Multisystemic Adenovirus Infection in Broiler Chicks with Hypoglycemia and Spiking

Mortality
Author(s): Mark A. Goodwin, Donna L. Hill, Mark A. Dekich and Marshall R. Putnam
Source: Avian Diseases, Vol. 37, No. 2 (Apr. - Jun., 1993), pp. 625-627
Published by: American Association of Avian Pathologists
Stable URL: http://www.jstor.org/stable/1591701
Accessed: 21-06-2016 13:26 UTC

Your use of the JSTOR archive indicates your acceptance of the Terms & Conditions of Use, available at
http://about.jstor.org/terms

JSTOR is a not-for-profit service that helps scholars, researchers, and students discover, use, and build upon a wide range of content in a trusted
digital archive. We use information technology and tools to increase productivity and facilitate new forms of scholarship. For more information about
JSTOR, please contact support@jstor.org.

Allen Press, American Association of Avian Pathologists are collaborating with JSTOR to digitize,
preserve and extend access to Avian Diseases

This content downloaded from 104.239.165.217 on Tue, 21 Jun 2016 13:26:04 UTC
All use subject to http://about.jstor.org/terms
AVIAN DISEASES 37:625-627, 1993

Case Report-

Multisystemic Adenovirus Infection in Broiler Chicks

with Hypoglycemia and Spiking Mortality
Mark A. Goodwin,AB Donna L. Hill,c Mark A. Dekich,c
and Marshall R. Putnamc

AGeorgia Poultry Laboratory, P.O. Box 20, 4457 Oakwood Road, Oakwood, Georgia 30566
BDepartment of Veterinary Pathology, College of Veterinary Medicine, The University of Georgia,
Athens, Georgia 30602
CPerdue Farms, Inc., 1537 Old Ocean City Road, Salisbury, Maryland 21802

Received 2 November 1992

SUMMARY. The search for a solitary cause of spiking mortality (so-called spiking mortality
syndrome [SMS]) among broiler chicks has been thwarted by the fact that many agents will
cause similar mortality histograms. Recently, severe hypoglycemia has been said to be a
characteristic finding in chicks that die with SMS. In the present case study, we report ade-
novirus inclusions in the pancreas, small intestines, and liver of chicks with hypoglycemia
and spiking mortality. We attributed the hypoglycemia and mortality to hepatic insufficiency.

RESUMEN. Reporte de Caso-Infecci6n multisistemica por adenovirus en pollitos de

engorde con hipoglicemia y aumento en la mortalidad.
La b6squedad de una causa 6nica del llamado sindrome del aumento de la mortalidad en
pollitos de engorde ha sido enmascarada por el hecho de que existen muchos agentes que
causan una mortalidad similar. Recientemente se ha dicho que la hipoglicemia es una ca-
racteristica que se encuentra en los pollitos que mueren del sindrome de aumento en la
mortalidad. En el presente estudio de caso, reportamos inclusiones de adenovirus en el
pancreas, intestino delgado e higado de pollitos con hipoglicemia y aumento de la mortalidad.
Atribuimos la hipoglicemia y la mortalidad a la insuficiencia hepatica.
Key words: adenovirus, mortality, hypoglycemia, chicks.

So-called spiking mortality syndrome (SMS) CASE REPORT

is a malady of broiler chicks (3). The search for

an etiology has not been successful. Severe hy-
poglycemia is said to be a characteristic finding
in chicks that die with SMS (12). One naturally
occurring toxin (carboxyatractyloside) in cock-
leburs (Xanthium spp.) causes hypoglycemia
and sudden death in cattle, sheep, pigs, and rats,
but the toxin was proven not to be the cause of
hypoglycemia or SMS in chicks (7).
Hepatic inclusion bodies are characteristic for
group 1 adenovirus infections in chicks (inclu-
sion body hepatitis [IBH]) (2,6,8,13). The pur-
pose of the present report is to describe ade-
novirus inclusions in the pancreas, small
intestines, and liver of chicks with IBH, hypo-
glycemia, and spiking mortality.
Case history. Fourteen-day-old chicks in
one house on a poultry farm had been ill for 3
days. The mortality rate was calculated to be in
excess of three chicks per 1000 stocked chicks
per day. Upon examination, ill chicks were hud-
dling together and had climbed into and filled
the feed pans. They were frantic to get water
and had wet eyes (attributed to recent reaction
to a live vaccine administered in the drinking
water). Ill chicks had feed in their gastrointes-
tinal tracts and did not move when approached
by people. Dead and ill chicks had enlarged,
mottled livers that had disseminated red
splotches (interpreted to represent hemor-
rhage) and were tough to cut (interpreted to

