Farm Flashcards
predisposition of simple indigestion
most common in cattle, rare In sheep and goats
cause of simple indigestipn
sudden changes in food or “mistakes” of nutrition
aetiology of simple indigestion
- any dietary factor that can alter the intraruminal environment (spoiled or frozen feed too)
- introducing urea to a ration
- accumulation of excessive quantities of relatively indigestible feed that can impair function
- turning cattle onto a lush cereal grain pasture… etc
signs of simple indigestion
anorexia and moderate drop in milk production, rumen is fully, firm and dough, faeces are normal to firm but reduce and can be soft-watery and foul smelling
diagnosis of simple indigestion
history, often multiple animals affect, hypocalcaemia present, rule out ketosis, rumen fluid analysis: reduced activity and concentration of large and small protozoa
treatment of simple indigestipn
- re-establish normal GI motility, pH and flora: by ruminal transfaunation
- feeding long-stem fibre
- parenteral calcium solution
- evacuate the GI tract
- correct suspected dietary factors
prognosis of simple indigestion
good
acute ruminal lactic acidosis aetiology
most severe form of indigestion, cattle can accidentally gain access to large quantities of grain, improper mixing of TMR (total mixed ration)
cause of grain overload
: sudden change to a diet containing higher levels of finely ground, rapidly fermentable feeds
pathogenesis of grain overload
- within 6 hours of ingestion, easily fermentable and high – sugar + starch concentrate is broken down to VFA, D and L lactic acid
- number of gram-positive bacteria increased amount of lactate rumen falls to <5 destroying protozoa, cellulolytic organisms impairs rumen motility osmotic pressure rise substantially results in movements of excessive quantities of fluid into the rumen causing rise of fluid ruminal contents and dehydration
consequence of acidosis and dehydration
haemoconcentration, cardiovascular collapse, renal failure, muscular weakness, shock, death
pH < 5.5
- low ruminal pH causes chemical rumenitis
- endotoxin and bacteria escape into the portal circulation
- septic emboli, dissemination in the liver, lungs, joints and kidney and laminitis3
signs of grain overload
anorexia, drastically decreased milk production, dehydration, subnormal temperature, elevated heart, elevated respiratory rates, totally static and enlarged rumen, cool skin surface, diarrhoea, or loose manure, weakness, ataxia, recumbency, abdominal pain, laminitis, coma and death
diagnosis of grain overload
history, confirmed by CE, assessment of rumen pH,
- CBC: neutropenia with left shift
- biochemistry: marked azotaemia
- metabolic acidosis
- rumen fluid analysis: sedimentation rate is fast, with a delayed or absent secondary flotation, decreased number of protozoa
treatment with grain overload
slaughter for salvage should be considered, restoration of rumen microenvironment
Mild cases
- rumen lavage with large tubes, application of large volume of warm water (15-20x), emptying the rumen via gravity flow, magnesium hydroxide diluted with water PO, laxative and charcoal IR
Serious cases
- rumenotomy and washed rumen, with water and emptied several times to remove as much lactate as possible
- fresh hay
- ruminal transfaunation, parenteral calcium, flunixin meglumine, procaine penicillin G at least 5 days
- thiamine
prognosis of grain overload
- good – quality hay and no grain should be given during the convalescent period, then introduced gradually, if good appetite returns within 3 days, prognosis = good
- some bacterial endotoxins can escape into circulation causing embolic infection of liver, lungs and other organs, resulting in fever and in some cases, death
cause of SARA
feeding of excessive quantities of concentrate with low level of well-structured fibrous roughage
pathogenesis of SARA
results from continued indigestion of these feeds over a prolonged period rather than sudden exposure without adequate adaption
signs of sARA
reduced or cyclic feed intake, decreased milk production, reduced milk fat, poor BCS, loose faeces
diagnosis of SARA
assessing rumen fluid samples or from telemetric rumen pH boluses sensors
treatment of SARA
no specific treatment, rather secondary conditions may need to be treated and the focus should be on prevention
cause of ruminal alkalosis
prolonged anorexia, poorly digestible roughage, simple indigestion, moudly food, spooield silage- coliform + proteins, high protein diets
pathogenesis of ruminal alkalosis
excessive ammonia, high protein diet ammonia concentration rises decomposition of proteins releases large amounts of ammonia that is absorbed into the blood liver detoxifies it by converting it to urea when the amount of absorbed ammonia is high intoxication occurs
- alkaline ruminal fluid pH occurs most commonly when microbial fermentation is reduced while the animal continues to ingest saliva
signs of ruminal alkalosis
inappetence, anorexia, ruminal hypomotility, recurrent tympany, occasional diarrhoea with odour, weakness, salivation, tachypnoea, polyuria, CNS excitation, muscle tremors, incoordination, abortions
diagnosis of ruminal alkalosis
history, CE, rumen fluid analysis (pH 7.8, blackish green, strong odour and poor protozoal activity)
treatment of ruminal alkalosis
- normalisation of rumen pH via food changes, antihistamines, vitamins, Ca, 5% acetate
- supportive therapies: anticonvulsant therapy (phenobarbital, pentobarbital), IV fluid
- urea poisoning: rapid intervention
prognosis for ruminal alkalosis
prognosis is poor for recumbent animals
define tympayn
over distension of the rumen, resulting in left-sided abdominal distension in both dorsal and ventral quadrants
frothy bloat
- resulting from stable froth of dietary origin (usually higher in chloroplast membrane fragments and soluble protein)
- coalescence of the small gas bubbles is inhibited
- intraluminal pressure Increases because eructation cannot occur
- cattle – grazing legume
free gas bloat
- occur secondary to over ingestion of grain, which promotes excessive VFA production, lower pH and then lactic acidosis with rumen stasis
- in calves with clostridial abomastitis-rumenitis
- oesophageal motility, vagal indigestion, hypocalcaemia, listeriosis, tetanus
- oesophageal obstruction due to foreign body
