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PROGRESSIVE PARALYSIS OF CHICKENS

Thesis for Degree of M.S.
Jesse Francis_9£ggy

1926

 

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INTRODUCTION

Since 1921, numerous inquiries have been received
at the Michigan State College as to the cause of an
affection among chickens occurring at the age of
ten weeks to maturity. The disease is commonly
termed leg weakness with no attempt to differentiate
it from polyneuritis, rachitis and other leg troubles
known to occur in chickens. In reality, this malady is
one of incoordination and paralysis, and not a weakness
of the legs. It involves the legs and toes, and some
times the wings and neck, causing a mortality of five
to fifteen per cent of aflected flocks.

In the review of literature, some material on
diseases showing symptoms closely allied to those
of progressive paralysis has been used in an effort
to differentiate this paralytic disease from otner

forms of leg weakness.

REVIEW OF LITERATURE
De Marek (l) in 1907, reported a disease of chiCkens
of Budapest, the chief symptom being a progressive
paralysis of the legs. Nerves supplying affected
parts show considerable changes, often an almost
complete degeneration of nerve fibers, and an

infiltration with round cells. Similar lesions

126397

 

 

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'were found in the spinal cord, and the pia mater
was also found to be infiltrated. De marek stated
that he was unable to determine the cause of this
disease.

In 1924, (2) Van der Walle, Winkler and Lumius re-
ported a disease among fowls, the chief symptom being
that of paralysis. The appetite remains good, even to
the last stages of the disease, and the birds 100k
healthy, as indicated by the bright comb and the
carriage of the head. The temperature is Iound to be
normal. Affected birds generally die in a few weeks
after the onset of the disease. Diseased birds fed
on a ration containing yeast did not recover as did
those suffering with polyneuritis as a result of an
exclusive rice diet. These investigators confirmed
the pathological findings of De Marek. They also
found on cross section of affected nerves that the
nerve sheath was swollen and degenerated, and cross
section through the Spinal cord revealed that the
ganglion cells had lost their Nissl granules, and
many were reduced or degenerated. Extravasation of
blood around the blood vessels of affected nerves
was common. They believed the degeneration was not

a primary condition but the result of the infiltration.

Experiments were performed to ascertain the cause

of the disease. Of two birds, one fed the same ration
as the affected flock and given water used at the
experimental station remained healthy, while the
second bird fed the same ration and water from the
well from which the affected flock received their
supply, became paralyzed after two months. Blood
from the affected bird was injected into a normal
bird which later deveIOped paralysis. Cultures were
made from the blood and passed through a Chamberland
filter. The filtrate was injected into a normal bird
which showed symptoms after two months. Six birds
were kept in the same pen with affected birds and re-
mained healthy. They concluded that the cause of the
disease is probably a filterable virus. Considering
the pathological findings they decided that the most
characteristic name for the disease would be Neuro-
myelitis gallinarum.

Doctor Jull, senior poultry husbandryman of the
United States Department of Kgriculture, said in a
personal interview, that they were encountering more
or less trouble among their eXperimental birds with
a paralytic disease closely resembling the malady

generally termed leg weakness or rachitis, and that

 

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the disease could not be controlled by the use of
cod liver oil, green feed and sunshine as in the
deficiency diseases showing similar symptoms.

The idea of leg weakness in chickens held by
Knox and Lamb (4) is that it may be the result of a
number of causes. They say, "In some cases it is
apparently a nervous condition which results in a
lack of coordination in the muscles of the legs. In
other cases it is due to a poor develOpment of the
bone, which may be referable to the ration and whicn
may in some cases be corrected by feeding bone meal,
and which may be a rachitic condition. In still other
cases it may be merely a symptom of disease or general
condition of malnutrition, in other words merely a
sick chicken. In our Opinion leg weakness is not a
specific disease in chickens referable to definite
deficiency in ration, but is a general symptom caused
by any one of various disorders, such as a headache
in the human family."

Knox and Lamb (5) quote Halpin as saying that it
is his Opinion that leg weakness is a rachitic condition
and that it is prevented by the use of cod liver oil.

