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INCLUSION BODY DISEASE _HERPESVIRUS INFECTION_ OF

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									Journal        of       Wildlife         Diseases      Vol.     11,   January,         1975                                                                             83




INCLUSION                               BODY           DISEASE                 (HERPESVIRUS                                 INFECTION)
OF         FALCONS                         (IBDF)

DAVID         L. GRAHAM,EIJ                  C.     JOHN      MARE,EU         F. PRESCOTT                   WARDE

and       MALCOLM                  C.   PECKHAMi



Abstract:       Inclusion          body disease         of falcons          (IBDF)         is caused       by a herpesvirus.              The
clinical     course        is short,      24 to 72 hours             in duration,          and is characterized               by mild to
severe      depression            and    weakness         often        accompanied            by anorexia.            The       disease       is
invariably        fatal.      The virus has a marked                     affinity       for the reticuboendothelial                  system
and hepatocytes,               producing      focal      to diffuse         necrosis       of infected        tissues     accompanied
by the formation                   of intranuclear            inclusion          bodies.      The      virus      is pathogenic            for
American         kestrels         (Fa/co    sparverius)           and great          horned      owls      (Bubo      virginianus)           in
which      typical       lesions       of IBDF        are reproduced.               The lesions         of IBDF         are similar          to
those     produced           by some herpesvirus                infections         in other      avian      species.



     Necrosis        of various           components             of the                     regions.        A herpesvirus                was suggested         as
 reticuloendothelial               system            and       of     the                   the      etiological      agent.              Lesion      material
liver,      in some instances                  accompanied              by                  from the prairie           falcon            was found        to be
the development                  of intranuclear                  inclu-                    infectious        for embryonated                  chicken      eggs
sion       bodies       has been              recognized           as a                     and for American             kestrels             (F.     sparverius)
feature        of certain          diseases          occurring           in                 in which             the lesions              described            above
several        avian      species.         Among           these     dis-                   were       reproduced.
eases       are goose          hepatitis,         from       which        a                 Since      the appearance            of this first re-
parvovirus           has      been         isolated.”’3’             owl                port      eight      other     cases      of the      disease
hepatosplenitis”#{176}#{176}”               herpesvirus           infec-                have been           diagnosed        in captive      falcons.
tion      of pigeons,””’#{176}”                 and duck           virus                The purpose             of the present        report      is to
enteritis””8           for which              herpesviruses           are               summarize           the clinical        and pathological
known          to be etiological                   agents.        Other                 findings        in these      cases      and to describe
examples          are inclusion              body      hepatitis        of              the disease          as it was experimentally                 re-
chickens,”'””'#{176}          Pacheco’s            parrot       disease                 produced          in other    raptorial     species.
                and a disease              of muscovy             ducks
described         by Kaschula,’#{176} all of presumed
but unproven              viral etiology.                                                   CASE         REPORTS           OF    FIELD   CASES       OF     IBDF

     In  1971     Ward        and co-workers”’                de-                               The           clinical, pathological                   and viro-
scribed     a previously           unreported           disease                             logical          findings  are summarized                    in Table
in a prairie        falcon       (Fa/co        mexicanus).
The clinical        course      was short,           approxi-
mately     40 hours,         and was characterized                                          Clinical         Findings
by anorexia       and listlessness.           Post-mortem
findings     were      multiple        necrotic        foci     in                          Case        1

the liver,     spleen,      bone      marrow,         and in-                               A 4- to                       S-month        old   male   prairie
testinal   wall. Intranuclear            inclusions         were                        falcon    died                  following        a 72-hour    period
found     in cells      adjacent        to the necrotic                                 of anorexia,                     listlessness,     and weight     loss.


rn    Department               of Veterinary           Pathology,          Iowa    State      University,        Ames,      Iowa     50010.
E1    Department              of Veterinary           Microbiology           and   Preventive          Medicine,       Iowa    State    University,             Ames,
                Iowa.
J     Veterinary            Medicine         Department,         Medical        Research               Laboratory,          Edgewood      Arsenal,        Maryland.
      Department             of Avian          Diseases,        Cornell       University,              Ithaca,       New      York.
84                                                                                       Journal                   of        Wildlife                    Diseases           Vol.           11,   January,_1975