- stenosis of oesophagus or compression in lymphadenopathy or abscess
signs of tympany
- acute onset, commonly develops in 1st 3 days after on bloat producing pasture
- typically left sided distension extending dorsally to the midline with a full paralumbar fossa
- rectal examination: ruminal distension extending into the right abdomen dorsally and ventrally
diagnosis of tympayn
- frothy bloat is usually obvious clinically – not relieved by a stomach tube
- free-gas bloat is accompanied with signs of causative disorder – confirmed if stomach tube can be passed easily and relieves bloat
treatment of tympany
- relief of the ruminal distention and correction of the primary cause
- decompression with stomach tube
- additional treatment with antifoaming agents: poloxalene, polymerised methyl silicone (3.3$ emulsion, cattle 30-60mL, sheep 7-15mL), vegetable oil alone, mineral oil
- trocarisation for emergency relief: trocar and cannula can be inserted into the rumen through a small incision, if trocar fails then rumenotomy
prevention of tympany
- feeding hay before turning cattle on pasture
- mature pasture are less dangerous than rapidly growing pastures
- continual administration of an antifoaming agent during the risk period
ruminal drinking
Calves – have failure of the reticular groove reflex (milk flows into rumen + is fermented to lactate)
3–8-week-old dairy calves fed with milk mostly by bucket
aetiology of ruminal drinking
milk in reticulorumen is fermented and lactic acid is produced, drop in pH of rumen, absorption of organic acids metabolic acidosis
Chronic rumenitis hyperkeratosis/parakeratosis impairment of ruminal motility chronic and recurrent bloat
cause of ruminal drinking
stress
pathogenesis of ruminal drinking
fails to close milk flow directly into the rumen and is fermented to lactic acid
signs of ruminal drinking
depression, ataxia, weakness, diarrhoea/clay like faeces, dehydration
diagnosis of ruminal drinkin
history, CE, passage of stomach tube may cause reflux of a grey fetid fluid
treatment of ruminal drinking
removal of the contents and lavage with warm water via stomach tube. Flunixin meglumine (NSAIDs) to reduce inflammation from endotoxemia
prevention of ruminal drinkning
feeding small volume of milk from a nipple-bottle. Closure of reticular groove can be triggered by allowing the calf to suck a finger before the milk is offered
predisposition of traumatic reticuloperitonitis
dairy cattle, occasionally in beef, rarely in sheep and goats
cause of traumatic reticuloperitonitis
cattle don’t use lips to discriminate between fibrous feed + metabolic objects
pathogenesis of traumatic reticuloperitonitis
consequence of perforation of the reticulum with ingested foreign objects like nails and pieces of wire
- after ingestion, objects fall directly into the reticulum or pass into the rumen and in 24-48hr are propelled into the reticulum
- by ruminal contractions subsequently carried over the ruminoreticular fold into the cranioventral part of the reticulum
- reticulo-omasal orifice is elevated above the floor, which tends to retain heavy objects in the reticulum
- honeycomb like reticular mucosa traps sharp objects
- contractions of the reticulum promote penetration of the wall by the foreign object
signs of traumatic reticuloperitonitis
Local peritonitis:
- decreased milk production, sudden reticulorumen, atony, anorexia, increased temp, HR + RR, arched back (pain)
Diffuse peritonitis:
- fever, increased HR + RR, total rumen + GI stasis, grunting – diffuse persistent pain
Pleuritis
- depression, increased HR, pyrexia, muffled lung sounds
Pericarditis
- muffled heart sounds, splashing sounds, pericardial friction, jug vein distension
diagnosis of traumatic reticuloperitonitis
History, CE
- CBC
- Biochem: plasma fibrinogen, haptoglobin, amyloid A, total plasma protein
- metabolic alkalosis
- pain tests
- metal detectors, abdominal US and radiography
haptoglobin and amyloid A for inflammatory markers
treatment of traumatic reticuloperitonitis
- conservative medical treatment: oxytetracycline, antibiotics therapy (3-7days)
- symptomatic therapy (oral fluids, ruminotorics, calcium solutions, oral electrolyte)
- rumen transfuantes, magnet, stall rest
- metabolic alkalosis: potassium chloride orally
- surgical treatment: rumenotomy with manual removal of object from reticulum, drainage of reticular abscess into the lumen of reticulum
prevention of traumatic reticuloperitonitis
avoiding the use of bailing wire, keeping cattle away from sites of new construction, apply prophylactic magnets and electromagnetic plates
cause of vagal indigestion
traumatic reticuloperitonitis (anterior/posterior functional stenosis)
pathogenesis of vagal indigestion
Lesions affecting the ventral vagus nerve and its branches (injury, inflammation, or pressure) cause complex clinical signs of indigestion with intermittently or constantly ruminal distension
signs of vagal indigestion
decreased: appetite, milk production and HR but normal temp and RR
- L dorsal + R ventral distension distension = ‘papple’ shape
- fever, salivation, swelling abscess, neoplasia
diagnosis of vagal indigestion
- history of primary disorder, CE
- clinical pathology:
o persistent lymphocytosis lymphosarcoma
o elevated serum globulin may suggest reticular or liver abscess
o metabolic alkalosis - abdominal US
treatment of vagal indigestion (chronic indigestion)
surgery (rumenotomy), emptying the rumen, removing the foreign bodies, lancing abscess into reticulum, supportive therapy
prognosis of vagal indigestion
usually pooe
predisposition of abomasa displacement
during first 6 weeks of lactation, bull and calves at any age, most common in pluriparous cows, in 1st calf heifers, lactating cattle of any age
cause of abomasa dis[lacemetn
multifactorial, excessive production of VFA (increases gas production in abomasum), abomasal hypomotility (hypocalcaemia, ketosis, hypokalaemia, retained placenta, mastitis, metritis, indigestion)
LDA
- partially gas distended abomasum displaced upward along left abdo wall lateral to rumen
- fundus and greater curvature of abomasum primarily displaced
- which passes underneath rumen and retained
- abomasum obstruction is partial mild metabolic alkalosis
RDA
hypomotility, gas production and displacement of partially gas filled abomasum
abomasa volvulus
- serious, life threatening
