REVIEW OF RUMINANT DISEASES

NERVOUS SYSTEM

MENINGITIS

Neonates: Sequel to septicemia. Failed passive transfer (FPT) important predisposing factor to omphalophlebitis/enteritis
with hematogenous spread of inf to CNS. Various bacteria: (E.coli, Salmonella, Pasteurella spp, Pneumococcus spp). Clinical
signs (CS) - diffuse brain Dz (brainstem/cerebellar mostly): Tetraparesis, ataxia ! recumbency; head tilt/tremor, depression
Cryptococcus neoformans – inf CNS via peripheral nn; Mycoplasma mycoides subsp. mycoides – common cause in goat kids

Adults: Direct extension into calvaria – dehorning, skull fracture/trauma, sinusitis, otitis; Various recognized entities:
Thrombotic meningoencephalitis: Cattle (mostly feedlot 8-12mo / Dairy cows (DC) also) – Haemophilus somnus
Often stress associated; may affect multiple animals within few days. Acute, usually fatal septicemic disease. Can
involve nervous, musculoskeletal, circulatory, & respiratory systems, singly or together. Reproductive system often
affected but usually without involvement of the other systems. Dz may be characterized by fever, severe depression,
ataxia, weakness, blindness, coma, & death. Sporadic in individual beef & dairy cattle & is found nearly worldwide.
Carried in the sheath & prepuce of males, the vagina of females & nasal passages of both.
Colonizes respiratory tract after inhalation, & is frequently found in urine.
Causes: TME
Fibrinopurulent bronchopneumonia
Fibrinous pleuritis
Polyarthritis
Myocardial & skeletal muscle necrosis occur.
Suppurative vaginitis, cervicitis, & endometritis may occur after breeding.
Also causes sporadic abortion.
Lesions = vascular thrombosis & infarction of the surrounding tissue.

Vasculitis: Ataxia, paresis ! recumbency & severe depression; death may be sudden. Can have concurrent lesions –
pleuritis/pneumonia/synovitis/fever common

Listeriosis – Listeria monocytogenes; Multifocal brainstem meningoencephalitis – spreads to CNS via cranial nerves.
All ages susceptible – esp young adult>1yo
Enters brain via blood/trigeminal nerve – lesions most severe in pons & medulla
3 disease syndromes:
1) Placentitis and abortion, usually in the last trimester. Most common in ewes.
2) Septicemia with miliary abscesses, usually neonates.
3) Suppurative meningoencephalitis with microabscesses in the brainstem; common in all ruminants.
Occasionally as a diffuse meningoencephalitis or spinal cord myelitis.

CS can be acute: Depression, Medial strabismus, +/- FEVER EARLY ON, Vestibular (head tilt; nystagmus; circling)
Dysphagia, Facial paralysis, Weak jaw & tongue, Tetraparesis/Ataxia, Occasionally cerebellar signs
(Blindness & Seizures – Are NOT features of Listeriosis)

Coccidiosis- Calves, yearling cattle, small R: Ass with enteric Eimerial infections, esp feedlot animals in winter.
Mortality can be high (usually low with enteric); ?Parasitic neurotoxin?

ENCEPHALOPATHIES

RABIES Cattle – any age, susceptible if wildlife/wild dog exposure. Transmitted in saliva ! Moves along nerve trunks.
Progressive stages in clinical signs of rabies (variable)
a) Prodromal stage: 1. Temperament - normal
2. Slight rise in temperature
3. Dilatation of pupil
 b) Excitatory stage: 1. Irritability, hiding, nervousness
2. Snapping
3. Wandering, roaming
4. Attacking moving objects
5. Seizuring, convulsing
6. Tenesmus
7. Cattle: sexual stimulation

c) Paralytic form may appear in absence of other stages

1. Dropped jaw (virus grows in neurons of motor nerve roots; may seen uni/bilateral CN signs).
2. Cannot see or drink.
3. Paralysis
4. Dysphagia
5. Death ensues within several days.

Wildlife Rabies
1. In the S.E. the racoon & fox are responsible for the current epidemic.
2. Rabid skunks, foxes, and raccoons behave abnormally and attack.
3. Long incubation in skunks make it a key reservoir.
4. When inititated in skunks, the disease is self-replicating. Not so in other species.

Bat Rabies
1. Prior to 1953, only vampire bats were known to transmit rabies.
2. Derrengue (bat transmitted bovine rabies) - manifested by paralysis.
3. Non bite-transmitted in bat cases. (There are insectivorous bats which shed the virus in their urine.)

Diagnosis of Rabies
1. CS - nothing is as typical of rabies as its atypicalness. However, rabies is always fatal in domestic species.
2. Laboratory (submit brain)
a. FA on brain - accurate & will detect affected animals before their death.
b. Negri bodies (pink inclusion bodies – not black!) on histopathology.

Rabies Differential Diagnosis - could logically include all CNS diseases: In Cattle: Nervous acetonemia (ketosis),
Salt poisoning, Pseudorabies, Encephalitis, Toxicosis, Organophosphate, Chlorinated hydrocarbons, Lead, Mercury

Furious Form (acute) – rage, hyperesthesia, charging, ataxia, bellowing, sexual excitement. May collapse & die within 2d.
Dumb Form – depressed animals, inappetant, febrile..
Paralytic Form – milder form with ascending paralysis: HL paresis/ataxia ! tetraparesis. Hypersalivation. Die within 1w.

PSEUDORABIES / AUJESKYS Dz (α-Herpesvirus)

Short incubation time so can ! sudden death; Cattle can get: a) Pruritus with self mutilation; b) Paralysis & death in 1-2d
c) Mutilation of site of inoculation (vulva or perineum usually). Sheep - uncommon - some infected sheep may survive. Abortions
have been reported.

NEOSPORA CANINUM - Dairy Cattle abortion predominantly – necrotizing encephalitis in aborted fetuses

POLIOENCEPHALOMALACIA (Cerebrocortical necrosis) (Thiamine (Vit B1) deficiency)

All Ruminants (R) (mostly calves 3-18mo); Individual DC/outbreaks in grain-fed feedlot cattle
Acute onset ataxia ! blindness, depression, headpressing, recumbent within few hours, semicoma, rigid limbs
Metabolic encephalopathy due to problems with B1 levels - mostly due to excess (XS) thiaminolytic rumen bacteria – associated
with XS concentrate feeding / Some plants have thiaminolytic action / Sulfates can also interact to reduce B1 levels. Often
associated with changed pasture.

VIT A DEFICIENCY
Growing feedlot ruminants – Vit A (plants) – low in cereal grains; Retinal degeneration; blindness, convulsions, depression.

LEAD TOXICITY Mostly acute CS in cattle (all ages) / chronic polyneuritis in horses
Acute form (calves/adults): Seizures common; hyperactivity (twitch, mania, hyperesthesia, headpressing); Death within 24h
Subacute (adults): Blindness, depression/stupor, ataxia, headpressing, circling, bruxism, head bob, constipation

PRION DISEASES: Prions are small agents that have PrP (Proteinase resistant protein) which is an abnormal form of a host
cellular protein & can act to cause more of the host protein to be converted to the abnormal form. Characteristic histologic
lesion is neuronal & neuroparenchymal vacuolation. BSE & Scrapie: BSE is a progressive, fatal, neurologic disease of adult
domestic cattle that resembles scrapie of sheep & goats – was 1st diagnosed in GB in 1986. Occurred as a result of a food-
borne exposure to a scrapie-like agent via contaminated meat & bone meal included in cattle rations. The pathogenesis remains
poorly understood, but it is thought that after oral exposure, the agent replicates in the lymphoreticular system then migrates,
via peripheral nerves, to the CNS. CS initially are subtle but progress gradually & most animals reach a terminal state within 3-
4 months. Weight loss & reduced milk yield (MY) are common & animals may be apprehensive & eventually develop exaggerated
responses to various stimuli, hyperesthesia, ataxia, dysmetria, aggression.
Scrapie – Also fatal - sheep, goats, deer & elk: Intense pruritus & hyperesthesia, which often begins over the rump, is common
though it does not occur in all cases. The fleece is dry, separable, and brittle, which results in loss of fleece over large areas.
Other areas may be rubbed raw. In some cases, the pruritus makes it difficult for the animal to feed and rest normally, which is
a major factor in emaciation and weakness. Animals become excitable, nervous, aggressive. Goast tend to be pruritic but
without the hyperesthesia.

