Horse, cow and small ruminants Flashcards
Describe the grading system for equine lameness ?
Describe how to flex the fetlock and carpus in the forelimb of a horse ?
Describe how you would flex the spavin and fetlock in the hindlimb of a horse ?
In horses where would you inject to achieve a PDNB ?
In horses where would you inject to achieve ABSNB ?
Describe the FAFROICD complex ?
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
basic principles of a lameness
basic principles of a lameness of a lameness investigation in sheep ?
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
Describe the epidemiology and pathology of OID in sheep.
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
Describe the clinical signs of OID
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
Describe the epidemiology of Foot/heel abscess
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%
Describe the clinical signs of Foot abscess
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.
Describe how you would go about a diagnose, prevent or treat ovine Foot abscess ?
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
Describe the aetiology of foot rot
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.
Describe the epidemiology of Foot rot in sheep ?
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
Describe how you would go about diagnosing a case of foot rot in sheep?
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
Describe the process of scoring the lesiins in the foot of a sheep ?
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
Describe what you would observe in a foot rot score of zero and one ?
Describe what you would observe in a foot rot score two ?
Describe what you would observe in a foot rot score three ?
Describe what you would observe in a foot rot score of four ?
Describe what tests could be carried out to identify the virulence of Dichelobacter nodosus ?
Diagnostics
- Protease thermostability test, gelatin gel test
- Elastase test - digestion of elastin particles in agar
Describe the control phase for foot rot ?
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)
Describe the different methods for eradication of foot rot in sheep herds ?
Eradication foot rot
First is it neccessary
1. Destocking
- whole flock + replacement + expensive
- opportunity to reorganise you enterprise
- 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
Describe the pathology and clinical signs of a toe abscess ?
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
Define the clinical signs and cause of Shelly hoof ?
Describe the epidemiology and pathology of CODD ?
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
-
Describe the clinical signs of CODD
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
Describe the prevention and treatment of CODD
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
Describe the clinical signs and cause of strawberry footrot ?
Pink = CODD
Green = OID
Blue = FR
Describe the cause and clinical signs of post dipping lameness ?
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
Describe how you would diagnose and treat post dipping lameness ?
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
Describe the epidemiology of foot and mouth disease ?
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
Describe the clinical signs of foot and mouth disease ?
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
Describe how you would diagnose and control foot and mouth disease ?
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
Describe the epidemiology and clinical signs of scabby leg ?
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
Describe how you would diagnose and traet scabby leg ?
Describe the epidemiology of blue tongue disease ?
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.
Answer = C. cattle
Answer = B. Hyperaemia
Describe the clinical signs of blue tongue disease in sheep ?
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
Describe how you could diagnose and traet foot and mouth disease ?
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)
Identify the bacterial causes of fibrinous and suppurative arthritis in sheep ?
Arthritis in sheep
Fibrinous arthritis
- Erysipelothrix arthritis
- Chlamydial polyarthritis
Suppurative arthritis
- E.coli, Staph, Strep, Fusobacterium necrophorum, Truepurella pyogenes
Describe the pathology and clinical signs of Fribinous arthritis in lambs ?
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
Describe the clinical signs and pathology of suppurative arthritis ?
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.
Describe how you would carry out a nervous disease investigation ?
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
Answer =
E. Trigeminal nerve and facial nerve
Answer = B Oculomotor nerve
Describe the pathology of Polioencephalomalacia
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
Describe the epidemiology of Polioencephalomalacia ?
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
Describe the clinical signs of Polioencephalomalacia ?
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
Describe how a Veternarian would diagnose Polioencephalomalacia ?
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
What can be done to prevent or treat Polioencephalomalacia ?
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
Describe the aetiology and epidemiology of Listeria monocytogenes ?
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.
-
Describe the clinical signs of Listeria ?
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
Describe how you go about diagnosing Listeria in sheep ?
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)
Describe how you would diagnose and treat an outbreak of Listeria ?
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
Describe the pathology and clinical signs of a spinal abscess in lambs ?
