Mycotoxins &

Mycotoxicoses
Group 5
Ravelo, Mc Kjell
Sadural, Vincent
Santos, Frances Joergina
Tamayo, Christian Narf
Torres, Charles

3B
 Mycotoxins
➔ secondary metabolites of certain fungal spp, are produced when toxigenic strains of these organisms grow under
defined conditions on crops, pasture or stored feed.
➔ diverse group of heat-stable, low molecular weight compounds, non-antigenic.
➔ Mycotoxicoses- term used for acute or chronic intoxication following ingestion of contaminated plant material
➔ More than 100 fungal spp are known to elaborate mycotoxins. Many of these fungi belong to the gene
Penicillium, Aspergillus & Fusarium.
➔ Clinical diagnosis: presence of a number of toxigenic spp on a food source. Severity of clinical signs is
influenced by period of exposure to contaminated feed & amount of mycotoxin ingested.
➔ Clinical evidence of the targeting of particular organs such as liver or the CNS is a feature of mycotoxicoses.
Immunosuppression, mutagenesis, neoplasia or teratogenesis may also result from exposure.
➔ Diseases caused by mycotoxins (mycotoxicoses) are non-contagious, tend to be sporadic, seasonal & associated
with certain batches of feed.
Aflatoxicosis
- large group of difuranocoumarins produced by toxigenic strains of Aspergillus flavus, A. parasiticus &
some other Aspergillus spp. Encountered worldwide in many domestic species.
- Ducklings, turkey poults, calves, pigs & dogs are sensitive to toxic effects. Sheep & adult cattle are more
resistant.
- Maze & other cereals, groundnuts & soya beans are commonly contaminated by these saprophytic fungi.
- Aflatoxins B1, B2, G1 & G2 are particularly important in disease production. Aflatoxin B1 is the
component most often encountered in disease outbreaks, appears to be the most toxic.
- Hydroxylated metabolites of B1 & B2, aflatoxins M1 & M2 may be detected in milk & meat. After
absorption from the GIT, aflatoxins are metabolized by the liver to a range of toxic & non-toxic products.
Clinical findings:

- subacute aflatoxicosis, associated with prolonged exposure to low concentrations of toxin, presents as slowly
developing ill thrift & reduced growth rate.
- Ataxia, opisthotonos & sudden death are features of acute disease in ducklings. Acute aflatoxicosis in cattle
may rapidly result in death (Cockcroft, 1995).
- Hepatopathy is a common finding and, in birds more than 3 weeks old, subcutaneous hemorrhages may be
evident.
- In affected calves, blindness, circling, tenesmus, diarrhea & convulsions have been recorded.

Diagnosis:
- Epidemiologic features & postmortem findings
- ELISA & radioimmunoassay procedures
- Biologic assays; bile duct proliferation in ducklings, chick embryo bioassay, bring shrimp larvae tests & trout
embryo bioassays.
Control & prevention:

- Batches of food for human & animal consumption may be monitored for aflatoxin
contamination
- Treatment with ammonia gas at high temperature & pressure has been used to detoxify
contaminated batches of feed.
- Dilution of contaminated feed with uncontaminated supplies can be used to reduce
aflatoxin concentration & minimize toxicity.
- Addition of hydrated sodium calcium aluminosilicate to feed is reported to reduce
aflatoxin toxicity (Harvey et al., 1989).
Facial eczema
This economically important disease of sheep and cattle occurs in Australia, New Zealand
and South Africa.
The skin lesions develop as a result of photosensitization following exposure to the
hepatotoxin sporidesmin in the spores of the saprophytic fungus Pithomyces chartarum
fungus sporulates prolifically on pasture litter during warm humid conditions in late summer
or early autumn.
Hepatobiliary lesions develop as a result of the accumulation and concentration of
sporidesmin in the bile.
The consequent atrophy, necrosis and fibrosis reduce the capacity of the liver to excrete
phylloerythrin, a potent photodynamic compound formed from chlorophyll by enteric
organisms, which is distributed to many tissues including the skin
The photo- Mycotoxins and dynamic activity of phylloerythrin when exposed to solar
radiation produces skin lesions typical of the disease.
Clinical findings
There is a latent period of 10 to 14 days between ingestion of a toxic amount of
sporidesmin and the development of photosensitization. In sheep, lesions develop
in non-pigmented areas which are not covered by wool.
The eyelids, muzzle and ears are inflammed and swollen.
Serous exudation and scab formation may be followed by necrosis and sloughing
of skin.