- rotation of abomasum on mesenteric axis, impairs circulation and causes ischemia
- large quantity of chloride-rich fluid accumulates in abomasum
- moderate-severe dehydration
- it doesn’t follow in all cases of RDA
signs of abomasal displacement
- anorexia, decreased milk production, dull appearance, mild dehydration, TRIAS normal, rumen motility normal, LDA (ping 9-13th rib), RDA (ping 10-13th, dilated caecum, presence of fluid – splashing and tinkling sounds)
- AV: depressed, tachycardia
- if fever and pneumoperitoneum in cow with LDA abomasal perforation
- weakness, toxaemia, ping louder, caudal abomasum palpable rectally
diagnosis of abomsal dispalcemtn
- history: recent parturition, partial anorexia, decreased milk production
- rectal exam
o LDA medially displaced rumen and left kidney
o RDA occasionally palpable
o insert 9cm 18G spinal needle 2 inches below bottom of “ping” and aspirate, if pH < 5 = abomasal fluid - KB in milk and urine
- hypocholermic, hypokalaemia, metabolic alkalosis
- US
- L – lactate concentration: with AV <2mmol/L
treatment of abomasa displacement
- medically: oral laxatives – after eat as much hay as possible to fill rumen with roughage
- ruminotoric, antacids
- cholinergic medications
- supportive therapy: calcium solution, potassium chloride, electrolyte solution
- rolling: only for simple LDA, never for RDA or AV
- surgically: right flank omentopexy, left flank abomasopexy, right paramedian abomasopexy, left paralumbar abomasopexy
prevention of abomasa displacement
- ensuring rapid increase in rumen volume after calving
- maintaining adequate roughage in diet, feeding total mixed ration
- avoid rapid dietary changes and post parturition hypocalcaemia
predisposition of abomasa ulcers
dairy cattle and calves (first 4-6 weeks after parturition), prolonged inappetence, high volumes of milk, NSAIDs
cause of abomasa ulcers
multifactorial, intensive management, highly acidic, high-energy, finely ground diets consisting of concentrates and silage, high milk production, stress
pathogenesis of abomsal ulcers
when the thick layer of mucus that protects abomasum from digestive juice is reduced digestive acids eat away at the tissues that line the abomasum ulcer
classification of abomasa ulcres
- Type 1: is an erosion or ulcer without haemorrhage
- Type 2: is haemorrhagic
- Type 3: is perforated with acute localised peritonitis
- Type 4: is perforated with acute diffuse peritonitis
- Type 5: is perforated with peritonitis within the omental bursa
signs of abomasa ulcers
mild abdominal pain, bruxism, tachycardia, melena, severe haemorrhage (pale MM, cold)
- perforating ulcers (localised peritonitis): anorexia, fever, pain, rumen hypomotility/stasis
- diffuse peritonitis: anorexia, complete stasis, fever, cold skin, dehydration, grunt or groan
- progression to recumbency
diagnosis of abomsal ulcers
- history, CE
- occult blood test of faeces to confirm melena
- PCV can be used to determine degree of haemorrhage
- X-rays, US
- inflammatory exudate and evaluation of peritoneal fluid (confirms peritonitis)
- WBC, serum albumin and TP = low
treatment of abomsal ulcers
- local peritonitis: stall rest, broad spectrum ATB, histamine type 2 blockers IV, PPI
- corticosteroids and NSAID are contraindicated as they may contribute to further ulceration
- bleeding ulcers: blood transfusion and fluid therapy
prognosis of abomsal ulcers
- localised peritonitis: good, takes about 1-2 weeks recovery
- diffuse peritonitis: grave – if they recover, usually have massive abdominal adhesions
prevention of abomasa ulcers
avoid prolonged periods of inappetence and low abomasal pH
abomasa impaction predisposition
pregnant beef cows during winter month, rare in dairy, calves (idiopathic)
cause of abomasa impaction
probably related to abomasal hypomotility or dietary impaction due to ingestion of poorly digestible material
signs of abomasal impaction
complete anorexia, scant faeces, moderate distension of abdomen, weakness, weight loss, decreased milk production, grinding teeth
diagnosis of abomasa Impaction
- Rectal exam: enlargement of the rumen dorsal and ventral sacs
- metabolic alkalosis and haemoconcentration
- objective: during right/left side exploratory laparotomy or rumenotomy
treatment of abomasa impaction
- idiopathic abomasal impaction massage via right flank laparotomy and administration of mineral oil, coffee or magnesium products
- rumenotomy: empty rumen and infuse mineral oil directly into abomasum through orifice, often poor prognosis
- prokinetic agents: erythromycin, bethanechol, lidocaine constant rate
prognosis of abomasa impaction
good if primary disorder or dietary impaction treated early, but often poor
predisposition of Abomasitis, abomasal tympany and abomasal ulceration in calves
beef calves, lamb and dairy calves, more common in bucket fed calves than bottle
cause of Abomasitis, abomasal tympany and abomasal ulceration in calves
clostridium perfingens type A, sarcina, salmonella typhimurium DT104
signs of abomasitis, abomasal tympany and abomasal ulceration in calves
acute abdominal bloat, anorexia, shock, diarrhoea, distension of both sides, gas filled abdomen
abomasitis, abomasal tympany and abomasal ulceration in calves diagnosis
metabolic acidosis, respiratory acidosis
- low serum chloride, azotaemia, elevated PCV
- immature and toxic-appearing neutrophils
- US: fluid + gas may be seen throughout right and left ventral abdomen
- oedematous and thickened wall of abomasum
treatment of abomasitis, abomasal tympany and abomasal ulceration in calves
intensive: colloids, crystalloids, systemic antibiotics
prevention of abomasitis, abomasal tympany and abomasal ulceration in calves
routine disinfection of equipment, feeding milk at body temperature, isolation of affected calves, use of bottle rather than bucket
cause of obstructive diseases of SI
- intussusception of jejunum and ileum
- volvulus of duodenal sigmoid flexure or caecocolic
- luminal occlusion of jejunum (blood clot, mural thickening, extramural mass, herniation)
- atresia coli, recti and ani
- faecal impactions of small intestine
signs of obstructive diseases of SI
acute onset of anorexia and GI stasis, milk production in lactating cows drops suddenly, abdominal distension, colic, absence of manure production
diagnosis of obstructive diseases of SI
