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142 Cards in this Set

  • Front
  • Back
What are the cardinal signs of pregnancy in a bovine?
As early as 35 days, can palpate amnionic vesicle (blister-like) and fetal slip (shoestring) and a fetus.
At 90 days, can feel the placentomes.
35 – pea
45 – large grape
55 - egg
65 – mouse
75 – rat
120 – cat
150 – small dog
270 large dog
Dystocia management in bovine
1. Give epidural to stop straining
2. Make stand up to get rumen off of uterus
3. Decide whether or not to do a C section (if is alive, may do a C section)
4. If pull, then decide the Three ‘Ps’, presentation, position and posture
Presentation – cranial, caudal, dorsal, ventral, lateral
Position – (all cranial presentation) describe what part is dorsal: dorso - sacral, pubic, ilial left, dorsoilial right
Posture – of limbs extended, retained, or flexed
Pull calf with chains ½ hitch above and below the pastern and pull
Fetotomy if not successful – percutaneous, subcutaneous, decapitation
5. If do C section, then can do:
a. Ventral midline – good exposure, chance for dehis
b. Left flank - Put in right lateral recumbancy and do left flank – must physically elevate uterus
c. Left standing flank – inverted L local; easiest restraint
6. Drug induction of parturition
a. Cow has injury
b. Give PGF2A and Dex (short acting steroid)
Retained placentas in bovine
• Retained if present > 24 hours after parturition
• Can induce a Post-partum metritis
• Can be confused w/ Ketosis, LDA, RDA, milk fever, peritonitis, indigestion and mastitis
• Suggested not to give ecbolic drugs (prostaglandins, ergots, oxytocin or 2 antagonists
• May be induced by low selenium and Vit E
• Treatment:
a. Placenta is usually expelled on own w/in 4-6 days
b. If loose, can manually extract
c. Abs (LA200)
d. Intra-uterine infusion controversial b/c of residues
DDx of infertility in bovine
Three categories of infertility:
1. Decreased conception rate
a. Timing, Timing, Timing
b. Inadequate energy – look at ration
c. Maternal gene abonromalites
d. Neoplasia – granulosa cell tumor
e. Infectious diseases
- Tritrichomonas fetus – pyometra, collect w/ Diamond’s media THREE times, ‘Peter pan’ of bull (asymptomatic carrier); no treatment
- Campylobacter fetus ss. veneralis – endometritis and salpinitis; collect with Clark’s medium, cows become carriers, tx bull with dihydrostriptomycin, vaccinate cows before breeding season
- Leptospirosis interrogans hardjo – zoonotic; mastitis and abortion, urine, placenta and discharge contact; vaccinate 2x a year
- IBR – bobine herpes virus-1; nose to vulvar contact; papules on V,V and V
- BVD – EED and abortion
- Brucellosis abortus – zoonotic; AI dz b/c cannot penetrate the cervix
- Mycoplasma – nodular, adhesions and lots of exudate
- Ureaplasma, Hemophilus, Chlamydia – AI dzs, double sheath or double rod AI pipette to prevent
2. Fertilization failure (semen can’t get there)
a. Bull semen
b. AI technique
c. Segmental aplasia
d. Intralumenal adhesions
e. Paraovarian cysts – prevents follicle from dropping
f. Double cervical os – cervix dioelphis
g. Persistent hymen
3. EED (semen gets there, but fetus dies)
a. Trichomonas or Campylobacter
b. Heat stress
c. High cortisol
d. Aged gametes
e. Lethal genes
f. Growth implants – endometrial glands don’t develop properly and creates a toxic environment for embryo
Bovine Respiratory Disease Complex
• Shipping makes animals susceptible to viruses: Bovine respiraotyr syncytial virus, Infectious bovine rhibotracheitis (bovine herpes virus-1), bovine viral diarrhea and Parainfluenza 3
• Bacteria infection via Mannheimia hemolytica, Pasteurella multocida, Haemophilus somnus, Mycoplasma and Arcanobacter pyogenes
• Fever is the first sign
• At necropsy see fibrinous pneumonia and coagulative necrosis
• Many antibiotics approved for BRDC treatment – LA200, PPG, TMS, Mictil, and Forfenicol
• Prevention is best
a. Metaphylaxis of LA200 to feedlot cattle on arrival
b. Don’t mix ages
c. Avoid overcrowding
d. Avoid drastic change in temperature during change
e. Give adequate ventilation
f. Wean calves before shipping
g. Vaccine with Pasteurella bacterin and Viral vaccinations
Pasteurellosis (aka Shipping fever)
• Pasteurella multocida - Gram negative aerobic coccobaccili; septicemic pasteurellosis
• Mannheimia hemolytica – pneumonic pasteurelosis
• Caused by transport and expousre to other animals
• P. multocida causes Acute fibrinous brochopneumonia
• M. hemolytica causes a coagulation necrosis
• Fever is the first sign
• Dx Serology (ELISA) and can culture blood or nasal swab
• Pathogenesis – part of normal flora that becomes virulent when the animal is stressed and obtaines a virus in the respiratory complex
• Four virulence factors:
a. Fimbriae – of organism enhances colonization in the upper resp tract
b. Polysaccaride capsule – inhibits complement and phagocytosis and  seg infilatration into the lung
c. LPS (endotoxin) – directly toxic to bovine endothelium
d. Leukotoxin – exotoxin that directly destroys cow’s cells
Calf Diarrhea

Villus absorbs
Crypts secrete
Ages of onset of D+ in calves
< 3 E coli
5-15 Rotavirus (tips – maldigestion, malabsorption)
5-21 Coronavirus (entire villus destroyed – more severe D+)
5-35 Cryptosprodiosis (villus blunting – malabsorption, maldigestion, acid fast stain, ‘flat calves’ b/c hypoglycemia)
5-42 Salmonella (typhimurium in environment and dublin is carrier) Bloody D+
5-15 Clostridium perfrengens – Type C Beta toxin;
> 30 Coccidia (Eimeria)
Ages of onset of D+ in pigs
<3 E coli
1-7 Clostridium perfringesn Thype C
5-25 Coccidiosis (Isospera suis)
TGE (corona virus) water D+, villus atrophy
1-5 w Rotavirus
(remember the previous card was about PIGS...not sure why that was thrown in!)
E coli
• Major cause of diarrhea in calves
• < 3 days old
• ETEC (enterotoxigenic E coli) has a K99 fimbriae that attaches to the mucosal surface via receptors at a very young age
• ETEC also produces a heat stable enterotoxin (ST) inhibits absorption by the villus but has no effect on secretion
• Inhibits NaCl absorption causing a loss of Na, Cl Bicarb, K and water
• Clinical signs:
a. Profuse, watery diarrhea
b. Dehydration
c. Metabolic acidosis b/c underperfused kidney
d. Hyperkalemia (but cells are hypokalemic)
• Dx
a. Age of onset very young (under three days old)
b. Profuse, watery D+
c. Fecal bacteriology
• Tx
a. rapid isolation
b. Rehydration w/ electrolytes to combat acidosis
c. Oral Ab
Abscesses in cattle
Abscesses in cattle
Brodie’s abscesses
Brodie’s abscesses
• AKA chronic fibrous osteomyelitits and chronic bone abscess
• A specific form of osteomyelitis that is circumscribed lined w/ granular membrane surrounded by sclerotic bone
• Fusobacterium necrophorum and Actinomyces pyogenes have been involved
Iatrogenic SQ injections
Iatrogenic SQ injections
• Mostly causes by Actinomyces pyogenes
• Caused by dirty syringes, or non-sterile preparation
• Inject in the neck according to BQA (beef quality assurance) in the middle third of the neck, about 1/3 of the way down instead of the gluteal region
Abscesses of the jaw
Abscesses of the jaw
• Confirm it is an abscess via paracentesis
• If the abscess is hard all over, then delay treatment until it softened and pittling of one area is noticeable (called Pointing of the abscess)
• Abscesses that are opened and drained prematurely have a tendency to recur
• Tx via incising the abscess, remove the pus and flush w/ clean water ONLY IF A SOFT AREA IS PALPATED ON THE MASS
Retropharyngeal abscess
Retropharyngeal abscess
• May be caused by Actinobaccillosis (wooden tongue) or infection entering pharyngeal wound
• Tx is same as jaw abscesses as above
Liver abscesses
Liver abscesses
• Caused by Actinomyces pyogenes or Fusobacterium necrophorum
• Due to Rumen acidosis
• May cause peritonitis, rupture of a major vessel causing hemorrhage and sudden death, or vena cava thrombosis
• Vena cava thrombosis may pro9duce pulmonary thromboembolism leading to pulmonary abscess (painful cough, dyspnea w/ rupture of abscesses into blood vessels producing severe and recurrent epistaxis and blood out of the mouth)
Myocardial abscess
Myocardial abscess
• Produces a similar clinical picture to chronic vegetative endocarditis, but with a slower temperature rise and slower course
Abscess in the preputial epithelium
Abscess in the preputial epithelium
• Caused by Actinomyces pyogenes and Staphylococcus aureus
• Angus, Hereford and Bos indicus breeds and crosses
Lice (pediculosis)
Lice (pediculosis)
• Biting lice (Anoplura) – Bovicola (Damalinia) bovis located on neck, withers and tail head
• Sucking lice (Mallophaga) – Hematophinus eurysternus, Linognathus vituli and Solenopotes capilatus have a more generalized infestation
• Entire life cycle on the host
• Higher populations in the winter (coat is long and transmission from animal to animal is easier)
• Cardinal sign is pruritis
• Tx is various antiparasitics including organochlorine, organophosphurus, pyrethroid, Coumaphos, Diazinon and permethrin
• Ivermectin injectable gets sucking lice but not biting spp
Postparturient paresis
• AKA Milk fever, hypocalcemia, Eclampsia
• Most common metabolic disorder affecting cattle
• Predispositions to milk fever:
a. Dairy cattle
b. Increases w/ age and milk yield
c. High prepartum calcium
d. Low magnesium – restricts ability to absorb calcium
e. Estrogens – can inhibit Ca immobilization
f. Low feed intake at partutrtion
g. Fatty liver
Postparturient paresis

• Pathophysiology –
• Pathophysiology –
a. hypocalcemia stimulates PTH which increases kidneys ability to synthesize 1,25, OH2D3 from Vit D3.
b. 1,25 OH2D3 stimulates increases gut absorption of Ca and Ca from bone
Postparturient paresis

• Clinical signs
• Clinical signs
a. Recumbancy
b. S bend to her neck
c. Incordination, ataxia
d. Dystocia
e. Low Ca, Low Ph and high Mg (even though milk fever is due to low Mg intake
Postparturient paresis

• DDx for a recumbant cow are:
• DDx for a recumbant cow are:
a. Acute toxic mastitis – examin milk from all 4 teats
b. Calving paralysis – obturator paralysis at L4-L6, abduction of hindlimb or straddled
c. Pelvic fxs – may be due to osteoprosis in dairy cattle but is rare
d. Grass tetany – hypomagnesia
e. Downer cow syndrome
f. Inanition – starvation, lack of food and water
g. Pregnancy toxemia – primarily dz of sheep; starvation, acetonemia b/c of lack of energy
h. Acidosis
i. Hypothermia
j. BSE
• Tx – Slow IV Calcium borogluconate warmed to body temperature
• Prevention – Feed Mg or high anionic diets to prepartum cows
Metritis-Pyometra complex
Metritis-Pyometra complex
• Induced by dystocia, retained placenta and milk fever b/c of delayed return to cyclicity
• Metritis will delay involution after calving, and develop into pyometra
• If the uterus is still infected after calving and ovulation and CL still develop, the progesterone created by the uterus reduces normal uterine defense mechanisms
• Defense mechanisms inhibited by progesterone:
a. Decreases protection against purulent infection
b. causes cervix to close tightly
c. reduces myometrial contractions
IBK – Infectious Bovine keratoconjunctivits (IBKC)
IBK – Infectious Bovine keratoconjunctivits (IBKC)
• AKA pinkeye
• Moraxella bovis is most common known cause
• May also be induced by IBR (infectious bovine rhinotracheitis) and Mycoplasma bovirhinits and M. laidlawii
• Caused by UV light, flies and dust
• Tx includes isolation, Abs topically, subconjunctival and parenterally
• Pedersen’s suggests sulphadimidine IV injection
• Sx – Third eyelid flap (membrana nictitans) to protect ulcerated cornea
• Eimeria zuernii and bovis
• Affects groups of cattle less than one year old
• Occurs three or four weeks after groups of purchased calves are mixed or sudden stress of extreme temperature reductions
• Sprozoite ingested  Trophozite in intestinal epithelial cell  Merozoites ruptures the cell  invade other cells  Gametocytes (new eggs) hatch and cause severe hemorrhage of the CECUM
• Tx:
a. Sulpha drugs (Albon)
b. Amprolium – is a thiamine antagones so can produce polioencephalomalacia
• Prevention:
a. Monensin
b. Deconquinate
Causes of physiologic (normal ) anestrus:
1. Pregnancy – farmer may not have known there was contact with a bull
2. Postpartum anestrus - Suckling – especially beef cattle, won’t cycle for 45-60 days, dairy will cycle back in 18 days
3. Prepubertal – not reached puberty yet; should be cycling by the time 65% of body weight

