Food Animal Med

PHYSICAL EXAM

Age, breed, sex, pregnancy status, production status/stage of production cycle
INTENDED OR CURRENT USE

Onset/duration/progression of signs
When was the animal last normal?
Body functions
Prior medical history
Management factors

Hands-off exam

Animal gets less stressed

Attitude
Apparent BCS
Gait, lameness
Resp rate
Muscle atrophy/asymmetry
Distribution of lesions
Posture and abdominal contour

Fat
Fluid
Foetus (low bulge)
Flatus (gas) (will probs have resp trouble and can feel ribs)
Food (look in paralumbar fossa)

At the rear

"Ping" the animals abdomen and listen for distinctive sound

The animal will lordose away from the pinch indicating that there probably is no cranial abdominal or thoracic pain

Bovine respiratory syncytial virus

Endotoxaemia

The use of a drug in a way other than specified by the manufacturer

1. As a treatment
2. Prophylaxis
3. Metaphylaxis - during high risk of disease development
4. Concurrent infection
5. Infection of structures in surgical field/tissue of interest

They only work if the patient's cellular and humoral defences are intact

Macrolides (erythromycin, tylosin, tilmicosin)
Tetracyclins
Sulfonamides

Lipid soluble - but they tend to cause granulomas at the injection site

Aminoglycosides
Vancomycin
Fluoroquinolones (restrictions)

Rumen flora metabolise most of the antibiotics

In the neck, in front of the scapula

15-20ml

White

Penicillins
Cephalosporins

Penicillins & Cephalosporins
Sulfonamides

Beta lactams

Third gen Cephalosporins
Florfenicol

Incorporation of PABA into dihydrofolic acid

Once animal starts ruminating drugs will be degraded

Macrolides
Lincosamides
Florfenicol

Macrolides - good for getting into diseased tissue like pneumonic lungs
Rifamycin - used for chronic granulomatous or purulent disease

Tetracyclins
Aminoglycosides

Tetracyclins
Lincosamides
Rifamycins
Florfenicol
Macrolides

Nephrotoxicity caused by the administration of degraded tetracyclins

Aminoglycosides

FALSE

It is ILLEGAL to use them for anything other than respiratory disease in beef cattle!!

Bacterial DNA gyrase

DNA-dependent RNA polymerase

Florfenicol
Fluoroquinolones (beef only)
Tetracyclines if caught early

Swine

Relief of minor pain
Can be used to treat DIC, endotoxic shock and sepsis as it inhibits platelet aggregation

Flunixin meglumine

Alleviate pain
Bind endotoxin
Reduce fever and inflammation

Sodium iodide IV

FLUID THERAPY

Adult - 50ml/kg
Calf can be up to 70ml/kg

80-90ml/kg

Severe - 11-12%

Moderate dehydration 8-10%

Endotoxaemia

USG = 1.015-1.045
TS = 6-8
PCV = 25-35%
BUN = 10-25
Cr = 0.5-2.0
Lactate = <1
Osmolality = 280

Feel tube moving down oesophagus
Listen at left para lumbar fossa while someone blows down the tube

4ml/kg - must follow with oral fluids e.g. 2L of saline followed by at least 10 gallons of fluids

10-20 gallons

To use isotonic, non-irritating solutions and no dextrose

Overhydration especially in camelids and neonates as they can get severe hypoproteinaemia - check the eyes to see if puffy

10ml/kg

Litres needed = body weight (kg) x % dehyradration

Diarrhoea or oesophageal choke

Calcium

Weight x 0.6 x base deficit

(0.3 adults)

25mEq

Bicarb and glucose

You need to supplement potassium because even though they appear to be hyperkalaemic - they will be whole body depleted after the fluids

0.5-1.0mEq/kg/hr

Start supplementation once K gets <3

Risk of cerebral oedema due to the brain being hypertonic compared to the rest of the body

Slowly give the calf serial dilutions of hypertonic saline to gradually reduce its tonicity

"Rat tailed" appearance to the tail

Hair loss on extremities, anaemia, weight loss

As a single hairless lesion, treatment not necessary

In the skin and cause a pustular erythematous dermatits

Biting or sucking lice

In the winter time when it's cold

Ivermectin for sucking lice
Powdered insecticides for biting lice
Treat every 2 weeks for at least 2 treatments

Yes in the United States

As for live but repeated treatments are not necessary

Between 1st October - 1st March as it will kill the larvae in their mobile state either in the oesophagus of the spinal canal and cause paralysis

Chorioptic (in cattle)
Psoroptic (in all ruminants)
Sarcoptic (in cattle) also zoonotic

Demodectic - head, neck and topline

Sarcoptic - starts on head and neck and spreads to rest of body

On the feet and the backs of the legs

Commonly in the ears, in other ruminants it starts on ribcage of shoulders/rump and spreads to the rest of the body

Rain scald, strawberry foot rot

"paint brush" appearance to scabs

Penicillin or oxytetracyclin

Sheep and goats

Around the eyes, lips, muzzle, udder, teats and feet

6

If its just a small area will usually clear up, if not can remove them.

The teats of cows, look like orf lesions

When housed indoors during the winter

No

Alopecia with broken hair shafts around the head and neck.

Treatment not usually necessary

Zinc deficiency

OCULAR PROBLEMS

Moraxella bovis

Sheep = Chlamydophila pecorum
Goats = Mycoplasma spp.

Sticks to the cornea via pili and these are constantly mutating which means vaccines are type specific

Spontaneous healing with a scar

However corneal rupture and blindness can occur

Blepharospasm, epiphora and photophobia.
There will also be a central corneal ulcer in one or both eyes

Subconjunctival injection of water soluble antibiotic e.g. procain Penicillin G

A lipid-soluble antibiotic and NEVER use steroids with corneal ulcers

Can give SQ long-acting lipid soluble antibiotics

Fly control!

