STUDIES ON FOWL PARALYSIS (NEUROLYMPHOMATOSIS
I. CLINICAL FEATURES AND PATHOLOGY.
BY ALWIN M. PAPPENttEIMER, M.D., LESLIE C. DUNN, PH.D., AND
VERNON CONE, M.D.
(From the Storrs Agricultural Experiment Station, Storrs, and the Department of
Pathology, College of Physicians and Surgeons, Cobumbia University,
l~Ax~S 6 xo 12.
(Received for publication, August 23, 1928.)
The disease known to poultrymen as fowl paralysis or range paraly-
sis is one whidh, in spite of its economic importance and great biological
interest, has been little studied.
The first account of the disease to which we have found reference is that of
Marek (1) in 1907. In four roosters, three of them Orpingtons, and all from the
same farm, there developed during the winter months, symptoms of paresis of
the legs and wings, unequal on the two sides, and accompanied by more or less
muscular atrophy. The diet was adequate, comprising potatoes, barley, bran,
clover and mixed grains, and the chickens were allowed free range. Two of the
birds made a partial recovery, one died after 25 days, one was killed 5 weeks after
the onset of symptoms, and the description of the pathology is based upon the
careful study of this bird.
Grossly, there was noted marked thickening of the right lumbar plexus (the
side on which the paralysis was more marked).
especially on the right side, were also thicker than normal.
Microscopic examination was made of four segments of the cervicodorsal and
lumbosacral regions of the cord with their nerve roots, of the lumbar plexus, sciatic
and femoral nerves and the extensor quadriceps femoris muscle. The tissue was
Most of the spinal nerve roots,
* Preliminary reports of this work have been presented at the November meet-
ing of the New York Pathological Society, 1925; at the Cleveland meeting of the
American Society of Experimental Pathology, December 28, 1925; and at the
World Poultry Congress in Ottawa, August 2, 1927. Much of the material in
this and the following paper has been included in Bulletin 143 of the Storrs
Agricultural Experiment Station, 1926.
64 FOWL PARALYSIS. I
fixed in Mueller's fluid, stained with Weigert-Wolters and counterstained with
alum-cochineal and Van Gieson.
In the plexus and sciatic nerves, there was almost a complete loss of nerve
fibers. There was a dense and uniform infiltration of mononuclears, in places
aggregated into dense clumps. The perineurium was but slightly thickened and
contained only scattered cells. Nests of mononuclears were present in the sur-
rounding connective tissue, chiefly in the vicinity of small blood vessels.
The spinal cord and the nerve roots, especially upon the right side, were also
infiltrated. In the cord, the cellular infiltrations were almost limited to the white
matter, but in one segment, there was a perivascular accumulation in the central
The degeneration of the nerve fibers was regarded by Marek as secondary to
the cellular invasion. The cause of the polyneuritis could not be determined, but
the disease was obviously not identical with the neuritis described by Eijkman
(2) in chickens fed on polished rice. In the latter condition, death ensued within
10 days, and the changes in the nerves were purely degenerative.
Kanpp (3) in 1921 reported rather fully upon observations first made in 1914.
In this paper, reference is made to outbreaks occurring in North Carolina, Mary-
land, Virginia, New Hampshire, New ~ersey, Connecticut and Massachusetts.
No information could be obtained by him as to the occurrence of a similar disease
in foreign countries.
The clinical features as described by Kaupp are lameness in one or both legs,
drooping of wings, partial blindness, finally diarrhea, complete paralysis and death
days or weeks after the onset. Recovery, in Kaupp's experience, never occurred.
All breeds were susceptible.
As regards the lesions, Kaupp found no changes in the cerebellum, medulla,
crura or brachial plexus. In the cord, however, corresponding segmentally to the
paralysed part, there was congestion of peripheral veins, round cell infiltration in
both ganglionic and non-ganglionic portions of the cord, chiefly perivascular.
There was degeneration of the ganglion cells, atrophy of the fibers and at times
a liquefaction necrosis. The process was interpreted as a transverse myelitis.
Kaupp studied the disease experimentally, but without arriving at any definite
results. Repeated efforts to isolate a causative organism were without success.
Inoculation of heart blood, liver, kidneys, spleen, various parts of brain and cord,
espedally of the affected segments, into rabbits, guinea pigs, young and year old
fowls all failed to reproduce the disease.
Kaupp regarded the disease as infectious.
An interesting paper treating of an apparently identical disease occurring in
the Netherlands, is that of Van der Walle and Winkler-Junius (4). The authors
studied an epizootic which occurred in the months of October and November,
1921. A large number of fowl were affected with paralysis, which ended acutely
after a few days or weeks. Most of the affected birds died, but the appetite and
general appearance of the chickens was unchanged even in the last stages of the
In spite of these negativeexperiments,
A. M. PAPPEN~IMER, L. C. DUI~N, AND V. CONE 6S
copper, lead nor zinc.
Two of the cases were examined pathologically. Inflammatory infiltrations
of polynuclear and mononuclear leucocytes were found in the swollen dorsal
ganglia; the meninges and spinal cord were likewise infiltrated, and in one of the
birds, the sacral and lumbar plexus showed mononndear infiltration.
The alterations of the nerve elements were regarded as secondary to the infil-
trations, and the apparently inflammatory nature of the lesions suggested the
term "neuromyelitis gaUinarum" for the disease.
of the brain.
A number of experiments to demonstrate the infectious nature of the disease
led the authors to conclude that this epizootic was due to a filtrable virus. We
shall discuss these in connection with our own experiments on transmission of the
May, Tittsler and Goodner (5) in December, 1925, issued a preliminary report
of field observations and laboratory findings in paralysis of the domestic fowl.
The lesions are very briefly and incompletely described.
microscopic examination of brain and spinal cord has given little information in
regard to the seat of the disease. Sections of brain and cord confirmed Kaupp's
findings, but the lesions are not described in detail, and no mention is made of
alterations in the peripheral nerves. Both aerobic and anaerobic cultures from
the tissues of infected birds consistently failed to show any infective organisms.
Attempts to transmit the disease by association and contact, by feeding material
from paralysed birds or by inoculation of blood, emulsified brain or spinal cord,
intravenously, intraperitoneally or intraspinally were all negative. None of the
inoculated animals developed paralysis during an observation period of 2 months.
The authors discuss the possible r61e of intestinal parasites and reach the con-
clusion that there is no relation, or at least that the presence of intestinal worms
or coccidia does not necessarily produce paralysis.
The most recent paper on the subject is that of Doyle (6) from the Indiana
Agricultural Experiment Station. Both the symptoms and the pathology of the
disease are very completely described. The disease occurs in birds from 4 to 8
months old, and is more prevalent in s~lmrqer and fall. The symptoms depend
upon the portion of nervous system involved. The occurrence of encephalitis is
responsible for the lethargic symptoms frequently noted. Iritis, when present,
causes a contracted, non-responsive pupil. There is a good description of the
histopathology of the brain, cord and peripheral nerves.