Causes of abnormal anestrus:
1. Nutrition
2. Cystic ovaries
a. not enough GnRH from hypothalmus, not enough LH receptors on ovary, not producing or releasing LH;
b. Will NOT show nymphomania
c. Tx is give GnRH or hCG to create luteal tissue, give PGF2 10 days later to destroy luteal tissue
d. If continues put on progesterone to suppuress the hypothalmus and create a hyperactive state when progesterone is removed
3. Free martin – bilateral gonadal aplasia (cotwins w/ males)
4. Ovarian hypoplasia
5. Retained fetal membranes, dystocia, and milk fever
6. Dystocia
7. Milk fever
8. Excess feeding
9. Metritis and pyometra due to prolonged progesterone production and decrease in uterus defense mechanisms
• Two types: Free gas and frothy
• Clinical signs:
a. Severe distention of Left paralumbar fossa
b. Respriatory distress
c. Circulatory compromise
d. Death
Free Gas Bloat (Secondary Rumen tympany)
• Esophageal obstruction or interference with eructation
• Usually only one animal is affected
• Caused secondary to:
a. Vagal dysfunction – omasal or pyloric transport failure, salmonella
b. Impaction/ choke
c. Abscess
d. Tumor or enlarged lymph nodes
e. Choke
f. Milk fever
g. Tetanus
h. Rumen acidosis
i. Rumenitis
• Pass a stomach tube, or (only when a tube won’t go down) put in a rumen fistula or trocar to relieve tension
Frothy Bloat (Primary Rumen tympany)
• More common than gas bloat
• Associated with pasture feeding – legumes such as alfalfa, clover or green chop
• Usually more than one animal is affected
• Is not relieved by passing a stomach tube (a trochar and cannula will become blocked if used)
• Tx is given when froth is seen on stomach tube of surfactants (Therabloat), mineral oil
• May perform an emergency rumenotomy in the middle of the sublumbar fossa
Downer Cow Syndrome
Many causes:
• Mastitis, milk fever or metritis – due to decreased Ca, P, Mg & K (LOOK AT THE VAGINA AND TEATS)

• Good nursing care – soft bedding, physical therapy, hoist, Aqua Cow (best for muscles)
• Prognosis decreases dramatically each day she is down
• Avoid IM injections b/c of muscle damage

• Injury to spine or legs – sacroiliac or coxofemoral luxation, or pelvic fx (NEED RECTAL PALPATION)
• LSA infiltration to spinal canal
• Toxic infectious – septic metritis or acute coliform mastitis
• Compartmental syndrome – increased pressure develops in an osteofascial compartment
• Crush syndrome – release of myoglobin from muscle damage
• Pressure syndrome – ischemic necrosis if cow is sitting in same position for 6 hours or more
• Calving paralysis – obturator or sciatic nerve damage
Many causes of abortion in cattle:
1. Salmonella dublin
2. Listeriosis – feeding contaminated silage, zoonotic
3. Brucelosis abortus – Bang’s dz
4. Campylobacteriosis fetus spp venerealis or spp fetus – Clark’s medium
5. Leptospirosis hardjo and pomona – mainly pomona in US
6. Candidia – contaminated foodstuffs causes this yeast
7. BVD
8. IBR
9. Tritrichomonas fetus – Diamond’s media
10. Drug inducted – PGF2 before day 150
11. Toxic plants – Ponderosa Pine, Broomweed, Montery cypress, Sumpweed
12. Braddica - inhibits iodine into thyroxine inducing a hypothyroidism
13. Trauma/stress
14. Fusarium spp
15. Nutrition
16. Twin pregnancy
17. Genetics

Samples should include entire aborted calf w/ associated fetal membranes
• The ticks and diseases that infest cattle are:
a. Babesia bigemina and Babesia bovis
- Boophilus (Texas Cattle Tick fever tick)

b. Anaplasma marginale
- Boophilus – Texas Cattle fever tick
- Argas – fowl tick
- Dermacentor variablis – American dog tick; also transmits RMSF
- Ixodes scapularis – Black legged tick
- Rhipicecephalus sanguineus – Brown dog tick; also host for Babesia canis
c. Epizootic bovine abortion – Spirochete; Ornithodorus coriaceus
d. Theileria – foreign countries

Ticks in general:
• Serve as intermediate hosts for Babesia, Thelieria and Cytauxzoon
• Serve as vectors for RMSF and lyme
• Cause tick paralysis
Flies (Myiasis)
• Simuliidae – blackflies or buffalo flies; around swiftly flowing streams; Ginsu-like knife biting; intermediate hosts for Leukocytozoon, Onchocerca, and vectors for EEE and vesicular stomatitis
• Phlebotomus – Old world sand flies; intermediate host for Leishmania
• Cullicoides – biting midges; vector for bluetongue
• Tabanus – horseflies – anthrax, anaplasmosis, trypanosomiasis, EIA, tularemia, ricketsial
• Deerflies – Chrysops, hematopota, Pangonia
• Houseflies – Musca domestica
• Face fly – Musca autumalis; pinkeye (Moraxella bovis); Thelazia eradesii (eyeworm)
• Stable fly – Stomoxys calcitrans; Habronema musca
• Glossina – Tsetse fly; Trypanosoma transmission
• Horn fly – Haematobia irritans, Siphoma irritans
• Heel flies – Hypoderma bovis and lineatium; gadding; cattle gallop madly to water; Warbles
Hypodermatosis (Warbles or Grubs)
Hypodermatosis (Warbles or Grubs)
• Hypoderma bovis and lineatum
• Look like bumble bees
• Life cycle
a. active in the spring and lay eggs on lower legs of cow in a row of six or more on a hair
b. Cattle becomes irritated by the flies and will “Gadding” or gallop madly to water
c. Eggs hatch in 4 days and crawl to skin surface and penetrate to C.T. and migrate to esophagus (lineatum) or spinal canal and epidural fat (bovis)
d. Remain here for autumn and winter
e. Produce large domed nodules under the skin on either side of the spine and produce a ventral breathing pore
f. In the spirng the larva emerge from the cyst and fall to the ground and pupate
• Cattle should NOT be treated between December and March b/c the larva are migrating through the esophagus or spinal cord and can cause bloat or paralysis if killed then.
BSE of bulls
BSE of bulls
Four biggest parts of a BSE:
1. PE
2. Minumum scrotal circumference based on age
3. Minimum progressive motility of sperm of 30%
4. Minimum morphology of 70% normal cells
BSE of bulls
• PE – 60 days prior to breeding season; musculoskeletal; foot
• Sheath – hematomas, lacerations, abscesses, adhesions
• Penis – papillomas, hair rings, persistent frenulum
• Rectal exam:
a. Urethralis muscle – covering the urethra, massage to feel pulsations
b. Prostate – firm like a wedding band
c. Vesicular glands – most problems here
d. Ampullae – enlarged end of the vas deferens near the urethra
e. Internal inguinal rings – not larger than 3 finger sizes
f. Bladder, kidneys, LN, peritoneum, omentum
• Scrotal exam – shape, symmetry, dermatitis, scars, injury
a. Size – at 1 year old, should be at least 30 cm, at 2 years old, should be at least 34 cm
• Testicles – firmness, size, symmetry, pain, swelling, fibrosis (palpate deeply), tone should be a flexed muscle
• Epididymis – head is readily palpable at proximal pole of testicle on anteriolateral surface, sperm granulomas found here; tail on distal pole
• Ductus deferens – 2-3 mm cord ascending on medial surface of testicle
• Electroejaculation
a. Evaluate libido
b. Minimum progressively motile sperm is 30%
c. Should have only 1-2 spheroids (immature sperm that are large, grainy & non-segmented nucleus)
d. Classify as normal, 1degree or 2 degree
e. 1degree - head or midpiece or tail rolled; bigger problem b/c can compete with normal sperm
f. 2degree - tail or loose, normal head
g. Abaxial attachment is problem in ruminants only
Abomassal disease
Abomassal disease
LDA, RDA and ulcers
Normal anatomy and Local anesthesia:
1. On left side, mostly rumen with some abomassum and most of reticulum
2. On right side, liver covers the omassum, with the abomassum and reticulum below; the descending duodenum in immediately in the right paralumbar fossa
3. Anesthesia –
a. Line block – Inverted L; T13, L1 & L2
b. Regional – Over and under L1, L2 and L4
4. GRID:
External Transverse Internal

Causes of ping on the left side:
1. LDA – variable pitch ping
2. Gas cap on rumen
3. Pneumoperitonitis
4. Rumen void
Abomassal disease
LDA – variable pitch ping b/c of peristalsis
• Left displaced abomassum (IT IS NOT TORSED)
• Dairy cattle
• Can have concurrent disease (milk fever, metritis, mastitis, hardware, ketosis, fatty liver, abomasal ulcers)
• Clinical findings:
a. Off feed/ milk
b. Variable pitch ping on left side
c. Ballotment
• Tx
a. Rolling – put on right side, and tie Grymer Sterner toggle suture loosely while cow is in dorsal recumbancy
b. Left flank laparotomy
- Preplace abomaspexy suture in Ford continuous pattern w/ Braunamid cranial from pylorus
- Decompress gas in abomassum
- Blindly put sutures between xyphoid and milk well and tie the sutures
- Explore abdomen last
- Contraindicated in occult LDA (has gone away); will have a low ping line

