Toxicology Flashcards
Name five plants which have the potential to cause nitrate poisoning ?
Nitrate poisoning
Example of plants
Avena sativa oats
Sorghum sp
Lolium spp. Rye grass
Portulaca spp (pig weed)
Dactyloctenium (button grass).
The nitrates are concentrated in plants stems and stalks.
Describe the pathology of nitrate poisoning ?
Why are horses not susceptible to nitrate poisoning ?
Pathology nitrate poisoning
Species affected = ruminants
Nitrates are converted to nitrites by the rumen bacteria (or by bacterial and fungal action in stored plant materials).
High levels of nitrates oxidises haemoglobin to methaemoglobin Fe3+, which renders red blood cells unable to transport oxygen (reducing the oxygen carrying capacity of blood.
Clinical signs will be observed at 50-60% conversion to methaemoglobin, with death above 75% conversion.
Horses are not susceptible
Monogastric are unable to convert nitrate in their digestive tracts to nitrite. They may be susceptible after microbial conversion of nitrate to nitrite in swill or wet hay.
Describe the clinical signs you would observe with nitrate poisoning ?
Clinical signs of nitrate poisoning
Acute death death 15mins+
Heart and lungs
- rapid deep breaths
- irregular weak heart beat
Nervous
- muscle spasm coma
At post mortem
- chocolate brown blood (presence methaemoglobin).
Note - Nitrate also acts as a vasodilator which may reduce peripheral perfusion and circulation to the uterus. Reduced blood flow to the uterus along with reduced oxygen carrying capacity contributes to placental hypoxia. = abortion observed in many cattle which survive.
What factors could affect plants to increase animal susceptibility to nitrate poisoning ?
Plant associated factors associated with accumulation of nitrate.
- low light volumes / low temperatures (reduces photosynthesis)
- high nitrate content in the soil (fertiliser)
- most nitrate is contained within the stems stalks (high nitrate conc)
- naïve rumen bacteria + massive feed intake = nitrite absorption
- immature plants, lush, low, fibre.
Plant nitrate content >1.5% KNO3 equivalent in dry matter is hazardous.
Describe what test could be used for nitrate poisoning ?
Nitrate poisoning
Phenylamine test
- suspect plants (>1.5% KNO3 in dry matter considered potentially toxic to ruminants)
Test aqueous humour of the eye (at post mortem) (>20mg NO3/L is diagnostic)
Commercial strips for nitrate MERCK / test plants or urinalysis
- the test detect nitrate levels, even though nitrite is the real culprit
Describe how you could treat nitrate poisoning ?
Nitrate poisoning
Methylene blue IV
- off label drug
- not currently registered for use in food producing animals
- vets are only allowed to treat a single animal within a herd
- withdrawal times must be advised
- treat the less severely affected animals first.
Greater emphasis of prevention
- feed adequate carbohydrate (grain)
- check suspect crops
- avoid circumstances promoting rapid intake of hazardous plants
Describe the MOA of cyanogenic glycoside poisoning ?
MOA Cyanogenic glycoside poisoning
Enzyme = beta glucosidase hydrolyses amygdalin
Plants store cyanide as cyanogenic glycosides in vacuoles which are separated from the activating enzymes beta glucosidase enzymes in the cytosol.
When the animal chews the plant the two are mixed producing toxic HCN (prussic acid).
The HCN is rapidly absorbed into the animals blood and spreads to it cells.
HCN blocks the mitochondria cytochrome oxidase > mitochondria cant make ATP > the body goes into energy starvation.
HCN results in tissue anoxia, as oxygen is retained in the blood
Describe the clinical signs of cyanide poisoning
Clinical signs of cyanide poisoning ?
Acute = sudden death (most common)
Post mortem = cherry red blood
Rarely chronic effects attributed to cyanide poisoning are reported, including
Cattle
- posterior ataxia and urinary incontinence
- foetal arthrogryposis
- sulphur responsive reduced production
- muscle spasms
- coma
- deep rapid breaths and a weak heart beat
Sheep
- selenium deficiency
- congenital goitre
Describe the potential factors of the animal and plant which could lead to cyanogenic glycoside poisoning ?
