A Case of Acute Pulmonary Edema Splenomegaly and Ascites in

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					A Case of Acute Pulmonary Edema, Splenomegaly, and Ascites in Guinea Fowl
Author(s): B. S. Cowen, H. Rothenbacher, L. D. Schwartz, M. O. Braune, R. L. Owen
Source: Avian Diseases, Vol. 32, No. 1 (Jan. - Mar., 1988), pp. 151-156
Published by: American Association of Avian Pathologists, Inc.
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AVIAN DISEASES32:151-156, 1988

Case Report-

                A Case of Acute Pulmonary Edema, Splenomegaly,
                           and Ascites in Guinea Fowl

                       B. S. Cowen, H. Rothenbacher,L. D. Schwartz,A
                               M. O. Braune,and R. L. Owen

                       Departmentof VeterinaryScience, Collegeof Agriculture,
                 The PennsylvaniaState University, University Park,Pennsylvania16802
                                          Received 7 August 1987

           SUMMARY. Acutepulmonaryedema,splenomegaly, asciteswereobservedin a disease
        outbreakin adult white and pearlguinea fowl. The clinical historyand gross and microscopic
        lesions resembledthose describedfor marblespleendiseaseof pheasantsand avian adenovirus
        groupII splenomegaly chickens.A small numberof intranuclear
                                of                                        inclusionbodies werefound
        in liver, spleen,andlungsectionsof affectedguineafowl.Attemptsto isolatevirusand serological
        tests to detect the presenceof viral antigenswere unsuccessful.
          Adult female pearl guinea fowl experimentallyexposed to pheasantand turkeyisolates of
        type II avian adenovirusesdeveloped gross and microscopiclesions similar to those seen in
        the field outbreak.The pheasantisolate was the more virulent. Intranuclear  inclusion bodies
        were observedin liver, spleen, and lung sections of pearlguinea fowl inoculatedwith either of
        the virus isolates, and direct immunofluorescent   examination revealed viral antigen in the
        spleen and lung.

          RESUMEN. Reportede Caso-Edema pulmonaragudo,esplenomegalia ascitisen gallinas
        de Guinea.
          Se present6 un brote con edema pulmonaragudo, esplenomegaliay ascitis en gallinas de
        Guinea adultas blancas y pintadas. La historia clinica y las lesiones macro y microsc6picas
        fueronsemejantesa las observadasen la enfermedaddel bazo moteado de faisanesy la esple-
        nomegaliacausadapor adenovirusaviar grupoII en pollos. Se encontr6 un nfimeropequenio
        de cuerposde inclusi6nintranucleares seccionesde higado,bazo y pulm6n.No fructificaron
        los intentosparaaislarel virus o paraidentificar antigenosviralespor medio de las pruebas
          Gallinasde Guinea pintadasexpuestasexperimentalmente cepas del tipo II de adenovirus
        de faisany pollo desarrollaronlesiones macroy microsc6picassimilaresa las observadasen el
        brotede campo, siendo la cepa de faisanla mas virulenta.Se encontraron   cuerposde inclusi6n
        intranucleares seccionesde higado,bazo y pulm6nde gallinasde Guineapintadasinoculadas
        con cualquierade las cepas y el examen por inmunofluorescencia   directaidentific6el antigeno
        viral en bazo y pulm6n.

   A literature search failed to reveal any reports      (HE) of turkeys are caused by type II avian ad-
of a guinea fowl disease resembling marble spleen        enoviruses (1), and pheasants, chickens, and
disease (MSD) of pheasants (5) or avian ade-             turkeys are the only known natural hosts (5).
novirus group II splenomegaly (AAS) of chickens          However, fowl adenoviruses (type I avian ade-
(5). These diseases plus hemorrhagic enteritis           noviruses) (1) have been isolated by Pascucci et
                                                         al. (15) from guinea fowl with pancreatitis.
                                                            No antibody to type II avian adenoviruses has
  Paper No. 7512 in the JournalSeries of the Penn-
                                                         been detected in wild bird sera (2). Laboratory
sylvania Agricultural
  ACurrentaddress:Animal Health Diagnostic Lab-          studies have demonstrated that pheasant and
oratory, College of VeterinaryMedicine, P.O. Box         chicken isolates of type II avian adenoviruses
30076, MichiganState University, East Lansing,MI         will infect turkeys and that turkey isolates will
48909-7576.                                              infect pheasants (3,6,7,12). Additionally, exper-

152                                               B. S. Cowen et al.

               w                                                                   wI



                         ltilmlllu.illill'l'                ll6l/34            5rl""67
                   <, "-"-"~      ^,'        --      '/,~         -,,, ~_DA'TE--
                    SPECIMENg           :-           e        l