Emmett and Peacock (6) and later Halpin, Hart and

Steenback have proved the causual relation exsisting
between dietary deficiency and leg weakness. These
investigators found that chicks fed from the time
they are hatched with a ration of corn and skimmed
milk, with few exceptions, cease to grow in four to
six weeks and soon die often showing symptoms of leg
weakness. Upon adding five per cent cod liver oil
to this ration uniform rates of growth were made up
to seven hundred grams in weight.

Mitchell, Kendall and Card (7) state, "That
whether the beneficial effects of cod liver oil are
due to its content of vitamin A or to its content
of anti-rachitic vitamin is not known, but cod
liver oil is known to be a potent curative in in-
fantile and experimental rickets."

Gwatkin, (8) a Canadian investigator, has reported
a form of leg weakness occurring during the late sum-
mer and autumn months, when apparently everything
necessary to a complete diet is available with sanitary
conditions of the best.

Bushnell and Hinshaw (9) describe the symptoms
produced in fowls, by a lack of vitamin 5 (anti-
neuritic) and vitamin D (anti-rachitic) as follows:

Vitamin B, "In birds the disease is characterized by

 

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extreme nervous symptoms and inability to coordinate
certain muscular movements. Sometimes there is a
paralysis of the legs and a slight paralysis of the
muscles of the neck. The internal organs appear
shrunken and darker in color than normal. The
muscles also appear to be darkened as 11 they had been
exposed to the air. Symptoms other than those due

to emaciation and nervous incoordination do not seem
to be marked. The disease develOps rapidly and the
bird dies in about fifty-four days. Vitimin D (anti-
rachitic) the most characteristic symptom of vitimin
D deficiency in the diet is that of leg weakness in
young chickens. This vitimin is present to some ex-
tent in green leaves, milk and in cod liver oil in
large amounts. One to five per cent of cod liver

oil added to the feed will prevent the appearance of
this trouble in young chickens. "

Hart, Halpin, Steenbock and Johnson (10) state,
"Leg weakness is rachitis. The chicken, and especially
the baby chick, is very sensitive to leg weakness or
rickets. This one malady is the occasion of tremendous
losses in baby chick rearing. With the recognition
that leg weakness is rachitis, a ready cure for the
malady is forthcoming. There are certain food

materials now recognized as having distinct anti-

rachitic prOperties, namely, the fish liver oils

and hen's egg yolk. It finds its equivalent also

in effect in sunshine or in ultra violet light."
Johnson((ll) states, "It is well recognized that

leg weakness, or going down on the legs,i of chicxens

may be due to a number of causes. Differentiating

the various types of leg weakness makes it better

possible to apply more scientific measures for relief

and also to distinguish between important and unim-

portant leg weakness troubles. Present knowledge shows

that one type of leg weakness is accompanied by rickets,

but information relative to the practical dianosis

of this condition among chickens is worthy of further

mention. While the common leg weakness of young

fowls is a problem of lack of mineral deposition in

bones, it is at the same time often accompanied by

an arrested development of the soft tissues of the

body. Examination of young fowls up to about six weeks

of age, received at this station, reveals that the

great majority of these chickens showing the condition

which might be regarded as distinctly a leg weakness

disturbance. evidence abnormal5bone'f0rmation. Leg

weakness in growing stock, of this section, older

than this is not likely to be accompanied by this ab-

normal bone formation. One of the most striking

 

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changes noted externally accompanying leg weakness
symptoms is a buckling or inward curvature of the
ribs at the junction of the vertebral and sternal
portions associated with a distinct lack of rigidity
of the distal portion of the bones."

Stafseth (12) makes the following statement,

"Leg weakness is not, as the name would imply, a
disease in itself out merely a symptom which may

be seen in a number of diseases such as: tuberculosis,
polyneuritis, enteritis, rachitis, articular gout, lim-
ber neck, asthenia, and diseases of the liver and per-
haps others."

A paralytic disease of ostriches resembling that
of chickens was observed by Marx (13), in 1900, in
the Frankfort Zoological gardens.

In 1910, Robertson (14) describes a paralysis a
occurring in ostriches near Cape Town. The symptoms
of the diseaé described are: sudden'onset, inability
to rise, paralysis of the toes, which are flexed
on themselves. The paralysis often involves the wings
and neck. The appetite remains good, and there is no
apparent pain. Young birds are the most often affected.
The only constant lesion.observed by Robertson is a
congestion of the duodenum. An organism was isolated

from the mucosa by ordinary cultural methods. This

 

 

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organism is aerobic and does not stain by Gram's method.
A suspension of the organisms in physilogical salt
solution when injected into a normal ostrich produced
symptoms in seven days, and death in one month.

