Bovine health Flashcards
Bill Tranter
Demonstrate and explain how to clinically examine the bovine abdomen ?
Clinical examination of the bovine abdomen
- visual assessment of the oral cavity and palpation of the tongue
- visual examination of the left abdomen
- palpation
- auscultation
- percussion and simultaneous auscultation
- ballottement
- auscultation and simultaneous ballottement (succussion)
- rectal examination.
Describe an LDA and its aetiology?
Left displaced abomasum
The abomasum becomes enlarged with accumulation of fluid and gas.
The abomasum then becomes mechanically displaced from its normal position to the left side of the abdominal cavity, between the rumen and left abdominal wall.
Left displacement of the abomasum is more common than right displaced abomasum.
Risk factors
- high producing adult dairy cow
- within a month of partuition
- heavy grain feeding or low levels of fibre
- poor management of the transitional period
What risk factors could lead to an LDA ?
LDA left displaced abomasum
(left displacement is more common then right displacement)
This usually occurs in high producing dairy cows within one month of partuition.
- incidence increases with heavy grain feeding
- low levels of fibre (high concentrate / low fibre rations)
- increasingly seen in recently calved heifers, reflecting poor nutritional management prior to entering the milking herd
- rare in beef cattle
Describe the presenting signs of an LDA ?
LDA left displaced abomasum
Presenting signs
- significant weight loss post calving
- low milk when should be firing
- potentially treated for other condition metritis with no recovery
- disinterested in eating grain, whereas would normally be ravenous
- gaunt appearance
Describe the clinical signs of an LDA ?
Left displaced abomasum
Clinical signs
Dilated abomasum sometimes visible as a small bulge behind the last rib in the paralumbar fossa. (sprung rib cage)
Usually high pitched metallic ping is heard over upper aspects of the 9th to 12th rib on the left side.
- decreased rumen contraction
- ketosis common
- faeces softer + reduced (occasional diarrhea)
- sunken sides / small rumen
- hypochloraemic, hypokalaemic metabolic alkalosis
- generally not possible to palpate a displaced abomasum on rectal examination.
Describe how LDA could potentially result in hypochloraemia and hypokalaemia ?
Abomasal displacements - biochemical changes
Dehydration and metabolic alkalosis
- low chloride and K
- this is due to continual secretion of hydrochloric acid, sodium and and chloride, potassium into the abomasum
- abomasum gradually becomes distended, but does not evacuate its contents into the duodenum ( - no or little absorption further down the GI tract).
You identify a left sided ping on clinical examination, provide a list of differentials ?
Left sided ping - differentials
Ping requires a gas / fluid interface
- left displaced abomasum
- atonic rumen
- pneumopertoneum
- air in the uterus
Describe the pathothology of an LDA ?
Pathology of an LDA
There are many risk factors (managerial, enironmental, and hereditary) playing a role in the development of DA.
- void left by involuting uterus post partuition, which is not taken up by the rumen
- permits movement of the abomasum
- decreased food intake in the peri-parturient period; reduced rumen volume, allows abomasum to become displaced left or right
The major risk factor poor feeding during the transition period
- excess concentrates prior to calving result in decreased rumen full
- minimal concentrate results in failure of papillae to develop, which is needed to increase rumen absorptive capacity (failure of microbes to adapt to new diet)
- decreased rumen motility due to low rumen fill and high VFA concentration
- decreased abomasal motility and emptying due to high VFA concentration
Describe the two ways in which you can correct a LDA ?
Treatment for LDA
Minimally invasive / closed procedures
- rolling
- percutaneous tacks ‘ blind tack Gryner method)
Right paralumbar fossa abomasopexy
Right paramedian abomasopexy (for a recumbant animal)
- surgical prep + paravertebral block
- incision paralumbar fossa
- descending duodenum pulled ventrally
- deflate abomasum with large bore (14 guage needle) + plastic tubing attached
- apply traction to greater omentum
- identify pylorus by its firmness (near pig’s ear)
Three suture layers
- include greater omentum in first suture layer (internal and transverse abdominal muscles, omentum, abomasum)
- 2nd layer external abdominal muscles
- finally the skin is stitched (forward interlocking pattern.
Supportive care
- oral or systemic calcium
- electrolytes
- propylene glycol for concurrent ketosis
- NSAIDS for pain relief
- antibiotics for any concurrent infectious conditions.
Describe the pathology of an RDA ?
Right displaced abomasum and volvulus
Right sided abomasal dilation and volvulus
RDA
Abomasal hypomotility
- associated with hypocalcaemia
- also with high concentrate, low roughage diets
- atony of abomasum followed by accumulation of feed, fluid and gas, produces a grossly distended organ.
Abomasum then becomes displaced dorsally on the right side of the abdomen.
- the abomasum may then rotate 180-270 around its axis which runs through the centre of the lesser omentum
- mostly cases in a counter clockwise direction
- this positional change has the potential to produce complete luminal obstruction and irreversible neurovascular damage if not corrected
A more acute condition (abdominal catastrophe) then a simple RDA.
Describe the presenting signs of an RDA ?
Presenting signs of an RDA
Usually adult dairy cows in the first few weeks after calving (but can occur at any time)
- similar to LDA weight loss, low milk
- not fully responsive to other treatments
- disinterested in grain
- faeces reduced, sometimes diarrhoeic
Describe the clinical signs of an RDA or volvulus?
The clinical signs of an RDA
- animal is dull and afebrile
- varying degrees of ketosis
- rumen contractions are weak and irregular
- HR elevated 80-90 bpm
- there may be abdominal pain, occassional lifting of hind limbs and looking at right flank
- sometimes abdominal distension (deep palpation behind and below the right costal arch.
Ping with percussion
- 15-20cm area cranial to the right paralumbar fossa
Right volvulus of the right abomasum (AV)
- often follows right sided dilation and displacement of the abomasum
- sudden onset of abdominal pain
- HR increases rapidly
- abdomen distended on right side
- rectum usually empty but may contain autolysed blood (black faeces)
- distended abomasum may be palpated by rectum
ping area > 60 cm in diameterwith abomasal volvulus
What signs would indicate to a clinician the RDA has evolved to Av, and what could this mean for the animals prognosis ?
Percussion with auscultation
RDA
- 20cm area
- elevated heart rate
- potential abdominal pain and shifting of legs
- ‘fluid splashing sounds’ ballottement and auscultation
RDA and VA
- prognosis is poor
- > 60 cm area associated with abomasal volvulus
- sudden onset abdominal pain
- distended abomasum may be palpated by rectum
- rectum empty but may contain autolysed blood (black faeces)
-
Describe the treatment for a RDA or AV ?
Treatment RDA
Surgical intervention (emergency)
- right flank omentopexy or pyloropexy (care must be taken to avoid accidental incision of the distended abomasum when opening the abdomen.
- inverted L block 2% lignocaine
- palpate abomasum (ensure no volvulus)
- insert 14 guage needle to remove excess gas + plastic tubing
- reposition abomasum
Post operative care
- antibiotics oxytetracycline 25ml SID for 5 days
- propylene glycol orally
- oral fluids
AV - Do not untwist euthanase animal
Describe the aetiology of abomasal ulceration ?
Aetiology abomasal ulceration
High producing dairy cows in the first six weeks of lactation, feedlot cattle and veal calves
- often well nourished suckling calves
- increased risk in calves on a high fibrous diet or when converting milk to high fibrous diet
- increased risk with silage adult dairy cows
Most likely cause is prolonged inappetence resulting in sustained periods of low abomasal PH.
