Mycotoxicosis in animals (and vitamin deficiency)

[Guest guest]

Your answers about the inability to absorb vitamins helped me do some more

research. I found this information in the Merck Veterinary Manual.

http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/203500.htm

A

mycotoxicosis is a disease caused by a toxin produced by a fungus. In

poultry, this usually results when fungi grow in grains and feeds.

Hundreds of mycotoxins have been identified and many are pathogenic.

Mycotoxins may have additive or even synergistic effects with other

mycotoxins, infectious agents, and nutritional deficiencies. Many are

chemically stable and maintain toxicity over time. (See also mycotoxicoses,

Mycotoxicoses: Introduction.)

The significance of mycotoxin

problems in poultry is probably considerable but yet insidious. The

impact on poultry production may be best measured indirectly by the

improvements in weight gain, feed efficiency, pigmentation, egg

production, and reproductive performance that accompany effective

control programs for mycotoxins.

Aflatoxicosis:

The aflatoxins are toxic and carcinogenic metabolites of Aspergillus flavus , A

parasiticus , and others. Aflatoxicosis in poultry primarily affects the liver,

but

can involve immunologic, digestive, and hematopoietic functions. It

affects weight gain, feed intake, feed conversion efficiency,

pigmentation, processing yield, egg production, male and female

fertility, and hatchability. Some effects are directly attributable to

toxins, while others are indirect, such as reduced feed intake.

Susceptibility to aflatoxins varies, but in general, ducklings,

turkeys, and pheasants are susceptible, while chickens, Japanese quail,

and guinea fowl are relatively resistant.

Clinical signs vary from general unthriftiness to high morbidity

and mortality. At necropsy, the lesions are found mainly in the liver,

which can be reddened due to necrosis and congestion or yellow due to

lipid accumulation. Hemorrhages may also occur. In chronic

aflatoxicosis, the liver becomes yellow to gray and atrophied. The

aflatoxins are carcinogenic, but tumor formation is rare with the

natural disease, probably because the animals do not live long enough

for this to occur.

Fusariotoxicosis:

The genus Fusarium produces many mycotoxins injurious to poultry. The

trichothecene

mycotoxins produce caustic and radiomimetic patterns of disease

exemplified by T-2 toxin and diacetoxyscirpenol (DAS). Deoxynivalenol

(vomitoxin, DON) and zearalenone are common trichothecene mycotoxins

that are relatively nontoxic for poultry, but may cause disease in

pigs.

Fusariotoxicosis in poultry caused by

the trichothecenes results in feed refusal, caustic injury of the oral

mucosa and areas of the skin in contact with the mold, acute digestive

disease, and injury to the bone marrow and immune system. Lesions

include necrosis and ulceration of the oral mucosa, reddening of the GI

mucosa, mottling of the liver, atrophy of the spleen and other lymphoid

organs, and visceral hemorrhages. In laying hens, egg production

decreases, accompanied by depression, recumbency, feed refusal, and

cyanosis of the comb and wattles. Ducks and geese develop necrosis and

pseudomembranous inflammation of the esophagus, proventriculus, and

gizzard.

Other Fusarium mycotoxins cause defective growth of long bones. The fumonisin

mycotoxins produced by F moniliforme impair feed conversion without causing

specific lesions. Moniliformin is also produced by F moniliforme and is

cardiotoxic and nephrotoxic in poultry. F moniliforme causes ear rot, kernel

rot, and stalk rot of unharvested corn and is

found in stored high-moisture shelled corn, and on other grains that

appear sound.

Ochratoxicosis:

Ochratoxins are among the mycotoxins most toxic to poultry. These nephrotoxic

metabolites are produced chiefly by Penicillium viridicatum and Aspergillus

ochraceus in grains and feed. Ochratoxicosis causes primarily renal disease but

also affects the liver, immune system, and bone marrow. Severe

intoxication causes reduced spontaneous activity, huddling,

hypothermia, diarrhea, rapid weight loss, and death. Moderate

intoxication impairs weight gain, feed conversion, pigmentation,

carcass yield, egg production, fertility, and hatchability.

Ergotism:

Toxic ergot alkaloids are produced by Claviceps spp , which are fungi that

attack cereal grains. Rye is especially

affected, but also wheat and other leading cereal grains. The

mycotoxins form in the sclerotium, a visible, hard, dark mass of

mycelium that displaces the grain tissue. Within the sclerotium are the

ergot alkaloids, which affect the nervous system, causing convulsive

and sensory neurologic disorders; the vascular system, causing

vasoconstriction and gangrene of the extremities; and the endocrine

system, influencing the neuroendocrine control of the anterior

pituitary.

In chicks, the toes become discolored

due to vasoconstriction and ischemia. In older birds, vasoconstriction

affects the comb, wattles, face, and eyelids, which become atrophied

and disfigured. Vesicles and ulcers develop on the shanks of the legs

and on the tops and sides of the toes. In laying hens, feed consumption

and egg production are reduced.

Citrinin Mycotoxicosis:

Citrinin is produced by Penicillium and Aspergillus and is a natural contaminant

of corn, rice, and other cereal grains.