Last rib


LDA Pylorus

c. Right flank laparotomy
- will see duodenum first
- Explore the abdomen first
- Decompress abomassum completely
- Pull abomassum around
Abomassal disease
• Right sided abomasal dilation and torsion (not displacement)
• Dilitation precedes torsion
• Clinical signs:
a.  rumination and contractions and fecal quantity
b. distension of right flank
c.  HR
d. Signs become peracute once torsion occurs
e. Cold extremities and extreme dullness (shock)
f. Ping on right side
g. Metabolic alkalosis b/c of loss of Cl ions
• Tx
a. Correcting dilatation without torsion is much easier
b. Reports of metochlopramide to tx dilatation w/o torsion
c. IV fluids w/ Ringers or isotonic (lactated ringers Nabicarb should not be used) b/c of loss of Cl- ions
d. Right standing laparotomy technique:
- decompress w/ 12 g needle, the direction of the torsion should be identified and an attempt made to correct the torsion w/out removing the fluid
- Performe abomasopexy as LDA
Abomasal ulcers
Abomasal ulcers
• May be due to hypocuprosis (low copper)
• Black tarry feces
• Anemia, increased HR
Teat/udder injury
Teat/udder injury
• Colonized by Staph and Strept aggalacita
• Emphasize hygiene b/c mastitis can easily start
• Repair surgically if within 12 hours
• Evaluate if the injury enters the teat cistern
IBR – Infectious Bovine Rhinotracheitis
IBR – Infectious Bovine Rhinotracheitis
• Bovine herpes virus –1
• Source of infectious is nasal, eye, vaginal or preputial discharge, semen and fetal tissue
• Spread via aerosol or venereally
• Latent infection – shed during times of stress
• Respiratory dz:
a. Most common
b. Mild, subacute, acute to peracute
c. Discharge out of nose
d. Mild rise in temp
e. Short, expressive cough
f. Rapid and shallow breathing
• Reproductive dz
a. Ifectious pustular vulvovagintits – discharge of pus from vulva
b. Infectious bovine penoposthitis – purulent discharge form prepuce
c. Endometritis
d. Abortion
• Alimentary form – newborn calves due to FPT
• CNS – calves less thant six months old; rare
• Inclusion bodies may be seen
Acetonimia (Ketosis)
Acetonimia (Ketosis)
• High yielding lactating cows
• Caused by negative energy balance
• LOW prprionic acid or HIGH butyric acid
•  milk yield, Wt loss, inappetance and nervous signs
• Pathophysiology:
a. Negative energy balance causes the mobilization of fat reserves to meet the energy deficit
b. Fatty acids are broken down to acetyl-CoA, which enter the citric acid cycle
c. Medium and short chain Fas enter the mitochondria (long chain Fas are bound to Carnitine from lysine and methionine)
d.  oxidation removes two carbons from the FA to produce a lot of energy
e. If there is a decrease in acetyl CoA entering the citric acid cycle b/c of  supply of glucose metabolites, OR if there is an accumulation of acetyl CoA, then more acetate is formed in the liver. The ability of the tissues to oxidize the ketones is soon exceeded and they accumulate in the blood
f. Ketone bodies are:
- Acetate - ketogenic
- Butyrate – ketogenic
- Proprionate – glucogenic
• Clinical signs
a. Hypoglycemia
b. Wt loss
c. Decrease milk yield
d. Sweet smell (pear drops) of acetone on breath and in milk
e. CNS signs
• Tx
a. 500 mL of 50% dextrose
b. Propylene glycol
c. One dose of steroids to increase appetitie and increase glucose
d. Monensin – 300-500 mg SID PO; selects for proprionic acid
• Prevention
a. Prevent excess fat at calving
b. Good transition
c. Niacin
d. Decrease Cereal grain silaages containing high butyric acid
Calf coronavirus
Calf coronavirus
• 1-3 weeks old
• More watery and more severe than rotavirus
• Loss of Na, K, Cl and bicarb
• Yellow, watery feces
• Effects entire villus – malabsorption
Traumatic reticulopericarditis (Hardware dz)
Traumatic reticulopericarditis (Hardware dz)
• Cow ingests metal object and it lodges in the reticulum due to the releative mass and position of the reticulum; Ruminal and reticular contraction the wire penetrates until it reaches the peritoneum
• A localized peritonitis occurs causing a local abscess and adhesion
• The diaphragm and pericardium may be punctured
• Clinical signs:
a. Anorexia
b.  milk production
c. Arched back and tucked abdomen
d. Grunt positive, scootch negative
e. Fever
f. Shallow resp (may even look like pneumonia)
g. Jugular pulse
h. Muffled heart sounds – splashing and tinkling sounds over the heart
i. Secondary ketosis
• Tx and prognosis depends on whether or not pericarditis is present
a. Magnet or sx if pericarditis is NOT present
b. If it is present, then immediate slaughter must be recommended
Cystic follicular degeneration
Cystic follicular degeneration
• Causes:
a. Not enough GnRH from hypothalamus
b. Not enough LH receptors on ovary
c. Not producing or releasing LH from pituitary
• Can be luteal (thick walled) or thin walled (follculrar ccyst)
• Will not have a crown or papillair
• Uteruse is flacid when has a cyst, but may have a CL on other ovary or may even be pregnancy
• More common in dairy cows during high lactation (rare in heifers or beef cattle)
• Biggest sign is anestrus
• Tx:
a. Give GnRH or hCG to create luteal tissue, give PGF2alpha 10 days later to destroy luteal tissue
b. If cyst is still there, put on progesterone to suppress the hypothalamus, then remove progesterone and hypothalamus becomes hyperactive and proeduces GnRH on own
Early embryonic death
Early embryonic death
• Causes:
a. heat stress
b. high cortisol (stress)
c. Endometritis - A pyogenes, Campylobacter fetus, Ureaplasma, H somnus, Tritrichomonas fetus, IBR
d. Aged gametes
e. Trauma from hand of palpator
f. Lethal genes
g. Growth implants – endometrial glands don’t devleop properly when embryo embeds in uterus, has toxic envirnonment ito embryo
Squamous Cell Carcinoma (cancer eye)
Squamous Cell Carcinoma (cancer eye)
• Most common bovine neoplasm
• Contributing factors:
a. Long term exposure to intensive sunlight
b. Herford most common breed (lack of pigment or melanin around eye)
c. IBR
d. Dust
e. Flies
f. High level of nutrition
• Tx;
a. Sx excise, enucleation
b. Cryosurgery
c. Hyperthermia
d. Radiation therapy
e. Immunotherapy
Bovine rotavirus
Bovine rotavirus
• Calves at about 10 days old
• Yogurt-like feces
• Fuses and stunts tips of villi causing columnar epithelium to become cuboidal or squamous oreven completely flat
• Prevention via dam vaccination
• Dx virus antigen in feces – examine four affected calves and four normal calves and compare b/c healthy calves can excrete the virus
• Perfusion problem to the claw
• Different forms:
a. Arched back
b. front legs are crossed and hind legs wide apart
c. Shifts weight, painful walking
d.  HR and RR
e. warm hooves
f. Lateral hind claws are most seriously affected
• Rumen acidosis most common cause
• Fattly liver – can’t detoxify endotoxins
• Locally released mediators in inflammation and perfusuion in capillary circulation causing degeneration of the stratum germinatinum
• Tx:
a. Alter initial process – mastitis, endometritis, lactic acidosis
b. Abs
c. Bute and banamine
d. Soft bedding
e. Warm water bats
f. Steroids
g. Corrective shoeing
h. Sulphur-containing aas
i. Claw blocks
Hamophilus Somnus complex
Hamophilus Somnus complex
• Part of respiratory complex
• Most commonly affect feedlot cattle
• Complex is characterized by pleuritis, myocarditis and pneumonia
• Causes meningoencephalitis, pleuropneumonia and mycarditis (septicemia)
• Clinical signs:
a. Fever
b. Ataxia
c. Joint swelling
d. Fundic lesions
e. Weakness
f. Recumbency
g. Death
h. Pleuropneumonia
i. Myocarditis
Bovine respiratory syncytial virus
Bovine respiratory syncytial virus
• Causes viral pneumonia in dairy and beef calves under 6 months old
• Ideal sample is virus isolation or FAvia TTW in early stages
• Causes necrosis of type I pneumocytes and type II pneumocytes show hypertrophy, hyperplasia and syncytial formation
Corynebacterium spp
Corynebacterium bovis – Mastitis
• Mildly pathogenic
• Shows major break in hygiene – spreads rapidly from cow to cow in absence of adequate teat dipping
Corynebacterium spp
Corynebacterium renale – Contagious Bovine Pyelonephritis
• Causes pyelonephritis or balanoposthitis
• Found on vagina or prepuce of carrier animals
• Spread by trauma (breeding or catheterization)
• Type I and III most pathogenic
• Clinical findings – hematuria, pyuria, colic, straining to urinate, fever
• increased Crea and urea
• pH urine alkaline (> 8.5)
• May stimulate production of Ab that gives cross reactions w/ complement fixing test for Johne’s
• Culture urine for confirmation
• Aqueous fluid from eye? (BUN)
• Tx w/ PPG for three weeks

Corynebacterium renale – Enzootic Posthitis; Pizzle Rot; Balanoposthitis
• More common in sheep; only occasionally in bull
• Pustules and scabs at preputial orfice
• Flies are mechanical vectors
• Sheep on lush, improved high legume pasture
• Cytototoxic effect of ammonia produced from urea in the urine + high protein diet + continuous wetting
Corynebacterium spp
Corynebacterium pseudotuberculosis – Ulcerative Lymphangitis of horses and cattle
• More common in the horse
• Lymphangitis of lower limbs
• Dz in workhorse era
• Occurs through abrasions on lower limbs when horses are crowded together in dirty, unhgenic quarter
• Infection of skin wounds followed by invastion of lymphatic vessels and development of abscesses
• Cattle have lymph node enlargement
Staphylococcal spp.
Staphylococcal spp.

Staphylococcus aureus – Mastitis
• Contagious udder pathogen
• Coagulase positive
• Intracellular pathogen
• Abnormal milk primary clinical sign
• Vaccination available; but not extremely successful
• Need thre negative tests to have 95% confidence that cow is clean of staph
• Heifer rearing – milk fed to heif3rs and then comingeled w/ adults perpetuates problem
• Will go into remission by itself regardless of Ab
• Dry cow therapy is most effective (double dry tx may be necessary)

Coagulase-negative Staphylococci (epidermidis, chromogenes, hyicus, warneri, xylosus, simulans, sciuri)
• Coagulase negative
• Environmental pathogens
• Minor, considered ormal skin residents
• Unhealthy teat, hand and skin conditions promote growth, especially in the winter
• Dry cow therapy very effective
• Lactic acidosis causes a chemical rumenitis
• This can induce a mycotic rumenitis w/ (Mucor, Rhizopus and Absidia) 4-6 days later
• These mycotic agents invade the ruminal vessels and cause a thrombosis and infarction
• Widespread necrosisi and gangrene may affect the entire ventral half of the ruminal walls leading to acute peritonitis
• Hepatic abscesses can result b/c F. necrophorum and A. pyogenes can enter directly into ruminal vessels and spread to the liver
Umbilical hernias
Umbilical hernias
Most common in Holstein or Fresian (dominant, or recessive)
Five categories (see production notes)
1. Uncomplicated – omentum, intestine or abomassum, completely reducible w/ ring; no systemic signs
2. With fibrous core or abscess – one part will be reducible, the other will not;
3. Infection of umbillical cord remnants
a. Omphalophelbitis - umbillical vein, connects to liver
b. Omphaloarteritis – umbillical artery
c. Urachal abscess – most common, abscess in urachus
4. Umbillical abscess – feels warm, painful, non-reducible, firm; no hernia ring palpated; systemic signs seen; lance, drain and flush
5. Enlarged umbillical stalk – usually only cosmetic issue; usually secondary to omphalitis, persistent patent urachus, or post tx w/ chemical retraint
Papillomatosis – Warts
Papillomatosis – Warts
• Bovine Papilloma virus 1, 2, 3, 4, & 5
• Spread by direct contact or by fomites
• Clinical signs – small, smooth, hairless, firm, button-like elevations from skin
• May become coarse and cauliflower-like, sessile or pedunculated
• Head, neck, brisket and sometimes udder and teats and eyelids
• Histo shows epithelial proliferation w/ or w/o C.T. proliferation
• BPV I & II sponaneously regress
• BPV II, IV, and V tend to be persistent
• Autogenous vaccines are doubtful value
• Cryosurgery or cold steel surgery
• Lithium antimony thiomalate 6% solution 15 mL by deep IM injection every other day 4-6 times
Interdigital fibroma
Interdigital fibroma
• Common in sheep
• Mass of fibrous tissue between the toes; resembles papilloma
• If detected early, sx removal (cryosurgery and electrocautery) is successful
Hairy heel warts
Hairy heel warts
• Aka Bovine digital dermatitis, Papillomatosis digital dermaitis, Mortellaro’s dz, Foot warts, heel warts
• Between the heel bulbs of the plantar surface at the junction of skin and periople
• Red, granular appearance
• Most common in dairy cattle
• Spirochetes (Treponema denticola)
• Causes lameness, wt loss,  milk production
• Tx is topical oxytetracycline and bandaging
• Footbaths w/ tetracycline, lincomycin, spectinomycin, or 5% Cu sulfate can be used for control, but must be watched for contamnation
• Ostertagia ostertagi
• Type I
a. profuse watery D+ of calves on grass
b. Caused by immature adults leaving the gastric glands
c. Fall in the north; winter in south
• Type II
a. Yearlings following their first season of grazing
b. Caused by arrested L4 resuming development after hypobiosis
c. Spring in north; fall in the south
• Hypobiosis
a. L4 accumulate in gastric glands b/c of harsh weather conditions
b. Winter in the north, Summer in the south
• Animal ingests L3 and encysted larvae invade the gastric gland of the abomassum causing a ‘morrocan leather’ appearance. The gastric glands (parietal- HCL and chief – pepsinogen) are affected and the tight junctions that maintain the integrity of the epithelial sheet in diminished.
• The alkaline pH in the abomassum causes bacterial overgrowth and hypoproteinemia b/c of lack of pepsinogen.
• Tx: ivermectin, doramectin and moxidectin
Broad spectrum anthelmintics can be broken down into three major chemical groups:

