Avian Pathology

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Gizzard erosion and ulceration syndrome in

chickens and turkeys: a review of causal or
predisposing factors

Anne-Gerd Gjevre , Magne Kaldhusdal & Gunnar Sundstøl Eriksen

To cite this article: Anne-Gerd Gjevre , Magne Kaldhusdal & Gunnar Sundstøl Eriksen (2013)
Gizzard erosion and ulceration syndrome in chickens and turkeys: a review of causal or
predisposing factors, Avian Pathology, 42:4, 297-303, DOI: 10.1080/03079457.2013.817665

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Avian Pathology, 2013
Vol. 42, No. 4, 297
303, http://dx.doi.org/10.1080/03079457.2013.817665

REVIEW ARTICLE

Gizzard erosion and ulceration syndrome in chickens and

turkeys: a review of causal or predisposing factors
Anne-Gerd Gjevre1*, Magne Kaldhusdal2 and Gunnar Sundstøl Eriksen3
1
Section of Veterinary Public Health, 2Section of Pathology, and 3Section of Chemistry and Toxicology, Norwegian
Veterinary Institute, Norway

Gizzard erosion and ulceration syndrome (GEU) was described for the first time in the 1930s. The main
focus of early studies was on nutritional deficiencies and peroxidation of highly polyunsaturated fatty acids
as causative factors. During the 1970s and 1980s the focus was moved towards toxic substances in the feed.
Scott’s review in 1985 concluded that overproduction of gastric acid induced by gizzerosine was a major
cause of GEU. During the last decades, serotype 1 of fowl adenovirus A and Clostridium perfringens have
been implicated as important pathogenic agents in the development of GEU in chickens. Although GEU is
globally distributed and its subclinical form appears to be common in commercial poultry flocks, the
condition is rarely mentioned in standard textbooks on poultry health. This regrettable fact is probably due
in part to the lack of one definitive cause of the syndrome.

Introduction
In the early 1930s Holst & Halbrook (1933) observed
dark erosion spots in the gizzard lining of 3-week-old
chickens in a nutritional study. This was one of the first
descriptions of ‘‘gizzard erosion and ulceration syn-
drome’’ (GEU). During the next few years the main
focus was on nutritional deficiencies (Holst & Halbrook,
1933; Almquist & Stokstad, 1936, 1937; Almquist,
1938a). However, in 1985 Scott concluded that the
major cause of GEU was overproduction of gastric
acid induced by a substance in overheated fish meal
(gizzerosine). He also emphasized the neutralizing effect
of bile in the gizzard under normal production of gastric
acid, and mentioned peroxidation of highly polyunsatu-
rated fatty acids as a causative factor for GEU (Scott,
1985). The syndrome has been variously termed ‘‘gizzard
erosion and ulceration’’ (Randall, 1991; Fletcher &
Abdul-Aziz, 2008), ‘‘ventriculitis’’ (Randall & Reece,
1996), ‘‘black vomit’’ (Becker et al., 1998; Herrera et al.,
1999), ‘‘vomito negro’’ (Fulton, 2008; Shlosberg, 2008)
and ‘‘Muskelmagenerosionen’’ (Fries et al., 2001) in
scientific papers, textbooks and atlases of poultry
diseases. The expressions ‘‘black vomit/vomito negro’’
have been used because black or blood-stained liquid
may dribble from the beak of severely affected birds if
lifted by their legs. During experimental studies on
necrotic enteritis in Norwegian broilers, erosions in the
koilin layer of the gizzard have been observed frequently
(Novoa-Garrido et al., 2006). We have also observed
that GEU is prevalent in clinically healthy broiler
chickens and slaughter turkeys from Norwegian farms
(unpublished data). These observations have made clear
the need for a new review of possible causative factors.
Anatomy of the gizzard mucosa
The mucosa of the gizzard is covered by a solid layer of a
carbohydrate
protein complex called the koilin layer,
also termed keratinoid layer, cuticle, and gizzard lining
(Figure 1a). Proteins constitute about 80% of the koilin
weight, with high levels of glutamic and aspartic acids,
leucine and arginine (Pivnenko et al., 1998). The surface
of the koilin layer and the underlying cellular mucosa are
arranged in rows of ridge-like folds except in the lateral
and medial tendon regions, which have a smooth surface.
The remaining mucosa of the gizzard form transverse
ridges in the blind sacs and longitudinal ridges in the
body regions. The koilin layer is composed of rodlets of
hard koilin secreted by the epithelial cells of the tubular
glands, and soft koilin secreted by the surface epithelial
cells (Akester, 1986).
Definition and scoring of GEU
GEU is characterized by macroscopic defects in the
koilin layer and often also in the mucosa of the gizzard
(Figure 1b). Defects that affect the koilin layer but not
the integrity of the underlying mucosa are easy to
identify grossly simply by removing the koilin layer
and inspecting the mucosal surface. In most of the
reviewed papers on GEU in chickens, neither ‘‘erosion’’
nor ‘‘ulceration’’ is clearly defined, but most workers
appear to consider defects affecting the koilin layer as
‘‘erosions’’ whereas gross lesions affecting the mucosa
have been designated ‘‘ulcers’’. Such a classification is
not in accordance with the terminology of mammalian
(including human) pathology, where an ‘‘erosion’’ is a

