Model answers to VETS 5002 Exam- May 2003
SECTION A
(Note that each question in this section is marked out of five for convenience,
giving a total of 75 marks for Section A, which is then reduced to a total out of 40
(= approximately 2.7 marks per question)
Question 1. In a 10-month-old dairy heifer, how would you differentiate
haemoglobinuria due to Leptospira pomona infection from haemoglobinuria due
to Babesia bovis?
L.pomona
(1) Mainly affects young calves around 2 months of age
(2) Presence of pigs in area, may have caused transmission of the disease
(3) What is the vaccination status of the calf in relation to Lepto?
(4) Have their been any abortions in the adult herd due to L.pomona
(5) Note that antibodies to L.pomona would be unlikely to be present in the calf as
antibodies appear some time after the period of leptpspiraemia
Babesia bovis
(1) Mainly affects young cattle from 9-36 months of age( that is, correct age group for
this calf
(2) Only occurs in Qld- that is, signs of haemoglobinuria in young cattle in other
States, would not be Tick Fever
(3) Check vaccination status of calf and whether there have been problems with this
organism on the farm previously
(4) Has the heifer been bought or was it born on the property?
(5) Clinical signs of both diseases could be similar, BUT organisms present in a tail
tip smear in the case of B.bovis
(6) Calf in Qld would also need to be located in the cattle tick area
Question 2. Discuss important aspects of the general epidemiology of
leptospirosis in dairy cattle and list ways in which Leptospira hardjo
(L.borgpetersonii serovar hardjo) is transmitted
Note that there are two parts to this question (a) the general epidemiology of
leptospirosis and (b) the transmission of L.hardjo
(a) General epidemiology of leptospirosis
Two types of hosts-maintenance hosts and incidental hosts
 Maintenance hosts
(1) Each serovar has one or more maintenance hosts
(2) These maintenance hosts don’t show acute disease
(3) In these hosts, the organisms persist with long term shedding (in urine)
(4) They have low antibody titres and are thus difficult to diagnose
 Incidental hosts
(1) Includes all mammals except the maintenance host
(2) Acute severe disease is common
(3) The organism is cleared quickly with little shedding
(4) They have high antibody titres and are thus easily diagnosed
(5) They are epidemiologically irrelevant
(b) Transmission of L.hardjo
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(1) Horizontally between animals by contact with infected urine
(2) Venereal transmission-natural service can spread the disease
(3) Vertical (in utero) transmission
Question 3. Why is foot lameness more common than leg lameness in dairy cattle
and how can the incidence of foot lameness be minimised?
(Note that in answering this question, you need to talk about foot lameness, leg
lameness and then ways of minimising foot lameness)
 Foot lameness is more common because:
(1) The feet bear the majority of the cow’s weight and are responsible for pivoting the
cow
(2) The hind feet propel the cow and are more exposed to abrasion
(3) The feet are in contact with the ground and thus exposed to uneven surfaces,
muddy conditions, concrete, stones etc
(4) The hind feet are predisposed to injury in early lactation because they are
displaced laterally by the udder
 Leg lameness
(1) Is less common than foot lameness for the above reasons
(2) Leg lameness tends to be a chance or incidental event and is related to the cow
slipping on concrete, being mounted by another cow etc
(3) It is usually not directly related to the cow’s environment, with the possible
exception of hip dislocation if there is a lot of slippery cement in the dairy
 How can foot lameness be minimised?
(1) Farmer patience in the way he/she handles the cows, particularly when they are
brought up to be milked
(2) Farm track design
(3) Farm track maintenance
Question 4. List the infectious causes of neonatal calf diarrhoea that are also
zoonoses. How can you differentiate between these on clinical grounds?
(1) There are only two infectious causes that are zoonoses as follows:
 Salmonellosis
 Cryptosporidiosis
(E.coli diarrhoea in calves is not a zoonosis, however E.coli in food can cause public
health problems)
(2) These two diseases can be differentiated on clinical grounds as follows:
 Crypto is confined to calves aged 1-3 weeks
 Salmonella is not confined to calves in this age group, but can occur in older
calves
 In contrast to Cryptosporiosis, Salmonellosis in calves is accompanied by
fever and severe systemic signs, often with blood in the faeces and can cause
dysentery
 In other words, in most cases it should be possible to clinically differentiate
Salmonellosis on the basis of the severity of clinical signs and the nature of the
diarrhoea, however in individual calves, taking samples for lab analysis may
be necessary
Question 5. Briefly discuss the pathogenesis of the anterior functional stenosis
form of vagus indigestion in cattle
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(1) The anterior stenosis form of vagus indigestion is characterised by interference
with the flow of ingesta through the reticulo-omasal orifice, that is, it is an outflow
abnormality
(2) So that disturbances in the particle flow of ingesta occur due to mechanical
inhibition of RR motility
(3) Normally, RR motility results in the stratification of rumen contents with high
density particles preferentially leaving the RR
(4) Vagus indigestion thus results in disturbances in (a) particle retention time and (b)
flow of ingesta
(5) Three phases can be seen with respect to anterior stenosis:
(a) first phase
  RR motility due to pain and inflammation
  flow of ingesta due to this impairment
(b) second phase
 ’d impairment to flow of ingesta
 loss of stratification
 ’d volume of rumen
 rumen may become hypermotile
(c) third phase relates to pyloric stenosis
(6) Thus, anterior functional stenosis causes:
 ’d flow of ingesta and ’d volume of RR
 Atonic rumenmild bloat
 Hypermotile rumenmarked distension of the RR, rumen moving 4-6
times/minute and sound reduced
 The rumen enlarges and fills most of the abdomen
Question 6. How would you differentiate right-sided dilatation of the abomasum
from caecal torsion?