- rectal examination: distended loops of bowel may be palpable and intussusception and fibrous bands
- fluid may be heard on simultaneous ballottement and auscultation of right side of abdomen
- US: distended loops of small bowel
- biochemistry: hypokalaemia, hypocholermic, metabolic acidosis
treatment of obstructive diseases of SI
- right sided exploratory laparotomy
- supportive therapy
prognosis of obstructive disease of SI
varies, economically may dictate slaughter
what is fat necrosis
Hard masses in the mesentery and omentum that gradually causes partial or complete extraluminal intestinal obstruction
predisposition of fat necrosis
usually over conditioned middle-aged to old
pathogenesis of fat necrosis
fat necrosis rectal constriction occurs establishing a risk for iatrogenic rectal injury during rectal palpation
signs of fat necrosi
partial anorexia, loose manure, occasional abdominal distension or mild colic
diagnosis of fat necrosis
rectal exam: hard mass around S.I, rectum or colon. US: biopsy or exploratory laparotomy to confirm
treatment of fat necrosis
exploratory laparotomy and surgical removal
prognosis of fat necrosis
bad
predisposition (+ predisposing factors) of caecal dilation and volvulus
dairy cattle, early lactation
: hypocalcaemia, indigestion and endotoxemia
cause of caecal dilation and volvulus
hypocalcaemia, endotoxemia secondary to metritis or mastitis and indigestion
pathogenesis of caecal dilation and volvulus
- In simple caecal dilatation, the caecum distends with gas and fluid and the apex begins to rise in the abdomen from its normal location toward or into the pelvic inlet
- Further distension of the caecum leads to rotation of the caecum (CW direction) as viewed from the right side or a ventral or dorsal retroflexion
signs of caecal dilation and volvulus
inappetence, reduced manure production, mild/moderate abdominal distension, < milk production, colic, dehydration
diagnosis of dilation
- right sided ping by simultaneous percussion and auscultation (paralumbar fossa to 1-3rd rib cranial)
- right paralumbar fossa appears “full”
- rectal: dilated caecum easily palpable in right caudal abdomen, apex of caecum is directed into pelvic inlet
diagnosis of volvulus
- signs more remarkable + metabolic alkalosis
- large ping in R caudal abdo
- rectal = dilation + volvulus, maybe distended ileum
treatment of caecal dilation ad volvulus
- medical: caecal dilatation with stable patients
o laxative ruminotoric (mixed with warm water using a stomach tube)
o transfaunation
o calcium and potassium solution
o diet: avoid highly fermentable feeds
o treatment must continue for 3-7 days - surgical treatment: right flank laparotomy followed by typhlotomy
what is downer cow syndrome
Non-ambulatory cattle recumbent for at least 24 hours without obvious reason
predisposition of downer cow syndrmoe
dairy cows (with previous episodes of milk fever), beef (after prolonged/difficult calving), delay of >4hr in treatment for recumbent milk-fever cows, hypophosphatemia and/or hypokalaemia
cause of downer cow syndrome
ischemic myopathy of large muscles of pelvic limb, ischemic neuropathies, secondary to prolonged recumbency, traumatic injury
compartment syndrome (downer)
Compartment of the body is composed of muscle and nerves within an anatomically defined area that is surrounded by a rigid muscle fascia layer 6 hours
mechanical constriction of the venous draining leads to ischaemic muscle and nerve necrosis.
crush syndrome (downer)
Refers to the sum of the systemic effects of extensive muscle tissue injury and is attributed to the massive release of muscle-tissue breakdown products into the blood circulation
muscle breakdown releases myoglobin, which can cause renal failure, and potassium which can cause heart failure.
signs of downer cow
Alert downer:
- unable to stand, sternal recumbency, normal mental status, appetite and thirst normal/mildly decreased
Non-alert:
- persistent recumbency, altered mentation and vital signs, unable to maintain sternal recumbency, abnormal position of legs
Creeper cows
- alert recumbent, cows unable to bear weight on hindlimbs but use forelimbs to crawl
diagnosis of downer cow
- increased serum activity of CK and AST
- Serum P and K conc may be decreased/increased
- proteinuria, myoglobinuria
- ischemic necrosis, edema and haemorrhage of large medial thigh muscle
treatment of downer cow
- roll animal from side to side every few (24)hrs
- NSAID fluid and electrolyte therapy hoist cows making them stand
- hip lifters, body slings, water flotation tanks
prevention of downer cow
treat all high risk cows with Ca salts PO to decrease change of milk fever
control of downer
observed 12-24hr before and after calving, if recumbent – don’t delay treatment for more than 1 hr, can treat all high risk cows with calcium salts orally to prevent clinical milk fever
gastric ulcers in swine predisposition
sows and growing pigs
Usually pars oesophagus of stomach
cause of gastric ulcer in pig
- multifactorial
- nutritional factors (low protein, low fibre and high energy diet, high level of wheat, high levels of unsaturated fats, low zinc, high iron, copper and calcium)
- physical aspects of feed (size, pelleted, high moisture)
- managemental factors (irregular feeding patterns, transportation, increased stocking density, poor management, inconsistent temperature, excessive aggression)
signs of gastric ulcer in pig
Anaemia, dehydration, grinding of the teeth, dark faeces, vomiting, healthy animals found dead and very pale, nutritional deficiencies
diagnosis of gastric ulcer in swime
clinical signs and PM exams, ulceration always differential in pale sow, faecal exam for blood and parasites and exam of stomach at slaughter
treatment of gastric ulcer in pigs
separating the pig, pale/anaemic (Vit K and antihematinics), access to fibre, ranitidine
prognosis of gastric ulcer in pig
poor
heat stroke cause in pig
extreme temperature and water shortages
signs of heat stroke in pig
panting, lethargy, reduced feed intake, reduced growth and milk production, diarrhoea, increased water consumption, increased urination, rectal temp 43C<
diagnosis of heat stroke in pig
increased respiration and loss of appetite
treatment of heat stroke in pig