From the literature revived in this paper, it will
be seen that the followig points appear to be established:

1. There are several separate and fairly distinct
diseases often referred to as leg weakness.

2. Vitamins play a very important part in rickets
and polyneuritis.

3. God liver oil and green feed are potent factors
in preventing and curing leg weakness caused by a laCk
of vitamins.

4. There is a paralytic disease of chiCkens,
commonly called leg weakness, which is not referable

to the nutrition, and the cause of which is unknown.

SYMPTOMS OF THE DISEASE
The first symptom of the disease is often a
flexion of the toes of one or both feet (Fig. 1) pro-
gressing as the disease deve10ps until the entire
leg is involved; sometimes the reverse is noted the
entire leg showing incoordination. The foot and leg
on the Opposite side may or may not become involved.

In the last stages of the disease one leg may be drawn

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forward fully extended, the other retracted posteriorly.
(Fig. 2) Thus it appears that the nerves controlling
the extensor muscles of one leg and the flexor muscles
of the other were the only nerves completely paralyzed.
This no doubt accounts for the lack of coordination

seen in the early stages of the disease. The wings

may become involved, also the neck which may be

drawn into an S shaped curve and at times in the last
stages is found drawn around until the head is in a
ventro-dorsal position. The bird appears alert and

has a good appetite for weeks and even months if well
fed, unless weakened by infestation with coccidia, worms
or tther parasites which are often found in tremendous
numbers in the last stages of the disease; but this is
by no means constant. The disease resembles, in some
reSpects, the leg weakness caused by the lack of certain
vitamins, which in some cases is a rachitic condition
while in others it is a polyneuritic condition. This
disease is not prevented nor cured by the use of cod

liver oil.

PRESENT WORK
The observations recorded in this paper have been
made from four flocks, one a commercial flock, the

other three were of the small flock type seen on the

11

average farm. Post-mortem examinations were made on
'forty-six birds in various stages of the disease, and
histo-pathological examinations were made of the
nervous system. Bacteriological cultures were made
from the intestinal tract of a number of birds.
Particular attention was paid to the vitamin content
of the ration fed to these flocks, to eliminate the
chance of confusing this disease with rachitis and poly-
neuritis.
HISTORY OF AFFECTED FLOCKS
Flock No. l. A commercial flock of one thousand
white leghorns had a mortality of one hundred fifty
birds from this disease during the summer and autumn
of 1924. It was found that during the early part
of the season they were fed on a commercial mash
and scratch feed, sprouted oats and semi-solid
butter milk. After the trouble manifested itself
the ration was changed to the following:
80 pounds corn meal
20 ” meat scraps
1 pound sodium chloride
5 pounds bone meal
5 " lime stone
They were given Sprouted oats and all the semi-solid

butter milk they would eat.

12

The change in ration had no affect upon the disease,
and the birds continued to become paralyzed during the
autumn and winter. many of the pullets came down with
the paralysis after they had been laying for some time.
Strong vigorous birds were as susceptible as those that
were not as thrifty.

In the spring of 1925, a large number of eggs
were hatched from this flock. many of the baby
chicks were sold to various parties in the state,
and about two thousand chicks~were kept by the
owner of the flock. These were fed on a ration
composed of mash, salt mixture and scratch feed.

Mash was composed of equal parts of the following:

Bran,

Middlings,

Oats,

Glutin feed,

Corn meal,

Meat scraps.

Salt mixture was added to the mash as follows:

3% Calcium carbonate,

3% Acid phosphate,

1% Sodium chloride.

Scratch feed composed of the following:

Wheat,

Cracked corn.

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The ration was supplemented with all the semi-solid
butter milk the chicks would eat, to which cod liver
oil was added in the following proportions:

One part of cod liver oil to sixteen parts of semi-
solid butter milk. They were also given lettuce,
rape, and sprouted oats. When the chicks were about
six weeks of age the flock was divided, half of the
chicks were placed on an alfalfa meadow where chickens
never had been raised. In spite of the cod liver

oil and plenty of green feed and free range, paralysis
deveIOped as soon in the experimental flocx as in the
home flock. The disease appeared when the birds were
about ten to twelve weeks of age. The birds, sold

as baby chicks and going to different parts of the
state, were not troubled with this disease. Birds
continued to become paralyzed until the last of

December when it seemed to almost disappear.
HISTORY OF INDIVIDUAL BIRDS

Bird No. 1.— White leghorn pullet about twelve
weeks of age with paralysis of both legs.
Autopsy-

Heart, normal.