Efforts to demonstrate the infectious nature of the disease were fruitless; the
author's experiments will be considered in detail in the second paper, but it is
interesting to note here that in spite of his failure to establish the transmissibility
of the disease, he is still convinced that it is due to an infectious agent.
Avitaminosis could be excluded, and the food contained neither arsenic,
No mention is made of lesions
The authors state that
66 FOWL PARALYSIS. I
Clinical Features of the Disease.
The first appearance of the disease is usually signalized by drooping
of a wing on one side, a lack of coordination in walking, followed by
a lame or limping gait, and ending in complete prostration. The
limbs are not symmetrically affected, even in advanced cases. The
chickens usually lie upon the side showing the greater paralysis, and
the impairment of mobility is at first unilateral, or at least more
marked upon one side than the other.
In the earlier stages of the disease, there is little muscular atrophy,
but after the chicken has been helpless for a longer period, the wasting
may become extreme. Whether the atrophy is due to the affection of
the nerves, to the inactivity or to the inability of the chicken to pro-
cure food has not been determined.
The paralysis is more often spastic than flaccid, and sometimes
accompanied by increased reflexes or even by clonlc spasms. The
paralysis is only exceptionally complete, and even in birds which lie
immobile and helpless, the struggles during anesthetization are at-
tended by vigorous movements of flexion or extension. Reflex move-
ments and muscular reaction to mechanical nerve stimulation have
been noted in the paralysed limbs after death.
assumed by the paralysed birds are illustrated by Figs. 1 and 2.
The duration of the disease, as judged from the onset of the paralytic
symptoms to the termination in death or rarely in recovery, is very
variable. With proper care, life may be prolonged indefinitely, and
the nutrition and general condition is often surprisingly good, even
after months of complete helplessness when the birds are kept in
confinement with access to food and water. Thus one of ten early
cases in the station flock at Storrs became prostrated early in October,
1922. With careful feeding in an individual coop, it lived until
January 1, 1923. Recovery has been noted in several instances, and
we have gained the impression that there frequently occur periods of
transient improvement. On the other hand, death may suddenly
occur with few premonitory symptoms, the diagnosis being revealed
only by the pathological study of the cases.
The onset of the paralysis may be very sudden. We have observed
one case in which complete toss of power in the legs developed in less
than 3 hours.
The curious postures
A. M. PAPPEN-AIEIMER, L. C. DI~, A_N'D V. CONE
Partial or complete blindness in one or both eyes, accompanied by
a change in the color of the iris from yellow-brown to slate-grey, was
observed in several paralysed chickens, and in two non-paralysed
birds from the same flock. The alterations which underlie this
condition will be described below.
As regards the age incidence, it would appear that young birds are
most frequently affected. In our experience, the earliest symptoms
in a spontaneous case were observed at 12 weeks, and the oldest case
in our records developed paralysis at 15 months, 18 days. In the
experimental material, the earliest clinical case was observed at 10
weeks of age. As will become apparent later, the characteristic lesions
do not always reveal themselves in typical paralytic symptoms. We
shall show also that mild cases exist in which the diagnosis cannot
be made from symptoms alone.
Epidemiology and Distribution.
The records of the Storrs Experiment Station flock of White Leg-
horns in which each year about 1500 growing chicks and 800 adult
chickens come under observation, have yielded data of some value in
regard to the natural history of the disease, and instructive information
has been obtained from visits to affected farm flocks. It is impossible
to present an analysis of these data within the confines of this present
article, but we may refer briefly to some of the more interesting
(1) The disease appears to be epidemic and to reappear year after
year on the same farm. In cases where its origin has been observed,
it has appeared suddenly and has thereafter persisted and become
endemic in certain foci. Efforts to prevenf its recurrence by rearing
new flocks on new ground on the same farm, have, in several cases,
shown no significant effect on the persistence of the disease. (2)
Paralysis occurs in both sexes and in all of the chief breeds of fowls.
There is some indication of breed differences in susceptibility to the
disease, although the observations on which these are based are in no
sense experimentally controlled and the difference may have been due
to other conditions. (3) The disease first appears usually in growing
chickens from 3 to 6 months of age, and new cases continue to de-
68 ~'OWL PARALYSIS. I
velop throughout the first 18 months of life. It is probably rare in
older fowls although a few clinical cases have been observed.
flocks in which an outbreak has occurred, paralysis usually causes an
appreciable mortality each year thereafter.
from a few per cent, up to 60 per cent and over.
Mortality may range
The following description is based upon a study of 60 spontaneous
cases in all stages of the disease.
in the course of the experimental work. The chickens were obtained
from a number of different sources, and characteristic lesions have
been found in material from Maine, New Hampshire, Massachusetts,
Pennsylvania, New Mexico, California and Ontario.
breeds are represented: White Leghorns, Silkies, Silver-Spangled
Hamburgs, Plymouth Rocks, Buff and White Wyandottes and
Rhode Island Reds. In this series, the lesions were identical, ir-
respective of breed.
Numerous chickens presenting no clinical evidence of paralysis,
have been studied.
Many more have been autopsied
The brain after fixation in Zenker's was cut in serial blocks so as to include
sections of cerebrum, optic lobes, cerebellum, pOllS and medulla. The entire
spinal cord was removed, and longitudinal sections examined at all levels. The
dorsal root ganglia, and the brachial plexus and sciatic nerves were also taken for
study, and routine sections from all the principal viscera. Zenker's fluid, and
10 per cent formol or Bouin's fluid in special cases, were used as fixatives. In
addition to routine histological stains, sections from individual cases were studied
by the Marchi and Pal-Weigert methods, and a variety of staining methods were
used in the attempt to demonstrate microorganisms in the tissue.
The general nutrition of the birds varied, depending upon the duration of the
disease and the care which the chickens had received. Many typical examples
showed excellent nutrition; others extreme emaciation.
the cloaca were matted with excrement, owing to a terminal diarrhea or
No recognizable alterations were found in the brain, or its covering. The pos-
terior root ganglia of the cord were found enlarged, and in the majority of cases,
to such a degree that, after a little experience, the histological changes could be
Often the feathers about
A. x¢. PAPPEN'R-ErSg~.R, L. C. DUNN, AND V. CONE
predicted with fair certainty. Not only were the ganglia enlarged, but they
appeared abnormally translucent, and usually they had a slightly yellowish tinge
in comparison with the cream-white of the cord itself. On dose inspection, one
could frequently discern a translucent strip extending into the contiguous tissue
of the cord. The enlargement of the ganglia, in most cases, was not symmetrical
In one case there was found a translucent, tumor-like enlargement of the
acoustic nerve. In another, one of the trigeminal nerves was thickened. We
have made no systematic study of the cranial nerves.
