Peter Gazdzinski
Cuddy Farms, Strathroy Ontario, Canada N7G 3H6
Proceedings of the 24th Technical Turkey Conference p29
Hepatic lipidosis has been observed in laying chickens since 1956. It
has been called fatty liver syndrome if there is an egg production drop and a
little mortality, or fatty liver hemorrhagic syndrome (FLHS) if there is little
effect on production but increased mortality. This condition affects older and
heavier layers in egg production, causing them to die from massive hemorrhage
of the liver (13). Another condition associated with liver failure because of
fatty degeneration of the liver is called fatty liver and kidney syndrome
(FLKS). This syndrome affects both broiler and layer-type chicks usually
between 10 and 40 days of age. Fatty infiltration of the tissue, caused by
dietary deficiency of biotin, occurs not only in the liver but also in the
kidneys, muscles and even the central nervous system (4). Turkey breeder hens
are grown almost every year to heavier weights. At lighting time they now
achieve an average body weight of 12.4 kg compared to 11.0 kg 10 years ago.
This progress puts high requirements on management and nutrition of turkey
breeder hens and it
may also predispose them to certain health problems. In the early
nineties, we started to observe increased mortality (0.7% – 4.5%) in turkey
breeder hens between the age of 20 and 25 weeks. In total, there have been 6
cases of unexplained mortality. Numerous trials and investigations were
conducted in order to explain the reasons of this mortality and it was found
that affected hens come down with fatty degeneration of the liver, which has
been called Hepatic Lipidosis of Turkeys (7). The Hepatic Lipidosis is still
causing significant losses in turkey breeder hen candidates in many countries
of the world. Therefore it is very important to describe the existing data
about this syndrome.
Clinical Signs and Mortality
Hepatic
lipidosis has been described for the first time in 1994 (7). It affects turkey
breeder hen replacements between 12-25 weeks of age with most cases being
between 20–24 weeks. It is observed either during the hot summer in North
America or the winter in Europe (2). It affects both BUT–Big 6 and
Nicholas–N700 breeds and is mainly observed in birds with body weights above
the target. The syndrome doesn’t affect toms. The mortality is very sudden and
can vary from 1% to 15% over a 2-week period, depending on many contributing
factors. A few hours before death, the affected hens are unable to walk and
show signs of dyspnea and cyanosis (7).
Gross Lesions
On post-mortem examination the birds are in good body condition with
dark breast muscles. A straw colored transudate is found in the abdominal
cavity. The most
consistent lesions are in the liver, which is enlarged and has a mottled
appearance because of numerous small hemorrhages. Occasionally, large white
areas of lipid
accumulation are observed. Petechial and ecchymotic hemorrhages are also
observed on the epicardium and abdominal fat. Lung congestion and edema are
prominent. In heart and larger blood vessels, an uncoagulated blood is present
(7). Bacteriological examinations show small number of E. coli isolated from
the liver (7). In one case an avian encephalomyelitis (AE) virus was isolated;
however, this was believed to be a vaccine strain. Inoculation of turkeys with
virus isolated from affected hens did not
result indisease (1).
Histopathology
On histopathological examination the liver structure is distorted by
large vacuoles present in hepatocytes. These vacuoles contain fat since they
stain red in the samples
prepared by the Herxheimer’s method (7). The nuclei are displaced from
their central position and show signs of degeneration. Central veins are
dilated with small to massive hemorrhage around them. Tissues adjacent to this
hemorrhage are degenerated and necrotic. In some parts of the liver, rupture of
intrahepatic vein sections is prominent. In the spleen, pancreas and kidney
there are no specific lesions except for a different degree of congestion (7).
Laboratory Investigations
In some cases of hepatic lipidosis feed samples were tested for
mycotoxins or heavy metals with negative results (7). Liver samples were tested
for the presence of malondialdehyde (MDA). The levels of MDA ranged from 31 to
38 ug/g in the livers of affected hens and from 11 to 25 ug/g in normal hens
(7). Feed samples tested for methionine and cysteine levels showed decreased
concentration of these aminoacids (7). Blood sera of affected breeder hens
tested for AST showed increased levels 2923-5453 u/l compared to 795-1544 u/l
in normal hens.
Pathogenesis
Based on history and investigations of hepatic lipidosis this syndrome
has a nutritional etiology with numerous factors contributing to its outbreak.
The most important and common mechanism by which fatty liver is produced is
enhanced lipogenesis in the liver and reduced transport from the liver. Some
authors (6, 15) showed that high feed consumption or force-feeding and high
energy-low protein
diet cause an increase fat content in the chicken liver. Other authors
(3, 5, 9, 10) showed big build-up of lipids in the liver if the diet doesn’t
supply adequate amounts of protein and amino acids (methionine, cysteine)
required for
synthesis of apolipoproteins. Other factors contributing to outbreak of
hepatic lipidosis are:
As soon as the liver accumulates excessive amounts of lipids, they are
subjected to lipid peroxidation (14). Peroxidation process generates toxic
compounds such as
aldehydes, alkanes, epoxy fatty acids and hydroxy fatty acids (12).