Jaundice is usually present.

In cattle, lesions are limited to areas of non-pigmented skin. Milk production may
be severely reduced. Although mortality due to severe liver damage is limited,
economic losses arising from debilitation may be considerable.
Diagnosis
In ruminants, photosensitization accompanied by jaundice is suggestive of the
disease.

Environmental temperatures above 12°C along with heavy rainfall over a 48

hour period provide suitable conditions for the growth of P. chartarum on
pasture and are likely to precipitate disease outbreaks.
Counts of the characteristic spores of P. chartarum in pasture samples can be
used for prediction of disease outbreaks. Pastures with high spore counts are
toxic for grazing animals.

Elevated serum liver enzymes such as gamma-glutamyl transferase are found in

affected animals.

Competitive ELISA techniques have been developed for field use. Sporidesmin
may be detected in bile, urine, plasma or whole blood
Control and prevention
Routine monitoring of pasture spore counts can be used to evaluate their safety for
grazing.

Growth of P. chartarum can be controlled by spraying pastures with fungicides.

Accumulation of pasture litter can be controlled by pasture management techniques.
Breeding programmes which select sheep resistant to the toxic effects of sporidesmin,
are employed in some countries.

The daily administration of zinc salts reduces the toxicity of sporidesmin for liver. A
zinc-containing intraruminal device for preventing the disease in sheep is available
Fescue toxicosis
This mycotoxicosis affects cattle and sheep in the USA, New Zealand and
Australia where tall fescue (Festuca arundinacea) is common in pastures. An
endophytic fungus, Neophytodium coenophialum (formerly Acremonium
coenophialum), found in the foliage and seeds of tall fescue, produces the
alkaloid ergovaline which has been implicated in the aetiology of fescue
toxicosis (fescue foot) which resembles ergotism in herbivores.

During winter months, the vasoconstrictive effects of ergovaline are exacerbated

by low ambient temperatures.

Dry gangrene develops on the distal extremities of hind limbs, tail and ears.
During warm months, summer fescue toxicosis which occurs in cattle, sheep and
horses, is characterized by hyperthermia and unthriftiness. Induced low serum
prolactin leads to a drop in milk production. In addition to agalactia, prolonged
gestation, weak neonates and thickened placentae are features of this toxicosis.
Clinical findings
Vasoconstriction / Dry gangrene in cold weather in cattle and sheep (fescue foot)
hyperthermia and low milk yeild (fescue summer toxicosis)

Some other symptoms of fescue toxicosis can include fever, tachypnea, or rapid
breathing, rough hair coat, excessive salivation, lameness, poor reproductive
success, and increased water intake. Not all tall fescue is endophyte-infected
Diagnosis
Erythema and swelling of the coronary region occur, and cattle are alert
but lose weight and may paddle or weight-shift. The back is slightly
arched, and knuckling of a hind pastern may be an initial sign.

There is progressive lameness, anorexia, depression, and later, dry

gangrene of the distal limbs (hind limbs first).

Signs usually develop within 10–21 days after turnout into a fescue-
contaminated pasture in fall. A period of frost tends to increase the
incidence.
Low environmental temperature may exacerbate the lesions of fescue
lameness; however, high temperatures increase the severity of a toxic problem
known as epidemic hyperthermia or summer syndrome, in which a high
proportion of a herd of cattle exhibits hypersalivation and hyperthermia

The animals seek wet spots or shade. Lowered reproductive performance also
has been reported. Agalactia has been reported for horses and cattle.
Thickened placentas, delayed parturition, and birth of weak foals have been
reported in horses. The severity increases when environmental temperatures
are >75°–80°F (24°–27°C) and if high nitrogen fertilizer has been applied to
the grass.
Control and prevention
Removing the seed head can help prevent fescue toxicosis. Stockpiling forage
for winter consumption can also decrease the risk of fescue toxicosis. If you are
not interested in managing through the Kentucky 31 variety, eliminating the
variety can be an option, if done correctly
Leukoencephalomalacia
➔ A mycotoxic disease of the CNS that affects primarily horses, donkeys and mules.
➔ Occurs sporadically in North and South America, South Africa, Europe and China.
➔ The fungus that is most commonly associated with the disease is Fusarium moniliforme
which produce three toxins, fumonisin B 1,B2, and B3.