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Journal           of     Wildlife         Diseases   Vol.   11,   January,   1975                                                              85


Case       2                                                                  Case    7

      A              female
                mature           red-headed          falcon                       A male       prairie     falcon      was being flown
(F.        chicquera)   became       listless     and de-                     at liberty       with its 2 siblings,           a male and
pressed       and was treated         empirically          for                a female.          The     birds     routinely        returned
trichomoniasis         with    Emtryl#{174} and Ter-                          twice a day to feed on a ledge                          outside
ramycin.#{174} The bird died 72 hours                   after                 the nest         box     in which         they     had       been
the     onset     of signs      having        maintained                      reared.       At 41 days of age the male                          in
both its appetite        and body weight.                                     question        was absent          and was obviously
                                                                              ill upon       his return        and recapture           2 days
Case       3                                                                  later.    He was anorexic,                weak,      had ruf-
                                                                              fled     feathers,       and      watery       green       feces.
     A   14-week      old male     prairie      falcon       in               The bird was fed pureed                   meat by gavage
training      for falconry     was observed            to be                  and was treated             daily     with an oral anti-
flying     less vigorously       than       normal.       Le-                 biotic but died 3 days after recapture.                         Its
thargy      and depression        progressed          rapid-                  siblings      remained        healthy.
ly. Because          of anorexia        the     bird     was
force-fed        a small   amount        of meat          and                 Case    8
egg yolk          but died   within       48 hours          of
the onset of signs of illness.                                                    A 10-month          old female prairie falcon
                                                                              had     a decreased          appetite      one evening.
Case        4                                                                 The      next     morning       it ate a few              small
                                                                              pieces      of meat       which      were     regurgitated
      An        immature                     peregrine
                                        female                 falcon         within       2 hours.       The      bird    was      treated
(F.        pergrinus                tundrius) was banded              on      empirically        with     Emtryl.#{174} On the sec-
Assateague            Island,       Maryland,           during       fall     ond day of illness           the falcon        was treated
migration            and      was released              in an ap-             with      Fungizone#{174}      on      the    basis       of    a
parently         healthy        state.     Sixteen       days later           presumptive          diagnosis          of   aspergillosis.
the bird           was again            trapped          250 miles            The      results    of fecal        examination            were
south of the original                  capture       location.        At      negative       for parasites       or their      eggs. The
recapture          the bird was thin, appeared                        ill,    bird died after 63 hours of clinical                   illness.
and was taken                into captivity.           Three       days
later    its appetite            decreased         and it began
to lose weight.                One week            following          re-     POST-MORTEM              EXAMINATION

capture         radiographs            were      taken       and re-
                                                                                  Necropsies          were performed             upon fresh
vealed         intrathoracic             nodules          suggestive
                                                                              cadavers         (cases      3, 4, and 8), and upon
of a mycotic               infection.        The       falcon       was       cadavers        that had been frozen                and rapid-
treated      with Amphotericin-B                     on the basis
                                                                              ly thawed           (cases      1, 2, and 7). In 2 in-
of a presumptive                 diagnosis        of pulmonary
                                                                              stances      (cases       5 and 6) only           histological
aspergillosis.          The bird died about                  2 hours
                                                                              material       and necropsy          reports       were avail-
later.
                                                                              able to the authors;              photographic           records
                                                                              of the lesions          and virus isolation            attempts
Case        5
                                                                              were      thus       precluded.        A report           on the
    A prairie    falcon     of unreported      age and                        parasitological            diagnosis        (serratospiculi-
sex      became       suddenly       depressed      and                       asis) on case S has been published.’
anorexic      and died within       24 hours     of the
onset     of clinical      illness.                                           Post-mortem           Findings

