Horse, cow and small ruminants

Question 1

Describe the grading system for equine lameness ?

Answer 1

Question 2

Describe how to flex the fetlock and carpus in the forelimb of a horse ?

Answer 2

Question 3

Describe how you would flex the spavin and fetlock in the hindlimb of a horse ?

Answer 3

Question 4

In horses where would you inject to achieve a PDNB ?

Answer 4

Question 5

In horses where would you inject to achieve ABSNB ?

Answer 5

Question 6

Describe the FAFROICD complex ?

Answer 6

Confusion between Foot rot, foot abscess and OID

• producers have their own terminology
• some professionals ascribe clinical syndrimes to specific agents
• othere concentrate on the symptoms themselves, and treat the cases based upon thses signs

There is likely an interplay between the 2 main organisms
1. Fusobacterium necrophorum
2. Dichelobacter nodosus

Question 7

basic principles of a lameness

basic principles of a lameness of a lameness investigation in sheep ?

Answer 7

Lameness examination
1. History
2. Examination of the environment
3. Examination of animals
- from a distance
- close up inspection
4. Use of ancillary aids
5. Data analysis and decision making
6. Reporting and further monitoring

Question 8

Describe the epidemiology and pathology of OID in sheep.

Answer 8

OID Ovine Interdigital Dermatitis

Ascribed to Fusobacterium but is clinically indistinguishable from Dichelobacter.
Favourable conditions
- wet perhaps warm environmnet (long wet grass or boggy paddock)
- occurs as an interdigital dermatitis that does not underun the horn of the hell or invade deeper tissues
- affects all classes 10-80% of the mob
- may cause a tail in the mob but is self limiting
- often all four feet affected
- can foot bath but the condition reduces as the environmnet dries

Question 9

Describe the clinical signs of OID

Answer 9

OID Ovine Interdigital Dermatitis
Fusobacterium necrophorum

Clinical signs
- interdigital skin red swollen, covered with a moist film, loss of hair
- occurs between heels and where skin rubs
- can have all four legs affected
- usually lameness is moderate
- no odour or seperation of the horn from underlying tissue

Question 10

Describe the epidemiology of Foot/heel abscess

Answer 10

Foot abscess
If fusobacterium invades into deeper tissues, it sets up a severe inflammatory response of the soft tissues.

• well of pus
• smaller numbers of sheep affected 15%

Question 11

Describe the clinical signs of Foot abscess

Answer 11

Clinical signs of foot rot
- acute severe lameness
- foot red, swollen, painful
- usually only one claw affected
- contains creamy/ white pus - may break open between digits or around the coronary band
- extreme lameness and pain

In advanced cases the bacteria may invade the distal interphalangeal joint and erode the joint structures.

Question 12

Describe how you would go about a diagnose, prevent or treat ovine Foot abscess ?

Answer 12

Ovine foot abscess

Diagnosis
- clinical signs
- history eg environmnet

Prevention
- limit predisposing factors dry paddocks for late pregnant ewes
- foot bathing (10% ZnSO4)
- foot bath during routine husbandry procedures
- No vaccine

Treatment
- Drainage and flushing of pedal joint
- Amputation
- Parental antibiotics Oxytetracycline and NSAIDS
- Most recover within about two months permanent joint damage very possible

Question 13

Describe the aetiology of foot rot

Answer 13

Foot rot = Dichelobacter nodosus
This is a nessary cause but potentially not a sufficient cause

• gram negative
• anaerobe
• fragile
• obligate animal parasite of the interdigital skin and soft tissue of the hoof
• environmental survival <7 days
• strain - refers to whether an isolate is virulent, intermediate or benign
• serogroup = antigenic variation conferred by fimbrial antigens - confers immunity in vaccines.

Question 14

Describe the epidemiology of Foot rot in sheep ?

Answer 14

Foot rot epidemiology
= a wet warm environment and foot damage
Transmission requires moist wet warm conditions (>10C)

Environmnetal factors
A feature of high rainfall areas (NZ), but may occur sporadically in drier areas after high rain fall
- <7 days survival on pasture
- Usually a spring disease with reduced incidence over winter
- perenial wet pastures favour ID skin maceration and damage facilitating colonisation by D.nodosus

Host factors
- merino, dryland sheep - Dorpers
- huge variation within mob susceptability
- goats capable of transmitting and sustaining very virulent strains (hot strains in sheep may only cause OID in goats)
- deer carrier

Pathogen factors
- virulence is determined by the strains capacity to elaborate heat stable proteass and elastases
- virulence is a continuum totally benign to underrun
- benign to virulent

Question 15

Describe how you would go about diagnosing a case of foot rot in sheep?

Answer 15

Diagnosis of foot rot
Difficult as the bacterium D. nodosus is present in nearly every sheep flock in the worlds

The virulence of any strain is critical
- Rapid PCR typing
- collect smears from underrun lesions
- benign to intermediate strains are almost impossible to eradicate

Epidemiological diagnosis
- Inspect sheep after a period for transmission or repeat inspection in four weeks
- score the lesions 1-4 / 5

Laboratory test for virulence
- pressence of D. nodosus
- protease thermostability test/ gelatin gel test
- Elastase test

Question 16

Describe the process of scoring the lesiins in the foot of a sheep ?

Answer 16

Score foot rot lesions on a scale of 1-4 /5
a. <1% Sc4 lesions = benign
b. 1-5% Sc4 lesions = intermediate
c. >5% lesions = virrulent
Use the highest score of any one foor of the inspected sheep

To obtain a foot score
SC1 = redness deep in the interdigital space, hair loss maby some moisture, slight lameness
SC2 = redness hairless and moist - inflammation extends to the junction of the interdigital skin and heel
SC3 = underrun of the soft horn of the caudel heel
SC4/5 = Underrun across the sole and up the walls

Question 17

Describe what you would observe in a foot rot score of zero and one ?

