fungal

1. Mycotoxin Mycotoxin
Defination: A mycotoxin (from the Greek mykes, "fungus" and toxikon, "poison") is a
toxic secondary metabolite produced by organisms of the fungus kingdom and is capable of
causing disease and death in both humans and other animals. The term 'mycotoxin' is
usually reserved for the toxic chemical products produced by fungi that readily colonize
crops.
Examples of mycotoxins causing human and animal illness
include aflatoxin, citrinin, fumonisins, ochratoxin A, patulin, trichothecenes, zearalenone,
and ergot alkaloids such as ergotamine.
 Fungi and substrate associationwithmycotin:
Toxin Fungus substrate
1.Aflatoxin  Aspergillus flavus
 Aspergillus parasiticus
Cotton,seed,corn
2.Ochratoxin-A  Aspergillus ochraceus
 Penicillium
viridicatum
Corn, Rye,Barley
3.Citrinin  Penicillium citrinin
 Penicillium
viridicatum
Barley,Oat
4.Zearalenone  Fusarium roseum
 Fusarium moniliforme
Barley,Cron,Milo
5.Ergot alkaloids  Claviceps perpura Oat,Barley
6.Paspaliterm  Claviceps paspali Dallis,Grass
Source of aflatoxin:
 Cron
 Milo
 Cotton seed
 Peanuts
Factors favouring productionof aflatoxin-
a)Temperature:The optimum temperature range for aflatoxin formation is 25-32 degree c
although temperature as low as 55*c for 2 days can support aflatoxin formation.

2. b)Drought stress: Enhence aflatoxin flavus formation by prolonging the survival of fungal
spore and reducing the host mechanical barrier.
c)High relative humidity or grain moisture : Supports fungal growth and enhance the
aflatoxin formation.
d)Continued fungal respiration uses O2 and CHO to from CO2 and H2O . Providing additional
support for fungal growth.
Mode ofaction:
Aflatoxininhibitproteinsynthesisbymodifyingthe DNA templet&depressingmRNA synthesis.Thus
interferingwithtranscription,Impairedproteinsynthesisinterfere withthe formationof enzyme
necessaryforenergymetabolism&fatmobilization.
Toxicity:
 Cattle,sheepand otherruminantsare lesssusceptiblethanmonogasticanimal.
 Young animal of mostspeciesare more susceptible toaflatoxin.
 Nutritional deficiencyspeciallyprotein,selenium&vit-Edeficiencyincrease susceptibilityof
aflatoxin.
Clinical sign:
a)acute
 Depression
 Anorexia
 Reducedmilkproduction
 Subnormal bodytemperature
b)Chronic
 In poultry-
 Decreasedgrowthrate
 Reduce feedefficiency
 Steatorroea(Impairedfatdigestion)
 Increase capillaryfragility
 Loss of tissue strength
 In swine –
 Anorexia
 Unthriftiness
 Slowgrowth
 Icterus

3.  Mildanemia
 Ascites
 In cattle – Aflatoxinathighconcentration( 1-4ppm)mayreduce rumenmotilityfor24-48
hours.
Lab diagnosis:
1.Blood-
 Mildanemia
 Serumbi-acidsare elevated
 Serumalbumin&albuminglobulinratioare decreased
 Prothrombinactivitymaybe reduced
2.Tissue analysisandurinalysis-
 Aflatoxin –M1can be detectedinmilkandurine afterseveral daysof
exposure of aflatoxin
3.Feedanalysis-
 Black lighttest- Brightgreenishyellow fluorescenceisseenincontaminated
grain.
 Additionspecifictest- Gasliquid,thinlayerchromatography.
Treatment:
1) Detoxification
2) HSCASreduce aflatoxinM1 inthe milkof dairy cow
3) HSCAScorrect impairedgrowthof liverlesion
4) supportive treatment –supplementvitaminEandseleniumhave beenused
Prevention:
1) Use of moldinhibitor
2) Treatmentof grain witherhydrusammoniumfor10-14 daysreducingaflatoxingrowth.