                                                                              Gross       Lesions
Case        6

    A male    gyrfalcon       (F.   ruslico/us),           ap-                    The lesions   in the livers and spleens           of
proximately       18 months        old and trained                            all 8 birds were similar.       There     was slight
for falconry,        suddenly       became          listless                  to marked       hepatomegaly          and     spleno-
and    easily   fatigued.      Anorexia          occurred                     megaly.     The   normally      concave      visceral
and the bird died about              72 hours           after                 surfaces    of the liver     lobes    were     flat in
the illness   was first noted.                                                some of the birds,       or in some cases, con-
86                                                                Journal         of   Wildlife         Diseases      Vol.   11,     January,      1975


vex. Both organs                 were     heavily        studded                 Examination            of the tibial        bone      mar-
with many            pale tan, yellow,              or yellow-               row of cases           2, 3, 6, 7, and 8 revealed
grey      punctate,           spherical,        and       stellate           innumerable            white       to tan      nodules          or
foci ranging            from       pinpoint       size to 1.5                granules        (0.5      to 1.0 mm)            distributed
mm in diameter                  (Fig.     1). Small           focal          throughout          the light         reddish    brown          to
lesions       were      visible       in the immediately                     purple      brown       marrow         matrix.    The light
subcapsular          parenchyma;            the larger          soli-        granular       foci were         relatively     more       firm
tary     foci     as well         as larger         regions         of       than,      and     thereby        separable      from         the
apparent          lesion        coalescence           produced               softer    marrow         tissue.
dome-like         elevations           on the surfaces             of            There      were        seevral        adult        air      sac
the organs.                                                                  worms      (Serratospicu/uni               atnacu/ata)             in
    Gross        examination         of cut surfaces            of           the abdominal           and posterior            thoracic        air
the livers          and spleens        revealed       that the               sacs of two of the prairie                   falcons        (cases
focal       lesions       were     heavily       and     evenly               1 and 5). These             are considered              by the
distributed           throughout         the    parenchyma                   authors    to be incidental              findings.         In the
of both          organs.       The larger       lesions     con-             peregrine       falcon        (case      4),       plaque-like
tained       friable,      caseous    material.                              air sac lesions           and      focal      caseous         lung
                                                                             lesions   of aspergillosis            were found.
    In cases 1, 2, and 8 the small intestines
were reddened          and there were several
                                                                             Microscopic               Examinations
to many        light tan puncta    (Fig.  2) and
short    transverse     streaks visible  through                                All tissues                were fixed         in 10% forma-
the serosa.                                                                  lin and were                  processed         by the standard




FIGURE       1.    Multiple      foci   of    necrosis      in   the     spleen        (held      in    forceps)      and    liver     of   a   prairie
falcon     (case     8).
Journal     of        Wildlife         Diseases        Vol.    11,    January,         1975                                                                87

paraffin       section       technique.         The      sections                       condensed     chromatin                by      a clear     or       at
were stained           with hematoxylin               and eosin                         least hypochromatic                 halo      (Fig.    3).
 (H and E).                                                                                 The       splenic       lesions      were      essentially
    The     livers        contained          many         discrete                      identical       to those        of the livers       described
non-zonally          distributed         spherical         foci of                      above.       They      were sometimes             so numer-
coagulation            necrosis         characterized              by                   ous     that      the    reticuloendothelial             paren-
karyolysis       and homogeneous                  eosinophilia                          chyma,        as well as the stromal              and vascu-
of the granular             to amorphous               cell rem-                        lar scaffold         of the organ         were obliterated
nants.      Occasional            pycnotic         nuclei        and                    by the coalesced                 foci.   Intranuclear          in-
                                                                                        clusions,        though       present,      were generally
basophilic       nuclear        fragments        were sparse-
                                                                                        less numerous             than      in the livers.
ly scattered          through        the necrotic            areas;
in the centers            of some        foci, particularly                                  In the bone           marrows           the grossly           ob-
the larger         ones,      there      was a dense              ac-                   served       focal      lesions        were      found         to be
cumulation          of nuclear         debris.                                           islands       of     coagulative            necrosis,          often
                                                                                        containing           much        nuclear         debris,        in a
    Intranuclear            inclusion         bodies       were
                                                                                        sea of degenerating                  erythroid         and mye-
found       in the hepatocytes              and histiocytes                              bid      elements.          The        marrow           sinusoids
adjacent        to the periphery            of the necrotic                             and      vessels       were       intact       except        in the
regions.        There      was a continuum              of in-                          areas       of coagulation                necrosis.         In the
clusion       morphology           and staining       ranging                           gyrfalcon         (case     6) there         was necrosis            of
from      large      pan-nuclear         basophilic      inclu-                         the bone          marrow        in the myeloid                spaces
sions     to centrally            disposed      eosinophilic                            of the ossified             tracheal        rings.       Inclusion
bodies        separated        from       the peripherally                              bodies       were present            but not numerous.