a. interfere w/ nerve transmission by opening Cl channels
b. very broad spectrum including some ectoparasites but are inactive against cestodes (tapeworms) and trematodes (flukes)
c. excreted in the feces and may affect insects colonizing the dung

a. bind to tubulin and disrupt nutrient uptake
b. some are effective against cestodes (tapeworms)
c. Albendazole is active against liver flukes

a. cholinergic antagonists

Cestodes – tapes
Nematodes – rounds, strongyles, ascarids
Trematodes – flukes
Lactic acidosis
Lactic acidosis
• AKA acute CHO engorgement, rumen overload
• Caused by ingestionof large amounts of highly fermentable CHO (cereal gains, corn, grapes, apples)
• Pathophysiology – The increase in CHO causes a marked change in microes, specifically Streptococcus bovis which utilize the CHO to produce large quantities of lactic acid, causing the rumen pH to be < 5. This causes destruction of bacteria and protozoa in the rumen. Both D and L forms of lactic acid are produced. This increases ruminal osmolality and water is drawn in from the circulation, causing hemoconcentration and dehydration. L lactic acid is utilized much more rapidly than D, so it accumulates and causes a severe D-lactic acidosis.
• Clinical signs
a. Profuse D+ w/ sweet/sour odor of feces – may have undigested kernels
b. Anorexia
c. Depression
d. Dehydration
e. Rumen stasis
f. Ataxia leading to recumbency
g. Fluid splashing sounds on ballotment\
• Complications: (3 Ls)
a. Liver abscess – Fusobacterium necrophorum and Arcanobacter pyogenes from rumenitis break down of vessels
b. Laminitis – unknown pathogenesis
c. Lactic acidosis
d. Fungal hepatitis – Mucor, Rhizopus, Absidia
• Clin path:
a. Ruminal fluid pH < 5
b. Rumen microbes abscent
c. Dehydration
d. Hypocalcemia – temproary malabsorption
e. Hypochloride – loss of serum Cl due to sequestration in the rumen
f. Hyperphosphatemia – renal failure
g.  blood lactate
• Tx if animal is found engorging herself (before clinical signs)
a. Off water for 12-24 hours
b. Offer good quality hay at ½ day ration
c. Exercise every hour for 12-24 hours to encrouage movement of ingesta through GI tract
• Tx if animal is showing clinical signs
a. Rumenotomy – severe cases; empty rumen w/ a siphon and replace with cud transfer and few handfuls of hay
b. Sodium bicarb – systemic acidosis
c. Rumen lavage – rubber tube and warm water pumped in until obvious distension of L paralumbar fossa, then empty via gravity
d. Alkalinizing agents – Mg hydroxide or Mg oxide pumped into rumen, then kneading to promote mixing
e. Antihistamines form lamintits
f. NSAIDs – shock therapy
g. Thiamin or brewer’s yeast to promote metabolism of lactic acid
h. Parasympathomimetics – Ach-like effect, cholinergic drugs; stimulates smooth muscle contraction
- Choline
- Ach
- Methacholine
- Carbachol
- Bethanechol
- Pilocarpine
i. Ca borogluconage – tx hypocalcemia
Classification of Drugs
Adrenergic agonists – Sympathomimetic (alpha and beta adrenoceptors)
Metabolism of norepinephrin – COMT and MAO

• beta (low dose) & alpha(high dose
• incr HR, mydriasis, relax the bronchioles
• Used for hypersensitivity reactions and anaphylactic shock, localized hemorrhage, open angle glaucoma; restores cardiac activity following cardiac arrest

• no B2 receptor
• Same as epinephrine except will increase mean blood pressure more than epinephrine b/c can’t relax skeletal blood vessels at B2
• Will decrease cardiac output b/c of stronger baroreceptor activation and vagal reflex
• corrects hypotension induced by spinal anesthesia

• no B 2
• D receptors on renal, mesenteric and coronary circulation
• D1 receptors causes vasodilation of renal and mesentaric vasculature at low rates of infusion (diuresis)
• D2 in CNS decr blood pressure and HR causing vasodilation in renal and mesenteric vasculature
• At higher concentrations, activates A1 and B1, which incr HR and causes vasoconstriction

• nonselective B agonist
• incr cAMP
• Decreases mean blood pressure, increases cardiac output, relaxes tissues w/ B receptors, inhibits histamine release
• Used for acute bronchial contstriction and complete AV block

• direct A 1agonist
• Used as a topical nasal decongestant
• Used to dilate the eyes

• A & B
• Short term tx of heart failure – inotropic effect; increases cardiac output

• Mixed acting agent
• Scheduled drug
• Treats asthma-like condition, used as a mydriatic, preimary urinary bladder sphincter incompetence

• Indirect sympathomimetic
• Primary urinary bladder sphincter incompetence
• Nasal decongestant

• Direct acting B2 agonist
• Bronchodilator, especially w/ animals w/ heart disease, hyperthyroidism or hypertension
Classification of Drugs
Alpha Adrenergic antagonists - Sympatholytics

• Binds covalently to A receptor
• Causes hypotension and decreases total peripheral resistance
• Reduces hypertonus at urethral sphincter in dogs and cats
• Can tx laminitis and secretory D+ in horses (but NOT to be used in horses w/ colic)

• Competitive and selective A1 receptor antagonist
• Decreases total peripheral resisitance and relaxes arterial and venous smooth muscle
• Used in congestive heart failure and hyertension

• Competitive A1 and A2 antagonist
• Increases HR and lowers blood pressure
• Used to tx hypertension
• Used to tx sympathomimetic amine overdose

• Competitive A antagonist
• Reverse the effects of xylazine and amitraz
Classification of Drugs
Beta adrenergic antagonists - Sympatholytics

• Competitively blocks both B receptors
• Decreases HR, cardiac output, myocardial oxygen demand, automaticity of the heart, Increases airway resistance
• Used to tx hypertension association w/ thyrotoxicosis
• Used to tx pheochromocytoma
• Used to tx arrhythmias – VPCs, tachcardia
• Long term therapy can induce up regulation of B receptors
• Abrupt cessation of therapy may lead to excessive stimulation of B receptors, exacerbating symptoms

• Competitive B antagonist
• Used to tx supraventricular arrhythmias, HCM (hypertrophic cardiomyopathy) in cats, and hypertension
Classification of Drugs
Cholinergic agonists - Parasympathomimetics

Acetylcholine (Ach)
• Ach stimulates muscarinic and nicotinic receptors
• Produces vagal stimulation – decreases blood pressure, vasodilation
• Increases GI motility and secreation
• Causes contraction of the uteruse, ureters, bladder , bronchi and sphincter muscles of the iris
• Increases salivary and lacrimal gland secretions
• Little or no use as a therapeutic drug

• Hydrolyzed much more slowly than Ach, so a more useful drug

Carbachol – carbamylcholine
• Produces miosis in ophthalmology

• Agonist of muscarinic receptors
• Used to tx abdominal distension, esophageal reflux and distention of the urinary bladder

• Produces miosis and lowers intraocular pressure in glaucoma
Classification of Drugs
Anticholinesterase agents – indirect cholinergic agonists

• Crosses the BBB
• Glaucoma tx
• Counteracts intoxication by atropine

• Reverses tubocurarine-like blockades of NBA (neuromuscular blocking agents)
• Used to tx paralytic ileus, atony of urinary bladder, myasthenia gravis conditions
• Contraindicated in bowel or bladder obstruction