4. Ergot Alkaloids
 Source:
 Rye
 Oats
 Barley
 Wheatand grasses
Toxicity: (Ergotism)
Animal mayshowearlysignof-
 Lamness
 Irregulargait
 Paininthe feet
 Posteriorextremitiesbeingchieflyaffectedasearlyaswithin10days.
There are two forms ofergotism-
1.Gangrenousergotismorchronicergotism.
2.Nervousorconvulsive ergotismoracute ergotism.
Gangrenous ergotism or chronic ergotism pathogenesis:
Clavicepsperpureadue todisturbancesinthe vasomotorsystem
Ergot alkaloidspotentsmoothmusclestimulents
Cause -intense vasoconstriction, elevate bloodpressure &induce stronguterine contracions
Excessive vasoconstrictiondamage endothelium
Cause – vascularstasisandblockade of capillariesflow
Results–indry gangrene formation
Due to thrombosisandsubsequently sloughingoff of hooves,ears& tail
Afterseveral weeksof ingestionof small amountsof ergotalkaloids.
Clinical sign:-
 Reddening
 Swelling
 Coldness

5.  Loss of hair or wool
 Lameness
 Lack off sensationof the affectedpart
 Irregulargaitand evidence of paininthe feet
Convulsiveor nervous form of ergotism:-
Acute- acute ergotpoisoningiscomparativelyrare inanimals,still commonlyoccursincarnivores,
horse & sheepandonlyrarelyincattle whenanimalshave free aecesstoparasitizedseedheadsof
grass withclavicepspaspali forfeworseveral days.Thisformof ergotism notonlydependsonthe
rate of ingestionbutalsovarieswiththe climate locationandspecies.Indolesandlysergicacid
derivativesprobablyresultinstimulationof CNSbyinterferingwiththe functionof brain
neutotransmitters.Ergotalkaloids mimicthe actionof dopamine inCNS.
Clinical sign:-
 Hyperirritability
 Excitability
 Muscular incoordination
 Ataxia
 Increase heartrate
 Aggressiveness
 Intermittentblindness
 Kicking
 Weakness
 Recumbency
 Tremors
 Fatal convulsions
 Respiratoryfailure
Diagnosis:-
 History
 Clinical sign
 Examinationof the hay,straw for the toxigenicfungi ormycotoxins
 Detectionof the ergotalkaloidsinbodyfluidsandtissue
 Abortioninpregnantanimalsalongwithothersign
Post-mortem lesions:-
 Necroticlesions-gangrene of the extremitiesisalmostdiagnosticof the
condition
 Ulcerationandnecrosisof the oral,pharyngeal,ruminal &intestinalmucosa
are characteristicinsheep.

6. Differential diagnosis:-
 Rule outthe infectiousdiseases,trauma,abscess.
 Deficiencyorexcessof seleniumfromchronicergotism.
 Othermycotoxicosesdue toFusariumsp.
Treatment:-
 No specificantidoteisthere.
 Offendingfeed,forage etc shouldbe immediatelywithdrawn.
 Provide awarm , clean& stressfree environment.
 Broad spectrumantibacterials- preventsecondarybacterial infections.
Mycotoxin
Defination: A mycotoxin (from the Greek mykes, "fungus" and toxikon, "poison") is a
toxic secondary metabolite produced by organisms of the fungus kingdom and is capable of
causing disease and death in both humans and other animals. The term 'mycotoxin' is
usually reserved for the toxic chemical products produced by fungi that readily colonize
crops.
Examples of mycotoxins causing human and animal illness
include aflatoxin, citrinin, fumonisins, ochratoxin A, patulin, trichothecenes, zearalenone,
and ergot alkaloids such as ergotamine.
 Fungi and substrate associationwithmycotin:
Toxin Fungus substrate
1.Aflatoxin  Aspergillus flavus
 Aspergillus parasiticus
Cotton,seed,corn
2.Ochratoxin-A  Aspergillus ochraceus
 Penicillium
viridicatum
Corn, Rye,Barley
3.Citrinin  Penicillium citrinin
 Penicillium
viridicatum
Barley,Oat
4.Zearalenone  Fusarium roseum
 Fusarium moniliforme
Barley,Cron,Milo
5.Ergot alkaloids  Claviceps perpura Oat,Barley
6.Paspaliterm  Claviceps paspali Dallis,Grass