                     Fig. 1. Lungswith acute edema;enlargedand mottled spleens.

imental HE virus infection of golden pheasant,               guinea fowl were observed to be affected. No
peafowl, chickens, and chukars produced en-                  vaccines or antibiotics had been administered,
larged and mottled spleens but no mortality (5).             and no significant disease problems had been
  The following is a case report of acute pul-               encountered previously by either of these guinea
monary edema, splenomegaly, and ascites in adult             fowl flocks.
guinea fowl. Results of experimental type II avi-              Eight dead and four live guinea fowl hens were
an adenovirus infection of guinea fowl are also              submitted to the Livestock and Poultry Veteri-
discussed.                                                   nary Diagnostic Laboratory at The Pennsylvania
                                                             State University for examination. Dead and sick
                                                             birds were cyanotic, and a greenish diarrhea was
                CASE REPORT
                                                             observed on vent feathers. Several birds had dis-
  An eastern Pennsylvania game farm experi-                  tended abdomens which contained copious
enced a sudden onset in mortality (33 of 1500;               amounts of straw-colored fluid. Affected hens ap-
2.2%) among white guinea fowl breeders in late               peared to be of normal weight and were ovulat-
April 1983. An egg-production drop of 30-50%                 ing, but the ovarian follicles were hemorrhagic,
was calculated for these breeders, which were                and some had ruptured, causing egg-yolk peri-
maintained in four different houses. Collected               tonitis. The lungs were edematous, and spleens
eggs were of normal size, shape, and color. Ap-              were enlarged (2-4 x) and mottled (Fig. 1); le-
proximately 1 week following the disease onset,              sions were similar to those described for MSD
pearl guinea fowl housed adjacent to the white               and AAS (5). The lungs also exhibited acute
                       Pulmonaryedema, splenomegaly,and ascites in guinea fowl                      153

                  A?     ~..

  Fig. 2. Lung (field case): A congested and edematous lung exhibiting a histiocyte with an amphophilic
           inclusion body (arrow).H&E. 1000x.

congestion, and serosanguineous fluid exuded            Bacterial culturing of liver sections, abdomi-
from the cut surfaces. Livers were swollen, and      nal fluid, and swabs of the abdominal cavity of
some had areas of greenish discoloration on the      both dead and moribund birds resulted in a mixed
surface. Most hens had a mild to moderate ca-        flora of Escherichia coli, Staphylococcus epider-
tarrhal enteritis, which was not grossly hemor-      midis, Streptococcusfaecalis, and Bacillus sp. Be-
rhagic. The intestinal walls of several hens were    cause of the suspected viral nature of this disease,
thickened, and cecal worms were present.             acute and convalescent sera were evaluated by
   Histopathologic examination of hematoxylin-       double immunodiffusion (DID) (4) and enzyme-
and-eosin (H&E)-stained sections of spleen           linked immunosorbent assay (11) and were found
showed characteristic multifocal histiocytic hy-     to be free of reovirus, reticuloendotheliosis virus
perplasia and necrosis. The pulmonary lesion was     (REV), and type I and II avian adenovirus an-
acute congestion and edema (Fig. 2). Periportal      tibodies (1,4). Spleens were examined for the
hepatitis and cholangitis with multifocal necrosis   presence of type II avian adenovirus antigen by
was observed in the liver. Nuclear changes re-       DID and direct immunofluorescence (DIF; fluo-
sembling those of type II avian adenovirus in-       rescein isothiocyanate conjugate) (8) and were
fections (nuclear vesiculation and inclusion body    also found to be negative. An attempt to isolate
formation) were seen in histiocytes of the spleen    a type II avian adenovirus from spleen homog-
and lung (Fig. 2) and in hepatocytes (Fig. 3). The   enates was made in a B-lymphoblastoid cell line
enteritis ranged from catarrhal to erosive-hem-      (MDTC-RP19) (13,14) with no success. At-
orrhagic. Capillaria cross-sections were found in    tempts to isolate other viruses by yolk-sac in-
the mucosa. Glomerular and tubular nephritis         oculation ofspecific-pathogen-free (SPF) chicken
was present in the kidneys. No brain lesions were    embryos (10) and inoculation of SPF chicken-
detected. Special staining techniques (Jenner-       embryo-liver-cell culture (16) were also unsuc-
Giemsa and Warthin-Starry) for spirochetes re-       cessful.
vealed nothing.                                         In an effort to obtain additional information
   A hematological evaluation of four affected       about the etiology of the above described disease,
guinea fowl hens revealed a relative lymphope-       three clinically normal 18-week-old pearl guinea
nia, monocytosis, and heterophilia. Red blood        fowl hens were inoculated intravenously (0.5 ml)
cells had hypochromic nuclei and immature            with approximately 5 x 104 TCID50 of pheasant
shapes.                                              or turkey type II avian adenoviruses. Two hens
154                                      B. S. Cowen et al.


nuclearvesiculation(N). H&E. 1000x.

