mycotoxins

MYCOTOXINS
JESSIL JOSEPH
20MVM52

INTRODUCTION
Mycotoxins are secondary fungal metabolites that cause illness or
death in other species
Mycotoxins are metabolites that are not essential to the normal
growth and reproduction of fungus
When temperature, moisture, and aeration are favourable
>>>>> TOXINS>>>>>> Animals >>>>>Toxic effects
Poisoning by mycotoxin – Mycotoxicosis

CHARACTERISTICS
 Not transmissible from one animal to other
Seasonal outbreaks – particular climate favours fungal growth and
toxin production
Specific association with a particular feed
Treatment with drugs or antibiotics have no effect
May allow secondary diseases by viruses, bacteria or parasites
because several mycotoxins are immunosuppressive

• Presence of large number of fungi in feedstuff doesnt
indicate excessive toxin production
• Mould infested feed along with nutritionally poor ,results in
more susceptible to Mycotoxin induced deterious
effects
• Environmental stress, insect damage, and plant
diseases encourage toxin production

CLASSIFICATION
Classified according to the main system that they affect
1. Hepatotoxic – aflatoxins, rubratoxins, sporidesmin & sterigmatocystin
2. Nephrotoxic – ochratoxin & citrinin
3. Oestrogenic – zearalenone (F2) toxin
4. Cytotoxic – trichothecenes (T2) toxin, diacetylnivalenol
5. Neurotoxic – tremorgens, penitrem, roquifortine
6. Miscellaneous – ergot & fescue

AFLATOXINS
• fungi Aspergillus flavus and closely related A.parasiticus
• 18 compounds in aflatoxin family.
• Some occur naturally in feedstuffs & other are metabolites formed
in body after contamination food
• Food animals can retain residues of aflotoxin or their
metabolites in tissues

• Aflatoxins – B1 , B2 ,G1 & G2
• Aflatoxin B1 – most abundant and most toxic
• Lipid soluble
• heat resistant & not soluble in water
• and they can grow rapidly when moisture content of feedstuff
exceeds 15%
• Unstable , when exposed to sun light

 Pea nut, soybean and cotton seed
meal
 Corn, cornmeal, silage, wheat,
barley, oats, rice and other cereal/
grain
 Remain in feed products for years
 Contamination can occur in the field,
during harvest, or in storage and
processing

Factors affecting toxicity
1. Species – dogs, rats, guinea pigs , ducklings,swine
2. Duration – cattle, sheep & goats are relatively resistant to acute form
of the disease but susceptible to toxic diet fed over a long period
3. Dosage – high doses produce severe hepatocellular necrosis and
prolonged low dosages produce reduced growth rate and liver
enlargement
4. Age – young ones are more susceptible than mature
5. Nutrition – deficiency of selenium, vit. C & protein increases
susceptibility
6. Sex – males are more susceptible than females ( except during
pregnancy)

TOXICITY
Carcinogenic, mutagenic, teratogenic & immunosuppressive to most
mammals
Dairy cattle exposed to more than 200 ppb will result in appearance of
carcinogenic M1 metabolite in milk
Aflatoxins & active metabolites binds covalently and cause dysfunction
or destruction of hepatocytes and other metabolically active cells
B1 is most toxic ( twice as active as G1 & M1)
 Metabolite of B1 found in animals urine, milk or tissues
 LD50 Value : 0.5 to 10 mg/kg body weight

Ingestion water soluble conjugate by rumen flora
deconjugated in acidic stomach release
original toxins
 Absorbed from GI tract>>>>>.bound to serum
albumin>>>>>>.liver remove toxins from
blood>>>>>metabolites are produced by cytP450

Mechanism
 Aflatoxin or their active metabolites bind covalently to cellular
macromolecule such as DNA, RNA, Protein
 Cause dysfunction or destruction of hepatocyte and other
metabolically active cells
 Hepatocellular damage leads to impaired liver function, bile
duct proliferation, bile stasis and liver fibrosis

• Aflatoxins directly affect the endocrine system resulting in hormonal
imbalances
• Aflaotxin B1 has been found to cause chromosomal aberrations & DNA
breakage to produce mutagenic effects