*To whom correspondence should be addressed. Tel: 47 23 21 64 29. E-mail: anne-gerd.gjevre@vetinst.no
Received 21 March 2013
# 2013 Houghton Trust Ltd
298 A.-G. Gjevre et al.
Figure 1. Gizzards from turkeys with normal koilin layer (1a)
and erosions and ulcerations (1b).
mucosal lesion that may reach but not penetrate the
muscularis mucosae and an ‘‘ulcer’’ affects tissues deeper
than the muscularis mucosae (Day et al., 2003). A likely
cause of this difference in lesion classification is the
anatomical differences between poultry and mammals.
Whereas mammals lack the koilin layer of birds, the
muscularis mucosae of the mammalian stomach is
absent in the poultry gizzard (Hodges, 1974). Further-
more, scoring of gizzard lesions has been based mainly
on gross examination, which may not allow for a clear-
cut distinction between categories based on histopatho-
logical criteria, in particular because no attempts to
correlate gross and microscopic gizzard lesions appear to
have been published. Similar definition and scoring
problems have been described in human (Laine &
Weinstein, 1988) and equine (Martineau et al., 2009)
gastroenterology studies. Species differences in anatomy
may dictate modifications in scoring systems (Martineau
et al., 2009) and may also be an argument in favour of
modified definitions of ‘‘erosion’’ and ‘‘ulceration’’.
Gizzards with erosive lesions often show areas with a
thickened, soft koilin layer that is lighter in colour than
normal. Bird et al. (1937) suggested that this is a
condition distinct from erosions/ulcers, but most workers
do not mention this distinction and we propose that such
lesions are considered part of GEU.
Over the years different methods for evaluation
of gizzard lesions have been published (for example,
Lansing et al., 1939; Okazaki et al., 1983; Wessels &
Post, 1989). The evaluation criteria are, in the authors’
opinion, often inadequately described. For example, they
do not include examination of the mucosal surface.
Therefore, we have recently developed a new scoring
method for gross gizzard lesions that includes examina-
tion of both sides of the koilin layer and the mucosal
surface (Kaldhusdal et al., 2012).
Poultry species affected by GEU
In the literature GEU appears mainly as a problem in
chickens (Fossum et al., 1988; Pfeiffer, 1992), and above
all in broilers (Johnson & Pinedo, 1971; Janssen &
Germs, 1973; Okuda et al., 2004; Novoa-Garrido et al.,
2006). GEU in young turkeys has very rarely been
described in the scientific literature (Sherwood & Sloan,
1954; Fletcher & Abdul-Aziz, 2008), although it is well
recognized as sub-lethal lesions, as a cause of sporadic
increase in mortality, and as a cause of gizzard con-
demnation at slaughter in Norway (unpublished data
from our laboratory and from the Norwegian Food
Safety Authority).
Gizzard erosions and ulceration caused by nema-
todes belonging to the genus Amidostomum (primarily
Amidostomum anseris) have been reported in geese, ducks
and pigeons. Chickens and turkeys are not natural hosts
of Amidostomum spp. (McDougald, 2008), and parasitic
infestations are not discussed further in this review.
Causative or predisposing factors
Numerous factors have been associated with GEU in
chickens. In the following we will give a review of the
possible role of congenital factors, starvation, feed
structure and fibre, nutritional deficiencies, toxic sub-
stances, infections and microbial colonization.
Congenital factors. Gizzard lesions have been detected in
chick embryos (Bird et al., 1937; Good et al., 1968) and
koilin lesions have been observed in embryos and newly
hatched broiler chicks in several European countries in
2012 (Johanna van der Stroom, personal communica-
tion, 2012), indicating that GEU may be congenital and
therefore caused and influenced by factors present before
hatch. Data have been published suggesting that the
occurrence of GEU in newly hatched chicks may be
associated with breeder diet (Tepper & Bird, 1942a, b;
Mushett & Ott, 1949), breeder age (Good et al., 1968)
and capillary fragility combined by transient increase
in blood pressure during hatching (Tepper & Bird,
1942a, b).
Starvation. When newly hatched chicks were deprived of
feed and water, the proportion of ulcerated gizzards
increased from about 3% (on incubation day 20 and on
the day of hatch) up to 68% on day 4 post hatch (Good
et al., 1968). Bierer et al. (1966) demonstrated that feed
and water deprivation induced erosions in broilers
starved from 1, 2, 4 and 8 weeks of age. These
observations indicate that restriction or deprivation of
feed and/or water may be associated with increased
frequency and severity of lesions whether this is initiated
from day of hatch or later in the rearing period.
Good et al. (1968) also demonstrated that gizzards
from 1-day-old chicks that were starved until day 3
post-hatch followed by access to feed showed only traces
of old ulcers on day 7 post hatch. This finding suggests
that starvation that is restricted to the first few days of
rearing cannot alone explain gizzard ulceration that
persists after 2 weeks of age.
Feed structure and fibre. Grit and feed particle size. Grain-
eating birds such as chickens and turkeys ingest small
stones if available. These stones are kept in the gizzard
lumen and assist effectively in the important grinding
function (Nickel, 1977). In spite of this, many broiler
farms do not provide access to grit as a part of their
management programme. The significance of grit has
been controversial (Bird et al., 1937), but published data
suggest that the frequency and severity of GEU lesions