No striking gross changes were found in the spinal cord itself. The peripl~ra~
nerres, in particular those of the brachial plexus and the sciatic nerves, were
frequently thickened and the same smoothness, translucency and yellowish dis-
coloration were noted as in the posterior root ganglia (Fig. 3). Small hemorrhages
were occasionally seen.
Lymphomatous tumor-like masses were discovered in six birds of this series,
or about 10 per cent. These appeared to originate in the ovary, but growths were
seen in the liver, kidneys, hmgs, adrenals and muscle, and in one instance, the
spinal cord was infiltrated with the same type of tissue. The finer structure of
these lymphomatous masses and their possible relation to the lesions of the
nervous system, will be discussed below.
None of the lesions occasionally met with, such as edema and atelectasis of the
lung, suppurative bronchiectasis, ulceration of the intestine associated with
severe coccidiosis, etc., seemed to be related to the disease under consideration.
tteterakis papillosa was present in the ceca in variable numbers in practically
every case, Heterakis perspicillum in several and cestodes occasionally.
Striking alterations were found in the brain, spinal cord, dorsal
root ganglia, spinal nerve roots and peripheral nerves.
tion and intensity of the lesions varied from case to case, but in gen-
eral the lesions resembled one another sufficiently to establish a
definite pathological entity.
The most severe lesions were seen in the peripheral nerves and nerve roots.
They consisted essentially of an infiltration of smaller and larger mononuclear
ceils between the nerve fibers, separating the individual fibers and accompanied
by more or less edema. This infiltration was at times so massive as to replace
almost completely the nerve tissue. More commonly, the cells were loosely dis-
tributed and in some areas, very sparsely. It was rare for all the bundles of the
nerve to be affected, and never did the infiltration extend uniformly throughout
the entire length of the section (Figs. 4 to 6).
70 FOWL PARALYSIS. I
Degenerative changes in the nerve fibers varied greatly in the different cases
examined, and were roughly correlated with the extent and intensity of the
cellular infiltration. In many instances, where the lymphoid invasion was sparse
and scattering, the degeneration of the nerve fibers was not detectable with the
usual stains. At the other extreme, many of the fibers had disappeared, their
places being taken by a vacuolar or foamy tissue, often filled with coagulated
edema fluid, and containing free fat globules and numerous fat-laden phagocytes,
derived in part from the swollen sheath cells. The myelin sheaths appeared
collapsed, and Pal-Weigert preparations gave evidence of advanced degeneration
(Figs. 7, 8). In some sections, there could be noted a proliferation of the
spindle-shaped sheath cells, amongst which mitotic figures were abundant.
Even when these degenerative changes were well advanced, the persistence of
the neuraxones in the infiltrated nerves could be demonstrated in silver carbonate
preparations (method of Rio del Hortega), and it is probably due to this fact that
paralysis, even in advanced cases, is rarely complete.
The smaller forms of infiltrating cells appear to be morphologically identical
with lymphocytes. In the nodular accumulations which crowd aside the adjacent
nerve fibers, the center of the mass is composed of somewhat larger elements, with
more vesicular nuclei, and here mitoses are frequent. In addition to cells of the
lymphocytic type, which predominate, there are numerous cells with more abund-
ant basophilic cytoplasm, peripherally disposed chromatin and a juxtanuclear
clear space, which closely resemble mammalian plasma cells. These are vividly
brought out in sections stained with Pappenheim's methyl green pyronine. There
are also large mononuclear cells with vacuolar cytoplasm corresponding to the
fat-laden phagocytes derived from the cells of Schwann's sheath. In paralysed
chickens stained intravitally with trypan blue, many of the large mononuclears in
the infiltrated nerves, particularly in the vicinity of the blood vessels, were found
to accept the dye though less intensely than the Kupffer cells, or the clasmotocytes
of the spleen and other tissues.
In a case recently studied, most intense lymphoid infiltrations were present
in the macroscopically thickened vagus and mesenteric nerves.
In the spinal cord, in addition to the regional infiltrations accompanying the
entrance of the nerve roots, there are found focal accumulations of wandering
cells most commonly in the white matter, but in some instances also in the central
grey. Lesions of this type, which may be termed submiliary nodules, seem to be
limited to the vicinity of small blood vessels.
part definitely lymphoid in type, in part, cells with paler, less spherical and some-
what larger nuclei, the origin of which could not be accurately determined. They
are most probably mobile glial elements. A very constant feature of these
nodules is the presence of spherical, deeply stained chromatin particles of varying
size and shape interspersed amongst the intact nuclei. These appear to be derived
The ceils composing them are in
A. M. PAPPENHEIMER, L. C. DUNN, AND V. CONE
by a massing of the chromatin against the nuclear membrane and its subsequent
extrusion; often they are surrounded by a narrow clear zone.
In no case was there definite necrosis in the center of the nodules, nor have we
observed the occurrence of giant cells.
Degenerative changes in the ganglion cells of the cord were seen only where the
lymphomatous infiltration was so massive as to bring about extensive destruction
of the cord tissue. The most obvious type of degenerative change was a hyaliniza-
tion of the cytoplasm, with chromatolysis, and karyolysis.
.Posterior Root Ganglia.
The posterior root ganglia, as one might expect from the alterations in the
gross appearance, frequently show an intense infiltration with mononuclear cells
(Figs. 10, 11). This was sometimes diffuse, sometimes rather circumscribed.
The extent and intensity of the infiltrations varied greatly in different ganglia
from the same case. The ganglion cells were usually intact, even when the
lymphoid infiltrations were extreme.
The majority of the birds showed lesions in the cerebrum, cerebellum, optic
thalamus and pons. These were always exquisitely focal in distribution. The
massive and diffuse infiltrations seen in the nerves and spinal cord were never found
in the brain. The lesions found were of the two types; either compact perivascular
rings of small densely staining lymphoid cells, or submiliary nodules composed
of lymphoid cells and paler elements, like those described as occurring in the
white matter of the cord. In two cases, the lesions seen in the molecular layer
of the cerebellum had a slightly different character. They were very sharply cir-
cumscribed, and composed almost exclusively of pale epithelioid elements showing
a more or less definite radial arrangement. There were very few lymphoid cells
in the nodules, which gave the impression of healing lesions.
The foci of cellular infiltration in the cerebrum were often very scarce, and in a
few of the birds, even careful study of a number of sections at different levels
failed to disclose them.
Although perivascular infiltration of the meningeal vessels was repeatedly seen,
in only one case were there observed a more diffuse infiltration and thickening,
accompanied by the presence of foamy, fat-containing cells.