wallows, cool, wet towel on the neck, consider diluted vinegar on skin as it evaporates quickly, dibble cold water into rectum, feed electrolyte rebalancing solutions (never use cold/freezing water as sends them into shock)
prognosis of heat stroke in pig
good with cooling down, otherwise death
cause of Porcine stress syndrome
stress or transport myopathy, anaesthetics, depolarising muscle relaxants, following muscle activity
pathogenesis of porcine stress syndrome
Group of conditions associated with autosomal recessive gene (acute stress induced sudden death ((malignant hyperthermia)), pale soft exudative muscle, dark firm dry meat, back muscle necrosis
- after muscle activity metabolism changes to anaerobic, acidity in muscle increases, temp increases
signs of porcine stress syndrome
muscle tremor, muscle rigidity, inability to walk, rapid respiration, hyperthermia, acute right heart failure, death within 20 minutes
diagnosis of porcine stress syndrome
accelerated onset of rigor mortis (5 mins), halothane test, genetic testing (PCR)
treatment of porcine stress syndrmoe
- malignant hyperthermia (under anaesthesia) – by hyperventilating with oxygen
- metamizole, beta-blockers, bicarbonate and cooling
- farm animals, treatment is not possible
- hetero- and homozygous carried should be culled
prognosis of porcine stress syndrome
variable, can appear as sudden death
cause of back muscle necrosis
porcine stress syndrome
pathogenesis of back muscle necrosis
degenerative changes take place in the back muscles along each side of the spine
signs of back muscle necrosis
sudden onset after exercise, severe pain in lumbar muscles, incoordination, lameness, dog sitting position, temp normal, discolouration of skin over the affected area
diagnosis of back muscle necrosis
PCR
treatment of back muscle necrosis
- inject with phenylbutazone/other painkiller
- inject with corticosteroids provided animal isn’t pregnant
- if temperature – injection of long-acting penicillin
predisposition of nutritional myopathy in pig
animals 3- 7weeks of age, no breed or sex predilections, pigs 5-06okg
cause of nutritional myopathy in spig
ingestion of plants high in inhibitors or vit E, fed diets from plants that grown in selenium deficient soils or soils containing selenium antagonists
pathogenesis of nutrtional myopathy in pig
generalised myopathy in skeletal muscles
signs of nutritional myopathy in pig
ataxia, stiff gait, staggering gait, weakness, paralysis, depression, anorexia and recumbency prior to death, chronic cases have lameness and shedding of hooves
predisposition of mulberry heart disease
weavers and growers
cause of mulberry heart disease
vit e deficiency
signs of mulberry heart disease
alternating areas of necrosis and haemorrhage throughout the myocardium, pericardial sac is distended with fluid and fibrin strands, straw-coloured fluid often present in pleural cavity and lungs are oedematous
prolapse of rectum predispotiion
growing pigs (8-20weeks)
cause of prolapse of rectum
increase in abdominal pressure, sex hormone levels, trauma, tail docking, diarrhoea, respiratory disease (excessive coughing), cold weather, slippery floors, stalls with steep slope
pathogenesis of prolapse of rectum
causes increase in abdominal pressure which forces rectum to the exterior
signs of prolapse of rectum
initially red coloured mucosa of rectum protrudes from anal sphincter, after few days it gets swollen and damaged and often haemorrhagic, often cannibalised
treatment of prolapse of rectum
reposition of the prolapse, purse string/mattress suture, return the pig to the pen, long acting ATB
prognosis of prolapse of rectum
sudden onset of death
consequence of prolaspe of rectum
sometimes scarring leads to strictures
predisposition of salt poisoning
uncommon in piglets
cause of salt poisoniing
water shortage/deprivation with normal or excess salt in the diet
signs of salt poisoning
develop in 24-48h, inappetence and dehydration, trying to drink from nipple drinkers
- nervous signs: fits, animals wandering around appearing blind, head pressing, incoordination
- signs of meningitis
- nose twitching just before a convulsion starts
diagnosis of salt poisoning
clinical signs with documented lack of water, brain histologically at PM
treatment of salt poisoning
response to treatment is poor when pig develops fit
- dehydration: rectal with flutter valve, oral, peritoneal infusion
prognosis of salt poisonnig
bad if condition progressed
prevention of salt poisoning
daily routine check of all water sources in the pens
predisposition of thin sow syndrmoe
BCS between 1 and 2
cause of thin sow syndrome
quantative or qualitative inadequate nutrition of sows
pathogenesis of thin sow syndrome
gradual decline in BCS, slow progression over a period of months, sow depletes body fat later muscle protein is degraded
signs of thin sow syndrmoe
very thin sow
diagnosis of thin sow syndrome
clinical signs, group faeces sample for parasitology and blood, eliminate chronic disease
treatment of thin spw syndrome
immediately raise feed intake, very thin sows should be housed in warm, extremely lean sows can have irreversible condition
prognosis of thin sow syndrome
progessive leading to death
predispositon of hypoglycemia in pigs
weak, new-born pigs who don’t nurse regularly
- gluconeogenetic enzymes aren’t developed in 1st days after birth
cause of hypoglycaemia in piglets
sow factors (nutrition, presence of disease, fewer functioning mammary glands)
signs of hypoglycemia in piglets
tachycardia, tremor, nervousness, vocalisation and irritability, hypothermia, mental dullness, confusion, depression and seizure
diagnosis of hypoglycmei In piglets
loss of condition, weak vocalisation, faltering gait, cold skin and recumbency
treatment of hypoglycemia in piglets
: immediately remove piglet and warm up, feed piglet with sow, colostrum/20% dextrose solution by syringe or stomach tube every 20minutes then reintroduce
cause of iron deficiecny anaemia in piglets
large excess of other trace minerals can decrease iron absorption, low iron stores, sows have a low permeability of the transplacental barrier, pigs raised in confinement without access to soil/faeces
iron def in piglets pathogenesis
rapid expansion of plasma volume due to colostrum, insufficient iron supply = microcytic hypochromic anaemia
signs of iron deficiency anaemia in piglets
poor weight gain and pale, anaemic, tissue hypoxia, hypothermia, GI inflammation, decreased appetite, stunted growth, tremors, pulmonary edema, death