Lungs, normal.

Liver, slightly enlarged, dark in color.

l4

Gall bladder,distended.
Spleen, normal.
Kidneys appeared normal.
Gizzard, normal.
Intestines- numerous coccidia and congestion of
the mucosa.
No tape worms present.

No round worms found.

Bird No. 2. White leghorn pullet, age twelve
weeks, right leg and toes of left leg paralyzed.
AutOpsy-

Liver, normal.

Heart, normal.

Gizzard, normal.

Proventriculus, normal.

Intestines- congested throughout the entire length.

No coccidia present.

No intestinal worms present.

Bird No. 3. White leghorn rooster, age fourteen
weeks. When received the bird showed paralysis of
the right wing, right leg to the hook joint and the
toes of the left leg.

Autopsy-

 

 

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Heart, normal.

Lungs, normal.

Liver, normal.

Spleen, atrOphied.

Intestines- showed inflammation of the duodenum.
No tape worms present.
Three ascaride present.

No coccidia found.

Bird No. 4. Both legs were paralyzed, left leg
drawn forward, right leg backward.
AutOpsy-
Heart, normal
Lungs, normal
Gizzard, normal.
Liver showed a few necrotic areas.
Intestines- hemorrhages of the duodenum.
Numerous coccidia were found.
No tape worms found.
No ascarides present.

Ceca- numerous coccidia.

Bird No. 5. White leghorn pullet died in pen,

left leg was drawn forward, right leg backward.

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AutOpsy-

Heart, normal.

Spleen somewhat smaller than normal.

Liver slightly enlarged.

Gall bladder very large.

Intestines- badly congested throughout the entire
length.

Numerous tape worms about three-fourths of

a centimeter in length were found.

Bird No. 6. White leghorn pullet.
The bird was slightly paralyzed in the toes of the
right foot when received at the college, and was
kept for observation. Ten days later the entire leg
was paralyzed and drawn backward and the left leg
showed signs of paralysis. At.the end of three
weeks both legs were completely paralyzed. The
bird was unable to move even a few inches for
food and water but retained a good appetite.. At
the end of the fourth week it was necessary to hold
the bird while it drank water. However, it was able
to pick grain from the floor.
AutOpsy-

Heart, normal.

Liver, normal.

l7

Lungs, normal.

Intestines- hemorrhagic ares throughout the
entire length. Two ascarides were found. No
tape worms were found.

Ceca- a few coccidia.

Sciatic nerve enlarged and of a pink color.

Bird No. 7. White leghorn pullet.
Both legs paralyzed from feet to hook Joint. The
bird could move about but showed considerable in-
coordination. Post-mortem examination was made during
the early stages of the disease.
Autopsy-

Heart, normal.

Liver, normal.

Spleen, normal.

Gizzard, normal.

Kidneys, normal.

Lungs, normal.

Intestines- badly congested, fifteen tape worms,

each about two inches long, were found. No coccidia.

Bird No. 8. White leghorn pullet. Right leg
paralyzed and drawn backward, left leg apparently

normal. Diarrhea was present.

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Autopsy-
Heart, normal.
Liver slightly enlarged with a few necrotic foci.
Intestines- hemorrhages of the duodenum and of
the ileum. No tape worms and no round worms were found.
Coccidia were found in the duodenum, and also in the

ceca. o

Bird No. 9. White leghorn pullet. The right leg
paralyzed from foot to hook Joint, left leg paralyzed
entire length and extended in a lateral position.
Autopsy-

Heart, normal.

Liver larger than normal.

Gall bladder very large.

Spleen atrOphied.

Lungs normal.

Intestines- congested. No coccidia nor tape
worms were found. Sciatic nerves and perineal nerve

of the left leg were enlarged and pink in color.

Bird No. 10. White leghorn pullet about three
months of age. When received, the toes of the left

leg were flexed, otherwise the bird appeared normal.