• Used to dx myasthenenia gravis dz
• Antagonizes tubocurarine-like drugs

• Used to tx myasthenia gravis

• Glaucoma tx

• Used to control flease

• DFP, Echothiophate, Malathion, Parathion, Dichlovros
• Causes SLUD
• Miosis and bradycardia
• Antidotes is atropine and 2-PAM, pralidoxime)
Classification of Drugs
Parasympathetic antagonists – anticholinergics (antimuscarinic)
Scopolamine (hyoscine) – tx motion sickness
Propantheline – Tx D+ in small animals and used to relax the rectum prior to rectal exam in horses
Tropicamide – induces mydriasis and cycloplegia in ophthalmology, has a shorter duration than atropine
Prirenzepine – reduces gastric acid secretion
• RNA pestivirus; related to Hog Cholera and Border dz
• 2 genotypes – Type I (Ia & Ib) and Type II
• Most are Type I
• 2 biotypes:
a. Cytopathic – cell death in culture
b. Noncytopathic – does not cause death in culture
• Naïve animals exposed to BVD will show:
a. D+
b. Fevere
c.  RR
d.  milk production
e. Abortions, Eed; fetal wastage
• Fetus will show:
a. Micro-phthalmia
b. Juvenile cataracts
c. Cerebellar hypoplasia
d. Arthroporosis
e. Curly hair coat – like border dz in sheep
• 1 virus to set up 2 infection of Mannheimia and Pasteurella along w/ stress and shipping
• Persistently infected animals – calf exposed in utero
a. Caused by noncytopathic biotype exposure to cow at < 150 days of gestation
b. Could abort, develop congenital lesions, develop persistent infection, or nothing could occur
c. PI infected animals are smaller, chronic poor-dooers or could be normal
• Mucosal dz
a. When persistently infected aniamsl are expposed to a cytopathic virus you get ‘mucosal dz’
b. Looks similar to Foot and Mouth
c. Must be similar strain of NCP and CP
d. Can be induced by modified live vaccin, mutation inside the calf changes from NCP to CP, or animal gets an acute infection of CP
• Dx
a. Virus isolation on whole blood
b. Test poor dors
c. Test again in 3 weeks
d. EAr notching – punch biopsy IMHC (immunohistochemistry)
e. If BVD +, then test every animal via virus isolation or ear notch. Cull all +; retest when born.
f. Retest w/in a year and cull the positive
g. Herd screening - >5 months old calves b/c after maternal antibodies but has not been vaccinated yet; “Canary in the mineshaft”
• Prevention
a. Vaccinate w/ killed or MLV
b. Close the herd – test incoming pregnant heifers via ear notch and test fetus when born; isolate her until she gives birth and then quarantine for 3 weeks
Clostridial enterotoxemia
Clostridial enterotoxemia
• Clostridium perfringens types B,C & E (beta toxin)
• Causes enterotoxemia in calves, lambs, foals and piglets
• Occurs in calves 5-15 days old
• Acute and highly fatal in all species
• The  toxin is readily inactivated by trypsin, but b/c the young animal has absence of mature flora, C. perfringens colonizes
• Bacteria are capable of forming spores
• D+, abdominal pain, nervous signs (tetany, opisthotonos); Violent bellowing and aimless running
• Type B – more localized lesions
• Type C – more extensive lesions
• Tx is hyperimmune serum
• All pregnant animals should be vaccinated to provide colostral immunity to babies.
• Antiserum will protect susceptible animals and is give immediately after birth
• AKA Navel ill
• Is inflammation of the external aspects of the umilicus
• Occurs commonly in calves w/in 2-5 days of birth and often persists for several weeks
• The umbilicus is enlarged, painful on palpation and may be closed or draining purulent material through a small fistula
• The affected umbilicus may become very large and cause subacute toxemia
• The calf will be moderately depressed
• Tx: sx exploration and excision
Winter dysentery
Winter dysentery
• Bovine corona virus
• Northern climates in adult lactating dairy cows during winter months
• Sudden, explosive D+ affecting almost entire herd w/in several days
• May have mild respiratory signs
• Dx via detection of virus in feces (ELISA)
• No tx or control available
Fatty liver – Fat Cow syndrome
Fatty liver – Fat Cow syndrome
• Mobilization of excessive body fat to liver during periods of negative energy balance at time of parturition or in early lactation in dairy and beef cows
• Predisposition includes:
a. High producing dairy cows
b. Over-conditioned beef cows just before or after calving (when energy intake suddenly decreases)
c. Twins
d. Lead or challenge feeding during dry period
e. Milk fever, detosisi and LDA can complicate fatty liver
f. Starvation diet of dry cows right before calving b/c farmer thinks is too fat which may increase dystocia (untrue)
• Highly fatal
Fatty liver – Fat Cow syndrome
• Pathogenesis – After calving there is a large increase in fat accumulation in the liver; b/c of the metabolic demands of lat pregnancy and early lactation, there is a gradual increase in NEFAs (nonesterfied FA) and glucose during final days of gestation and a decrease in BHBA (betahydroxyburtyrate). Immediately after parturition, there is an  in energy demands. This causes a mobilization of fat from body reserves (SQ fat) to the blood which transports fat to the body tissues (particularly the liver) but also muscle and kidney
a.  NEFAs and glucose and  BHBA pre-parturition
b.  energy demands immediately after parurtion
c. Mobilization of fat from SQ fat to blood to liver, muscle and kidney
d. If there is a decreases in energy intake (she can’t eat enough or there is not enough food) then there is an excess mobilization of FFAs to the liver
e. Hepatic lipogeneissi – enlarged hepatocytes,  liver glycogen, inadequate lipoprotein transport
f. Most lipids in the liver are triacylglycerols b/c  NEFAs and  deacylglycerol acyltransferase (enzyme activated by FA)
g. May be exacerbated if the liver has  ability to export VLDL (very low density lipoprotein)
• Clinical signs
a. High BCS
b. Anorexia
c. Recumbancy
d. Scant feces
e. Unresponsive ketosis
f. Nervous signs – especially beef cows
g. Increase in liver enzymes, increase in blood ketones
• Tx
a. IV glucose and electrolyes
b. Transfaunation
c. Dexamethasone
d. BSE
e. Propylene glycol – promotes gluconeogenesis and inculin
f. Offer good quality hand and water
g. Steroids
• Control
a. Prevent pregnant cattle from becoming fat during last trimester (especially during dry period)
b. BCS often to monitor nutrtional starus of herd
• Coccidia in calves 1-2 weeks old)
• Excreted oocysts are directly infective to new hosts
• Not host specific – can spread to man and other species
• Unaffectd by existing anticocccidial drugs
• Ingests oocytsts w/ sporozoites  Trophozoites  mature to Schizones w/ 8 merozoites  2nd generation merozoites (sexual phase) to form zygotes in the enterocyte
• Profuse watery green D+ w/ occasional mucus and blood
• Dehydration
• Destroys mature enterocytes in small and large intestine causing a malabsorption and secretory dz
• Giemasa, Acid fast and Auramine to stain oocysts in fecal smear from flotation technique
• No specific tx, but sulfaquinooxaline w/ Vit B & K may decrease mortality
• Steam cleaning and good hygiene as best control
Grass tetany; hypomagnesemia
Grass tetany; hypomagnesemia
• Lactating cows (beff or dairy) when grazing grass in spring or autumn
• Clinical signs are hyperastesia, incorrdination, tetany and convulsions; reluctance to enter the parlor (subclinical); sudden death
• Most common around peak lactation b/c of increased secretion of Mg in milk
• Pathophysiology – there are no Mg stores in the body, so if there is a reduction in the amount of Mg in the diet w/ an increase in milk production, grass tetany can occur
• Clovers have high Mg
• Ryegrasses have low Mg
• K+ fertilizers in late winter/early spring will reduce abdorption of Mg
• Ca, K and ammonium (Nitrogen) ions interfere w/ body uptake of Mg
• Milk tetany can occur in calves 2-4 months old fed whole milk diets w/o Mg supplement
• Any level below normal (0.85) is hypoMg
• Hypocalcemia and Hyperkalemia is common
• After death, blood or tissue levels are meaningless b/c Mg rises after death. However, CSF and vitreous humor will be depressed even after death
• Tx:
a. Be quiet and gentle – can die from any stress or sudden stimulus
b. IV 6% Mg salt (Mg sulfphate) slowly– can cause resp or cardia failure
c. Ca borogluconate – hypocalcemia
d. Sodium pentobaritone (euthaniasia) solubiont IV to reduce convulsions
e. Relapses are common – SQ Mg sulfphate solution
f. Orally give 4 Mg bullets
Bovine Leukemia Virus - Bovine lymphosarcoma (LSA) or Enzootic bovine leukosis
Bovine Leukemia Virus - Bovine lymphosarcoma (LSA) or Enzootic bovine leukosis
• Most common in 3-8 years old; Hereford
• Description
a. Exogenous C-type RNA oncovirus in retroviridae family
b. Present in circulating B lymphocytes
c. P24 internal protein antigen and gp51 glycoprotein antigen is important for dx
• LNs, right side of heart, abomasum, uterus, kidney, eye, spinal cord
• Iatrogenic transmission – needles; multidose syringes can spread, same rectal gloves, dehorning and ear tattooing
• Contract transmission via saliva, vaginal disharges, tracheal fluids
• Clinical signs
a. 60% are asymptomatic
b. May show persistent lymphocytosis
c. Enlarged LNs
d. Depression, indigestion, chronic bloat, LDA, lamness or paralysis
• Dx
a. Persistent lymphocytosis
b. AGID Ab to viral antigens p15, p24, and gp51
c. ELISA to detect BLV Abs
• Control
a. isolate and separate BLV positive cows
b. Test all incoming cows
c. Separate and raise calves on BLV-free milk, if serologically negative at 7 months then can join negative herd
Sporadic bovine leukosis
Sporadic bovine leukosis
• LSA in young animals in absence of BLV
• Three forms:
a. Juvenile - < 6 months old LNs, liver , spleen and bone marrow; death
b. Thymic – 6-30 months old; massive tumor in thymus and nods of neck and thorax; death
c. Cutaneous – 18 months-3 years; nodular lymphocytic neoplasia in seen in the skin; if animal survives, will recover in several weeks but will have remission and die
White muscle disease – aka Subacute enzootic muscular dystrophy
White muscle disease – aka Subacute enzootic muscular dystrophy
• Selenium and Vit E deficiency causes a myopathy
• Myodegeneration in calves and lambs of dams that received selenium-deficient feed during or before gestation
• Legumes are low in selenium
• Clinical signs:
a. sternal recumbency but will attempt to stand
b. The hocks will rotate
c. Muscle tremor
d. Dyspnea
e. ‘Flying scapula’ – scapula protrudes above the vertebral column and is widely separated from the thorax; bilateral rupture of the serratus ventralis muscles
f. Paralytic myoglobinura – stiffness, recumbancy, myoglobinuria, hyperpnea, and dyspnea
• Selenium is component of GSH-PX enzyme needed to protect RBC membranes and a component of thyroid gland hormones to convert T4 - T3
• Selenium contouracts toxicty of heavy metals
• Vit E is an antioxidant that prevent oxidant damage by decreasing hydroperoxid formation
• Tx is a mixture of selenium and alpa-tocopherol (Vit E)
Actinobacillosis – Wooden tongue
Actinobacillosis – Wooden tongue
• Actinobacillus lignieresii
• Infection through abrasion of the tongue (ulcer, teeth, spiny awns, prickly forage) ; it is a normal inhabitant of the oral cavity and rumen
• Clinical signs:
a. salivation and gentle chewing
b. Tongue is swollen and hard particularly at the base
c. Manipulation of the tongue causes resentment
d. Lymphadenitis
e. Loud, snoring respiration
• Can also occur in sheep but involves the lower jaw, face and nose (not the tongue)
• Tx w/ Iodides (Potassium iodide, Sodium iodide) until iodism develops
Signs of iodism
Signs of iodism
• Lacrimation
• Anorexia
• Coughing
• Appearance of dandruff
Actinomycosis – Lumpy Jaw
Actinomycosis – Lumpy Jaw
• Actinomyces bovis
• Caused by wounds to the buccal mucosa through wounds or dental alveoli
• Clinical signs:
a. Iniatially painless, hard, immovable bony swelling on mandible or maxilla at the level of the central molars
b. Eventually discharge small amounds of pus through one or more openings in skin
c. Can spread to esophageal groove and even reticulum
• Clin path show ‘club’ colonies of Gram-positive filaments
• Tx is debridement w/ antibacterial therapy
Streptococcal diseases
Streptococcal diseases

Streptococcus agalacia
• Contagious udder pathogen
• CAMP positive, esculin negative
• Dry cow therapy will 100% eradicate

Environmental Strepts: S. uberis, dyslactia
• Non-ag, CAMP test and esculin fermentation
• Dry cow therapy is highly effective
• Eradication is not possible b/c is ubiquitous

Neonatal Streptococcus
• Streptococcus genitalium
• Causes acute painful swelling of joints, lameness, and fever
• May show signs of meniingitis, omphalophlebitis, and ophthalmitis
• Source is contaminated uterine discharged from infected dams through umbilicus
• Tx w/ PPG
Paratuberculosis – Johne’s disease
Paratuberculosis – Johne’s disease
• Mycobacterium avium paratuberculosis (MAP)
• Related to Crohne’s dz
• Clinical signs:
a. D+ - often contains bubbles
b. Progressive wasting dz over several weeks or months
c. Bottle jaw
d. Normal to increased appetite (parasites will have a decreased appetite)
e. 3-5 years old
• Transmitted via feca/oral, colostrum or transplacental
• Dx:
a. Clumps of acid fast bacteria in smears of feces stained w/ Ziehl-Nielsen stain of rectal mucosa
b. Culture – 16 weeks; positive is useful (high specificity)
• Tx is not recommended; Control via:
a. Test everybody w/ ELISA
b. Those that are positive, culture to confirm positive
c. Cull fecal culture cows
d. Cull offspring of culture positive cows
e. Multiple/yearly testing – cull accordingly
• In gray matter of brain
• Caused by thiamin inadequacy or ingestion of thiaminase plants in cattle and sheep
• OR caused by sulfate toxicity
• Clinical signs
a. Sudden blindness
b. muscle tremors
c. opisthotonus
d. nystagmus
e. convulsions
f. staggers
• Plants containing thiaminase (will also cause bone marrow suppression)
a. Bracken fern
b. Horstail.
• Thiamin hydrochloride (there is no tx for sulfate toxicity)
Dermatophilosis – aka lumpy wool and Strawberry foot rot, cutaneous streptotrichosis
Dermatophilosis – aka lumpy wool and Strawberry foot rot, cutaneous streptotrichosis
• Dermatophilus congolensis
• Infection of the epidermis characterized by exudative dermatitis w/ scab formation
• Seen in cattle, sheep and goats most commonly (occasionally horses)
• A few human cases have been reported
• Prolonged wetting by rain, high humidity, high temp and flies and ticks can increase it
• Carbon dioxide released from breaks in the skin attact the zoospore
• Most recover w/in 3 weeks of initial infection or during dry weather
• Scabs look raised and circular
• Lumpy wool – pyramid-shaped masses of scabs on wool
• Strawberry foot rot – skin from coronet to carpus or hock
• PPG or streptomycin injections
• Seen in housed calves fed milk substitute or wened animals fed high concentrates
• Occur most commonly at the sigmoid flexure of the penis
• Housed animals - Ca or Mg ammonium phosphate, Struvite or oxalate
• Pastured animals – Ca carbonate, Mg carbonate and Ph carbonates
• Factors:
a. High concentration of grain
b. Vit A deficiency has been suggested a factor
c. Estrogesn from plants or growth promoters
d. Pelleted ration
e. Castrated males
• Clinical signs:
a. Palpate preputial hairs, will feel gritty
b. Straining to urinate
c. Colic – kicking at belly, paddling movement, tail swishing
d. If there seems to be a sudden relief, probably a urethral or bladder rupture (will see abdominal distension)
• Tx is sx
• Enterobacteria – anaerobic Gram negative rod
• Zoonotic dz – food contaminated w/ animal products
• The two types that affect cattle are S dublin and S typhimurium
• Occurs in calves (> 5 days old; or 2-6 weeks old) and cattle
• Signs are severe D+ in adults
• Putty-like D+ in calves, may become dark brown and watery and foul smelling
• Three syndromes:
a. Peracute systemic infection
b. Acute enteritis
c. Chronic enteritis
• All serotypes are pathogenic to man & animals