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
Describe how to diagnose and treat a spinal abscess in lambs ?
Answer = d. navel cord
Describe the pathology and clinical signs of a brain abscess ?
Describe the pathology of Gudair staggers ?
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.
Describe the clinical signs of injecting Gudair vaccine into muscle ?
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.
Describe prevention and treatment after Gudair vaccine is injected into muscle ?
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).
Describe the pathology of Clostridium Tetani ?
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)
Describe the clinical signs of Tetanus
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).
Describe how you can diagnose and treat a case of Tetani ?
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
Answer = C Gabba
Describe the pathology of Botulism in sheep ?
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)
Describe the clinical signs of Botulism ?
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
Describe how you would diagnose and treat a case of Botulism ?
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
Describe the aetiology and epidemiology of Perennial ryegrass staggers ?
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.
Describe the clinical signs of Perenial ryegrass staggers ?
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
Describe how to diagnose and treat perenial ryegrass staggers ?
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
Describe the pathology and epidemiology behind annual ryegrass staggers ?
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
Describe how t dignose annual ryegrass staggers ?
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
Describe how you can treat or manage ryegrass toxicity ?
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)
Describe the epidemiology and pathology of phalaris staggers ?
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
Describe the clinical signs of Phalaris staggers ?
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
Describe how we could diagnose, prevent or treat a case of Phalaris staggers ?
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
Describe the epidemiology and clinical signs of lumpy back ?
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
Describe how you can diagnose and treat hump back ?
Describe the clinical signs of Scrapie
Describe how you would go about making a diagnosis of Scrapie ?
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.
Describe how you could carry out an investigation in Lingering death ?
Describe the epidemiology of Ovine Johne’s disease ?
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)
Describe the factors that can affect the long incubation period of ovine Johne’s disease ?
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.
Describe the clinical signs of Ovine Johne’s disease ?
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%
Describe the observations you would make on a post mortem of a OJD infected sheep ?
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
Describe how you would go about making a diagnosis of Ovine Johne’s disease ?
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
Describe the surveilance of OJD at the abattoir ?
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
Describe all the steps that may be taken to prevent OJD introduction onto a property ?
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
Describe correct vaccination practivce with the Gudair vaccine ?
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
Describe the epidemiology and pathology of urolithiasis ?
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)
Describe the clinical signs of Uroliths in sheep ?
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)
Describe how you would go about diagnosing Urolithiasis ?
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
Describe the best method for the prevention and treatment of uroliths ?
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
Describe the epidemiology and pathology of Maedi-visna ?
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
Describe the clinical signs of Maedi Visna ?
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).
Describe how to diagnose, prevent and treat cases of Maedi Visna ?
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
Describe the epidemiology and pathology of mastitis ?
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)
Describe how you could diagnose mastitis in sheep ?
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
Describe the features which characterise enzootic Pneumonia, and its common causes ?
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.
Describe the epidemiology and pathology of enzootic Pneumonia
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)
Describe the clinical signs of Enzootic pneumonia ?
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
Describe how you would go about diagnosing and treating a case of enzootic pneumonia ?
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
Describe how you would prevent Enzootiv Pneumonia ?
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
Describe the pathology and clinical signs of aspiration pneumonia ?
Describe the pathology and clinical signs of Oestrus ovis ?
Describe the epidemiology and pathology of Melioidosis ?
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
Describe the clinical signs of Melioidosis ?
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)
Describe the diagnosis, prevention and control of Melioidosis ?
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.
Describe the pathology and clinical signs of Jaagsiekte ?
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).
Describe how you could diagnose and treat Jaagsiekte ?
Jaagsiekte
Diagnosis
- history, CS
- Post mortem
- Histopathology
- Immunohistochemistry
Control
- Quaratine with slaughter of all infected and supect stock
- No vaccine available
Describe the pathology and clinical signs of Rift Valley fever ?
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
Describe how you could go about diagnosing and treating an out break of Rift Valley fever ?
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
Describe the pathology and clinical signs of Peste des Petits Ruminants ?
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%