Factors cyanogenic glycoside poisoning
Plants
- age young growth and regrowth is more toxic
- genotype (certain families more toxic)
- plant nutrition (prussic acid increases with nitrogen fertiliser, phosphorous deficiency and decrease with sulphur fertiliser)
- stress
- dry matter more dangerous than source plant
Animal factors
- feed intake - hunger
- time since last feed - HCN production more rapid in a fasted rumen high rumen PH
- exposure history
Describe how you would diagnose and treat a case of cyanogenic glycoside poisoning ?
Cyanogenic glycoside poisoning / prussic acid
Diagnosis
- clinical signs
- post-mortem findings
- known access to a source of cyanogenic glycoside containing plants
Treatment
Sodium thiosulphate IV or PO
Describe how you would diagnose and treat a case of cyanogenic glycoside poisoning ?
Cyanogenic glycoside poisoning / prussic acid
Diagnosis
- clinical signs, post mortem findings
- known access to a source of cyanogenic glycoside containing plants
Prevention
- graze sorghum >75cm
- supplement sorghum with sulphur
- reduce hungry animal access
- feed cyanogenic plants as silage to reduce abolish toxicity
Treatment
sodium thiosulphate IV and PO (per oral)
Describe the MOA for oxalate poisoning ?
Oxalate poisoning
Sheep, goats and cattle
Plant oxalate can be found in both the soluble and / or the insoluble form at a neutral PH.
Soluble oxalates affects the homeostasis of calcium
- primarily by sequestering with calcium ions
- resulting in hypocalcaemia (and hypomagnesaemia)
Insoluble oxalates is generated by binding and precipitating crystals in tissues which it then damages, nephrosis as an example.
Hypocalcaemia and nephrosis with oxalate calcium crystals in tubules.
Describe the pathology and clinical signs of calcium oxalate poisoning ?
Calcium oxalate poisoning
- Rumenitis
- Blood - hypocalcaemia, azotaemia (increase) in nitrogenous products creatine)
- Kidneys calcium oxalate crystals nephrosis
- lungs dyspnoea and oedema
- Neuromuscular system, stiff gait staggering collapse
Describe the diagnosis and treatment of calcium oxalate poisoning ?
Calcium oxalate poisoning
Diagnosis
- clinical pathology
- kidney histopathology
- soluble oxalate assay on plants
Treatment
Calcium borogluconate IV SC
Nephrosis is a serious syndrome resulting in a guarded prognosis.
List five plants which contain cardiac glycosides, and the poisoning circumstances ?
Cardiac glycosides with the plants
Species affected = horses and ruminants
- Nerium Oleander
- Thevetia peruviana yellow oleander
- Rubber vine
- Mother of millions
- Cape tulips
- Foxglove
- Adonis microcarpa (pheasents eye)
- Chorchorus olitorius (jute)
Poisoning circumstances
- plants are generally not palatable
- hunger or lack of alternatives
- plants retain toxicity when dried and are more toxic at certain times eg flowering
- contaminated garden clippings
- some pharmaceuticals eg digoxin can cause cardiac toxicity
Describe the clinical signs of cardiac glycoside poisoning ?
Clinical signs of cardiac glycoside poisoning in animals
- Sudden death
- Cardiac arrhythmia (bradychadia, tachycardia, focal necrosis)
- diarrhoea with blood
- azotaemia
- focal myocardial necrosis
- dyspnea, atelactasis and oedema
Ruminants = rumen atony and omasa ulcerations
Horses will show signs of abdominal pain coli
Dogs and pigs may vomit
Describe the mechanism of action for cardiac glycoside poisoning ?
MOA Cardiac glycoside poisoning
Cardiac glycosides inhibit the Na+K+ pump on cardiac and other tissues
- intracellular Na+ increases followed by the concentration of Ca2+ through the effect of the Ca2+ exchange mechanism
The increased concentration of Ca2+ causes over activation of the myosin/actin filaments.
Describe how you would go about diagnosis and treatment of cardiac glycoside poisoning ?
Cardiac glycosides
Diagnosis
- plant access
- myocardial histopathology
- cardiac arrhythmia
Treatment
- activated charcoal
- electrolyte replacement fluid PO
- Atropine
- Propranolol
Note - some pharmaceuticals might not be available for use in food producing animals. Also chasing a large group of cattle causing stress may not be practical.
Describe the poisoning circumstances Bufogenins / bufotoxins ?
Bufogenins / Bufotoxins
The cane toad has parotid glands on the back of the animal behind the eyes. The poison can also be produced in other areas of the skin.