These toxic substances cause liver cell and blood vessel damage leading to
necrosis of hepatocytes, hemorrhages,
lung edema and death. High levels of MDA in liver samples indicate a lipid
peroxidation process whereas higher levels of AST in blood serum reflect a
severe degree of liver tissue damage. In cases of hepatic lipidosis turkey hens
die from liver failure. Fatty liver hemorrhagic syndrome in chickens differs
from the hepatic lipidosis of turkeys but also bears some similarities. FLHS
occurs in mature laying chickens, whereas the turkeys are about 20 weeks of
age. The
mortality levels are similar. Histopathological lesions are also
similar, although the lesions are more focal in chickens (4). The gross lesions
are different between turkeys and chickens. Chicken layers affected with FLHS
seem to die from massive hemorrhage and rupture of the liver. Usually they show
the signs of hemorrhagic anemia with pale combs while turkeys die from liver
failure.
Treatment and Prevention
During some outbreaks of hepatic lipidosis in turkey hens, different
attempts were investigated to control mortality. The methionine level should be
checked in the feed. If the level of methionine in low protein diet (<12%)
is below 0.22% it should be adjusted to that level. Vitamin E in the drinking
water at the level of 25 IU per hen seemed to reduce mortality (7, 13).
Administration of liquid methionine (87%) in a dose of 1 l per 500 US gal
stopped mortality after 3 days of treatment. Increased levels of methionine in
the feed by 0.5 kg per tonne of feed and Vitamin E up to 50 IU/kg of feed seem
to prevent the incidence of this syndrome. Diets should also contain ethoxyquin
and 0.3 ppm of selenium as antioxydants.
References
1. Barns, J. Hepatic Lipidosis of Turkeys in Diseases of Poultry.10 th ed. by B.W. Calnek et.al. 1042-1044, 1997.
2. Bentley, J. 2001. Personal communication
3. Blair, R., C.C.Whitehead and P.W. Teaque. The effect of dietary fat and
protein levels, form and cereal type on fatty liver and kidney syndrome in
chicks. Res.Vet.Sci. 18: 76-81. 1975.
4. Butler, E.J. Fatty liver diseases in the domestic fowl, a review. Avian
Pathol. 5:1-14, 1976.
5. Flores, H., W. Sierralta, and F. Mankeberg. Trigliceride transport in
protein depleted rats. J. Nutr. 100: 375-379. 1970
6. Ivy, C.A., and M.C. Nesheim. Factors influencing the liver fat content
of laying hens. Poult. Sci. 52: 281-285. 1973
7. Gazdzinski, P., E.J. Squires and R.J. Julian. Hepatic Lipidosis in Turkeys.
Avian Dis. 38: 379-384, 1994.
8. Gazdzinski, P.,and B. Hunter. Hypothyroidism in turkey breeder candidate
hens. Proc. Of 3rd International Symposium on Turkey Diseases. Berlin 2000 pp.
105-112.
9. Marion, J.E., and M. Edwards. Observation on the influence of diet and
age upon liver lipid changes in the chick. J. Nutr. 77: 23-27. 1962.
10. Pearson, A.W. and E. Butler. Pathological and biochemical observation
on subclinical cases of fatty liver hemorrhagic syndrome in the fowl. Res. Vet.
Sci. 24: 65-71, 1978.
11. Pearson, A.W., and E. Butler. Environmental temperature as a factor
in the etiology of fatty liver hemorrhagic syndrome in the fowl. Res. Vet. Sci.
25: 133-138, 1978
12. Poli, G., M.U. Diazani, K.H. Cheeseman, T.F. Slater, J. Long, and H.
Esterbaue. Separation and characterization of the aldehydic products of lipid
peroxidation stimulation by carbontetrachloride or
ADP-iron in isolated rat hepatocytes and rat liver microsomal suspensions.
Biochem. J. 227: 629-635. 1985.
13. Squires, E.J. Causes and treatments for fatty liver hemorrhagic syndrome.
Proc. BASF Technical Seminar. St. Hyacinthe, Quebec, 1993.
14. Squires, E.J., and S. Leeson. Aetiology of fatty liver syndrome in laying
hens. Br.Vet.J. 144: 602-609. 1988.
15. Wolford, J.H., and D. Murphy. Effect of diet on fatty liver hemorrhagic
syndrome incidence in laying chickens. Poult. Sci. 51: 2087-2094. 1972.