Answer 17

Question 18

Describe what you would observe in a foot rot score two ?

Answer 18

Question 19

Describe what you would observe in a foot rot score three ?

Answer 19

Question 20

Describe what you would observe in a foot rot score of four ?

Answer 20

Question 21

Describe what tests could be carried out to identify the virulence of Dichelobacter nodosus ?

Answer 21

Diagnostics

1. Protease thermostability test, gelatin gel test
2. Elastase test - digestion of elastin particles in agar

Question 22

Describe the control phase for foot rot ?

Answer 22

Control
The control phase consits of any treatments given to reduce production loss and clinical signs within the herd.

Keep it down and set the stage for elimination.
Eradication
- regulatory requirement of WA and NSW

Foot bathing
- Foot bathing formalin, chloride/copper or zinc sulphide (effective for surface infection).
- frequency of foot bathing is the critical element - very labour intensive

Vaccination
Reduces the number of uninfected feet becomming infected and reduces lesion severeity.
- mostly used during transmission summer lambing

Antibiotic treatment
- Oxytetracycline, penicillin, Erythromycin
- use to reduce prevalence prior to elimination
- salvage a disaster
- biosecurity (new ram introductions)

Question 23

Describe the different methods for eradication of foot rot in sheep herds ?

Answer 23

Eradication foot rot
First is it neccessary
1. Destocking
- whole flock + replacement + expensive
- opportunity to reorganise you enterprise

2. Eradication through inspection and culling
   - must start with a low prevalence <5%
   - no transmission hot dry environmnets
   - infustructure and resources to complete repeat inspections (smaller flock)
   - pare flock to facilitate inspection
   - do not use suppressive treatment we want to see it if its there.

Biosecurity
FR one disease you can do without
- boundary fencing
- quarantine
- walk through foot bath of transports
- do not buy from sale yards

Question 24

Describe the pathology and clinical signs of a toe abscess ?

Answer 24

Toe abscess = white line disease
Fusobacteriumnecrophorum, Trueperella pyogenes
The bacteria may gain entry through cracks in the hoof, usually in the area of the white line.
- often only one foot affected

Clinical signs
- acute severe lameness
- no obvious lesions, but hot and painful
- abscess may break over coronet
- pus and fluid released from the point of toe if pared
- seperation of the front half of the sole in chronic cases

Diagnosis
- history and clinical signs
Treatment
- drainage

Question 25

Define the clinical signs and cause of Shelly hoof ?

Answer 25

Question 26

Describe the epidemiology and pathology of CODD ?

Answer 26

Contagious ovine digital dermatitis This is an exotic disease - UK and EU countries Causes - one or more Treponema spp - potential spill over from the dairy industry -

Question 27

Describe the clinical signs of CODD

Answer 27

CODD contagious ovine digital dermatitis Clinical signs - severe lameness - typically affecting only one digit of one foot (biosecurity - not all sheep with CODD are lame). - primary lesion is at the coronary band of the outer wall with subsequent invasion and underrunning of the hoof wall - coronary band twards the toe - causing detachment and shedding of the horn capsule - no interdigital skin involvement

Question 28

Describe the prevention and treatment of CODD

Answer 28

CODD contagious ovine digital dermatitis Prevention - strict biosecurity Control (exotic to Australia) - isolate infected sheep - parental tetracyclines, amoxicillin - NSAIDS - zinc sulphate foot baths - some feet are permantly affected cull animal

Question 29

Describe the clinical signs and cause of strawberry footrot ?

Answer 29

Question 30

Answer 30

Pink = CODD Green = OID Blue = FR

Question 31

Describe the cause and clinical signs of post dipping lameness ?

Answer 31

Post dipping lameness Erysipelothrix rhusiopathia It is cellulitis of the lower legs following dipping with skin wounds in dip fluid contaminated with faeces. Clinical signs - outbreak of acute lameness - depression - hot and swollen limbs - may progress to non supprutive arthritis

Question 32

Describe how you would diagnose and treat post dipping lameness ?

Answer 32

Erysipelothrix rhusiopathia Diagnosis - history, clinical signs - bacterial culture Prevention and treatment - dip hygiene - correct use of bacteriostsat in dip - minimize faecal contamination of the dip - treat with parental penicillin

Question 33

Describe the epidemiology of foot and mouth disease ?

Answer 33

Foot and mouth Highly contagious viral disease 7 serotypes Exotic disease in Australia - affects cattle, sheep, goats and deer (species variability in susceptability) - transmission all secretions of affected animals - milk, urine, faeces and saliva etc - may secrete virus 4 days prior to CS - virus may survive in the environmnet for upto seven days Transmission = inhalation of virus, ingestion contaminated feed (swill) or skin abrasions

Question 34

Describe the clinical signs of foot and mouth disease ?

Answer 34

Foot and mouth disease High morbidity, low mortality - mild to no symptoms sheep / goats - fever and mild lameness - vesicles on feet - vesicles in and around the mouth - vesicles on teats - abortions may occur

Question 35

Describe how you would diagnose and control foot and mouth disease ?

Answer 35

Diagnoses - CS - Post mortem - PCR, ELISA Treatment - ban on swill feeding of pigs - quaratine - If outbreak stamping out procedure - slaughter of infected/ suspect animals and quaratine

Question 36

Describe the epidemiology and clinical signs of scabby leg ?

Answer 36

Contagious ecthyma Scabby leg Most common in young sheep grazing lush wet pastures (late winter, spring) Clinical signs - Lesions most common on the lips (scabby mouth) - lesions interdigital spacescab formation - if removed mass of raw spongy tissue - no involvement of horny layers

Question 37

Describe how you would diagnose and traet scabby leg ?

Answer 37

Question 38

Describe the epidemiology of blue tongue disease ?

