DPT 511 - Production animals

Bovine Pathology Case studies 2021

Instructions

1. Provide one or more morphological diagnosis

2. Provide an aetiological diagnosis or develop a list of differential diagnosis – to know what samples to focus on
3. List key epidemiological features for the diagnosis or each of the DD’s
4. List the specimens to be collected and diagnostic tests to be performed to confirm a diagnosis for each DD.
What is normal and abnormal and the lesions

Case 16 – acute heart failure, with the heart failing over a couple of hours – LHF - GIFBLAAR

Caudal dorsal area of the lungs – has a white appearance of the visceral pleura of the lung – NORMAL
(Caudal dorsal part of the lung in a bovine – explands more than the cranial part – when the lung
collapses – the pleura thickens and appears white – NORMAL

Vets make the mistake – by looking at this and jumping to the conclusion of it being pneumonia – you
need to be careful (rather take samples for histopathology to see or do impression smears – to see if
you have inflammatory cellular component)

Image – Acute heart failure – with heart failing Macroscopically

- Opened thoracic cavity
- focus on the lung and mediastinum
- diffuse purple discoloration of the lung and on the mediastinal
part/cranial mediastinum – there is fluid accumulation and not
yellow (watery and translucent) - oedema
Lungs like this = 2 things
- congestion – common change
simple/passive acute congestion of the lungs
- active congestion in the form of hyperemia – referring to
inflammation – pneumonia
- You can look at the surface of the lungs
- On cut surface of the lung in an animal with interstitial pneumonia = rubbery consistency and
heavy lungs – way above normal – loses spongy feel
If you cut into it – will ooze oedematous fluid – part of exudate in interstitial pneumonia =
foamy on cut surface
In acute passive congestion
- The lung maintains its spongy and dense purple – this lung in the image is spongy and not
heavy, but is congested
what you have in this image and with congested lungs – mediastinal
oedema takes place
- think of a cardiogenic mechanism at work – this is all the
hallmarks of acute heart failure
- acute heart failure – heart stops in per acute and may not have
congested or may take time to fail and it would be more intense
congested lung, or you may get a lung takes a bit longer to fail
and is still in acute and fails in 2 to 3 hours and intense
congestion of the lung, as well as enough time that the heart is
failing with increase hydrostatic pressure
this is a sign of acute heart failure with the heart failing over a couple of
hours in a period
Gifblaar intoxications
- region in the country – gifblaar areas
Has indicators
- Wild syringa (Burkea africana),
- silver terminalia (Terminalia sericea), lek-kerbreek (Ochna
pulchra),
- grysappel (Parinari capensis)
When the left heart takes longer to fail -> see oedematous fluid in pericardium and in chest cavity- LHF
Cardiotoxicities – LHF more as appose to FHF with pulmonary hypertension (ascites and liver
centrilobular fibrosis and oedema in abdomen)
Combination of the 2 – ascites and hydrothorax – the whole heart is failing
LHF image – typical in cattle with cardiotoxicities which give acute heart failure
- Cardio glycosides – tulp, others
- Gifblaar – dichapetulum
- Ionophore toxicity
- Gossypol – chronic left heart failure
Key features
- On soil - small little shrub that grows in patches on the ground
- Alternate leaves and fruit (rare)
- Leaves can be hairy or smooth
- Venation of the leaves – curvature – primary and secondary veins that curve adjacent
When leaves are chewed – all the green disappears, and u get a netted appearance
Gifblaar
- Acute heart failure -> you can predict the amount of pathology is not much great
- Congestion is not specific and acute heart failure can be many things
- Conditions affect the heart intrinsically
Ionophore toxicity Diagnosis
- take feed content
- rumen content will not suffice - Histopathology – samples of choice – but not clear due to per acute and acute conditions – not
- heart muscle and diaphragm – will affect skeletal muscle much time for lesions to occur in the heart – morphologically on microscope there is little to
tissue see
Cardioglycosides - Tulp and ionophore you can see lesions in the heart
- toxicology test - Take HEART – sample the apex and include the internal ventricular septum and left pupillary
- rumen contents muscle and free wall and the right ventricular wall and the 2 atria (1cm cubic blocks –
- but many labs do not test for it anymore throughout the myocardium) – formalin jars
- History in a herd

Gifblaar being acute -> the leave remnants in the rumen contents (only plant)
-Cardioglycosides – everything chewed up and digested