FIGURE       2.        Pale      tan       foci   in    the    submucosa         are      visible     through       the    serosal      surface      of   the
intestine        of     a     red-headed          falcon      (case    2).
88                                                                  Journal         of   Wildlife          Diseases        Vol.    11,   January,         1975


      In   the intestinal          tract    the focal necro-                          No bacteria     or mycoplasmas                              were iso-
tic     lesions       were      limited        to the la,nina                     lated  from      the liver,     spleen                         and   bone
propria         and were          poorly        circumscribed.                    marrow     lesions    examined.
There        were      discrete        foci of necrosis             in                 Tissue        emulsions         were       prepared        from
the      lympoid         cell accumulations                 of the                 liver     and       spleen       (cases        1, 2, and           4),
vestigial        ceca      (“cecal       tonsils”)      of cases                   liver    (cases        7 and 8), or bone                   marrow
7 and 8. Inclusion                  bodies      were    not con-                   (case      3) and were used to inoculate                           the
sistently        found       in the intestinal             lesions.               chorioallantoic                membrane             (CAM)             of
    The ovarian           stroma       of the red-headed                          embryonated               chicken         eggs,     or cell cul-
falcon      (case      2) contained          one small       fo-                  tures        of      chicken          embryo           fibroblasts
cus of necrosis.                                                                   (CEF)            or     duck         embryo           fibroblasts
    There       were      several      areas     of the ad-                       (DEF).          On primary             inoculation          or sec-
renal     glands       of one prairie          falcon    (case                    ond      passage          in chicken            embryos         focal
8) in which             large     pale     magenta      intra-                    white thickenings               of the CAM and multi-
nuclear        inclusion         bodies       were    locally                     focal      necrotic         lesions       in the livers            and
numerous          but were not accompanied                    by                  spleens         of the embryos                were       observed.
necrosis.                                                                         Intranuclear            inclusions          occurred         in and
                                                                                  around         the lesions.         In cases        1 and 2 the
Microbiological          Examinations
                                                                                  initial       virus      isolations         were       performed
                                                                                  by chicken              embryo          inoculation           as de-
    Lesion     material  suitable  for microbio-                                  scribed        above.       Suspensions           of the CAM
logical     examination      was available   from                                 lesions       were used to inoculate                     CEF       and
cases     1, 2, 3, 4, 7, and 8.                                                   DEF cell cultures.                In cases 3, 4, 7, and 8




FIGURE       3.   Intranuclear       inclusion      bodies     in     a   liver       lesion        from     a   prairie      falcon     (case      3).   H&E
x 750.
Journal      of   Wildlife        Diseases    Vol.    11,   January,     1975                                                                     89