These diseases can be differentiated in three ways as follows:
 Clinical signs
(1) RDA runs a subacute course with impairment of appetite, dullness, possible
increase in heart rate, ’d ruminal movements, possible abdominal distension
(2) Caecal torsion is an acute syndrome with anorexia, increased heart rate, rumen
stasis, decreased or absent faeces and distension of the right paralumbar fossa
 Rectal findings
(1) In RDA, the distended abomasum may be palpable in the lower right quadrant of
the abdomen
(2) In caecal torsion, the distended body of the caecum is palpable in the upper right
quadrant of the abdomen as a sausage-shaped mass
 Pings
(1) In RDA, a ping is audible from the 9-12 (or 13th) rib, but rarely extends into the
right paralumbar fossa
(2) In caecal torsion, a ping is present in apart or all of the right paralumbar fossa and
also extends under the last two ribs
Question 7: How would you differentiate localised peritonitis associated with
abomasal ulceration from the localised peritonitis associated with perforation of
the reticulum by a foreign object?
(1) Both these conditions show similar clinical signs as follows:
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 Sudden onset of anorexia and ’d milk yield
 Abdominal pain
 ’d ruminal motility with decreased intensity of sounds
 slightly elevated heart rate (80-90 beats/minute)
(2) They can be differentiated on the location of the abdominal pain
 Type 3 ulceration will have the pain restricted to the lower right quadrant
of the abdomen
 The pain in TRP is localised to the lower left quadrant of the abdomen
(xiphysternal region)
(3) Note that cows with type 3 ulceration may also show anaemia and occult blood in
the faeces detectable by faecal occult blood tests
Question 8: Discuss the differential diagnosis of acute enteritis due to Salmonella
spp in adult dairy cattle
Salmonellosis in adult dairy cattle needs to be differentiated from:
(1) Yersiniosis- would look very similar but less common
(2) Winter dysentery
(3) Acute mucosal disease
(4) Acute bracken fern toxicity
(5) Acute arsenic poisoning
(6) Plants causing diarrhoea
A brief discussion of the first three would also be in order
Question 9: Discuss the differential diagnosis of second stage milk fever
(parturient paresis) of cattle
The differential diagnosis includes the following: (for details on each category, see
pages 4-5 of lecture 13)
 Diseases associated with toxaemia and shock
(1) Here you need to include peracute mastitis, peracute metritis and acute diffuse
peritonitis
(2) The heart rate in these conditions will be 120 beats/min and the heart sounds will
be louder than normal
 Injuries to the hind limbs
 Maternal obstetric paralysis
With both these categories the cow’s demeanour will be unchanged-that is, bright and
alert and the cow will be interested in her surroundings and eating and drinking
 Other metabolic diseases
 Non-parturient hypocalcaemia
Note that I am simply listing the various categories-some discussion of conditions
within each category would be called for
Question 10: Outline your treatment for a case of the wasting (or digestive) form
of ketosis in a lactating dairy cow
There would be three parts to the answer as follows:
 Replacement therapy
(1) 500ml 50% glucose given I/V using a flutter valve
(2) Propylene glycol or glycerine (both glucose precursors), given orally for 2-4 days,
or until appetite returns
 Hormonal therapy
20mg (10ml) of a glucocorticoid such s dexamethasone I/M
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Combined therapy
Most vets administer 500ml 50% glucose I/V plus 20mg dexamethasone I/M and may
also recommend the use of a glucose precursor as a drench

Question 11: Milk fever and the downer cow syndrome are closely related. What
advice would you give a dairy farmer who was getting a high incidence of both
milk fever and downer cows in his dairy herd?