CLINICAL SIGNS
ACUTE TOXICITY
 High to moderate amount of toxin is consumed
 Weakness, anorexia, vomiting, depression, dyspnoea, coughing, nasal
discharge, anaemia, epistaxis, petichiae on MM, bloody faeces, icterus,
possible convulsions and death
 Cattle : debility, ascites, diarrohea and hepatic insufficiency
 Birds : anorexia, ruffled feathers, ataxia, circling, opisthotonus,
convulsions, ecchymosis, oedema and rapid death

SUBACUTE TOXICITY –
 jaundice
 Hypoprothrombinaemia
 Haematomas
 Haemorrhagic enteritis
 death

chronic
 Most common in domestic animals
 Continuous intake of low level of toxins ( weeks/months)
 Gradual decrease in feed efficiency, productivity and weight gain, rough hair coat,
mild jaundice, depression and anorexia
 Abortion
 Ruminants : reduced rumen motility
 Poultry : interfere with absorption of lipids and transportation of yolk
 High risk of concurrent infectious disease
 Liver damage and blood coagulation defects

Postmortem lesions
• ACUTE CASES
 Widespread haemorrhage and icterus, gastro enteritis, ascites, hepatic
necrosis and hepatomegaly
 Microscopically : fatty liver, centrilobular necrosis and haemorrhage
SUBACUTE CASES
 Hepatic changes are not pronounced
 Microscopically : liver show proliferation and fibrosis of bile ductules
CHRONIC TOXICITY
 Diffuse liver fibrosis, hydrothorax, ascites, oedema on the wall of gall
bladder
 Hepatic neoplasm

Diagnosis
 History, clinical signs, necropsy findings
 Microscopic examination of liver
 Detected in milk or urine for several days
 Liver function tests
 Prothrombin activity may reduced
 Serum bile acids are elevated
 Hyperbilirubinemia
 Laboratory testing of feed

TREATMENT
 No specific Rx
 Hydrated sodium calcium aluminosilicate as feed additive ( 5 kg/ tonne)
 Vitamin E and selenium, decrease the effects
 Treatment of grain with anhydrous ammonia for 10-14 days
 Feeding of chronically poisoned animal with easily digestible, low fat diet
containing adequate protein
 Treat secondary infection

RUBRATOXINS
• Acute toxins produced by fungi Penicillium rubrum , P.
purpurogenum
• First recognised as haemorrhagic syndrome in poultry ( 1950s )
• Rubratoxins often grow in feed stuff along with Aspergillus sp.
• Occurs in 2 forms – A & B toxins
• Rubratoxin A – minor metabolite
• Rubratoxin B – major metabolite & most toxic – hepatotoxic,
mutagenic & teratogenic

Properties
 Poorly soluble in water, alcohol and esters and Insoluble
in oils
 Toxin stable at room temperature
 Heating > 85-1000C for 2 hrs destroy the toxins

Toxicity
 Domestic animals, such as dog, cat, goat and horse are
susceptible
 Much less toxic than aflatoxins
 Usually along with aflatoxin in mouldy feeds
 Acute oral LD50 of rubratoxin B : 400-450 Mg/kg

Toxicokinetics
 After absorbtion in to systemic circulation
 Metabolised in liver & produce number of metabolites
 Glucuronidation and Sulphate conjugation
 Excreted in bile : Enterohepatic recycle after deconjugation
 Toxins excreted unchanged in urine and feaces

Mechanism of action
• Mechanism of action of rubratoxins in some aspects is similar to that of
aflatoxins.
• Rabratoxin B or its toxic metabolites due to the presence of lactone
moiety can bind to cell macromolecules like DNA, RNA and others
• binding of rubratoxin B might alter DNA, RNA polymerase or protein
functions
• There is also depression of oxidation of citrate, malate and pyruvate,
possibly because rubratoxin or its metabolites block the electron transport
chain
• Rubratoxin B also inhibits adenosine triphosphatases (ATPases).
• The lethality of rubratoxin B is related to these basic effects on ATPases
and the electron transport system

Clinical Signs
• Clinical signs of rubratoxicos are related to severe liver
damage and include anorexia
• Dehydration, depression, diarrhoea, jaundice and weight loss
• Swine may manifest head pressing, colic and ventral
erythema
• Acute poisoning in horses is characterised by anorexia
depression, profuse bloody diarrhoea, foul smelling faeces,
incoordination, recumbency and terminal convulsions.
• Death occurs after 12 hours or more