primary        isolations         were accomplished                on     Post-mortem           Findings
cell culture.            All 6 isolates              were      main-
                                                                                The     lesions observed                    in the kestrels
tained      in cell culture             in which        they pro-
                                                                          and       owls         were         similar.           There         were
duced       the      typical        cytopathic          effect      of
                                                                          myriad          focal       tan      to yellow-tan                lesions
herpesviruses            consisting         of cell rounding,
                                                                          in the livers,            spleens         and bone marrows.
syncytium          formation,             and the develop-
                                                                          Histologically               the lesions             were      qualita-
ment       of intranuclear                 inclusion        bodies.
                                                                          tively     identical           to those         observed           in the
Physical,           chemical,               and       serological         previously           described           field cases,          i.e. foci
characterization              studies       have shown           that
                                                                          of necrosis           with the formation                     of intra-
these     virus       isolates       are members             of the
                                                                          nuclear          inclusion           bodies         in cells          peri-
herpesvirus          group        (20).
                                                                          pheral       to the limits              of necrosis.            Similar
                                                                          lesions,       which         had apparently                originated
TRANSMISSION                 STUDIES
                                                                          in      accumulations                   of       lymphoreticular
                                                                          cells,     were       found         in a variety             of other
    Cell-culture-propagated                    virus     isolated         organs        although           no one bird had lesions
from      case 1 (FHV            S-18)        was inoculated              in all sites.           Lesions           were       found        in the
into 8 kestrels,           3 great horned             owls, and           submucosa              or /amina               propria          of the
3 pigeons         (Co/umba          /ivia).       The dose of             tongue,        pharynx,           esophagus,             esophageal-
virus     ranged        from      10”#{176} TCID         to 10’’          proventricular                 junction,           proventriculus,
TCID          per inoculum.               A suspension             of     ventriculus,           small       intestine,         cecum,        bron-
liver tissue        from     case 5 containing                virus       chioles,        the thymus              gland,        the subepen-
FHV        2-A was inoculated                    into   a great           dymal         connective            tissue        in the choroid
horned       owl and a suspension                  of CAM         le-     plexus,        and the interstitium                     of the kid-
sions      from        embryonated              eggs    infected          ney, pancreas,              thyroid         gland and gonads.
with      FHV        2-A     was       inoculated          into     a     Intranuclear             inclusions           but       no necrosis
kestrel      and      2 pigeons.            All inoculations              were      observed             in some          adrenal          glands.
were      administered          intramuscularly.                          Organs           which          were        examined             but       in
                                                                          which        no lesions             were       found        were        the
                                                                          parathyroid            gland,       heart,      eye, and uropy-
Clinical     Observations                                                 gial gland.
                                                                                There     were      no     lesions       in the      pigeons.
    The      kestrels       died     4 to 6 days              post
inoculation         (P1). Clinical           signs of illness
were      mild     (anorexia        and listlessness           for        DISCUSSION
24 to 48 hours                ante-mortem),            or were
                                                                              Herpesvirus          infection       of falcons     is a
altogether        absent.       One kestrel         ate a full
                                                                          disease      with     a short         (24 to 72 hour)
meal       S hours        before      it died.       The     owls
                                                                          clinical    course       characterized       by the rela-
died 7 to 10 days P1 having                      shown      anor-
                                                                          tively     non-specific           signs    of partial      or
exia during         their terminal          24 to 72 hours.
                                                                          complete         anorexia        and listlessness.      The
The pigeons            remained         clinically       normal           mild nature         of the signs belies          the rapid-
until they were killed                60 to 90 days P1.
                                                                          ly fatal course           of the disease.       In experi-
                                                                          mental      cases      the incubation         period     was
Hematological          Studies                                            likewise       short,     the P1 interval          to death
                                                                          ranging      from 4 to 6 days for kestrels               and
     Blood      samples     were collected         by jugu-               7 to 10 days for owls.
lar venipuncture            from     3 of the kestrels
                                                                              The       lesion        distribution           in the       field
from       1 to 6 hours           ante-mortem.          Total
                                                                          cases      and experimental                 cases     indicate         a
leukocyte          (WBC)         counts      were       made
                                                                          strong      affinity        of the virus for reticulo-
using      the method          of Rees-Ecker          as de-              endothelial          tissues,        particularly         for the
scribed       by Lucas        and Jamroz.”'         Two       of          lymphoreticular                elements,          and also         for
the birds         had 350 WBC’s/mm”                 and the               hepatocytes.              “Inclusion            body       disease
third      had      600    WBC’s/mm”.           Pre-inocu-                 (herpesvirus            infection)           of falcons”             is
lation      blood     samples      contained      from     6.8            suggested          as a more              appropriate          name
x 10” to 22.5            x 10’ WBC/mm’.                There              for the disease.              Destruction           of the bone
was no anemia.                                                            marrow         and of the various                lymphoreticu-
90                                                                  Journal         of     Wildlife        Diseases        Vol.     11,     January,         1975


lar cell         foci      throughout            the body           ac-        for the field cases are not known.              We
counts       for the severe             terminal       leukopenia              agree with the suggestion of Ward et a/.”’
and for the conspicuous                        absence         of in-          that certain of the falcon’s prey species
flammatory               cell     response         in the         peri-         (or food     species  in the case of captive
pheral       regions        of the necrotic             foci. Fail-            falcons)    may be subject        to mild or sub-
ure of the birds                 to evidence           a terminal              clinical  infection   with the FHV        and thus
anemia         in spite of necrosis                  of the cry-               serve as sources      of infection    for the fal-
thropoietic           tissue      is a reflection             of the           cons.
relatively        longer        half-life      of erythrocytes                    The striking       qualitative         similarities        be-
compared           to that of leukocytes.                  That the            tween the lesions of falcon                     herpesvirus
birds      which         were       experimentally             inocu-          infection    and       those        described          in owl
lated      with FHV             undoubtedly            received         a      herpesvirus      infection,        pigeon       herpesvirus
far      higher         infecting         dose      by a more                  infection,      duck         virus        enteritis,         and
direct      route       than did the field cases pre-                          Pacheco’s      parrot        disease        indicate        that
sumably          explains          the wider          distribution             comparative         studies on the pathogeni-
of lesions in the former group.                                                city and serological interrelationships of
    The       sources         and       routes      of infection               these viruses are warranted.