Polyarthritis (stiff lamb disease)

Parenteral oxytetracycline

Entropion

Polyarthritis, septicaemia, mastitis and abortions in the herd

It can take a long time to clear up as Mycoplasma can mutate to avoid the immune response. An outbreak can last 3-6 weeks

Ocular Squamous Cell Carcinoma

Genetics, UV light exposure, white faces, age >4yrs

It can invade the conjunctiva, cornea, sclera, 3rd eyelid and/palpebral skin

Usually slow to grow and slow to metastasize

Cryotherapy or hypertharapy

Debulk and cryotherapy for any remaining tissue. May need to completely remove 3rd eyelid

If there is not enough eyelid left to cover the eye, if the eye is bind and painful

A 4 point retrobulbar block

The socket will bleed A LOT so just let it fill up with blood and it will eventually clot and form granulation tissue. NEVER leave gauze in the socket

Pre- and post-op antibiotics and NSAIDs

BONES, JOINTS & CONNECTIVE TISSUE

Primary
Secondary or
Tertiary

From infection introduced directly into the joint by puncture wounds or septic joint injection

An extension of infection into a joint from adjacent tissues (e.g. associated with foot rot)

Tertiary e.g. neonates with failure of passive transfer are prone to septicaemia

Arcanobacter pyogenes

- always found in wounds that are older

Chlamydia psittaci

-stiffness, fever, abortions, keratoconjunctivitis. In 1-8mth old lambs

1. Bacterial invasion
2. Polymorphonuclear cells
3. Synovitis
4. Cartilage destruction

Damage to the articular plate resulting in permanent impairment of joint function

Lameness, heat, pain and swelling of affected joints

Bacteria
Nucleated cell count >10000 with >80% neutrophils
Total protein >4mg/dl

2-3 weeks

Penicillins, cephalosporins, tetracyclins, clindamycin etc.

Joint drainage and lavage
Anti-inflammatory drugs

Progressive deterioration of articular cartilage with variable degrees of periarticular osseous remodeling

Often related to direct or indirect trauma
Also can be secondary to osteochondrosis

An early microscope fibrillation of the cartilage, which leads to degeneration and necrosis of chondrocytes, which results in decreased production of proteoglycans in the matrix of the cartilage.
The decrease in proteoglycan content leads to a decrease in water content, decreased elasticity and an increase in fibrillation. This decreases the ability of the cartilage to withstand stress.

Full thickness erosions of the cartilage and damage to the subchondral bone. Eventually there is fibrosis of the joint capsule and marginal osteophytes which interfere with movement of the joint.

Larger weight-bearing joints - hock, stifle and carpus

Change in management
Anti-inflammatory agents
Intraarticular therapy (hyaluronic acid, polysulfated glycosaminoglycan)

Lack of mineralization of rapidly growing bones

A deficiency of phosphorus of vitamin D

Camelids

Winter months

Lameness, stiffness, joint enlargement.
Palpating the ribcage = "string of pearls" feeling of costochondral junctions

ALP is elevated
Vit D is decreased
Ca and P often normal

Adequate dietary calcium and phosphorus
Injectable Vit D
Crias born during winter need Vit D supplementation - care incase of toxicosis

One of the most frequently encountered congenital diseases characterised by deformity of the interphalangeal, metacarpophalangeal, carpal and/or metatarsophalangeal joints

Beef breeds e.g. Charolais, Herefords, Simmental.
Incidence is higher in bull calves

Irreducible and rigid flexural deformity of affected joints.
Dystocia in cattle
Scoliosis and cleft palate often

Euthanasia as it is usually severe

Minor tendon contracture can be treated with splinting and stretching

With contracted tendons you should be able to flex the joints a bit

If animal can stand - straighten manually
In moderate cases splinting can work
In severe cases they may need a complete or partial tenotomy

Laxity of periarticular supporting structures
Imcomplete ossification
Asynchronous growth rate

Camelid crias

Suffolk Sheep - a semi-lethal autosomal RECESSIVE trait

Where the lamb is abnormal at birth
Or lamb develops abnormalities 3-8 weeks after birth

Kyphosis
Scoliosis
Concavity of the sternum
Lateroventral deviation of the maxilla (Roman nose)
"knock kneed" appearance at carpus and lateral deviation and rotation at metacarpus/tarsus

Carrier rams should be destroyed, carrier ewes are fine because the trait is recessive. They can be used to test rams

A retrovirus that infects cells of monocyte-macrophage lines

Synovium, mammary glands, CNS and lungs

1. Leukoencephalomyelitis - kids up to 6 months, rear leg paresis then paralysis which can spread to front legs
2. Polysyynovitis-arthritis - from 6 months +, chronic joint enlargement - may walk on their knees, can have mammary gland involvment and decreased milk

May have red-tinged fluid, increased cell count (monocytes) and decreased/normal protein

AGID (agar-gel immunodiffusion)

No treatment for leukoencephalomyelitis form
NSAIDs and supportive care for arthritic form

Through milk and colostrum to kids. Positive dams shouldn't be allowed to nurse their kids and milk should be pasteurized

Endotoxaemia as a result of peripartum diseases e.g. metritis, retained membranes etc.