Postmortem findings
Haemorrhages in various organ with,
 Severe haemorrhagic necrotic hepatitis
 Jaundice, haemorrhagic enteritis and mild renal damage
 Horse > brain haemorrhage

Diagnosis
History, clinical signs
 Identification of fungi
 Presence of toxins in urine & faeces
Presence of rubratoxin in urine & feed may help in diagnosis
by means of chromatographic procedures

TREATMENT & MANAGEMENT
• No specific treatment
• Withdraw contaminated feed
• Symptomatic treatment

SPORIDESMINS
• Produced by soil fungus Pithomyces chatanum (Sporidesmium bakeri) infests
dead plants
• which can get consumed by grazing ruminants
• Sheep are most susceptible followed by cattle
• Goats are least susceptible
 Grow and sporulate on perennial rye grass
 Intoxicated by graizing
 Common in cattle and sheep
 Commonly called “ Ruminant facial eczema”

• Sporidesmin is a potent hepatotoxin
• Causes extensive damage to liver and biliary epithelium
• leading to acute biliary obstruction resulting in severe hepatic
insufficiency
• Also causes photosensitization & blistering of skin

Properties and toxicity
 Group of Epipolythiadioxo piperazine mycotoxin(Sporidesmin A – H)
 Poisoning depends on climatic conditions
 Fungus require warm, humid weather and light rain for growth
 Spores contain sporidesmin
Animal grazing on short pasture on greater risk
 Sheep most susceptible followed by cattle
 Goats are less susceptible
 Rats are resistant

Toxicokinetics
 Readly absorbed from intestine after ingestion
 Reaches liver causes liver damage

Mechanism
 Potent hepatotoxin
 It causes extensive damage to liver and biliary obstruction
 Resulting severe hepatic insufficiency
 As a result chlorophyll absorbed from the gut is not completely metabolised and
excreated
 Phylloerythrin reaches the blood stream
 Photosensitization and blistering of skin commonly in lightly pigmented area
 This condition “Facial eczema”

Clinical signs
• The clinical signs appear 10-20 days
• Dullness,anorexia, jaundice, facial eczema and photosensitive
dermatitis
• The skin reddened and then becomes crusty and dark eventually
peels off
• leaving large raw areas are susceptible to infections
• The photosensitization is often accompanied by watery swelling
the underlying tissues.
• Jaundice
• Other signs are hyperirritability, lachrymation, nasal discharge
and haemolysis with hemoglobinuria
• Many animals die during acute stage and the survivors conditions
become poor.

Post-mortem findings
• Swollen mottled liver,
• Thickened bile duct walls and necrotic lesion on
face and other lightly pigmented areas
• Chronic cases, liver is tough and Microscopically, there is
perilobular fibrosis .
• Obliteration of bile duct and atrophy of hepatocytes
• Spongy vacuolation of brain

Diagnosis
• Diagnosis should be based on history of exposure
contaminated pasture, clinical signs and necropsy lesions
• Detection of sporidesmin on the feed ,urine of affected animal

• No specific treatment
• Only supportive care
• Animals should be shifted to shaded areas out of direct sunlight
• Antibacterials & antihistaminics to control secondary infections
• Zinc sulphate : 6g/ 100L In drinking water

OCHRATOXINS
• Produced by Aspergillus ochraceus & Penicillium viridicatum
• Potent nephrotoxin
• Produces renal damage in animals & birds – mould nephrosis or
mycotoxic nephropathy
• Ochratoxin A is the most common of all ochratoxins and has the
greatest toxicological importance

Ochratoxigenic fungi and ochratoxin A in defective coffee beans

Properties:
Toxin production can continue during long term storage of grains
especially when moisture content is 16% and relative humidity
>85%
The optimal temperature range for toxin production is 12°C -25°C,
Ochratoxin A is a colourless crystalling compound
exhibiting blue fluorescence under UV light
 It can be stored in ethanol for at least a year and refrigeration
and protected from light.
Ochratoxin A is a moderately stable molecule that survives most
food processing to some extent

Toxicokinetics:
 Absorbed from GI tract
 Distributed mainly in liver and kidney
 A accumulate in body tissue and fat of pig and poultry
 In Liver,metabolized by microsomal enymes
 Metabolites : ochratoxin Q and phenyl alanine
 Half life : 30 days
 Cross placental barrier