can be reduced by use of grit (Bird et al., 1937; Almquist,
1938a).
A limited amount of research on optimum particle
size of poultry feeds has been conducted. Available data
indicate that relatively coarse grinding to a uniform
particle size improves the performance of birds offered
mash diets (Amerah et al., 2007). It has been postulated
that this effect may result from the positive effect of
increased particle size on gizzard development, and
inclusion of at least 20% cereal particles larger than 1
mm in size has been recommended (Svihus, 2011). We
have not, however, found studies focusing on the effect
of grit and feed particle size on GEU.
Pelleted versus mash feed. In an experiment comparing
pelleted and mash feeds based on the same formulation,
an outbreak of severe GEU was detected in broilers fed
pellets but not in those offered mash (Ross, 1979). Both
groups of birds were kept on litter. The author repeated
the experiment; this time also comparing groups of
broilers kept on wire-floors and on litter, and found that
a combination of pelleted feed and lack of access to
litter was associated with significantly increased gizzard
score.
Non-soluble fibres. Ingestion of non-soluble fibres has
been shown to exert strong effects on the structure and
function of the gizzard, and inclusion of at least 3%
coarse fibres has been proposed as a measure to
stimulate gizzard development (Svihus, 2011). Starck
& Rahmaan (2003) demonstrated that quails fed 40%
oat beards (non-digestible fibre) for 14 days developed a
gizzard mass that was 182% of the gizzard mass in the
control group. Inclusion of much more moderate
amounts of fibre (3% oat hulls) in the feed improved
production performance in broilers, increased the rela-
tive weight of the gizzard and reduced the pH of the
gizzard contents (Jimenez-Moreno et al., 2009). Inclu-
sion of 6% wood shavings in a broiler diet based on
ground wheat improved feed utilization when the data
were corrected by subtracting the amount of wood
shavings from the total feed consumption. Wood
shavings increased the relative gizzard weights and
improved ileal starch digestibility (Amerah et al.,
2009). Further, Hetland et al. (2005) published data
suggesting that layer chickens may eat feathers to
compensate for the lack of structural components in
the feed.
The effect of ingestion of non-soluble fibres on GEU
does not appear to have been much studied. Almquist
(1938a) presented data suggesting that hempseed meal
and hempseed hulls reduced GEU scores, and ascribed
this property in part to a grit-like action of the hempseed
hulls, and Thompson & Wilcke (1941) published an
abstract suggesting a preventive effect on GEU of oat
hulls. In a recent study performed in our laboratory, 5%
oat hulls reduced GEU scores and access to litter
reduced GEU scores when oat hulls were included in
the feed (Kaldhusdal et al., 2012).
Nutritional deficiencies. Early research on GEU focused
on nutritional deficiencies. Many studies were conducted
to identify the ‘‘anti-gizzard erosion factor’’ (Mushett &
Ott, 1949). Vitamin E has been proposed to be protective
against GEU if substantial amounts of highly polyunsa-
Gizzard erosion and ulceration syndrome: a review 299
turated fatty acids are present in the feed (Scott, 1985).