Dogs are poisoned by mouthing the toad
- more cases in warmer months of the year (may be all yaer round in Northern QLD)
- small dogs more frequently affected / more inquisitive
What is the pathology and clinical signs of Bufogenins / Bufotoxins poisoning ?
Bofugenins / Bufotoxins poisoning cane toads
MOA
- Same mode of action as cardiac glycosides by inhibiting the Na+K+ ATPase in myocardial cells and subsequent intracellular Ca2+.
Clinical signs
- ptyalism excessive salivation
- cardiac arrhythmia
- seisures
What is the pathology and clinical signs of Bufogenins / Bufotoxins poisoning ?
Bofugenins / Bufotoxins poisoning cane toads
MOA
- Same mode of action as cardiac glycosides by inhibiting the Na+K+ ATPase in myocardial cells and subsequent intracellular Ca2+.
Clinical signs
- ptyalism excessive salivation
- cardiac arrhythmia
- seisures
Identify the cane toad toxin, how would you diagnose and treat the clinical signs?
Bufogenins / Bufotoxin
Diagnosis
- exposure history and clinical signs
Treatment
- flush the mouth out with water
- monitor ECG in severe cases
- atropine for bradycardias <50 beats a min
- esmolol or propranolol for tachycardias
- diazepam or anaesthesia for seizures
Activated charcoal and diuretics
What plants contain fluroacetate and what are the poisoning circumstances ?
Fluoroacetate poisoning 1080
affects dogs, ruminants, horses, pigs and rodents
1080 is used as a fluoroacetate poison
- Gastrolobium heart leaf
- Georgina Gidyea
- Afrikans gifblaar
Poisoning circumstances
- pods are far more toxic then leaves
- drought / dry season
- signs of poisoning often occur when stock are moved / forced exercise often preceeds death
- secondary poisoning of dogs scavenging carcasses
- plants can be highly palatable and readily eaten
- placements of baits
Describe the mechanism of action of fluoroacetate poisoning ?
Fluoroacetate poisoning
Fluoroacetate is converted to fluorocitrate
which is potent inhibitor of the TCA cycle (Krebs cycle).
The cells are deprived of an essential source of ATP resulting in cellular death.
Various metabolic disturbances for instance metabolic acidosis, occur through the accumulation of citrate and blood.
Describe the pathology and clinical signs of Fluoroacetate poisoning ?
Fluoroacetate poisoning
Pathology
Multifocal myocardial degeneration and necrosis sheep
- there may be myocardial scarring in survivors of Acacia Georgina poisoning.
As with most sudden death syndromes lesions may not be apparent, non existent or subtle.
- it takes time to manifest in the body
- 6hrs electron micrographic changes, a entire day for histological changes
Clinical signs (sudden death)
Dogs
- excitement hysteria
- wild running
- barking
- tonic convulsions, paddling
- dypsnea frothing
- repeated vomiting and diarrohea
Ruminants
- arrhythmias
- focal necrosis
- defaecation and urination
- hypersensitivity
- depression
Describe how you would diagnose and treat a case of fluoroacetate poisoning ?
Fluoroacetate poisoning
Diagnosis
Assay stomach contents
Myocardial histopathology - multifocal myocardial degeneration necrosis
Treatment
There is no specific treatment and the prognosis is generally poor
- anaesthesia for convulsions
- ethanol
Prevention is the better option
- muzzle dogs in areas with bait
- new methods of delivering baits reducing the possibility of accidental non target species poisoning
- manage livestock access to plants especially during drought
- genetically engineered rumen bacteria for detoxification
Describe the poisoning circumstances of Grayanotoxins ?
Grayanotoxins
Species affected = ruminants, camelids, equids, dogs and cats
Poisoning circumstances
Rhododendrons Azaleas
These species are common ornamental garden plants;
- access to garden waste
- humans consuming contaminated honey
Describe the mode of action of Grayanotoxins ?
MOA cyanotoxins
Binds and modifies the cell membrane Na+ channels, increasing the permeability of Na+ into the cell. affecting the cell potential.
This also leads to increased intracellular Ca2+ having a positive inotropic effect on myocardial cells.
Describe the clinical signs of Grayanotoxin poisoning?