Cow will stand with arched back, will lie down most of the time, swelling and tenderness over the coronet

White line abscesses or sole ulcers
Subacute is recognised by solar haemorrhages and broadened or bloodies white lines

Chronic form - hooves widen and flatten, ventral deviation of the pedal bone, sole thins and softens and haemorrhages appear beneath the cranial portion of the sole
Pasterns and heels tend to drop

Often problems in nutrition - subacute rumen acidosis

5lb of effective fibre and it must be at least 1.5 inches ling minimum

Acute - NSAIDs, supportive care and treat primary condition
Chronic - routine foot trimming and are more susceptible to other foot problems

Fusobacterium necrophorum

Dichelobacter nodosus

Swollen interdigital space, coronet and bulbs.
Mild to severe lameness in one or more limbs
Fetlock and pastern usually held in a flexed position with only light weight on the toe

Septic arthritis

Systemic antibiotics - tetracyclins, penicillins, sulfonamides
Local wound cleaning

That the infection has spread to deeper structures and further dignostics are required e.g. radiographs

Drain and clear wet areas and remove slurry more frequently

More it is highly contagious and is a leading cause of lameness in small ruminants. Even foot trimmings and tools are infective

Archanobacter pyogenes

Infection spreads from interdigital space or sole into distal interphalangeal joint. Severe swelling at the coronet results in lameness, pressure builds within the joint and fistula develop on abaxial region of digit

Drill out the necrotic bone and material, place a block on the other claw to raise the injured one off the ground

12-18 months - the suspensory apparatus of the other claw breaks down over time

Dairy cows

Muddy pens & poor biosecurity - new cows always coming and going

Sharply demarcated, round, ulcerated, strawberry-like appearance on the plantar/palmar surfaces of the feet

Up to 2 inches and raised with hair-like tissue projections

Topical abx - spraying the feet, tetracycline infused bandages, foot baths

Thickening of interdigital skin causing a mass to protrude between the claws.

Front feet of cows
Rear feet of bulls

No therapy unless they are causing a problem, then you can surgically remove

A sole/subsolar abscess

Debride sole to establish drainage

A circumscribed loss of horny sole from solar corium to weight bearing surface

Might not be severe until granulation tissue develops from exposed corium and prolapses through the defect in the sole

To reduce/prevent formation of granulation tissue

Remove the undermined sole at the edges of the lesion including excessive granulation tissue
Apply copper sulfate powder to control granulation and bandage the foot
Place the unaffected claw on a block to raise affected claw

A subsolar abscess involving the white line

Infection of navicular bursa

As for subsolar abscesses

Once it gets lower down the hoof wall it can snap off and expose P3 - should be trimmed away

Vertical crack in the hoof usually of the forefeet
Can go deep enough to cause pain

Place a horizontal groove at the cracks proximal limit
Trim crack with grinder and place acrylic cement

Endophyte fungus produces toxins, these cause vasoconstriction which results in blood stasis, endothelial damage and thrombosis in peripheral vessels.
As a result the distal extremities become ischemic and gangrenous

Begins as hindlimb lameness
Cattle are underweight, have a dull, rough hair coat
Feet and pasterns become cold and coronary bands are red and swollen
Hair can be rubbed off the pastern and limb oedema may be present

When a sharp line of demarcation at the level of the pastern or fetlock appears distal to which the skin becomes dry and gangrenous and eventually sloughs

Tips of the ears and the tail

Abdominal fat necrosis can also happen

Remove animals from pasture asap, once the foot has gone cold there is nothing that can be done

Corkscrew claw

1. Minimise standing time
2. Good quality environment
3. Limit rumen acidosis
4. Biosecurity

1. Foot rot
2. Infection of the deep structures
3. Fracture

MUSCLE DISEASES

A peracute-subabcute myodegenerative disease of cardiac and skeletal muscle caused by a deficiency of selenium or vitamin E

Selenium

Cardiac - sudden onset, severe debilitation or death. Lesions in the heart, diaphragm and intercostals. Pulmonary oedema and dyspnea
Skeletal - slower onset, muscular weakness or stiffness. Animals may be unable to stand, tongue muscle may not work making it hard to eat

Creatinine
AST
LDH

Blood mineral analysis
Selenium-dependent glutathione peroxidase (GSH-Px) level

From the destruction of cell membranes
Vit E acts as an antioxidant

Cardiac form generally isn't responsive
Skeletal form can be treated if caught early enough - injectable selenium and vit E

Clostridium chauvoei

Rapid progression from muscle tremors, ataxia and dyspnoea to recombancy, coma and death

Severely depressed
Febrile
Tachypneic
Anorexic
Muscle will be hot and then go cold
Crepitus within the muscle

Spore-forming characteristics allow it to remain in the environment for a long time
Once spores are in the muscle they convert to toxin-producing bacteria

Penicillin
Debride the area as clostridium are anaerobic and you want to get as much oxygen to the site as possible

Yes get a 7- or 8-way vaccine

C. septicum
+/- C. novyi type B

Microabrassions in the mucosa of the vulva and vaginal vault at calving

Local inflammation of skin, SQ and muscle +/- crepitation
Cusion-like swelling of vulvar region with foul-smelling reddish discharge
Swelling may extend down between the legs

With penicillin and local irrigation with 3% hydrogen peroxide

A Downer cow - just a term doesn't indicate disease/prognosis

1. Metabolic disease - low Ca, P, Mg, K, pregnancy toxaemia
2. Metritis
3. Mastitis - severe acute coliform
4. Musculoskeletal/nervous
5. Miscellaneous - spinal lumphosarcoma, peritonitis, starvation

Sick downer cows tend to have signs of endotoxaemia - low temp, tachypnoea, tachycardia, injected sclera, depression
Alert cows are generally normal and maintain themselves sternally

Crush injury to the muscles - myonecrosis
Ulcers
Loss of muscle and nerve function

Creatinine kinase and AST

Big increase in CK
Small increase in AST

Px = guarded

Smaller increase in CK
Big increase in AST

Px = fair

Big and persistent elevation in CK
Big increase in AST

Px = poor

Float tank
Lift with a sling and use inflatable mattress

Piedmontese
Belgian Blue and White

Dystocia

Affects older dairy cows, weird intermittent leg kicking
No treatment it is neurological cow will be fine