SALT TOXICITY
Salt/water imbalance – upsets CNS osmolality - Cerebral CS: Dullness/hyperesthesia, tremors, muscle spasms, seizures,
blindness, death may be sudden

MALIGNANT CATARRHAL FEVER

Sheep = reservoir of the infectious agent - Affects many organ systems – primary lesion is fibrinoid necrotizing vasculitis
Head & Eye Form involve CNS: Nonspecific CS - Depression, ataxia, paresis; Ocular lesions mostly in cornea & conjunctiva
Persistent fever, Diarrhea, RT Dz

OTHER POSSIBLE CAUSES OF ENCEPHALITIS

HEPATIC ENCEPHALOPATHY – CNS signs secondary to liver Dz
COENURUS CYST – “Gid” Dog tapeworm Taenia multiceps has intermediate stage Coenurus cerebralis can develop in R brain
HYDROCEPHALUS - Congenital (Hereford, Ayrshire, Charolais); BVDV; Bluetongue; Cache Valley Virus; Vit A deficiency
NEOPLASIA - Lymphoma
IBRV in young calves (BHV-1): ! CNS via trigeminal nerve (its dendrites in pharynx / tonsils)
Otitis media/interna
In utero BVD
Akabane Virus in utero / bluetongue virus
Pituitary abscess – occasional in R (A.pyogenes) (Bull nose ring insertion); High mortality rate
Brain abscess – A.pyogenes – extension of sinus infection thru calvaria
Sarcocystis – infection usually asymptomatic
Babesiosis –Transmitted by Boophilus tick
Cowdria ruminantium – Heartwater; Transmitted by Ambylomma tick.
Theileriosis – Piroplasma parasite; SW USA, relatively nonpathogenic; Transmitted by Hyalomma ticks
Trypanosomiasis – Tstetse fly transmission
Ethylene glycol toxicity – Ruminants less prone because can metabolize oxalates in rumen

BRAINSTEM & CRANIAL NERVE (CN) DYSFUNCTION

BACTERIAL OTITIS MEDIA-INTERNA

Common in cattle & sheep following Resp Tract inf with M.haemolytica, P.multocida, C.pseudotuberculosis, P.aeruginosa, H.somnus
Bacterial ear infections common in feedlot lambs. CS of peripheral vestibular Dz

LISTERIOSIS (Mostly V & VII - X) (CN V - XII)

TEME (Haemophilus somnus)
CEREBELLAR SIGNS (Incoordination, ataxia, head tremor)

CEREBELLAR ABIOTROPHY – Inherited Dz in Holstein heifers (seen 3-9mo)

BVDV – Infection of dam 90-170d gestation
GRASS STAGGERS - Toxic products of plant metabolism; Many animals simultaneously.
HYPOMAGNESEMIA
LYSOSOMAL STORAGE DISEASES

SPINAL CORD / PERIPHERAL NERVE SIGNS

TRAUMA Vertebral fracture – most common cause of SC injury – Deficiencies in young R up to 6mo – Ca / Vit D / Cu
SPINAL ABSCESS Extends from vertebral o/myelitis 2ndry to hematogenous spread from septic focus (endocarditis etc)
SPINAL NEOPLASIA LSA
PARASITIC MIGRATION - Hypoderma bovis cattle; Parelaphostrongylus tenuis (Sheep/goat [S&G]) – near white-tailed deer.
TETANUS Cl.tetani ! Toxic proteins; From uterine infections in DC; castration, docking wounds etc; Toxin inhibits GABA
release ! disinhibition of motor neurons with subsequent muscle spasms & hypertonia

MOTOR NEURON DYSFUNCTION

BOTULISM Cl.botulinum toxin; Hypotonia in cattle – all skeletal muscles ! progressive generalized weakness & ataxia

PERIPHERAL NERVE DYSFUNCTION

FEMORAL N – Dystocia; Fall
RADIAL N – Blunt trauma
SCIATIC N – Dystocia; Pelvic fracture; Space occupying lesion along nerve; Downers
OBTURATOR N - Dystocia
DOWNER COWS
Hypocalcemia / Dystocia / SC lesions / Orthopedic Dz / Muscle Dz

HYPOCALCEMIA – Milk Fever

High producing lactating dairy cows – paresis/paralysis 1st 3d postpartum (pp): The sudden onset milk production ! ↓ Serum Ca
Twitchy, excitable, tremors ! Sternal recumbency, flaccid paralysis, depression ! Coma
S – Last month pregnancy - Huge Ca need for fetus (much moreso than cows – can have paralysis; also more tetany than in cows
G – Lactation in high yielding dairy goat – CS like cattle

HYPOMAGNESEMIA (Mg – maintains nerve RMP)

Lactating beef cattle 1st 2m lactation (Sheep & dairy goats too). Grasses in the cool season – mostly a spring-calver thing.
Predisposing factors to hypomag tetany ! lactation, transport, any stress, animals on all-milk diets; Spring/winter – grasses
relatively lo Mg ! Hypomag ! CS: Excitable, twitch, tremor, staggering, quite violent behavior & convulsions.

SMALL RUMINANTS

MAEDI-VISNA VIRUS (Ovine progressive Pneumonia) (Lentivirus- Retrovirus)

Immunosuppressive virus ! 2ndry bacterial inf !Eventual chronic Dz (RT / Nervous system / Mammary / Musculoskeletal)
CS – Ataxia, twitching, CP deficits, convulsions – some only emaciated with no other signs
Slowly progressive – years – thus serum Ab considered diagnostic

CAEV (Retrovirus); Neuro form: young goats – paresis, plegia, head tilt, gait disturbance, nystagmus, tremors, depression coma.
Various regions of CNS can be affected. Dx - AGID
Systemic viral inf may also ! lameness, fever, swollen joint, weight loss, tachypnea

BORDER DISEASE VIRUS (Pestivirus – akin to BVDV) “Hairy Shakers” (Dx – FA test for viral Ag)
Congenital inf – HUGE problem ! abortion, infertility, fetal malformations.
Naïve ewe infected in pregnancy ! infected lamb is immunotolerant & persistently viremic
CS – pronounced in lambs infected <50d gestation: Coarse long hair / abnormal pigmentation / arthrogryposis / tremor / ataxia
Infection between days 50-90: Teratogenic
Affects goats – but kids don’t have the “hairy” coat like lambs
OCULAR DZ

CONJUNCTIVITIS
IBR, MCF, Bluetongue, Mycoplasmosis
Infectious Bovine Keratoconjunctivitis - Moraxella bovis - “Pinkeye”
Listeria monocytogenes, Haemophilus somnus (TEME) (septicemia & ocular vascular damage)
Chlamydia psittaci (S), Branhamella ovis (S&G)

UVEITIS - Septicemia induced in youngsters; Bovine-specific recurrent uveitis (Dz similar to that in horse - ?Etiology)

RETINAL DEGENERATION - Scrapie in S&G; BVDV in cattle

PARASITES – Cute but usually zebras on the DDx list!

Oestrus ovis larval migration in sheep
Thelazia nematodes in the conjunctival sac – usually asymptomatic, but can ! keratoconjunctivitis in ruminants
Elaeophora schneideri – transferred from deer to rumninants by biting flies – migrate into ocular blood vessels ! inflammation
Trypanosomes, Babesia, Theileria – blood protozoans – conjunctival hemorrhage & edema

NEOPLASMS – SCC; Ocular manifestations of Enzootic Bovine Leukosis

GASTROINTESTINAL TRACT DISEASE

FUSOBACTERIUM NECROPHORUM – Calf diphtheria/Necrobacillosis ! Oral cavity ulcers

VESICULAR STOMATITIS VIRUS (Rhabdovirus) ! Oral cavity ulcers
IBRV (BHV-1) ! Oral cavity ulcers
MCF (Herpesvirus) ! Oral cavity ulcers
RINDERPEST: Morbillivirus – Cattle fatal (S&G less severe). Virus in via RT ! target lymphoid tissue & GI mucosa !
immunosuppression & GI mucosal damage (diarrhea & wt loss). Acute onset fever, depression, anorexia, ulcers etc !
diarrhea/emaciation ! death. Highly contagious – transmission via direct contact, fomites, airborne; wild ruminants !
livestock. Hi morbidity & mortality.
BLUETONGUE (Sheep orbivirus) - Orbivirus carried by Culicoides. Endemic in USA. Disease of sheep, cattle, goats, and wild
ruminants. Cattle are the reservoir. Inappetance in cattle and goats, severe disease in sheep and deer.Clinical signs - Sheep-
hyperemia of muzzle, lips, ears; dyspnea, erosion/ulceration of oral mucosa; muscle necrosis, cyanotic tongue. Abortions,
congenital defects. Mortality 0-30%. Cattle - usually asymptomatic. If develop clinical signs, same as sheep. If infected
during gestation, may abort or give birth to abnormal calves. Diagnosis and Prevention – IFA. Vaccinate sheep. Insect control
BOVINE PAPULAR STOMATITIS - Cattle (Parapox virus); Asymptomatic; Can ! papules/ulcers: mouth/esoph/nose/muzzle

FMD
Aphthovirus (Multiple types: A, O, C, Asia 1, SAT-1/2/3) - Cloven-hoofed animals – Cow/Pig most susceptible. CS –
Fever, depression, inappetance, lameness, salivation. Vesicles appear ! rupture quickly ! Ulcers – Feet, Mouth,Teats. Dz at an
age – Hi morbidity/Lo mortality - ↑ mortality in young due to cardiac involvement. Viral inf & replication – epithelium of
GIT/pharynx/udder ! local spread & wide dissemination when it enters bloodstream. Transmission – aerosol / fomites / cows
milk. Hardy wee virus – survives milk pasteurization & freezing of meat. Some animals harbor virus in URT for many months.