➔ Fumonisin B1 and B2 appear to have similar toxicity, while fumonisin B 3 is mostly nontoxic.
➔ The toxin fumonisin has associated with both Central Nervous System and Liver damage.
➔ Horses may develop leukoencephalomalacia from prolonged exposure to fumonisin at
concentrations greater than 10 μg/g of feed.
Clinical findings

➔ Neurological signs include apathy, drowsiness, pharyngeal paralysis, blindness, circling,

difficulty backing, staggering, hyperexcitability, seizures and eventual recumbency.
➔ However, in some cases, sudden death may be the only clinical sign observed. Once
animals show the neurological signs, death usually occurs within 48-72 hours.
➔ If an animal survives the acute syndrome, neurological deficits are observed. A
recovered horse is sometimes referred to as a “dummy” because of its loss of
intelligence.
➔ The signs associated with the hepatic form include petechial or ecchymotic hemorrhages
of the mucous membranes, icterus, edema of the head and neck, decreased appetite,
depression, lingual paralysis, clonic convulsions, and coma.
Diagnosis
➔ Histopathological examination
➔ Mycotoxicology analysis of the food given to the animals

Treatment
➔ There is no specific treatment and, in most cases, the affected animals either die
or are euthanized due to neurological sequelae
➔ Supporartive care include gastrointestinal protectants such as activated charcoal
and laxatives to aid elimination of the toxin, fluids, and dextrose for hydration and
energy.
➔ If the clinical signs have progressed to recumbency, euthanasia may be needed.

Prevention
➔ Minimizing exposure to fumonisin-contaminated feed.
➔ Good storage practices, such as keeping the feed dry and appropriate
temperatures
➔ Regular testing of feed for mycotoxin contamination.
Mouldy Sweet Potato Toxicosis
➔ Sweet potatoes (Ipomoea batatas) infected with the common mold, Fusarium solani,
are the source of 4-ipomeanol a lung edema factor, and exposure to this chemical is
solely by ingestion.
➔ Acute interstitial pneumonia in cattle has been attributed to eating mould-damaged
sweet potatoes.
➔ It is responsible for the poisoning of cattle fed moldy sweet potatoes in USA, New
Zealand and Australia, and the result of this poisoning is often fatal respiratory
distress.
➔ 4-Ipomeanol is a highly specific pulmonary toxin in rats, guinea pigs, and rabbits.
Clinical findings

-Dyspnoea is the principal clinical sign -Breathlessness

-Coughing
-Grunting

-Hypersalivation and frothing at the mouth -Anorexia

Diagnosis

➔ Examination of suspect sweet potato for evidence of damage and mold.

Gross autopsy findings:

➔ Gelatinous edema and severe emphysema

➔ Airways may be partially filled with white foam and copious fluid oozes from cut
Histopathology Findings

➔ Interstitial emphysema, eosinophilic fluid in the lymph nodes and alveolar lumens
containing fibrinous exudates with macrophages and mononuclear cells.
➔ Lymph nodes can be enlarged due to the presence of air and the larynx may be
edematous

Treatment

➔ There is no specific treatment for sweet potato toxicosis

➔ Treatment is supportive such as diuretics, non-steroidal anti-inflammatories and
corticosteroids

:
Treatment

➔ There is no specific treatment for sweet potato toxicosis

➔ Treatment is supportive such as diuretics, no-steroidal anti-inflammatories and
corticosteroids

Control and Prevention

➔ Removal of damaged sweet potato

➔ Careful examination of sweet potato for damage, moisture and possible fungal growth
before feeding
➔ Proper storage and handling of sweet potatoes
➔ Regular inspection of signs of mold and mycotoxin production
Mycotoxic lupinosis
➔ It has been reported in sheep that grazes growing lupins with blight stem. It is an
important mycotoxicosis in Australia and South Africa.