Describe the cinical signs of moderate to severe abomasal ulceration ?
Describe the cinical signs of abomasal ulceration
Abomasal ulcers may haemorrhage into the GI tract resulting in melaena
- may perforate leading to peritonitis and sudden death
- may also be sealed by omental adhesions
Clinical signs
- impaired appetite and rumen function
- decrease milk yeild
- loss of condition
- intermittent diarrhoea
- ketosis
- pain with grinding of the teeth and when pressure applied low in abdomen behind last rib on right side
- haemorrhage
- localised peritonitis
- moderate fever
- loud fast HR
- rapid shallow respiration
- weakness and collapse
- passage of stale fould smelling tar like faeces (melaena).
Describe the management process for abdominal ulceration ?
Abomasal ulceration
Supportive therapy
- intravenous fluids
- some cows recover slowly over a period of several weeks
- blood transfusion in valuable cows 4-6 L
No NSAIDS may exacerbate the problem
Describe the aetiology and pathology of indigestion in cattle ?
Cattle and indigestion
Aetiology
Occurs when new feeds are suddenly introduced (which the animal is not accustomed to).
- indigestable roughage
- very wet grass
- overheated, frosted or mouldy stale feeds
- sudden introduction of concentrates
- intake of large quantities of antibiotics, disturbs rumen microflora
Pathology
This causes an upset in rumen microflora - needs time to adapt (1-2 weeks)
- can induce rumen stasis through an acute fall in rumen PH.
Describe the clinical signs of indigestion in cattle ?
Indigestion in cattle - clinical signs
- enlarged doughy rumen
- reduced and weaker rumen contractions
- partial or complete anorexia
- slight drop in milk production
- slight to moderate ruminal tympany
- animal typically afebrile
Initially faeces reduce in quantity and drier than normal, followed by malodorous diarrhoea.
Describe how you can confirm a diagnosis of simple indigestion ?
Diagnosis simple indigestion.
We suspect due to
- abrupt change in the nature or amount of feed
- multiple animals affected
- exclusion of other causes of forestomach dysfunction
Confirmation via
- diagnosis by examining rumen fluid (PH <6.0 or >7.0)
- decrease in the number and size of protozoa in rumen fluid.
Describe the strategies to prevent and treat simple indigestion in cattle ?
Simple Indigestion
Prevention
- avoid abrupt changes in the diet
- introduce new feeds in small quantities at first, with intake being gradually increased.
Treatment of sick animals (5)
- often have spontaneous recover
- provide good quality hay
- magnesium sulfate (epsom salts 1-2 grams/Kg BW) stimulates outflow of rumen contents from reticulo rumen
- gastric stimulant powder orally
- multivitamin B injections (assist with processing of proteins)
Describe the two types of ruminal tympany ?
Ruminal tympany
(An excessive accumulation of gas in the rumen = bloat)
Primary frothy bloat (pasture bloat)
- excessive production of gases and raising of rumen fluid viscosity
- small bubbles become entrapped
- stable and persistant foam
Secondary gaseous (free gas float)
- accumulation of free gas in dorsal sac of rumen
- physical or functional defect in eructation of free gas
- inability to eliminate free gas
What is the normal PH of the rumen ?
Rumen PH = 6.2-7.0
Describe the pathology behind primary bloat ?
Pathology primary bloat
Excessive production of gases and raising of rumen fluid viscosity
- bubbles trapped in stable and persistant foam
- eructation prevented by accumulation of froth (cardia not cleared), fails to relax preventing gas entering the eosophagus.
associated with feeding lush, immature rapidly growing legumes (clover, lucerne or thinly ground grain).
Gases are trapped by fine particles of feed
Describe the presenting signs and clinical signs of primary bloat ?
Primary bloat (frothy bloat)
Presenting signs
- severe distension of left paralumbar fossa following feeding
- somtimes within in an hour of commencing grazing
- signs of pain bellowing, frequent lying down, kicking at ventral abdomen
Clinical signs
- initially rumen contractions increase followed by hypomobility
- severe respiratory distress / open mouth breathing
- protrusion of tongue
- possible vomiting of frothy rumen contents
- recumbancy and death.
How would you diagnose a case of primary bloat vrs secondary bloat ?
Bloat diagnosis
Primary bloat / Pasture bloat
> one animal; very likely to be primary or frothy bloat
On post mortem
- severe distension of abdomen
- blood tinged fluid exuding from body orifices
- ‘bloat line’ in oesophagus
- oedema, congestion and haemorrhage in muscles of the head and neck.
Secondary blaot
Usually only one animal affected and it may be relieved via a stomach tube
Describe the treatment of a cow suffering from primary bloat
Treatment for primary bloat
Non life threatening
- remove gentle from offending pasture and supplement good quality hay
- drench antifoaming agent (paraffin, vegetable oil) 500ml
Life threatening case
Indication cow is in severe distress, mouth breathing, tongue protruding and lieing down
emergency rumenotomy
- stab incision ‘bloat stab’ trocar
- large ones may need stictches or antibiotics
Describe reasonable management strategies to prevent bloat ?
Bloat control and prevention
Gradual introduction to at risk pasture (limited time access or strip grazing)
- avoid immature rapidly growing legumes
- oral administration of anti-foaming agent bloat oil, paraffin oil and tallow
- fermentation modifiers such as monensin
- (individual drenching, spraying pasture, mix with grain / molasses, water trough application, bloat blocks)
- apply atleast seven days before anticipated risk.
Alcohol ethoxylate based compounds are favoured because of their extended persistency of action.
- genetic selection for bloat safe pastures and bloat tolerant cattle
Describe the pathology behind secondary bloat ?
Secondary gaseous bloat pathology.
(Accumulation of free gas in dorsal sac of the rumen).
Pathology
- usually recurrent and chronic
- occurs when there is physical or functional defect in eructation of free gas.
The inability to eliminate gas is secondary to some other condition or disease.
- acute form - physical obstruction to the oesophagus ‘choke”
- chronic lesions affecting the cardia (fibro-papilloma)
- vagus indigestion
Describe how you would diagnose and treat a case of secondary bloat ?
Secondary bloat
Gastric intubation
Diagnosis - pass a stomach tube feel some resistance than release of gas.
Describe the pathology behind ruminal acidosis ?
Rumen acidosis - pathology
Results from sudden unaccustomed ingestion of large quantities of carbohydrate rich feeds.
(grains, concentrates, potatoes, bread etc)
Rapid fermentation of readily available carbohydrate and inadequate saliva production.
- large amounts of VFA produced
- natural PH regulators overwhelmed
- streptococcus bovis and lactobacillus sp multiple producing lactic acid
- intraluminal acidosis with increases in D and L lactate (D isomer)
Increase in rumen liquor osmolarity (hypertonic) draws fluid in from extravascular space causing dehydration.
- low rumen PH reduces motility causing stasis and mild bloat
- lacatae absorbed into circulation causing the development of metabolic acidosis.
- some cows develop laminitis due to vasoconstriction.
What is (Per) acute rumen acidosis ?
(Per) acute rumen acidosis
Results from a sudden unaccustomed ingestion of large quantities of carbohydrate rich feeds (grain, concentrates, potatoes)
Definition
- Ph drop <5.0 of rumen fluid
- accumulation of lactic acid in the rumen- upto 300 mmol/L (normal <5mmol/L)
- defaunation of rumen fluid (absence of protozoa
- rumen microbial flora is dominated by acid tolerant lactic acid producing bacteria gram +ve Streptococcus bovis and Lactobacillus spp.