LUMPY JAW – ACTINOMYCOSIS

Actinomyces bovis (normal inhabitant of oral cavity) – Mostly cattle (S&G occasionally). Bug enters bone (puncture wounds due
to rough plants; Abrasions in mouth; Dental Dz) ! Granulomatous lesions – Mandible, horizontal ramus ! If untreated can
progress to involve tooth roots etc. Non-painful thickened, swollen bumpy jaw

WOODEN TONGUE – ACTINOBACILLOSIS

Actinobacillus lignieresii (oral cavity inhabitant; also found in some plant awns) – Gains entry to soft tissues of mouth via
abrasions, as with A.bovis. Cattle – Tongue; Sheep – lips & face. Generalized involvement of internal organs & LNs is possible.

BOVINE VIRAL DIARRHEA – MUCOSAL DISEASE

BVDV = Pestivirus: 2 strains. A Dz syndrome with many faces
(1) Noncytopathic – Important in transplacental infections ! Abortion, Congenital anomalies, Persistently infected animals
(2) Cytopathic – Responsible for Dz in cows with Mucosal Dz
Most infected animals develop mild fever, leucopenia & will seroconvert. Transmission is horizontal (ingested/inhaled) within a
herd or vertical (in-utero) – also Indirectly via fomites/biting flies.

Acute BVD: Dz in animals that are immunocompetent but not PI – usually cows 6mo-2yo. CS – depression, anorexia, leukopenia,
diarrhea, oculonasal discharge, oral erosions, ↓ MY – don’t forget Viral Shedding. Causes a general non-specific
immunosuppression ! ↑ susceptibility to other Dz. Animals outside the age range can obviously also be affected – infected
neonates can ! Diarrhea / Pneumonia - so consider BVDV as a DDx for either condition somewhere on your list.

In-utero infection: Many repro effects. Abortion – Days 50-100 - V crosses placenta ! fetal infection & death ! Abortion,
Mummification. Days 100-150 – Fetal infection as before ! Congenital abn – Cerebellar hypoplasia, Hydrocephalus, Cataracts,
Microphthalmia, Retinal Degeneration, Hypotrichosis. Animals infected in-utero before Day 125 can be PI & immunotolerant –
even if born normal, can still develop MDz & die. Other repro effects: ↓ bull semen quality, ↓ Conception / Pregnancy rate.

Dz In PI Animals: Generous Viral Shedding from these beasts is a huge source of evil. Calves born PI - frequently poor-doers
(immunosuppressed etc), weak, small – occasionally some are OK & make it thru to the breeding herd. Mucosal Dz is the most
striking syndrome that occurs in PI cattle. PI cattle are infected with NCP strain – MDz results from these animals
becoming infected with CP strain – usually due to Mutation of NCP ! CP in the animal. CS – Fever, anorexia, ↓MY, diarrhea
+/-blood, Erosions - oral cavity, udder, oculonasal discharge, bloat, immunosuppression ! 2ndry inf: pneumonia, mastitis, metritis
Animals are progressively debilitated, dehydrated – Animals with Acute cases can die within 1—2w. Cows with Chronic MDz are
those that survive the acute phase – are poor-doers, lose wt, diarrhea on & off, frequently have continuously loose poop – sadly
progressively deteriorate - usually die within 1-2y. BVDV damages epithelial tissues & hence causes problems.
ORF – CONTAGIOUS ECTHYMA
S&G – Zoonotic; Parapox virus. Infection is usually self-limiting – 1m. High morbidity in naïve animal, Low mortality – Infection
! Solid immunity. Hardy virus – persists well in environment. Lesions start as papule/vesicle/pustule ! proliferative &
scabby. Typical Sites – mucocutaneous junctions of face/mouth. Can be seen on teats, interdigitally, coronary band, eyes & if
overwhelmed by infection, can extend to involve respiratory tract/GIT. Usually no systemic involvement.

OSTEODYSTROPHIA FIBROSA (Nutritional 2ndry Hyperparathyroidism) – Seen mostly in Goats

Teeth & bone poorly mineralized due to bone lysis to normalize Ca levels – swollen, soft jaw & teeth. Generalized skeletal Dz:
XS P intake relative to Ca - Thus XS P causes hyperphosphatemia & secondary hypocalcemia – this stimulates PTH secretion
which mobilizes Ca reserves (bone lysis) to revert to normocalcemia.

HYPERSALIVATION Mouth trauma, Choke, Dental Dz, Chemicals – “accidental” ingestion

Pharyngeal swelling/Trauma: Injury - stomach tube/dosing gun; Retropharyngeal FB/Neo/Abscess – C.pseudotuberculosis in S&G
Rabies, Aujesky’s Dz, Vesicular Dz – FMD / VS

Uncommon things – Developmental lesions (Dentigerous cysts) Periodontal Dz, Dental Caries, Tooth Root Abscesses,

ESOPHAGEAL CHOKE – Common, can be fatal if untreated due to rumen bloat. Usually chunky feeds - potatoes, apples
– don’t forget other lesions in/near esophagus that reduce lumen size – neo, abscess etc. Potential sequelae – esophageal
inflammation / stricture / diverticulum / perforation / metabolic acidosis / dehydration

FORESTOMACHS

RUMEN INDIGESTION
PRIMARY INDIGESTION = RR dysfunction induced by problematic (1) Rumen Contents or (2) Rumen Wall / Its Motor Control
SECONDARY INDIGESTION = Consequence of systemic Dz (Endotoxemia ! anorexia, inappetance ! motility probs)

2 independent RR contractions: Primary – Optimizes fermentation process - mixing action. Includes a biphasic reticular
contraction ! Caudal direction across dorsal rumen sac ! ventral sac. Toward end of reticular contraction, omasal orifice
allows fluid in. Secondary – For eructation. Cranial direction of contraction, begins in rumen caudal blind sac ! dorsal rumen
! takes gas bubble to cardia. Reticulum not involved.
Usually one primary every minute / One secondary for every 2 primary = Totals 3 contractions every 2 mins

PRIMARY: Motor Problems & Wall Dz

(1) Ruminitis/Reticulitis: Wall damage – Chemical – Grain overload ! Acidosis ! Ulcers (can also be caused by acorn tox) !
Bugs (A.pyogenes; F.necrophorum) invade damaged mucosa. Physical – Tumors, Traumatic reticulitis: Accidental hardware
ingestion ! Settles in rumen ventral sac ! taken into reticulum with contractions ! Penetrates (a) cranial wall !
diaphragm/heart or (b) medial wall ! liver ! abscesses etc. Rumen contents leak out ! peritonitis.

(2) Vagal Indigestion: Syndrome involving motor dysfunction – controversial pathogenesis. Most cases involve hypermotile
rumen with failed omasal function (mostly due to traumatic reticulitis) ! Reticulorumen (RR) overdistension ! ↓ Appetite ! ↓
Fecal output
Pyloric failure may also occur (Mostly due to abomasal volvulus) – Failed outflow here ! fluid accumulates in
omasum/abomasums ! can overflow back into RR if prolonged. Sequelae – accumulation of Cl-rich fluid in RR & lack of
movement thru GIT ! dehydration & hypochloremic metabolic alkalosis.

(3) Rumen Parakeratosis: Hi conc, fine rations ! ↑ Pr/Bu relative to Ac ! ↓ pH ! Thickening & clumping of rumen papillae.

PRIMARY: Fermentation Disorders - Usually involve nutritional discrepancies.

(4) Indigestion: Sudden food change ! Bugs unprepared ! Usually diarrhea & inappetant 1-2d ! self limiting as bugs adapt.

(5) Poor Quality Roughage with Lo protein & digestible carbs ! Rumen bug inactivity ! Retained longer in RR for digestion !
Hypomotility, distension & tympany.
(6) Acute Acidosis: Sudden Grain overload ! XS highly fermentable CH ! Rapid fermentation with lactate production & ↓ pH.
Striking problem – can be rapidly fatal.

