Gizzard and proventricular

Day-old chicks have been Figure 1 - Gizzard ulcers and Figure 2 - Proventricular haemorrhage
found to have confluent haemorrhage
HATCHERY

haemorrhages and erosions

in the mucosal lining of their
gizzard. Often affected birds
did not recover and had to be
culled. What is it and what
can be done?

1 1
By Dr 2Joseph J Giambrone
2
, TV Dormitorio
3
,
Dr LLi Dr Fred J Hoerr , and Don Poole
1
Department of Poultry Science, Auburn
University, Auburn, AL, USA
2
Alabama Department of Agriculture and
Industries, C. S. Roberts Veterinary Diagnostic
Laboratory, Auburn
3
Degussa Corporation, Kennesaw GA
lines maybe be hatchery related (insuffi-
cient atmospheric conditions within the
machines). She reported that eggs were
overcrowded, embryos were smaller, and

D uring 2004 day-old broiler chicks

from the south-eastern United
States, Delmarva, and Mexico were
observed by Don Poole, a consultant for
the Degussa Corporation, to have focal to
confluent haemorrhages and erosions in
the mucosal lining (koilin) of the gizzard.
The condition spontaneously affected
many broiler flocks in a production com-
plex and involved chicks from multiple
breeder flocks of various ages. The lesion
occurred in chicks in the hatchery before
placement in the broiler house and prior
to feed consumption. In the broiler
house, stunted broilers were observed
with faecal-soiled feathers around the
cloacae. At necropsy, affected chicks had
focal to confluent or linear erosions and
roughening of the gizzard lining, fre-
quently with brown or red discoloration
indicative of haemorrhage (Figure 1). The
proventriculus often had yellow coagu-
lum adhered to gland openings (Figure2).
Affected birds (1 to 5% of the flock) did
not often recover and some were culled
before processing.
had enlarged hearts. Dr Bob Kiers from
Mississippi State University reported in
Applied Poultry Research in 2004, a 176%
increase in embryonic abnormalities af-
ter a switch to high yielding broiler
strains. Neither study reported on the in-
cidence of gastrointestinal lesions.
Dr John Brake, from North Carolina
State University, has also seen broiler
chicks with gizzard ulcerations in the
hatchery. He claims that the lesions ap-
pear commonly in chicks, which hatch
too early and is more prevalent in males
than females. He sees more of the lesions
in the colder months of the years, when
hatchers must work harder to keep the
proper temperature. Don Poole has so not
come to these conclusions on hatch rate,
gender incidence, or seasonality. So far
Don has seen only a normal hatch, body
weight, and heart size in affected flocks.
Experimental procedures
During 2004, Don Poole brought to
Auburn newly hatched chicks from 2
broiler complexes, one in Georgia and
the other in Alabama, which were show-
ing this problem. We examined chicks di-
rectly from the hatchery from 15 broiler
breeder flocks, ages 28 to 63 weeks of
age. Gizzards with gross lesions were di-
vided, with proventriculus attached, for
viral studies and portions were fixed in
neutral buffered formalin for
histopathology. Tissues were similarly col-
lected from three-day-old broilers with
gizzard lesions from four flocks. At
necropsy, gross lesions in the gizzard
were as described above.
Histologic examination showed multifo-
cal to confluent haemorrhage in the
koilin. Affected regions of koilin had in-
complete fusion and were discontinuous
(Figure 3). Many sloughed epithelial cells
were also present. In some, the haemor-
rhage was represented by nuclei of degen-
erated erythrocytes (Figure 4) occurring
in a laminar pattern with normal koilin
forming between the haemorrhage and

History
In 1968, Dr Bob Good and others reported
in Avian Diseases that gizzard ulcers and
haemorrhages occurred in white leghorn
embryos as early as 18 days of age. He
noted that the lesions were strain related.
He found no organism associated with
the condition. He asserted that the nor-
mal emptying and shrinking of the giz-
zard during incubation caused the le-
sions. In 2004 Dr Donna Hill with Hatch
Tech, Inc. reported in Poultry Digest that
an increase incidence of broiler malfor-
mations and lower hatch in high yielding
Future work
The authors used a $10,000 mini-grant from Degussa, Inc. to help solve this important problem, and
now they have more questions than answers. They will continue this important work with the help of
Don Poole to first establish the pathogeneses and second the cause of this disease. Giambrone: “We
would like to take eggs from several hatcheries within several companies, which have experienced the
problem, at various stages of incubation to determine the onset of the lesions. Once we have determined
the onset of the lesions, it will be easier to determine the etiology. We want to perform electron mi-
croscopy on lesion sites, homogenate inoculation to examine for transmissibility, infect chick embryos
and allow them to hatch, and try to reproduce lesions by altering incubation environment. If grants per-
mit we would also like to submit affected organs to laboratories for toxin analysis.”

WORLD POULTRY - Vol. 21 No 3. 2005 www.AgriWorld.nl 28

lesions before & after hatch
Figure 3 - Regions of koilin had incom-
plete fusion and were discontinuous.
Sloughed epithelial cells were present
the mucosa. In others, acute haemor-
rhage occurred at the interface of the
mucosa and the fused koilin layer. Some
sections of pancreas had infiltrates of
heterophils in periductal interstitial tis-
sue; duodenum and proventriculus had
no conclusive findings. In three-day-old
broilers, the haemorrhages were less ob-
vious in most gizzards available for exam-
ination, however, acute, locally extensive
haemorrhage and koilin disruption oc-
curred in some.
Figure 4 - Degenerated erythrocytes
occurring in the Lamina propria
Serological data using commercial ELISA
kits showed antibody titres against NDV,
IBV, IBDV, and reoviruses. The titre levels
were within the normal range for day-
old broiler chicks. Attempts to isolate
bacteria or viruses from the lesions, or
show inclusion bodies, have so far not
been successful. PCR and RT PCT have
not shown the presence of reovirus, ade-
novirus, infectious bronchitis virus, or
infectious bursal disease virus.
Epidemiology discounts broiler feed or
infectious agents from the broiler farm.
Microscopic observation indicated that
the lesions occur about 2 to 3 days prior
to hatch.
Possible causes
Our working hypothesis is that gastric
haemorrhages are from hatch-related
stress. Heavy meat birds have pro-
nounced metabolic demands at hatch.
Gas exchange stress can promotes anaer-
obic metabolism and stress on heart, liv-
er, and muscle to meet energy demands.
Overcrowding of hatching eggs can cre-
ate temperature extremes (99-106°F).
Energy depleted chicks are slow, diffi-
cult to hatch, energy deficient, and
prone to early stunting.
Gastric haemorrhage may be an indica-
tor of stress rather than a cause of clini-
cal disease.
Another possible cause could be myco-
toxins in the breeder feed. Lesions seen
herein are similar to those seen with
birds that have consumed various myco-
toxins. It is possible that small amounts
of feed toxins consumed by the hen,
could be passed from the gut of the hen
to the ovary, and then to embryo from
the ova. ■