Answer 38

Blue tongue disease Bluetongue virs (orbivirus) - 26 different serotypes Australia is free from blue tongue disease. Transmission = biting midges (Culicoides sp) - clinical disease occurs primarily in sheep - cattle show no CS, but midgees preferentially feed on cattle and the cattle can shed the virus for upto 100 days. - virus may persist in surviving sheep for upto 30days.

Question 39

Answer 39

Answer = C. cattle

Question 40

Answer 40

Answer = B. Hyperaemia

Question 41

Describe the clinical signs of blue tongue disease in sheep ?

Answer 41

CS blue tongue - high morbidity - mortality - 30% - widespread damage to the endothelial cells - haemorrhages, oedema and tissue necrosis - high fever - depression - salivation - erosions and ulcers of the mouth - respiratory distress and panting

Question 42

Describe how you could diagnose and traet foot and mouth disease ?

Answer 42

Foot and mouth disease Diagnosis - history - clinical signs - post mortem haemorrages at the base of the pulmonary artery and ulceration of mucous membranes - PCR and ELISA Treatment Eradication - insect control - movement restrictions - culling of infected aniamls (overseas there are vaccines available)

Question 43

Identify the bacterial causes of fibrinous and suppurative arthritis in sheep ?

Answer 43

Arthritis in sheep Fibrinous arthritis - Erysipelothrix arthritis - Chlamydial polyarthritis Suppurative arthritis - E.coli, Staph, Strep, Fusobacterium necrophorum, Truepurella pyogenes

Question 44

Describe the pathology and clinical signs of Fribinous arthritis in lambs ?

Answer 44

Fribrinous arthritis Erysipelothrix and Chlamydial Principally affects lambs 1 to 4 months of age through contamination of wounds (mulesing, marking, navel). - many recover spontaneously, a proportion develop a chronic arthritis - commonly affects higher limb joints; hip, stifle, hock and shoulder - affected joints warm and painful - <1% prevalence - no systemic illness - in chronic cases joints may become ankylosed

Question 45

Describe the clinical signs and pathology of suppurative arthritis ?

Answer 45

Suppurative arthritis Strep, Staph and Fusobacterium Infection occurs through contaminated wounds Generally perinatal event, but can affect up to 10% lambs 2-3 weeks post mulsing. Clinical signs - markedly lame with hot joints - severely distended joints with pus - chronic lesions permanent joint damage - often absesses in internal organs Usually to late for treatment - penicillin Best to prevent the disease through higiene at lambing, marking, shearing or dipping.

Question 46

Describe how you would carry out a nervous disease investigation ?

Answer 46

Nervous disease investigation steps 1. History - age, breed of sheep, sex, changes in management or grazing, environmnetal examination 2. Onset of disease, intermittent or continuous, progressive or non progressive 3. Physical examination of the animal Initially observe from a distance - behaviour, mental status, head position, head tremors, gait, posture and balance, apparent blindness - response to approach - TPR, - mental status (hypo or hyperaesthesia) - ocular responses, auditory, facial sensation and facial muscles (palpebral reflexes, corneal reflex) - pharynx and larynx - tongue - gait posture reflexes withdrawal, patellar, perineal, panniculus - proprioceptive tests (knuckling over) ANCILLARY AIDS - CSF collection - POST mortem (+sample collection) - may need to carfully dissect brain and complete spinal cord

Question 47

Answer 47

Answer = E. Trigeminal nerve and facial nerve

Question 48

Answer 48

Answer = B Oculomotor nerve

Question 49

Describe the pathology of Polioencephalomalacia

Answer 49

Polioencephalomalacia PEM or cerebrocortical necrosis (CCN) or polio Star gazing Is an acute central nervous disease of ruminants caused by a deficiency of thiamine (vitamin B1) Thiamine is produced in the rumen, thiamine deficiency is probably caused by the microbiological production of thiaminase Thiamine plays an essential role in carbohydrate metabolism (which provides ATP to the brain); deficiency leads to lesions in the brain PEM

Question 50

Describe the epidemiology of Polioencephalomalacia ?

Answer 50

Polioencephalomalacia Thiamine deficiency Star gazing Epidemiology In most cases this results after a dietary change (feedlot - change of diet to lower roughage, higher concentrates) In some cases it may result from plant toxins thiaminase nardoo rock fern - sheep/goats and other ruminants - all ages and sex - usually low percentage of herd affected <5% - been asociated with diets high in sulphur

Question 51

Describe the clinical signs of Polioencephalomalacia ?

Answer 51

Clinical signs Polioencephalomalacia Initially the sheep appear blind and may isolate themselves - wander aimlessly - fine muscle tremors - star gaze or head lowered to the ground Later sheep will go down - opisthotonus, nystagmus and extensor rigidity - periodic convulsions - animals usually die within 2-3 days of CS becomming apparent

Question 52

Describe how a Veternarian would diagnose Polioencephalomalacia ?

Answer 52

Diagnosis of Polioencephalomalacia Diagnosis - History and Clinical signs - Response to treatment - Post mortem - Histopathology - Blood thiamine concentrations below 50 indicates deficiency (normally 75-185nmol/l). Post mortem findings - cerebral hemisphers will become swollen, aple and soft - yellow discolouration of some gyri - lesions bilateral symetrical and restricted to grey matter Affected areas may fluoresce under UV light Cerebrocortical necrosis

Question 53

What can be done to prevent or treat Polioencephalomalacia ?