diagnosis of iron def anaemina in pig
based on clinical signs, lack of iron supplements and Hb levels in blood below 8g/100ml
- CBC + Biochem will show reduced serum iron and transferrin saturation + low haematocrit
treatment of iron def anaemia in pig
injected with iron dextran
pthogenesis of selenium
absorbed in SI increased by good vitamin A + E levels
decreased by large dietary quantities of Ca, Cu, Vit C, unsaturated fats
signs of selenium
retained placenta, nutritional muscular dystrophy, poor growth, weakness, mastitis, metritis
diagnosis of selenium
serum selenium concentrations reflect dietary intake over the past 2-4 weeks, whole blood selenium reflective of dietary selenium intake over the past 100+ days, liver biopsy is the most accurate method
treatment of selenium
diets containing 0.1-0.3ppmof selenium, injectable Vit E and selenium
zinc predisposition
growing pigs
zinc cause
fed diets high in phytic acid, more than recommended amount of calcium
zinc signs
parakeratosis + dermatitis, decreased milk production, decreased growth and decreased hair on head and legs
zinc diagnsosi
- sample all constituents of the diet
- serum or plasma should be properly collected into tubes specifically designed for trace mineral
- haemolysis (RBC have high zinc concentrations)
- liver samples yield the most reproducible measurements of the zinc status of the animal
copper cause
primary deficit in forage (alkaline soils, liming of soil), secondary (high conc of dietary cadium, iron and selenium and zinc)
signs of copper
depressed growth rate after weaning often with diarrhoea, lighter or faded-looking hair or fleece colour with poor quality
- Microcytic anaemia, depressed milk production, heart failure, infertility, increased susceptibility to disease, enlarged joints, lameness
diagnosis of copper
- copper status in blood or liver tissue
- liver storage gets depleted first, so levels fall
- blood – easier to collect, but delayed significance
treatment of copper
- copper glycinate injection
- addition of copper sulphate or copper lysine in salt/mineral mix
- standard salt mix
- ruminal boluses (copasure) releases Cu for 6 months
prognosis of copper
good
Extras: sheep have liver reserves for 6 months
cause of cobalt
Used by rumen bacteria in formation of B12
Cause: deficient in highly organic or poorly drained soils
pathogenesis of cobalt
low phosphorus and copper, chronic parasites play roles in pathogenesis
signs of cobalt
loss of appetite, emaciation, anaemia, wasting diseases, ulcer discharge, pale skin and fatty liver
diagnosis of cobalt
- difficult
- serum/urinary methylmalonic acid increased
- serum vitamin B12 and liver cobalt concentration depressed
- dietary levels below 0.06ppm should be considered deficient
iron
Predisposition: rare in grazing animals and adults
Cause: can be exacerbated when fed milk replacer low on iron, young animals in total cofinement
Signs: microcytic hypochromic anaemia
Treatment: IM iron dextran, dietary requirement 30-40ppm
iodine predisposition
more common in certain geographic regions
cause of iodine
availability is reduced by methylthiouracil, nitrates, perchlorates, soybean meal and thiocyanates, Rubidium, arsenic, fluorine, calcium and potassium interfere with iodine absorption
signs of iodine
goitre, poor growth, depressed milk yield, pregnancy toxaemia, reproductive abnormalities
diagnosis of iodine
measure serum or plasma thyroxine levels
treatment of iodine
3-6 drops of iodine daily for 7 days, mixed mineral feed supplements, iodine to the skin of a pregnant female once each week for preventing iodine deficiency-induced hypothyroidism
viatmin A is needed for
growth, skeletal development, normal reproduction + vision
liver store is enough for 6 months, plants contain carotenoid precursors of Vit A,
- supplements with oxidising agents (Cu or Fe) can decrease Vit A actvitiy
cause of Vitamin A
supplements that also contain oxidising agents may result in Vit A that is of severely reduced activity
signs of Vitain A
weight loss, depressed immune function, microoftalmia in calves, night blindness, decreased fertility, and hair loss
vitamin D
Predisposition: heavy wooled lambed (reduced sunlight)
Cause: reduced sunlight exposure
Pathogenesis: needed for bone integrity
Signs: rachitis
Treatment: exposure to sunlight or supplemented if housed 24/7, plants fresh + hay contain sufficient D2 and D3 levels
Disease: = rachitis
vitamin K
Cause: corn, feeds containing high levels of sulphur and onions decrease vitamin E availability
Pathogenesis: needed for blood clotting and vision
Signs: white muscle disease, depressed immune function, subfertility
Treatment: no need to supplement in healthy rums as rumen produces it
Extras: farm animals can synthesis Vitamin B
vitamin E
Needed for: maintaining cell membrane integrity (is an antioxidant)
Deficiency: white muscle disease, decrease immunity and decrease fertility
Treatment: no need for supplementation in healthy ruminants, lambs given Vit E and selenium injections in deficient areas
predisposition ketosis
periparturient period of cow (due to marked nutritional, metabolic, hormonal and immunological changes)
pathogenesis of ketsosi
- feed intake doesn’t meet energy demand
- insufficient ruminal production of propionic acid
- not enough glucose = hypoglycaemic
- hypoglycaemia causes metabolism of FA and glycerol supplies
- FA and glycerol’s are oxidised to form Acetyl-CoA
- excess of Acetyl-CoA is converted to KB KETOSIS
prevention ketosis
- avoid overcrowding
- inappropriate stall design for lying time
- first lactation heifers should be housed in separate fresh pen to reduce social stress
- nutritional management
type 1 ketosis
Predisposition: between 3-6 weeks post calving, component-fed herd, primary (starved, not enough food), secondary (decreased intake due to disease/stress)
Cause: overcrowding, stress, limiting factor = supply of glucose precursors,
Pathogenesis: blood KB conc, becomes very high and blood glucose very low
Signs:
- clinical ketosis = both hyperketonaemia and abnormal clinical signs
o reduced feed intake (1st sign), decreased milk production, rapid weight loss, emptying appearing abdomen, acetone breath, normal TRIAS, rumen motility, weakness
- subclinical ketosis: BHB values greater than threshold without clinical signs