Note that this question is not a roundabout way of asking about milk fever prevention,
it also requires some comment on the high downer cow incidence
(1) The advice would include ways of preventing milk fever with the most effective
being alteration of the DCAD in the ration by the addition of anionic salts to the
dry cow/transition cow ration
(2) The other advice would be to treat cases of milk fever early and preferably get a
vet to give Ca I/V as farmer-administered subcutaneous Ca may not be enough to
get the cow up. I would be happy these days as a vet to train the farmer on how to
find the jugular vein and give I/V calcium
Question 12: How would you treat a case of peracute mastitis due to
Staphyloccus aureus in a freshly calved dairy cow?
Treatment regime is as follows: (note that peracute Staph mastitis is always
gangrenous):
(1) Early treatment with short-acting oxytetracycline I/V will save the life of many
cows but the affected quarter will still be lost
(2) Intrammamary infusion of antibiotics is of little value
(3) Supportive treatment includes the use of 10-20 litres of electrolyte solution I/V 
the injection of NSAID’s such as Finadyne or ketoprofen
(4) Other treatments include (a) amputation of the teat to aid drainage and (b)
amputation of the quarter of ligation of the mammary vessels to the affected
quarter (historical treatment only)
Question 13. List the important elements in a mastitis control program. Why
don’t these measures work as well in cases of environmental udder pathogens?
(1) The important elements can be grouped as follows:
 Measures to reduce the new infection rate and
 Measures to reduce the duration of infection
(2) Measures to reduce the new infection rate are mainly hygiene measures and
include teat dipping or spraying, hygiene during milking and regular maintenance
of the milking machine
(3) Measures to reduce the duration of infection include dry cow therapy, treating
clinical cases and culling chronic cases
(4) Note that your answer should include some brief discussion of each of the above
including mentioning the use of teat sealants when talking about DCT
(5) These measures are all designed to control contagious mastitis pathogens spread
during milking and will not prevent infections that the cow picks up away from
the milking shed and in the latter part of the dry period.
Question 14. Discuss important features of the epidemiology of anthrax in cattle
in Australia. What possible explanations exist for occurrences of the disease
outside recognised “anthrax belts”
 Epidemiology
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(1) Anthrax is a soil borne infection
(2) The disease in Australia occurs mainly in well defined endemic areas where soil
and climate favour survival of the bacillus
(3) Geographic distribution
 occurs in ‘anthrax belts’ in parts of NSW and Vic (endemic areas above)
 has also been reported in south-Western Australia, Rockhampton (1 case) and
in the Wandoan area of Qld
(4) Outbreaks are more common in the warmer months of the year
(5) Cattle become infected by ingesting spores from contaminated pasture or soil and
through contact with infected carcases
(6) Spread of infection
 not spread directly by contact
 any activity (ploughing etc) that spreads or disturbs spores in the soil can
result in the exposure of more animals
 spread can occur by movement of animals that are incubating the disease
 Occurrences outside recognised “anthrax belts”
Could occur due to the following:
(1) Movement of cattle as outlined above
(2) Disturbance of soil by agricultural practices where the spores have lain dormant
for many years and are now brought to the surface
(3) Major climate change such as flooding where spores are moved from one area to
another
Question 15 How would you confirm a clinical diagnosis of botulism in a dairy
herd?
(1) The disease commonly affects a number of animals at once with clinical signs of
flaccid paralysis (more commonly, animals are simply found dead)
(2) There are no specific lesions found at necropsy exam
(3) An attempt can be made to demonstrate the toxin in suspect food, water or animal
tissues (gut contents, serum, liver, spleen, faeces) by injection of this material into
mice
(4) The suspect feed can be fed to experimental animals such as lab animals or cattle,
however the toxin can be very patchy in its distribution in feed
(5) Use of ELISA tests as follows:
 T-ELISA (toxin ELISA) is used as a screening test on feed samples and/or
animal tissues
 A-ELISA (antibody ELISA) is used as a herd test for botulism diagnosis,
particularly in extensive beef herds
SECTION B
Question 1.
The following is an abbreviated answer
What is your differential diagnosis?
(1) Pyloric stenosis form of vagus indigestion
(2) Possible abomasal impaction
(3) Not RDA/RDA because there are no pings
(4) Not metritis-good uterine tone on rectal exam
(5) Not mastitis- question says it has cleared up
What is your prognosis?
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Answer: Unfavourable (or poor)
What is your treatment?
This cow is probably unlikely to respond to treatment, however the following could
be tried:
(1) Rumen lavage using a wide bore stomach tube (more for anterior functional
stenosis)
(2) Administration of 5-10 litres of mineral oil via stomach tube daily for 2-3 days
(3) Administration of 20 litres balanced electrolyte solution I/V (more for anterior
functional stenosis)
(4) Consider euthanasia
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