S typhi, partype A and sendai
• Host adapted and cause dz only in man

S abortusovis
• Sheep specific

S pullorum
• Poultry specific

S cholerasuis
• Causes dz in pigs, but are opportunist pathogens for other spp

S dublin
• Causes dz in cattle but is opportunist pathogen for other spp

S typhimurium
• Ubiquitous
• Causes dz in many animals including cattle and humans

• Fecal samples (not swab) before Abs for culture
• Control:
a. Uncontaminated food and water
b. Control of rodents and birds
c. Biologic control
d. Vaccination
Stifle injuries - Patellar luxation
Stifle injuries - Patellar luxation
• Dorsal
a. intermittent in adult cattle
b. hindlimb remains extended caudally longer than usual, then pulled forward and upward (looks like stringhalt)
c. Tx is medial patellar desmotomy if signs persist form more than one week
• Medial– rare; congenital
• Lateral
a. mature cattle and young calves
b. secondary to quadriceps atrophy from femoral paralysis
c. Lateral and medial fixation show characteristic posture of a markedly flexed stifle and the limb collapses on weight bearing (exactly as in femoral paralysis)
d. Bilaterally affected calves may be recumbant
e. Both medial and lateral fixation are tx w/ a joint capsule overlap procedure
Stifle injuries – Cranial cruciate ligament rupture
Stifle injuries – Cranial cruciate ligament rupture
• Heavy weight, sudden twists and falls (mounting, being mounted by cows in estrus)
• Subluxation of femarotibial joint, CrCL rupture, damage to tibial menisci, secondary osteoarthritic changes
• Soft tissue swelling and creptus
• Can get tibial drawer sign
Other stifle injuries:
Other stifle injuries:
1. Collateral ligament torn
2. Patellar fx
3. Proximal tibial epiphyseal separation – young cattle
Clostridial myositis – Blackleg
Clostridial myositis – Blackleg
• Clostridium chauveoi
• Gram positive, spore bearing anaerobic bacillus
• Highly resistant to environmental conditions and can remain viable for many years
• Localize in spleen, liver and muscles
• Clinical signs:
a. Initial – hot and painful lameness on a limb
b. Cold and emphysematous limb
c. Respiratory distress if involves the tongue
d. Stiffness and reluctance to move when sublumbar muscles are involved
e. Depression, anorexia, incr HR and incr temp
f. Death occurs in 12-24 hours
• After death, carcass becomes bloated and putrefaction occurs rapidly
• Bloodstained froth exudes form all body orfices
• Muscle is black, dry and crepitant w/ spongy and rancid odor
• Dx:
a. Anthrax must be ddx
b. FA stain
• Tx Ab of PPG only if early
• Prevent via vaccines of all animals > 6 months old
Clostridial myositis – Malignant edema
Clostridial myositis – Malignant edema
• Acute wound infection caused by Clostridial organsism
• C. novyi, C perfringens, C septicum, C sordelli
• Caused by deep puncture wounds, sx operations, injections, parturition
• Affects individual or small number of animals
• Swelling, tense and emphysematous
• Lameness, stiffness, and muscle tremors may be evident – can die w/in 48 hours
• At necropsy, all body cavities contain blood stained fluid
• The side of infection is surrounded by an extensive edema of SQ tissue and IM fascia
• FA tests or culture
Pregnancy toxemia
Pregnancy toxemia
• Considered primarily a dz of sheep
• Similar to ketosis only during 7-9 months of gestation
• Problem w/ beef cattle in late pregnancy
• Starvation, energy deficient diet in fat cows induces causing massive mobilization of fat reserves
• Same clinical signs as ketosis
• Clin path shows hypoglycemia, hyperketonemia and ketonuria
• Dx via clinical signs, nutritional status and stage of pregnancy
• Tx is same as ketosis
• Even though it is more common in fat cows, it is essentially the result of starvation; therefore, supply good quality forage throughout gestation
Leptospirosis (serotypes icterohemorrhagica and canicola)
Leptospirosis (serotypes icterohemorrhagica and canicola)
• L interrogans serovar icterohemorrhagica and serovar canicola
• Rodent is carrier
• Spread via feed or water
• Fever, dullness & anorexia
• Jaundice and hemoglobinuria
• Synovitis and dermatitis
• Tx: Dihydrostreptomycin, tetracycline, blood transfusion
Leptosprirosis (serotypes hardjo)
Leptosprirosis (serotypes hardjo)
• Leptospira interrogans serotype hardjo
• Common cause of abortion
• Transmitted to humans by contact via urine by milking
• Spread cow to cow via urine, fetus and uterine discharge and semen
• Two main syndromes:
a. Udder – sudden drop in milk in all quarters, udder secretion is thickened and clotted; Flabby bag
b. Abortion – second half pregnancy
• Culture urine to dx
• Tx: dihydrostreptomycine
• Vaccination w/ killed, but should use Ab in all cattle before vaccination program b/c infected cows may still excrete vacteria
Coxofemoral luxation – hip joint
Coxofemoral luxation – hip joint
• 2-5 year cattle w/ parturition and early postpartum
• Obturator or other nerve injury during dystocia
• Craniodorsal displacement most common
• Sudden onset of lameness is only consistent sign
• Leg may be rotated outward, hock medial and stifle more lateral
• Leg may appear shortened and asymmetrical femoral trochanters
• Rectal palpation may locate crepitance
• Tx:
a. Manipulative reduction – position cow so that the body is fixed while the affected upper leg can be extended in various direction (deep sedation is advisable)
Retropharyngeal abscess
Retropharyngeal abscess
• Same as abscesses of the jaw, wait until there is a softening to lance open
• May be induced by balling gun, actinobacillosis or foreign object
• Apples and potatoes most common
• Fed in groups where cows will hoard food
• Signs include:
a. Profuse salivation followed by bloat (prevents swallowing and eructation)
b. Head extended
c. Frequent attempts to swallow
• Dx pass a stomach tube to see if there is an obstruction (or will dislodge it!)
• DDx rabies (excess salivation is either choke or rabies!)
• Tx
a. cannula for rumen tympany
b. spasmolytics (hyoscine butylbormide and dipyrone)
• Prevent by cutting food into small pieces
Mycoplasmosis - mastitis
Mycoplasmosis - mastitis
• Mycoplasma bovis most common cause of mastitis
• Not a bacteria, lack a cell wall
• Multiple quarters
• Refractory to Ab tx – cull postitive cows
Mycoplasmosis – respiratory; Contagious bovine pleuropneumonia
• Mycoplasma mycoidies
• Eradicated
• Sudden pyrexia and respiratory distress and pain
Contagious bovine pyelonephritis
Contagious bovine pyelonephritis
• Corynebacterium renale
• Urinary tract of cattle causing inflammation of kidneys, ureters and bladder
• Caused by ascending infection, females are far more susceptible than males
• > 3 years old
• Hematuria, colic, painful urination w/ progression to anemia and uremia
• Gram stained urine shows the organism
• Tx w/ PPG
• Acidification of urine w/ Na phosphate
• Caused by intravascular hemolysis
• True hemoglobinuria causes a deep red to brown coloration of urine and giva a positive raction to hemoglobin tests

DDx for Hburia
Red maple – wilted leaves (BUT ONLY IN HORSES)
Scented thorn
Cereal rye
Babesiosis (bigemina and bovis) – severe jaundice
Tropical theileriosis – Hyalomma ticks, LN enlargment
Postparturient Hburia – no jaundice, 2-4 weeks postcalving in cows 3-6th lactation
Bacillary Hburia
Leptospriaotiss (interrogans pomona) – mostly in young calves, jaundice, petechia, pallow, adults have orange milk
Chronic copper poisoning – copper supplement in swine diet by mistake
Bacillary hemoglobinuria
Bacillary hemoglobinuria
• Clostridium hemolyticum
• Beta toxin grows in a single necrotic infarct in theliver
• Summer and autumn in endemic areas (irrigated or poortly drained pastrue)
• Causes toxemia, Hburia, and jaundice, brisket edema, sudden death, urine is dark red
• Tx is immediate PPLG or tetracyclines
• Antitoxic serum if available
• Vaccination available
Campylobacteriosis and Trichomoniasis
Campylobacteriosis and Trichomoniasis

In calves
• Campylobacter jejunia and coli are most common causes of disease in man, but are NOT implicated to cause D+ in calves

• Campylobacter fetus spp venerealis – venereal infection
• Campylobacter fetus spp fetus – ingestion
Tritrichomonas fetus
Tritrichomonas fetus
Protozoan w/ 3 anterior and 1 posterior falgella and an undulating membrane
Venereal dz of cattle
Transmitted by coitus

Shed via coitus, bull sprays semen on cervix, then trich migrates to the uterus

Lives in crypts of preputial cavity of bulls or vagina and uterus of cows

Must persist >7 wks to cause endometritis, placentitis & fetal loss

DOES NOT prevent conception, but EED (early embryonic death)

Asymptomatic in bull

Herd hx of gradual ‘infertility’

Conceive, but then return to estrus 40-45 days later

Get a ‘scattered calf crop’

**Causes postcoital (not post partum) pyometra

If only ONE T. fetus is found, then entire herd is considered infected.

Pyometra fluid will be FULL of T. fetus.

Cow w/o pyometra will spontaneously recover and temporary immunity

1. Pass sterile pipette into prepuce fold, massage till hemorrhage. Aspirate w/ saline. Inoculate w/ Diamond’s media so will multiply, & culture for 24-48 hrs. THREE TIMES

2. Retract penis and scrube till bleeds w/ sponge. Pan below catches drippings (Peter Pan)

3. Fetal fluids, pyometra fluid, cervico-vaginal mucus

If only ONE T. fetus is found, then entire herd is considered infected.

Pyometra fluid will be FULL of T. fetus.

Cow w/o pyometra will spontaneously recover and temporary immunity

1. Pass sterile pipette into prepuce fold, massage till hemorrhage. Aspirate w/ saline. Inoculate w/ Diamond’s media so will multiply, & culture for 24-48 hrs. THREE TIMES

2. Retract penis and scrube till bleeds w/ sponge. Pan below catches drippings (Peter Pan)

3. Fetal fluids, pyometra fluid, cervico-vaginal mucus
Campylobacter fectus ss. Veneralis
Campylobacter fectus ss. Veneralis
(ss fetus and jejuni are not venereal dzs – but only cause sporadic abortions)

Not zoonotic in cattle (zoonotic in sheep)

Microaerophilic (candle jar method)

Spread by genital contact in vagina and cervix and progresses to uterus and oviducts in 7 days causing endometritis and salpinitis

Affects developing embryo at the time of maternal recognition of pregnancy (DOES NOT affect conception)
Same as above only some cows become CARRIERS from one breeding season to the next
Same as above only isolate in CLARK’s medium

To test bull, breed to virgin heifers, then culture the heifers

Once dx, need lifelong vaccination program

Tx bull w/ Dihydrostriptomycin
C jejuni – cattle, swine, fowl
C jejuni – cattle, swine, fowl
C fetus, hyointestinalis – swine

C coli – fowl

C jejuni most common, thermophilic, thermoduric
Survives refrigeration and freezing well and has low infective dose

Commercial poultry and eggs, cattle, swine are reservoirs

Person to person (daycares and mental institutions)
Young puppies or kittens w/ D+ can serve as source in children

Raw foods of animal origin (water, milk, meat, eggs and seafood)are the major sources of these pathogens via mishandling and recontaminating foods
Highest risk in children 0-5 years old, young children and young adults also at risk

*Major pathogen of college students in US

Enteric form in children:

Disseminated form:
Chills, sweats, cough, headache, meningitis (esp in babies), wt loss, poor appetite, V+, D+