(7) Chronic Acidosis: Prolonged access to hi levels grain ! bugs adapt ! ↑ lactobacilli / ↓ Cellulolytic bugs ! Food thus rapidly
fermented without lactate accumulation since lactobacilli utilize it ! Hi conc VFAs result in lo pH with ↑ Pr/Bu relative to Ac !
Pr/Bu stimulate rumen papillae to proliferate ! can become parakeratotic at worst scenario. Changed rumen papillae – are more
susceptible to trauma & less able to absorb VFAs. Trauma can ! bac entry & dissemination to liver ! Abscesses

(8) Rumen Alkalosis: When saliva is produced & swallowed but rumen fermentation has ceased. Alkaline saliva not buffered
due to ↓ VFA levels. Due to (4),(5), Anorexia. Also due to XS NPN supplements but SEVERE ! NH3 toxicity & CNS signs
Bloat: Involves gas accumulation because unable to be eliminated – Many causes, including all of above!
Free-gas bloat: Diet ! XS gas / ↓ pH. Usually with concentrate levels to which animal not accustomed.
XS gas accumulates due to external cause – Choke, Hypocalcemia
Frothy bloat: Diet ! Froth formation. Legumes/Hi grain rations

ABOMASUM

ABOMASAL IMPACTION - Food lo in energy & poorly digestible ! Need to eat more to meet needs ! Impaction ! Outflow
obstruction ! Accumulation of ingesta in abomasum then RR. Calves due to (a) Hairballs – result from hair licking due to
acidosis; (b) Lo quality milk replacer ! eat bedding. Adults ! indiscriminate eating/lo fiber diet ! eat baler twine etc!

ABOMASAL ULCERS - Stress, Hi conc diet, Postparturient dairy cow. CS: Asymptomatic ! Melena ! Perforation/ peritonitis

DISPLACED ABOMASUM - Dairy cow early postpartum; Due to hi VFA level with continued fermentation (hi conc ration / lo
roughage) ! atony with gas accumulation; Usually LDA; RDA can ! Volvulus (?Etiology). CS: Anorexia, ↓ Feces, ↓ Rumen motility
RDA alone – hard to distinguish from volvulus – Sx intervention important. Volvulus (+/- RDA) will ! complete rumen stasis.

INTESTINE

INTUSSUSCEPTION Calves – SI or LI – Enteritis ass’d; Adults – Jejunum - ?Mass/polyp ass’d.

VOLVULUS All ages, especially neonates.

ATRESIA/STENOSIS Calves, lambs – Congenital. Jejunal atresia inherited (auto rec) in Jerseys. Malformations more orad
in location – quicker onset CS than those caudal rectum/anus. CS: No poop, Intestinal distension, colic ! CV collapse eventually

MESENTERIC FAT NECROSIS Channel Island dairy breeds / Fattening cattle & any animals on hi levels saturated LCFAs;
Usually adults. Starts with degeneration of a clump of adipocytes ! induces inflammatory response ! Necrosis. CS: Often
none; Symptomatic cases present as GIT obstruction as hard, necrotic fat surrounds & compresses lumen.

CECAL DILATION & VOLVULUS Adult dairy cow, early lactation - Less common than DA. Change to a hi conc / roughage
poor diet ! escape of highly fermentable carbs from RR to LI – Cecum metabolizes them into VFAs - ↑ VFAs in cecum ! ↓
Motility & ↑ Gas production ! Dilation ! Predisposes to volvulus.

WINTER DYSENTERY - Cattle – acute, explosive diarrheic Dz, contagious, epizootics. Most susceptible animals affected
worst & 1st ! spreads ! self-limiting within a couple of weeks. Bovine coronavirus implicated.

JEJUNAL HEMORRHAGIC SYNDROME – Acute hemorrhagic diarrhea in cattle & sudden death. Clostridia implicated.

CLOSTRIDIAL ENTEROTOXEMIA Cl.Perfringens types A-E ! Toxins (alpha - hemolytic/beta/epsilon/iota)

TYPE A (α) Yellow lamb Dz

TYPE B (α β ε) Lamb Dysentery / Foal enterotoxemia (Both UK)
TYPE C (α β) Necrotic Enteritis – calves, lambs, piglets, foals (“Struck” UK) Sudden death +/- diarrhea
TYPE D (α ε) Sudden death – well-fed, growing animal; Sheep (cow/goat); Vascular damage ! Edema: ”Pulpy Kidney”
TYPE E (α ι) Rabbit Enteritis; rarely a problem for farm animals
SALMONELLA
Important veterinary pathogen – famed for nosocomial infections, zoonosis, multi-drug resistance. Many serotypes – mostly
nonhost-specific, some host-adapted. Dz also maintained by rodents, environmental contamination, carriers. Important Dz-
promoting factors include: Intensive systems - Large units, Overcrowded housing, Hi protein diets. CS – Diarrhea, fever. Can
produce significant mucosal damage ! PLE & Endotoxin absorption ! Endotoxins can produce shock, fever. S.dublin &
S.typhimurium especially can ! acute bacteremia in neonates, & acute septicemia can ! systemic lesions. Calves – 6wo classic
age – Sudden death, respiratory probs, occasional diarrhea; Adults – Abortion / Diarrhea
Orofecal transmission – Ingested bacteria attach to mucous membranes ! invade & stimulate inflammatory response

JOHNES Dz
Mycobacterium paratuberculosis – enters GIT & infects ileum 1st – Most inf occur as calves (drink milk/colostrums
contaminated with the bug). Organism causes gradual thickening of the intestine ! ↓ absorption nutrients & PLE ! CS of Wt
loss / Diarrhea (not seen for 1st few years). Sheep & Goats mostly have wasting with Johnes, not diarrhea, unlike cattle.
Public health – Crohns Dz (IBDz) in humans. Organism may be present in pasteurized milk.

HEPATOBILIARY Dz

Damage needs to exceed reserve capacity before CS of Hepatic failure (HF) seen.

CNS: Hepatoencephalopathy (HE) – Imbalance of circulating neurotransmitters since liver can’t eliminate
them ! Cross BBB ! CNS dysfunction
DERM: Icterus - Bilirubin metabolism fails – pigments deposits in skin - Less common in
Ruminant than Horse unless have biliary obstruction.
Photosensitization Dermatitis - Failing liver can’t detox chlorophyll-derived phylloerythrin !
Accumulates in skin ! uv exposure renders unpigmented skin
susceptible to dermatitis.
(Pruritus - Bile salts accumulate in skin)
(Non-specific - Weight loss, Diarrhea)

DIAGNOSTICS Clinical Parameters reflect ↓ anabolic function ↓ Blood glucose

↓ Albumin → Edema / Wt loss / Ascites

Enzymology (Acute): ↑ AST / SDH / GGT

(Chronic) SDH of little use - ↑ GGT most useful

LIVER ABSCESSES
Common – arise from a septic process elsewhere (mammary gland/uterus etc). Can invade into vena cava & subsequently
disseminate hematogenously anywhere else ! frequently lung

CHRONIC ACTIVE HEPATITIS

Prolonged hepatic inflammatory Dz – Etiology uncertain, but cases unrelated to flukes documented in cattle. CS – progressive
Wt loss, fever,

LIVER FLUKE
Fasciola hepatica – Cattle develop resistance (thus subclinical infections), sheep don’t (suffer more acute Dz). CS – non-
specific with Diarrhea, Wt loss, Icterus, PLE, Anemia. Dx – Trematode eggs in feces, Serum Ab’s, Serum parasitic Ag’s
Metacercariae ingested ! Juvenile flukes invade GI mucosa ! Migrate in peritoneal cavity to liver ! Invade liver – migration
of the fluke larvae in this way can ! BLACK Dz – Cl.novyi Type B ! Toxins: Especially grazing sheep ! Sudden death.
Commensal in GIT – Concurrent liver damage provides anaerobic env for Cl.novyi to proliferate ! produce toxins (α – Lethal
necrotizing toxin; β – Lethal & hemolytic lecithinase activity; z – Hemolytic)
Cl.novyi type D “Clostridium haemolyticum” ! BACILLARY HEMOGLOBINURIA (Red water) ! Cattle - Sudden death
Toxins (β – Lethal/Hemolytic; Eta – Tropomyosinase; Theta – lipase) ! Hemolysis & Liver Necrosis. Organism found in soil !
Ingested by animal ! again concurrent liver damage – flukes – necessary for germination & toxin elaboration.
HEPATIC LIPIDOSIS (HL)
NEGATIVE ENERGY BALANCE (NEB) ! ↓ Blood Glu & ↓Ratio Insulin:Glucagon → ↑Hormone sensitive lipases ! FFA & Glycerol
released from tissue fat: Glycerol converted in liver to glu/TGs; FFA ! TGs or shunted thru β-Ox to produce A-CoA !
Combines with Oxaloacetate to subsequently enters TCA ! ENERGY

FFAs – OK, so XS are being produced & entering the liver for TG production ! So more TGs are stored in hepatocytes:
Normally they are transported out of the cell in plasma on the VLDL boat – BUT- HL occurs if TG production > β-Ox of FFA &
release of VLDLs for TG transport.

Oxaloacetate is an important little character – If in short supply, A-CoA can’t enter TCA cycle to produce energy – so instead
takes the alternative pathway toward KETONE BODY production. OK for short term energy solution but hi levels can suppress
food intake & thus exacerbate the NEB.

WHAT DOES ALL THIS MEAN?