CS Grayanotoxin poisoning
Early onset drooling followed by regurgitation in ruminants
- choking
- laboured breathing and cyanosis
- aspiration pneumonai
- cardiac arythmia
- sudden death
Describe how you would diagnose, treat and prevent Grayanotoxin poisoning ?
Grayanotoxin poisoning
Prevention
- reduce access to garden plants and their disposal
Diagnosis
- CS and history of access to plants or garden clippings/ waste containing the plants
Treatment
- Remove from source
- rehydrate, absorbants
- antiarrhythmics atropine
Describe the poisoning circumstances of Galegine
Galegine
Animals affected = ruminants and pigs
Plants containing the toxin
- Goats rue (Galega officinalis)
- Crown beard (Asteraceae)
- Poison sedge ( Cyperaceae)
Poisoning circumstances
- hungry stock and dense plant population
-
Describe the MOA, pathology and clinical signs of Galegine poisoning ?
Galegine poisoning
MOA
Increases pulmonary permeability - fibrin rich effusion ( straw coloured and solidifies into a gel-like substance at room temperature)
Pathology
Severe hydrothorax (very distinctive find)
Pulmonary oedema
Clinical signs = sudden death
- dyspnoea rapid breath
- oedema
- hydrothorax
Describe how you would go about diagnosing and treating Galegine poisoning ?
Galegine poisoning
Diagnosis
Pathology ( straw coloured effusion into the hydrothorax)
access to plants
Treatment
There is no therapy
To prevent deny access and control plants
Describe the MOA and cause of poisioning when animals consume ironbark ?
Consumption of ironbark
Poison = Erythrophleum / Diterpenoid alkaloids
All parts of the pants are toxic
- root suckers are a great risk for grazing animals
- any consumption is a risk
Clinical signs
- acute death
- cardiac arythmia
Describe the poisoning circumstances of Cyanobacteria ?
Cyanobacteria = called blue- green algae
The factors which increase the risk of cyanobacterial blooms
- nutrient concentrations in water ways (livestock waste fertilisers)
- seasonally reduced flow rates
- wind could concentrate alage blooms
- irrigation with water contaminated with cyanobacterial blooms
Describe the pathology of Cyanobacteria poisoning ?
Cyanobacteria produce two groups of toxins
Pathology
Hepatotoxins (microcystin , nodularins)
- inhibits proteins phosphatase 1 and 2A in the liver - this disrupts the cytoskeleton of hepatocytes and endothelial cell.
- liver disintegrates and the cells lose their archetecture and die
- necrosis and haemorrhage
In acute to severe cases = Peri acinar liver necrosis
Subacute cases
- more prolonged and less severe lesions
- fatty liver
- biliary hyperplasia
- cholestasis
- fibrosis
Characterised by a swollen pale liver with generalised petechial haemorrhage
Neurotoxin
- no gross post mortem abnormalities observed
Describe the clinical signs of Cyanobacterial alkaloid neurotoxins and hepatotoxins ?
Clinical signs of cyanobacteria poisoning
Neurotoxic alkaloid
“Fast factor death syndrome” neurotoxin
Neurotoxins may lead to respiratory arrest, hepatotoxins can lead to death and sudden death due to massive hepatic necrosis.
- tremors, staggers and recumbency
- hypersensitivity to stimuli
- abdominal pain
- diarrhoea and dyspnoea
“Slow death factor syndrome”
- severe liver damage noticed as jaundice and photosensitivity
Describe the pathology and clinical signs of acute liver necrosis ?
Acute liver necrosis
Pathology and clinical signs
Icterus/photosensitization = inability to excrete substances into bile
Hepatic encephalopathy = inability to remove toxic substances
haemorrhage = failure to sythesise sufficient clotting factors
Sweeling and inflammation of the liver = abdominal pain (saw horse stance, teeth grinding, colic kicking at the belly.
Describe the poisoning circumstances of Furanosesquiterpenes poisoning ?
Furanosesquiterpenes poisoning
Animals affected = ruminants
Plants
Native fushia
Turkey bush
Myoporum laetum (New Zealand)
Describe the pathology, diagnosis and treatment of Furanosesquiterpenes poisoning ?
Furanosesquiterpenes poisoning
Animals = ruminants
Pathology
Acute hepatic necrosis
Lesion distribution in the liver can centrilobular, midzonal or periportal necrosis.