What if animal only eats 1 or 2 leaves

- Highly potent toxin

- Monofluoroacetate – couple of leaves needed to kill an animal
- If it eaten 1 or 2 – it is still lethal – animal will survive the acute stages and ruminate the leaf
remnant and disappear from rumen content
- Animal can eat other leaves and can be found in rumen – u need to submit leaves for diagnosis
by a botanist

However, you can take the suspicious leaves and dip in formalin for histopathology

Lab tests for Monofluoroacetate

- Not common anymore

- In its chemical form – used to kill vermon/predator farm s- not much exists – but can be asked
to taken rumen contents for Monofluoroacetate analysis
- Do not take a negative report with negative results
 DPT 511 - Production animals

Bovine Pathology Case studies 2021

Instructions

5. Provide one or more morphological diagnosis

6. Provide an aetiological diagnosis or develop a list of differential diagnosis – to know what samples to focus on
7. List key epidemiological features for the diagnosis or each of the DD’s
8. List the specimens to be collected and diagnostic tests to be performed to confirm a diagnosis for each DD.
What is normal and abnormal and the lesions

Case 17 – Pesticide poisoning

Pesticide intoxication/poisoning

- more common than we think

Image
- Kidney of sheep
- Maize present
Do not focus on kidney, but what else is happening
- the flies are dead and, on their backs, – do you expect to have
dead flies while doing a pm – BE AWARE of other things and see
what is normal at a PM
- flies which sit on tissues and die, and your PM is negative, and u
do not see much but signs of acute heart failure with congestive
heart failure – YOU NEED TO CONSIDER PESTICIDE POISONING
-
- accidently in feedlots, as well as malicious poisons by workers – feedlots and farms and poison
the cattle
- feed particle that the cows and sheep may like
- maize are whole Kernels– used for planting and maize crop production
- You need to ask the owner the history about feed and what type of maize and if he fed the
animal maize and if it was crushed or white/yellow maize
If he says no – RED FLAG – malicious poison
Maize for crop production is normally catered with pesticide production automatically – sometimes
you see a colour code (blue or pink – but not seen here as its washed by rumen fluid)
-Red flag – foreign chemical substance ingested
Diagnosis
- Rumen contents/ organs (kidney/liver) – for pesticide screening and analysis
(you don’t need to tell the lab – what pesticide you suspect, you can but you often get asked
what is this pesticide used for)
Organophosphate poisoning CS Other items that are poisoned
- Acute death
- Tremors, tenesmus and diarrhea, worms - Water troughs – no indication in the rumen -take rumen contents
- Sudden mortalities of same duration – typical intoxication Any acute heart failure/ acute condition that stems from gifblaar or organophosphate poisoning
pattern
(pesticide poisoning) – rumen samples to collect
- No typical bell curves
-
Anything taking longer to digest before it causes the problem – rumen content not a good sample to
collect
 DPT 511 - Production animals

Bovine Pathology Case studies 2021

Instructions

9. Provide one or more morphological diagnosis

10. Provide an aetiological diagnosis or develop a list of differential diagnosis – to know what samples to focus on
11. List key epidemiological features for the diagnosis or each of the DD’s
12. List the specimens to be collected and diagnostic tests to be performed to confirm a diagnosis for each DD.
What is normal and abnormal and the lesions

Case 18 – Microcystic aeruginosa

Epidemiological pattern

- more common in the country

- animal mortalities – does not discern any animals – any animals which drink the water will die
- cattle or sheep or buffalo – multis species
- die quickly and found close to the source of what causes the mortality
- accidently in feedlots, as well as malicious poisons by workers – feedlots and farms and poison
Image the cattle
- Dam
- Buffalo that is floating If you see all species and dead animals close to the water hole – do not only look into organic cause
- Green coloration of the water – Microcystis aeruginosa – like algae bloom, but it can also be malicious poisoning with organophosphate or cyanide poisoning
cyanobacteria
(highly potent -blue green algae/ algae blooms)
Did the buffalo drown?
- it is possible, but not likely
- the animal may have been poisoned
 Diagnosis