Mechanism of action
• Ochratoxins have main action or renal proximal tubule where they
cause decrease metabolite clearance and urine concentration
ability
• Inhibit anion transport and release of renal brush border enzymes
(eg leusine aminopeptidase)
• At cellular levels, they have multiple actions like binding to proteins
(eg. albumin), interferwith synthesis of transfer RNA and
messenger RNA, interference with protein synthesis , disruption
of carbohydrate metabolisin, and increase in generation of free
radicals via cytochrame P-450 reductase
• Kidneys of affected pigs become larged and greyish in colour

Acute toxicity
Acute toxicity relatively rare
Anorexia, vomiting, diarrhea, dehydration and depression
Poultry : listlessness, crowding together, diarrhea, ataxia,
prostration and death

Subacute and chronic
chronic cases are Common
Weigh loss, redused feed efficiency, polyuria, polydipsia,dehydration and
anaemia
Immunosupression, teratogenecity, carcinogenecity and haemorrhages
Poor sperm quality in boar
Foetal death, foetal resorption and abortion in sows

Postmortem findings
PM findings includes Renal lesions are predominant : pale, enlarged, rough
irregular surface
Cut surface : pale cortical streaking & multiple cystic areas of fibroplasia
Enteritis, gastric ulcers and oedema
Microscopic : renal tubular swelling, degeneration of proximal tubule,
atrophy of tubular epithelium, interstitial fibrosis in renal cortex
Hepatic necrosis and lymphoid depletion

Diagnosis
History of feeding mouldy feeds, clinical signs, lesions and laboratory
analysis
Chemical analysis of grain and feed : thin layer chromatography or
HPLC
Ochratoxin A can also detected in renal, hepatic and adipose tissues
Blood analysis : elevated BUN and serum creatinine levels

• No specific therapy
• Activated charcoal may be used to reduce absorption from GIT
• Remove contaminated feed immediately

CITRININ
P. citrinum, P. viridicatum, P. verrucosum, A. ochraceus and A. terreus
Barely, oats, rye, wheat and corn
Co- contaminant with ochratoxin : mycotic nephropathy
Pigs are highly susceptible
Kidney damage and mild liver damage
Vasodilation, constriction of bronchi and increased muscular tone
Also affect domestic birds
No specific treatment

ZEARALENONE
Potent non-steroidal oestrogenic mycotoxin
Zearalenone contaminated feed can produce hyperestrogenism with
reproductive disorders in affected animals
Swine is most commonly affected
Also known as F2 toxin or RAL
Toxic metabolite- by mould Fusarium roseum
Swine- commonly affected

No structural similarity with oestrogen
But produces uterotropic & metabolic effect
similar to that of exceesive steroidal and
synthetic oestrogens
Toxin is heat stable & not destroyed by long storage
or mould retardants or roasting

Properties
Zearalenone is a white crystalline compound, which exhibits blue-green
fluorescence when excited by long wavelength UV light and a more intense green
fluorescence when excited by short wavelength UV light
Fusarium infest maize, wheat, sorghum, milo and oats and proliferate in warm weather
Fungal infections of corn and wheat are commonly known as “ pink ear rot” and
“scab” respectively
It is heat stable and not destroyed by long storage, roasting, or by addition of
propionic acid or mould retardants

Toxicity
Widespread and economically important mycotoxins that affect swine, cattle, sheep, poultry
and other species.
Condition in pigs is commonly called porcine vulvovaginitis or hyperestrogenic syndrome.
Toxic effects usually related to the concentration in the diet of domestic animals.
In prepubertal gilts, dietary zearalenone concentrations of 1-3ppm may produce
hyperoestrogenism, vulvovaginitis and vaginal and rectal prolapse.
In cattle, conc >10ppm cause infertility, reduced conception rate and repeat breeding.
Very high doses required to produce disease in poultry.

TOXICOKINETICS
Readily absorbed from GI tract.
Metabolised to alpha and beta zearalenols, which conjugate with
sulphate or glucuronides and are excreted to bile, faeces and urine.
Limited amount excreted in milk.
Alpha-zearalenol- major metabolite in pigs- 3-10 times more potent
than the parent compound
Beta-zearalenol major metabolite in cattle.