(1) PREGNANCY TOXEMIA IN SHEEP/GOATS – Ketosis/Twin Lamb Dz – Final month pregnancy; Depression, anorexia,
weakness ! CNS signs. NEB: Relative underfeeding - hi fetal growth at this stage > intake ability . Can have ↓Ca ↓Glu ↑KBs
(2) FATTY LIVER IN DAIRY COWS – Postparturient – Well-conditioned cows – Periparturient NEB & hormonal changes !
mobilize fat reserves to liver ! lipidosis. During this phase, also important to remember concurrent Dz that will ↓ food
intake & ↑ energy requirements & so exacerbate the NEB - RFM / Metritis / Mastitis / DA / Paresis.
(3) PREGNANCY TOXEMIA IN BEEF COWS – Pregnant beef cow on a marginal diet – often a winter thing – especially
heifers that are still growing & pregnant. Energy needs for growth of fetus & heifer, & coping with cold weather > intake.

TOXINS

Pyrrolizidine alkaloids – Senecio, Crotolaria plants ! Chronic progressive intoxication CS – Diarrhea, Weight loss, Ascites in
cattle mostly, & tenesmus & rectal prolapse. Can have CNS signs, but icterus unusual. Other hepatotoxic plants include
Trifolium (Alsike clover) & Cottonseed (Gossypol)

Mycotoxins (aflatoxin B) Moldy feed ! Liver necrosis, bile duct hyperplasia

Cu Toxicosis Hemolytic crisis ! Liver necrosis

DIARRHEA DDx (To name a few)

NEONATES ADULTS
Rotavirus (villus tips) Parasites - flukes
E.coli BVD-MDz
Coronavirus (crypts) Coccidiosis
Cryptosporidiosis Cu / Se / Co deficiency or even toxicity
Clostridiosis Jejunal Hemorrhagic Syndrome
Salmonellosis Rumen Acidosis
Campylobacter Winter Dysentery
BVDV Food related indigestion
Johnes Dz
RESPIRATORY TRACT

URT Dz

CALF DIPHTHERIA (up to 2yo) (Poor environmental conditions)

Ulcerated larynx ! Fusobacterium necrophorum invades
Common Dz – feedlot calves: painful cough, stertor, open-mouth breathing, salivate, swallow, anorexia, depression, fever
Death within 7d if not Tx – URT obst / toxemia; Sequelae: aspiration pneumonia, chronic poor-doers

IBR - BHV-1. Seen in cattle of all ages in crowded situations. URT infections & late term abortions. CS - Nasal discharge, red
nose, ulcers of nasal mucosa, dyspnea, conjunctivitis. Abortions late term. Genital infections. Lesions in upper respiratory
tract and trachea. Serofibrinous exudate.

ATOPIC RHINITIS & ENZOOTIC NASAL GRANULOMA

Allergic rhinitis can be chronic & ! Granuloma: Antigenic stimulant – fungal spore/plant pollen – seasonal.
Especially Friesians & Channel Island breeds – familial predisposition
Rhinorrhea/sneezing/stertor/rubs nose/nasal discharge. Chronic (granuloma) – constant CS with seasonal exacerbation.

TRAUMA Passing large NGT / Fights / Restraint / Machinery – swelling & stertor / Dosing guns etc damage pharynx/larynx

SINUSITIS (Mostly cattle, less common S&G): Frontal – dehorning / Maxillary – dental Dz

OESTRUS OVIS (Sheep Nasal Bots) (S>G) / Warm weather; Eggs deposited in nostrils. Larvae migrate into nose ! adults
emerge – headshaking etc

ENZOOTIC NASAL ADENOCARCINOMA Sheep & goats predominantly – arise from ethmoidal conchae of nasal cavity due to
Retroviral infection of respiratory epithelial cells. Typically invasive but don’t met.

LESS COMMONLY…..
FB: Cattle > S&G – rubbing nose or snorting things while rooting for food ! can lodge in trachea if inhaled
Nasal Polyp
Nasal Tumor: Cattle - Adenocarcinoma / OSA / SCC; Sheep – (Adenoma / Adenocarcinoma)
Fungal Granuloma: Rhinosporidium, Aspergillus
Laryngeal masses: Abscesses (A.pyogenes), papillomas, granulomas, FB; edema due to restraint trauma

LRT Dz

PNEUMONIA
BOVINE RESPIRATORY DISEASE COMPLEX (RDC)
General term used by clinicians to describe any acute, severe bovine respiratory illness of undetermined etiology
Includes: Enzootic pneumonia of calves (Multifactorial)
Mannheimia haemolytica
Haemophilus somnus
Viral infections (IBR/PI3/BRSV)
Noninfectious causes such as Atypical Interstitial Pneumonia (Fog Fever)

Various infectious agents, usually in combination, interact with host & environmental factors to ! Bronchopneumonia
Housed dairy cattle / Beef cattle after transport
Dairy Calves <2mo usually affected: Predisposed by – Neonatal diarrhea / Nutritional deficiencies / FPT
Beef Calves: Wean, creep feed & do routine Sx as long as poss in advance of shipping (at least 3w) to reduce incidence; also
stresses such as multiple auctions, long transport time will predispose. Cold stress is important in lambs – shearing etc)
IBRV (BHV-1)
Various entities: IBR / Conjunctivitis / IPV / Balanoposthitis / Abortion / Mastitis
Respiratory manifestations – Rhinitis / Tracheitis / Pyrexia / ↑ RR / ↓ MY – abortion may occur concurrently, or up to 100dpi.
Dz is more frequent, severe and likely fatal in dairy than beef cattle
Dz, however, usually non-fatal unless during severely stressful time or 2ndry bacterial pneumonia complications
Viral latency in neural tissues ! recrudescence & viral shedding
?role of herpesviruses in S&G

PIV-3 (Paramyxovirus) PREDISPOSES RT TO DAMAGE BY OTHER AGENTS

↑ RR, fever, oculonasal discharge
Dz severity ↑ with 2ndry bacterial pneumonia which can ! death (usually lesions less extensive than BRSV)
Also sheep, probably goats too

BRSV (Paramyxovirus)
This virus has a high frequency of occurrence & the LRT is its predilection site – makes it an important cause of the RDC
Mostly calves, also sporadically in adults
Hi morbidity & varied mortality rates.
Colostral Abs do not prevent Dz but can reduce Dz severity – also ↓ humoral response of immune system to vacc / inf
Fever, depression, inappetance, ↑ RR common ! pronounced dyspnea & mouth breathing later on
Frequent 2ndry bacterial pneumonia
S&G isolates of RSV exist - ?role in RTi

BVDV (Pestivirus) IMMUNOSUPPRESSIVE ROLE

Often associated with Mannheimia haemolytica in cattle with shipping fever pneumonia - ?synergistic action of organisms
Most frequent viral associate in calves with multiple viral RTi’s

MCF
A clinicopathological syndrome caused by related herpesviruses & acquired from persistently infected wildebeest & sheep.
Highly fatal - usually within 1wk; Usually sporadic Dz with one animal affected; Mortality high; Cattle = dead-end hosts.
Wildebeest ass’d MCF: Alcelaphine HV-1 BHV-3 (γ-HV) – Transmission to cattle hazy – occurs +/- contact. (? Carriers)
Sheep ass’d MCF: OHV-2 – Sheep spread it to cattle by contact – lambing season etc.
Incubation 1-2m ! viral attack on endothelial cells (Vasculitis) of all epithelial surfaces:
CS ! Keratoconjunctivitis / oral ulcers / diarrhea / fragile skin / ↑↑ LNs / oculonasal discharge / encephalitis

BACTERIA ET AL – Many are URT inhabitants – hop on board the disease wagon when defence mechanisms are low…
Mannheimia haemolytica (Serotyope A-1) - Commonest bacterium isolated from cattle with RT Dz in N.Am
Pasteurella multocida – less “popular” & Dz is less severe.
Haemophilus somnus increasingly common.
Arcanobacterium pyogenes – abscesses.
Mycoplasmas – frequent pneumonia isolates – not hugely significant pathogens - subclinical infection, unless other stresses/bugs

S&G – M.haemolytica/P.multocida/Haemophilus spp/Salmonella spp/Mycoplasma ovipneumoniae

AND FINALLY……..
Adenovirus / Reovirus / Rhinovirus / BHV-4 / Enterovirus / ?Cornonavirus / Chlamydia – may enhance pathogenicity of others

Dx: Paired sera Ab titers. Swab nasopharynx – bacterial C&S & in VTM for viral isolation – special medium for mycoplasmas

CONTAGIOUS BOVINE PLEUROPNEUMONIA

Mycoplasma mycoides ssp.mycoides (small colony type) ! highly fatal fibrinous bronchopneumonia: vasculitis important in
pathogenesis. Severe acute illness – painful cough, shallow respiration, pleural friction on ausc
Hi morbidity & mortality; carriers possible in survivors (CFT to detect carrier)

CONTAGIOUS CAPRINE PLEUROPNEUMONIA – Mycoplasma F38 currently implicated – highly contagious for goats only
MYCOPLASMA PNEUMONIAS OF YOUNG GOATS
Some caprine pneumonias not contagious among adults: M.mycoides ssp. mycoides (large colony type) – imp cause of kid mortality
Most have pneumonia & swollen joints. Can be febrile with acute death, others have CNS signs.