7. Source of aflatoxin:
 Cron
 Milo
 Cotton seed
 Peanuts
Factors favouring productionof aflatoxin-
a)Temperature:The optimum temperature range for aflatoxin formation is 25-32 degree c
although temperature as low as 55*c for 2 days can support aflatoxin formation.
b)Drought stress: Enhence aflatoxin flavus formation by prolonging the survival of fungal
spore and reducing the host mechanical barrier.
c)High relative humidity or grain moisture : Supports fungal growth and enhance the
aflatoxin formation.
d)Continued fungal respiration uses O2 and CHO to from CO2 and H2O . Providing additional
support for fungal growth.
Mode ofaction:
Aflatoxininhibitproteinsynthesisbymodifyingthe DNA templet&depressingmRNA synthesis.Thus
interferingwithtranscription,Impairedproteinsynthesisinterfere withthe formationof enzyme
necessaryforenergymetabolism&fatmobilization.
Toxicity:
 Cattle,sheepandotherruminantsare lesssusceptiblethanmonogasticanimal.
 Young animal of mostspeciesare more susceptible toaflatoxin.
 Nutritional deficiencyspeciallyprotein,selenium&vit-Edeficiencyincrease susceptibilityof
aflatoxin.
Clinical sign:
a)acute
 Depression
 Anorexia
 Reducedmilkproduction
 Subnormal bodytemperature
b)Chronic

8.  In poultry-
 Decreasedgrowthrate
 Reduce feedefficiency
 Steatorroea(Impairedfatdigestion)
 Increase capillaryfragility
 Loss of tissue strength
 In swine –
 Anorexia
 Unthriftiness
 Slowgrowth
 Icterus
 Mildanemia
 Ascites
 In cattle – Aflatoxinathighconcentration( 1-4ppm)mayreduce rumenmotilityfor24-48
hours.
Lab diagnosis:
1.Blood-
 Mildanemia
 Serumbi-acidsare elevated
 Serumalbumin&albuminglobulinratioare decreased
 Prothrombinactivitymaybe reduced
2.Tissue analysisandurinalysis-
 Aflatoxin –M1can be detectedinmilkandurine afterseveral daysof
exposure of aflatoxin
3.Feed analysis-
 Black lighttest- Brightgreenishyellow fluorescenceisseenincontaminated
grain.
 Additionspecifictest- Gasliquid,thinlayerchromatography.
Treatment:
1) Detoxification
2) HSCASreduce aflatoxinM1 inthe milkof dairy cow
3) HSCAScorrect impairedgrowthof liverlesion
4) supportive treatment –supplementvitaminEandseleniumhave beenused

9. Prevention:
1) Use of moldinhibitor
2) Treatmentof grain witherhydrusammoniumfor10-14 daysreducingaflatoxingrowth.
Ergot Alkaloids
 Source:
 Rye
 Oats
 Barley
 Wheatand grasses
Toxicity: (Ergotism)
Animal mayshowearlysignof-
 Lamness
 Irregulargait
 Paininthe feet
 Posteriorextremitiesbeingchieflyaffectedasearlyaswithin10days.
There are two forms ofergotism-
1.Gangrenousergotismorchronicergotism.
2.Nervousorconvulsive ergotismoracute ergotism.
Gangrenous ergotism or chronic ergotism pathogenesis:
Clavicepsperpureadue todisturbancesinthe vasomotorsystem
Ergot alkaloidspotentsmoothmusclestimulents
Cause -intense vasoconstriction,elevate bloodpressure &induce stronguterine contracions
Excessive vasoconstrictiondamage endothelium
Cause – vascularstasisandblockade of capillariesflow

10. Results–indry gangrene formation
Due to thrombosisandsubsequently sloughingoff of hooves,ears& tail
Afterseveral weeksof ingestionof small amountsof ergotalkaloids.
Clinical sign:-
 Reddening
 Swelling
 Coldness
 Loss of hair or wool
 Lameness
 Lack off sensationof the affectedpart
 Irregulargaitand evidence of paininthe feet
Convulsiveor nervous form of ergotism:-
Acute- acute ergotpoisoningiscomparativelyrare inanimals,still commonlyoccursincarnivores,
horse & sheepandonlyrarelyincattle whenanimalshave free aecess toparasitizedseedheadsof
grass withclavicepspaspali forfeworseveral days.Thisformof ergotism notonlydependsonthe
rate of ingestionbutalsovarieswiththe climate locationandspecies.Indolesandlysergicacid
derivativesprobablyresultinstimulationof CNSbyinterferingwiththe functionof brain
neutotransmitters.Ergotalkaloids mimicthe actionof dopamine inCNS.
Clinical sign:-
 Hyperirritability
 Excitability
 Muscular incoordination
 Ataxia
 Increase heartrate
 Aggressiveness
 Intermittentblindness
 Kicking
 Weakness
 Recumbency
 Tremors
 Fatal convulsions
 Respiratoryfailure