Answer 53

Polioencephalomalacia Thiamine deficiency Prevention - prevent further cases by adding good quality roughage - SC injection of thiamine to all remaining at risk sheep Treatment Bypass rumen thiaminases by giving thiamine systemically, or flood rumin fluid with thiamine - IV 10mg/kg - good response in early cases - should be able to stand within 24 hrs but may remain blind for a week - humanely destroy unresponsive animals

Question 54

Describe the pathology and clinical signs of focal symmetricalencephalomalacia (FSE)

Answer 54

FSE Focal symmetrical encephalomalacia result from Clostridium perfringens type D toxins Chronic form of enterotoxaemia Clostridium perfringens type D toxins The bacteria are a normal commensal of the GI tract in healthy sheep. If the bacteria multiple into large numbers they rapidly produce toxins causing brain damage - occurs sporadically - usually affects lambs - seen in animals with partial immunity or who suffer partial intoxication Clinical signs Blindness aimless wandering Circling Head pressing Tremors Go down can be very difficult to differentiate from Polioencephalomalacia

Question 55

Desribe how you would diagnose and treat a case of Focal symetrical encephalomalacia ?

Answer 55

Focal symetrical encephalomalacia Diagnosis - History, clinical signs - Post mortem - bilaterally symmetrical haemorrhage and softening of the internal capsule, basal ganglia - haemorrhages focal area of malacia There is no treatment Vaccinate in an outbreak or preferable prevent through vaccination

Question 56

Describe the aetiology and epidemiology of Listeria monocytogenes ?

Answer 56

Listeria monocytogenes Listeria causes three syndromes in sheep; abortion in ewes, septicaemia in lambs and focal encephalitis in sheep (any age sex) It is unusual for different presentations of the disease to occur in one flock. - commensal of normal sheep gut flora - can survive for long periods in contaminated feed, soil and water Transmission The transmission of Listeria is often associated with feeding poor quality silage (PH<5.5) - sheep wet pasture, rotten vegetation - route of infection = mouth lesions - teeth eruptions and ascending peripheral nerves in particular the trigeminal nerves to the brain. -

Question 57

Describe the clinical signs of Listeria ?

Answer 57

Listeriosis Clinical signs Depends upon the sight of lesions - severe depression - fever - anorexia - isolation The lesions usually have a unilateral nature and reflect loss of the function of multiple cranial nerves. Head tilt = trigeminal Unilateral facial paralysis = facial nerve Unilateral tongue paresis = hypoglossal n

Question 58

Describe how you go about diagnosing Listeria in sheep ?

Answer 58

Listeria diagnosis History Clinical signs - unilateral brain disease, but not pathognomonic Collect Cerebrospinal fluid Cloudy appearance, elevated protein concentrations incrased WBC count - culture of CSF or PCR is often unrewarding Post mortem Gross lesions of the brain Histo - multiple micro abscesses and neuronal necrosis in the area of the brainstem (lesions usually unilateral)

Question 59

Describe how you would diagnose and treat an outbreak of Listeria ?

Answer 59

Listeria Prevention = good quality silage Treatment Antibiotics - penicillin - oxytetracycline - erythromycin Treatment may be effective in very early cases but often unrewarding for advanced cases. Supportive therapy = fluids

Question 60

Describe the pathology and clinical signs of a spinal abscess in lambs ?

Answer 60

Spinal abscess in lambs Pathology All ages are affected but most commonly seen in lambs following marking or lambing (hygiene) Common cause Trueperella pyogenes Staphyloccocus aureus Fusobacterium necrophorum The clinical signs feverish Slight ataxia to complete hindlimb paralysis Common site for abscess is the lumar vertebrae

Question 61

Describe how to diagnose and treat a spinal abscess in lambs ?

Answer 61

Question 62

Answer 62

Answer = d. navel cord

Question 63

Describe the pathology and clinical signs of a brain abscess ?

Answer 63

Question 64

Describe the pathology of Gudair staggers ?

Answer 64

Gudair staggers Gudair staggers is caused by the injection of the Gudair vaccine directly in to muscular tissue instead of subcutaneously. - The Gudair vaccine contains a Freund's adjuvent containing non soluble oil and other agents to stimulate immunity. - persist in muscle tissue and causes a sterileabscess which often tracks down the spinal column where it may compress the spinal cord. The out come can vary from mild incoordinatin to quadriplegia. Vaccination site Under the skin on the side of the neck 5cm from the base of the ear - keep well away from the atlas and atlanto occipital joint true subcutaneous 6mm needle recommended.

Question 65

Describe the clinical signs of injecting Gudair vaccine into muscle ?

Answer 65

Wrong injection of the Gudair vaccine clinical signs Can vary from mild incoordination to quadriplegia granulomatous reaction There is also a risk to operators - accidental injection into human muscle will cause a severe granulomatous reaction similar to that of sheep.

Question 66

Describe prevention and treatment after Gudair vaccine is injected into muscle ?

Answer 66

Gudair vaccine Sheep Treatment - none - affected animals should be humanely destroyed if losing conditon and no longer feeding Prevention - review vaccine techniques - subcutaneous injection requires injection between the skin and musculature. Humans seek immediate medical attention ( vaccine must be surgically removed by a cmpetant surgeon).

Question 67

Describe the pathology of Clostridium Tetani ?

Answer 67

Clostridium Tetani Highly fatal disease Pathology - spores present in soil for many years, enter the body usually through a wound - tail docking, mulesing, castration (rubber rings), dehorning - sporadic result f contaminated puncture wounds in adults Incubation 1-3 weeks, being longer in adults than in lambs. Under suitable anerobic conditions, spores vegetate, proliferate and produce neurotoxins (tetanospasmin), which reaches the central nervous system via peripheral nerves (bacteria stay at the site of orgnal infection)

Question 68

Describe the clinical signs of Tetanus

Answer 68

Tetanus = Clostridium Tetani clinical signs Hyperaesthesia - spasm of voluntary muscles (head tremors, restricted jaw movements) - general stiffness to extremeties - recumbant - erect ears retraction of lips - bloat and aspiration pneumonia may develop - Tetanic convulsions and opisthotonus Death occurs 3-7 days after the onset of CS (usually as a result of respiratory failure).