Affects calves
Walk with straight hind limbs which often shake or are on their toes
Don't breed these animals and will have to eventually euthanise

MAMMARY SYSTEM

Most stays in the alveoli but a small fraction is held in the gland cisterns

2

Prolactin & ACTH - secretion

Oxytocin - Let down

Primary physical barrier to microbial invasion

Epithelial cells produce keratin to line the canal - this physically plugs the end of teat trapping microbes and preventing milk leakage

2 hours

It may take weeks, increasing her risk of mastitis in that time. Barrier teat dips can be used

Macrophages

Neutrophils

No glucose in milk
Decreased glycogen
Deficiency of opsonins and complement in milk
Neutrophils get coated in casein
Loss of PMN pseudopods due to ingestion of fat
PMN has less hydrolytic enzymes after ingestion of fat and casein

Immunoglobulins
Lactoferrin - prevents multiplication of iron-dependent bacteria - coliforms
Cytokines

In the periparturien period (just before and after calving)

Depressed neutrophil function
Macrophages not as efficient
This is due to high levels of circulating cortisol
Also the cow tends to lie down in dirty areas and udders are really full and get dirty

Bacteria effect the milk secreting cells in the alveoli which die and cause alveolar atrophy
Chunks of clotted milk and cells mix with normal milk

Pain
Heat
Loss of function
Swelling

Stall side test to detect subclinical mastitis

Milk is stripped from each quarter into the chambers
Reagent is added to lyse cells and agglutinate the DNA

The more WBCs that are present = more agglutination = more gel

Graded from negative, trace, +1, +2, +3

Colostrum
Late lactation
Illness
First stripping of the day
Residual milk
Trauma to the udder

<100,000/ml

Individual quarter - Best results
Composite sample
Bulk tank sample - coliform or strep +ve indicates pre-milking problem as these live on teats

Staphylococcus aureus
Streptococcus agalactiae

Corynebacterium bovis
Mycoplasma sp

Contaminated milking equipment
Nursing calf
Hands of dairy staff

Post-milking teat disinfectant
Antibiotic treatment of all quarters at dry off
Culling of chronic cows
Prompt recognition and treatment
Proper use and maintenance of milking equipment

Gram negative coliforms such as E. coli, Klebsiella, Enterobacter

Less commonly
- Pseudomonas, Serratia, Proteus and Strep uberus

Gland in swollen, painful and may be oedematous or very hard

Clinical signs - anorexia, depression and fever. Hypocalcaemic in severe cases

Flakes or clots; watery or serous

Anorexia
Dehydration
Depression
Fever
Signs of toxicity

Usually Staph. aureus

Clostridium can too

Initially it is red, warm and swollen but then teats become cold and secretions watery.
Then sharply delineated blue discolouration extends from the teat
Tissues begin sloughing in 10-14days

May have no clinical signs

SCC usually elevated and milk might have flakes, clots or fibrin

Bulk tank >250,000
>15% of cows have DHIA score >4.5
>2% new clinical cases per month
Acutely ill cows in the herd are >1% a year

Severe and also gangrenous mastitis
Resists phagocytosis - invades mammary epithelial and interstitial tissues
Fibrosis of tissues and abscesses can occur
Often resistant to B-lactams

Staphylococcal alpha toxin

Coagulase-+ve

It can never truly be cleared up by antibiotics so flare ups occur

Highly contagious
Subclinical mastitis with periodic acute local inflammation
Remains on epithelial surfaces resulting in tissue damage

Penicillin

Intramammary treatment is usually fine

Decreases it as it causes necrosis and fibrosis of secretory tissue

Staph. aureus - younger "springing" heifers

Strep. agalactiae - older cows

The exposure of bacterial populations in the environment

Pink lactose fermenting colonies on MacConkey agar

In the late dry period, they remain subclinical and then become clinical at calving when the immune system is compromised

Spontanous recovery without treatment

However can become very severe with acute toxicity and sometimes death

Dehydration
Fever followed by subnormal temp
Tachycardia and tachypnoea
Injected sclera
Rumen atony
Death

They do not adhere to mammary epithelial tissue
They multiply quickly and die in the mammary gland which can result in the release of endotoxin

Haematogenous spread of bacteria to lungs and heart resulting in pneumonia and vegetative endocarditis

Frequent milking to eliminate toxins
Intramammary abx
NSAIDs
Supportive care - fluids, feeding
Supplements - vit C, calcium as needed

Mycoplasma bovis

They may also get bronchopneumonia, otitis or polyarthritis

No effective treatment and cows become lifelong carriers

Cull infected cows

Do NOT feed it to calves as they can have haematogenous spread to other body systems

Corynebacterium bovis

1. Consider the pathogen
2. The cow's history - cull chronic
3. The severity
4. Alternatives? Dry off?
5. Start tx promptly
6. Choose appropriate antibiotic
7. Realise limit of sensitivity testing
8. Consider pharmacokinetics and dynamics - e.g. in milk? systemic?