11. Diagnosis:-
 History
 Clinical sign
 Examinationof the hay,straw for the toxigenicfungi ormycotoxins
 Detectionof the ergotalkaloidsinbodyfluidsandtissue
 Abortioninpregnantanimalsalongwithothersign
Post-mortem lesions:-
 Necroticlesions-gangrene of the extremitiesisalmostdiagnosticof the
condition
 Ulcerationandnecrosisof the oral,pharyngeal,ruminal &intestinalmucosa
are characteristicinsheep.
Differential diagnosis:-
 Rule outthe infectiousdiseases,trauma,abscess.
 Deficiencyorexcessof seleniumfromchronicergotism.
 Othermycotoxicosesdue toFusariumsp.
Treatment:-
 No specificantidoteisthere.
 Offendingfeed,forage etc should be immediatelywithdrawn.
 Provide awarm , clean& stressfree environment.
 Broad spectrumantibacterials- preventsecondarybacterial infections.
Mycotoxin
Defination: A mycotoxin (from the Greek mykes, "fungus" and toxikon, "poison") is a
toxic secondary metabolite produced by organisms of the fungus kingdom and is capable of
causing disease and death in both humans and other animals. The term 'mycotoxin' is
usually reserved for the toxic chemical products produced by fungi that readily colonize
crops.
Examples of mycotoxins causing human and animal illness
include aflatoxin, citrinin, fumonisins, ochratoxin A, patulin, trichothecenes, zearalenone,
and ergot alkaloids such as ergotamine.
 Fungi and substrate associationwithmycotin:
Toxin Fungus substrate
1.Aflatoxin  Aspergillus flavus Cotton,seed,corn

12.  Aspergillus parasiticus
2.Ochratoxin-A  Aspergillus ochraceus
 Penicillium
viridicatum
Corn, Rye,Barley
3.Citrinin  Penicillium citrinin
 Penicillium
viridicatum
Barley,Oat
4.Zearalenone  Fusarium roseum
 Fusarium moniliforme
Barley,Cron,Milo
5.Ergot alkaloids  Claviceps perpura Oat,Barley
6.Paspaliterm  Claviceps paspali Dallis,Grass
Source of aflatoxin:
 Cron
 Milo
 Cotton seed
 Peanuts
Factors favouring productionof aflatoxin-
a)Temperature:The optimum temperature range for aflatoxin formation is 25-32 degree c
although temperature as low as 55*c for 2 days can support aflatoxin formation.
b)Drought stress: Enhence aflatoxin flavus formation by prolonging the survival of fungal
spore and reducing the host mechanical barrier.
c)High relative humidity or grain moisture : Supports fungal growth and enhance the
aflatoxin formation.
d)Continued fungal respiration uses O2 and CHO to from CO2 and H2O . Providing additional
support for fungal growth.
Mode ofaction:
Aflatoxininhibitproteinsynthesisbymodifyingthe DNA templet&depressingmRNA synthesis.Thus
interferingwithtranscription,Impairedproteinsynthesis interfere withthe formationof enzyme
necessaryforenergymetabolism&fatmobilization.

13. Toxicity:
 Cattle,sheepandotherruminantsare lesssusceptiblethanmonogasticanimal.
 Young animal of mostspeciesare more susceptible toaflatoxin.
 Nutritional deficiencyspeciallyprotein,selenium&vit-Edeficiencyincrease susceptibilityof
aflatoxin.
Clinical sign:
a)acute
 Depression
 Anorexia
 Reducedmilkproduction
 Subnormal bodytemperature
b)Chronic
 In poultry-
 Decreasedgrowthrate
 Reduce feedefficiency
 Steatorroea(Impairedfatdigestion)
 Increase capillaryfragility
 Loss of tissue strength
 In swine –
 Anorexia
 Unthriftiness
 Slowgrowth
 Icterus
 Mildanemia
 Ascites
 In cattle – Aflatoxinathighconcentration( 1-4ppm)mayreduce rumen motilityfor24-48
hours.
Lab diagnosis:
1.Blood-
 Mildanemia
 Serumbi-acidsare elevated
 Serumalbumin&albuminglobulinratioare decreased
 Prothrombinactivitymaybe reduced
2.Tissue analysisandurinalysis-