Describe the factors which would increase the risk of your herd developing (per) acute rumen acidosis ?
(per) acute rumen acidosis
The risk increases with:
- lack of previous exposure to offending feed
- reduced NDF content of total ration
- rate of fermentation of feed
(wheat>triticale>oats>barley>maize>rice>sorghum
- fineness of milling
Describe the clinical signs of (Per) acute rumen acidosis ?
Clinical signs Ruminal acidosis
Signs develop within 8 hrs of excess carbohydrate ingestion
- Increased HR 120bpm
- anorexic weak ataxic
- colic
- teeth grinding bruxism
- decreased rumen motility + distension
- profuse foul smelling diarrheoa (sweet sour odour) which may contain whole grains.
- enophthalmos
- nervous signs of staggering, head pressing and posterior paresis + recumbancy
Fluid splashing on ballottement / auscultation of distended rumen
Describe how you could go about treating a case of (Per) acute acidosis ?
(Per) acute acidosis PH<5.0
Treatment
- administer alkalising agents
MgO via a stomach tube/ 10L of water repeated every 12 hrs
- provide access to good quality grass hay
- keep away from water
- keep animals who are ambulatory moving
- rumenotomy and lavage in severe cases
Procaine penicillin - reduce lactate producing bacteria
Vitamin B - prevent polioencephalmalacia
NSAIDS
Rumen transfaunation
Define a rumen transfaunation ?
Describe SARA and its pathology ?
SARA Subacute rumen acidosis
(rumen PH falls to between 5.0 and 5.5 + usually occurs early lactation)
Pathology
- sudden change to lactation ration with larger amounts of starch
- insufficient effective fibre in ration being fed
- productions of VFA exceeds absorptive capacity of rumen mucosa
- increased propionate and butyrate and less acetate
- rumen microbial flora remains dominated by gram negative bacteria, although gram +ve may slightly increase
The risk of SARA is less when the concentration / forage ratio is kept well below 60:40
Describe the clinical signs of SARA ?
The clinical signs of SARA
Intermittent diarrhoea, often containing undigested food particles
- lowered milk fat (sometimes even lower than milk protein %)
- low milk fat syndrome SARA
- proportion of cows cud chewing is decreased <50%
- increased incidence of lameness, with increasing herd locomotion score
>30% of cows sampled have rumen PH <5.5
Describe how you would go about making a diagnosis of SARA ?
SARA Sub acute rumen acidosis
Diagnosis - Obtain samples of rumen liquor from live cows (herd test);
- oral or nasal intubation
Rumenocentesis
- insert needle into the main body of the rumen and aspirate a sample of rumen liquor.
- no saliva contamination
- landmarks; left side, horizontal line with the level of the petalla 15-20 posterior to the last rib. (must positively identify ventral sac of rumen prior to sampling).
Rumen fluid 5.0-5.5 = ruminal acidosis
Describe strategies we can employ to prevent SARA ?
SARA Sub acute ruminal acidosis
Prevention strategies
- adapt cows gradually to carbohydrate rich feeds
- provide adequate effective fibre (eNDF) in the ration >32% concentrate forage ratio < 60:40
Can utilise additives when the risk of SARA is great
- buffers (sodium bicarbonate)
- neutralising agents (magnesium oxide)
- rumen modifiers (eg. monensin sodium)
- oral antibiotics such as virginiamycin
Describe the pathology underlying Traumatic reticulo-peritonitis ?
Also describe the presenting signs of the cow ?
Traumatic reticulo - peritonitis
Pathology
Penetration of the reticular wall by a sharp foreign body:
- discarded nails, fence staples or fencing wire
- common in lot or stall feed cattle
- uncommon in pastured animals
- related to standards of management of the farmout break have been reported after disintegrated car tyres were used on silage clamps.
The foreign object can
- sit on the floor of the reticulum
- penetrate the reticular wall, cause acute inflammation and mild clinical disease
- perforate reticular wall causing peritonitis
- migrate into peritoneal or thoracic cavity
Describe the presenting and clinical signs of Traumatic reticulo peritonitis ?
Traumatic reticulo-peritonitis
Presenting signs
- distension of jugular veins
- oedema (submandibular, brisket, ventral)
- anorexia
- dramatic drop in milk production
- reluctance to move - grunt test
- shallow and rapid breathing
- slight rumen tympany
The clinical signs may only last for a few days, after which adhesions restrict reticular movement
Clinical signs
- shallow and fast respiration
- fever (40-40.5 C)
- Increased HR >90bpm
- taught rigid abdomen (defense musculaire)
- constipation
- heart muffled sounds - friction
- fluid splashing sounds (washing machine noises).
-
Describe how you could go about making a diagnosis of Traumatic reticulo-peritonitis ?
Diagnosis of Traumatic reticulo-peritonitis
On clinical pathology
- history and clinical signs
- elevated leukocyte cout
- neutrophilia - with a marked left shift
- increased plasma protein and fibrinogen levels
- low protein : fibrinogen ratio (P:F)
- increased white blood count in the peritoneal fluid
Describe how you would go about treating a case of Traumatic reticulonitis ?
Traumatic reticulo-peritonitis treatment
Medical treatment
- antibiotics 5-7 days
- oral magnet
- ‘cage rest’ confinement to a small area or loading race
- exploratory laparotomy, with rumenotomy and removal of the foreign body
Describe the pathology underlying Vagus indigestion ?
Vagus indigestion
(chronic condition of mainly adult cattle)
Pathology
Vagus indigestion is caused via damage to the vagus nerve, or mechanical impairment of reticular motility and oesophageal groove dysfunction.
- slow insidious onset
- mechanical impairment of reticular motility - failure of passage of normal ingesta through reticulo-omasal orifice and pylorus
Large quantities of ingesta, fluid and sometimes gas accumulates mainly in the rumen
- Abdominal distension ‘papple”
Describe the presenting signs of vagus indigestion ?
Vagus indigestion presenting signs
- chronic fore stomach distension
- ‘papple
- reduced appetite
- gradually reduced milk production
- weight loss (often masked by abdominal distension)
- pasty faeces or diarrhoea
- reduced faecal output
- sometimes bradycardia (<50bpm) characteristic.
Describe the clinical signs of vagus indigestion ?
Vagus indigestion clinical signs
Rumen enlarges to fill most of the abdomen
- ventral sac progressively enlarges and extends into the right ventral abdomen (L shaped rumen)
- papple ‘ 10 - 4’ shape
- rumen contractions weak and difficult to hear
- failure of ingesta to exit the stomach typically results in rumen contents being mixed into a froth
There are three classification
1. obstruction of oesophagus / cardia
2. failure of omasal transport
3. failure of abomasal outflow
Describe how you would go about diagnosing a case of vagus indigestion ?
Diagnosis vagus indigestion
History and clinical signs
- papple, distended L shaped rumen
- bradycardia (if present)
- small quantities of pasty or runny faeces
- chronic weight loss
An exploratory laparotomy may confirm anterior abdominal adhesions/ pathology.
Describe how you would manage and treat a case of vagus indigestion ?
Treatment vagus indigestion
Determine cause and provide
Specific treatment
- antibiotics, NSAIDS
- many of the underlying causes are non reversible and not easily treated
- relieve distension with stomach tube
- perform a rumenotomy and explore rumen, reticulum and rumen reticular groove
- rumen fistulisation for chronic bloat
Overall the prognosis is poor - salvage slaughter is the best option
(No recognised control measures)
Provide a differential list and clinical signs of colic in cattle ?