Mechanism of action
Mechanism of action Similar to oestrogens
Zearalenols and its active metabolite bind to cytosolic receptors for oestradiol-17β.
The alpha isomers of zearalenone metabolite have greater affinity of oestrogen receptors than the beta
isomers.
After binding, zearalenone-receptor complex migrate to the nucleus and bind to oestradiol sites on DNA,
initiating specific RNA and protein synthesis.
It causes increased water and lowered lipid contents in muscles and increased permeability of uterus to
glucose, RNA and protein precursors.
It inhibits secretion and release of FSH, which inhibits preovulatory ovarian follicle maturation.

Clinical signs
Clinical signs vary acording to the animal’s species, age and reproductive status.
In pigs induces porcine “vulvovaginitis syndrome”
It affects primarily weaned and pubertal gilts in which it causes hyperaemia and enlargement
of the vulva.
Hypertrophy of the mammary gland and uterus with occasional vaginal and rectal prolapse.
Clinical signs appear 2-7 days after exposure and subside 4-10 days post-exposure.
Mature sows- nymphomania or anoestrus and pseudopregnancy.
Multiparent sows- diminished fertility, anoestrus, reduced litter size, neonatal mortality,
small foetal size, foetal malformation and probably foetal resorption.

Dairy heifers- weight loss, vaginal discharge, nymphomania, uterine
hypertrophy
Pregnant heifers- abortion in 1-3 months
Young males- infertility with atrophy of testes
Casterated male- enlargement of prepuce and nipples
Poultry- reduced fertility, lowered spermatogenesis
No report in man

Diagnosis
Diagnosis based on the reproductive performance in the herd,
together with clinical signs and history of diet-related
occurrence
Chemical analysis of feed
Chromatographic analysis
Feed should contain more than 10ppb of zearalenone

Treatment and management
No specific treatment
Recovery of reproductive functions and regression of signs generally occur 1-4 weeks after the intake of
zearalenone stops in less severe cases.
Supportive therapy
Administration of one 10 mg dose of PGF2α or two doses on successive days usually resolves retained CL
and corrects anoestrus in sows
Activated charcoal binds zearalenone in GI tract and helps to prevent enterohepatic cycling
Dehydrated alfalfa feed (15% in ration) protective as fibre reduces absorption from GI tract
Offending feed should be withdrawn immediately

TRICHOTHECENES
Produced by various species of Fusarium ,
Myrothecium, Trichothecium, Trichoderma,
Cephalosporium & Stachybotrys
Very large family of chemically related toxins
Most toxic mycotoxin
Most common : vomitoxin and diacetoxy scirpenol
T2 toxicosis or fusariotoxicosis
Affect all species including humans
Warfare agent : yellow rain attacks in South east Asia
S

Properties
Growth favoured by alternating cool and warm temperature(5-150C)
Poorly soluble in water
Soluble in organic solvents and fats
Resist chemical and environmental decomposition
Cat appear to be most sensitive to T2 toxin

Toxicokinetics
 Lipophilic agents
 Easly absorbed through skin, gut and pulmonary mucosa
 Reach systemic absorption
 Don’t accumulate preferably in any tissues
 Metabolised by liver microsomal enzyme
 don’t require any metabolic activation
 Excretion : bile ( faeces ) & urine
 May present in egg and milk

Mechanism of action
 Highly toxic at subcellular, cellular and organic system levels
 Pennetrate lipid bilayer and gain acesse to DNA, RNA, cellular organallae
 Inhibition of protein synthesis
 Effects of these toxins are much more diverse
 Higher dose : Inhibit DNA and RNA nucleic acid synthesis
 Lower dose : inhibit membrane transfer of glucose, calcium and some amino acids
 Induce alteration in membrane structure, stimulate lipid peroxidation
 Stimulated alteration in mitochondrial membrane contribute to effect on cellular
energetics and cellular cytotoxicity

 Potent inhibitor of protein synthesis
 T2 toxin interact with 60S ribosomal subunit
 lack of essential protein and enzymes impair various cellular activities
( mitochondrial electron transport ) resulting in cell death
 Affect immunity>>.immunosuppression>>>T suppressor cell
 affect functions of helper T cells, B cells or macrophages
 Depression of cloting factor>>>>haemorrhage, thrombocytopenia and inhibition of
platelet function
 Irritant to skin and mucous membrane and produces gastroenteritis

Acute clinical signs
 Vomiting, colic, poor appetite or anorexia, lethargy,
weakness, mucous or bloody diarrhea, dehydration,
hypothermia, unthriftness, abortion, haematuria,
 Death mainly due to hypotension and shock
 Direct contact : cutaneous area become red, tender,
swollen, painful, pruritic or necrotic