14.  Aflatoxin –M1can be detectedinmilkandurine afterseveral daysof
exposure of aflatoxin
3.Feedanalysis-
 Black lighttest- Brightgreenishyellow fluorescenceisseenincontaminated
grain.
 Additionspecifictest- Gasliquid,thinlayerchromatography.
Treatment:
1) Detoxification
2) HSCASreduce aflatoxinM1 inthe milkof dairy cow
3) HSCAScorrect impairedgrowthof liverlesion
4) supportive treatment –supplementvitaminEandseleniumhave beenused
Prevention:
1) Use of moldinhibitor
2) Treatmentof grain witherhydrusammoniumfor10-14 daysreducingaflatoxingrowth.
Ergot Alkaloids
 Source:
 Rye
 Oats
 Barley
 Wheatand grasses
Toxicity: (Ergotism)
Animal mayshowearlysignof-
 Lamness
 Irregulargait
 Paininthe feet

15.  Posteriorextremitiesbeingchieflyaffectedasearlyaswithin10days.
There are two forms ofergotism-
1.Gangrenousergotismorchronicergotism.
2.Nervousorconvulsive ergotismoracute ergotism.
Gangrenous ergotism or chronic ergotism pathogenesis:
Claviceps perpureadue todisturbancesinthe vasomotorsystem
Ergot alkaloidspotentsmoothmusclestimulents
Cause -intense vasoconstriction,elevate bloodpressure &induce stronguterine contracions
Excessive vasoconstrictiondamage endothelium
Cause – vascularstasisandblockade of capillariesflow
Results–indry gangrene formation
Due to thrombosisandsubsequently sloughingoff of hooves,ears& tail
Afterseveral weeksof ingestionof small amountsof ergotalkaloids.
Clinical sign:-
 Reddening
 Swelling
 Coldness
 Loss of hair or wool
 Lameness
 Lack off sensationof the affectedpart
 Irregulargaitand evidence of paininthe feet
Convulsiveor nervous form of ergotism:-
Acute- acute ergotpoisoningiscomparativelyrare inanimals,still commonlyoccursincarnivores,
horse & sheepandonlyrarelyincattle whenanimalshave free aecesstoparasitizedseedheadsof
grass withclavicepspaspali forfeworseveral days.Thisformof ergotism notonlydependsonthe
rate of ingestionbutalsovarieswiththe climate locationandspecies.Indolesandlysergicacid
derivativesprobablyresultinstimulationof CNSbyinterferingwiththe functionof brain
neutotransmitters. Ergotalkaloids mimicthe actionof dopamine inCNS.

16. Clinical sign:-
 Hyperirritability
 Excitability
 Muscular incoordination
 Ataxia
 Increase heartrate
 Aggressiveness
 Intermittentblindness
 Kicking
 Weakness
 Recumbency
 Tremors
 Fatal convulsions
 Respiratory failure
Diagnosis:-
 History
 Clinical sign
 Examinationof the hay,straw for the toxigenicfungi ormycotoxins
 Detectionof the ergotalkaloidsinbodyfluidsandtissue
 Abortioninpregnantanimalsalongwithothersign
Post-mortem lesions:-
 Necroticlesions-gangrene of the extremitiesisalmostdiagnosticof the
condition
 Ulcerationandnecrosisof the oral,pharyngeal,ruminal &intestinalmucosa
are characteristicinsheep.
Differential diagnosis:-
 Rule outthe infectiousdiseases,trauma,abscess.
 Deficiencyorexcessof seleniumfromchronicergotism.
 Othermycotoxicosesdue toFusariumsp.
Treatment:-
 No specificantidoteisthere.
 Offendingfeed,forage etc shouldbe immediatelywithdrawn.
 Provide awarm , clean& stressfree environment.
 Broad spectrumantibacterials- preventsecondarybacterial infections.
Mycotoxin

17. Defination: A mycotoxin (from the Greek mykes, "fungus" and toxikon, "poison") is a
toxic secondary metabolite produced by organisms of the fungus kingdom and is capable of
causing disease and death in both humans and other animals. The term 'mycotoxin' is
usually reserved for the toxic chemical products produced by fungi that readily colonize
crops.
Examples of mycotoxins causing human and animal illness
include aflatoxin, citrinin, fumonisins, ochratoxin A, patulin, trichothecenes, zearalenone,
and ergot alkaloids such as ergotamine.
 Fungi and substrate associationwithmycotin:
Toxin Fungus substrate
1.Aflatoxin  Aspergillus flavus
 Aspergillus parasiticus
Cotton,seed,corn
2.Ochratoxin-A  Aspergillus ochraceus
 Penicillium
viridicatum
Corn, Rye,Barley
3.Citrinin  Penicillium citrinin
 Penicillium
viridicatum
Barley,Oat
4.Zearalenone  Fusarium roseum
 Fusarium moniliforme
Barley,Cron,Milo
5.Ergot alkaloids  Claviceps perpura Oat,Barley
6.Paspaliterm  Claviceps paspali Dallis,Grass
Source of aflatoxin:
 Cron
 Milo
 Cotton seed
 Peanuts
Factors favouring productionof aflatoxin-
a)Temperature:The optimum temperature range for aflatoxin formation is 25-32 degree c
although temperature as low as 55*c for 2 days can support aflatoxin formation.
b)Drought stress: Enhence aflatoxin flavus formation by prolonging the survival of fungal
spore and reducing the host mechanical barrier.