Sympathetic Nervous System.
A systematic study of the sympathetic nervous system was not undertaken,
but sympathetic ganglia and nerves were frequently included in the visceral
sections, particularly in the section of adrenal (Fig. 12).
mononuclear infiltrations more or less intense were present in the ganglia and
nerve trunks, so that it may be said with certainty that the disease involves the
In a number of cases,
~2 :FOWL PARALYSIS. I
sympathetic system. To what extent this affects the clinical picture of the disease,
can only be surmised.
Thickening and cellular infiltrations have also been repeatedly found in the
vagus nerves and in the nerve trunks accompanying the mesenteric vessels.
In three birds showing partial or complete blindness, there was observed in the
living animals a change in the color of the eye, from a yellow-brown to a bluish
grey. This was readily explained by the microscopic changes. The iris was found
to be thickened, edematous and infiltrated with wandering ceils. These were of
two distinct types--small, deeply staining lymphoid cells with little cytoplasm, and
larger mononuclears resembling mammalian plasma ceils, the nucleus being
eccentric, and the cytoplasm strongly basophilic. These larger elements were
aggregated into compact clusters, situated especially near the anterior surface.
Occasional eosinophilic polymorphonulcears were also seen. There was slight
edema, and a granular coaguhma, and in some sections mononuclear cells of various
types were present in the anterior chamber (Fig. 13).
The cornea was normal in structure.
nerve heads showed only a minimal infiltration.
however, were present in the conjunctiva and in the extraocular muscles.
The retina was unaltered and the optic
Groups of lymphoid cells,
Lungs.--No lesions were found which could be correlated with the cellular infil-
trations present in the central nervous system. The only exception to this
statement is in the case of chickens in which there were present lymphomatous
masses in the abdominal viscera. In several of these, the lungs were also the
seat of lymphomatous growths in the form of diffuse infiltrations in the walls of
the bronchi and perivascular areolar tissue. In general, however, the lymphoid
tissue which is normally found in the mucosa of the larger bronchi, was not
Myocardium.--In the routine study of sections both from paralysed and normal
chickens, one finds almost without exception, focal aggregations of wandering
cells amongst the muscle fibers or ill the loose connective tissue about the larger
blood vessels. Sometimes these are composed entirely of lymphoid or larger
mononuclear cells, with basophilic cytoplasm; at times there is a predominance
of eosinophilic polymorphonuclears or of larger mononuclears with coarse eosin-
ophilic granules--presumably, myelocytes. So frequently are these small cell
aggregations to be found that it seems difficult to regard them as the expression
of an infectious lesion, and still more difficult to believe that they are in any
way related to the disease under consideration. It seems more probable that
they are merely extramedullary leuco- and lymphopoietic loci.
On the other hand, we have encountered instances in which the myocardial
infiltrations are so intense and widespread that they cannot be interpreted merely
A. M. PAPPENHEIMER~ L. C. DUNN, AND V. CONE
as areas of heterotopic blood formation. Two types of changes have been seen.
The first is a simple accumulation of small round cells crowding apart the intact
muscle fibers, mantling the small arterioles and at times forming large oval aggre-
gations which completely replace the muscle tissue over a considerable area.
The other type of lesion is more definitely inflammatory, and has been seen
but once. It occurred in a Barred Plymouth Rock, which presented somewhat
atypical lesions. There was iritis with blindness. The brain and cord were the
seat of intense lesions of the usual character. The nerve trunks were not involved,
but there was extensive perineuritis. A cross-section of the ventricle showed that
a large part of the myocardial tissue was replaced by granulomatous areas contain-
ing a variety of cell forms--fibroblasts, giant cells, often surrounding remains of
necrotic muscle fibers, lymphocytes, many of them fragmented and pycnotic, and
rare eosinophilie polymorphonuclears. Although the individual muscle fibers in
the affected areas were degenerated or necrotic, there were no larger areas of
coagulative necrosis, nor tubercle-like lesions. The pericardium was invaded by
the granulomatous tissue, leaving the overlying serous cells intact. It is of course
possible that in this case the myocardial lesions, which are frankly inflammatory
in type, may have been due to some other agent than that causing the lesions in
the iris and central nervous system. It seems possible, however, that we are
dealing with an unusual and atypical reaction to the same agent.
Ziver.--In this organ, also, it is difficult to draw a sharp line between the normal
and the pathological. Infiltrations of the periportal connective tissue with
lymphoid cells, and not infrequently with eosinophilic, mono- and polymorphonu-
clear leucocytes, are present in practically every section examined, whether of
normal or paralysed fowl. One finds also small, compact spherical masses of
small mononuclears in any portion of the liver lobule, and these appear to be a
normal feature of the chicken liver.
In certain of the paralysis cases, these infiltrations have become so massive as
to leave no doubt as to their pathological nature (Fig. 14). They may even
reveal themselves macroscopically as greyish areas obliterating the normal archi-
tecture of the liver lobule, and in several of the birds with large lymphomatous
masses in the region of the ovary, the liver lesions were of a distinctly nodular char-
acter, grossly and microscopically suggesting a neoplasm. It would seem, there-
fore, that the same agent which is responsible for the infiltrations of the nervous
system may at times incite the lymphoid tissue of the liver to abnormal and
Pancreas.--Interstitial lymphoid masses were present in a few cases. There
were no lesions of the parenchyma.
Spleen.--We have found neither gross nor microscopic lesions.
Kidney.--The situation here is analogous to that in the liver.
of kidney, lymphoid infiltrations of variable extent may be found between the
tubules. In certain cases, these may be so extreme as to separate widely or
actually replace the parenchymal elements. In several of the birds with large
In every section
74 1,OWl~ PARALYSIS. I
tumors arising about the ovary, there was direct extension into the kidney
Adrenal.--Here again in routine sections, one finds very frequently compact
aggregations of lymphoid cells in any portion of the gland, and such lymphoid
foci, as in the adult human adrenal, may be looked upon as a normal histological
feature of the gland. In many of the paralysed fowls, these infiltrations are
very extreme. They appear to take their origin in the sympathetic ganglia and
nerve trunks, which, in the chicken adrenal, are intimately incorporated with the
glandular elements. We have already referred to the periadrenal nerves as very
frequently and characteristically involved.
Ovary.--In the majority of the typical cases the ovary showed no pathological
changes. In a certain proportion of the cases, this organ, as has been stated, gave
origin to large lymphomatous masses of an invasive character.
Testes.--No infiltrations have been found in the testes of normal or paralytic
fowl, and the male gonads seem to be, of all the viscera studied, the least favorable
site for a localization of the lesions.