This depends on the metabolic state of the toxin
Can cause sporadic secondary photosensitisation
Diagnoses
Pathology and identification of plant in accessed pastures
Treatment
NIL - deny access to these plants to prevent plant poisoning
Describe the poisoning circumstances, mode of action and pathology of MAMS ?
MAMs = Methylazoxymethanol
Animals affected = ruminants and dogs
Ingestion of plant
Cycad seeds or leaves ingested
Cycads Macrozamia, Bowenia and Lepidozamia
Mode of action
Cycasin is broken down into glucose plus MAM in the rumen.
MAM is absorbed by the intestines and is transported to the liver.
In the liver MAM is transformed into a highly reactive and damaging methylating agent.
Pathology
- acute hepatic peri acinar necrosis
- vascular damage
- necrotic gastroenteritis
- megalocytosis
Describe the poisoning circumstances and pathology of Gossypol ?
Gosspol
Gossypol is contained within the pigment glands of cotton seeds
- excess gossypol in rations
Pathology
- MOA cardiomyopthy
- heart failure
- liver necrosis
- hen’s egg yolk discolouration
To prevent poisoning add iron and calcium to the diet
DO NOT FEED
pre-ruminants, chickens and pigs
Describe the poisoning circumstances of Aflatoxins ?
Aflatoxins
Aspergillus flavus (fungus) often grows on carbohydrate rich foods
-peanuts, grain, bread
- the distribution of toxins is not uniform (may only affect the bottom of a bag of dog food).
Animals affected
Poultry are the most susceptible
followed by dogs>pigs>cattle>sheep
Describe the MOA of Aflatoxin poisoning ?
Aflatoxin poisoning
MOA
Aflatoxins are metabolised in zone 3 of the liver by cytochromes.
- the metabolites are highly reactive and bind up nucleic acids including DNA
- binding of DNA inhibits cell division
- binding of RNA inhibits protein synthesis
- the cell eventually dies /stops mitosis
In severe cases you will see liver necrosis
Long term binding of the DNA can be carcinogenic
Describe the pathology and clinical signs of poisoning From the fungus Aspergillus flavus ?
Aspergillus flavus = Aflatoxin
Pathology
Binding of the DNA prevents the cell from undergoing mitosis.
In the liver hepatocytes compensate for the inability to divide by becomming really large
- megalocytosis (big cell)
- widespread haemorrahge
- jaundice
- chronic liver lesions such as fatty change, biliary duct hyperplasia and fibrosis
Note the pale liver and distended gall bladder
Clinical signs
- hepatic encephalopathy nervous signs such as circling, head pressing and stumbling
- aggression
- teeth grinding
- convulsions
- photosensitive dermatitis
- pregnant animals may abort
gastrointestinal signs such as diarrhoea, tenesmus (straining)
- rectal prolapse
saw horse stance and kicking at the belly
Describe the poisoning circumstances of Phomopsin poisoning ?
Phomopsin poisoning circumstance
Diaporthe toxica is a fungus which produces Phompsin
- grows on dead lupins
- poisoning is concentrated in the seeds of plants
Lupinosis is a mycotoxicosis - pathology caused by the fungal toxin.
- Lupinosis associated myopathy (LAM)
Describe the pathology and clinical signs caused by the ingestion of Phomopsin ?
Diaporthe toxica = Phompsin
Pathology
- jaundice and swollen pale liver and distended gall bladder
- individual hepatocyte necrosis
- numerous mytotic figures and fibrosis
- chronic liver damage
Clinical signs
- weight loss
- jaundice
- stiff gait
- skeletal muscle degeneration
-
Describe how you would diagnose and treat a case of Lupinosis ?
Phompsin = Diaporthe toxica
Diagnosis
- lupin stubble or seed access
- phompsin assay
- liver histopathology
Prevention as there is no therapy
- diaporthe resistant cultivars
- grazing and plant management to minimise stubble intake
- potential vaccine but it is not commercially available
Describe the poisoning circumstances of Cylindrospermopsin ?
Cylindrospermopsin
The most important pathogen responsible for poisonings of this toxin = Cylindrospermopsis raciborski
Blooms are dispersed through out the water column.
Describe the pathology and clinical signs of Cylindrospermopsin ?
Cylindrospermopsin
Pathology
The toxin is a potent inhibitor of protein synthesis in mammals. Toxin production peaks in winter in Northern Australia
The clinical signs
- sub acute to chronic liver damage
- nephrosis
- palor
- distended gall bladder
- focal myocardial necrosis
- swollen hepatocytes
What can be done to stop the Clydrospermopsin poison ?