Colic in cattle
Clinical signs
- animal is uneasy; hindlimb treading, leaning against stationary objects
- kicking at abdomen
- repeatedly twisting and turning
- getting up and down, throwing themselves to the ground
- in cattle colic signs are not as clear and severe as in the horse (usually only last for a short period and is often not observed).
Differential list colic
- Ruminal tympany (bloat)
- (Per) acute ruminal acidosis - grain overload
- intestinal volvulus
- intussusception
- intestinal phytobezoar
- constricting band (incarceration)
- abomasal volvulus
- caecal dilation and volvulus or caecal torsion
What is spasmodic colic and its signs ?
Spasmodic colic - the most common form of colic in cattle.
Occurs when the bowel contracts in an abnormal manner
- usually following grazing lush green pasture in cold weather
- most frequently observed at milking
The clinical signs of Spasmodic colic
- colic signs are often severe
- spontaneous recovery occurs quite quickly (+/- treatment)
- treatment with a spasmolytic drug or sedative
You need to distinguish from a real GI disorder through a thorough clinical exam.
Describe the aetiology of an intussusception ?
Intusssusception
Invagination of one segment of bowel into the lumen of an adjacent segment (intussusipiens) of bowel
- usually jejuno - ileum
- often also occurs through the ileo caecal valve
- obstruction of intestine follows
- sporadic condition, but most common cause of small intestinal obstruction in cattle
- in calves related to diarrhoea and strong peristaltic activity.
Describe the presenting signs of an intestinal Intussusception in cattle ?
Intussusception presenting signs cattle
- Sudden reduction in milk yeild to virtually nothing
- colic ‘saw horse stance’
- early pain is intense, but lessens when desensitisation and sloughing of the intussusceptum occurs
- small amounts of faeces at first, with some blood and mucous - then only tenacious blood stained mucous.
Describe the clinical signs and diagnoses of Intussusception ?
Intussusception
A diagnosis may be made from the clinical signs
Clinical signs
- Right abdomen enlarges as intestines distend
- fluid splashing sounds ballottement / auscultation of right abdomen
- inappetence and litle rumen activity
- rectal examination - multiple loops of tightly distended small intestine in right abdomen
- rectum - empty of faeces, but contains blood and thickened mucous
- HR and RR increase with colic - then fall to normal, but HR increases again as condition progresses
Describe how you would go about treating a case of Intussusception ?
Intussusception surgical treatment
Heroic or try another table at the casino
- fluid therapy
- pre opertive analgesia and antibiotics
- right flank laparotomy with paravertebral anaesthesia in standing patient
- identify and exteriorise intussusception (difficult)
- recognise as spongy or more solid bowel, cylindrical or coiled, usually painful segment of bowel
- ligate mesenteric blood supply close to affected bowel
- apply towel clamps (occlude intestinal lumen) and resect affected segment of lumen with wide margins
- rejoin sisde to side anastomosis single interrupted crushing sutures
- rinse intestine with saline and replace into abdomen
Describe the aetiology of intestinal volvulus ?
Intestinal volvulus
Pathology
This results from twisting of a segment of intestine upon itself - causing obstruction as well as stragulation of the blood supply.
- rapid distension of the bowel segment enclosed in volvulus and distension of intestine proximal to lesion.
- - caused by sudden fermentation of lactose with gas production and subsequent torsion.
Aetiologogy
- calves 3-6 weeks old condition is more common
- red gut
- associated with ad lib milk feeding systems (uncontrolled and excess intake).
-
Describe the clinical signs diagnosis of intestinal volvulus ?
Intestinal volvulus - the clinical signs
- temperature usually elevated
- HR increased
- animal dehydrated and recumbent (circulatory failure)
**Rectal examination = multiple gas distended loops of small intestine
**
- may be palpable
Definitive diagnosis
- Affected calves - severe unrelenting pain, with death following within 12 hrs
- sudden death
Describe how you would go about treating a case of intestinal volvulus ?
Intestinal volvulus - Treatment
Surgical correction
- right paralumbar fossa in standing animal
- make liberal vertical incision
- determine site and direction of twist by following mesentery to its root
- manipulate and reposition involved intestine within abdominal cavity
- surgery may be successful if a diagnosis is made early
- intravenous fluids and antibiotics indicated.
Describe the aetiology behind a phytobezoar ?
Phytobezoar - aetiology
Phytobezoars are fibre balls
- may occur when fibrous feeds make up a large part of a cow’s diet
- pastures with a large amount of onion grass (onion weed)
- large phytobezoars usually lodge in the abomasum
- smaller phytobezoars pass abomasum into small intestine (largely lodging in ascending part of duodenum
- small phytobezoars may occurs in any part of the small intestine.
Describe the presenting and clinical signs of a phytobezoar ?
Phytobezoar - fibre balls
Presenting signs
- loss of fluids and electrolytes
- sudden reduction in milk yeild to virtually nothing
- colic in early stages - restlessness - kicking at abdomen
Clinical signs
- faeces reduced and somewhat pasty
- more advanced disease = grey yellow faeces that are pasty and foul smelling (like inspissated mayonaise) / pathognomonic
- greenish rumen fluid discharge from nostrils
- fluid splashing sounds ballottement / auscultation of lower right abdomen
It is rare that a phytobezoar can be detected on rectal exam.
Describe a Trichobezoars and theirs clinical signs ?
Trichobezoars
Hair balls form in the rumen or abomasum - caused by frequent ingestion of hair.
This is a common incidental finding at postmortem
- variable found PM poor grwon calves
- seen in older cattle with lice (licking and shedding)
- rarely blockage of the pylorus may occur - same clinical picture as a physical obstruction of the pylorus
Describe the risk factors leading to dilation, volvulus and torsion of the caecum ?
**Dilation, volvulus and torsion of the caecum
Risk factors**
Occurs sporadically in cattle fed restricted roughage and high levels of concentrates + may also occur following a change in pasture.
Dilation: distension without a twist
Volvulus: apex of caecum rotated cranially and caecal body becomes distended (not a real torsion / a kink upon itself)
Torsion: rotation of caecum along its axis (relatively rare condition).
Describe the pathology underlinging dilation, volvulus and torsion of the caecum ?
Dilation, volvulus and torsion of the caecum
Pathology
- low fibre / high concentrates
- incompleted fermented starches escape from the fore stomaches and are metabolised in the caecum
- resulting VFA cause hypomotility
- PH of caecal contents is lowered / more acidic, further inhibiting motility
- this results in an accumulation of fluid and gas in the caecum
- dilation - displacement, impaction and possible torsion follow
Describe the presenting signs of dilation and volvulus of the caecum ?
Presenting signs Dilation and volvulus
- well feed high producing dairy cow
- usually within 60 days of partuition
- reduced milk yeild
- reduced appetite
- mild abdominal discomfort
- decreased amount of faeces
Describe the clinical signs of Dilationof the caecum in cattle ?
Dilation and volvulus in cattle
Clinical signs
- right abdomen distended
- ping typically extends tuber coxae to 11th or 12th rib
- fluid splashing sounds may also be heard with simultaneous ballottement/auscultation
- rumen activity is usually normal
Rectal examination
- distended caecum / palpated as a tubular movable organ 12-20cm in diameter
- palpation of dilated blind end of caecum protruding into pelvic cavity is diagnostic
- (not possible with retroflexed caecum)
Describe the clinical signs of volvulus and torsion of the caecum ?