 Recovery is seen but long convalescence
 Exposed animals are susceptible to secondary infections
 In horse : bradycardia, disturbed respiration, cyclic movement,
convulsions and death
 Poultry : neurological signs ( ataxia, abnormal posture ) poor feathering,
abnormal wing positioning
 Secondary infections may mask the primary injury

chronic
 Alimentary Toxic Aleukia ( ATA)
 Characterised by weakness, salivation, abdominal pain, leucopenia,
granulopenia and progressive lymphocytosis
 Bright red or dark cherry red petechial rashes on skin
 In severe case : ulceration and gangrenous process developed on
larynx
 Death by strangulation

Postmortem lesions
Oral, oesophageal, abomasal and
ruminal erosions
Haemorrhagic enteritis and necrosis
Lymphatic organs are smaller than
normal
Chickens : yellow-white caseous plaque
at beak margin, on hard palate or
tongue edges
Spleen decrease in size

diagnosis
History
Clical signs are non-specific
Chemical analysis also difficult
From grain by : TLC, HPLC, ELISA
Laboratory animal tests

treatment
No specific treatment for T-2 toxicosis
Symptomatic treatment ( GI infections, skin, toxemia, shock)
PROGNOSIS : Grave

TREMORGENS
Group of mycotoxins produced by fungi belonging to genera
Penicillium, Aspergillus and Claviceps
Also Includes paspalitrems, lotitrems, alfatrem, verruculogen,
fumitremorgens, roquefortine and penitrems

Primarily affect central nervous
system
Penitrem A – most toxic tremorgen
Isolated from grains, cheese,
silage and various forages- pose
health threat to animals and
humans

Properties and toxicity
 Contain an indole moiety, derived from tryptophan
 Penitrem A,B and C, verruculogen and roquefortine are produced from Penicillium
spp
 Fumitremorgens A and B from Aspergillus spp.
 Common in cattle and dogs
 In cattle, paspalitrems, lotitrems, alfatrem and verruculogen – neurological disease-
“staggers syndrome”
 Oral and intraperitoneal LD50 of penitrem A in mice is 10 and 1.1 mg/kg respectively.
 Oral dose of 0.175 mg/kg is sufficient to produce severe muscle tremors in dogs

TOXICOKINETICS
Tremorgenic indole alkaloids are lipophilic- readily absorbed from GI tract
Cross blood brain barrier
Penitrem A in dogs is excreted unchanged, some unmdergo some hepatic
transformation
Enterohepatic recirculation and continued reabsorption may contribute
to the prolonged recovery
Excretion of penitrem A and roquefortine are primarily through the bile

Mechanism of action
 Multiple effect on receptors and neurotransmitter release mechanism at
central and peripheral levels
 Penitrem A affect presynaptic acetylcholine release, antagonize
production of glycine, or at as a surrogate od GABA.
 Increased levels of excitatory neurotransmitter glutamate and
decreased levels of inhibitory transmitter GABA in the brain
 Acute exposures to toxins may result in degeneration of neuronal fibre
processes

CLINICAL SIGNS
 Clinical signs of penitrem A in dogs- within 30 minutes after exposure
 Early signs- irritability, weakness, vomiting, muscle tremors, rigidity, hyperactivity and
panting
 Eventually tremors become more severe and there is opisthotonus, seizures, nystagmus, paddling movements, hyperpyrexia,
dehydration and exhaustion
 In cattle- staggers syndrome different aetiologies and named rye grass staggers, paspalum (dallis grass) stagger,
corn staggers and Bermuda grass staggers
 Characterised by ataxia, muscle tremors, gait incoordination, rigid stance, falling on ground, recumbancy and convulsions
 Nystagmus and profuse salivation

Postmortem
No specific gross and histopathological changes
Trauma from seizures observed

Diagnosis
History and clinical signs
Increased muscle activity and seizures
Elevated levels of plasma creatinine phosphokinase, lactic
dehydrogenase and aspartate aminotransferase
Detection of mycotoxin in vomitus, stomach contents or bile

Differential diagnosis
strynchnine, metaldehyde, bromethalin and OP and OC
insecticide poisonings