Clydrospermopsin
There is no treatment
To prevent disease
- reduce ran off off fertiliser and faeces into the water
- reduce nutrient load
- vegetate margins of the small reservoir dams
- aerate bottom
- reduce P inflow (minimise fertiliser use, vegetation buffer zones, minimise sewage)
- improve flow rates and disrupt stratification
Describe the poisoning circumstances of Tannins (hydrolysable) ?
Tannins hydrolysable
Animals affected = cattle > sheep
Yellow wood Terminalia oblongata
Oak (Quercus spp)
- acorns young leaves
- large intake of suckers or fallen leaves
- overwinterings period
Pictures = yellow wood
Describe the pathology of tannins (hydrolysable) ?
Tannins (hydrolysable)
Pathology
Protein binding (astringency) nephrotoxic and hepatotoxic
Clinical signs
- grey green pigmented kidneys
- chronic nephrosis (renal fibrosis) = progressive weight loss, polyuria, alimentary erosions/ ulcers
- Acute liver damage = jaundice, photosensitization, ascites and hydrothorax
- perineal oedema - fluid accumulation
- pale kidneys with subtle white mottling
- ulcers erosions in the abomasum
Describe the cause and pathology of Iforrestine poisoning in shepp and cattle ?
Iforrestine poisoning
Source = Isotropis forrestii, Isotropis atropurpurea
Highly palatable plant
Pathology
The main effect is nephroisi
- the animal’s urine out put slows over time until it eventually stops
- animal becomes weak and collapse
- death within 2-7 days
diarrhoea that may contain mucous and blood
Describe the poisoning circumstances of 3-methoxy-2(5H)-furanone and its pathology ?
Describe a treatment plan for a cat who has consumed 3-methoxy-2(5H)- furanone ?
3-methoxy-2(5H)-furone
Common sources = Lillium sp + Hemertocallis spp (day Lily)
Animals affected = cats
Main effect = nephrosis
Treatment
Treat before 18 hours post ingestion
- decontaminate (emesis, activated charcoal, cathartic)
- fluid diuretic (lactated ringers solution)
- deny access to plant always
Define photosensitization and its clinical signs ?
Photosensitization
Photosensitization is the development of an abnormally reactivity of the skin to sunlight (UV radiation) due to the presence of a photodynamic agent in the dermis.
Photosensitization may be primary, secondary or congenital.
- melanocytes, thick hair or wool can block the UV rays and photosensitization may be prevented in some individuals.
- unpigmented skin without a thick covering is susceptible to photosensitisation.
UV rays result in the formation of free radicals that cause damage to the blood vessels and capillaries resulting in leakage of plasma and cells from the blood vessels.
When sensitiser molecules lodge in the capillary walls, the skin undergoes the same sunburn effect but with lower amounts of UV exposure - the skin has become photosensitised.
Clinical signs
- lesions of unpigmented skin
- pruritus
- photophobia
- subcutaneous oedema
- corneal oedema
- lameness
Only secondary photosensitization = jaundice and increased in serum associated enzymes of the liver
Define primary photosensitization its and its potential causes ?
Primary photosensitization
Animals = ruminants, horses, pigs and poultry
Primary photosensitization occurs when the ingestion of a sensitiser compound (fluorescent plant pigment) causes photosensitization directly (without involvement of the liver).
Cause
- Dianthrone derivatives: hypercin Saint John’s wart
- Fagopyrin buckwheat
- Furanocoumarins parsley, celery and cullen sp.
Define secondary photosensitisation and identify potential causes ?
Secondary photosensitization
Animals affected = ruminants»_space;> horses
Secondary photosensitisation may be referred to as “hepatogenous” (originating from the liver.
In the rumen chlorophyll porphyrin
is converted to sensitizer compound which is photodynamic pigment.
Normally this photodynamic pigment is excreted from the body without any ill effects through detoxification in the liver.
However dysfunction of the liver can cause sensitiser molecules to accumulate in the body including the skin as a result of liver damage.
Secondary photosensitization is by far more common.
Cause
- Lantedenes (Lantana camara)
- Sporidesmin (phitomyces chartarum)
- Steroidal saponins caltrop)
Tannins (terminalia oblongata)
- PAs pyrrolizidine alkaloids
- furanosesquiterpenoids
Describe what recommendations you could make to farmer to prevent , treat photosensitization ?