18. c)High relative humidity or grain moisture : Supports fungal growth and enhance the
aflatoxin formation.
d)Continued fungal respiration uses O2 and CHO to from CO2 and H2O . Providing additional
support for fungal growth.
Mode ofaction:
Aflatoxininhibitproteinsynthesisbymodifyingthe DNA templet&depressingmRNA synthesis.Thus
interferingwithtranscription,Impairedproteinsynthesisinterfere withthe formationof enzyme
necessaryforenergymetabolism&fatmobilization.
Toxicity:
 Cattle,sheepandotherruminantsare lesssusceptiblethanmonogasticanimal.
 Young animal of mostspeciesare more susceptible toaflatoxin.
 Nutritional deficiencyspeciallyprotein,selenium&vit-Edeficiencyincrease susceptibilityof
aflatoxin.
Clinical sign:
a)acute
 Depression
 Anorexia
 Reducedmilkproduction
 Subnormal bodytemperature
b)Chronic
 In poultry-
 Decreasedgrowthrate
 Reduce feedefficiency
 Steatorroea(Impairedfatdigestion)
 Increase capillaryfragility
 Loss of tissue strength
 In swine –
 Anorexia
 Unthriftiness
 Slowgrowth
 Icterus
 Mildanemia
 Ascites

19.  In cattle – Aflatoxinathighconcentration( 1-4ppm)mayreduce rumenmotilityfor24-48
hours.
Lab diagnosis:
1.Blood-
 Mildanemia
 Serumbi-acidsare elevated
 Serumalbumin&albuminglobulinratioare decreased
 Prothrombinactivitymaybe reduced
2.Tissue analysisandurinalysis-
 Aflatoxin –M1can be detectedinmilkandurine afterseveral daysof
exposure of aflatoxin
3.Feed analysis-
 Black lighttest- Brightgreenishyellow fluorescenceisseenincontaminated
grain.
 Additionspecifictest- Gasliquid,thinlayerchromatography.
Treatment:
1) Detoxification
2) HSCASreduce aflatoxinM1 inthe milkof dairy cow
3) HSCAScorrect impairedgrowthof liverlesion
4) supportive treatment –supplementvitaminEandseleniumhave beenused
Prevention:
1) Use of moldinhibitor
2) Treatmentof grain witherhydrusammoniumfor10-14 daysreducingaflatoxingrowth.
Ergot Alkaloids

20.  Source:
 Rye
 Oats
 Barley
 Wheatand grasses
Toxicity: (Ergotism)
Animal mayshowearlysignof-
 Lamness
 Irregulargait
 Paininthe feet
 Posteriorextremitiesbeingchieflyaffectedasearlyaswithin10days.
There are two forms ofergotism-
1.Gangrenousergotismorchronicergotism.
2.Nervousorconvulsive ergotismoracute ergotism.
Gangrenous ergotism or chronic ergotism pathogenesis:
Clavicepsperpureadue todisturbancesinthe vasomotorsystem
Ergot alkaloidspotentsmoothmusclestimulents
Cause -intense vasoconstriction,elevate bloodpressure &induce stronguterine contracions
Excessive vasoconstrictiondamage endothelium
Cause – vascularstasisandblockade of capillariesflow
Results–indry gangrene formation
Due to thrombosisandsubsequently sloughingoff of hooves,ears& tail
Afterseveral weeksof ingestionof small amountsof ergotalkaloids.
Clinical sign:-
 Reddening
 Swelling
 Coldness
 Loss of hair or wool
 Lameness
 Lack off sensationof the affectedpart
 Irregulargaitand evidence of paininthe feet