This view is underpinned by experiments (Dam, 1946)
demonstrating increased gizzard erosions by adding
either 5 or 10% cod liver oil or 0.5 to 1% of a highly
unsaturated fraction of fatty acids from menhaden oil.
Further, experiments based on use of diets with 15% fish
meal containing 8 to 14% crude fat have demonstrated
a variable but usually clearly protective effect of supple-
mentary vitamin E against GEU (Janssen & Germs,
1973).
Studies on the effect of experimental vitamin B12
deficiency on GEU have produced contradictory results
(Mushett & Ott, 1949; Sherwood & Sloan, 1954; Daghir
& Haddad, 1981). Sherwood & Sloan (1954) found a
protective effect against GEU in turkeys of choline, and
Daghir & Haddad (1981) detected a significant increase
in GEU severity among vitamin B6-deficient chickens.
The severity of GEU among vitamin B6-deficient chick-
ens was reduced by adding taurocholic acid to the diet.
This finding offers a potential explanation for the
mechanism behind an effect of vitamin B6 deficiency.
The role of vitamin B6 in taurine synthesis has been well
documented in rats, and the authors suggest that the
vitamin deficiency may contribute to taurine insuffi-
ciency and presumably also to insufficiency of tauro-
cholic acid, which is a bile acid. This reasoning is
consistent with Almquist’s (1938b) report indicating a
protective effect of whole bile and bile components
(including sodium taurocholate) against gizzard ero-
sions. Further, Miller et al. (1975) demonstrated experi-
mentally that gizzard erosions were prevalent and severe
when chickens were fed inadequate methionine, which is
an intermediate in the biosynthesis of taurine. GEU
lesions were improved considerably, but not totally
prevented, by inclusion of 0.70 to 1.25% levels of
sulphur-containing amino acids in the diet.
Toxic substances. Biogenic amines. These are amine-
group-containing substances produced by biological
organisms. The most studied and most commonly found
biogenic amine is histamine, primarily produced in fish
and fish products by time-dependent and temperature-
dependent bacterial processes (Hungerford, 2010). Free
histidine is the precursor of histamine while other amino
acids are precursors of other biogenic amines (Shalaby,
1996). Biogenic amines have also been reported from
meat products as well as dairy products, so the potential
source in feed is not restricted to fish meal.
Histamine has been associated with gizzard erosions
and ‘‘black vomit’’ observed in poultry (for example,
Johnson & Pinedo, 1971; Harry & Tucker, 1976), but has
generally received less attention as a causal agent for
these lesions since the discovery of gizzerosine in the
early 1980s. Pure histamine is only able to induce gizzard
erosions when present in high concentrations in poultry
feed. Levels exceeding 200 mg/kg induced gizzard
erosions in some studies (Barnes et al., 2001), but not
in others (Bermudez & Firman, 1998; Friday et al.,
1999). In a 6-week trial, chickens were given four
biogenic amines alone or in combination. All in-feed
concentrations were at or above levels occurring in the
USA. No effects were found on performance or gizzard
health. The authors concluded that these biogenic
amines are unlikely to be of any concern in any practical
