if tissue has become necrotic, dry, friable surgical amputation needed
  • Prognosis depends on cause, extent of prolapse, timeliness of intervention
213
Q

Trichobezoars, Phytobezoars, Enteroliths

A

Cattle that are maintained
on a low-roughage diet, that lick their coats frequently, that have long hair coats from outdoor housing, or that have heavy lice or mite infestations will often develop trichobezoars
-Younger calves with abomasal ulcers more likely to also have abomasal trichbezoars
-Enteroliths can form from consumed indigestible material
-Clin signs: mild to severe; ruminal trichbezoars rarely cause clinical signs; obstruction - pain, bloat, decreased appetite, fecal production
-Dx: abdominal auscultation, rectal palpation, US
-Tx: surgical - paracostal laparotomy (for abomasal),
rumenotomy, or right paralumbar celiotomy (for
obstruction of the duodenum, jejunum, or spiral colon); supportive care as necessary
-Prognosis generally good if condition diagnosed and treated before dehydration & imbalances become severe and peritonitis develops
-Prevention: good-quality roughage, treating lice & mange, avoiding incorporation of plastic materials into mixed rations

214
Q

Traumatic health issues in ruminants

A
  • Frontal sinusitis is a potential complication of dehorning
  • Abscesses may occur in soft tissues of hooves d/t entrapped foreign bodies or hoof cracks filling with dirt
  • Paraphimosis may be seen in male ruminants assoc w/ hair rings around penis
  • Treatments: tetanus antitoxin, antibiotics, cleaning of wounds; improve housing facilities, predator control, monitoring hierarchies among animals penned together
  • Seasonal fly control to avoid infestation of wounds
215
Q

Anaphylactic Reactions

A
  • In sheep, goats, cattle - often clinical referable to the respiratory system
  • Lung is major target organ in cattle for Type 1 hypsensitvity
  • Anaphylactic vaccine reactions cause acute lung edema
  • Clin signs: anxious, shivering, hyperthermic, salivation, diarrhea, bloat
  • Tx: epinephrine IV, corticosteroids (dexamethasone), NSAIDs, furosemide may be beneficial to reduce edema, tracheostomy if pharyngeal or laryngeal edema
  • Prognosis usually guarded
  • Recovery can occur within 2 hr
216
Q

Heath Issues Related to Experimental Manipulations

A
  • In research environment, catheter & surgery sites can be sources of iatrogenic infection
  • Traumatic injuries to peripheral nerves or improper injection techniques can cause acute lameness; ‘dropped elbow’ = traumatic injury to radial nerve
  • Husbandry procedures - tail docking, castration, dehorning, shearing, dosing with balling gun - may result in superficial lesions, dermal infections, tetanus
  • Balling gun injuries may lead to celluitis with coughing, decreased appetite, sensitivity to palpation
  • Tx: swelling around peripheral nerves: diuretics, antiinflammatories; wounds: antibiotics
217
Q

Neoplasma in ruminants

A
  • Neoplasia relatively rare in ruminants
  • In sheep lymphoma/leukemina has been shown to result from infection by a virus related (or identical) to BLV
  • Pulmonary carcinoma (pulmonary adenomatosis) & hepatic tumors are found in sheep
  • Pulmonary adenosarcoma in sheep is a transmissible viral disease
  • Virus-induced papillomatosis
  • Squamous cell carcinomas have been reported in sheep
  • In goats, thymoma & cutaneous papillomas most common tumors; papillomas most common skin & udder tumor, no wart virus has been identified; persistent udder papillomas my progress to squamous cell carcinoma; lymphoma reported rarely in goats
  • Lymphoma of various organ systems & bovine squamous cell carcinoma (BSCC, ‘cancer eye’) most common neoplasia in cattle - lymphoma d/t BLV; lack of periocular pigmentation, amount & intensity of exposure to solar UV light, age important factors in BSCC - genetics may also be involved as many cases occur in Herefords - mets to LNs and major organs; tx for either lymphoma or BSCC is enucleation for BSCC is still local or palliative; papillomatosis also common in cattle
  • Forms of bovine lymphoma NOT assoc w/ BLV = Calf/Juvenile; Thymic/Adolescent (animals 6 mth-2 yrs) & Cutaneous (any age). Calf = rare, generalized lymphadenopathy, may be sudden onset, progresses rapidly, lymphadenopathy, anemia, weight loss, weakness; some animals may be paralyzed d/t spinal cord compression from subperiosteal infiltration of neoplastic cells. Adolescent = rare, progression rapid; most often seen in Hereford, characterized by space occupying masses in the neck or thorax - loss of condition, dysphagia, rumen tympany. Cutaneous = longer course & may wax & wane; masses at anus, vulva, escutcheon, shoulder, flank - masses painful when palpated, raised, often ulcerated; anemia, neoplastic involvement may affect cardiac function; lymphadenopathy
218
Q

Amyloidosis

A
  • Occurs in adult cattle d/t accumulations of amyloid protein in kidney, liver, adrenal glands, GI tract
  • Assoc w/ chronic inflammatory disease & other unknown factors
  • Clin signs: chronic diarrhea, weight loss, nonpainful renomegaly, generalized edema; loss of protein in urine = abnormal plasma albumin & foaming urine
  • PROTEINURIA - distinguishes amyloidosis (& glomerulonephritis) from other causes of weight loss & diarrhea like Johne’s disease or parasitism
  • Diffuse nature and insidious onset makes amyloidosis difficult to diagnose
  • Prognosis - poor; no treatment
219
Q

Dental Wear

A
  • Ruminants have an intermandibular space that is narrowed than the intermaxillary space
  • Dental wear is seen most commonly in sheep - as sheep age, excessive dental wear may result in weight loss, unthriftiness
  • Dietary contamination with silica will lead to mechanical wear on teeth; animals in sandy environments will similarly have excessive teeth wear
  • Sheep older than 5 years especially prone - check teeth frequently
  • Prevent: manage content and consistency of diet