May be confused w/ appenticitis

Pasteurization of milk
Water tx
Proper cooking of food
Stray voltage
Stray voltage
• Low voltages of 110-220 volts are sufficient to kill a cow
• At 2 volts, cattle are expected to respond
• Measured point to point (2 contact points that the cow mich touch simultaneously) or point to reference point (measures the ground and a cow).
• Anaplasma marginale
• Carrer animals are the source of infection
• Transmitted by ticks (Boophilus microplus, Dermacentor), tabanids, iatrogenically and transplacentally
• Anemia, jaundice, severe debility, death
• Disease Anaplasmosis ovis in sheep and goats is usually subcliical
• Will see organism in red cells by microscopy
• Detection via blood smear, serology, PCR
• Tx: Tetracycline or imidocarb, blood transfusion
• Weekly dipping in acaricides is vacciantion inendemic arease
• Listeria monocytogenenes
• Ubiquitous in farm enviroment
• Rumeinants, particularly sheep, assocaiated w/ feeding silage w/ high listerial growth and management induced stress
• Can see multiple cases in a group
• Causes encepthalitis w/ brainstem and CN dysfunction or abortion in last trimester
• Can also cause septicemia in pregant and neonatal sheep and goats, enteritis in weanlings, spinal myelitis, ophthalmitis and occasionally masitis
• CSF – pleocytosis of mononuclear cells and lymphocytes &  protein
• No difinitive dx except for at necropsy
• Microabscesses in brainstem, spinal cord, intestin or viscera
• Tx is chlortetracycline or PPG EARLYin clinical dz
• Zoonotic implications
Listeria monocytogenes
Listeria monocytogenes
Gram pos, nonspore forming facultative anaerobic rod

Can survive in the soil & in the animal in both carrier and active states
Serious dz in man b/c:
* Ubiquitous
* Apparent resistance b/c psychrophilic and thermoduric

Animals, birds, insects & environment are reservoirs

Foodborne most imp

Milk & dairy products
Raw vegetables
Mexican soft cheese
Coleslaw (cabbage)
Pasteurized milk
Vegetation from contaminated soil, sewage, stream water, slaughter house waste, milk of normal mastitis cows & feces of healthy humans
Hotdogs & sausages
Meat & fish
Pregnant women
I/S individuals
Debilitating dzs
Farmers who consume raw milk

Spontaneous abortion
Septicemia (flu-like)
Localized abscesses
Dermatitis w/ papular or pustular rash following infected dystocia cases and aborted fetuses

Pasteurization – may survive if present in fresh milk in sufficient quantities b/c found in WBCs which provide protection

More heat resistant than many vegetative forms of bacteria
• Schistosomes – blood fluke, important parasite in humans and in cattle, sheep and goats in the Orient (Schistosome bovis)
• Fasciola hepatica Flukes
a. Liver fluke
b. water snail is host
c. in sheep causes traumatic hepatitis ‘Black Dz’
d. causes migratory tracts and hepatic fibrosis and thrombus in sheep and cattle
e. Causes hyperplastic cholangitis – where the biliary mucosa becomes permeable to albumin
f. Most pathogenic fluke in cattle – major cause of liver condemnation
g. Predisposes cattle to Clostridium hemolyticus (red water dz) see above
• Paramphistomum and Coylophron – rumen flukes
a. Water snail is host
b. Not pathogenic – irritant to intestinal mucosa especially the duodinum, lose appetite and condition
• Clostridium tetani produced in necrotic tissue
• Almost all mammals are susceptible to the disease but cats seem resistant (Birds are quite resistant) and horses are most susceptible
• Anaerobe w/ terminal spherical spores found in soil and intestinal tracts and introduced via deep puncture wounds
• Releases neurotoxin that is abosrbed by motor nerves in the area and passes up the nerve tract to the spinal cord causing asceingin tetanus (tonic contractions of volutary muscles by interfering w/ release of neurotransmitters)
• Clincal signs are – tonic spasms, hyperesthesia, lockjaw, thrid eyelid prolapsed, sawhorse stance
• Immuze w/ toxoid
• Boost annualy w/ toxoid or give another toxoid shot if deep penetrating wound occurs
• If animal has not been vaccinated, then give anti-toxin and toxoid in different locations
Systemic mycoses
Aspergilosis, Candiasis, Zygomycosis (Mucor, Rhizo)
• Moldy hay or straw
• Causes abortions via placentitis
• Transmitted via inhalation of dust or ingestions
• Also causes pneumonia, pharyngitis, gastroenteritis, dermatitis, preputial catarrh and cutaneous mycotic granulomata
• PCR, ELISA, immunoblotting and monoclonal Abs in histochemistry

• Coccidiodes immitis
• All specides including humans
• Benign dz of farm animals, but most common in dogs and cattle
• Major dz in humans but is not contagious
• Leukocytosis

• Histoplasma capsulatum
• Rare
• Mississippi river area
• Pneumonia, hepatic insufficiency, placentitis
• Skin test to dx

• Rhinosprodidium seeberi
• Chronic dz of nasal mucosa in cattle and horses
• Causes large polyps of nares and interferes w/ respiration

• Cryptocossus neoformans
• Generalized dz or granulomatous meingoencephalitis
• GM - CNS, blindness, siffness, hyperestesia, incoordination
• Generalized dz – pneumonia, pulmonary abscess, jejunal granuloma, lymphadenitis, placentitis w/ abortion
• Can be a cause of bovine mastitis

• Blastomyces dermatitidis
• Most common in dogs
• Has been recorded once in a horse – perineal abscess, emaciation and death
• Cutaneous or pulmonary granuloma
• Small intestine telescopes into the small intestine or the ileo-cecal valve into the cecum
• Mild signs of colic, constipation
• Rectal shows empty rumen & hard, sausage-shaped mass in right abdomen
• Oil and see if passes feces
• Tx is exploratory laparatomy in right sublumbar fossa – it may look like a bloodstained tumor
• Sx remove and anastomosis performed – DO NoT UNRAVEL
• D+ will be the sign in calves – same tx
Lead toxicosis
Lead toxicosis
• Most common source is electric storage batteries
• Brain will be pale, swollen, w/ flattened gyri (no herniation)
• Cattle become frenzied, bellow, staggering, and crashing into obstacles, from central blindness
• Liver will show lead concentrations
• Tx Mg sulphate, Ca EDTA, thiamine
Ammoniated feed toxicosis
Ammoniated feed toxicosis
• Anhydrous ammonia is added to hay to improve digestibility and nitrogen content
• If forage is high quality and has a high CHO content, it may undergo chemical change to 4-MEI causing hysteria
• Hyperesthesia, rapid blinking, ear flicking, frequent urination and defecation, dyspnea, circling and convulsions
• Blood ammonia levels are normal
• Tx – sedation and dilute toxic forage w/ normal feed is NOT recommended b/c can get an accumulatory effect
• Maximum rate of ammoniation to avoid toxicity is 3% for poor quality forage and 1% for high moisture forage
Ergot toxicosis
Ergot toxicosis
• Includes:
a. Neothypohdium (Acremonium) - ergovaline (fescue toxicosis), lolitrem (ryegrass staggers via tremorgens)
b. Clavicepts paspali – paspalum staggers; dallis grass, bahiagrass, CNS
c. Claviceps purpurea – ergotism; ergotomine; cereal rye grasses, ingestion of large quantities
• Claviceps purpura
a. Gangrene of extremities
b. Hyperthermia syndrome
c. Reproductive syndrome – abortion, rare, pigs more common by lack of udder development and agalactia
100% mortality
Affects all warm blooded animals
Biting, intimate contact transmission introduced into striated muscle
Replicates until reaches nerve ending (tropism for Ach)
Migrates 50-100mL/day in nervous system toward brain (the longer the bite is from the brain, the longer it takes to be fatal!)
Then replicates in limbic system of lower brain – behavior modifications
Then moves to cortex – ‘Dumb rabies’
The moves to salivary gland & is excreted via a bite in extremely high concentrations

DDx: distemper in racoons; pseudorabies in swine

Clinical signs
Prodomal stage – humans, vague changes in temperament 1-3 days before clinical signs
Furious stage – Dogs, cats, horses, CNS ; loses emotional control – bizarre behavior; will move after anything that moves, will break teeth
Dumb stage – cattle, pharyngeal paralysis, ‘choke’
Wild animals – aberrant behavior, animals come out in middle of day
Drool b/c swallowing is painful

Dx: IFA test of head to state lab

Protocol –
Confine dog/pet for 10 days after bite; rabies animal will shed virus for 6 days before showing signs. (4 extra days are precautions)
Need to differentiate between provoked and non-provoked attack and natural behavior of the breed
If vaccinated pet bitten by rabid animal, revaccinate immediately, release to O, and observe for 45 days
If unvaccinated pet bitten by rabid animal, isolate for 6 months and vaccinate 1 month before release

Susceptibility –
Coyotes, Foxes, Skunks > racoons > Dogs > Pigs > Human > Opossums

• Most common sign in cattle is bellowing
Brucelosis – Bang’s dz, contagious abortion
Brucelosis – Bang’s dz, contagious abortion
Causes abortion in cattle
• Bacteria may be found in the uterus during pregnancy
• Brucella is NOT transmitted when AI semen is deposited mid-cervix
• Dx via stomach and lungs of aborted fetus
• Test cow via serum agglutination test from milk, whey and plasma or ELISA Abs in milk and serum and vaginal mucus
• No tx – vaccinate w/ B abortus strain 19
• Chronic infection from soil borne organisms
• Causes generalized, purulent granulomatous nodular lesions
• Cattle are affected most frequently – although seen in many spp
• Mastitis is most common sign
• ADR, fever,  salivation, lacrimation
• Metastasis to lungs and supramammary LNs
• Can cause bovine farcy – puruelent lymphadentitis and lymphangitis
• Beaded, Gram positive branching filaments, certain degree of acid fast
• Easily cultured on blood ro brain-heart agar for more than 3 days
• Tx successfully w/ udder infusion; Erythromycin and miconazole are most effective

Chlamydial Abortion
• Chlamydia psittaci
• Fecal oral transmission
• Causes seminal vesiculiis syndrome – semen contain chlamydia
• Causes an endometritis and infertility and abortion
• Severe placentitis
• Intracytoplasmic chlamydial inclusion or elementary bodies in chorionic placental epithelial cells
• ELISA via AB, rise in titier in paired serum sample

Sporadic bovine encephalomyelitis
• Chlamydia psittaci
• Intestinal infection that penetrates the intestinal barrier and established a blood-infectious phase
• Fever w/ good appetite
• ADR, incoordination and staggering
• Vascular damage in many organs – peritonitis, pleuritis, pericarditis
• Tx tetracyclines and tylosin

• Has been isolated in intestine of normal cattle
• New born calves can cause an enteritis along w/ E coli
• Part of FPT – mucoid watery D+

• Infectious dz of cats, lambs, goats and guinea pigs
• Chlamydia psittaci
• Eye infectiouns occasionally transmitted toman

• Enzootic pneumonia in calves
• Chlamydia psittaci
• GI tracts may be source

• Infectious dz of sheep, calves, goats and pigs
• Chlamydia psittaci
• GI tracts is important source, and cay replicate in synovial membrane
• Stiffness, lameness, anorexia and concurrent conjunctivitis
• Calves 4-30 days old are hunched while standing, joints swollen and painful on palpation
• Navel involvment and nervous signs not observed
• Joint contains excessive, gray/yellow fluid w/ fibrin flakes and plaques, thickened joint capsule
• Arthritis!! In calves!
Ionophore/Monensin/Lasalocid toxicity
Ionophore/Monensin/Lasalocid toxicity
• Used as an coccidiostat and growth promotant in cattle
• Monensin is also used to tx ketosis, lactic acidosis and bloat
• Cause myopathy
• Horses have highest toxicity – fed in mixing mistakes (cow feed fed to horse)
• Potentiated by Abs and sulfonamides
• Anorexia, cardiac failure, dyspnea, D+, myoglobinuria
• Myocardial necrosis and pulmonary congestion
Sodium poisoning
Sodium poisoning
Na chlorate
Na chloride
Na fluoroacetate
Na fluorosilicate

Na chlorate
• Herbicide
• D+ and black erosions of abomasal and duodenal mucosa
• Hburea, anemia and methemoglobinemia
• Somnolence (drowsy) and dyspnea
• Blood , muscle and viscera are very dark
• Tx w/ Na thiosulfate and methylene blue

Na fluoroacetate
• Compound 1080 as a reodenticide
• Is cumulative
• Inhibites aconitase – Myocardial depression w/ ventricular fibrillation and CNS causing convulsions

Na chloride poisoning
• Caused by ingestion of excessive amounts of NaCl OR normal intake but limited water intake
• V+/D+, dehydration, opisthotonus, nystagmus, blindness, convulsions, death
• Polioencephalomalacia