Question 69

Describe how you can diagnose and treat a case of Tetani ?

Answer 69

Tetani = Clostridium Tetani Diagnosis - History, particularly recent wounds (eg present one week post marking). - Post mortem - identification of C.tetani in the wound. Treatment Culling of animal - treatment is expensive, antitoxin - sedation and muscle relaxants - elimination of infection = parental and local antibiotics

Question 70

Answer 70

Answer = C Gabba

Question 71

Describe the pathology of Botulism in sheep ?

Answer 71

Botulism Clostridium botulinum toxins Pathology Botulism = caused by ingestion of preformed Clostridium botulinum toxins - present in soil - toxin production usally occurs under warm moist anaerobic conditins - decomposing plant matter animal carcasses - sheep most commonly affected by type C and D - rumen microflora inactivates the majority of ingested toxin Cause phosphorus deficiency (stock chew bones) rotting vegetation water contaminated with rotting vegetation or carcasses rain damaged mouldy hay Toxin is absorbed from the small intestine and adheres to the neuromuscular junctions, blocking transmission of nerve impulses (by inhibiting the release of acetylcholine)

Question 72

Describe the clinical signs of Botulism ?

Answer 72

Botulism Variable incubation period of 1-7 days - weakness, reluctance to move, and a stumbling gait can be seen - - weakness and ataxia - ataxia most prominabt in the hind legs - low head carrage, head bobbing - protrusion of tongue and salivation - decreased rumen motility, bloat and constipaton Sheep eventully go down but remain conscious, abnormal breathing followed by death due to respiratory paralysis Death usually 3-5 days after first CS Post moretem no specific signs

Question 73

Describe how you would diagnose and treat a case of Botulism ?

Answer 73

Botulism Diagnosis - no specific lesions on post mortem - identification of toxin (suspect feed, rumen fluid) - ELISA (herd test) - ending of mortalities after vaccination Prevention Avoid the feeding of rotten hay/silage supplement phosphorus in deficient areas Vaccnation Removal / burning of carcasses Treatment Nursing care Vaccinate remaining sheep at risk

Question 74

Describe the aetiology and epidemiology of Perennial ryegrass staggers ?

Answer 74

Ryegrass staggers Lolium perenne Aetiology Produced by the perenial ryegrass endophyte fungus Neothypodiumnlolii - ingestion mycotoxin lolitrem B - unknown mechanism of action suspected to block calcium activated potassium channels. Epidemiology Prevalence is highest in late summer / autumn under close grazing conditions - particularly late season rainfall causing abundant pasture growth - toxin primarily in the green leaf sheath, flowering stem - morbidity variable 10-80% - all ages are affected, but weaners and hoggets most severely affected.

Question 75

Describe the clinical signs of Perenial ryegrass staggers ?

Answer 75

Perenial ryegrass staggers Clinical signs CS develop within 1-2 weeks after introduction to toxic pastures - head tremor, mild muscle fasciculations, head nodding - severe muscle tremor head shaking - staggery - uncoordinated gait - collapse rigid extension of legs - convulsions If left quietly sheep may recover and walk away The sheep are more difficult to move and may interfere with normal management practices - may reduce reproduction if ewes/rams are affected during joining post mortem - nospecific pathological changes

Question 76

Describe how to diagnose and treat perenial ryegrass staggers ?

Answer 76

Managment Perenial ryegrass staggers - Remove sheep from toxic pastures (recover within three weeks) - minimise any handling and disturbance - provide safe watering system - the onset of autumn break brings fresh pasture growth with subsequent recovery of affected animals

Question 77

Describe the pathology and epidemiology behind annual ryegrass staggers ?

Answer 77

Pathology Annual ryegrass staggers Annual ryegrass Lolium rigidum The ryegrass is infested with a nematode Anguina Funesta containing a neurotoxin Corynetoxin producing baceria. = corynetoxins ARGT like disease known as flood plan staggers - SA, wheat belt of WA - outbreaks October to January The Anguina nematode lies dormant over summer in galls. During autumn break the nematodes migrate to annual ryegrass plants, climb a tiller and are then brought - Nematodes move to seed head feed on developing ryegrass seeds and form galls within the seed heads. - Bacteria multiply within the nematode gall, producing a yellow sime and corynetoxins

Question 78

Describe the clinical signs of annual rygrass toxicity ?

Answer 78

Annual ryegrass toxicity Corynetoxins Clinical signs - all ages are susceptable - CS of cerebellar dysfunction - mildly affected anmals fall behind the mob and have a high stepping gaut - uncoordinated gait - fall over convulse when driven - neck arched back with stiff legs If left undisturbed they get up and stagger away - most severely affected sheep remain down - convulsons, opisthotnus, limb paddling untl death - morbidity and mortality high

Question 79

Describe how t dignose annual ryegrass staggers ?

Answer 79

Annual ryegrass staggers Diagnosis - History, CS - Pressence of infected ryegrass seed heads + yelow bacterial slime on heads - Nematode galls - Lab test for bacteria ad nematode Histopatholgy - Histopathology brain (pressence of pervascular oedema) - no characteristic lesion on post mortem

Question 80

Describe how you can treat or manage ryegrass toxicity ?

Answer 80

Annual ryegrass toxicity Corynetoxins Treatment - No effective treatment - Remove sheep from toxic psture (new cases may still appear upto 4 days post removal) (deaths can still occur upto 7 days post removal) Prevention Herbicides to kill annual ryegrass in crops and pasture - heavy grazing in winter to decrease ryegrass - spray topping to reduce seed set - resistant cultivars (safeguard) - biological control (twist fungus)

Question 81

Describe the epidemiology and pathology of phalaris staggers ?