➔ The blight stem was caused by Phomopsis leptostromiformis, it also produces

natural toxin phomopsis A and B that causes total anorexia, jaundice, and
lethargy, as well as mitotic arrest in hepatocytes' metaphase and liver damage.
➔ Ingestion of lupine plants infected with Diaporthe toxica (formerly known as
Phomopsis leptostromiformis) results in lupinosis, a liver disease or
hepatotoxicosis.
➔ Acute lupinosis are represented as hepatic encephalopathy with stupo, stumbling
and recumbency that results to death. Animals that survive develops jaundice and
photosensitization.
➔ A skeletal myopathy associated with phomopsin toxicity has been reported in
Western
Australia (Allen et al., 1992).
Disease / Mycotoxins Fungus / Crop or Species affected / Functional or structural
substrate Geographical distribution effects / Clinical findings

Mycotoxic lupinosis / Phomopsis Sheep, occasionally Hepatotoxicity /

Phomopsins A, B leptostromiformis/ cattle, horses, pigs i lnappetence, stupor,
growing lupins with Worldwide jaundice, ruminal stasis,
stem blight often fatal
Clinical finding:
➔ In sheep and cattle, the first clinical indications are inappetence and listlessness. Ketosis is prevalent, as is
complete anorexia and jaundice. Lacrimation and salivation may occur in cattle. Ketosis is a common
complication in pregnant or recently calved cows. Surviving patients may acquire hepatic cirrhosis.

➔ Icterus is prominent in acute disease. The livers are big, orange-yellow in color, and fatty. More chronic
cases have bronze- or tan-colored livers that are solid, small, and fibrotic. Transudates can be seen in large
quantities in the abdominal and thoracic cavities, as well as the pericardial sac. Spongiform lesions in the
brain have been observed in some animals.

Diagnosis:
➔ Diagnosis is based on history of feeding moldy lupine material.

➔ Clinical signs and increased levels of serum liver enzymes, is an strong indication of lupinosis.

Control of Mycotoxic Lupinosis in Animals

➔ Use of resistant lupine cultivars and surveillance for fungal infection
➔ Good sheep management practices
Liver of sheep with lupinosis
Ochratoxicosis
➔ Penicillium viridicatum and Aspergillus ochraceus toxigenic strains produces
ochratoxins, a group of related isocoumarin derivatives, when growing on
stored barley, maize or wheat.

➔ The heat stable ochratoxin A is a potent nephrotoxin which is also

immunosuppressive and carcinogenic. It also interferes protein synthesis.
Citrinin, a mycotoxin produced by A. ochraceus enhances the nephrotoxic
effects of ochratoxin.

➔ Adult ruminant are able to detoxify ochratoxins; pigs and poultry are more
susceptible. (Hoerr, 2019)
Disease / Mycotoxins Fungus / Crop or Species affected / Functional or structural
substrate Geographical distribution effects / Clinical findings

Ochratoxicosis / Aspergillus ochraceus Pigs, poultry / Degenerative renal

Ochratoxins A, B, C other, Worldwide changes / Polydipsia
Aspergillus species, and polyuria in pigs, fall
Penicillium viridicatum, in egg production in
other Penicillium birds
species / Stored barley,
maize and wheat
Ochratoxicosis effects on poultry:
➔ decreased weight gain and poor feed conversion
➔ reduced spontaneous activity, hypothermia and huddling
➔ diarrhea, rapid weight loss, and death
➔ decreases in carcass yield, egg production, fertility and hatchability

Ochratoxicosis effects on swine:

➔ Inappetence
➔ Depression
➔ Loss of weight
➔ Polydipsia and polyuria are features of mycotic nephropathy.
Prevention
Probiotics: Adding probiotics can reduce the amount of OTA by 55% : Slizewska et al., 2014
Purchase quality poultry feed
Properly store poultry feed, for no longer than a month in duration and in an air-tight container that
is free from moisture accumulation and not exposed to sunlight, insect contamination, or rodents.
Inspect feed daily :
Look over quality of feed prior to giving to birds. Do not feed anything to birds that is suspected of
contamination with mold, insects, spoiled, or has been continuously refused by your chickens.