Fluids and electrolytes
Anti-inflammatory drugs - NSAIDs, steroids
Oxytocin and frequent milk out
Others such as Vit C and hydrotherapy

Staph. aureus

Gangrenous S. aureus found more commonly in heifers than older cows

Mycoplasma mycoides

Ovine progressive pneumonia
CAE

During the periparturient period

Oedema is symmetrical, pits on pressure and is cool to the touch

Reduce salt in the diet
Administer a diuretic

As a result of trauma
When 'bagging up'
Severe mastitis - poor prognosis

They are agammaglobulinaemic at birth and rely on colostrum

During the first 24hrs only

IgG

Older cows have more immunoglobulin
High producing cows have lower quality
Leaking of milk or pre-milking

A colostrometer

Measure the milk at room temperature

CARDIO

Low incidence
Cattle rarely do strenuous exercise
Difficult to examine CVS

Mucous membranes
Oedema
Presence of jugular pulses
CRT

Facial
Coccygeal
Caudal auricular
Lingual

Fever
Excitement
PDA
AV shunt

Hypovolaemia
Electrolyte abnormalities
Arrhythmias

Pulse should not extend beyond 1/3 of the way up the neck
If you occlude the vein at the caudal border of the mandible the vein should not distend caudal to your hand or have pulses
When occlude at thoracic inlet vein should rise but not have pulses

Hypomagnesiaemia
Cranioventral bronchopneumonia
Thin animal

Displacement of the heart by a mass
Changes in pericadial/pleural spaces
Hypocalcaemia

Cattle:

Adult: 60-80 bpm

Calves: 100-120 bpm


Sheep, goat: 80-100 bpm


Pig: 60-90 bpm


Llama, alpaca: 40-60 bpm

Bradycardia

Fear and stress
Drugs
Pyrexia
Pain
Increased CO2 or decreased O2
Metabolic diseases

Atrial fibrillation

Absence of P waves
+/- fibrillation (F) waves

A primary cardiac disease

Ultrasound guided
Left side, 5th intercostal space with a 20cm needle

Pericardial effusion

Intracardiac masses

Enlargement and displacement of the heart

Thickened myocardium

Congenital abnormalities

Narrow rib spaces
Large triceps muscle mass

Ventricular septal defect

Atrial Septal Defect (ASD)
Patent Ductus Arteriosus

Tetralogy/Pentology of Fallot

Poor growth, lethargy, dyspnea, exercise intolerance,

None - not viable economically or practically

Limousine and possibly Herefords

It is an opening in interventricular septum - communication b/w left and right

Changes in left and right
atrial pressures fail to
produce functional
closure of the foramen

Common in calves

Machinery

Ectopia cordis cervicalis

Usually in the cervical region, they don't survive long

Heat stress

Radiation
Conduction
Convection
Evaporation

The first 3 only work if there is a temp gradient b/w the animal and the environment

Breed, night-time temp, alpacas are more tolerant than llamas, poor nutrition, over conditioning and fescue toxicosis

Decreased milk
production

Reduced reproductive
performance

Reduced feed intake

Altered respiration

Abnormal GI function

Increased water loss

Delivery of low birthweight
calves

High ambient
temperature and
humidity

Overexertion

Fighting

Breeding

Transportation

Prolonged restraint

Fever

Dehydration

Depression and ataxia
Recumbancy
Tachycardia/pnoea
Increased temp
Dehydration
Colic
Scrotal oedema
Neuro signs
Congested MMs

Fibre coat can generate heat at high humidity and impedes evaporative cooling from the skin
Exacerbated by
dehydration

Multiple organ failure

Disseminated
intravascular
coagulation

Early recognition
Rapid cooling

Apply cold water to
thermal window (hairless areas)

Soaking fleece is
ineffective

Intravenous fluids
Oxygen therapy

Right heart failure

Secondary to other diseases with cause cardiac insufficiency but go undiagnosed until full blown heart failure is happening

Tachycardia
Submandibular and brisket oedema
Jugular and mammary vein distension
Jugular pulses

Endocarditis
Pericarditis
Lymphosarcoma
Cor pulmonale (Brisket dz)
Myocardial dz - dilated cardiomyopathy, myocarditis

Bacterial - A. pyogenes

Tricuspid valve

Chronic weight loss
Intermittent fever
Transient response to antibiotics
Lameness - nidus of bacteria break off and settle in feet

High globulins

Also
High fibrinogen
Anaemia
Variable WBCs

Rarely curable
Long term Abx (6-8wks)

Poor prognosis

Septic form

Usually accompanied by traumatic reticuloperitonitis (hardware disease)

Pain! - elbows abducted, teeth grinding
Muffled and/or splashing sounds

Metal such as nails rest within the reticulum, resulting in FB perforation through the diaphragm and into the pericardium

Radiographs
Echocardiography
Pericardiocentesis

Give the cows a magnet at 15 months old, clear up the farm.

All treatments have grave prognosis - repeated drainage and levage, 5th rib resection

Enzootic

Right atrial myocardium

Older cow
Dairy>beef

Less than 5%

Seropositive for life

RHF +/- murmur

99% positive for BLV

Symptomatically

Terminal disease

Decrease transmission of the virus - minimise blood transfer, control insect vectors, don't feed colostrum/milk from infected cows which have very high cell counts, cull positive animals

High altitude disease as a result of living at greater than 6000 feet

In the winter and if there is any ingestion of locoweed

Calves are more commonly affected

Right ventricular hypertrophy and subsequent RHF secondary to pulmonary hypertension and increased pulmonary vascular resistance

Alveolar hypoxia causes vasoconstriction of pulmonary vessels

Airway obstruction
Pneumonia
Pulmonary oedema
Lung worms
Pulmonary thromboembolism secondary to liver abscesses

Remove from high altitude
Treat primary lung dx if present
Digoxin
Diuretics

Px - guarded once in RHF

No

May be bacterial, viral, parasitic or inflammatory

Focal myocardial infacts, necrosis and fibrosis

A primary myocardial disease characterised by ventricular dilation and myocardial systolic dysfunction that may result in congested heart failure

Ingestion of monensin, gossypol, cassia, phalaris, Vit E/selenium deficiency and copper deficiency

Sudden death in association with Histophilus somni
Fever
Tachycardia +/- arrhythmias
May have a mumur
May have no signs of heart failure