19

One week later the paralysis had prOgressed to the
hook joint, and the right toes became paralyzed.
The paralysis steadily progressed until the end
of the third week the left leg was extended forward
and the right leg drawn backward. The appetite was
good until the bird was killed.
AutOpsy-

Heart, normal.

Liver, normal.

Gall bladder very large.

Spleen very small.

Intestines- badly congested the entire length.
No tape worms, round worms or coccidia were found.

Ceca contained few worms.

Sciatic nerve of right leg was swollen and pink in

color. Perineal nerve of left leg was swollen.

Bird No. ll. White leghorn pullet.
Both legs totally paralyzed. It was noted that in
the right leg the sciatic nerve was enlarged, and pink
in color while the perineal nerve appeared normal
macrosc0pically. The leg was drawn backward fully
retracted. The left perineal nerve was much larger
and pink in color. The leg was drawn forward

fully extended.

2O

Autopsy-
Heart, normal.
Liver, normal.
Spleen enlarged.
Intestines- congested.
No tape worms, round worms or coccidia

were found.

Bird No. 12. White leghorn pullet.
Both leg and right wing were paralyzed.
Autopsy-

Heart apparently normal.

Liver slightly enlarged.

Spleen atrOphied.

Intestines- congested in duodenum. No intestinal
parasites. Nerves were swollen and inflamed as given

in bird No. ll.

Bird No. 13. White leghorn pullet. Right leg
paralyzed and drawn outward in a lateral position and
left leg showed considerable incoordination.

Autopsy-

Sciatic and perineal nerves of the right leg

were swollen and pink in color. The correSponding

nerves of the left leg appeared normal.

Heart, normal.

Liver very dark in color.
Spleen under sized.

Gall bladder, normal.

Intestines- congested and no parasites found.

Bird No. 14. Black Minorca pullet.
Right leg normal, left leg paralyzed and drawn back-
ward. Muscles appeared atrOphied.
AutOpsy-
Sciatic nerve slightly swollen and pink in color.
Heart appeared normal.
Spleen anemic and small.
Liver apparently normal.

Intestines- normal. No parasites were found.

Bird No. 15. White leghorn cockerel.
This bird showed incoordination in both legs.
Autopsy-

Sciatic and perineal nerves were apparently
normal.

Liver slightly discolored.

Intestines- congested and numerous tape worms

each about two inches in length were found. No

other parasites present.

Bird No. 16. Black Minorca
Right leg showed incoordination
apparently normal.

Autopsy-

Sciatic and perineal nerves

Heart, normal.

Liver slightly enlarged.

Intestines congested and no

Bird No. 17. White leghorn
Incoordination of both legs.
Autopsy-

Heart, flabby.

Liver enlarged.

Gall bladder distended.

Spleen normal.

pullet.

and left leg

appeared normal.

parasites were found.

pullet.

Intestines- very few round worms and no tape worms

found.

Bird No. 18. White leghorn pullet.

Both legs were paralyzed and drawn backward.

Autopsy-

Heart, normal.

23

Lungs, normal.

Spleen, anemic.

Liver, normal.

Intestines- numerous coccidia but no other parasites
found.

Ceca- numerous coccidia were found.

Rectum greatly distended.

Flock No. 2. The owner of this flock reported
incoordination and paralysis of both legs in a few
birds during the latter part of the summer and autumn
of 1924. The first birds to become affected, during
the summer of 1925, occurred the first of August. The
birds were on free range with access to an alfalfa
meadow and were fed on a ration composed of mash and
scratch feed. Mash was composed of egual parts of
the following:

Corn meal,

Middlings,

Ground oats,

Meat scraps.

Scratch feed was composed of the folmowing:

Wheat,

Cracked corn.

Ten birds were examined, by the writer, and with but

24

one exception showed the same symptoms as those of
flock No. 1, and the lesions found were not unlike
those of the first flock. The exception will first be
considered. A photograph was taken of this bird in
the early stages of the disease Fig. 3, it will be
noted that the neck is affected being drawn into an S
shaped curve and the head is rotated. One week later
the head was drawn around into a ventrodorsal position.
This was the only bird, observed by the writer, to
show these symptoms of the neck.