- secondary ketosis: occur due to decreased appetite caused by other diseases (eg, peritonitis, metritis, septic mastitis)
Diagnosis:
- KB in blood, urine or milk
- physical exam
- without clinical signs, results indicate subclinical ketosis
- urine KB conc are always higher than in milk
- positive milk tests for BHB usually indicate clinical ketosis
type 2 ketosis
Predisposition: fat cows are at higher risk
Cause: cow develops NEB and begins mobilising body fat prior to/ at calving, stress (hepatic lesions)
Pathogenesis: NEB decease glucose glucagon, ACTH, catecholamine, glucocorticoids = increase, insulin decrease lipase activation
3 forms:
- subclinical
- chronic fat mobilisation after early periparturient ketosis
- ketosis in obese ow with massive lipid accumulation in liver
Aetiology:
- insulin + glucose increase but insulin resistance because they’re obese
- obese = increased lipolysis in peripartal period = decrease DMI NEB, increased adipose sensitivity mobilise fat very quickly under stress
- excessive mobilisation of fat increased fatty liver infiltration ketone production decreased DMI
- NEB decreased glucose increased glucagon, AcTH, catecholamines + glucocorticoids lipase activation
Signs:
- non-specific: depression, anorexia, weight loss, weakness, hypoactive rumen motility, decreased milk production, enlarged liver on palpation
- dystocia, retained placenta, endometritis, mastitis, SARA, hypocalcaemia puerperalis, abomasal dislocation, ketosis, HE
Diagnosis:
- nonspecific clinical signs
- lab tests
o CBC: leukopenia
o Biochem: increased (NEFA, BHB, pyruvate, AST, ALT, LDH, SDH, GGT and ammonia), decreased (triglycerides, cholesterol, insulin, glucose, albumin)
- US on liver
- very persistent ketosis
- blood ketone conc are not as high as type 1
Treatment – really hard to treat
- non-encephalopathic severe ketosis type II
o 1-2 weeks after calving
o constant rate infusion (CRI) – 5-10% dextrose + balanced electrolyte solution containing supplemental KCl
o IV insulin 200IU q24-36h P21
o force feeding
o 12g/day niacin PO
o if not working after 3- 5 days, milk 1 min 2xday until NEB broken
- Hepatic encephalopathy in severe ketosis type II
o advanced cases, euthanasia is recommended
o depressed consciousness
type 3 ketosis
Cause: feeding ketogenic silages. Hay crop silages are chopped too wet/low in water soluble carbs (favour growth of clostridium)
Pathogenesis: clostridium ferment some carbs to butyric acid (instead of desired lactic acid)
Diagnosis:
- silage fermentation (VFA) analysis confirms present and amount of butyric acid in silage
- silage with clostridial fermentation – can smell
Treatment: divert, dilute and destroy
- divert this feed away from the pre- and post-fresh cows, can be fed to replacement heifers, late lactation cows and/or far-off dry cows
- aerating the forage prior to feeding with it, silage that are over 2% butyric acid should be destroyed
- 50% dextrose solution (IV)
- propylene glycol (PO) should be given as a drench and not mixed in feed, overdosing = CNS depression
- glucocorticoids: dexamethasone/isoflupredone acetate (stimulate hepatic gluconeogenesis)
- neurological form of ketosis: IV glucose + PO chloral hydrate
preganncy tozemia and fatty liver syndorme in ewes and does predisposition
during last month of gestation, multiple foetuses. Females with poor BCS or over conditioned
cause of fatty liver syndrome / pregnancy toxemia
stress, anorexia caused by other diseases
pathogensis of pregnancy toxemia and fatty liver syndrme
anorexia or lack of sufficient energy intake NEB animals mobilise body stores of fat and transport them to the liver hypoglycaemia, hyperketonaemia fatty liver
signs of pregnancy toxemia
decreased appetite, anorexia, dullness, altered behaviour, recumbency, constipation, bruxism, acetone breath, frequent urination, incoordination, circling, dystocia
diagnosis of pregnancy toxemia
presence of multiple foetuses, clinical signs
- Increases serum BHB levels
- positive urinalysis for ketone and protein biochemistry: hypoglycaemia, azotaemia, occasionally hypocalcaemia, hypokalaemia
eamtnet of pregnancy toxemia
Early cases (before onset of recumbency)
- propylene glycol PO
- single injection of 50% dextrose, followed by balanced electrolyte solution with dextrose + calcium borogluconate
- potassium, flunixin meglumine
Recumbent animals
- comatose animals – human euthanasia
prevention of pregnancy toxemia
- good feeding management
- adequate feeder space for pregnant animals
cause of hypocalcaemia/mik fever
usually 3rd lactation
pathogenesis of hypocalcemia
- need for Ca during dry period is low so GI absorption + mobilisation from bone decreases
- late pregnant cow needs 30g/d Ca, lactating around 50g/da
- huge sudden demand for Ca which test homeostatic mechanism
- occurs when cows don’t extract enough Ca from bones to diet to replace Ca lost in milk
signs of hypocalcemia
Stage 1 : cows still standing, hypersensitivity, excitation, ears twitching, muscle tremor, mild ataxia, open mouth breathing
Stage 2: sternal recumbency, depression, dry muzzle, decreased temp, cold extremities, heart sounds quieter, tachycardia, smooth muscle paralysis
Stage 3 : lateral recumbency, disturbance of consciousness, complete flaccid muscle paralysis, ruminal bloat, filiform pulse
diagnosis of hypocalcemia
- ca: normal 2.2-2.5 mmol/L, milk fever = < 1.9, stage 1 = 1.4-1.9, stage 2 = 0.9-1.6, stage 3 = < 0.9
- p, Mg decrease, CPK and AST increase
- stress leukogram: neutrophilia, lymphopenia, eosinopenia
emergency = flaccid paralysis
treatment of hypocalcemia
ca-borogluconate IV (500ml slowly over 10-20mins) , slow application for teat canal: ca-propionate, give Vit D, wrap knees
prognosis of hypocalcemia
favourable in simple cases, grave if: cow lying down for long time, mastitis, musculoskeletal trauma, ischemic muscle necrosis
prevention of hypocalcemia
dietary cation anion difference, diet high in Na + K and low in Cl + sulphur, vit D 1 week before calving, Ca gel PO after calving, PTH IM 6 days before parturition
redisposition of parturient paresis
occurs 6 weeks prior and 10 weeks after birth
cause of parturient paresis
: exact cause unknown, stress
signs of parturient paresis
ataxia, tremor, constipation, rumen atony, tachycardia, tachypnoea, bloat, depression, opisthotonos
