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77 Cards in this Set

  • Front
  • Back
What are the 6 clinical signs for weaner ill thrift syndrome?
•failure to thrive
•poor growth rates
•low BCS
•poor coat
•reduced reproductive potential
What are the energy requirements for weaners?
Energy(MJ/ME/kgdrymatter) =
What are the 3 causes for copper deficiency?
•dietary insufficiency but Mo, Zn, S and Fe are Cu antagonists
•reduce bioavailability
•particularly on improved pastures
What are the clinical signs for copper deficiency?
•rough coat
•reproductive failure
When does cobalt deficiency occur? What are the clinical signs?
•Co required by microbes to synthesise vitamin B12
•need a constant supply from pasture
•fast growing spring pastures deficient
•therefore often occurs with Cu deficiency
Clinical signs
•same as for Cu
•occasionally PEM
Co deficiency: list the treatments.
•Co sulfate added to pasture
•B12 injections
•Co in drench or water
What are the clinical signs and diagnosis for cobalt deficiency?
Clinical signs
•reduced fertility
•White muscle disease
•clinical signs
•blood –GPX
•liver –reflects selenium ingestion
What are clinical signs that suggests phosphorus deficiency?
Poor body condition
Sunken eyes
Dull, woolly coats
Low growth rate
Low milk yield
Low pregnancy rate
High incidence of broken bones (ie. backs and limbs broken easily in the race or crush)
Shifting lameness, stiff gait, arched backs
Chewing bones
what is the gold standard eay for measuring P deficiency?
Chemical analysis of rib bone
Gold standarddiagnosis of chronic P deficiency
Measure mg P/ cm³ fresh bone& specific gravity
what is the best way to address P deficiency?
Top dressing not possible in pastoral areas
what is the causative agent for wooden tongue?
Actinobacillus lignieresii
What is the treatment for wooden tongue?
Sodium iodide (not in milking animals)
what is the causative agent of lumpy jaw?
Actinomyces bovis
what is the treatment management for lumpy jaw?
• Treatment is often unrewarding
• Better success if identified and treated early
• Local and systemic iodide treatment
• Antibiotics - penicillin preferred
• Surgical curettage with packing
what is the ddx for vesicular stomatitis?
what does Bovine Papular Stomatitis resemble?
Contagious Ecthyma and pseudocowpox
describe the wualities of rumen fluid
• pH - check immediately
• Normal 5.8-6.2, increased with
anorexia, decreased with
indigestion, grain overload
• Colour - olive to dark green
• Odour - pungent VFA
• Untreated wet mount
• Iodine treated wet mount - starch
granules (at least 50% of protozoa)
• Gram stain (50:50 ratio) - increased
G +ve in grain overload
name 4 disease states that alters rumen fluids
• Anorexia - increased pH (>7.0)
• Urea poisoning - over-production of ammonia, ties up free H+,
therefore pH rises (Rx - 5% acetic acid or vinegar)
• Grain engorgement - decreased pH, increased G +ve bacteria
• High protein ration - increased rumen pH in a feedlot
what are the treatments for indigestion in cows?
• Ruminotoric-laxatives as powder or bolus
• MgOH (1 gm/kg)
• Forced exercise
• Calcium
• Free choice hay
what ferments grain the cow stomach?
Streptoccocus bovis
and Lactobacillus acidophilus
what would u except on bloods with lactic acidosis
High anion gap acidosis
• Hypocalcemia
• Hypomagnesemia
• Hyperglycemia
• Hemoconcentration (↑ PVC and Hb)
• CBC – neutropenia and toxicity
what are the 4 therapy for lactic acidosis?
• IV fluids (without lactate)
• Rumenotomy and transfaunation
• Calcium, magnesium, thiamine, NSAID
• Antibiotics as alternative to transfaunation
what is the sequelae to lactic acidosis?
Sequelae include:
• Fungal or bacterial rumenitis
• Rumen necrosis and gangrene
• Peritonitis
• Hepatic abscesses and vena caval thrombosis
what is secondary gas bloat caused by?
Recurrent problem in individual animals on a high grain
• Eructation or rumen outflow failure
how do u treat free gas bloat?
• Treatment involves passage of stomach tube
and removal of gas
• Administer antiacid-ruminotoric mixtures
• Tie stick in mouth
• Avoid trocharization if possible
• Secondary peritonitis
• Explosion and fire hazard
what causes frothy bloat?