Flocks No. 5 and 4. It was reported that there was
no paralysis in these flocks until the summer of 1925.
Both were on free range and the rations were not
materially different from that of flock number two.
Symptoms and lesions were true to type as observed in
flock No. 1. Six birds were examined from each flock.

The ration fed to flocks 2, 5, and 4 contained plenty
of green feed but no cod liver oil. Birds of these
flocks were given cod liver oil or fresh ox gall as
a curative to differentiate the disease under study
from rachitis and polyneuritis. The fresh ox gall
treatment was first used by Kapsinaw and Jackson’fit
as a prenentative and cure for rickets in rats. The
writer has found it to be a very effective treatment in

rickets among chickens. A number of birds, which

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had completely lost the use of their legs, were

given 8 cubic centimeters of fresh ox gall daily,

and recovered in a week to ten days. Cod liver oil

is usually recognized as an agent for the prevention
and cure of these cases. The use of fresh ox gall

in the early stages of this paralytic disease resulted
in an improvement for a few days after which the disease.
progressed as before. Results with cod liver oil

were negative.

DISCUSSION OF POST MORTEM FINDINGS

In the post-mortem examinations of the first
paralyzed birds, coming to the laboratory, no attempt
was made to examine the nerves. Those examined later,
however, showed varying degrees of enlargement of
the sciatic or perineal nerves and sometimes of both.
In the majority of cases the heart, liver, lungs,
gizzard and kidneys appeared normal. A small anemic
spleen was common. Of the abdominal organs, the in-
testines showed the most constant lesions; congestion
or hemorrhage of the duodenum was present in nearly
every bird examined. The presence of parasites was
not constant, and the large numbers found in some
birds can no doubt be accounted for by the lowered
resistance of the bird, thus breaking down the pro-

tective forces of the body and permitting the para-

sites to develop.

BACTERIAL ISOLATION
This disease, resembles that described by Marx and
Robertson not only in the paralysis of the legs, but

\

also in the congestion or hemorrhages of the duodenum
from which they isolated organisms capable of repro-
ducing the disease. It was thought that an organism
causing the paralysis of chickens might be isolated
from the contents or mucosa of the duodenum. The
following technique was used:

l.- Varying dilutions were made of the intestinal
contents in physiological salt solution and inoculations
were made from each dilution into the following:

Nutrient agar plates.

Liver agar plates.

Blood agar plates.

Endo agar plates.

Brilliant green agar plates.

Lactose agar tubes (shake cultures) to which sterile
petrolatum was added to produce anaerobic conditions.

Liver agar tubes (shake cultures) were cultivated

anaerobically under a two inch layer of sterile petro-

latum.

2.- The contents of the duodenum were washed out

carefully with physiological salt solution, VA small
piece of the duodenum was washed in ten changes of
physiologicxl salt solution, using about 250 cc to
each washing. The mucosa was then scraped with a
sterile knife, the scrapings being suspended in
physiological salt solution, which was re-diluted
several times and inoculations were made as given
under one.

3.- The intestinal contents were washed and a
small section of the duodenum was washed again in
saline solution, after which it was iodized with
colloidal iodine just long enough to sterilize the
surface. The mucosa was then scraped with a sterile
knife and the scrapings were placed in a sterile
physiological salt solution. Inoculations were made
as given under one.

The plates and tubes were incubated at thirty-
seven degrees centigrade and observed after twenty-
four hours, at which time colonies were picked from
the plates and transferred to liver agar slants.
After twenty-four hours the agar slants were washed
with physiological salt solution and the suSpension
of organisms was injected into normal white leghorn

pullets about three months of age. At the end of

three months there were no symptoms of paralysis,
among the birds injected. No attempt was made to
classify the organisms isolated, as there was no in-

dication of their connection with this disease.

TRANSMISSION OF THE DISEASE

1. Blood of two affected birds was drawn into

sterile test tubes; the clots were loosened with a
sterile needle and the serum Was separated by centri-
fuging. Three normal white leghorn pullets, about
eight weeks of age, were each injected with 5 cc of
the serum. One was injected intravenously, one sub-
cutaneously and one intraperitoneally. Results were
negative after three months.

2.- Blood of two affected birds was drawn into
physiological salt solution containing citric acid
to prevent blood from coagulating. Injections were
as given above into three normal white leghorn
pullets. Results were also negative after three
months.