Our material does not provide a certain answer to the question as to whether
the presence of the disease arrests or suppresses spermatogeI~esis. In the series
of 60 spontaneous cases, there were but four males; three of these showed immature
testes, but the exact ages were not known. In the fourth case, the testes were not
examined. Amongst the positive cases uncomplicated by coccidiosis, which
occurred in experimentally inoculated chickens, there were but two males, one
killed on the 122nd day, the other killed on the 137th day, or 132 days after in-
oculation. The testes in these cockerels were also immature, the seminal
epithelium being almost wholly undifferentiated. By the 122nd and 137th days,
spermatogenesis should be well established. Selecting from our control material
healthy cockerels killed on the 109th, lllth, 122nd, 125th (2), 128th (2), 131st,
135th and 137th days, we find active spermatogenesis, with ripe spermatozoa in
the tubules, in every instance. It would seem that the disease in these two cases,
which was of a severe type, definitely delayed or suppressed the onset of sperma-
togenesis. To what extent this is a characteristic effect cannot be decided without
Alimentary Tract.--No lesions have been found in proventriculus or gizzard.
The great majority of the birds, both in the spontaneous and experimental cases
of the disease, showed no lesions of the intestinal tract. In a few instances in
which there were lymphomatous tumors of other abdominal viscera, the intestinal
mucosa, especially that of the duodenum, was thickened by diffuse infiltration of
mononuclear cells. Lymphomatous plaques also occurred in the subserous
The relation of worm infestation and coccldiosis to the disease will be discussed
Thymus, Thyroid and Parathyroid.--Examined in a few of the cases, showed
A. M. PAPPENHEIME.R, L. C. DUNN, AND V. CONE 7S
Visceral L ymphomala.
Visceral tumors, as has been stated, were found in six of the 60
spontaneously paralysed birds. Four additional cases occurred in a
group of 120 chickens used in experiments.
Histologically, these were all identical in structure. They were composed of
closely packed, small round cells with deeply stained nucleus and relatively scant
cytoplasm. In the more actively proliferating areas where mitotic figures were
extremely numerous, the cells were larger in size, the nuclei more vesicular, with
distinct chromatin structure, and the cytoplasm more abundant (Fig. 15). Such
cells are perhaps comparable to the larger lymphoid elements present in the
centers of the germinal follicles.
With special stains (Foot's modification of the Bielschowsky method, J. Lab.
and Clin. ]fled., 1924, ix, 3), a delicate reticulum surrounding almost every individ-
ual cell was demonstrated.
The manner of growth of these tumors into adjacent healthy tissues was char-
acteristic of that of the malignant lymphoblastomata. The cells invaded the
stroma of the organs, pushing apart the parenchymal elements, and eventually
replacing them completely. Thus, in the kidney, one found glomeruli and tubules
widely separated by dense masses of the tumor cells, but showing little or no
degenerative change. So, too, in the ovary, liver and lung, the normal elements
remained intact until entirely replaced by the tumor tissue.
Necroses occurred in some of the larger tumor masses, in which case there usually
remained a broad collar of living cells about the blood vessels.
The ovary has been the apparent site of origin of the main tumor
mass in all instances, no males being included in our tumor cases.
The growths have shown regional invasiveness into oviduct, kidney,
adrenal, adjacent fat and muscle; in one case, the tumor grew directly
through the vertebral column into the spinal cord.
cases, there have been nodules in the liver, lungs, peritoneum and
other situations. Whether these were true metastases, or whether
the agent which incited the local proliferation of lymphoid cells in the
ovary produced the same effect upon the lymphoid tissue in other
situations, it is impossible to say.
What does seem plain, however, is the fact that these visceral
lymphomata--in spite of their apparently neoplastic appearancc are
but a manifestation of the same unknown agent which brings about
the infiltrations in the nervous tissues.
in the case alluded to, in which the ovarian tumor had penetrated the
In several of the
This is very clearly shown
76 ZOWL PARALYSIS. I
spinal canal. In the region where the growth had invaded the cord,
the closely packed cells with numerous mitoses destroyed and replaced
the nervous tissue after the manner of a malignant neoplasm. But
as one passed away from this site, the cellular infiltrations became
distinctly perivascular, and in the remainder of the cord and brain,
the lesions were identical with those found in the paralysed birds in
which no tumorous growth was associated with the nervous lesions.
The scattering infiltrations of the peripheral nerves were also like those
Usually found in the paralysis chickens, and, as is shown by our tabu-
lated protocols, they were present in every case of visceral lympho-
matosis included in our material.
We shall reserve for our final discussion the interpretation of this
Because of the obvious resemblance of the lesions to leucemlc infil-
trations, careful attention was given to the blood within the vascular
channels. In no instance did there appear to be an excessive pro-
portion of lymphoid cells or other leucocytic elements, even in situa-
tions where the infiltration of the tissues was most intense.
more, a study of stained smears, from paralysed birds and healthy
controls, showed no significant differences in the percentage of the
various types of leucocytes. Time did not permit a systematic study
of the blood, but even with the data at hand, it seemed that the
lesions were not associated with a leucemic blood picture. I That the
cells forming the infiltration are not derived wholly from the circulat-
ing blood is shown by the fact that the capillaries in the infiltrated
areas contain no excessive number of leucocytes, and the occurrence
of numerous mitoses is proof that the cells proliferate in situ.
Lesions Encountered in Non-Paratysed Chickens.
One of the puzzling facts which has made the experimental study
of the disease very confusing and difficult, is the frequent occurrence
of lymphoid infiltrations in the nervous tissue of chickens which are
not paralysed, and which betray no clinical evidence of disease.
While it is true that in most of these apparently healthy birds, the
x Through the kindness of Dr. H. F. Pierce, we have had the opportunity to
compare our blood smears with two cases of fowl leucemia, from the material of
Professor Ellermann of Copenhagen.
A. M. PAPPENHEI~R, L. C. DLrNN, AND V. CONE
lesions are trifling, and indeed may fall within the range of normal
variation, in others they are so intense and widespread that they can-
not but be regarded as pathological. It has thus been of interest to
study carefully birds from various sources, so as to obtain a clear
idea of what one may consider "normal."
In 32 non-paralysed birds of various ages, and from various locali-
ties, lymphoid infiltrations of the nervous system were found in ten--
approximately one-third of the cases. The brain was most fre-
quently affected, the spinal cord next and in only one case were
infiltrations present in the peripheral nerves.
Fifteen of the 32 examined came from farms or experiment stations
where paralysis had occurred during the present year. 2 Lesions were
Occurrence ~ Lesions in Non-Pard
From localities where paralysis occurs..
From localities where paralysis is absent...
Brain Cord Dorsal
12 10 3
found in six of these fifteen; or if we exclude two which were less than
2 months old, in five out of seven.
Seventeen birds were obtained from sources where paralysis is
definitely stated not to occur. In this group, infiltrations occurred
in five birds.