• Feeding of lush pasture
• High in chloroplast membrane fragments and
soluble protein
• Production of a stable foam that traps gas
• Blocks cardia and prevents eructation
what is the difference with frothy bloat on exam?
Signs are as for free gas bloat except usually an
absence of large auscultable “ping” despite
despite marked left flank distention
How do u treat frothy bloat?
• Administration of anti-foaming agents such as:
• Poloxalene (Therabloat® or Bloatguard®)
• Dioctyl sodium succinate (DSS, 500 ml of 5%
• Vegetable oil (1 liter)
• Oral ruminotorics-laxative-antacid powders
• Calcium therapy
how do u treat frothy bloat?
• Frothy Bloat is prevented by:
• Gradual access to dangerous pastures
• Avoid pastures with >50% legume content
• Feed additives (e.g., poloxalene @ 5-10 gm/BID/cow)
• Spray pasture with oils
• Pre-feed ionophore antibiotics (monensin, lasalocid)
what are the clinical signs of vagal indigestion?
• Reduced feed intake with normal water consumption
• Decreased milk production
• Bradycardia (<60 bpm) due to reflex retrograde irritation of
the vagus nerve
• Variable rumen sounds (absent, hypomotile, or hypermotile)
• Usually increased (3-6/min) but ineffective contractions
• “Papple” or L-shape from behind
• Rumen gas cap and ventral filling
• Vomiting - also TRP, hypocalcemia, listeriosis
what does the lab data for vagal indigestion suggests?
• Lab data
• Normal with failure of reticulorumen emptying
• Hypochloremic metabolic alkalosis with abomasal transit
what are the vagal indigestion ddxs?
• Important DDx
• Indigestion
• Bloat (Gas or Frothy)
• Ruminal acidosis
• Omasal or abomasal impaction
• Small intestinal obstruction
Describe how LDA occurs?
• Abomasum migrates from normal position right ventral
abdomen to lodge between rumen and left abdominal wall -
results in partial pyloric obstruction
• Any ruminant at any age but most common in older lactating
dairy cattle in the first 3 months after calving (80% within
first month)
What are the 4 causes for LDA?
• Diet - often inadequate dietary fibre
• Hypocalcemia
• Inherited predisposition
• Concurrent illness - approximately 40% of animals will have a
retained placenta, mastitis, or metritis
what are the 7 clinical signs for LDA?
• Decline in milk production
• Capricious appetite – eat hay and grass but refuse
grain and silage
• Altered feces (volume and consistency)
• “Ping” on left side of abdomen
• Fluid may be succussed
• “Sprung” rib
• Distant rumen contractions
what are the DDX for left sided ping?
• Left displacement of the abomasum
• Rumen gas cap
• Pneumoperitoneum
what are the lab result of LDA?
• Ketosis
• Hypochloremia
• Hypokalemia
• Aciduria
• Metabolic alkalosis
• Hypocalcemia
• Increased rumen chloride concentration (>50 mEq/L)
what are the treatments for LDA?
• Fluid therapy
• Saline supplemented with 40-100 mEq/L of KCl
• Calcium 500 ml of 23% Ca borogluconate IV or SQ
• Glucose or propylene glycol (5-8 oz b.i.d or t.i.d)
• Replacement of organ:
• Rolling
• Right paramedian abomasopexy
• Right paralumbar omentopexy/pyloroplasty
• Left flank abomasopexy
waht is RDA?
• Abomasum migrates dorsally on the right side
• Results in partial pyloric obstruction
• Diagnosis
Name 8 Differential Diagnoses for
Right-Sided Ping
• Volvulus
• Cecal dilatation/volvulus
• Gas in spiral colon
• Gas in duodenum
• Pneumorectum
• Physometra
• Rumen
• Pneumoperitoneum
Tx for RDA?
Right flank omentopexy
“Bleeding ulcers do not perforate and
perforating ulcers do not bleed”
what are the clinical signs of ulceration?"
• Bleeding, non-perforating ulcers
• Chronic focal abdominal pain
• Dark, tarry feces
• Reduced feed intake
• Bruxism
• Pale mucous membranes, rapid pulse rate,
weakness, cool extremities
• Anemia and hypoproteinemia
How do you treat ulceration?
• Treatment
• No grain, lots of roughage
• Stall confinement
• Antibiotics
• Anti-acid drugs (IV, efficacy ?)