625

This content downloaded from 104.239.165.217 on Tue, 21 Jun 2016 13:26:04 UTC
All use subject to http://about.jstor.org/terms
626 M. A. Goodwin et al.
represent fibrosis). Glucose levels were mea-
sured in blood samples taken from 15 ill chicks
and 15 healthy counterparts by following in-
structions for measuring blood glucose that ac-
company Chemstrip bG reagent strips (Boeh-
ringer Mannheim Corp., Indianapolis, Ind.).
When color block readings were made on the
color scale, ill chicks always had glucose read-
ings of 20-40 mg/dl. Their healthy counterparts
always had glucose readings of 240 mg/dl.
Portions of duodenum, jejunum, ileum, ce-
cum, liver, pancreas, heart, spleen, and kidney
were collected in 10% neutral buffered forma-
lin. Portions of submitted specimens were pro-
cessed through graded alcohols, embedded in
paraffin, sectioned, stained, and examined with
a light microscope. Other organ portions were
post-fixed in osmium tetroxide, dehydrated
through a methanolic series, embedded in
Spurr's resin, thin-sectioned, mounted on cop-
per grids, stained, and examined with a trans-
mission electron microscope.
Treatment consisted of nursing care and vi-
tamins in water. A decision was made to with-
hold vaccinations until the chicks were normal.
Histologically, significant lesions were found
only in the liver, pancreas, and small intestine.
Multifocal coalescing areas of coagulative ne-
crosis (liver, pancreas) were accompanied by
hemorrhage and fibrin pools. Hepatocytes in
and around the necrotic areas contained solitary
large basophilic inclusion bodies. In segments
of small intestine, enterocytes over the distal
one third of the villus finger commonly con-
tained similar inclusions. Inflammation and ne-
crosis were not apparent in these sections. In-
clusion bodies consisted of crystalline arrays of
particles diagnostic for adenovirus among gran-
ular material (4).
DISCUSSION
Adenovirus inclusions have not been de-
scribed in the pancreas or small intestines of
chicks with spontaneously occurring IBH. Ex-
perimentally, infections with group 1 adenovi-
rus can result in intranuclear inclusion bodies
in chick liver (13), pancreas (14), and trachea
and lungs (10). Although adenovirus infections
might be latent and activated by stress or other
immunosuppressive events (13,16), there is in-
creasing evidence that several serotypes of ad-
enovirus are primary pathogens in chicken gas-
This content downloaded from 104.239.165.217 on Tue, 21 Jun 2016 13:26:04 UTC
All use subject to http://about.jstor.org/terms
trointestinal, respiratory, and genitourinary tracts
(2,5,6,13) (C. M. Lamichhane, D. B. Snyder, G.
Paul, M. A. Goodwin, S. Scholler, and S. Mengle,
University of Maryland and Georgia Poultry Lab-
oratory; observation not published). Clinicians
and pathologists should be aware that adeno-
virus inclusion bodies might be found in the
pancreases, small intestines, and livers of clin-
ically ill broiler chicks.
Spiking mortality histograms are expected in
outbreaks of IBH (13). We attributed the chick
mortality in the present study to hepatic insuf-
ficiency that resulted in hypoglycemia (5). Se-
vere hypoglycemia is said to be a characteristic
finding in chicks that die with SMS (12). Al-
though it is tempting to use commercially avail-
able rapid direct blood tests to determine glu-
cose levels, results of the present report should
be interpreted with caution until studies are
done to determine the relationship between
these rapid tests and standard methods under
field and laboratory conditions. In addition,
blood glucose levels have a circadian pattern
(15) and can be affected by age (11), genetic