21. Convulsiveor nervous form of ergotism:-
Acute- acute ergotpoisoningiscomparativelyrare inanimals,still commonlyoccursincarnivores,
horse & sheepandonlyrarelyincattle whenanimalshave free aecess toparasitizedseedheadsof
grass withclavicepspaspali forfeworseveral days.Thisformof ergotism notonlydependsonthe
rate of ingestionbutalsovarieswiththe climate locationandspecies.Indolesandlysergicacid
derivativesprobablyresultinstimulationof CNSbyinterferingwiththe functionof brain
neutotransmitters.Ergotalkaloids mimicthe actionof dopamine inCNS.
Clinical sign:-
 Hyperirritability
 Excitability
 Muscular incoordination
 Ataxia
 Increase heartrate
 Aggressiveness
 Intermittentblindness
 Kicking
 Weakness
 Recumbency
 Tremors
 Fatal convulsions
 Respiratoryfailure
Diagnosis:-
 History
 Clinical sign
 Examinationof the hay,straw for the toxigenicfungi ormycotoxins
 Detectionof the ergotalkaloidsinbodyfluidsandtissue
 Abortioninpregnantanimalsalongwithothersign
Post-mortem lesions:-
 Necroticlesions-gangrene of the extremitiesisalmostdiagnosticof the
condition
 Ulcerationandnecrosisof the oral,pharyngeal,ruminal &intestinalmucosa
are characteristicinsheep.
Differential diagnosis:-
 Rule outthe infectiousdiseases,trauma,abscess.
 Deficiencyorexcessof seleniumfromchronicergotism.

22.  Othermycotoxicosesdue toFusariumsp.
Treatment:-
 No specificantidoteisthere.
 Offendingfeed,forage etc should be immediatelywithdrawn.
 Provide awarm , clean& stressfree environment.
 Broad spectrumantibacterials- preventsecondarybacterial infections.
Defination: A mycotoxin (from the Greek mykes, "fungus" and toxikon, "poison") is a
toxic secondary metabolite produced by organisms of the fungus kingdom and is capable of
causing disease and death in both humans and other animals.The term 'mycotoxin' is
usually reserved for the toxic chemical products produced by fungi that readily colonize
crops.
Examples of mycotoxins causing human and animal illness
include aflatoxin, citrinin, fumonisins, ochratoxin A, patulin, trichothecenes, zearalenone,
and ergot alkaloids such as ergotamine.
 Fungi and substrate associationwithmycotin:
Toxin Fungus substrate
1.Aflatoxin  Aspergillus flavus
 Aspergillus parasiticus
Cotton,seed,corn
2.Ochratoxin-A  Aspergillus ochraceus
 Penicillium
viridicatum
Corn, Rye,Barley
3.Citrinin  Penicillium citrinin
 Penicillium
viridicatum
Barley,Oat
4.Zearalenone  Fusarium roseum
 Fusarium moniliforme
Barley,Cron,Milo
5.Ergot alkaloids  Claviceps perpura Oat,Barley
6.Paspaliterm  Claviceps paspali Dallis,Grass
Source of aflatoxin:
 Cron

23.  Milo
 Cotton seed
 Peanuts
Factors favouring productionof aflatoxin-
a)Temperature:The optimum temperature range for aflatoxin formation is 25-32 degree c
although temperature as low as 55*c for 2 days can support aflatoxin formation.
b)Drought stress: Enhence aflatoxin flavus formation by prolonging the survival of fungal
spore and reducing the host mechanical barrier.
c)High relative humidity or grain moisture : Supports fungal growth and enhance the
aflatoxin formation.
d)Continued fungal respiration uses O2 and CHO to from CO2 and H2O . Providing additional
support for fungal growth.
Mode ofaction:
Aflatoxininhibitproteinsynthesisbymodifyingthe DNA templet&depressingmRNA synthesis.Thus
interferingwithtranscription,Impairedproteinsynthesisinterfere withthe formationof enzyme
necessaryforenergymetabolism&fatmobilization.
Toxicity:
 Cattle,sheepandotherruminantsare lesssusceptiblethanmonogasticanimal.
 Young animal of mostspeciesare more susceptible toaflatoxin.
 Nutritional deficiency speciallyprotein,selenium&vit-Edeficiencyincrease susceptibilityof
aflatoxin.
Clinical sign:
a)acute
 Depression
 Anorexia
 Reducedmilkproduction
 Subnormal bodytemperature
b)Chronic
 In poultry-
 Decreasedgrowthrate

