Facial Eczema (Pithomycotoxicosis)

Abstract

facial eczema

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Facial Eczema (Pithomycotoxicosis)
Clinical ,hematological and biochemical studies of facial eczema syndrome in
local sheep breeds of Basrah Govornorate
Facial eczema (FE) is a disease of sheep, cattle and deer, but can affect
other grazing animals. It had a significant impacts on animal productivity,
health and welfare and is considered as a common seasonal problem in
farm animals .
The condition is caused by ingestion of spores of the fungus Pithomyces
chartarum, which lives mainly on ryegrasses. Under favorable conditions
the fungus can rapidly multiply in pastures. The spores of the fungus
release a potent mycotoxin known as sporidesmin in the gastrointestinal
tract, which causes damage to the liver, bladder and mammary gland.
Facial eczema is named for the visible signs of photosensitisation that
affect non-pigmented areas of skin exposed to sunlight and result in
severe skin irritation,dermatitis and fly strike like lesions , However, in
some outbreaks of the disease ,animals might show little or no visible
skin lesions, but have suffered liver damage, Therefore the disease
considered as not well named or misnomer .
Production losses in dairy cattle arise from animal deaths, weight losses
or reduced weight gain, reduced milk yield and reproductive performance
are more common in this disease .
Predisposing factors enhance the occurrence include…
1-Higher temperatures
2-Increase rainfall
3-Autumn.summer and may be winter time of the year
Which provide suitable conditions for germination and sporulation of
Pithomyces chartarum over longer periods and more widespread
outbreaks of the disease .
4-Increase genetic susceptibility
Etiology …..
The fungus Pithomyces chartarum, was originally believed to have a
tropical habitat and been found across the world, including temperate
climate zones, saprophytic organism and is found on a wide range of
decaying plant matter and in soil and air. it is characterized by hand-
grenade shaped spores.
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Pathogenesis
Sporidesmin the fungal toxin is released from ingested spores in the
upper digestive tract, absorbed into the portal bloodstream and taken to
the liver where it generates oxygen free radicals which damage cell
membranes.
Concentration of sporidesmin in the bile ducts lead to severe necrosis of
their mucosal surfaces, resulting in rapid reduction of biliary secretion,
bile duct thickening and blockage ,Cholangiohepatitis, ductular
hyperplasia and fibrosis are also seen histologically.
Thickening of ducts.
The liver become shrunken
Finally the end results is obstructive jaundice and hepatic
photosesitization followed by shrunken and fibrosis of the hepatic tissue
due different stages of liver damage .
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Clinical sings ….
1-The first signs of ingestion of the sporidesmin toxin may be an initial
transient diarrhea and sudden milk production drop.
2-Presenting sign is photosensitization, arising from liver damage and
bile duct blockage which characterized by allergic dermatitis with itching
and alopecia with redness and scratching over the head ,ears ,lips , face
,udder, Moreover mild swelling and edema of the affected area starting in
the head and face but it also can affected udder ,back ,sides ,legs
3-Third eyelid commonly appears sunburnt .
4-Diseased animals may be restless, seek shade and lick or rub affected
areas and if photosensitisation is acute, collapse showing extreme pain
5-Skin lesions may progress further and eventually lead to large sheets of
skin peeling off
6-Some cows may also suffer photodynamic coronitis. This eventually
grows out with the horn of the hoof, sometimes resulting in painful
horizontal fissures of the hoof wall.
7-In severe cases, cystitis may also occur, with affected animal specilly
cows exhibiting prolonged and frequent urination. Haemoglobinuria and
jaundice may also occur, associated with an acute haemolytic crisis, often
as a prelude to a severe outbreak of FE However, they are not seen in
many herd outbreaks.
Post mortem findings ….
1-Since the biliary tract rather than the hepatocytes is the principal target
for sporidesmin, it is common for affected animals to show clinical signs
of cholestasis (i.e.photosensitivity) without other signs of liver failure.At
post-mortem examination there may be macroscopic evidence of oedema
and fibrosis of the biliary tract.
2-Cholangiohepatitis, duct hyperplasia and fibrosis may be seen
histologically.
3-Chronic cholangitis eventually leads to left lobe atrophy in the livers of
ruminants. Therefore, a bovine liver in which the right lobe is enlarged
while the left one is pale, thin, tough and small, should always signal the
possibility of chronic sporidesmin toxicity.
Clinical pathology ….
Treatment ….
There is no specific treatment for this disease , and any therapy
considered is only symptomatic and palliative. Ideally, affected animals
should be kept indoors in darkened buildings during daylight hours and
allowed to graze at night. At a minimum they must be given access to
shelter. This will prevent the development of further skin lesions and
allow the existing lesions to heal while the liver regenerates. Areas where
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skin is peeling should be dressed with sun-blocking ointments. It may be
necessary to dry off severely affected lactating dairy cattle.
Zinc does not prevent FE if given after the sporidesmin challenge, nor
does it have a therapeutic effect when given orally to animals that are
displaying clinical signs of FE.Zinc cannot reverse liver damage, but can
help reduce the risk of further liver damage due to sporidesmin.
Note : Zinc works by forming a complex with sporidesmin, which
inhibits sporidesmin’s ability to form oxygen free radicals and cause cell
damage. Zinc also inhibits intestinal absorption of copper which catalyses
the reaction.
Note: Copper seems to activate sporidesmin toxin in the process of
metabolism in the liver.
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