5.- The muscles, liver, Spleen and heart of a
paralyzed bird were gbound up and fed to normal
birds without results.

4.- The intestinal tract was cut into short pieces

and fed to normal birds which remained healthy after

three months.

5.- Brains, Spinal cord and nerve trunns were
removed as quickly as possible and ground in a sterile
mortar with fine sterile quartz , and suSpenSion was
made in warm physiological salt solution and injected
into normal birds as given in No. l. The results were
also negative.

6.- It was observed that a great number of
birds in flock No. l, were roosting out of doors in
apple trees, on fences, and on irrigation pipes. It
appeared that the birds out of doors remained healthy
while those resting in the c00p continued to become
affected. It was found that the coops were infested
with red mites. This fact together with the fact that
there are very few cases of the disease during the
winter months when the mites are inactive. This
suggests that the mites may play some part in the
transmission of the disease, either acting as an inter-
mediate host or as a carrier.

ten normal birds were placed in a brooder coop with
six diseased birds. The coops were infested with red
mites. The result of this work was negative, but un-
fortunately this work was carried on during the latter
part of September and October, 1925. The weather

turned cool and it is doubtful if the mites were

30

sufficiently active to have transmitted the disease
even if they were the infective agent.

HISTOLOGICAL TECHNIQUE

AND
EXAMINATION OF TISSUES
The following technique was employed in preparing
the sections for histo-pathological study of the brain
The bird was quickly killed by cutting off the head

with a sharp knife, for it was important that the
bird should be killed with minimum shock, and without
the use of drugs. The brain was immediately re-
moved by carving away the skull with a knife. The
brain tissues were cut into four parts and dropped
into warm fixing solution, which consisted of four
per cent formaldehyde in saturated aqueous solution
of corrosive sublimate, and allowed to remain for
twenty-four hours. The tissues were then washed for
twenty—four hours in running water, after which they
were carried through 60, 70, and 80 per cent alcohol
to which a few drOps of five per cent alcoholic
iodine was added, until the excess corrosive sublimate
was removed. The alcohol was changed as frequently
as it becomes decolorized. The tissues were then de-
hydrated, cleared, imbedded and sectioned. The sec-

tions were cleared in the various grades of alcohol

31

and stained with methylene blue in saturated anilin
oil water. They were hurriedly rinsed in a large
volume of water after staining, and placed in 95 per
cent alcohol until sufficiently destained. They were
cleared in xylene, and mounted in neutral balsam.

The cerebellum being one of the centers of co-
ordination, the Purkinje cells were studied very
carefully, by comparing sections made from diseased
birds with those of the normal which were passed
'through the same solutions and at the same time.
There was apparently no change in these cells.

Brain tissues were also fixed by Zenker's method
and were stained with eosin and methylene blue.
Punctate cerebral hemorrhages were found.

The Spinal cord was also fixed by Zenker's method
and were stained with eosin and methylene blue. Sections
Show what appears to be a degeneration of the ganglion
cells. Some appear to have lost the Nissl granules
while others Show no nucleus.

Examination of the sciatic and perineal nerves in
sections fixed by Zenker's method and stained with
‘eosin and methylene blue, Show a degeneration of the
nerve fibers, and an infiltration of round cells and
in many places a complete disappearance of the fiber.

These changes depend upon the stages of the disease.

32

In the early stages very little degeneration can be >
noticed by this method of staining. However, de-
generation can be seen by osmic acid fixation, even
in nerves that Show but slight infiltration of
mononeuclear leucocytes. In the advanced stages in-
filtration of leucocytes is extensive. Areas thickly
infiltrated with leucocytes are seen in the affected
trunks, in the early stages as well as in the latter
stages of the disease. ChromOphilic granules re-
sembling microorganisms can be seen in these densely

infiltrated areas.