More likely to have heart failure signs
Tachycardia
Jugular pulses. brisket and submandibular oedema
Increasing lung sounds, dyspnoea
Murmurs and arrhythmias

Calf/juvenile
Thymic
Cutaneous

No

Signs from 1mth-3yrs

Depression, weight loss, weakness, lymphadenopathy - cervical and parotid especially
Tachypnoea/cardia, increased lung sounds
Microcytic hypochromic anaemia

Death in 2-8wks

Rare

Signs usually from 6-24mths

Space occupying mass in the neck
= Brisket oedema, dysphagia, bloat, tachycardia/pnoea

Fatal soon after signs

Anus, vulva, shoulders and flank

Raised and may be ulcerated, 1-3yo

Heart - right atrium, RHF
Abomasum - diarrhoea, weight loss
Uterus - infertility
Lymph nodes
Spinal cord - ataxi
Retrobulbar - exopthalmus

BLOOD DISEASES

Milk vein

Tachycardia/pnoea
Cold extremities
Pale mms
Weakness

Hypertonic saline followed by crystalloids
Blood if needed - first transfusion does not need to be cross matched

When PCV is <15% - the body has time to adapt to chronic hypoxia

Natural coumarins get converted to dicoumarol if the the forage is improperly stored and mould forms

Interferes with synthesis of factors 2, 7, 9 & 10 because of inhibition of vit K

Epistaxis and melena 2-7 days after ingestion

Remove feed and administer injectable vit K

Haemolytic
Depression
Aplastic - rare

Increased rate of RBC destruction

Inadequate erythropoiesis or bone marrow suppression

Extravascular - diseased RBCs are removed by splenic and hepatic macrophages

Cattle - anaplasma marginale

Sheep and goats - anaplasma ovis

Adults over 2yo
High fever 12-24hrs
Anorexia and drop in milk production
Lethargy and decreased ruminations
As PCV drops animal becomes more hypoxic and may start to stagger or be aggressive

15-30days

Constipation, pollakiuria with dark yellow urine

Haemoglobinuria does NOT occur!! - extravascular

Because they may collapse and die if stressed

Ticks, stable flies and direct blood transfer

Because PCV drops quickly in the first 24-48hrs and the cow doesn't have time to adapt

Anaplasma can be detected within RBC with a blood smear during the acute stage
ELISA can be used only in a subclinical/chronic stage

Tetracyclines - oxytetracyclin

Insecticides, safe dehorning practices etc. to reduce iatrogenic blood transmission

B. bigemina

B. bovis - most virulent

INTRAvascular

Fever, icterus, anorexia, tachycardia/pnoea, haemoglobinuria
Hyperexcitability, convulsions, opistotonis, coma and death

Up to 9mths

Once haemaglobinuria or cerebral signs are seen prognosis is poor

Diminazine aceturate or phenamidine disethionate can be used for treatment

Mycoplasma haemolamae

Organism is associated with the outer edge of the erythrocyte

EXTRA-vascular

Camelids - lethargic, poor growth, weight loss. Can lead to severe anaemia and death

Tetracycline is antibiotic of choice, long course

Organisma remains in the spleen and will become active if the animal is stressed

Pomona and icterohaemorrhagiae

Fever, lethargy, icterus, anaemia, petechial haemorrhages

It is immune mediated - cold-reacting immunoglobulin M (IgM) antibodies

Clostridium haemolyticum

After liver fluke migration
Clinical signs develop so rapidly you may only notice a dead animal

Phenothizine
Red Maple Leaf
Onions
Brassica plants
Some nutritional imbalances

Weakness, lethargy, pale mms, exercise intolerance and marked icterus

Lethargy, muddy or cyanotic mms, icterus, brown coloured blood and pigmenturia

Formation of methaemoglobinuria

Oxidative denaturing of haemoglobin results in aggregation of globin which appears as a Heinz body inclusion

Reduced glutathion
Methaemoglobinaemia
Elevated liver enzymes

Remove source of toxicity and provide supportive care

- fluids, blood, vit C

Intravascular haemolysis
Neurological signs - coma, convulsions
Hyponatraemia
Hypoosmolality
Haemoglobinuria
Hyposthenuria

In milk fed calves that are given free access to water

Hypertonic saline and mannitol

Happens sporadically in dairy cows during the first month after calving

Intravascular haemolysis and haemoglobinuria

Hypophosphataemia

Tx - supportive care and correction of nutrition deficiencies

In growing lambs

Can occur in adult sheep, goats and cattle also. Merino sheep are more resistant

Diet = 4-6ppm

Toxicity = 10-20ppm

It is stored in the liver, which has a large capacity.
When the hepatocytes are saturated with copper or if there is environmental or dietary stress, hepatocytes die and release large amounts of copper into the blood

Improperly mixed feeds and supplements

>6:1

Molybdenum binds with copper and prevents storage in the liver
Too much sulphur can reduce molybdenum absorption and also cause toxicity

Asymptomatic while copper is building up

After rapid release of copper - anaemia, myopathy, renal and heptic disease
Anorexia, tachycardia/pnoea, icterus, dark red/brown urine

Pale yellow with "gun metal grey" appearance

Only just before the acute crisis

Serum mineral analysis, fecal copper levers or blood smear will be more helpful during acute stage

GGT and AST

Start supportive care immediately

Treatment of choice = D-penicillamine $$$

Anhydrous sodium sulphate
Ammonium molybdate
Ammonium tetrathiomolybdate

Do NOT feed horse or cattle feed to small ruminants

If you suspect that excess Cu has been fed then add sodium molybdate or sodium sulfate to the ration