From these small numbers, it is impossible to draw conclusions as
to the comparative incidence of lesions in non-paralysed chickens
from affected and unaffected localities. One may, however, make
the definite assertion that perivascular lymphoid infiltrations of the
brain and cord are often found in seemingly healthy chickens from
sources where paralysis is known not to occur, and in certain instances
they may be of considerable intensity and wide distribution.
There is no qualitative distinction between the infiltrations found
2 In one instance, no data as to the source of the chicken were obtainable.
78 FOWL PARALYSIS. I
in the healthy birds and in those with frank paralysis; and it would
seem that only when the infiltrations implicate the peripheral nerves
to such a degree as to block motor impulses, or to bring about actual
destruction of nerve fibers, do paralytic symptoms become manifest.
One is driven to the conclusion that the condition exists in masked
form in a very considerable number of seemingly healthy chickens.
We cannot, from our experience, state whether or not these birds
with unrevealed lesions are on their way to develop obvious paralysis.
The fact that such cases have been found on farms where paralysis
does not occur suggests that the birds with mild lesions are immune
to the more severe forms of the disease.
The question may be raised at this point as to whether the presence
of lymphoid tissue about the meningeal and cerebral vessels may not,
after all, be a normal histological feature in the chicken. It is not
easy to reach a definite decision as to this, and we have found no refer-
ence in the literature to guide us. In a certain number of birds, a
thorough and systematic study of numerous sections from all parts
of the brain and cord has failed to disclose any perivascular lymphoid
tissue. On the other hand, as has been indicated, we have frequently
found small lymphoid nodules in the walls of the cerebral and spinal
vessels, and in the dorsal root ganglia, in well nourished, healthy
stock from unaffected sources. Such small compact focal masses
of lymphoid cells have been arbitrarily regarded within the range of
"normality." The line between these and the milder grades of
pathological infiltration, it must be admitted, is not a sharp one, and
the difficulty becomes especially troublesome in attempting to inter-
pret the effects of experimental inoculation.
Bacteriology. Attempts to Demonstrate an Infective Microorganism.
Efforts to identify an infecting organism in smears and sections of
the brain, spinal cord, peripheral nerves and heart blood have thus
far proved unavailing. Sections have been stained by the Gram-
Weigert method, with toluidine blue, Giemsa's method, Wright's
stain, Levaditi's method and Jahnel's modification of Levadifi's
method for spirochetes. None of these procedures has disclosed any
structures which can with reasonable certainty be recognized as
bacterial or protozoan. We have had in mind the possibility of
A. M. PAPPENHEIMER, L. C. DUNN, AND V. CONE
rickettsial infection, and we have carefully searched our preparations
for intranuclear or cytoplasmic inclusions.
We have made numerous attempts to obtain cultures of organisms
from the nerve tissue of paralysed chickens. Among the media used
were peptone and meat extract-broth, with and without addition of
glucose; plain and glucose agar, with and without addition of inacti-
vated chicken serum or whole blood, and adjusted to various pH
ranging from 7.4 to 6.0; beer-wort agar; chopped chicken meat broth,
and potato. Cultures were incubated at 37 ° and at room temperature.
Following a suggestion of Dr. Rettger, we tested the possible stimu-
lating effect of an atmosphere of approxirnatdy 10 per cent CO~.
Although diphtheroids, sarcin~e, yeasts and torula~ were occasionally
obtained, none of the strains isolated appeared to be of etiological
significance and they were regarded as accidental contaminants.
Fowl Paralysis and Coccidlosis.
The view that coccidial infection may play a r61e in the etiology of
paralysis has been expressed by a number of poultrymen and experi-
ment station workers. Thus Beach and Davis (7) describe and picture
(Fig. 3 of their article) paralysis as a form of chronic coccidiosis occur-
ring in older birds between the ages of 4 and 8 months. The authors do
not refer to "fowl paralysis" as an independent disease, but appear to re-
gard it merely as a late symptom of the coccidial infection. The op-
posite point of view is represented by May, Tittsler and Goodner (5),
who state that coccidia are frequently present in paralysed birds but not
in all cases; and that birds may die from coccidiosis without exhibiting
symptoms of paralysis.
Our material, we believe, affords a decisive answer. As a routine,
sections were taken from duodenum and ceca in practically every
case examined; during the past summer, we have also checked the
80 !~OWI, PARALYSIS. I
histological findings by the examination of fresh scrapings of the
duodenal and cecal mucosa~. There is, in general, close agreement
between the findings of coccidia in fresh preparations and in the stained
tissue sections. This is brought out in Table IL
Thus, in only six out of 83 examinations was there any discrepancy
as regards the presence or absence of coccidia between fresh prepara-
tions and the stained sections. From this one may conclude that
the absence of coccidia in histological sections is strong presumptive
evidence against the existence of coccidial infection.
In 60 spontaneous cases of paralysis, coccidia were found in the
sections in ten, or roughly, 16 per cent; in 33 non-paralysed birds
from various sources, coccidia occurred in four, or approximately 12
per cent. Obviously, there is no significant difference in the two
Our experimental material is also instructive. In Experiment VI,
only one of thirteen cases of paralysis was infected with coccidia. In
83 chickens which did not develop paralysis, coccidial infection oc-
curred in eleven, or roughly, 13 per cent, about the same ratio as
in the non-experimental material. In Experiment VII, coccidiosis
appeared in both inoculated and control animals during the 3rd and
4th months. Of the four positive cases, two showed coccidia, and
two were free. Fifteen of the non-paralysed chickens were affected,
and 33 were free. The higher incidence of coccidiosis in this experi-
ment may be attributed to the crowding and close confinement.
From the foregoing data, it is very evident that there is no correla-
tion whatever between infection with Eimeria avium and the incidence
of fowl paralysis.
The disease as thus described is one with striking and characteristic
pathology, and one which has no close counterpart, so far as we are
aware, in mammalian pathology. The essential changes are cellular
infiltration of the nervous tissues, peripheral nerve trunks of the
extremities and viscera, spinal ganglia and cord--less strikingly of
the brain and rarely of the cranial nerves. In the nerves, the cells,
which are predominantly of the lymphoid type, but mixed with
plasma cells and clasmatocytes, push apart the nerve fibers and
A. M. PAPPENHEB~.R, L. C. DUNN~ AND V. CONE S~
eventually cause considerable destruction of the myelin. The axis
cylinders tend to be preserved so that it is not surprising that paralysis
is rarely complete. That sensation as weU as motion is affected, is
evident from the involvement of the spinal ganglia and posterior
spinal roots in most of the cases.
In the cord and brain the infiltrations are largely confined to the
vicinity of the vessels and the lesions often bear a close resemblance
to those found in various types of mammalian encephalomyelitis.