conditions in the USA (Bermudez & Firman, 1998;
Friday et al., 1999). This conclusion was supported by
300 A.-G. Gjevre et al.
Barnes et al. (2001). The possibility of an interaction
with gizzerosine, if present in the same feed, cannot be
ruled out, particularly because both histamine and
gizzerosine are reported to bind to and activate the H2
receptors, leading to an increase in acid production and
reduced pH (Hino et al., 1987; Ito et al., 1988; Guinotte
et al., 1993).
Gizzerosine. This substance was identified as the causal
agent of GEU when it was isolated from heated fish meal
causing the disease (Okazaki et al., 1983; Scott, 1985).
Gizzerosine was assumed to be formed during heating of
brown fish meal, especially when overheated (1308C).
Gizzard erosions were also found when a heated mixture
of casein and histidine was fed to chickens (Masumura
et al., 1981). An apparent dose-dependent increase in
gizzard erosions was observed in chickens given concen-
trations from 0.15 mg gizzerosine/kg feed, but no statistics
were provided (Sugahara et al., 1988).
Later studies of the effects of gizzerosine in poultry
confirm its potential toxicological effects, including
gizzard lesions (Grabarević et al., 1998; Tisljar et al.,
2002; Artuković et al., 2005). The papers do not,
however, provide any information about safe levels of
gizzerosine in poultry feed since only high daily oral
doses by gavage were used and no detailed information
about the gizzard lesions was provided.
There are very limited data on the occurrence of
gizzerosine in poultry feed, partly due to lack of reliable
analytical methods. Until now it has therefore been
impossible to compare the levels of gizzerosine needed to
induce gizzard erosions with the level in feed on the
market. However, a liquid chromatography
tandem
mass spectroscopy method for quantification of gizzer-
osine has been published recently (Uhlig et al., 2011). In
this study a limited number of samples of Norwegian
poultry feed was analysed with negative results. Accord-
ing to the Norwegian fish meal and feed industry, the
modern processing of fish meal has to a large extent
changed the drying process, lowering the maximum
temperature well below the temperature said to be
associated with the formation of high levels of gizzer-
osine. It is therefore likely that the levels of gizzerosine in
general would be lower at present than previously.
However, the old processing methods may still be in
use in some parts of the world.
Mycotoxins. None of the well-studied mycotoxins seem
to primarily affect the gizzard in poultry, but some
widespread mycotoxins may affect the gastrointestinal
tract.
Trichothecenes constitute a large group of Fusarium
mycotoxins, including deoxynivalenol (DON) and T-2
and HT-2 toxins that are frequently found in feeds and
grains (NFSA, 2005
2011; Langseth & Rundberget,
1999). Gizzard erosions following exposure to DON
have only been reported from chickens given very high
levels in the feed (49.4 and 83 mg/kg feed). Increased
relative gizzard weights have been reported from poultry
consuming feed containing DON levels from 16 mg/kg
feed (reviews in EFSA, 2004; Eriksen & Pettersson, 2004).
Concentrations of DON rarely reach these levels in
processed feed (Placinta et al., 1999; NFSA, 2005