See more at: https://www.poultrydvm.com/condition/ochratoxicosis

Tremorgen intoxications:
● Perennial ryegrass staggers/ Lolitrem B
- problem in livestock grazing perennial ryegrass pasture during the summer and autumn months.
- caused by a group of toxins that accumulates in the leaf sheaths of perennial ryegrass/ Acremonium lolii
- most commonly seen in cattle, pigs, poultry, sheep, horses & deer.

Clinical findings:
Neurotoxicity/ Muscular tremors, incoordination, convulsive seizures, collapse.

Diagnosis:
- Clinical signs & a prevalence of ryegrass in the pasture
- Laboratory tests can identify endophyte and alkaloid levels.
- A post-mortem may typically reveal a microscopic swelling of neurons within the brain and haemorrhage
of the heart, rumen and lymph nodes.

Prevention:
- avoiding overgrazing, restricting spread of infected grass & seed
Tremorgen intoxications:
● Paspalum staggers/ Paspalinine, paspalitrems A,
-seen in cattle, and more rarely in sheep and horses grazing paspalum grass or water couch seed heads
infested with fungus, or ergot, Claviceps, paspali.
- Outbreaks usually occur in autumn when warm wet weather promotes the ergot's growth

Clinical findings:
- Neurotoxicity/ Muscular tremors, incoordination, convulsive seizures, collapse.

Diagnosis:
- made via a combination of observing typical clinical signs,
- finding a history of exposure to ergot-infected paspalum pasture

Treatment :
- fluids and electrolytes if animals have physical injuries or are compromised from dehydration or lack of
eating
Penitrem staggers
Many Penicillium species, including P. crustosum and P. verruculoswn, and some
Aspergillvv species, including A. flavus and A. fumigatus, produce tremorgens
when growing on pasture plants or stored feed. The clinical signs produced by
these mycotoxins, mainly the penitrems verruculogen and paxilline, are similar to
those of ryegrass staggers (di Menna and Mantle, 1978). The disease, which can
affect many domestic animal species, has been reported in New Zealand,
Australia, the USA and South Africa.

In mice, dogs, sheep, and humans, tremorgenic dosages of penitrem A produce a

neurological syndrome characterized by generalized tremors and ataxia. Higher
dosages may produce vomiting and seizures.
Clinical Findings
Symptoms of ryegrass staggers include initial head tremors, muscle
fasciculation of the neck and legs, and hypersensitivity to external stimuli as
a result of the neurotoxic effect.