Acknowledgments

        The    authors         are indebted       to Dr.  C. H. Bigland,                 University       of     Saskatchewan,            Saskatoon,          Sas-
katchewan,         and       to Dr.     M. Berthrong,     Penrose       Hospital,            Colorado          Springs,     Colorado          for    providing
histological        material       from     cases   5 and   6, respectively.



LITERATURE           CITED


  1.     ANDREWES,                   C. H. and H. G. PEREIRA.    Viruses                                       of Vertebrates.              2nd        ed. The
              Williams               and Wilkins Co., Baltimore, 1967.
  2.      BIGLAND,              C.    H., S. LIU and M. L. PERRY.                     Five cases of                                 Serratospicu/uni
                 amacu/ata            (Nematoda:         Filarioidea)      infection      in prairie                                   falcons          (Falco
                 mexicanus).            Avian    Disease       8: 412-419.      1964.
  3.      BREESE,            S. S. and A. H. DARDIRI.                          Electron                microscopic            characterization                   of
               duck          plague  virus. Virology 34:                      160-169.                1968.
  4.     BURTSCHER,          H. Die       virusbedingte         Hepatosplenitis        infectiosa     strigorum  I.
              Mitteilung:     Morphologische            Untersuchungen.          Pathologia        Veterinaria  2:
              227-255.    1965.
  5.     BURTSCHER,         H. Uber eine virusbedingte Einschlussk#{246}rperchen-Hepatitis und
              -Lienitis     bei Eulenv#{246}geln.       Zentralblatt f#{252}r   Algemeine         Pathologic und
              Pathologish     Anatomic       107: 96. 1965.
  6.     BURTSCHER,         H. Die virusbedingte          Hepatosplenitis          infectiosa       strigum    II.                                         Mit-
              teilung:   Kultur-und   Infektionsversuche.             Zentralblatt               Veterinarmedizen
                                                                                           f#{252}r
              Reihe    B 14: 540-554.    1968.
  7.     BURTSCHER,         H. and A. SCHUMACHER.                                                 Morphologische                    Untersuchungen
              zur Virus#{228}tiobogie der Hepatosplenitis                                  infectiosa     strigum.                Pathobogia      Veter-
              maria   3: 506-528.      1966.
  8.     CORNWELL,     H. J. C. and A. R. WEIR.         Hcrpesvirus      infection                                                     of pigeons   III.
             Use of embryonated     eggs for the growth      and characterization                                                        of the virus.
             Journal of Comparative      Pathology   80: 509-515.        1970.
  9.     CORNWELL,                H. I. C. and A. R. WEIR.             Herpesvirus         infection     of pigeons     IV.
             Growth             of the virus    in tissue    culture     and comparison              of its cytopatho-
             genecity            with  that   of the viruses         of laryngo-tracheitis            and   pigeon-pox.
             Journal           of Comparative      Pathology      80: 517-522.        1970.
Journal        of   Wildlife       Diseases       Vol.    1 1,     January,          1975                                                               91