Inadequate erythropoiesis or bone marrow depression

Normocytic normochromic

Except iron and copper deficiencies

Bone marrow evaluation

Piglets

Chronic blood loss, bleeding GI ulcers and haemostatic defects

Microcytic hypochromic

Remove the underlying cause and supplement with oral or dietary iron

Milk fed animals and those on pasture

Decreased growth rate
Rough, depigmented hair coat
Diarrhoea
Osteoporosis with spontaneous fractures

"Swayback" or "Enzootic ataxia"

- a demylinating syndrome

Bacillus anthacis

Protective antigen (PA)
Lethal factor (LF)
Oedema factor (EF)

Elevated pH and higher levels of calcium and magnesium

A drought followed by heavy rain

Fever, depression, respiratory distress, bloody diarrhoea, haematuria, tissue oedema

Bloody exudates from orifices
Incomplete rigor mortis
"Blackberry jam" consistency to the spleen

OPEN THE CARCASS!

Anthrax can easily be spread to humans. Report it!

Lightening strike
Clostridium
Oleander poisoning

Penicillin and tetracyclin

Vx in endemic areas and burn carcasses

Casous lymphadenitis

External or Internal abscesses

Contact of exudates from draining abscess or from contaminatede equipment

Mandibular, parotid, prefemoral and prescapular lymph nodes are most commonly afftected
Thick inspissated pus

Lungs, kidneys as well as mediastinal, bronchial, mesenteric and lumbar lymph nodes
Chronic weight loss most common sign
Pneumonia, azotaemia and bloat may occur

A cutaneous excoriated granuloma
Large ulcerated granulomas with necrotic centres usually on the head, neck, thorax and flanks

Abscesses in submandibular and cervical area

Elevated white count
Hyperproteinaemia from high globulins
ELISA test of cell wall antigens
Abdominocentesis, Rx, U/S

External
Establish drainage once abscess matures
Collect and dispose of exudates
Lavage with antiseptic

Internal
Poor prognosis
Weeks-months of Abx

Isolate infected animals
Fly control
Good sanitation and cleaning of equipment

RESPIRATORY DISEASES

Tracheobronchus
Complete mediastinum
Pulmonary secondary lobules
Limited respiratory exchange capacity

Reduced heat tolerance
Decreased resistance to infections, toxic or noxious substances
High air flow rates transport more bacteria to lung

Bronchovesicular tones

Pulmonary emphysema
Pulmonary mass or consolidated lung
Pleural fluid, pneumothorax, mass in pleural space
Thick body wall

Thin body wall
Rapid, deep or laboured respiration
Pulmonary inflammation or oedema

Pleural inflammation

Transtracheal wash
Bronchoalverolar lavage

Irregularities in the pleural surface
- comet tails, abscesses, consolidated areas
Presence of free fluid

There is fibrin attached to the pleural surface

Virus isolation

Pick a cow and sacrifice it and submit it for necropsy

Rhinosporidium spp

Epistaxis
Stridor
Dyspnoea
Granulomas

With difficulty
Surgical removal
Sodium iodide

Type 1 (mast cell damage)

Granulomatous inflammation

Channel Island breeds and Friesians

Dyspnoea and stertorous inspiration
Bilateral nasal discharge
Intense pruritis - nose rubbing
Multiple granulomas

Antihistamines
Dexamethasone 5 days

Nasal adenocarcinoma

Limited to secretory epithelial cells of nasal turbinates

Progressive inspiratory dyspnoea
Stridor
Exercise intolerance
Open mouth breathing
Head shaking sneezing

It will grow back

Nasal foreign bodies
Trauma and fractures
Nasal polyps
Condential cystic nasal turbinates

TRUE

Dehorning
Infected teeth
Extension of infection in oral cavity
Trauma

Anorexia, lethargy, fever, frontal bone distortion, exophthalmos, abnormal posture, nasal discharge, neuro signs

Drilling a hole in the skull to release exudate

Flush daily with weak betadine in saline
Systemic Procaine Pen G

Good if no CNS signs

Careless use of equipment
Rough feedstuff
Foreign objects
Migrating foreign bodies/medication

Anorexia
Fever
Smelly breath
Ptyalism
Dyspnoea & inspiratory stridor
Dysphagia & bloat

Antibiotics
NSAIDs
Open and drain abscesses
Temporary rumenostomy
Tracheostomy

Ventral midline at the junction of the cranial and middle third of the neck

This avoids thyroids and larynx cranially and you don't have to dig around in the the muscle ventrally

Remember to check the patency of the tube and remove any mucous and debris

Infection of the larynx as a result of Fusobacterium necrophorum

Acute onset of moist, painful cough
Inspiratory dyspnoea and stridor
Open-mouth breathing
Fever
Ptayalism
Fetid breath
Painful larynx

Can start as laryngeal contact ulcers
Upper respiratory viruses and reflex coughing which erodes swollen mucous membranes over the larynx

Antibiotics - sulfonamides, penicillin, oxytetracyclin
NSAIDs
Tracheostomy

Cattle are usually poor doers and they are at risk of aspiration pneumonia

Tracheal oedema

Cause unknown

Acute dyspnoea

Chronic cough

Fat feeder cattle due to hot weather, trauma and fat

Honking, open mouth breathing, head and neck extended and oedema of lower trachea. Death

Lighter cattle

Continuous, non-productive cough and oedema of tracheal not as severe

Broad spectrum Abx and steroids for acute, avoid stress and provide shade

No treatment for chronic form

Pneumonia

Bovine Respiratory Disease complex (Shipping fever)
Enzootic calf pneumonia

Interstitial
Metastatic

Viral disease
Bacterial disease
Transportation
Co-mingling
Weaning
Handling
Processing
Nutritional deficiences