(representing one of each inoculum type) were       and congested edematous lungs (pheasant virus
sacrificed at 4 days postinoculation for patho-     only). Gross lesions were more marked in the
logical evaluation. No clinical signs were ob-      pheasant virus (PV)-inoculated hen.
served before euthanasia. One hen-was held for        Microscopic lesions were similar to those de-
assays of antibody stimulation.                     scribed for the reported field outbreak and were
   Sacrificed hens exhibited distended gas-filled   more intense in the guinea fowl exposed to the
intestines and ceca, enlarged marbled spleens,      PV isolate. The spleen of the PV-inoculated fowl

         q        ?w                                    !&                           V


             Ib            t"

                                                         inclusion bodies in pulmonaryhistiocytes (ar-
                             Small amphophilicintranuclear
  Fig. 4. Lung (experimental):
rows). H&E. 1000x.
                        Pulmonaryedema, splenomegaly,and ascites in guinea fowl                  155


         | 3!
         rowFrte                                                                          w
             w          d+lPa      ;-
 Fig. 5. Liver (experimental):                       inclusion body in a hepatocyte(arrow).Note the
nuclear vesiculation (N). H&E. 1000 x .

exhibited multifocal necrosis, and nuclei of his-                      DISCUSSION
tiocyteswere found to be vesiculatedand to con-         Thegrossandmicroscopic     lesionsin the spleens
tain amphophilic inclusion bodies. Acute             and lungsof white and pearlguineafowl plus the
congestion and mononuclear pneumonitis was           clinical history of this case are similar to those
detected in the lung of the PV-inoculatedfowl.       describedfor MSD of pheasants(5) and AAS of
Pulmonary   histiocyteshadvesiculatednucleiwith      chickens (5).
eosinophilicto lavenderto slightlybasophilicin-         The histopathologic changesseenin guineafowl
clusions (Fig. 4). Cholangiohepatitiswas seen in     spleens (field case and experimental) included
the liver of the PV-inoculatedfowl. Numerous         lymphocyticdepletion and proliferationand ne-
hepatocytes had enlarged nuclei with eosino-         crosis of histiocytes.The type of intranuclear  in-
philic to lavender inclusion bodies (Fig. 5). The    clusion bodies observed in splenic histiocytes
pancreasof this bird had foci of hydropic de-        have been describedas pathognomonicfor MSD
generation.                                          of pheasants(18). Additionally,theseguineafowl
   The histopathologic findings for the turkey-      exhibited an acute pneumonic congestion and
virus-infected guineafowl weresimilarto but less     edema, which closely resembledsigns described
intense than those found in the PV-inoculated        for MSD and AAS (5).
guinea fowl; there was less necrosis and fewer          Although no virus could be isolated and no
vesiculated nuclei of histiocytes with inclusion     viral proteincould be detectedby DID and DIF
bodies. The microscopiclesions observed in the       in guinea fowl spleens from the field outbreak,
intestine and kidney of experimentallyinfected       the pathologicand DIF findingsof field and/or
guinea fowl (both viruses) were essentially the      experimentalcases are suggestive of a "type II
same as those found in the field case.               avian adenovirussplenomegaly"of guinea fowl.
   Viralproteinwas detectedby DIF in the spleen                       and
                                                     The hematology renalhistopathology also    are
and lung of experimentallyinfected guinea fowl       suggestiveof a viral etiology. Since the existence
(both virus isolates), which supports the gross      of virus and/or viral protein in type II avian-
and microscopicfindings.Weeklyassaysfor pre-         adenovirus-infectedbirds (9,17) is transient, it
cipitin formation in guinea fowl experimentally      is understandable   that virus might be missed in
inoculated twice (3 weeks apart) with the PV         field cases. Type II avian-adenovirus-induced
isolate were negativethrough3 months post pri-       precipitincould not be detected in either field or
mary inoculation.                                    experimentally infected guinea fowl. In retro-
156                                             B. S. Cowen et al.