Although these lesions of the nervous system are the most distinctive
features of the disease, and probably the ones responsible for the more
obvious clinical symptoms, it seems probable that the massive lympho-
matous infiltrations and growths occurring in the ovary and other
viscera are integral features of the disease. They have been present--
and we refer here only to the grossly evident, tumor-like growths--in
I0 per cent of our spontaneous cases; and they have developed, as will
be pointed out in a following paper, in fowl experimentally inoculated
with suspensions of brain and cord from paralysed fowl. Although
these masses often take on the character of a malignant neoplastic
growth, pushing aside and invading normal structures, their cyto-
logical composition, and the frequent continuity of the neoplastic
tissue with the characteristic accumulation in the nervous tissues
make it highly probable that the same agent or stimulus is concerned.
This brings up the difficult questions d the relation of this disease
to the malignant lymphoblastomata on the one hand, and to the
leucemias and pseudoleucemias on the other.
Numerous tumors in fowls variously termed lymphoma, lymphosarcoma and
small round cell sarcoma have been described.
In certain cases these have been associated with a leucemic blood picture, and
considerable evidence has been presented by Ellermann and Bangs (8), Ellermann
(9), Hirschfeld and Jacoby (I0), Schmeisser (11) and others that the leucemia
of fowls is a transmissible disease. Of the non-leucemic lymphomatous cases,
we may cite those reported by Hathaway (12), Butterfield (13), Tyzzer and
Ordway (14), Wernicke (IS), Joest and Ernesti (16), Pentimalli (17), Beatti (18),
Hobmeyer (19), Eisner (20), Schuchmann (21) and Michalka (22). It is un-
necessary to review this literature in detail. That the disease which we have
studied is not a form of leucemia has been shown by the examination of blood,
smears and by the absence of enlargement of the spleen and liver, which has been
a characteristic feature of the reported cases.
82 FOWL PARALYSIS. I
It has seemed to us that the diagnosis of "pseudoleucemia" and "leucanemia"
used by Ellermann to describe cases in which lymphoid or myeloid infiltrations
were present in the viscera without a leucemic blood picture, must be accepted
with considerable reserve. Ellermann regards such cases as being produced by the
injection of his leucemic virus, and includes them amongst the positives. In our
experience, such visceral infiltrations occur in practically every chicken, although
there is considerable individual variation in the amount of lymphoid or myeloid
tissue present in the different organs. Neither Ellermann nor subsequent workers
with fowl leucemia appear to have made a systematic study of control "normal"
material. It is regrettable also, that none of the investigators of fowl leucemia
has included a study of the nervous system. We cannot state, therefore, whether
brain, cord and nerves in this disease may show lymphoid infiltrations such as we
have described in fowl paralysis. That such infiltrations may be found in human
leucemias, is well known; 30 such cases have recently been collected from the
literature by Fried (23). That they cannot involve the peripheral nerves to the
degree found in the paralysis of chickens, is obvious from the absence of neuritic
symptoms in leucemic birds.
Whether some of the cases which have been described as "pseudo-
leucemia" may have been instances of paralysis with visceral infiltra-
tions, it is impossible to say. The literature contains no references
to a careful study of the nervous system in these cases.
case reported by Beatti from Buenos Aires, is it recorded that the
chicken during life could not stand erect, but rested on the right foot,
using the left wing as support. The cause for this was a lympho-
blastomatous mass in the lumbosacral region, infiltrating the kidney,
and invading the lumbosacral plexus.
among the nerve fibers. There was no leucemic blood picture.
is probable that this was a true case of fowl paralysis, of the type
associated with regional lymphomatous growth, and that other cases
in the literature, if the nervous system had been carefully studied,
would have revealed themselves as examples of this disease.
A striking association between paralysis and a high tumor incidence
(12.9 per cent) was in evidence also in the "farm flock" cited by
Schneider (1926) (24). From a study of material supplied to us, we
have learned that paralysis was prevalent in this particular flock.
In the 60 cases of spontaneous paralysis here reported, macroscopic
ovarian tumors, usually with lymphomata also in the other viscera,
were found in six instances or 10 per cent and we have found a similar
high incidence in our experimental chickens.
Only in the
Tumor ceils were distributed
The abnormally high
A. M. PAPPENHEr~R, L. C. DUNN, AND V. CONE SS
rate in our paralysis material is in itself suggestive of a correlation,
and we have given pathological evidence for the view that the lympho-
matous masses in the ovary and other viscera are no different in their
cytological composition from the infiltrations found in the nervous
tissues. Our material does not permit us to state whether all cases
of visceral lymphomatosis in fowls are accompanied by lesions of the
nervous system, and this question demands further investigation.
Our studies at least indicate that the agent which is responsible for
the pathological changes in the nervous system is not exclusively
neurotropic; it may in certain cases stimulate the proliferation of
lymphoid cells in the viscera, and to a degree which makes them take
on the morphological character of a neoplasm. One of the most
interesting and as yet, wholly obscure phases of our problem, is the
undoubted transition between the lesions which histologically appear
to be inflammatory and those which assume the character of a true
No satisfactory designation for this disease has yet been suggested.
The term "polyneuritis" used by Marek in 1907, is open to several
objections--it is not sufficiently inclusive, leaving out of account the
lesions of the cord, ganglia and brain; and it does not distinguish this
disease from the nutritional polyneuritis gallinarum, which is etiologi-
cally and pathologically unrelated. Kanpp, and May, Tittsler and
Goodner speak simply of "paralysis of the domestic fowl"--a term
which is unsatisfactory, since paralysis is but a symptom, and one
which is inconstantly present in this disease, and which may be due
to a variety of other disorders. The term "neuritis" is used by
Doyle, and is open to the same objections as the term "polyneuritis."
Van der Walle and Winkler-Junius suggest the name "neuromyelitis
gallinarum" to differentiate this condition from the nutritional
It is perhaps not possible to find an altogether satisfactory
name for this disease until the cause of it shall have been definitely
established. The outstanding pathological features, as we have
seen, are the lymphoid infiltrations of the peripheral nerves, and
the frequently associated lymphomatous growths in other situations.
We wish, therefore, to propose tentatively the term neurolymphoma-
tosis gallinarum, as indicating more specifically than any of the
POWL PARALYSIS. I
terms previously suggested, the most striking pathological features
of the disease.
I. Fowl paralysis (neurolymphomatosis gallinarum) is a disease
entity, with characteristic clinical and pathological features.
2. The disease occurs in all parts of the United States, Holland,
Austria and probably South America.
3. The disease appears to be endemic in certain foci. Having once
appeared, the disease tends to persist through successive years.
4. It occurs with about equal frequency in both sexes; all common
breeds may be affected.
5. Symptoms appear between the 3rd and 18th months. Typical
clinical cases have not been observed outside of these limits.
