Clinical symptoms and pathomorphological changes of more important myc
otoxicoses of different poultry species have been reviewed. In case of
aflatoxicosis, inappetency, faintness, weakness and frequently ataxia
, opisthotonus and spastic retroextension of extremities can be observ
ed. The pathological investigation may reveal swelling, yellow coloura
tion of liver with heamorrhages on its surface (Fig. 2), swelling of k
idneys, dropsy in the pericardium and acute intestinal catarrh. The hi
stopathological investigation may reveal disorganization of hepatic st
ructure (dystrophy), and severe necrosis of parenchymal cells (fatty i
nfiltration, necrosis, Fig. 3) which can be accompanied by proliferati
on of bile vessels (Fig. 4), nodular hyperplasia of hepatic cells and
fibrosis. All avian species, except for domestic fowl (Gallus domestic
us) are sensitive for F-2 fusariotoxicosis. Zearalenone has no effect
on egg production, however the sperm cell production of males (drake,
gander, turkey cock, guinea cock) - similar to the mammalians - is dam
aged. It causes fatty degeneration of germi nal epithelium in the semi
niferous tubules and later on atrophy and ceasing of spermiogenesis (F
igs 5 and 6). The electron microscopic examinations revealed - besides
the presence of fat droplets - necrosis (appearance of so-called myel
in figurations), calcification of mitochondria (Fig. 7) in the cytopla
sm and chromatin degeneration in the head of matured sperm cells (Fig,
8). Fusariotoxicoses caused by T-2 and other trichothecene skeleton t
oxins (HT-2 DAS, NIV, FX, DON). It causes diminition of body-mass gain
, disturbed feathering and the flock will be ''scattered'' (Fig. 9). I
n case of higher toxin contamination, necrosis covered with crusted de
position develops on the bill, skin of the angle of mouth, on the tong
ue and palate (Figs 10, 11, and 12). Occasionally, motor disturbance a
nd nervous symptoms can also be observed. During the gross-pathologica
l examination,especially in case of mixed toxin contamination, a frequ
ent observation is an acute, haemorrhagic hepatic dystrophy and tubulo
nephrosis as well as atrophy of lymphoid organs (bursa of Fabricii, th
ymus, etc., Figs 13 to 17). Damage of immune system predisposes for th
e manifestation of other diseases (e. g. caecal coccidiosis) and worse
n the effect of vaccinations. In adult laying flocks, the egg producti
on decreases (Figs 18 and 19), hatching ability worsens (Fig. 25), fol
licular degeneration and necrosis can be observed on the ovaria (Figs
20 and 21) accompanied by the involution of oviduct (Figs 22 and 23) a
nd often amyloidosis of liver and spleen (Fig. 24). In case of stachyb
otryotoxicosis, smaller or larger areas are erythematous and oedematou
s and superficially necrotized on the head, wattle, neck (Fig. 26), as
well as plantar pulp (Fig. 27). Surface of ulcers are covered by crus
t-like exudate. Depletion and necrosis of immatured and matured cells
is characteristic in the lymphoid and myeloid haemocytogenetic organs,
as well as tissues. Ochratoxicosis affecting all animal species and m
an, caused by a mycotoxin and manifests in the primary damage of kidne
ys. Structural manifestation is. degeneration of renal tubules followe
d by interstitial fibrosis, while functional manifestation in the insu
fficient function of renal tubules. Uptake of ochratoxin predisposes t
o the development of renal uricosis in all avian species. Mass inciden
ce of renal injury was observed many times in growing geese (Fig. 28).
Worsening of hatching ability of eggs is caused by the uptake of even
a low, 1 to 2 mg/feed kg of toxin dose. Uptake of higher doses of the
toxin - similar to certain trichothecenes and aflatoxins - causes a r
achitic osteogenetic disturbance in chickens and turkeys. Diagnosis an
d practical conclusions. The above reported diseases develop in typica
l clinical symptoms and pathomorphological alterations mainly after th
e uptake of feeds with higher concentrations of mycotoxins. In the pra
ctice, however, only the lower developmental force, general resistance
, worse feed conversion and reproductive indices call the attention fo
r mycotoxin contamination of feed. In this case, besides the identific
ation and quantitative determination of toxins in the feed, carefully
should also be considered during the diagnosis that in the cause of de
tailed - non specific - clinical cymptoms other causes, as well as dis
turbances (management, infectious and deficiency diseases, etc.) may a
lso play a role. Thus, the diagnosis of diseases due to consuming myco
toxin containing feeds is always a very complex task.