 No specific antidote
 Gastric lavage
 If acid-base inbalance- administration of sodium bicarbonate
 Seizures controlled by diazepam; if fails IV pentobarbitone or phenobarbitone
 Central muscle relaxants like methocarbamol or guaiphenesin
 Fluids and corticosteroids for shock
 Elevated body temperature may be decreased by using ice packs or cold water baths

ERGOT
• Oldest known mycotoxin that affects animal and human health
• Caused by one or several alkaloids that are formed during the growth of Claviceps
purpurea & other Claviceps species & other Claviceps species
 Ergot alkaloids are derivatives of lysergic acid Affect both animals and humans
 Claviceps purpurea : alkaloids
 In livestock : By ingestion of fungus infested grasses
 In humans : Contamination of wheat flour with rye
 Occur more commonly in cattle
 Occur mainly in stall feed animals feeding on heavly contaminated feed

properties
Fungal spores are carried by insects or wind to ovaries of
young rye, which germinate into hyphal filaments and
penetrate deep into seed and geadually consume the entire
substance of grain and hardens to form a lightly curved black
to purple body called sclerotium
 Sclerotium contain varying quantities of ergot alkaloid

Important ergot alkaloids are
Ergotamine
Ergometrine
Ergocryptine
Ergocornine
Ergocristine
Ergosine

Toxicokinetics
 Poor oral bioavailability
 High first pass metabolism
 Absorption and distributed in various organs
 Effectively cross the blood brain barrier
 Metabolised in liver….biliary excretion (90%)
 Plasma half life : 2 hrs
 Vasoconstriction action for 24 hrs
 Ergotamine sequestrated in tissues

Mechanism of action
 Non selective toxicological agents
 Interact with numerous neurotransmitter receptor including adrenergic, serotonergic and
dopaminergic receptors
 Causes stimulation of smooth muscles
A. Ergot alkaloid act as a partial agonist and antagonist at alpha-adrenergic receptor in
vascular and other smooth muscles
B. Ergot alkaloid, particularly ergotamine, act as partial agonist and antagonist at some
serotonergic receptor subtype
C. Ergot alkaloid, particularly ergometrine has potent oxytocic action
D. Mimic the action of dopamine in CNS ( Stimulation of D2 receptor)
E. Inhibit prolactin release from pituitary

Acute/ nervous ergotism
 Commonly in carnivores, horse and sheep rare in cattle
 Vertigo, weakness, recumbency, tremor, spasm, hyperexcitability,
incoordination
 Nodding of head, tonic convulsions with opisthotonus and posture
paralysis
 Intermittened blindness and deafness
 Gangrenous extremities may also occur

Chronic/ gangrenous ergotism
 Most common in cattle
 Lameness may be the first sign
 Swelling and tenderness of fetlock joint and pastern
 Sharply demarcated necrosis of feet, ear and tail
 In severe cases the hooves or feet and tail may be sloughed off
 Condition exacerbated in cold weather

HYPERTHERMIC ERGOTISM
Hyperthermia : 105-1070F
Dyspnoea and hypersalivation
Milk production and growth rate are depressed
More severe in hot weather
Affected animal seek water or shade

Postmortem findings
Increased volume of CSF, on complete rigor, empty arteries
Subcutaneous haemorrhage and proximal necrotic area
Mammary gland become flaccid and no lacteal secreations
Microscopic : endothelial damage and coagulative necrosis

Diagnosis
History, clinical signs, necropsy findings and chemical analysis
Extraction and identification of ergt alkaloid
Identified by thin layer chromatography or mass spectrometry

Treatment
History, clinical signs, necropsy findings and chemical analysis
Extraction and identification of ergt alkaloid
Identified by thin layer chromatography or mass spectrometry

FESCUE
 Plant :Fescuta arundinacea
 Fungi : Neotyphodium coenophialum
 Ergopeptide alkaloid : ergovaline and peramine
 Mare and pregnant animals are highly susceptible
 Spontaneous abortion, still birth, retained placenta, agalactia
 Foals have overgrown hooves, poor suckling reflex, incoordination and hypothermia
 Poor immunity due to lack of colostrum

FESCUE SUMMER TOXICOSIS
 Decrease feed intake, poor weight gain, lower milk production, hyperthermia, poor reproductive
performance
 Agalactia due to decreased release of prolactin
 Cattle, sheep are more susceptible
 Ergovaline : potent vasoconstrictor
FESCUE FOOT : In sheep ( occur in winter )
 Similar to Gangrenous ergotism
 No effective treatment

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