line (11), and sex (11). Excessive dietary me-
thionine levels (9) can induce hypoglycemia,
and hypoglycemia accompanies diseases such
as fatty liver kidney syndrome (1).
Because hypoglycemia and spiking mortality
are not specific for any particular etiology, just
what does constitute SMS remains a dilemma.
Use of an imprecise acronym can encourage
grouping together of illnesses that might be
caused by different agents. In this case, a clin-
ical sign (spiking mortality pattern) does not
constitute a diagnosis.
REFERENCES
1. Bannister, D. W., I. E. O'Neill, and C. C. White-
head. The postmortem diagnosis of fatal hypogly-
cemia using the fatty liver and kidney syndrome of
chicks as a model. Br. J. Nutr. 47:235-241. 1982.
2. Christensen, N. H., and Md. Saifuddin. A pri-
mary epidemic of inclusion body hepatitis in broilers.
Avian Dis. 33:622-630. 1989.
3. Craig, F. R. Delmarva Mortality Task Force sum-
mary. Proc. 26th National Meeting on Poultry Health
and Condemnations, Ocean City, Md. pp. 12-28.1991.
4. Doane, F. W., and N. Anderson. Adenoviridae.
In: Electron microscopy in diagnostic virology-a
practical guide and atlas. Cambridge University Press,
Cambridge, Mass. pp. 69-74. 1987.
 Adenovirus, hypoglycemia, and spiking mortality
5. Duncan,J. R., and K. W. Prasse. Proteins, lipids,
and carbohydrates. In: Veterinary laboratory medicine
clinical pathology, 2nd ed. Iowa State University Press,
Ames, Iowa. p. 116. 1986.
6. Erny, K. M., D. A. Barr, and K. J. Fahey. Molec-
ular characterization of highly virulent fowl adeno-
viruses associated with outbreaks of inclusion body
hepatitis. Avian Pathol. 20:597-606. 1991.
7. Goodwin, M. A., E. T. Mallinson, J. Brown, E. C.
Player, K. S. Latimer, N. Dale, W. V. Shaff, and T. G.
Dickson. Toxicological pathology of cockleburs
(Xanthium spp.) for broiler chickens. Avian Dis. 36:
444-446. 1992.
8. Grimes, T. Cause and control of a peracute form
of inclusion body hepatitis. Proc. 41st Western Poultry
Disease Conference, Sacramento, Calif. pp. 42-44.
1992.
9. Katz, R. S., and D. H. Baker. Methionine toxicity
in the chick: nutritional and metabolic implications.
J. Nutr. 105:1168-1175. 1975.
10. Kawamura, H., and T. Horiuchi. Pathological
changes in chickens inoculated with Celo virus. Natl.
Inst. Anim. Health Q. (Tokyo) 4:31-39. 1964.
11. Leenstra, F. R., E. Decuypere, G. Beuving, and
J. Buyse. Concentrations of hormones, glucose, tri-
This content downloaded from 104.239.165.217 on Tue, 21 Jun 2016 13:26:04 UTC
All use subject to http://about.jstor.org/terms
627
glycerides, and free fatty acids in the plasma of broiler
chickens selected for weight gain or food conversion.
Br. Poult. Sci. 32:619-632. 1991.
12. Mallinson, E. T., C. T. Larson, M. Salem, D. W.
Murphy, E. Russek-Cohen, E. M. Odor, and G. Stein,
Jr. Severe, acute, idiopathic hypoglycemia of chicks.
Proc. 64th Northeastern Conference on Avian Dis-
eases, University Park, Pa. pp. 10-13. 1992.
13. McFerran,J. B. Adenovirus infections. In: Dis-
eases of poultry, 9th ed. B. W. Calnek, H. J. Barnes,
C. W. Beard, W. M. Reid, and H. W. Yoder, Jr., eds.
Iowa State University Press, Ames, Iowa. pp. 552-563.
1991.
14. Rinaldi, A., G. Mandelli, D. Cessi, A. Valeri, and
G. Cervio. Proprieta di un ceppo di virus CELO isolao
dal pollo in Italia. Clin. Vet. (Milan) 91:382-404.1968.
15. Saini, S. K., and A. K. Pati. Circadian features
of carbohydrate metabolism in domestic fowls ex-
posed to 120-degree shifts of synchronizer schedule.
Indian J. Exp. Biol. 30:87-89. 1992.
16. Ward,J. M., and D. M. Young. Latent adenoviral
infection of rats: intranuclear inclusion induced by
treatment with a cancer therapeutic agent. J. Am. Vet.
Med. Assoc. 169:952-953. 1976.