6. The conspicuous symptoms are (a) asynunetrical, partial and
progressive paralysis of the wings and both legs, and rarely of neck
muscles; (b) occasional grey discoloration of iris, with blindness.
Nutrition is usually preserved.
7. The duration is variable; the outcome is usually fatal, but
spontaneous recovery may rarely occur.
8. The principal pathological changes are found in the nervous
system. In the peripheral nerves, the essential feature is an intense
infiltration of lymphoid, plasma cells, and large mononuclears. This
is accompanied by a myelin degeneration in the more advanced lesions,
but the cellular infiltrations appear to precede the degenerative
changes. In brain, cord and meninges, there are similar infiltrations
Infiltrations of the iris with lymphoid and plasma cells are found in
the cases showing gross discoloration of the iris.
Visceral lymphomata, originating usually in the ovary, are associ-
ated in a certain percentage of the cases. Evidence is presented in
favor of the view that this association is not accidental, and that the
lymphomata are a manifestation of the disease.
9. Infiltrations of the spinal cord and brain, rarely of the peripheral
nerves, are frequently present in birds showing no clinical symptoms.
These are interpreted as mild cases of the same disease.
I0. No microorganisms of etiological significance have been dem-
onstrated in the tissues or by cultural methods.
A. M. PAPPENHEIME~R, L. C. DUNN, AND V. CONE
1. Marek, J., Deutsch. tier~rztl. Woch., 1907, xv, 417.
2. Eijkman, C., Geneesk. Tijdschr., 1890, xxx, 295; 1893, xxxiii, 163, 340; 1896,
3. Kaupp, B. F., J. Am. Assn. Instructors and In~. Poultry Husbandry, 1921,
4. Van der Walle and Winlder-Junius, Tijdschr. vergdijk. Geneesk. Enz., 1924,
5. May, H. C., Tittsler, R. P., and Goodner, K., RhodelslandAgric. Exp. Station,
Bull. 202, December, 1925.
6. Doyle, L. P., J. Am. Vet. Med. Assn., 1926, lxviii, 622.
7. Beach, J. R., and Davis, D. E., Univ. Calif. Agric. Exp. Station, Bull. 300,
8. Ellermann, V., and Bangs, O., Centr. Bakt., 1. Abt., Orig., 1908, xlvi, 4, 596.
9. Ellermann, V., Z. klin. Med., 1913, lxxix, 43.
10. I-Iirschfeld, I-I., and Jacoby, M., Z. klin. Med., 1910, lxix, 107.
11. Schmeisser, H., J. Exp. Med., 1915, xxii, 820; Johns Hopkins Hosp. Rep.,
1915, xvii, 1.
12. Hathaway, Brit. Med. J., 1883, i, 1226.
13. Butterfield, E. S., Folia tu~matol., 1905, ii, 647.
14. Tyzzer, E. E., and Ordway, T., J. Med. Research, 1909, xxi, 459.
15. Wemicke, Z. Kre~sforsch., 1911, x, 168.
16. J'oest, E., and Emesti, S., Z. Krebsforsch., 1916, xv, 1.
17. Pentimalli, F., Z. Krebsforsch., 1916, xv, 111.
18. Beatti, M., Z. Krebsforsch., 1916, xv, 452.
19. Hobmeyer, Mona~schr. prakt. Tierheilk., 1913, xxiv, 474.
20. Eisner, K., Inaugural dissertation, Leipsic, 1912, cited by Michal~s.
21. Schuchmann, K., Inaugural dissertation, Giessen, 1922, cited by Michalka.
22. Michalka, J., Virchows Arch. path. Anat., 1926, cclx, 399.
23. Fried, B. M., Arch. Path., 1926, ii, 23.
24. Schneider, M., J..Exp. Med., 1926, xliii, 433.
EXPLANATION OF PLATES.
Fie. I. Fowl paralysis. Showing weakness of legs and drooping of left wing.
FI~. 2. Fowl paralysis. Terminal stage, complete prostration.
FIO. 3. Fowl paralysis. Dissection of spinal cord and brachial plexus. On
the~right side there is massive nodular thickening of the nerve trunks, extending
into the corresponding segment of the cord.
86 FOWL PARALYSIS. I
FIG. 4. Section through sciatic nerve. Intense mononuclear infiltration of
upper bundle, moderate infiltration of lower.
FIG. 5. Fowl paralysis. Infiltration of peripheral nerve. High power.
FIQ. 6. Fowl paralysis. Section of sciatic nerve, showing intense cellular
infiltration. Note nodular loci.
FIG. 7. (A) Brachial plexus. Normal. (B) Advanced paralysis. Myelin de-
generation, fibrosis, mononuclear infiltration.
FIG. 8. Typical paralysis. Sciatic nerve. Pal-Weigert stain, showing ad-
vanced degeneration of myelin sheaths.
FIG. 9. Typical paralysis. Sciatic nerve stained by the Rio del Hortega silver
carbonate method. Persistence of neuraxones in infiltrated nerve.
FIG. 10. Low power photograph of spinal cord with attached ganglia and
nerve roots, showing asymmetrical enlargement and extension of infiltration into
adjacent tissue of cord.
FIG. 11. Spinal ganglion, showing lymphoid infiltration between ganglion
FIG. 12. Fowl paralysis. Infiltration of sympathetic ganglia and nerves about
FIG. 13. Section through cornea, anterior chamber of eye, iris and lens. Note
cellular infiltration of iris.
FIG. 14. Fowl paralysis. Massive lymphoid infiltrations in liver.
FIG. 15. Fowl paralysis. Section of ovarian tumor, associated with typical
lesions of the nervous system. Note numerous mitoses. High power.
THE. JOURNAL OF EXPERIMENTAL MEDICINE VOL. XLIX.
CPappenheimer et a/.: Fowl paralysis. I.)
THE JOURNAL OF EXPERIMENTAL MEDICINE VOL. XLIX.
(Pappenheimer el a/.: Fowl paralysis. I.)
THE JOURNAL OF EXPERIMENTAL MEDICINE VOL. XLIX.
(PappenheJmer et el.: Fowl paralysis. I.)
THE JOURNAL OF EXPERIMENTAL MEDICINE VOL. XLIX.
(Pappenheimer d d.: Fowl paralysis. I.)
THE JOURNAL OF EXPERIMENTAL MEDICINE VOL. XLIX.
(Pappenheimer e# a/.: Fowl paralysis. L)
THE JOURNAL OF EXPERIMENTAL MEDICINE VOL. XLIX. PLATE 11.
(Pappenheimer et al.: Fowl paralysis. I.)
THE JOURNAL OF EXPERIMENTAL MEDICINE VOL. XLIX.
(Pappenhelmer d at.: Fowl paralySiS. I.)