10.        CORNWELL,                   H. J. C. and N. G. WRIGHT.                                  Herpesvirus          infection          of pigeons
                  I. Pathology                and virus          isolation.          Journal        of Comparative                 Pathology           80:
                  221-227.            1970.
11.        CORNWELL,                   H. J. C., A. R. WEIR                         and E. A. C. FOLLETT.                           A herpesvirus
              infection         of pigeons           The Veterinary                 Record         81: 267-268.            1967.
12        CORNWELL,                   H. J. C., N. G. WRIGHT                             and H. B. McCUSKER.                            Herpesvirus
                  infection          of pigeons          II. Experimental                infection        of pigeons          and chicks.           Jour-
                  nal of Comparative                       Pathology             80: 229-232.             1970.
13.        FINDLAY,               G. M. Pacheco’s                    parrot       disease.        The Veterinary                Journal         89:      12.
                   1933.
14.        HELMBOLDT,                     C. F. and M. N. FRAZIER.                              Avian        hepatic       inclusion         bodies       of
                  unknown              significance.           Avian          Diseases         7: 446-450.             1963.
15.        HOWELL,              J., D. W. MacDONALD                                and R. G. CHRISTIAN.                           Inclusion          body
                  hepatitis          in chickens.           Canadian           Veterinary           Journal        11: 99-101.            1970.
16.        KASCHULA,                   V. R. A new virus                     disease       of the muscovy                duck       (Cairina         mos-
                  chata       L.) present            in Natal.         Journal         of the South             African       Veterinary           Medi-
                  cal Association                21: 18. 1950.
17.        LEIBOVITZ,                 L. Gross        and histopathologic                   changes        of duck plague                (duck       virus
                  enteritis).           American           Journal          of Veterinary               Research          32: 275-290.              1971.
18.        LEIBOVITZ,                L. Duck plague                (duck       virus enteritis).            Page 732 in M. S. Hofstad,
                   ed. Diseases              of Poultry.           6th ed. The Iowa State                        University           Press,       Ames,
                   Iowa.       1972.
19.        LUCAS,          A. M. and C. JAMROZ.                             Atlas      of avian         hematology.            U.S. Department
                  of Agriculture,                Agriculture            Monograph             25.     1961.
20.        MARE,          C. J. and D. L. GRAHAM.                                   Falcon        Herpesvirus,           the Etiobogic Agent
                   of Inclusion             Body Disease              of Falcons.           Infection         and Immunity              8: 118-126.
                   1973.
21.        PACHECO,                G. Nouvelles recherches sur la psittacose des perroquets. Comptes
                   Rendus Soci#{233}t#{233}      de Biologic 106: 372-374. 1931.
22.        PACHECO,               G. and 0. BIER. Epizootie chez les perroquets                                           du Br#{233}zil.     Relations
                   avec Ia psittacose.                Comptes          Rendus                       de Biologic
                                                                                      Soci#{233}t#{233}                   lOS: 109-111.              1930.
23.        PETTIT,          J. R. and H. C. CARLSON.                                Inclusion         body hepatitis            in broiler         chick-
                   ens. Avian              Diseases         16: 858-863.              1973.
24.        RIVERS,            T. M. and F. F. SCHWENTKER.                                          A virus         disease        of parrots           and
                  parakeets            differing       from psittacosis.               The Journal             of Experimental                Medicine
                   55:     911-924. 1932.
25.        SCHETTLER,                   C. H. Eine infekti#{246}se                  Leberentz#{252}ndung (Hepatitis) der Eulen.
              Tier#{228}rztliche         Umschau            163: 1-6. 1969.
26.        SCHETTLER,                   C. H. In vitro              Untersuchungen                          die
                                                                                                   #{252}ber Eigenschaften des Virus
                   der Hepatitis             et Splenitis         Infectiosa         Strigum.         Proc. XII Internationalen Sym-
                   posiums #{252}ber           die Erkrankungen                   der Zootiere,             Budapest.         205-209.           1970.
27.        SCHETTLER,                   C. H. Isolation                of a highly             pathogenic           virus      from        geese      with
                   hepatitis.          Avian      Dis. 15: 323-325.                  1971.
28.        SCHE1TLER,                   C. H. Virus hepatitis of geese II. Host range of goose                                                 hepatitis
                   virus.      Avian         Dis. 15: 809-823.                  1971.
29.        SCHETTLER,                  C. H. Goose             virus hepatitis            in the Canada              goose and snow goose.
                   Journal         of Wildlife           Diseases         7: 147-148.             1971.
30.        SENEVIRATNA,                        P. Diseases           of Poultry.           2nd ed. John             Wright         and Sons Ltd.,
                   Bristol.         1969.
31.        WARD,          F. P., D. G. FAIRCHILD                               and J. V. VUICICH.                      Inclusion          body hepa-
                   titisin a prairie falcon. Journal of Wildlife                                     Diseases        7: 120-124.             1971.

                                               Receised          for   publication          9   August   1973

								
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