spect, one additional virus-isolation technique               9. Gross, W. B., and C. H. Domermuth. Spleen
should have been attempted: the inoculation of             lesions of hemorrhagic enteritis of turkeys. Avian Dis.
                                                           20:455-466. 1976.
SPF turkey poults with the intestinal contents
and/or minced splenic tissue of dead or mori-                 10. Hitchner, S. B. Virus propagation in embryo-
bund guinea fowl (4,6).                                    nating eggs. In: Isolation and identification of avian
                                                           pathogens, 2nd ed. S. B. Hitchner, C. H. Domermuth,
  More research is needed to clarify the etiology          H. G. Purchase, and J. E. Williams, eds. Am. Assoc.
of the described guinea fowl disease.                      Avian Pathol., College Station, Texas. pp. 120-121.
                   REFERENCES                                 11. Ianconescu, M., E. J. Smith, A. M. Fadly, and
                                                           K. Nazerian. An enzyme-linked immunosorbent as-
   1. Cowen, B. S., and S. Naqi. Classification of avian   say for detection of hemorrhagic enteritis virus and
adenoviruses. J. Am. Vet. Med. Assoc. 181(3):283.          associated antibodies. Avian Dis. 28:677-692. 1984.
 1982.                                                        12. Iltis, J. P., R. M. Jakowski, and D. S. Wyand.
   2. Domermuth, C. H., D. J. Forrester, D. O. Train-      Experimentally transmitted marble spleen disease in
er, and W. J. Bigler. Serologic examination of wild        pen-raised wild turkeys. J. Wildl. Dis. 11:484-485.
birds for hemorrhagic enteritis of turkeys and marble       1975.
spleen disease of pheasants. J. Wildl. Dis. 13:405-408.        13. Nazerian, K., A. Elmubarak, and J. M. Sharma.
 1977.                                                     Establishment of B-lymphoblastoid cell lines from
   3. Domermuth, C. H., W. B. Gross, L. D. Schwartz,       Marek's disease virus-induced tumors in turkeys. Int.
E. T. Mallinson, and R. Britt. Vaccination of ring-        J. Cancer 29:63-68. 1982.
necked pheasants for marble spleen disease. Avian Dis.         14. Nazerian, K., and A. M. Fadly. Propagation of
23:30-38. 1979.                                            virulent and avirulent turkey hemorrhagic enteritis vi-
   4. Domermuth, C. H., and W. B. Gross. Hemor-            rus in cell culture. Avian Dis. 26:816-827. 1982.
rhagic enteritis of turkeys. In: Isolation and identifi-       15. Pascucci, S., A. Rinaldi, and A. Prati. CELO
cation of avian pathogens, 2nd ed. S. B. Hitchner, C.      virus in guinea fowl: characterization of two isolates.
H. Domermuth, H. G. Purchase, and J. E. Williams,           Proc. 5th International Conf. of World Vet. Poult. As-
eds. Am. Assoc. Avian Pathol., College Station, Texas.     soc., Munich, Germany. pp. 1524-1531. 1973.
pp. 106-107. 1980.                                             16. Purchase, H. G. Cell-culture methods. In: Iso-
   5. Domermuth, C. H., and W. B. Gross. Hemor-            lation and identification of avian pathogens, 2nd ed.
rhagic enteritis and related infections. In: Diseases of   S. B. Hitchner, C. H. Domermuth, H. G. Purchase,
poultry, 8th ed. M. S. Hofstad, H. J. Barnes, B. W.        and J. E. Williams, eds. Am. Assoc. Avian Pathol.,
Calnek, W. M. Reid, and H. W. Yoder, Jr., eds. Iowa        College Station, Texas. pp. 112-115. 1980.
State University Press, Ames, Iowa. pp. 511-516. 1984.         17. Silim, A., and J. Thorsen. Hemorrhagic enter-
   6. Domermuth, C. H., J. R. Harris, W. B. Gross,         itis: virus distribution and sequential development of
and R. T. DuBose. A naturally occurring infection of       antibody in turkeys. Avian Dis. 25:444-453. 1981.
chickens with a hemorrhagic enteritis/marble spleen            18. Wyand, D. S., R. M. Jakowski, and C. N. Burke.
disease type of virus. Avian Dis. 23:479-484. 1979.        Marble spleen disease in ring-necked pheasants: his-
   7. Domermuth, C. H., C. R. Weston, B. S. Cowen,         tology and ultrastructure.Avian Dis. 16:319-329. 1972.
W. M. Colwell, W. B. Gross, and R. T. DuBose. In-
cidence and distribution of"Avian adenovirus group
II splenomegaly of chickens." Avian Dis. 24:591-594.                   ACKNOWLEDGMENTS
   8. Fasina, S. O., and J. Fabricant. Immunofluores-         The authors acknowledge the excellent technical as-
cence studies on the early pathogenesis of hemorrhagic     sistance of Allan Schantz, Donna Marthouse, and
enteritis virus infection in turkeys and chickens. Avian   Charlotte Smith, and they thank Donna Smith for typ-
Dis. 26:158-163. 1982.                                     ing the manuscript.