2011). Even other trichothecenes, including T-2 toxin
and nivalenol, have been associated with gizzard lesions
(Harris, 1984; as cited in Hoerr et al., 1981; Hedman et al.,
1995; Hoerr, 2008). The concentrations of these toxins in
processed poultry feed are rarely reported (NFSA, 2005

2011; Placinta et al., 1999) or those in Norwegian grain
(Langseth & Rundberget, 1999).
Analyses of Norwegian poultry feed have revealed low
concentrations of trichothecenes (Norwegian Veterinary
Institute, unpublished data; NFSA, 2005
2011). These
toxins are therefore unlikely to be main explanations for
the occurrence of GEU in Norwegian commercial
poultry.
Other mycotoxins may also affect the gizzard.
Moniliformin, pure fumonisins B1 and B2, and extracts
of cultures of Fusarium proliferatum containing both
moniliformin and fumonisins caused gizzard ulcers
(Javed et al., 2005). This indicates that fumonisins may
have the potential to cause GEU. Analyses of Norwe-
gian poultry feed have revealed very low concentrations
of fumonisins (Norwegian Veterinary Institute unpub-
lished data; NFSA, 2005
2011). We do not therefore
consider fumonisins to be a likely cause for GEU in
Norway, demonstrating that other factors must be of
importance for the development of GEU.
Cyclopiazonic acid (CPA) is another mycotoxin that
caused mucosal necrosis in the gizzard in feeding
experiments where poultry were given 34 or 10 mg
CPA/kg feed (Gentles et al., 1999; Kamalavenkatesh
et al., 2005). Although the occurrence of CPA in feed has
rarely been reported, it seems that the levels associated
with gizzard lesions in experimental feeding studies are
high compared with the few available data on occur-
rence. No CPA above the detection limit of 0.02 mg/kg
was found in 44 samples of Norwegian poultry feed
(Moldes-Anaya et al., 2009).
Other little-studied mycotoxins, such as oosporein and
rubratoxin or rubratoxin-producing fungi, have been
shown to cause gizzard lesions in poultry (reviewed by
Hoerr, 2008). The occurrence of these toxins in poultry
feed is not known, and therefore the potential contribu-
tion from these to the occurrence of GEU cannot be
evaluated.
Infections and microbial colonization. Adenovirus. Tanimura
et al. (1993) and Goodwin (1993) reported the presence of
adenoviral inclusions in gizzard epithelium of chickens
showing GEU lesions, and Lenz et al. (1998) reproduced
gizzard lesions experimentally by inoculating specific
pathogen free Leghorn chicks with adenovirus isolated
from commercial US broilers with GEU. During the first
half of previous decade the widespread occurrence of
adenovirus-associated GEU in slaughtered broilers was
documented in Japan (Okuda et al., 2001a, b; Ono et al.,
2001, 2003), and similar findings have been reported
from Italy over the time period of 1995 to 2006 (Manarolla
et al., 2009). Both vertical and horizontal transmission is
important in the spread of adenoviruses. An adenovirus
infection can remain latent and be reactivated later
(Adair & Fitzgerald, 2008). Experimental data indicate
that adenoviral gizzard erosion can be reproduced by
horizontal transmission (Ono et al., 2007). Broilers
affected by adenoviral gizzard erosion usually show no
clinical signs and the problem is therefore mainly detected
at slaughter (Ono et al., 2001, 2003; Manarolla et al.,
2009). Most virus strains that have been isolated from
gizzard lesions belong to serotype 1 of fowl adenovirus A
within the genus Aviadenovirus (Ono et al., 2003; Adair &
Fitzgerald, 2008; Manarolla et al., 2009).