To date, no physical effects or gross lesions have been reported, and animals
completely recover when the toxin is eliminated from their systems.
Although, affected animals suffer poor weight gain and they may be
difficult to handle due to their hypersensitivity.
Death is rarely a consequence unless an accident, such as drowning, occurs
during an episode in which the animal loses voluntary control
Diagnosis
Diagnosis of tremorgenic mycotoxin exposure is based on the clinical signs of CNS
stimulation and can include vomiting and tremors. Tremors can be intensified by
handling or sound, intentional tremors, hyperesthesia, tachycardia, and seizures in
dogs. A differential diagnosis could include ingestion of strychnine, plant toxins,
acetylcholinesterase inhibitors or pesticides, metaldehyde, ethylene glycol,
methylxanthines, and illicit drugs. The patient history may include recent access to
moldy foods (walnuts, peanuts, dairy products), free-ranging behavior, access to
compost, and, in ruminants, possible ingestion of moldy silage.
A veterinary diagnostic laboratory can conduct mass spectrometry chemical testing
of source material, vomit or GI tract contents, and possibly serum or urine.
Several tremorgens (penitrem A and E and roquefortine C) have be detected in liver
and kidney tissue, and penitrem A has been detected in the brain. Analysis for
tremorgenic mycotoxins in tissues may not be routinely available.
Control and Prevention
One of the methods to control the disease centers on offering
alternative feed sources or removal of animals from drought-stressed
and overgrazed pastures during summer and early autumn when the
toxin levels are elevated and neurological signs appear
Aspergillus clavatus
Aspergillus clavatus is a species of fungus in the genus Aspergillus
with conidia dimensions 3–4.5 x 2.5–4.5 μm. It is found in soil and
animal manure.
The fungus can produce the toxin patulin, which may be associated
with disease in humans and animals. This species is only occasionally
pathogenic.
mostly affect cattle and sheep
Aspergillus clavatus is known as an agent of allergic aspergillosis and
has been implicated in multiple pulmonary infections. It has also been
labelled as an opportunistic fungus, as it is responsible for causing
aspergillosis in compromised patients. A. clavatus can also cause
neurotoxicosis in sheep and otomycosis.
Clinical signs
Neurotoxicity, degeneration of neurons / Frothing from mouth
and knuckling of limbs when forced to move
Chromatolysis in neurons of brainstem, spinal ganglia and
cord, Wallerian degeneration in cord.
Torticollis and disturbances of equilibrium occur when
infection disseminates to the brain. Yellow nodules of varying
size and consistency or plaque lesions are found in the
respiratory passages, lungs, air sacs, or membranes of body
cavities. Furlike mycelial growth of fungus may be found on
the thickened walls of air sacs.
In ruminants, infection may be subclinical, appear in a bronchopulmonary
form, cause mastitis, or cause placentitis and abortion. Mycotic pneumonia
may be rapidly fatal. Clinical signs include pyrexia; rapid, shallow,
stertorous respiration; nasal discharge; and a moist cough.
In the absence of pneumonia, infected cows generally have no clinical signs
except for abortion; a dead fetus is aborted at 6–9 months gestation
Mycotic mastitis often presents as a sudden decrease in milk production
from one or more quarters; the gross appearance of milk may not be
abnormal
In horses, epistaxis (sometimes fatal) and dysphagia are common
complications of guttural pouch mycosis.
In dogs, aspergillosis is typically localized to the nasal cavity or paranasal
sinuses
Diagnosis
Demonstration of tissue invasion
Guttural pouch endoscopy in horses
Antigen assays, immunohistochemistry, and molecular diagnostics
In dogs and cats, CT or MRI may be necessary
Control and prevention
Topical antifungal treatment for nasal and ophthalmic aspergillosis;
systemic azoles or amphotericin B for disseminated disease
Surgery possible for equine guttural pouch mycosis
First-line treatments: itraconazole, voriconazole, posaconazole,
liposomal amphotericin B, and terbinafine
Good sanitation.
Avoidance of mouldy feed.
Avoidance of mouldy litter.
Cleaning and disinfection of feed and water utensils.
Frequently relocating feeders and water dispensers to avoid mould build-
up.
Trichothecene toxicoses

● Food Refusal and Emetic Syndrome

➔ Affects pigs exposed primarily to vomitoxin (deoxynivalenol, DON).
Diacetoxyscirpenol (DAS) and T-2 toxin may also contribute to the
development of clinical signs
➔ Produced by Fusarium species, in particular Fusarium graminearum, when
growing in maize, barley grains or in mixed feeds containing cereals.

Clinical Findings

➔ Lethargy, malaise, Inappetence, decreased weight gain, vomiting, diarrhea

➔ There may be irritation of the oral mucosa
Diagnosis

➔ Feed source analysis for mycotoxin

➔ High performance liquid chromatography (HPLC)
➔ Enzyme-linked immunosorbent assay (ELISA)

Treatment and Control

➔ Removal of contaminated feed

➔ Activated charcoal may help if ingestion was recent
➔ Antiemetics
➔ Fluid therapy may be required
Haemorrhagic Syndrome
➔ Refers to a condition in which cattle experience bleeding disorder due to the
consumption of feed contaminated with the fungus Fusarium sporotrichioides.
➔ ­It has been reported in the USA
➔ Fusarium sporotrichioides is a plant pathogen that commonly infect grains, especially
corn, wheat, oat and barley.
➔ The mycotoxins T-2 toxin and DAS are potent epithelial necrotizing agents