Treatment of photosensitization
General principles
- avoid sunlight exposure (shady paddocks, buildings)
- offer feed with minimal chlorophil (secondary photo)
- remove from green feed
- offer limited amounts of grain and hay, with free access to clean water
- apply anti-inflammatory therapy in early cases
- long acting Dexamethasone (secondary photo), could cause abortion in cows over 5 months gestation
- maintain hydration oral electrolyte therapy
- nutritional support + hypocalcaemia therapy
Treat secondary bacterial infections of the skin and eye with topical or systemic antibiotics
Describe the poisoning circumstances of Lantadene poisoning ?
Lantadene poisoning
Source = Lantana camara
This is arestricted invasive plant biosecurity act 2014 (QLD Government.
Suscetability
- newly introduced animals
- lack of alternative feed
Describe the MOA, pathology and clinical signs of Lantadene poisoning ?
Lantadene poisoning (secondary photosensitization)
Lantana camara
MOA
Lantadene is absorbed in the small intestine and negatively affects the liver and kidneys.
Phylloerythrin is abosorbed is the large intestine and can no longer be excreted due to the damaged liver. Phylloerythrin accumulates in the skin leading to photosensitization.
Pathology
- hepatogenous photosensitisation
- gall bladder paralysis
- nephrosis
- jaundice
Clinical signs
- dermatitus
- sloughing of the mucosa
Describe your recommendations for the treatment and prevention of Lantadenes poisoning ?
Lantadenes poisoning
Prevention
Plant control
- burn, herbicides, mechanically remove
- improved pasture
- prevent access
Therapy (secondary photosensitization)
- shade
- hydration
- antibiotics and antiinflammatorys
- treat for hypocalcaemia
- remove green feed and access to Lantana
-
Describe the poisoning circumstances of facial eczema ?
Facial eczema = Sporidesmin
A toxin present in the sporse of Pithomyces Chartarum on Lolium spp (Ryegrass and decomposing leaves)
Poisoning circumstances
Weather and pasture conditions suiting rapid fungus growth and spore production
- heavy litter component in pasture
- warm humid weather ( minimum night temp 15 and high humidity >90%)
- light rain
- livestock management prmoting intensive grazing leads to ingestion of numerous spores.
Describe the pathology and clinical signs of Sporidesmin poisoning ?
Sporidesmin poisoning
Facial eczema = rye grass (Lollium) and Pithomycess chartarum
Main effects
Obliterating cholangitis (bile ducts inflamed to the point of blockage)
Clinical signs
secondary photosensitization
Describe how you dignose and prevent Sporidesmin poisoning ?
Sporidesmin poisoning
Facial eczema
Rye grass (lollium spp) and Pithomyces chartarum
Diagnosis
- Clinical signs
- Elevation of GGT concentrations in serum
- Elevated pasture or faecal spore counts
- Definitive diagnosis through histopathology of the liver
Preventative strategies
- Predicting danger periods
monitoring spore counts on pasture/faeces ( pasture >10000/g grass or faeces >75,000/g faeces)
- spraying pasture with a fungicide
- Administration of zinc sulphate in water / feed
forms inactive compound binding the toxin
inhibits intestinal absorption of copper (plays a role in catalysing the formation of free radicals that cause cell damage)
ZINC is only a preventative management strategy
Describe the poisoning circumstances of steroidal or lithogenic saponins?
Lithogenic or steroidal saponins
Animals affected = young animals particularly lambs
Source
Panicum sp
Hairy panic grass, native millet, gilvum swwet grass and bambatsi grass.
Caltrop Tribulus terrestris
Brachiara decumbes (signal grass)
Poisoning circumstances
- if the toxic plant comprises the majority of available feed
- stressed plants will be more toxic.
Describe the pathology and clinical signs of lithogenic steroidal saponins ?
Lithogenic / steroidal saponins
Animals affected = particularly young animals lambs
Pathogenesis
- Glucuronides combine with Ca2+ in bile blocking the ductiles and hepatocytes - insoluble crystals
- crystals blocking the intraheptaic bile ductiles, cholangitis
- secondary (hepatogenous) photosensitization
Diagnosis = histopathology
Clinical signs
- thick ear
- yellow sweeled head (caltrop)