• Blood transfusion
• Surgical resection of ulcerated tissue –
usually bad idea
who is at risk of caecal dilatation and volvulus?
• Post-partum animal at greatest risk
• Half within one month of calving
• Diet related - high concentrates
• Decreased motility and increased organ distention
How do you treat caecal dilatation with and without volulus?
• Treatment of simple dilation without volvulus
• High roughage diet, withdrawal of CHO
• Fluid therapy
• Calcium
• Treatment of simple dilation with volvulus
• Surgical correction
• Fluid and electrolyte therapy
• Prognosis related to degree & chronicity of organ
list 7 ddx for Acute diarrhoea without oral lesions
• Dietary (indigestion)
• Salmonellosis
• Winter dysentery
• Ostertagiasis
• Septic conditions
• Miscellaneous
• Plant, metal or mycotoxin poisoning
list 5 Acute diarrhoea with oral lesions
• BVDV / Mucosal disease
• Malignant Catarrhal Fever
• Rinderpest - 2011
• Ingested caustic agents
• Toxicoses (oak, lead)
list 6 causes of diarrhea
Johne’s disease
• Parasitism
• Chronic salmonellosis
• Copper deficiency/molybdenosis
• Toxins or poisonous plants
• Chronic mucosal disease
What is the causative agent for BVDV
• Pestivirus genus of the Flaviviridae family
• Closely related to the viruses associated with hog cholera
and border disease
• Two biotypes (based on cytopathicity in culture):
• Non-cytopathic (NCP)
• Cytopathic (CP)
• CP is a mutant of NCP
• NCP is the most common biotype in nature
How does BVDV spread?
Natural reservoir - persistently-infected (PI)
• Outbreaks often follow introduction of PI animal
into herd
• PI - infection with NCP in utero before 125 d
• Immunotolerance and failure to clear virus
• PI calves often appear clinically normal but shed
large numbers of viral particles into
• 1% of population are PI
How is BVDV transmitted?
• Transmission:
• Direct animal to animal contact
• Vectors (insect and/or mechanical)
when does Infection in immunocompetent animals occur? What happens?
• Infection in immunocompetent animals
• Usually affects animals 6-24 months of age
• Most infections are subclinical (up to 90%)
• Mild fever with transient leukopaenia
• Seroconversion (measurable antibody response)
What happends in infection in naive animals.
• Infection in naive animals
• Mild-to-moderate clinical signs
• Fever
• Oculonasal discharge
• Oral ulceration
• Diarrhoea
• Abortion
• Respiratory disease (primary, secondary agents)
• Decreased milk production
What happens with infection in immunocompetent animals with BVDV?
• Transient immune suppression
• Leukopaenia (primary neutropaenia) and
• Results in decreased resistance to secondary infections -
pneumonia, mastitis, metritis
• Type II BVDV - often high mortality
• Bloody diarrhoea
• Haemorrhagic syndrome (severe thrombocytopaenia)
What happens to the developing foetus with infection of BVDV?(days -9 to 45)
• Infection prior to conception through
embryonic stage (days -9 to 45)
• Reduced fertility
• Decreased conception rates
• Oophoritis, uterine inflammation
• Early embryonic loss
What happens to the developing foetus with infection of BVDV?(day 45 to 175)
1. Abortion
• Can occur in response to infection with either NCP
or CP biotypes
• Estimated at 7% in endemic herds
• Expulsion of dead foetus can be delayed (up to 50 d)
• Usually occurs 10-27 days after exposure

2. Immunotolerance
• Infection with NCP biotype only
• Days 18 - 125 (rare after day 100)
• Persistent infection
• Absence of neutralizing and non-neutralizing
What happens to the developing foetus with Infection after embryonic stage (day 45 to 175)?
Congenital defects
• Usually during period day 100 - 150
• CNS: Cerebellar hypoplasia, hydrocephalus,
hydranencephaly, hypomyelination
• Ophthalmic lesions
• Thymic lesions
What happens to the developing foetus with Infection in late gestation (125 - 285 days)
• Usually effective clearing
• Solid immune (antibody) response
• Susceptibility to post-natal infections (?)
Give 4 characteristics of Persistently-infected animals with BVDV
• High mortality rate
• <10% survive to 2 years of age
• Variable appearance at birth - often normal
but some are weak and ill-thrifty
• High rate of other diseases
Describe how does Mucosal disease develops?