Answer 81

Phalaris staggers Phalaris is a popular important improved pasture species in Sourthern Australia but can cause Two types of sudden death - Polioencephalomalacia - cardiac form Pathology - Dimethyltryptamine alkaloids accumulate in the CNS - usually seen in animals grazing Phlaris dominant pastures for several weeks - especially cobalt deficient areas - persist when animals are moved off the toxic pasture - morbidity / mortality are high

Question 82

Describe the clinical signs of Phalaris staggers ?

Answer 82

Phalaris staggers clinical signs - Hyperexcitability - Tremors of the head and body - Twitching of lips, tail and ears - Walking on kness and buckling over - Struggling to stand and convulsions

Question 83

Describe how we could diagnose, prevent or treat a case of Phalaris staggers ?

Answer 83

Phalaris staggers Diagnosis - History, clinical sgns - histopathology (brain, kidney) There is a characteristic greenish or golden brown pigmentation in neurons of the brain, spinal cord and kidneys Prevention - cobalt bullet ( better breakdown of phalaris toxins byrumen flora) - low alkaloid cultivars, sudden death and staggers may still occur Treatment There is no effective treatment Move animals quietly from affected pasture Recovery is slow withsome anmals not recovering - potentially cull

Question 84

Describe the epidemiology and clinical signs of lumpy back ?

Answer 84

Lumpy back Solanum esuriale (potato bush, wild tomato) Outbreaks follow significant summer/spring rainfall - prevalence increases with age Clinical signs The CS first appear when sheep are driven >1km - affected fall behind mob with a short, stiff legged gait - inadequate hock flexion - they stop and are unable to keep walking - Typically stand with head lowered and back arched - often are accompanied with hyperthermia Sheep go down and may attempt to rise again after a brief rest; but CS comes back - if forced to walk may die

Question 85

Describe how you can diagnose and treat hump back ?

Answer 85

Question 86

Describe the epidemiology and pathology of Scrapie in sheep ?

Answer 86

Scrapie Transmissible Spongiform Encephalopathy disease (TSE) Epidemiology - Scrapie can affect sheep and goats - vertical and horizontal transmission - the placenta is a major source of infection - ingestion of infected material Very long incubation period - CS most commonly seen in sheep aged 3-4 years. -susceptability influenced by genotype Pathology Slow prion infection of central nervous system - prions transmissable self replicationg proetin that lacks nucleic acid

Question 87

Describe the clinical signs of Scrapie

Answer 87

Question 88

Describe how you would go about making a diagnosis of Scrapie ?

Answer 88

Spongyform encephalopathy Histopathology - characteristic non inflammatory, vacuolar degeneration of grey matter of the brain Detection of PrP in brain tissue - immunohistochemistry, ELISA - electron microscope identification of Scrapie associated Fibrils (SAFS) in the brain.

Question 89

Describe how you could carry out an investigation in Lingering death ?

Answer 89

Question 90

Describe the epidemiology of Ovine Johne's disease ?

Answer 90

Ovine Johne's disease Caused by Mycobacterium avium subspecies paratuberculosis - S strain (sheep type, type 1) sheep and goats - C strain (cattle, type 2) cattle, goats, (dairy goats, dee. Epidemiology - affects younger animals < one year of age more susceptable - many clear the infection - some become subclinical carriers (source of pasture contamination - which may then become clinical cases (long incubation period) - able to survive in the environment for a long time (cool, shady) Transmission = faecal oral route, contaminated teats or soil (organism has been isolated in clostrum / milk)

Question 91

Describe the factors that can affect the long incubation period of ovine Johne's disease ?

Answer 91

Ovine Johne's disease The incubation period is influenced by many factors - infecting dose - age of exposure - breed - stress - vaccination status (Gudair vaccine) - Due to the slow and insiduous nature of OJD, the disease may remain unoticed for years in a naive flock.

Question 92

Describe the clinical signs of Ovine Johne's disease ?

Answer 92

Ovine Johne's disease Clinical signs Most clinical cases occur in sheep between 2 and 5 years of age - chronic progressive emaciation - the infected mob will have a 'tail' with animals in 0.5-1.5 CS where the majority of the mob are in good condition CS>2 Diarrhoea is not a common feature of OJD in sheep (contrast to cattle). - animals remain bright and maintain appetite - slow clinical progression - mortality variable 1-2%

Question 93

Describe the observations you would make on a post mortem of a OJD infected sheep ?

Answer 93

Post mortem OJD Post mortem gross pathology - many affected animals have no gross lesions - emaciated carcass - serous fat atrophy - effusion of body cavities Lesions usually limited to the terminal ileum, caecum, colon draining lymphatics - thickening mesenteric lymphatics - enlarged oedematous mesenteric and ileocaecal lymph nodes - thickening intestinal mucosa

Question 94

Describe how you would go about making a diagnosis of Ovine Johne's disease ?

Answer 94

Diagnosis Samples to collect One lot preserved in 10% buffererd formalin (for histopathology) One lot fresh for culture - ileocaecal valve and 2 ileocaecal lymph nodes - 2-4 caudal mesenteric lymph nodes - 5cm pice of the ileum - proximal colon - caecum - faecal sample - clotted blood sample Histopathology (ileum and or/ mesenteric lymph nodes) - Ziehl Neelsen stain - Granulomatous enteritis with pressence of red acid fast bacilli Culture from faeces or tissues - sensitivity is dependant upon the stage of infection - specificity considered 100% - Map media with mycobactin slow growing - PCR - requires follow up test Faecal smear Ziehl Neelsen stain - poor sensitivity in early stages of disease - Faecal 350 = flock test of 7 pools of 50 shepp or more over two years of age (,one pellet each) - Flock health screening - Market assurance program - the result is unaffected by vaccination status - three months to obtain results to obtain a negative result

Question 95

Describe the surveilance of OJD at the abattoir ?