SEPTIC EMBOLIC PNEUMONIA IN CATTLE

Septic Dz
(liver abscesses due to rumenitis / footrot / mastitis / metritis)
↓
Septic thrombi in caudal vena cava
↓
Pulmonary arterial septic thromboemboli
↓
Pulmonary abscesses & embolic pneumonia

Frequently feedlot cattle (Hi conc feeds ! lactacidosis ! rumenitis ! damage allows F.necrophorum / A.pyogenes to
penetrate epithelium, enter portal blood ! liver: filtered out & result in abscesses – if near CdVC ! thrombus etc
Respiratory signs, anemia, hemoptysis - Occasionally melena

INTERSTITIAL PNEUMONIAS
ATYPICAL INTERSTITIAL PNEUMONIA – “Fog Fever” - Adult (>2y) ARDS reaction: Abrupt change to lush green pasture
Acute onset severe dyspnea, usually no cough
L-Trp in pasture ! 3-MI in rumen ! absorbed into blood ! Lung cell damage: pneumotoxic - edema, emphysema

MOLDY SWEET POTATO TOXICITY - Due to 4-Ipomeanol produced by sweet potatoes infected by fungus Fusarium solani

EXTRINSIC ALLERGIC ALVEOLITIS - Hypersensitivity reaction like “Farmers Lung” – inhaled organic dusts from moldy hay

CHRONIC INTERSTITIAL PNEUMONIAS

FIBROSING ALVEOLITIS - Poorly understood - ?multifactorial pathogenesis ! diffuse inflammation
Many cases +ve for Ab to Micropolyspora faeni – poss a chronic Farmers Lung? Or chronic manifestation of other allergens?

BRONCHIOLITIS OBLITERANS - Chronic Dz – yearling/young adult cattle – ?sequel of RT virus/parasites/allergies

PARASITES
CATTLE – Dictyocaulus viviparus (young mostly – adults immune) / Aberrant migration of Ascaris suum
D.viviparus Primary inf – youngsters / previously unexposed adult
Reinfection – immune cattle (previously exposed) ! massive infection
Adults live in URT & lay eggs ! L1
L1 coughed up – swallowed – pooped out
LI ! Infective L3 stage ! hang out on grass ! ingested
In intestines, penetrate wall ! Mesenteric LNs & molt to L4:
L4 enter blood & lymphatics ! lung capillaries ! molt to L5 in alveoli

CS – ONLY AT ALVEOLAR STAGE OF L4 ENTRY: Causes cough of prepatent phase (late summer/fall)
CS gradually resolve – “self-cure” occurs in postpatent phase when adults expelled (Severe cases can be fatal at this stage)

S&G – Dictyocaulus filaria (young mostly – no immunity in adults)/ Protostrongylus rufescens / Muellerius capillaris
(M.cap – most common but least pathogenic)

OVINE PROGRESSIVE PNEUMONIA (OPP) – MAEDI-VISNA (Lentivirus/Retrovirus)

Chronic progressive Dz – wasting / pneumonia / mastitis – death within 6-12m
Emaciation in the face of good appetite frequently an early CS
Dx – AGID – usually Abs present 6m postinfection
Oral/respiratory route of inf – infects macrophages – dissemination of virus
CAPRINE ARTHRITIS – ENCEPHALITIS (Retrovirus)
Naturally occurring – goats.
Adults – chronic arthritis / Kids – Encephalitis
Various cases of CAE have also involved concurrent respiratory Dz

OVINE PULMONARY ADENOMATOSIS (Jaagsiekte) (LOWER RT)

Contagious carcinoma: Occurs naturally - sporadic / endemic in sheep & occasionally goats – young adults
?Retrovirus induced, but poorly understood cause & pathogenesis
Progressive weight loss & respiratory signs – sheep die in weeks-months
No antemortem test
REMEMBER THE OTHER Retrovirus-induced RT lesions- OPP & Enzootic Nasal Adenocarcinoma

TUBERCULOSIS (Mycobacterium bovis – cattle & goats susceptible)

Nonspecific CS – usually respiratory / Public health significance; granulomatous pneumonia & lymphadenitis
Intradermal tuberculin test

CASEOUS LYMPHADENITIS (Corynebacterium pseudotuberculosis / C. ovis)

Common in S&G / Lung = most frequently involved internal organ – Lung abscesses

PNEUMOCYSTIS CARINII – Pneumonia / death in goats; Predisposed by immunosuppression due to chronic Dz

SOME MORE ZEBRAS…..

MYCOTIC PNEUMONIA – Histoplasma, Aspergillus, Coccidioides
LISTERIOSIS – Pulmonary form – can resemble atypical interstitial pneumonias
ANAPHYLAXIS – Lung is the target organ for anaphylaxis in cattle
NEOPLASIA – Primary pulmonary carcinomas, multisystemic neo like LSA; Pleural mesothelioma;
PLEURAL Dz – Usually 2ndry involvement – bronchopneumonia / reticulopericarditis

CARDIOVASCULAR DISEASE

CONGENITAL DZ
Various types documented alone & in combination, VSD most common – reportedly inherited in Limousin & Herefords.

ENDOCARDIAL DZ
VEGETATIVE VALVULAR ENDOCARDITIS – Extra-cardiac infection & chronic bacteremia ! Bugs implant onto endocardium
! (1) Impaired cardiac function due to valvular insufficiency
! (2) Bacterial embolic dissemination to other sites

PERICARDIAL DZ
PERICARDITIS – Etiologies (1) Hematogenous spread in septicemic animals (2) Traumatic reticulopericarditis / external
penetrating injury (3) Extension from inf in lung/pleura (4) Neoplasia

MYOCARDIAL DZ
CARDIOMYOPATHY – Dz of the myocardium in the absence of other anatomic cardiac lesions / pulmonary Dz – Often idiopathic
DCM in large animals. Also CM ssociated with Vit E/Se deficiency, & one associated with curly haircoat in polled Herefords!
MYOCARDITIS – Myocardial inflammation can be bacterial (Staph/Strep/Cl.Chauvoei), viral (FMDV), parasitic (Toxoplasmosis,
Cysticercosis, Neosporosis, Sarcocystis)

NEOPLASIA – Rare. Most frequently LSA: Predilection for RA myocardium.

THROMBOEMBOLIC EPISODES – Mostly associated with bacterial (vegetative) endocarditis, omphalophlebitis,

thrombophlebitis
URINARY TRACT DISEASE

RENAL Dz

Congenital: Consider if young animal has renal Dz Cystic kidneys – common in cattle; Renal agenesis - common congenital
defect in lambs.

Acute RF: Causes mostly (1) Prerenal – hemodynamic: Shock, hemorrhage; (2) Renal – Nephrotoxins: Lead, Arsenic,
Aminoglycosides, Oak, Ethylene glycol, Oxalates.

Chronic RF: (1) Pyelonephritis (S&G) – C.renale / Chlamydia psittaci (2) Glomerulonephritis (S) – Usually membranous GN in
sheep, associated with chronic inflammation/infection (lung/liver abscess) ! immune complex deposition

Leptospirosis: Cattle – L.interrogans, serovars hardjo / grippotyphosa / pomona; S&G – L. pomona / icterohaemorrhagica
Highly infectious – penetrates mucous membranes. Hemolytic Dz, septicemia, multiorgan dissemination with nephritis; Icterus.
Hemoglobinuria. ZOONOTIC. May be asymptomatic or cause fever, renal failure, liver failure, infertility, abortion and death.
Leptospires can localize in kidneys and reproductive organs and shed in urine. Often waterborne, wet weather, ponds. Contact
w/ infected urine. Cattle - Redwater disease of calves. Abortion. Cattle natural hosts for L. hardjo (4 mos-term) and L. pomona
(3rd trimester). Acute hemolytic syndrome is seen with L. pomona and L. icterohaemorrhagiae. Dx w/ paired serum samples (or
titer>100 suspicious), IFA, culture. Vacc is short term. Sheep similar, though less prevalent.

Pulpy Kidney S&G - Clostridium perfringens type D: epsilon toxin ! enterotoxemia with hemorrhagic enterocolitis; Mostly
lambs on Hi conc diet. Toxin ! ↑ Vasc permeability ! renal & pulmonary edema. Frequently found dead. Glycosuria common.

Cu Toxicity: (S>G; Babies>Adults) – XS Cu accumulates in liver until hepatic capacity saturated ! Free Cu released which is
hemolytic ! Hemoglobin released is deposited in renal tubules – Hemoglobinuric nephrosis ! renal impairment

Oak Toxicity - Quercus toxin. Consumption of large quantities of young oak leaves or green acorns causes GI & renal
dysfunction. Causes pale swollen kidneys, perirenal edema, anorexia, depression, emaciation, rumen stasis, serous nasal
discharge.