Red flags! There is a serious herd problem

Cough, laboured breathing, depression and separation from the group, nasal dischage (dirty nose), peeling nose exercise intolerance

Lack of oxygen

Onset 6-10 days after insult
Depression, fever >105F initially
Ocular discharge
Cough, dyspnoea

Explosive onset (dairy and veal)
Fever
Harsh, dry cough, nasal discharge
Dehydration +/- diarrhoea

Calves with a suppurative pneumonia which never thrive

1. Stress and upper resp ciliary damage
2. Growth of normal bacteria in airways
3. Failure of mucociliary protection mechanism to clear ventral lung
4. Proliferation of normal nasal bacterial flora in ventral lung
5. Vicious cycle of infectious inflammation in dependent ventral lung

Infectious agents, dust and fumes, ammonia

= Sewer pipe trachea

The WBC components cause lung damage, releasing tissue fluid that more bacteria can grow in and attract more WBCs

Whole antigen bacterins - attracted even more WBCs

Viruses
IBR
BVDV
PI3
BRSV

Bacterial
Mannheimia haemolytica
Pasteurella multocida

High fever
Serous nasal discharge
More alert
Increased bronchovesicular tone

Mild to moderate fever
Purulent nasal discharge
Severe depression
Wheezes and crackles and pleural friction rub

Infectious Bovine Rhinotracheitis

BHV-1

FALSE

They are latently infected and reservoirs of disease

Cattle over 6mths

Feedlot cattle get it worse with higher attack rates, more severe disease and higher fatality rates

Hyperaemia of nasal turbinates and muzzle
Conjunctivitis
High fever
Anorexia
Profuse nasal discharge which becomes mucopurulent

On necropsy - congestion and haemorrhage in trachea, "sewer pipe trachea"

Serology from nasal swabs fluorescent antibody of tissues

Modified live

Noncytopathic
Cytopathic

BVDV-1
BVDV-2

2 positive virus isolation tests at least 3 weeks apart

Immunohistochemistry on skin biopsies or ear notching
PCR
Serology

Vaccines - MLV and killed

I.d. and remove persistently infected cattle. Biosecurity

Paramyxovirus

Infection is very common and is endemic. Considered a pthogen only for young calves

Fever, cough, nasal and ocular discharge. Very mild signs

Yes

Ruptured bulla may lead to SQ emphysema

Antibiotics
Dexamethasone
Antihistamines
Feeding (avoid 'fog fever' feeds)

FALSE

No vaccine for small ruminants

PI-3

Nasal discharge, cough, fever, no vaccine

Biotype A, serotype 1

Leukotoxin
Endotoxin
Fimbriae

Kills bovine blood leukocytes and alveolar macrophages. Drying out macrophages release inflammatory mediators with results in the deposition of fibrin

Fibrinous bronchopneumonia

Develops 10-14 days after stress

Depressed, fever, mucopurulent discharge, tachypnoea

Cranioventral

Abx
Anti-inflammatories
Supportive care

Toxoids BEFORE stress

Septicaemia, arthritis, otitis media
1st sign may be death

Enzootic calf pneumonia

Normally found in nasopharynx of healthy cattle

Has LPS and capsule

Purulent bronchopneumonia

CNS
Respiratory
Musculosleletal
Reproductive
Cardiovascular

Necrotic laryngitis, necrotic and polypoid tracheitis, fibrinous bronchopneumonia and fibrinous pleuritis
Fever, tachypnoea and increased lund sounds

Pneumonia
Arthritis
Tenosynovitis
Otitis media
Mastitis

Fever, tachypnoea, anorexia

Coughing and nasal discharge are not consistent

Unilateral/bilateral drooping of ear/s - facial nerve paralysis +/- vestibular signs

Animal did not respond to therapy as expected

Produces toxins which increase vascular permeability

Transmitted by aerosol and in the milk

Dark red, firm consolidated lobules of cranioventral lung lobs

May have white/yellow firm nodules - coaglation necrosis

Tulathromycin (Draxxin)

TRUE

Sheep - M. ovipneumoniae
Goats - M. mycoides

Via milk and ear mites

Adults
Fever, pleuropneumonia, mastitis, polyarthritis

Kids
Septicaemia, meningitis, arthritis

Not really, may just reduce clinical signs, they will likely shed it for life

BRSV
Acute bovine pulmonary oedema and emphysema
Parasites

"Fog Fever"

NONinfectious and NONfebrile!

Within 2 weeks of turnout from dry grazing onto lush pasture or alfalfa

L-tryptophan converted to 3-methylindole
Metabolism of 3-methylindole results in highly reactive intermediates which cause cellular damage in the lungs

Emphysema secondary to dyspnoea

Sudden onset
Afebrile
Flared nostrils
Frothing at the mouth and expiratory grunting
SQ emphysema

Forced movements may result in collapse and death

Hard
Remove cattle from feedstuffs
Steroids
Antihistamines
NSAIDs
Diuretics

Avoid sudden onset of hungry cattle onto lush pasture - give hay to fill them up first

Primary infection
Young stock

Reinfection syndrome
L4 and adults in respiratory tree

Ventral areas of caudal lobes

In severe cases indistinguishable from other AIPs

Baerman faecal

Tx - lavamisole, fenbendazole, ivermectin

Spread by close contact
Infected animals can spread it for years
Long incubation
Weight loss, intermittent pyrexia, debilitation

GI tract

Aerosols
Contaminated feed

Caudal fold test
Comparative cervical test

Test and slaughter policy

Septic emboli from other conditions break off and lodge in the microvasculature of the lungs

Fusobacterium necrophorum
Arcanobacterium pyogenes

Epistaxis and hemoptysis

May die suddenly from severe intrapulmonary haemorrhage or haemoptysis

Need long term antibiotics, poor px