Citrinin causes a diuresis that results in watery fecal droppings and

reductions in weight gain. At necropsy, lesions involve chiefly the

kidney. Citrinin acts directly on the kidney to transiently alter

tubular transport processes.

Oosporein Mycotoxicosis:

Oosporein is a mycotoxin produced by Chaetomium spp that causes gout and high

mortality in poultry. Chaetomium spp are found on feeds and grains, including

peanuts, rice, and corn.

Oosporein mycotoxicosis is seen as visceral and articular gout related

to impaired renal function and elevated plasma concentrations of uric

acid. Chickens are more sensitive to oosporein than turkeys. Water

consumption increases during intoxication, and fecal droppings become

unformed and fluid.

Cyclopiazonic Acid:

This is a metabolite of Aspergillus flavus , which is the predominant producer

of aflatoxin in feeds and grains.

In chickens, cyclopiazonic acid causes impaired feed conversion,

decreased weight gain, and mortality. Lesions develop in the

proventriculus, gizzard, liver, and spleen. The proventriculus is

dilated and the mucosa is thickened and sometimes ulcerated.

Sterigmatocystin:

This biogenic precursor to aflatoxin is hepatotoxic and hepatocarcinogenic but

is less common than aflatoxin.

Diagnosis:

Mycotoxicosis should be suspected

when the history, signs, and lesions are suggestive of feed

intoxication. Toxin exposure associated with consumption of a new batch

of feed may result in subclinical or transient disease. Chronic or

intermittent exposure can occur in regions where grain and feed

ingredients are of poor quality, and feed storage is substandard or

prolonged. Impaired production can be an important clue to a mycotoxin

problem, as can improvement due to correction of feed management

deficiencies.

Definitive diagnosis involves

detection and quantitation of the specific toxin(s). This can be

difficult because of the rapid and voluminous use of feed and

ingredients in poultry operations. Diagnostic laboratories differ in

the capability to conduct screening and confirmation tests for the

different mycotoxins and should be contacted before sending samples.

Feed and also birds that are sick or recently dead should be submitted.

A complete diagnostic evaluation including necropsy, histopathology,

bacterial and viral cultures, and serology should accompany feed

analysis if mycotoxicosis is suspected. Other diseases that occur

concurrently with mycotoxins can adversely affect production and should

be considered. A flock rarely has a single disease. Sometimes, a

mycotoxicosis is suspected but not confirmed by feed analysis. In these

situations, a complete laboratory evaluation can exclude other

significant diseases.

Feed and ingredient samples should be

properly collected and promptly submitted for analysis. Mycotoxin

formation can be localized in a batch of feed or grain. Multiple

samples taken from different sites increase the likelihood of

confirming a mycotoxin formation zone (hot spot).

Samples should be collected at sites

of ingredient storage, feed manufacture and transport, feed bins, and

feeders. Fungal activity increases as feed is moved from the feed mill

to the feeder pans. Samples of 500 g (1 lb) should be collected and

submitted in separate containers. Clean paper bags, properly labeled,

are adequate. Sealed plastic or glass containers are appropriate only

for short-term storage and transport, because feed and grain rapidly

deteriorate in airtight containers.

Treatment:

The toxic feed should be removed and

replaced with unadulterated feed. Concurrent diseases should be treated

to alleviate disease interactions, and substandard management practices

must be corrected. Some mycotoxins increase requirements for vitamins,

trace minerals (especially selenium), protein, and lipids, and can be

compensated for by feed supplementation and water-based treatment.

Nonspecific toxicologic therapies using activated charcoal (digestive

tract adsorption) in the feed have a sparing effect but are not

practical for larger production units.

Prevention:

The focus should be on using feed and

ingredients free of mycotoxins and on management practices that prevent

mold growth and mycotoxin formation during feed transport and storage.

Regular inspection of feed mills and feeding systems can identify flow

problems, which allow residual feed and enhance fungal activity and

mycotoxin formation. Mycotoxins can form in decayed, crusted feed in

feeders, feed mills, and storage bins; appropriate cleaning can be

immediately beneficial. Temperature extremes cause moisture

condensation and migration in bins and promote mycotoxin formation.

Ventilation of poultry houses to

avoid high relative humidity also decreases the moisture available for

fungal growth and toxin formation in the feed. Pelleting of feed also

reduces moisture. Antifungal agents added to feeds to prevent fungal

growth have no effect on toxin already formed but may be cost-effective

in conjunction with other feed management practices. Organic acids

(propionic acid, 500-1,500 ppm [0.5-1.5 g/kg]) are effective

inhibitors, but the effectiveness may be reduced by the particle size

of feed ingredients and the buffering effect of certain ingredients.

Sorbent compounds such as hydrated sodium calcium aluminosilicate

(HSCAS) are effective in binding and preventing absorption of

aflatoxin. Esterified-glucomannan, a cell wall derivative of Saccharomyces

cerevisiae , is protective against aflatoxin B1 and ochratoxin and has moderate

binding activity for fumonisins, zearalenone, and T-2 toxin.