Answer 95

Abattoir surveilance of OJD Practical and cost effective flock screening test, used for sheep health declaration and market assurance program. Inspec adult sheep >2 years of age, for visabls signs of OJD in intestine and lymph nodes - sheep identification NLIS - requires trained technicians - Negative abbattoir results can be recorded on the National sheep health declaration - Abattoir 500 status - Abattoir 150 status

Question 96

Describe all the steps that may be taken to prevent OJD introduction onto a property ?

Answer 96

Prevention of OJD Introductions - only buy sheep with a high assurance level - biosecurity (fencing, run off) - vaccinate your flock if there is a risk of OJD from neighbors properties (high prevalence district) - good nutrition and worm control Work with neighbors to minimize risk and join a regional biosecurity group

Question 97

What steps may be taken to control ovine Johnes disease once infected ?

Answer 97

Ovine Johnes disease out break Control methods = challenging 1. Total destocking for 18 months, incuding two summers and restocking. - limited success - limit further introduction of OJD - biosecurity, purchase sheep with high assurance, work with neighbors 2. On farm management Identify and eliminate infected animals mobs - cull all sheep with clinical symptoms - cull all positive reactors to serological or faecal tests - prevention of new infections - limit further spread of disease - Vaccination Gudair Hygiene and husbandry - place water troughs higher - adequate nutrition and good parasite control - avoid lambing in wet dirty paddocks - grazing management fence off low lying creeks

Question 98

Describe correct vaccination practivce with the Gudair vaccine ?

Answer 98

Gudair vaccine Gudair is a killed vaccine (oil based adjuvents) Single dose subcutaneous at 6-14 weeks of age, usually done at marking or weaning - provides lifelong immunity - reduces environmental shedding - reducing environmnetal contamination (hence opportunity for disease transmission) The vaccine is highly reactive Many sheep develop local reaction at injection site. Granulomatous need to be trimmed at the abattoirs) - OJD staggers neuro - vaccinated sheep = NLIS tag with PIC and letter V

Question 99

Describe the epidemiology and pathology of urolithiasis ?

Answer 99

Urolithiasis Primarily a problem in wethers; rams are occassionally affected It is multifactoral disease = diet, mineral composition of water, urine PH and body water balance. Urinary caculi in sheep occur under three cicumstances 1. Diet high in cereal (low calcium, high phosphorus; silica wheat belt) 2. Alkaline urine (calcium carbonate calculi) 3. Magnesium phosphate (struvate) complexes and calcium phosphate (apatite)

Question 100

Describe the clinical signs of Uroliths in sheep ?

Answer 100

Uroliths in sheep Clinical signs The clinical signs may be variable depending upon where the obstruction occurs. - off feed - straining to urinate, may not pass any - colic signs - Rupture of bladder (temporary involvement followed by death) - perforation of urethra ( due to leakage of urine into the urethra)

Question 101

Describe how you would go about diagnosing Urolithiasis ?

Answer 101

Diagnoses of Urolithiasis History (concentrate feeding, cereal, stubble) - CS - urine sample - Abdominocentesis (increase in creatine) - blood sample (azotaemia) - ultrasound (distended bladder) Post mortem rupture of bladder performation of urethra hydronephrosis pressence of calculi in urethra or bladder

Question 102

Describe the best method for the prevention and treatment of uroliths ?

Answer 102

Treatment of uroliths - euthanasia - may be able to milk out the calculus if located in the urethral process It is seldom economic and prognosis is poor Prevention is best - unrestricted access to water - add 2-4% salt to ration to increase water intake - reduce the level of concentrate feeding - adding of ammonium chloride - acidification of urine to prevent phosphate and calcium carbonate uroliths

Question 103

Describe the epidemiology and pathology of Maedi-visna ?

Answer 103

Maedi Visna Caused by lentivirus - worldwide distribution - affect sheep and to a lesser extent goats (cross species transmission is possible) Main route of transmission is from ewes to lambs through infected colostrum and milk - horizontal transmission aerosol - very long incubation period

Question 104

Describe the clinical signs of Maedi Visna ?

Answer 104

Maedi Visna Clinical signs This is a slowly progressive disease - Maedi (means dyspnoea) most common - progressive interstitual pneumonia - progressive wasting - animals > 3-4 years of age - progressive ataxia of the hind limbs - paresis and paralysis - Indurative mastitis (enlarged hard udder) - Ultimately fatal (sheep die from anorexia or secondary bacterial infection).

Question 105

Describe how to diagnose, prevent and treat cases of Maedi Visna ?

Answer 105

Maedi-Visna Diagnosis - history - post mortem (lung, brain, mammary gland). - ELISA, PCR Treatment there is none Prevention Identify infected flocks (serological testing) - reduce prevalence through sanitary procedures (seperate lambs from ewes immediately after birth and serological test lambs) - avoid iatrogenic transmission

Question 106

Describe the epidemiology and pathology of mastitis ?

Answer 106

Mastitis Greatest concern to dairy and sheep and goats The most important bacteria - Staph aureus "contagious" - Mannheimia (necrotising black mastitis) - Mycoplasma mycoides capri - Listeria, Klebsiella, some streps Predisposing factors - entry of microbes via the teat canal - environmnet, nutrition, cold/wet/windy conditions - nutritional stress drought / grain trail feeding - teat injuries - age (prevalence increases with age)

Question 107

Describe how you could diagnose mastitis in sheep ?

Answer 107

Mastitis Sheep Diagnosis - Clinical - Bulk and individual SCC counts > 800000 likely subclinical or clinical - bulk and individual counts tend to be higher than they are for cattle - Calibrate counters

Question 108

Describe what measures you should take for the treatment of mastitis in sheep ?