• Mucosal Disease
• Relatively uncommon but spectacular
• PI with NCP; NCP mutates to CP or animal
is exposed post-natally to CP
• Usually seen in animals < 2 years of age
List 4 Clinical signs of mucosal disease.
• Fever
• Profuse and watery diarrhoea
• Oral, nasal, interdigital, and gastrointestinal
• Severe leukopaenia
what is the prognosis for mucosal disease?
• High mortality soon after development of signs
• Prognosis hopeless
• Some will develop a chronic form of MD and may
survive for several months before eventually
how can you diagnose BVDV?
• Acute infection
• History
• Clinical findings
• Serology (serum neutralization, ELISA)
• Type I, Type II
• Detection of virus (isolation, capture-ELISA)
How do you detect PI cattle?
• Virus detection in whole blood or tissue (ear notch
test) - repeat sampling
• Detection in milk (antigen-capture ELISA)
• Serology - low or negative antibody titers
• Effective of colostrum (pre-suckle, >4 months)
• Antigenically-different strains (natural, vaccine)
List Control and Prevention for BVDV
• Biosecurity practices
• Vaccination
• Bega and Trangie Strains - inactivated virus with
• 2 doses 4-6 weeks apart followed by annual dose
• Pestigard, Pfizer Animal Health, Australia
• Detection and elimination of persistently-infected
animals is critical for control
List 8 Clinical Signs for malignant cattharal fever.
• Fever
• Oral erosions
• Diarrhea, may have blood
• Keratoconjunctivitis (blepharospasm, photophobia, corneal
• Nasal discharge
• Lymphadenopathy
• Lameness
• Encephalitis
What is winter dysenterry? What are the agents involved?
• Explosive outbreaks of diarrhea in adult cattle over
• Often housed or feedlot
• Camplyobacter; Breda virus (Europe)
• Coronavirus - EM and seroconversion
• Highly contagious – spread by fomites, including
• High morbidity (up to 100%), but low mortality
What are the clinical signs of winter dysentary ?
• Clinical signs
• Fever (39 - 41 C) - can be inconsistent finding
• Acute watery diarrhea that is dark brown and
malodorous. Young cattle infected for the first time may
have substantial blood loss in diarrhea
• Decreased appetite
• Hypolactia
• Signs resolve within 5 days (10-14 days across herd)
What causes Johnes disease? Where does the organism live? How long does it live in the environment?
• Mycobacterium avium subspecies paratuberculosis
• Slow-growing acid-fast bacterium
• Survives and replicates within macrophages
• Persistent in the environment
• 9-18 months in cool damp conditions
• Susceptible to sunlight, heat, disinfectants
what are the 5 clinical sings of Johnes?
Clinical signs
• Weight loss with normal appetite
• Normal vital signs
• Chronic, intermittent diarrhoea
• Cachectic, lethargic
• Oedema
List how Johnes is transmitted
• Infection occurs in the first few weeks of life
• Faecal - oral transmission (usually from dam)
• Infected cows can shed in colostrum and milk
• In utero transmission
• Resistance to infection increases with age
Pertinent pathophysiology 3 of Johnes
• Ingestion → MAP phagocytosed and proliferates in
macrophages in the wall of the distal small intestine
and regional lymph nodes
• Recruitment of additional macrophages to the site of
• Intestinal infiltrate → malabsorption and protein loss
What tests are needed for testing Johnes?
• Signalment and history; PE
• Hypoproteinemia (TPP, SP -albumin)
• Serology (AGID, CF, and/or ELISA)
• CF not recommended
• AGID - >95% sensitivity when signs are present
• ELISA - best test for detecting sub-clinical infection
• Detection of acid fast organisms in feces
• Fecal culture (3-4 months, > 50-100 CFU/gm feces)
• DNA probe - 2-4 days, high specificity, expensive
HOw do you control Johnes dz?
• Herds with high infection rates
• Takes many years
• Prevent new infections
• Separate calves from cows at birth
• Clean, dry birthing environment
• Use colostrum from negative cows
• Milk replacer
• Raised separately from adults
Hemorrhagic bowel
syndrome: who does it affect? What does it cause?
• Lactating diary cattle
• Increasing frequency
• Severe, segmental hemorrhage of the small
intestine with intraluminal blood
• High mortality (85-100%)
• shock, necrotic enteritis
Hemorrhagic bowel
syndrome: What is the causative agent?
Clostridium perfringens