Volvulus or torsion
Clinical signs
- onset is more acute
- abdominal pain
- sharp decline in milk production
- HR and RR increased
- right abdomen markedly extended
- dehydration
- very scant faeces
Ping in paralumbar fossa - extending over a greater area with than caecal dilation (tuber coxae - 9th rib)
rectal exam: distended body of caecum palpable
Describe the treatment for caecal dilation and volvulus ?
Caecal dilation and medical treatment
Can only be carried out in simple caecal dilation (not volvulus or torsion)
Medical treatment
- calcium borogluconate infusions
- feeding good quality hay
- spasmolyticum (Buscopan) i/v
- when using these drugs, feed should be withheld for atleast 24 hours - then gradually increasing amounts of good quality hay
- monitor animal closely
Surgical treatment (indicated HR >90, abdominal pain persist)
- preoperative analgesia
- right flank laparotomy
- grossly distended apex of caecum is exteriorised
- caecum drained
- contents are milked towrads enterotomy site and caecum rinsed
- incision is closed and caecum rinsed
- greater omentum is pulled caudally across the incision site
- wound closed
Describe the aetiology of Jejunal haemorrhage syndrome ?
Jejunal haemorrhagic syndrome
Massive progressive haemorrhage occurs in segments of jejunum - leading to obstruction and blood clots.
Aetiology
- relatively new disease of dairy cows
- risk factors include feeding silage and diets high in concentrates
- high production early in lactation
- usually sporadic, but may occur in clusters within herds
- very case fatality rate, often found dead.
Describe the presenting and clinical signs of Jejunal haemorrhage syndrome ?
Jejunal haemorrhage syndrome
Very high case fatality rate - often found dead.
Presenting signs
- acute + severe drop in milk production
- dark bloody faeces small volume of
- diarrhoea containing frank blood
- recumbant collapse
- weak depressed
- anorexia
- predominantly right sided distension
Clinical signsHR > 100pbm
signs of shock (pale mucous membranes, poor CRT sunken eyes)
tooth grinding vocalisation, kicking at abdomen
fluid splashing sounds
Diagnosis on exploratory laparotomy or post mortem
Rectal exam
- multiple loops of distended small intestine
- segments of sausage within each
Identify 6 aetiologies which could result in peritonitis ?
Aetiologies of peritonitis
- Traumatic reticulitis
- perforation of abomasal ulcer
- prforation of intestinal ulcer
- metritis, dystocia and uterine rupture
- penetrating abdominal wounds
- rumenitis secondary to acidosis
- abdominal surgery (eg caesarian, laparotomy)
Uncommon causes of
- intra peritoneal injections (eg calcium deposits)
- accidental toggling of small intestine.
Describe the clinical signs, which would make you suspect peritonitis ?
Describe how you woul;d confirm your suspicions ?
Peritonitis
(Inflammation of the peritoneum / abdominal walls)
Clinical signs
- toxaemia
- shock
- pain (grunt test)
- paralytic ileus
- bilateral abdominal distension
Fibrin deposition and adhesion formation
- may interfer with gut motility eg diarrhea
- mechanical or functional intestinal obstruction
How would you go about confirming peritonitis
Abdominocentitis
- healthy cows large volume 1-5 ml
- if nucleated cell count >12 -30,00 pep ml and protein >20g/L
Peritonitis can be classified as acute, chronic or peracute - describe the clinical signs of acute peritonitis ?
Acute peritonitis - Clinical signs
If untreated usually results in a gaunt appearance with a marked reduction in abdominal girth.
- initially fever
- elevated HR and RR
- grunting at expiration and painful expression
- rumen contractions are absent or reduced
- reluctance to move stiff gait (cautious and slow to rise)
- deep palpation reveals tense musculature / guarding of the abdomen.
- reduced faeces
Fibrin (roughening, sticking) and early adhesions - which may still be seperated on rectal palpation.
Describe the clinical signs of chronic peritonitis ?
Chronic peritonitis
Clinical signs
- severe weight loss “tucked up appearance”
- rumen contraction become weak
- abdominal distension (with peritoneal effusion)
- firm, fibrous adhesions may be felt upon rectal exam
- +/- diarrhoea
Describe what you would observe in the case of local peritonitis ?
Localised (focal) peritonitis
Clinical signs
Localised pain
- Pain on deep palpation of abdominal wall
- Positive grunt test (best heard by listening over trachea)
- firm upward push with closed fist
- pinching of withers
- kneeing or upward lift of xiphoid sternum
What is the prognosis and treatment for peritonitis ?
Peritonitis
Prognosis
Diffuse - related to severeity of clinical signs and degree of toxaemia but generally poor.
Localised (focal) - usually ok with aggressive and prompty treatment
Chronic - unfaveorable.
Treatment
Broad spectrum antibiotics (eg oxytetracyclines)
- confinement and ‘cage rest’
- peritoneal lavage is of limited value in cattle
- depending on prognosis no treatment euthansia or salvage slaughter
What are the most common causes of ascites in cattle ?
Ascites in cattle
(severe liver disease, cardiac disease or hypoproteinaemia)
bilateral distension of abdomen (submarine contour) or dependant odema brisket, ventrally or submandibular.
Severe liver disease
- portal hypertension arising venous blockagge
- increased hydrostatic pressure and leakage of protein in peritoneal cavity
- acute copper poisoning, cirrhosis, fasciolosis
Cardiac disease
- reduced cardiac out put - increased venous pressure
- passive venous congestion - leads to excessive capillary filtration (monensin toxicosis)
Hypoproteinaemia
- Johne’s disease
- reduction of albumin concentration gradient - fall in protein serum
What disease could you expect observing distension in these quadrants ?
Describe the pathology and clinical signs of a ruminal drinker
Ruminal drinker
Abdominal distension in a calf
Pathology
Milk entering the rumen sporadically or repeatedly
Rumen putrefication follows;
- rumen PH falls significantly
- overgrowth of proteolytic bacteria
- moderate rumen tympany
- may have bits of milk clot in rumen fluid - greyish in colour and rancid.
What are the common bacterial causes of diarrhea in cattle ?
What are the common causes of viral diarrhoea in cattle ?
What are the common parasitic causes of diarrhoea in cattle ?
What are the common nutritional and toxic causes of diarrhea in cattle ?
Bovine diarrhoea
Nutritional
- copper deficiency
- acute copper toxicity
- cobalt deficiency
- selenium deficiency
- lush rapidly grwoing pasture (low NDF), NZ
Toxicities
- arsenic
- salt
- mercury
- molybdenum
- mycotoxins
Describe how you would expect salmonella to present ?
Identify salmonella species ?
Salmonella
Presentation
The most common disease associated with acute diarrhoea in adult dairy cows.
- world wide distribution
- many animals affected
- carrier animals shed the organism when stressed
Species
S. Typhimurium
- predominate species in Australia
- zoonotic
- enteritis
- carriers for 3-4 months
S. Dublin
- reported some states (exotic NZ)
- host adapted to cattle
- latent carrier status, excrete during periods of stress
- liver fluke damage to bile ducts
- abortion
S. Brandenburg
- common NZ
- can spread from sheep to cattle
- enteritis and septicaemia
- sporadic abortions.
Describe the infectious route and pathogenesis of salmonella ?
Salmonella
Infection occurs through ingestion
- faecal oral route
- clinically affected and carrier animals
- feedstufffs contaminated with faeces
- fomites
- abortus material (Dublin)
- organism may persist in the environment for years
Pathogenesis
- bacteria invade enterocytes - and colonise the distal small intestine and colon
- produce enterotoxins
- which cause damage to villi - inflammation and necrosis of the mucosa - maldigestion and malabsorption
Carrier state
Organisms survive within macrophages mesenteric lymph nodes, gall bladder and bile ducts.