PHYSIOLOGICAL EXAMINATION

A bird, completely paralyzed in the right leg
which was drawn backward and the left leg badly
affected, was placed under ether anesthesia. The
muscles of the thigh and the sciatic and perineal
nerves were eXposed. Direct faradic stimulation of
the muscles of the right leg on the posterior side
of the femur produced contraction, lifting up the leg
which was held straight backward. Direct faradic
stimulation of the anterior muscles produced no con-
tractions.r The nerve was stimulated which produced a

contraction of the posterior muscles but no contractions

35

of those on the anterior side of the femur. The muscles
and nerves of the left leg were GXQOSBd in a similar
manner. Direct stimulation of the muscles, with an
induction coil, on the posterior and anterior side
of the femur responded to the stimulant, but the
contractions were not as strong as normal. The
nerve trunks were stimulated producing a contraction
of the muscles on the posterior part of the thigh

in the right leg. The nerve trunks were severed

and each end was stimulated. The lower end produced
contractions the same as before it was cut. Stim-

ulation of the proximal end produced no results.

DISCUSSION

Keeping in mind the pathological findings, the
results of the nerve stimulation were about what one
would expect. However, direct stimulation of the
muscles without response, indicates that the ganglion
cells and nerve trunks are not alone degenerated,
but the nerve endings and possibly the muscles them-
selves may be degenerated. '

This, however, is contrary to the findings reported
by May, Tittsler and Goonner (l5) in wnich they state,
"Stimulation of the sciatic nerve in a recently killed

bird produces a strong muscular reaction. This shows

54

that there is no incoordination between nerve and
muscle and that both nerves and muscles appear to

function normally."

EXAMINATION OF BLOC

Blood was drawn from a paralyzed bird and smears
were made on slides in the usual way. The smears
were stained by Wright's method.

The number of leukocytes of one bird appeared
normal in every respect. The other three birds
showed a marked leucocytosis. The number of
leucocytes of one bird were about three times the
number found in a normal fowl. The other two
showed an extremely high leucocytosis. The majority
of these cells were of the rod-bearing polyneuclear

type and small lymphocytes.

GENERAL DISCUSSION
It appears from the nature of the disease and the
pathological and physiological findings that the
malady is undoubtedly caused by some infectious micro-
organism. However, the eXperiments recorded in this
paper like those of other investigators, in this
country, have failed to Show the cause of the disease.

It also appears, from the eXperiments with chicks

in flock No. l, in the Spring and summer of 1925,
that there may be a long incubation period of six to
eight weeks or more.

The pathological findings of the brain and Spinal
cord confirm those of other investigators. The changes
found in the sciatic and perineal nerves and the re-
actions to electric stimulation seem to diSprove the
Opinion_of other investigators, that the incoordination
is purely of the central nervous System, would in-
dicate that the primary lesions were in these parts and
that the lesions of the central nervous system are
of secondary origin.

The increase of leucocytes also points to the

possibility of this being an infectious disease.

C NCLUSIONS
l. The disease is not due to a dietary deficiency.
2. The cause of the disease is unknown.
3. The seat of the disease is probably not in the

central nervous system but in the peripheral nerves.

 

 

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BIBLIOGRAPHY

I. Demarek, Deut. Ticrarztl Wchnschr. 15-1907

No. 30, Page 417-421.

2. Van der Walle and Winkler-Luminus, Tudschrift
Voor Vergelykende Geneeskunde, G. N. Z.

Nieuwe Reeks, Deel V. January 17, 1924.

3. Kapsinaw and Jackson, Soc. Expt.Biol. and Med.,
Proc 21 (1924) No. 5, Page 472-473

4. Knox.

5. Lamb, Poultry Science Feb. and March, 1924.

6. Emmett and Peacocx, Journal of Biol. Chem.

1921, Page 40

7. Mitchell, Kendall and Card, Poultry Science

April and May 1923.

e. Gwatkin, Canadian vet. Rec. July, 1925, Page 48.
9. Bushnell and Hinshaw, Agri. Expt. ey. Kansas State
College.

10. Hart, Halpin, Steenback and Johnson, “is. Bul.
371. Revised Oct., 1925.

11. Johnson, Poultry Science, Dec-Jan-l924-l925.

12. Stafseth, Mich. Agri. EXpt. St., Quarterly May 1922.

15 and 14. Marx and Robertson, Diseases of Domestic

F
Fowls by Ward-Gallagher, Page 251.

15. May, Tittsler and Goodner, Rhode Island Agri. EXpt.

St. Bul., Dec., 1925.

ACKNOWLEDGMENTS

I gratefully acknowledge the assistance of
Doctor Ward Giltmer, Doctor William L. Chandler,
Professor William L. Mallman and others for

suggestions and generous help in this work.

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