Answer 108

Mastitis is sheep Treatment Treat on the basis of culture and sensitivity - parental and or intramamary, use full tube of IM - NSAIDS if toxaemic - cull animals high SCC count - dry sheep therapy, limit to high SCC animals - shed procedual cleaness (milking machine maintenance) - Udder conformation and functionality (Udder scoring systems) - pre joining inspection of ewes $4-8 across the flock profit Perform inspection atleast 4 weeks after lambing when udder is involuted - palpate udders up the race. There is an increased awareness of udder health as part of the MLA's "Fit to join program".

Question 109

Describe the features which characterise enzootic Pneumonia, and its common causes ?

Answer 109

Enzootic Pneumonia This disease is characterised bu Summer pneumonia - high morbity / low mortality - CS are most common at weaning hence summer pneumonia - the disease generally has litle impact except for additional trimming at the abbatoir due to (pleurisy) - potentially reduced growth rates The common cause of enzootic pneumonia - Mycoplasm (nearly always involved - Parainfluenza (PI3) virus - with the appropriate stressors may also be infected with Pasteurella and Haemolytica.

Question 110

Describe the epidemiology and pathology of enzootic Pneumonia

Answer 110

Enzoomatic pneumonia Commonly; Mycoplasma, Parainfluenza (PI3). Enzootic pneumonia is detmined by - handling in dusty yards - shearing at weaning NZ - irrigated paddocks - long haul transport - feedlotting - stressors (transport and feedlotting)

Question 111

Describe the clinical signs of Enzootic pneumonia ?

Answer 111

Enzootic pneumonia Clinical signs - Coughing - Laboured breathing - Head extension (mostly in cases of Mannheimia/Pasteurellosis) - usually a mild non progressive pneumonia unless superinfected with bacteria - production loss limited to abbatoir trim

Question 112

Describe how you would go about diagnosing and treating a case of enzootic pneumonia ?

Answer 112

Enzootic pneumonia Diagnosis - clinical signs - autopsy - should only diagnose severe bacterial pneumonia if sheep are dead with severe PM signs Treatment No treatment for mild non progressive cases - Oxytetracycline for severe cases

Question 113

Describe how you would prevent Enzootiv Pneumonia ?

Answer 113

Enzootic Pneumonia Prevention 1. Dust reduction - handle sheep on concrete and dampen down the dust 2. Avoid post weaning shearing if possible 3. Feedlot acclimatation 4. Vaccination with cattle Mannhiemia 5. Long transport in accordance with land and transport. dust and stress reduction

Question 114

Describe the pathology and clinical signs of aspiration pneumonia ?

Answer 114

Question 115

Describe the pathology and clinical signs of Oestrus ovis ?

Answer 115

Question 116

Describe the epidemiology and pathology of Melioidosis ?

Answer 116

Melioidosis Burkholderia pseudomallei Aetiology Bacteria are acquired from the environmnet - ingestion, inhalation - wounds and abrasions - Transplacental transmission in goats Pathology - disease of sheep, goats, pigs and humans

Question 117

Describe the clinical signs of Melioidosis ?

Answer 117

Melioidosis Burkholderia pseudomallei The clinical signs Variable incubation periods days/months/years - subclinical infection is common - Respiratory - coughing, fever, respiratory distress - mucopurulent nasal and ocular discharge - weakness and recumbancy - lameness (arthritis - neurological signs (circling, incoordination, blindness)

Question 118

Describe the diagnosis, prevention and control of Melioidosis ?

Answer 118

Melioidosis Burkholderia pseudomallei Diagnosis - history and clinical signs - post mortem ( multiple abscess in a range of organs, pus) - PCR - serology Control/Prevention - eliminate all affected stock - rodent control - raise the remaining animals off the soil - avoid muddy or contaminated water - no vaccine available Make sure you have adequte PPE when investigating resp disease in the tropics.

Question 119

Describe the pathology and clinical signs of Jaagsiekte ?

Answer 119

Jaagsiekte Ovine pulmonary adenocarcinoma, ovine pulmonary adenomatosis Pathology Beta retrovirus (Jaagsiekte sheep retrovirus) - produces a tumor in the lung of sheep Clinical signs - long incubation - only seen in sheep >2 yrs of age - progressive respiratory disease associated with loss of weight - accumulation of fluid in the respiratory tract (wheelbarrow test) - death is inevitable (2-6 months after CS become apparent).

Question 120

Describe how you could diagnose and treat Jaagsiekte ?

Answer 120

Jaagsiekte Diagnosis - history, CS - Post mortem - Histopathology - Immunohistochemistry Control - Quaratine with slaughter of all infected and supect stock - No vaccine available

Question 121

Describe the pathology and clinical signs of Rift Valley fever ?

Answer 121

Rift Valley fever Viral disease Bunyviridae Epidemiology - affects humans, sheep, goats and cattle (humans usually afected by handling infected stock). - Transmission mosquitoes Clinical signs - mass abortions - high mortalities - fever - anorexia - thick nasal discharge - blood stained diarrhoea - jaundice - weakness - death

Question 122

Describe how you could go about diagnosing and treating an out break of Rift Valley fever ?

Answer 122

Rift Valley Fever Diagnosis - History CS - Post mortem (hepatic necrosis, generalised congestion) - Histopathology - Serology - Virus isolation Control Insect control, movement restrictions vaccines are available overseas

Question 123

Describe the pathology and clinical signs of Peste des Petits Ruminants ?

Answer 123

Peste des Petits Ruminants Goat plague (Paramyxoviridae) Viral disease of sheep and goats The virus is shed in tears, nasal discharge, faeces and urine Transmission = close contact / inhalation Clinical signs - fever - anorexia - nasal and ocular discharges - blood stained diarrhoea - morbidity and mortality reach 100%

Question 124

Describe how you could diagnose and treat a case of Peste des Petits Ruminants ?

Answer 124

Peste des Petits Ruminants Diagnosis History CS Post mortem Virus isolation Control Quarantine and slaughter Movement restrictions