What facotors on farm could predispose the herd to an outbreak of salmonella ?
Risk factors for salmonella
- overcrowding
- partuition (decreased immunity)
- concurrent disease (BVD, IBR, liver fluke)
- sudden dietary changes
- stress
- poor body condition
- magnesium oxide supplementation (PH buffer)
- dexmethosane (abortion)
- effluent on pastures
- following major surgery (may precipiate disease in carrier animals)
Describe the clinical signs of salmonella in cattle ?
Salmonella clinical signs mature cattle
(many cattle affected)
Syndromes
- acute septicaemia and death
- chronic diarrhea =/- dysentery, weight loss
- carrier state / asymptomatic
Clinical signs
The severeity of signs and morbidity + mortality may vary considerably
- dysentary (bloody diarrhoea) + mucosal shed
- sudden + severe drop milk production
- profuse foul smalling watery diarrhoea - sheds of mucosa and fibrin casts
- dullness loss of appetite
- usually marked elevated temperature
- dehydration, weight loss and possible death
- some will be less severe - less severe diarrhoea
Describe the clinical signs of samonella in calves ?
Salmonella calves
Usually 2-6 weeks of age, variable clinical signs
- fever
- dullness, loss of appetite
- usually an elevated temperature
brown / grey pasty scour - leads to foul smelling diarrhoea with blood, mucous, sloughed mucosa
- dehydration weight loss
- weakness, gaunt appearance
- septicaemia / bacteraemia leading to pneumonia and meningitis.
Describe how you would diagnose salmonella ?
Diagnosis salmonella
Faecal culture in live animals
- you must sample a number of animals due to intermittent shedding
Post mortem examination
- may have haemorrhagic enterititis
- watery malodorous intestinal contents - pseudomembranes in lumen
- take swabs from the gall bladder and intestines (bacterial culture)
- sample; liver, spleen, mesenteric lymph nodes and intestines (culture and histopathology)
Describe how you would treat cases of salmonella ?
Salmonella treatment
- parental broad spectrum antibiotics
- Trimethoprim, sulphonamide, ceftiofur and oxytetracycline
- prognosis is reasonable given prompt treatment
- fluid therapy (hypertonic saline) + water via stomache tube
- NSAIDS (flunixin)
remember during treatment there is a zoonotic risk.
Describe what practices could be implemented to prevent salmonellosis outbreak in mature cattle ?
Salmonella
- isolate clinical cases and treat
- reduce stocking rate
- prevent contamination of food and water supplies (faecal contamination)
- spell pastures for 4-5 weeks after spreading effluent
- closed herd policy - avoid carrier introduction
- rodent and bird control.
- take care MgO supplementation and with overall grain feeding.
- take care zoonotic observe personal hygiene (untreated milk not to be consumed).
Vaccination (Bovillis) only if an outbreak is likely + can be used to provide clostral immunity administer 8 weeks prior to calving
Describe how you could prevent salmonella in calves ?
Prevention of salmonella in calves
Careful sourcing of calves; closed herd policy; avoid sales yard
- quarantine newly introduced stock
- strict cleaning and hygiene, pens utensils and staff
- adopt an all in / all out policy
- isolate and treat clinical cases
- vaccinate calves at any age and boost 3-4 weeks later (from 8 weeks of age if vaccinating dams).
Describe the aetiology of Johnes disease in cattle ?
Aetiology Johnes disease
Paratuberculosis - Mycobacterium avium (MAP)
The most common disease causing chronic diarrhoea in adult cattle.
- zones abolished 2016 / QLD used to be free
- cattle sheep and bison affected (strict seperation of species)
- slow developing disease with clinical signs typically appearing after 4 years of age (may be earlier with severe challange)
- long prepatent period where large numbers of bacteria are excreted
- essentially an endemic problem of a particular herd: mortality 1%
Describe the transmission Johne’s disease ?
Johne’s disease
Transmission
Horizontal before 6months of age (calves<30days old are most susceptable/ adults above 12 months unlikely to become infected).
- faecal oral route
- colostrum and milk from infected calves (first 30 days of life)
- contaminated water, semen, faeces, respiratory route
Vertical transmission (transplacental)
Describe the pathology of Johnes disease ?
Johnes disease
Pathology
- chronic granulomatous enteritis
- lymphangitis of mesenteric lymphatics, enlargement of mesenteric lymph nodes
- generlised disease with most organs affected
All diagnostics tests have good specificity but low sensitivity esp during the early course of disease.
Describe the three broad categories of Johne’s disease ?
The three broad categories of Johnes disease
- Animal becomes resistant
- no clinical disease or faecal shedding (cell mediated immunity is detectable, but serum antibody response is poor) - Intermediate stage
- infection partially controlled - subclinical disease and intermittent shedding - Infection progresses
- to clinical disease and heavy shedding. (Serum antibody response is strong, but cell mediated immunity is weak)
Describe the clinical signs of Johne’s
Johne’s disease
The incubation period for Johne’s is prolonged typically exceeding several years.
Year 1, 2 = unlikely to be shedding
Disease is usually induced by stressors such as calving or poor nutrition
year >4 high doses infective bacteria are excreted into the environment.
Clinical signs
- hose pipe diarrhoea
- Chronic weight loss, despite normal appetite
- Diarrhoea initially intermittent but becomes continuous (malabsorption, protein losing)
- brisket oedema
Production losses (poor milk yeild, reduced fertility).
coat depigmentation in some cases
Describe your expected findings on post mortem of a Johne’s case ?
Johne’s post mortem
- Thickening and folding (corrugation) of intestinal mucosa
- granulomas develop at ileal sites
- spreads to lymph nodes - pronounced
lymphatic vessels, and enlarged oedematous mesenteric lymph nodes
large numbers of acid fast bacilli in macrophages on histopathology.
Describe how you could diagnose a case of Johne’s disease ?
Johne’s disease
Low sensitivity
- relatively easy at stage 4, 3 when there is obvious clinical signs and high numbers of bacteria
- no single reliable conformation test for Johne’s
Test
Post mortem examination and histopathology - sensitive + specific
- terminal ileum and lymph nodes are primary sites
Live animals
- positive faecal culture (can take upto 6 months) clumps of acid fast bacteria in faeces
- positive PCR (quicker)
- Serology to detect antibodies (not all cases ahve a detectable response).
- faecal culture and faecal PCR will not detect an infected animal if it is not shedding at the time of sampling (intermittent or early in infection)
- serology and bacteriology and only reliable in advanced cases
- ELISA
- AGID
Individual animal
Tests are limited by slow growth of bacteria or delayed immune response
- in early stages of disease may not be secreting sufficient bacteria for culture or have sufficient antibodies for detection.
Herds tests
- A large number of negative tests provides good evidence that infection is not present on the property
- animals sourced from this property are unlikely to be infected.
How many animals need to be tested to detect Johne’s ?
Test for large numbers
- sample test 200-300
- check test 50
- HEC - dairy only single sample of slurry
Describe management polices to implement in the control of Johne’s disease ?
Johne’s disease
Difficult to control due to long incubation, shedding by subclinical animals and low sensitivity of tests.
The options include;
- closed herd policy
- early identification and disposal of infected animals
- reduce faecal oral spread by minimizing exposure of calves to contaminated pasture and milk
- use commercial milk replacer
- do not allow new born calves to suckle
- prevent contamination of feed and water
- prevent young stock from having contact with faecal material of mature cows
- biosecurity plan (J bas assurance score)
- vaccination only available for heavily infected herds (Gudair)
What is the Johne’s disease 3 step program for calves ?