diagnosis o f paturient paresis
- low level of Ca in goats and sheep in high lactation with multiple foetus, decreased P, increased/decreased Mg
- history, clinical signs + response to therapy
treatment of parturient paresis
Ca-borogluconate 50-150ml IV or 50-150ml IV in 1L glucose
differeitnatil of parturient paresis
pregnancy toxaemia and fatty liver syndrome in ewes and does
prevention of parturient paresis
avoid alfalfa, application Ca postpartum, avoiding stress and parasite control
hypomagnesia predisposition
dairy and beef cattle during 1st 2 months after calving
low Mg + high N, K in rapidly growing grass causes hypoMg + HypoCa resulting in tetanic signs
cause of hypomagnesiua
animals grazed on lush grass pastures or green cereal crops
types of hypomagnesiua
Grass Tetany (grass staggers)
- in dairy cows during the spring
- grazing cold grass with deficient content of Mg
- grazing wheat, barley/oats treated with potassium and nitrogen fertilisers that reduce the absorption of Mg from rumen
- stress adrenaline hypoMg
Winter tetany
- animals are fed with a food deficient in Mg
- stress-extreme low temperature
Transport tetany
- low Mg in food and stress of prolonged transport
- typically in cows and ewes in late pregnancy
Milk tetany
- calves feeding only with milk
- milk < mg but resorption is good
- diarrhoea in calves contributes
signs of hypomagnesiua
: hyperexcitability, muscular spasms, convulsion, nystagmus, respiratory distress, collapse, elevated temp, tachycardia, loud cardiac sounds, tachypnoea, tetanic spasm
diagnosis of hypomagnesia
emergency, clinical signs, low Mg in serum and CSF, often hypo Ca and hypo P
treatment of hypomasnesia
sedation with xylazine, ca borogluconate + hypophosphate IV
prevention of hypomagnesia
mineral blocks, optimal intake of energy, prevent fertilisation with the K, avoiding stress
differentials of hypomagnesia
rabies, nervous ketosis, coccidiosis, hypoCa, tetanus, strychnine poisoning, salt poisoning, enterotoxaemia in calves, bloat, acute poisoning heavy metals
what is rickets
Disease of bony growth plate, failure of both vascular invasion and mineralisation in the area of provisional calcification of metaphysis of the long bones
predisposition of rickets
dogs, cats, pig, young, growing animals
cause of rickets
dietary insufficient (phosphorus/ Vit D), abnormal calcium:phosphorus ratio, animals fed all meat diets, during winter
signs of rickets
bone pain, stiff gait, swelling in the area of metaphysis, lameness, pathologic fracture, limb deformity
diagnosis of rickets
radiographic exam: thickening metaphysis
treatment of rickets
correction of the diet, exposure to sunlight increases Vit D3 precursors, high quality commercial food
prognosis of rickets
good in absence of pathologic fractures/irreversible damage to the physis
predisposition of osteomalacia
older cows
cause of ostemomalacia
cattle grazing on arid, infertile soils deficient in phosphorus, horses (bran/miller/big head disease), keeping animals indoors
pathogenesis of osteomalacia
similar to rickets but seen in mature bones, accumulation of excessive unmineralized osteoid on trabecular surfaces
signs of osteomalacia
nonspecific shifting lameness, spinal deformation, rough hair coat, weight loss, pica, limb deformities, spontaneous fracture
diagnosis of osteomalacia
history, CE, diet should be evaluated for calcium, phosphorus and Vit D content, X-ray (generalised demineralisation of the skeleton and fractures of long bones)
treatment of osteomalacia
proper nutrition prevents occurrence of significant bone damage and fracture
prognosis of ostemomalacia
favourable only in initial stage of the disease, medicine containing Ca, P and Vit D
predisposition of urolithiasis
feed a lot and range cattle, steers but also in some sheep and goats
cause of urolithiasis
high concentrate diets (increased solidification) , grazing on silica-rich soil, high in calcium, Vit A deficiency, hypervitaminosis, reduced water intake, chronic UTIs
pathogensis of urlothiasis
magnesium ammonium phosphate most common calculi
signs of urolithiasis
urethral obstruction, tenesmus, colic, inappetence, sandy calculi, bloody urine
diagnosis of urolithiassi
history, CE, rectal exam, abdominal US, radiography
treatment of urlothiasis
catheterisation usually impossible in most bulls (sigmoid flexure), surgical treatment: urethrostomy or urethrotomy
prognosis of urolithiasis
increase urinary chloride excretion, decrease urine pH, decrease dietary cation-anion difference, provide calcium: phosphorus ratio 2:1, free access to a source of non-frozen water
prevention of urolithiasis
correction of underlying cause, removal from offending pastures of feedstuffs
- to prevent struvite calculi:
o increase urinary chloride excretion, decrease urine pH, decrease dietary cation-anion ratio, free access to caean, non-frozen water
cause of pyelonephritis
Corynebacterium renale, E.coli, trueperella pyogens, stap and pseudomonas
- Physical/ chemical damage to the mucosa in the lower portion of the UT (dystocia or puerperal infection, bladder paralysis or catheterisation may predispose the cow to pyelonephritis)
pathogenssis of pyelonephritis
ascending infection from lower urinary tract
signs of pyelonephritis
urinary blood clots or fibrin, pyuria
- Acute pyelonephritis: fever, anorexia, decrease in milk production, sometimes colic, arched stance, stranguria, polyuria, haematuria
- Chronic pyelonephritis: anorexia and weight loss, poor hair coat, poor production, diarrhoea, polyuria, stranguria, anaemia
diagnsosi of pyelonpehritis
- history of recent parturition, CE
- Rectal exam (palpation of left kidney for enlargement, loss of lobulation and pain)
- US – kidney, ureters and bladder
- Endoscopic detection of cystitis
- urine exam: fibrin, blood clots, pus and haemorrhage
- positive blood and protein reactions on reagent test strips
treatment of pyelonephritis
- catheterisation, urine sample for urine culture penicillin
- if c.renale identified – penicillin
- E.coli ceftiofur
- azotaemia is present - gentamicin
prognosis of pyelonpehritis
good for cows with acute pyelonephritis that are treated with long-term antimicrobial therapy, severe bilateral and azotaemia is guarded
extra of pyeloneprhtisi
calves can get septic nephritis + renal abscessation from umbilical artery infection