LOWER UT

Small Ruminants
Corynebacterium renale – Normal resident of preputial / vulvar mucosa ! proliferates & causes probs when urinary urea conc ↑
(ie – Hi protein diets): Converts Urea ! NH3 ! mucosal ulceration ! scabs – Vulvitis/Balanoposthitis – “Pizzle Rot” (M>F)
Internal form: occurs in males from Dz extension along prepuce ! swelling, necrosis & UT obstruction. Venereal spread.

Urolithiasis – Urethral Obst mostly – (S&G & Cattle) - Common

Metabolic Dz: (1) Phosphate calculi - Hi conc, Lo roughage, Lo Ca:P, Hi Mg diets, & alkaline urine. On Hi Conc diet – XS
urinary P excretion due to overwhelmed salivary excretion. (2) Silica calculi – sandy soil grown plants. (3) Oxalate calculi – XS
oxalate-containing plants – bind Ca in rumen. (Often @ distal sigmoid flexure / urethral process)
CS – Frequently non-specific – depression colic (Stranguria, dysuria, hematuria, uremia, even death).

UTi (A.pyogenes, E.coli, Staph, Strep)

Ascending umbilical inf (due to omphalitis/patent urachus) ! urachal infection, abscess, adhesions ! UTi. Primary UTi rare.

ENZOOTIC HEMATURIA
Chronic bracken fern ingestion ! carcinogenic principles ! neoplasia (renal / bladder): hematuria – Usually >1 animal affected
MASTITIS

Most common problem in adult dairy cattle

(1) Environmental: Contaminant organisms in environment enter MG: Strep uberis / Strep dysgalactiae; Gram –ve - E.coli /
Pseudomonas / Enterobacter spp: ↑ incidence as ↓ incidence of contagious forms. Control - env hygiene.

(2) Contagious: Transfer of infectious organisms from infected cow to others at milking: Str agalactiae – obligate
mammary gland (MG) organism / S. aureus / Corynebacterium bovis / Mycoplasma bovis. Control –
transmission routes – milking time: hands, cloths, machines.

Subclinical Cases – MG & milk look normal – (California Milk Test) CMT will detect ↑ somatic cell count (scc); S. agalactiae,
S. aureus. Eventually ! MG fibrosis & ↓ MY
Acute Cases – MG hard, swollen, painful. Milk +/- changes. New infection or flare-up of a chronic problem.
Acute Gangrenous Cases – Usually Staphs – Cow is toxic, dehydrated, depressed. MG eventually becomes cold, blue & sloughs.
2ndry bac inf common. S. aureus ! alphatoxin / Clostridium perfringens.
Chronic Cases – Signs are intermittent in MG & milk Something triggers a flare-up. scc usually always ↑. Eventually MG
destroyed ! fibrotic. Commonly E. coli / S. aureus / Str. agalactiae
Summer Mastitis – A.pyogenes: Dry cow at pasture - ?Flies transmit infection to udder? Massive invasion of gland ! systemic
spread & loss of function of a quarter.

GOATS – Staphs commonly isolated; Less strep infections that dairy cattle. CAEV also ! fibrosis & agalactia
SHEEP – S. aureus / E. coli / Streps commonly isolated. S. aureus/M. haemolytica often ! acute toxic mastitis with gangrene.
Also OPP ! fibrosis & agalactiae.

HEMATOPOIETIC DZ

BOVINE LEUKOSIS VIRUS: Retrovirus. Lymphoma / Leukemia. Common cattle disease, 2nd most common bovine neoplasia
after SCC. Transmitted by transfer of blood between animals. Trauma & surgery most common mechanisms of transmission,
also insect vectors. Only 3-5% of those infected get LSA. 4 syndromes- calf, thymic, skin and adult forms. The first 3 are
SPORADIC & not contagious. The adult form is from BLV = ENZOOTIC BOVINE LEUKEMIA. Calf form - calves < 6 mo old;
widespread tumor metastasis. Generalized lymphadenopathy in calves. Thymic form – 6-8 mo old calves. Skin form - only
nonfatal form, seen in young adults 1-3y. Adult form - adults 4 -8 yrs old, wide distribution of metastasis. Dx - Clinical signs.
Serologic test (AGID test to detect circulating Ab’s to gp-51 Ag of BLV ) for BLV (adult form only). Severe lymphocytosis
(>30,000) is not enough to Dx LSA, need histology. Control - No treatment. Test for BLV & cull positive animals or segregate all
BLV reactors from nonreactors.

ANEMIA
Anemia of chronic Dz – Inflammation / Renal, Hepatic, GIT Dz / Neoplasia
Nutritional Deficiencies: Fe / Cu / Folate / Co - B12 (Imp in RBC production)

HEMOLYTIC ANEMIA ! Icterus & Anemia

Leptospira icterohaemorrhagiae/pomona – Hemolytic syndrome mostly calves/lambs
Bacillary Hemoglobinuria – Clostridium novyi type D ! toxins: cattle.

Cu Toxicity – Sheep (calves) (goats more resistant). Sudden release of large hepatic Cu store (eg/ with stress) - transport etc
Postparturient Hemoglobinuria – Sporadic in dairy cattle. Often high yielding multiparous cows - ? pathogenesis.
Water Intoxication - milk-reared calf – 1st access to large water vol – sudden ↓serum osmolality ! osmotic shock ! RBC lysis

Anaplasma marginale – Dz severity ↑ with age; Splenomegaly; Arthropod vector; (A. ovis - S&G: mostly asymptomatic; can ! CS)
Babesia bigemina (larger organism) / bovis (smaller but more virulent) – Tick-borne, intra-erythrocytic parasite.
(Haemobartonellosis – Eperythrozoon wenyoni (C) / E. ovis (S&G))
(Theileriasis & Trypanosomiasis – Africa)

CORYNEBACTERIUM PSEUDOTUBERCULOSIS
Caseous lymphadenitis (S&G) – LN abscesses – Internal abscesses (viscera/LN) = commonest cause chronic wt loss in S&G
Skin abscesses (Cattle)
The bacteria lives in soil ! enters body thru abrasions etc ! travels in lymphatic system & produces abscesses
SKELETAL DZ

MYOPATHIES
Clostridial Myopathy (“Blackleg”) – Spores into body via penetrating wound ! converted to toxin-producing form ! Acute
skeletal muscle inf ! necrosis: Rapid onset fever, toxemia, death. Often found dead. Mixture of Clostridial organisms common.

White Muscle Dz: Vit E/Se deficiency – (loss of antioxidant function – cell damage & necrosis). Progressive skeletal muscle
weakness, stiffness. Also can have acute cardiac dysfunction. Mostly youngsters, quickly growing animals.

Sarcocystis neurona ! Myositis, if heavy inf – often incidental cysts: Cattle eat dog poop-contaminated feed & ingest protozoan

Downer Cow ! Muscle damage, often due to ischemic necrosis. Heaps of differentials for the downer cow: Systemic Dz v
NonSystemic
Metabolic Dz: Hypocalcemia classically; Hypomagnesemia etc
Musculoskeletal: Postparturient peripheral nerve damage; Lameness for whatever reason; Myopathy; Spinal lesions; Trauma
(fractures etc) Etc etc etc!

Viruses: Some can affect muscle due to more general body system involvement – BVDV, MCFV, FMDV (myocarditis).

ORTHOPEDIC Dz

DEVELOPMENTAL DISORDERS
DOD - Umbrella term - various skeletal probs – multifactorial etiology; abnormal endochondral ossification considered pivotal:
OCD – Young growing cattle – Distal femur: lateral trochlear ridge (Hi Mo/Lo Cu also implicated)
Physitis – Show rams on hi nutritional plane for fast growth; Pregnancy-associated in S&G – ALDs ! resolve post-parturition

FLEXURAL DEFORMITIES: Calves – S&G less common. Rigidly flexed limbs. Beef animals, esp males. Multifactorial etiology –
other congenital probs often associated. Associated with Genetics, also Viruses - Bluetongue, Akabane, BVD, Cache Valley.

DEGENERATIVE CONDITIONS
SPONDYLOSIS – Degeneration/ankylosis of vertebral joints. Older bulls used for AI – prone to vertebral enthesiophytes.
DJD Cattle - Important cause of lameness – larger, wt bearing jts – carpus, hock, stifle
Goats – frequently associated with CAEV
Sheep – rare but has been associated with OPP

FRACTURES
PRIMARY – Traumatic – not uncommon, especially youngsters post-calving for example.
SECONDARY – Pathologic: (1) Osteoporosis from Cu deficiency (2) Rickets (3) Bone neo (4) Osteomyelitis (5) Osteomalacia

INFECTIOUS DISORDERS
SOLAR ABSCESS - Common cause of cow foot lameness – less in S&G. Predisposing factors – corkscrew claw, overgrown hoof,
poor hoof care, dirty underfoot conditions. Puncture wound ! dirt in ! contamination extends to soft tissue beneath sole.