Johne’s three step program for calves
Central to Dairy Australia’s reccomendations for controlling Johne’s
Three steps
1. Calves removed from cows within 12 hours of birth
2. Ensure no effluent from susceptable species comes into contact with calves in calving area
3. Calves upto 12 months of age should be reared on pastures that, during the past 12 months have not had adult stock or stock known to carry BJD.
What is JBAS ?
Johne’s Dairy score
J-BAS Johne’s beef assurance score = equates to dairy score.
Dairy score
7-8) Property actively managing to prevent infection entering.
High assurance.
2-6) Focus is to minimise impact of disease
1) No management of risk, or testing
Describe LPA ?
LPA accreditation
livestock production inssurance
- Australia’s inssurance program
- LPA accredited producers must have a biosecurity plan
- LPA national vendor declaration (NVD) is required for all livestock movements
- a biosecurity plan should include elements that identify the risk of entry of Johne’s and measures to protect against these risks
- JBAS score
note Johne’s has the potential to be zoonotic.
Describe the aetiology of Yersinosis ?
Yersinosis
(Yersinia pseudotuberculosis)
Sporadic cause of enteritis / ill thrift in cattle
- organism may be present as a normal gut inhabitant
- disease usually presents as single cases, although outbreaks do occur
- usually yearling cattle - occassionally younger cattle after weaning and in adults
- often animals of good condition
- often seen in inclement weather
Describe the spread of yersinosis and the risk factors ?
Yersinosis
Transmission
- faecal oral route
- pigs, rodents, and deer may be reservoirs of infection
Infection usually requires other risk factors such as
- inclement weather
- concurrent infection
- management stresses (mustering, parasitism)
- trace element deficiencies (Cu, Se) are also associated with the develooment of disease.
Describe the clinical signs of Yersiniosis ?
Yersiniosis clinical signs
- Diarrhoea - often chronic, green brown faeces with no smell without bad odour
- anorexia
- depression, dehydration and wasting
- potential high fever
- more often chronic than acute
- poor growth
- stunting or wasting
(not necessarily accompanied by diarrhoea)
Describe how you could diagnose and treat a case of yersinosis ?
Yersinosis
Diagnosis
- isolate organism from faces (+ve faecal) not nessarily diagnostic but a heavy growth is indicative of infection
- neutrophilia left shift
- anaemia
- hypoproteinaemia
Post mortem
- ulcerative enterocolitis on histopathology
Treatment
Parental antibiotics broad spectrum
- Trimethoprim
- Sulphonamide
- Oxytetracycline
- prognosis is good
- Fluid therapy
- Identify the most important clinical anatomical landmarks of the bovine head ?
- Demonstrate and explain how to clinically examine the bovine head and interpret findings ?
The most clinically significant anatomical landmarks of the bovine head
- teeth
- buccal mucosa
- tongue
- jaw
- oesophagus
Bovine head examination
- examine head for asymetry
- examine both eyes
- best using a mouth gag and torch
- if needed, can view by holding the tongue (if not painful to one side)
You treat examine a cow with excessive salivation but no oral vessicles or erosions.
Write down a differentials list ?
Excessive salivation and no vesicles or erosions
Differentials
Many animals involved
- heat stress (Bos taurus in tropics)
- botulism
- ephemeral fever
Individual animals affected
- woody toungue
- oral trauma/ foreign body
- early stages of hypomagnesaemia
- mal-eruption of incisors/ infected tooth pockets
- choke (upper and lower oesophagus); complete or partial obstruction following feeding on potatoes, turnips.
- botulism
- pharmaceuticals eg xylazine
You examine a cow with excessive salivation, and oral vesicles and erosisons.
Write a differentials list.
Cow excessive salivation, oral vesicles or erosions
Differentials list
Multiple animals involved
- Foot and mouth disease
- vasicular stomatitis (Rhabdoviridae, zoonotic)
- bluetingue
- rinderpest ( eradicated world wide)
- chemical irritants
- toxic plants eg lantana
Only individual animals involved
- bovine viral diarrhoea/mucosal disease (BVD?MD)
- malignant catarrhal fever (MCF)
What are the consequences of excessive salivation ?
Bovine saliva (50-150L produced per day)
Components
- water (rumen hydration)
- bicarb (rumen buffer)
- PO4-2 (higher than serum)
- Na+ (slightly higher than in serum
- K (higher then in serum)
The consequences of excessive salivation
- dehydration
- bi carb loss so rumen may become acidotic
Describe how you can age cattle, using the incisor eruption time frames as a guidline ?
Cattle aging through incisor eruption times.
(The age of an animal is often reffered to by the number of permenant teeth).
Incisor teeth
Two permenant teeth = two years old
6 permanent teeth = 3.5-4 years of age
Full set of permanent teeth (8 tooth) = 4-5 years of age
Describe the clinical signs, diagnosis of Fluorosis ?
Fluorosis
Is the chronic ingestion of excess fluride (industrial pollution, deep water wells, contaminated phosphate supplements or volcanic ash).
Clinical signs
- brittle, fast wearing
- calky instead of glistening
- cattle exposed < 3 years of age (ameloblast cell activity), older cattle are more resistant to dental lesions
- osteoporosis (bone weakness; lameness)
- wasting
Diagnosis
- coccygeal bone amputation and bone fluride content evaluation
- urine fluid concentrations
- post mortem; enlarged porous bones, chalky.
Describe this pathology and its potential management ?
Cleft palate
sporadically found in cattle and sheep
- failure of midline fusion during foetal development
- sometimes associated with other congenital defects
- heritability possible (Herefore, Charolais)
Presenting signs
- Difficulty in feeding and breathing: milk may reflux through the nostril
- consequential aspiration pneumonia
- subsequent poor growth/ ill thrift
Describe the aetiology and clinical signs of Actinobacillosis ?
Actinobacillosis - wooden toungue
The bacteria is normal inhabitant of the mouth
- infection follows abrasion / traumatic injury of the oral mucosa
- following teeth eruptions
- grazing abrasive pasture
- high prevalence in areas of copper deficiency
Clinical signs
- salivation
- gentle toungue chewing
- palpate toungue (swollen, hard)
- lymphadenitis (retropharyngeal lnn)
- atypical cutaneous form (abscess of moth, salivary glands)
- oesophageal groove involvement may result in rumen dysfunction.
Describe the most effective treatment for Actinbacillosis ?
Treatment for Actinobaccillosis
Treatment = sodium iodide
- Iv injection, diluted with sterile water usually only one dose is required
- occasionally a follow up dose 7-14 days later
In case of abscess
- surgical curette, irrigated with iodine and drainage if well circumscribed abscess
WATCH OUT FOR IODINE TOXICITY
- indicated by skin scaling, lacrimation, seromucoid nasal discharge, anorexia and coughing
Describe the aetiology, clinical signs and treatment of Actinomycosis ?
Actinomycosis - lumpy jaw
This is a G+ve anerobe and a normal inhabitant of the mouth
- gains access to bony structures through lymphatic drainage of oral trauma
- tooth root injury
- molar teeth eruption
Clinical signs
- Pyogranulomatous osteitis / osteomyelitis of mandible > maxilla > soft tissue > GIT > lungs
Treatment
- IV diluted sodium iodide
- prevent further bone growth
- if only bone growth - prognosis is good
- if animal is unable to eat the prognosis is grave (malalignment cheek teeth, fractured jaw).
Case study: cow with submandibular oedema.
The swelling under the jaw can be from several causes identify 5 ?