Caused by water deprivation and (rarely) ingestion of large amounts of NaCl

Caused by water deprivation and (rarely) ingestion of large amounts of NaCl

Hypernatremia causes water to move OUT of brain and into circulation. Circulation becomes hypotonic in relation to the brain, so water moves into the brain, causing osmotic edema. Eosinophilia appears to follow increased Na ion levels into the brain
• Rare, but Suid Herpesvirus 1 can be spread from the pig to cattle via nasal discharge in contact w/ abraded skin or nasal mucosa
• Causes sudden death
• Intense, local pruritis w/ violent licking, chewing and rubbing of the part
• May cause intesne excitiment including bellowing and convulsionsm manic behavior, circling and spasm and opsthotonus
• Most cause death
Vesicular stomatits
Vesicular stomatits
• REPORTABLE – like all vesicular diseases
• Disease of cattle, horses and pigs
• Vesicular lesions on oral mucosa, teats and prepuce
• Virus isolation or PCR, serology w/ rising titers
• Late summer and early autumn
• Latest outbreak in 1995 – in western states
• Humans are susceptible getting flu-like symptoms
• Windborne, black fly, Culicoides fly, eye gnats may transmit
• Vesicles only occur in 30% of cases – hard to detect
• FA Ab used to dx
• Mycobacterium bovis
• Infected cattle are main source of infection to pigs and all other spp (all ages and all spp!)
• Wildlife are also a reservoir which prevents eradication in some countries
• Transmitted by inhalation or ingestion – drinking water and feed troughs, infected milk, intrauterine infection, feeding TB cattle carcasses, stockmen urinating in cattle environment
• Zebu (Bos indicus) more resistant
• Important zoonosis – consumption of infected milk
• Spread by two stages:
a. Primary complex – lesion at point of entry and in local LN; calcification of lesion 2 weeks later; and spreads to lung or liver
b. Post primary dissemination – discrete nocular lesions in various organs or chronic organ tuberculosis
• Pathognomonic – monocytes and plasma cells surrounded by granulation tissue “tubercle’
• Clinical signs:
a. Progressive emaciation
b. Capricious appetite and fluctuating temperature
c. Chronic soft cough
d. Dyspnea – bronchopneumonia in sheep & goats
e. Crackles over caudal lobes
f. May have infertility or abortion – uncommon
g. Mastitis – important b/c cause of public health; palpate supramammary LNs
h. Painful osteomyelitis in cervical vertebrae in horses
• Tuberculin test
a. Single intradermal (SID) test – intradermal injection of 0.1 mL of tuberculin into a caudal tail skin fold made of bovine tuberculin purified protein derivative (PPD)
b. Reaction is read 48-72 hours later for sensitivity and 96 hours for specificity
c. NVLs – no visible lesion reactors and lack of specificity (M bovis, M avium, tuberculosis, paratuberculosis, Nocardia
d. May not be sensitive to to old cows or cows which ahbe rectnly calved
e. Cannot retest for 60 days
• Other tests:
a. Short thermal test – intradermal TB (4 mL) injected SQ in the neck which have NO temperature. If temp at 4,6 and 8 hours later goes above 104, the animals is a positive reactor
b. Stormont test – same as above, w/ further injection at same site 7 days later, an increase in skin thickness of 5 mm or more 24 hours after 2nd injection is a positive; cannot retest for 6 months
c. Comparative test – Avian and bovine TB are injected simultaneously into two separate sites on same side of neck and read 72 hours later. Good to differentiate between vaccination against Johne’s and TB
d. Serological tests – Interferone gamma assay
• Other spp:
a. Pigs – SID in base of the ear
b. Horses – SID – false positives occur; smaller doses required, may provoke an anaphylacitic rxn
c. Sheep and goats – Stormont test
• Eradication – test and slaughter
Atypical mycobacterium
Atypical mycobacterium
• Mycobacterium avium-intracelluar
• Domestic or wild birds are source
• Ubiquitous in nature
• Infection by ingestions
• Draining LNs of GI tacts; most are subclinical but can cause carcass condemnation
Skin tuberculosis
Skin tuberculosis
• Chronic tuberculoid granuloma lesions of the skin on lower limbs
• Acid fast organsism
• Not pathogenic
• Confused w/ bovine farcy – Mycobacterium farcinogens
Malignant Catarrhal Fever
Malignant Catarrhal Fever
• Caused by two agents: Alcelaphine herpes virus-1 (AHV-1) from wildabeast and Ovine herpes virus-2 from sheep
a. occurs in Africa in cattle comingled w/ wildabeast
b. Spread by inhalation or ingestion by young wildebeest in nasal and ocular discharges
a. occurs in USA in low incidence in cattle that comingle with sheep
b. Unknown how it is spread
• Both agents are fatal
• Some recovered cattle show a persistent viremia
• Considered one of the most important dzs of farmed deer
• Causes lymphoid hyperplasia and widespread vascular epithelial and mesothelial lesions
• Encephalitis, vasculitis, synovitis (espieciall tibiotarsal joint), Lymphadenopathy
• Different forms of clinical signs:
a. Head and eye form – ocular discharge w/ edema of eyelids, areas of necrosis on the hard palate, gums and gingiva, mucosa splits easily; opacity of the cornea is always present, and persistant bilateral ocular leukomata
b. Peracute – dyspnea, acute gastroenteritis
c. Alimentary tracct – looks like head and eye only with marked D_
d. Mild form – fever, milkerosions in oral and nasal mucosa
• Dx via whole blood, nasal swabs or washings, LN biopsy w/ pathognomonic histologic lesions of necrotizing vasculitis
• Dx serology w/ competitive inhibition ELISA or PCR for detection of viral nucleic acid
Gossypol toxicosis
Gossypol toxicosis
• From cotton seed seeds and hulls
• Causes damage to myocardium and liver
• Preruminant calves most susceptible
• Most outbreaks refere to pigs
• Thin, exercise intolerance, dyspnea, jugular vein distension, reduced fertility in bulls, generalized edema
• Feeding WCS meal to rams and bulls is not recommended b/c of risk of spermatogenic damage
• Adding to diet will protect:
a. iron to pig diet
b. cations
c. Ca carbonate – prevents repro effects in cattle
d. Cookiing in Ca hydroxide or Ferrous sulfate
• Clostridium botulinum neurotoxin
• Spore forming anaerobe can suvive in environment for 30 years
• Animal dz from subtypes B, C & D
• Type B – not found in south, horse
• Type C – acid soils in Gulf coast, cattle and sheep
• Type D – alkaline soils in the west, cattle and sheep
• Forage botulism
a. ingestion of preformed toxin in spoiled stored forages or decaying vegetable material
b. Usually cereal or big bale silage
c. Most type B
d. Horses are most susceptible
• Carrion associated botulism
a. Animals on pasture
b. Includes dead animals and birds
c. Most type C & D
d. Can persist in carcass for at least one year
e. Poultry manure and ensiled poultry litter used as feed or fertilizer
f. Phosphorus deficient diet (cattle) or Protein deficient diet (sheep)
g. Drinking from lakes w/ avian botulism has been a source
• Wound botulism
a. rare but recoded in horses following castration or injection abscess
• Causes Shaker foal syndrome in horses (type B)
• Most common in birds
• Txoin binds to receptros on nerve ending, is internalized and interferes w/ Ach at the neuromuscular junction causing lfaccid paralysis
• Animal dies of respiratory paralysis
• Progressive symmetric muscular paralysis
• ‘Limber neck’ in sheep
• Muscle tremor – foals
• Dx:
a. detection of toxin using mouse bioassay
b. spores in the feed or feces of affected animals
c. Ab via ELISA
• Tx
a. Supportive fluid therapy
b. Polyvalent antiserum – early
c. Mineral oil – constipation
d. Bladder catheterization
e. Avoid drugs that deplete neuromuscular junction (Ach)
Bovine Spongiform Encephalopathy (BSE)
Bovine Spongiform Encephalopathy (BSE)
• Occurred in United Kingdom when meat and bone rendering processing changed from organic solvent to steam
• Scrapie changed spp
• Possible zoonotic
• Incubation is 2-8 years
• Spongiform encephalopathies have also been identified in ungulates and domestic cats and zoo felids (Feline spongiform encephalopathy) and ther is a Transmissible mink encephalopathy in the US in subclinical form
• Clinical signs – nervousness, aggression, abnormal posture, incoordination, difficulty rising,  milk prod
• Case fatality is 100%
• Pathognomonic signs in the Brain will have bilaterally symmetric intracytoplasmic vacules in neurons and degeneration of gray matter
• Dx via demonstration of prion protein PrPSc
• Variant Creutzfeld-Jakob disease – human form similar to FSE and BSE
• Bacillus anthracis
• Reportable dz
• ‘Anthrax belts’ – enzootic
• Spores can be picked up directly from the soil, fodder from infected soil, contaminated bone meal or protein, or from infected excreta
• Transmission:
a. Inhalation – minor importance
b. Ingestion – causes most death
c. Through the skin
• Outbreaks occur after a major climate change
• Important cause of fatal human illness
• Organism is resistant to phagocytosisi b/c poly-D-glutamic acid capsule
• Produces a lethal toxin which causes edema and tissue damage and death
• Death from shock and acute renal failure and termnal anoxia
• After death
a. discharges of blood form orfices of the body
b. absence of rigor mortis
c. Gaseous decomposition
e. Blood will not clot
f. Spleen is soft, large and looks like blackberry jam
• Vacicnation w/ modified live ‘Sern avirulent spore vaccine does not present a hazard to humans
• Disposal of infected animals is the biggest single factor in the prevention of spread of dz – should be buried at least 2 meters deep or burned
Babesiosis – Texas cattle tick fever, Redwater dz
Babesiosis – Texas cattle tick fever, Redwater dz
• Babesia bigmina and bovis
• In the horse, is equine piroplasmosis
• Ticks (Boophilus) is natural vector
• Infected adults can be carriers for life
• Iatrogenic infections via contaminated needles and sx instrument
• Zebu are relatively resistant b/c they have a resistance to ticks
• Strong immunity occurs after natural infection
• Clinical signs:
a. Intravascular hemolysis
b. High fever
c. ADR
d. Jaundice
e. Dark-red to brown urine
f. Abortion
g. May show CNS signs w/ Bigemina w/ cerebral babesiosis
• Giemsa stain on blood smear in RBCs
• Complement fixation test most common serologic test
• Tx is a babesidcide - Diminazen aceturate, Imidocarb, Amicarbalide and phenamide
• Prevention includes giving the vaccination at the same time as a babesidide
• Cattle plague
• Rinderpest virus (morbillivirus)
• The need to combat the disease was instrumental in the establishment of the first veterinary school in 1762 in Lyon, France
• All ruminants and pigs are susceptible
• Virus is ecreted by infected animals in ruine, feces and nasal discharges and perspiration
• Transmission occurs through contaminated feed or by inhalation
• Cannot persist outside the body
• Clinical signs:
a. high fever
b. Oculonasal discharge
c. Slaivation
d. Ulcerative stomatitis
e. D+
f. Dehydration and death
• Causes necrotic stomatitis and esophagitis, ulcerative and hemorrhagic enterocolitis and massive necrosis of lymphocytes in Peyer’s patches, LN and spleen
• Dx via virus isolation, serology and immunohistochemistry
• Effectively controled by slaughter and rigic quarantine measures
• Annual vaccination and surveillance
• Fusobacterium necrophorum
• Necrotizing dermatitis in interdigital space w/ characteristic odor
• Caused by wet, unhyginic or abrasive conditions
• More common in dairy cattle in first month of lactation and beef cattle on irrigation
• Clinical signs of severe foot lameness, fever and swelling of coroent and claw
• Typical lesion in skin at top of interdigital cleft
• Long continued irritation may cause interdigital fibroma (see below)
• Tx Abs and local tx of foot lesion
• Cu sulfate may be used
• Bandage to keep clean and dry
Interdigital fibroma
Interdigital fibroma
• Inherited defect in food conformation in heavy animals
• Anterior part of the cleft; a wart-like mass of fibrous tissue
• Can be the sequela of foot rot