24.  Reduce feedefficiency
 Steatorroea(Impairedfatdigestion)
 Increase capillaryfragility
 Loss of tissue strength
 In swine –
 Anorexia
 Unthriftiness
 Slowgrowth
 Icterus
 Mildanemia
 Ascites
 In cattle – Aflatoxinathighconcentration( 1-4ppm)mayreduce rumenmotilityfor24-48
hours.
Lab diagnosis:
1.Blood-
 Mildanemia
 Serumbi-acidsare elevated
 Serumalbumin&albuminglobulinratioare decreased
 Prothrombinactivitymaybe reduced
2.Tissue analysisandurinalysis-
 Aflatoxin –M1can be detectedinmilkandurine afterseveral daysof
exposure of aflatoxin
3.Feedanalysis-
 Black lighttest- Brightgreenishyellow fluorescenceisseenincontaminated
grain.
 Additionspecifictest- Gasliquid,thinlayerchromatography.
Treatment:
1) Detoxification
2) HSCASreduce aflatoxinM1 inthe milkof dairy cow
3) HSCAScorrect impairedgrowthof liverlesion
4) supportive treatment –supplementvitaminEandseleniumhave beenused
Prevention:
1) Use of moldinhibitor

25. 2) Treatmentof grain witherhydrusammoniumfor10-14 daysreducingaflatoxingrowth.
Ergot Alkaloids
 Source:
 Rye
 Oats
 Barley
 Wheatand grasses
Toxicity: (Ergotism)
Animal mayshowearlysignof-
 Lamness
 Irregulargait
 Paininthe feet
 Posteriorextremitiesbeingchieflyaffectedasearlyaswithin10days.
There are two forms ofergotism-
1.Gangrenousergotismorchronicergotism.
2.Nervousorconvulsive ergotismoracute ergotism.
Gangrenous ergotism or chronic ergotism pathogenesis:
Clavicepsperpureadue todisturbancesinthe vasomotorsystem
Ergot alkaloidspotentsmoothmusclestimulents
Cause -intense vasoconstriction,elevate bloodpressure &induce stronguterine contracions
Excessive vasoconstrictiondamage endothelium
Cause – vascularstasisandblockade of capillariesflow
Results–indry gangrene formation
Due to thrombosisandsubsequently sloughingoff of hooves,ears& tail

26. Afterseveral weeksof ingestionof small amountsof ergotalkaloids.
Clinical sign:-
 Reddening
 Swelling
 Coldness
 Loss of hair or wool
 Lameness
 Lack off sensationof the affectedpart
 Irregulargaitand evidence of paininthe feet
Convulsiveor nervous form of ergotism:-
Acute- acute ergotpoisoningiscomparativelyrare inanimals ,still commonlyoccursincarnivores,
horse & sheepandonlyrarelyincattle whenanimalshave free aecesstoparasitizedseedheadsof
grass withclavicepspaspali forfeworseveral days.Thisformof ergotism notonlydependsonthe
rate of ingestionbutalsovarieswiththe climate locationandspecies.Indolesandlysergicacid
derivativesprobablyresultinstimulationof CNSbyinterferingwiththe functionof brain
neutotransmitters. Ergotalkaloids mimicthe actionof dopamine inCNS.
Clinical sign:-
 Hyperirritability
 Excitability
 Muscular incoordination
 Ataxia
 Increase heartrate
 Aggressiveness
 Intermittentblindness
 Kicking
 Weakness
 Recumbency
 Tremors
 Fatal convulsions
 Respiratory failure
Diagnosis:-
 History
 Clinical sign
 Examinationof the hay,straw for the toxigenicfungi ormycotoxins

27.  Detectionof the ergotalkaloidsinbodyfluidsandtissue
 Abortioninpregnantanimalsalongwithothersign
Post-mortem lesions:-
 Necroticlesions-gangrene of the extremitiesisalmostdiagnosticof the
condition
 Ulcerationandnecrosisof the oral,pharyngeal,ruminal &intestinalmucosa
are characteristicinsheep.
Differential diagnosis:-
 Rule outthe infectiousdiseases,trauma,abscess.
 Deficiencyorexcessof seleniumfromchronicergotism.
 Othermycotoxicosesdue toFusariumsp.
Treatment:-
 No specificantidoteisthere.
 Offendingfeed,forage etc should be immediatelywithdrawn.
 Provide awarm , clean& stressfree environment.
 Broad spectrumantibacterials- preventsecondarybacterial infections.