Five causes of submandibular swelling
- Injuries
- under toungue or pharynx; often caused by balling or drenching gun
- early signs = inappetance, abscesses, discharging sinuses
Grass seed abscess
- common in Aus summer/autumn
- seed penetrate buccal mucosa - abscess formation
- surgical drainage and iodine lavage
Blocked salivary ducts
- salivary ducts opens on ventral tongue, rostral to frenulum
- massage blocked salivary gland (push out foreign body), drainage of purulant fluid
Phlegmonous cellulitis
- Fusobacterium necrophorum
- subandibular swelling
- depression off milk
- high temperature and HR
- toxaemia and death
- palpation of fluid not oedema
- establish drainage and high doses of procaine penicillin
Clinical case. You are presented with a cow with a history of eating potatoes presenting with excessive salivation and bloat ?
What is your number one differential.
Choke
Choke is associated with feeding practice
- potatoes
- turnips, fruit
- this causes a complete or partial obstruction of the oesophagus
- secondary bloat
Clinical signs
- excessive salivation (severe)
- discomfort, chewing
- sudden bloat
Describe the pathology and clinical signs of Enzootic nasal granuloma ?
Enzootic nasal granuloma
Pathology
Nasal mucosa swelling causing difficult noisy breathing
- may be caused by a stuck foreign body
- nasal granuloma
Clinical signs
- progressive stertorous breathing (back of throat noise).
- acute onset bilateral nasal or ocular discharge
- head shaking and nose rubbing
- if nose is palpated feel firm polyps/nodules
- drop in milk production in affected cattle
- not fatal
Describe the pathology and clinical signs of sinusitis ?
Sinusitis
(Treat with local and systemic antibiotics)
flush sinus - rarely trepination of sinus is required
prevent by dehorning young animals in clean conditions.
Pathology
- usually as a result of dehorning older heifers or adult cattle
- most commonly trueperella pyogenes
- dirty conditions nad inclement weather
- poor technique
The clinical signs
might elicit a dull sound on frontal percussion
anorexia, lethargy
fever
frontal bone distortion
exophthalmos
abnormal posture
nasal horn / stump purulent discharge
Describe the aetiology of Infectious bovine keratoconjuctivitis (risk factor, causative agent, and transmission) ?
Infection bovine keratoconjuctivitis (IBK)
Haemolytic Moraxella bovis is the major causitive organism (G-ve)
- highly contagous disease
- rapidly spreads during the summer months via
Risk factors
- UV light
- dust
- long grass (irritation)
- flie (Musca spp)
- Host risk factors = breed Bos taurus, and pigmentation
Pathology
(Clinical signs exacerbated by concurrent infection IBR BOHV-1)
-bacteria utilize pili to adhere to the epithelial cells of the eye
- infected animals can remain carriers for upto 1 year - source of infection to others - disease may persist from year to year.
- outbreaks often follow the introduction of new cattle
Transmission
- direct contact
- face flies (mechanical vector)
- Inanimate fomites (grass, leaves, seed heads)
Describe the pathology underlying Infectious bovine keratoconjunctivitis ?
Infectious bovine keratoconjunctivitis - Morexalla bovis
Main causative organism is Moraxella bovis
(Chlamydia, mycoplasma, Rickettsia may also play a role).
Bacteria utilise pili to adhee to epithelial cells of the eye.
- neutrophils migrate to the site of infection - release enzymes
- corneal ulceration
- blood vessels grow from limbus towrds the centre of cornea; produces red/pink colour of eye
- granulation tissue
- accumulation of neutrophils result in creamy purulent material in center of lesion
- ulcer may rupture - collapse of eye (animal becomes permentantly blind)
Often there is spontaneous healing within 60 days
finally mild to severe scarring (white dot on eye-macule) - can lead to some problems with vision.
Describe the clinical signs of infectious keratoconjunctivitis ?
Infectious keratoconjunctivitis - Moraxella bovis
Clinical signs
- often unilateral but may be bilateral
- photophobia with (blepharospasm involuntary eyelid movements)
- epiphora lacrimation (tear staining of the face (initially serous becomming purulent)
- marked conjunctivitis
- negative effect on growth rate and production
- corneal oedema (opacity and temporary blindness)
Advanced cases have keratitis and corneal ulceration
neovascularistion in severe cases, with vessels progressing towards central lesion
Describe how you could go about treating a case of infectious bovine conjunctivitis ?
IBK - Treatment
Early treatment pinkeye ointment (cloxacillin)
- 2 treatments 48 hrs apart
- treat both eyes (ensure unaffected eye is treated first)
Subconjunctival injection 1-2ml procaine penicillin +/- dexmethasone
parental antibiotics; oxytetracycline
In severe cases provide aftercare
- cover eye with patch - reducing UV exposure, reduces pain
- in addition less chance of flies further spreading the infection
- third eyelid flap
- closure of eyelids temporarily by suturing
In a severe outbreak
- may consider a metaphylactic injection of oxytetracycline to all at risk cattle.
Describe the management strategies we could implement to prevent pink eye ?
Morexella Bovis - pink eye
Prevention
1. Control of flies - fly ear tags work well
2. seperation and isolation of infected animals
3. avoid grazing calves on long stalky pasture
4. avoid overcrowding
5. manage new stock seperately from the main herd
6. UV protection/ shade may help in severe outbreak
7. reject any new animals showing signs of pink eye
- Vaccinate Pilliguard
- vaccinate once 3-6 weeks prior to pink eye season
Describe the aetiology and clinical signs behind bovine irititis ?
Bovine irititis ‘silage eye’
This is associated Listeria monocytogenes
- common cause of uveititis in cattle fed baled silage or baleage
- conjunctival infection
Clinical signs
- uveitis = inflammation of the eye
- excess lacrimation
- blepharospasm
- photophobia
- miosis (pupil constriction)
- THERE IS NO CONJUNCTIVITIS = AND NO ULCERATION OF BOVINE IRITITIS
Describe how you could treat and prevent cases of bovine irrititis ?
Bovine irititis ‘silage eye’
Listeria monocytogenes
Without treatment the ocular lesions will regress after several weeks
- extremely painful condition
- Topical cloxacillin every 48hrs until it resolves
- subconjunctival injection procaine penicillin and dexmethasone
- attempting treatment of chronic cases has litle effect on resolution
Prevention
- rolling / spreading out big bale silage
Describe the aetiology and clinical signs and pathology of squamous cell carcinoma ?
Squamous cell carcinoma - cancer eye
Predisposing factors
- poor pigmentation eg at muco-cutaneous junctions, especially the eye but may also occur in the vulva or anus
- typically involves the third eyelid, medial canthus and lower eyelid margin and potentially the globe itself
- Poor pigmented cattle such as Holstein, Hereford, Ayrshire susceptable (attempt to cross breed with a dark faced sire).
Clinical signs
- initially unilateral blepharospasm and ocular discharge due to mechanical irritation of the cornea
- grows to obvious swelling / lesion
- local invasion of ocular tissues is common, but metastatic spread to regional lymph node is rare
Describe the pathogenesis underlying SCC of the bovine eye ?
Pathogenesis SCC - cancer eye
- arise following prolonged exposure to UV radiation
- tumour develops through a series of non malignant stages (plaques and papillomas). into invasive malignant carcinoma
- tumours of the globe spread relatively slowly
- tumours of the 3rd eyelid and lower eyelid - spread more rapidly into tissues of the orbit and orbits bony surroundings.
Malignant tumours are more irregular, haemorrhagic and often necrotic