Clostridium perfringens. Fossum et al. (1988) isolated
C. perfringens from the gizzard koilin layer of most
chicks that were examined from outbreaks of GEU in
11 flocks of White Leghorn birds submitted for autopsy
during 1981 to 1988. Clinical signs, including increased
mortality, usually appeared about 1 week after hatching,
but outbreaks could appear in chickens up to 4 weeks of
age. Addition of antibiotics to the drinking water as a
rule reduced mortality to normal within a few days.
Novoa-Garrido et al. (2006) summarized data obtained
from 1217 broiler chickens originating from six experi-
ments, and showed that caecal C. perfringens counts
increased significantly with severity of mucosal gizzard
lesions. Dinev (2010) investigated an outbreak of GEU
with increased mortality starting in a 38-day-old com-
mercial broiler flock. He demonstrated foci of bacteria,
including bacilli, within the changed koilin layer, and
isolated C. perfringens from all gastric samples exam-
ined. Kaldhusdal et al. (2012) demonstrated that the
antibacterial compound narasin, with a well-known
activity against C. perfringens (Martel et al., 2004),
reduced GEU severity when the feed was supplemented
with insoluble fibre.
C. perfringens is capable of hydrolysing the amide
bond of conjugated bile salts (Knarreborg et al., 2002)
and a protective effect of bile against GEU has been
proposed (Almquist, 1938b; Scott, 1985). It is therefore
possible that C. perfringens is more than an opportunis-
tic pathogen occupying a new niche following the
appearance of gizzard lesions.
Concluding remarks
Twenty-five years ago, gizzerosine in fish meal was
assumed to be the most important cause of GEU.
Gizzerosine may still cause GEU in regions where fish
meal used for poultry is exposed to high temperatures
during processing, but the importance of this toxin has
probably decreased because of improved drying meth-
ods. The recent publication of a convenient analytical
method for gizzerosine should enable the fish meal
industry and the scientific community to clarify the
present importance of this toxin.
Adenovirus infections have been the most frequently
discussed cause of GEU during recent years. Although
most reports originate from Japan, these viruses are
likely to play a role in several regions.
The importance of vitamin E deficiency is likely to
depend on the fatty acid composition of the diet. The
potential significance of factors stimulating gizzard
motility (e.g. dietary non-soluble fibres and grit) is an
aspect that deserves more attention from the research
community.
A protective role for whole bile or bile components
against GEU has been proposed, and more work is
warranted in order to test this assumption. Several
factors might increase the risk of GEU by reducing the
availability of bile components. C. perfringens may
contribute to GEU development by means of its bile
salt hydrolysing activity. Suboptimal levels of vitamin B6
and methionine may play a similar role, because these
nutrients are intermediates in the biosynthesis of the bile
component taurocholic acid.
Several mycotoxins have been associated with gizzard
lesions, but so far there is a lack of data confirming that
Gizzard erosion and ulceration syndrome: a review 301
any of these compounds are of major significance as
causative factors. Most of these toxins have other main
target organs than the gizzard and thus induce signs or
lesions distinct from GEU. In addition, experiments
demonstrating an association have been based on
toxin levels that are unlikely to be present in commercial
feeds.
Clinical GEU has been reported from many countries
and most continents. This review was prompted by our
detection that GEU lesions are prevalent in apparently
healthy flocks of Norwegian broilers and slaughter
turkeys, and by the fact that the cause(s) of these lesions
have not been established. Difficulties in establishing the
cause of GEU have been a persistent feature, and a high
number of proposed causative or predisposing factors is
another trait. These features explain why GEU is
designated as a syndrome, and probably also why this
condition, despite its wide distribution, is rarely men-
tioned in textbooks on poultry health.
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