OSTEOMYELITIS
Usually bacterial. Directly introduced (wound/Sx) – more usual in adults. Hematogenous – esp youngsters – often associated
with infection elsewhere – Umbilical / Respiratory / GIT. FPT may predispose. Typically associated with:
SEPTIC ARTHRITIS – Sequestration of infectious organisms in joints – (Routes as above) A.pyogenes mostly in cattle.
Chlamydia psittaci – also ! a polyarthritis in Cattle, S&G – different serotype to abortigenic one. Mycoplasma mycoides
polyarthritis in goats. Erysipelothrix rhusiopathiae in lambs. CAEV in goats – Most common manifestation of Dz caused
is the leg form – Polysynovitis/Arthritis in goats 6mo+ (most in adults). Carpal joints commonly affected – Enlarged.

PIII OSTEITIS - Chronic lameness. Usually a sequel to unnoticed/unresponsive foot infections.

INTERDIGITAL DERMATITIS – Bacteroides nodosus

FOOTROT
Infection, inflammation of interdigital space – Involves tissue trauma & organisms – Fusobacterium necrophorum (produces
exotoxins for suppuration & necrosis), Bacteroides (proteases to attack soft tissues), Spirochetes. Causes swelling, lameness.
Dairy > Beef; Sporadic cases > Epizootics; Any time but ↑ in wet season. Interdigital dermatitis may predispose.

VERTEBRAL OSTEOMYELITIS – Bacterial (or fungal) origin – Hematogenous in neonate when septicemic; Extension of local
wound. Omphalitis / Tail dock wounds / Traumatic reticulitis. Sequelae: ! paravertebral abscess / Meningitis / SC compression

DISCOSPONDYLITIS – Can result from direct injury to Intervertebral disk / vertebral end-plate ! damages blood vessels !
↑ Susceptibility to inf
A. pyogenes, F. necrophorum, E. coli, Pseudomonas spp

DEFICIENCIES & EXCESSES

RICKETS (Vit D/P deficiency) - Young growing ruminants – defective bone mineralization

FESCUE TOXICOSIS
Fescue grass – Infested with Acremonium fungus ! mycotoxins (Ergovaline, ergonine, ergosine) ! vasoconstriction
CS: Lameness ! dry gangrene of feet, distal limbs, ear tip, tail tip.

FLUORIDE TOXICOSIS
Acute toxicity rare. Sources of Fl – Water hi in Fl / Contamination of forages - volcanic activity or industrial plants. Dental
Fluorosis – Enamel hypoplasia, chalky mottled teeth, undercalcified / Osteofluorosis – thickened, irregular, roughened bones.

LAMINITIS
Inflammatory condition of dermal/epidermal hoof wall laminae. Mostly fat heifers post-calving – Hi conc diet / concrete floor.

COPPER DEFICIENCY (Cu-Mo-S interaction pivotal) (Cu = Enzyme cofactor)

Diarrhea, ↓weight gain, Swayback (lamb - HL ataxia), Anemia (Cu for Fe metabolism), Hair color change “Spectacles”, Weak Bone

COBALT DEFICIENCY (Co = integral part of Vit B12 molecule) (So long as ruminant has Co in diet, rumen makes Vit B12)
Hinders gluconeogenesis from Pr (Co-containing enzyme required for metabolism) ! wt loss etc. Another enzyme is necessary
for erythropoiesis ! Normocytic normochromic anemia.

TOXINS
Oak – Toxins = metabolites of oak tannins – in bud, twig, leaf, acorn ! Mouth, Esoph, GIT, Kidney. Toxins bind to epithelial
proteins ! Edema: Cavity fluids – ascites etc; Renal tubular necrosis ! Anuria.
REPRODUCTIVE DISORDERS
Remember the 21d cycle in cattle & that ovulation (& hence best time for AI) is 24h after estrus.

ANESTRUS
Pregnancy, Silent Estrus, Follicular Cysts, Pyometra (Ovarian neo - GCT / Fetal mummies / Freemartinism)
Causes of anestrus that involve prolonged luteal function & hence ↑ Progesterone – Pregnancy / Pyo / Mummified fetus

FREEMARTINISM – Cattle (rare in sheep)

Twins – genetic female born with a male – conjoined placental circulations: Since sexual differentiation of male occurs before
female, the male will subsequently sterilize the female – transfers HY antigen in circulation ! stops development of female
gonad. “Ovary” – poorly developed & has seminiferous tubules!
Twins common in goats but no conjoined circulations.

RETAINED FETAL MEMBRANES (RFM) (If not out by 12h – Cattle, S&G)
Dairy > Beef. Twins, Dystocia, Shortened or longer pregnancy. Cause poorly understood – nutritional deficiencies??
RFM (as well as dystocia, uterine prolapse, torsion or obstetrical manipulations) may ! METRITIS

In dairy cows, organisms will infect the uterus around/after birth ! ENDOMETRITIS (Usually mild, transient): If she
ovulates before these bugs are eliminated, may ! PYOMETRA (A.pyogenes again….) Uterine infections more common in cows
overfed & overconditioned (lipidosis)

UTERINE PROLAPSE – Most within a few hours post partum – often ass’d with Hypocalcemia, Dystocia.

INFECTIOUS PUSTULAR VULVOVAGINITIS VIRUS (BHV-1) Strain distinct from IBRV. Vaginal discharge & inflammation
of vulvar & vaginal mucosa ! pustules ! ulcers. Similalry on penile mucosa. Contagious.

ULCERATIVE DERMATOSIS IN SHEEP (Parapox virus – distinct from Orf parapox virus)
Ulcerated vulva, penis, prepuce. Venereal Dz.

ABORTION

Cattle - Herd problem: IBR, BVD, brucellosis, leptospirosis, campylobacteriosis, trichomoniasis, anaplasmosis, ureaplasmas,
mycoplasmas. Sporadic cases: Mycotic (Aspergillus, Mucor spp). Reach uterus hematogenously, cause late term abortion. Fetus
not affected or may have ringworm lesions; placenta severely affected with necrosis of cotyledons. Dx via culture of fetal
tissue. Also Listeria, Haemophilus, Corynebacterium pyogenes, Staphylococcus, bluetonque. Nitrates, lupine, locoweed,
mycotoxins. Akabane virus disease – arthrogryposis, hydrancephaly.

Sheep - Most common cause of abortion is campylobacteriosis. Campylobacteriosis - Infection via ingestion of organisms. Late-
term abortion of edematous fetus; liver with gray necrotic foci. Carrier sheep shed organisms in feces, uterine discharges,
aborted fetuses. Culture and ID organism in fetal abomasal fluid and liver. Vaccinate ewes at breeding; booster at second
month gestation. Toxoplasma gondii – protozoan; life cycle is completed in the cat. Abortion and still births in sheep, pigs, and
goats. White foci in cotyledons (intercotyledonary regions only minimal to mild necrosis), leukoencephalomalacia. Chlamydia
psittaci – late-term abortion. Exposure via ingestion, inhalation or venereal. Fetus well-preserved or mummified. Placentitis
most consistent finding. Leptospirosis - late-term abortions. Listeriosis - late-term abortion, birth of weak lambs. Slight to
marked autolysis of fetus, fluid in serous cavities, necrotic foci in liver, lung and spleen. Erosions in abomasal mucosa. CNS
deficits. Man can be affected. Coxiella burnetti – Intercotyledonary regions markedly necrofibrinous (Both cotyledonary &
intercotyledonary necrosis are seen in coxiellosis & brucellosis – difficult to DDx grossly).

NICE REVIEW: “Causes of caprine abortion: diagnostic assessment of 211 cases (1991-1998)”.
J Vet Diagn Invest. 2001 May;13(3):265-70.
CATTLE
Campylobacter fetus, ssp. venerealis EED (Early embryonic death)
Tritrichomonas fetus 1ST HALF
Neospora caninum MIDDLE
IBRV 2ND HALF
BHV-1 2ND HALF
Leptospira interrogans 2ND HALF JAUNDICED FETUS
Salmonella (typhimurium/dublin) LAST THIRD
Sarcocystis cruzi LAST THIRD
Aspergillus fumigatus LAST THIRD THICKENED PLACENTA
Brucella abortus LAST THIRD
Listeria monocytogenes LAST 2M
BVDV ANY TIME
Bluetongue Virus ANY TIME
Haemophilus somnus ANY TIME

SHEEP & GOATS

Chlamydia psittaci LAST 2M THICKENED/NECROTIC PLACENTA
Campylobacter fetus fetus (or C. jejuni) LAST MONTH
Listeria monocytogenes LAST MONTH
Coxiella burnetti LATE
Brucella ovis (S) LATE
Border Dz Virus ANY TIME
Toxoplasma gondii ANT TIME
Bluetongue Virus ANY TIME

October 2003; Dr Nicola Parry, Large Animal Pathology, NBC Ext 2451, nmparry@vet.upenn.edu