- Histopathology of the liver (both right and left lobes samples in formalin) – due to portal
streaming of blood from various parts of the intestine (1 lobe of the liver may have intense
lesions and the other may not have it) – if u take the wrong lobe – will not provide good
evidence
- Toxic heptoses on histopathology – but not specific, there are reports that microcystic causes
specific midzonal/ zonal to hepatocellular necrosis – Dr Steyls experience – not clear
- Reports should be taken further – by collecting water for toxic analysis – mouse assay – in vivo
assay (similar to botulism) – water injected interparental into mice to see what happens
- You can also look at the algae – on microscope – morphology – dark green black spots forming
PM colonies
- Principle hepatotoxin
- Hepatoxicities
- Macroscopically the liver will look like this -> zonal pattern or
zonal heptoses (white circles with center of circles being central
canal/vein of the hepatic acinus, and the white area around the
central canal area the injured hepatocytes which is diffusely
spread across the liver and causing massive acute liver failure
- MAIN CAUSE
 DPT 511 - Production animals

Bovine Pathology Case studies 2021

Instructions

13. Provide one or more morphological diagnosis

14. Provide an aetiological diagnosis or develop a list of differential diagnosis – to know what samples to focus on
15. List key epidemiological features for the diagnosis or each of the DD’s
16. List the specimens to be collected and diagnostic tests to be performed to confirm a diagnosis for each DD.
What is normal and abnormal and the lesions

Case 19 – Thiamine deficiency – VIT B 1

Lesion In cortex, whereby the darker areas may be haemorrhage and there is loss in distinguish
between grey and white matter – due to haemorrhage and necrosis
This specific gyrus is sunken – malacia
More older lesions – different time periods associated with all lesions

Typical for necrosis of the grey matter – polioencephalomalacia

- Cerebral cortical necrosis – differentiate with FEM (pulpy kidney) and with
leucoencephalomalcia (intoxications)
Image
- Bovine brain Thiamine deficiency
- Cross section of cerebral hemispheres
- Common seen
Underlying triggers - Associated with rumen acidosis -> proliferation of thiaminase producing bacteria in the rumen
- Acidosis – common in cattle - Thiamine/ B vitamins – not food items, but is produced in the rumen
- In cats/ animals with a fish diet – b1 diet – similar in cat – will be - Rumen produced vitamin B 1 and when it is low > problem with blood supply that is affecting
 low
Epidemiology
- High concentrate diets
- Feedlots
Signs typical of a CNS deficit – depending on the lesion location
- Occipital lobe -> blindness – animals head pressing into the
camps and drinking water
- Blindness also lead poisoning – clinically amaurosis – central
blindness (inspect the eyes they will be blind and nothing wrong
with the eyes and ocular tissue -> central blindness)
- Overdoses with rafoxanide – NB
- Extensive conditions – over grazed pasture - Helichrysum
argyrophyllum – little weeds flat on the ground – colored
flowers – clinically
- Aggression for CCN – D for rabies
Fungal plaques in inured ruminal mucosa – the fungi are saprophytic –
mucor mycosis – areas of necrosis -> emboli in rumen vasculature ->
punches out lesions (like LSD – but nothing wrong with rumen – not a
DD for this image), you need to consider similar mechanism whereby the
blood vessels are thrombosed causing infarcts and necrosis
Chronic to acute stages in rumen serosa – multifocal large foci of
hemorrhage and necrosis (typical infarcts)
-> submit sample for histopathology – confirmation of mucoid mycosis
(chronic of rumen acidosis)
the cortex of the brain
- Underlying mechanism – vitamin B is NB for the blood supply of the cortex and if it is low ->
ischaemic necrosis
CCN macroscopically
- Can be subtle
- Often visible when fixed in formalin
- Cut fresh brain and you do not see anything – put in formalin – sectioned 1cm widths apart – 2
quarters through the brain – fix in formalin for fixation and then couple of days later you will
see grey, yellow areas in cortex which is highlighted
- Histopathology will also help – brain
Acidosis being the common trigger
This is an acidosis condition
What are the chronic consequences of acidosis
- CCN with thiamine deficiency
- Rumenitis -.> predisposition to fungal growths (Mucoid mycosis)
- Hepatic abscess in liver -> Rupture -> peritonitis and fatal -> also can be in veins in caudal vena
cava and area compress – congestion of the liver -> rupture in caudal vena cava -> emboli -> in
right heart and right ventricles and into lungs -> lung emboli -> rupture -> haemorrhage in
lungs -> death and epistaxis
- Also, pulmonary endocarditis can cause emboli in lungs and haemorrhage in lungs