History of Nursing in Pacific Canada

The Vancouver Medical Association Bulletin: December, 1928 Vancouver Medical Association 1928

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 VoL V.
No.   J
The Bulletin
Vancouver Medical Association
'"Ked 'Water" in Qattle
Qongress of Ttydiology
^Published monthly atUancouver, ^B.Q., by
*^>Trice»> $1.50 per ytav^ DESHELL  LABORATORIES  OF
Deshell Laboratories of Canada     24TorontoT oS&ia
Limited Gentlemen:     Please   send   me   copy   of
the   new   brochure   "Habit   Time"    (of
„.,-,-> . —. it ir bowel movement) and specimens of Pet-
245 Carlaw Ave.    Dept. V.M.        roiagar.
Published Monthly  under the Auspices of the  Vancouver Medical  Association  in  the
Interests of the Medical Profession.
529-30-51 Birks Building, 718  Granville St., Vancouver, B.C.
Editorial Board:
Dr. J. M. Pearson
Dr. J. H. MacDermot Dr. D. E. H. Cleveland
All communications to be addressed to the Editor at the above address.
Vol. V. DECEMBER,  1928 No. 3
OFFICERS, 1928-29
Dr. T. H. Lennie Dr. W. S. Turnbull Dr. A. B. Schinbein
Vice-President President Past President
Dr. G. F. Strong Dr. J. W. Arbuckle
Secretary Treasurer
Additional members of Executive:—Dr. A. C. Frost and Dr. F. N. Robertson
Dr. W. F. Coy Dr. W. B. Burnett Dr. J. M. Pearson
Auditors:    Messrs. Price, Waterhouse & Co.
Clinical Section
Dr.  L.  H.   Appleby   Chairman
Dr. J. R. Davies Secretary
Physiological and Pathological Section
Dr.  C. E.  Brown Chairman
Dr. R. E. Coleman Secretary
Eye, Ear, Nose and Throat
Dr. W. E. Ainley Chairman
Dr. F. W. Brydone-Jack \ Secretary
Physiotherapy Section
Dr. H. R. Ross Chairman
Dr. J.  W.  Welch Secretary
Pediatric Section
Dr.  E.  D.  Carder   . : -_. Chairman
Dr.  G. A.  Lamont Secretary
Library Orchestra Summer School
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Dr. Lyall Hodgins Dr. L. Macmillan rjR- j. Christie
Dr. S. Paulin Publications dR- ^ l. Graham
Dr. W. A. Wllson Dr. J. M. Pearson dr- R. P. Kinsman
Dinner •^R" J- ^- McDermot
Dr. E. M. Blab* ^r- ^ ^- **• Cleveland Hospitals
Dr. L. Leeson Credentials Dr. F. Brodie
Dr. H. H. Pitts Dr. J. T. Wall Dr. A. S. Monro
Rep. to B. C. Med. Assn.   Dr. D. D. Freeze Dr. F. P. Patterson
Dr. Stanley Paulin Dr. W. A. Dobson Dr. H. A. Spohn
Sickness and Benevolent Fund   —   The President   —   The Trustees VANCOUVER MEDICAL ASSOCIATION
Founded 1898
Incorporated 1906
GENERAL MEETINGS will be held on the first Tuesday and
CLINICAL MEETINGS on the third Tuesday of the month at 8 p.m.
from October to April inclusive. Place of meeting will appear on the
December    4th—General Meeting:
Papers—Dr. B. D. Gillies; Dr. G. E. Gillies: "Peptic
Ulcer, its Medical and Surgical Aspect."
December 18 th—Clinical Meeting.
8th—General Meeting:
Paper—Dr.   Ralph   C.   Matson,   Portland,   Oregon:
"Surgical Treatment of Pulmonary Tuberculosis."
22 nd—Clinical Meeting.
5th—General Meeting:
Paper—Dr. R. P. Kinsman: "Focal Infections in Infancy and Childhood."
X-ray films to be shown by Dr. H. A. Rawlings.
19 th—Clinical Meeting.
5 th—General Meeting.
The OSLER LECTURE—Dr. H. M. Cunningham.
19 th—Clinical Meeting.
2nd—General Meeting.
Paper—Dr. F. P. Patterson: Subject to be announced.
16 th—Clinical Meeting.
23 rd—Annual Meeting. Jo quote another eminent authority
on ultraviolet trterapu    4
"The Quartz Mercury Vapour is the most
generally suitable lamp for employment
in private or in small clinics.
"It is easy to use, effective, rapid in its action, rich in ultraviolet light of therapeutic value, clean, economical both in first
cost and current consumption, suitable for
either a general light bath or local treatment. It occupies little space, and is easily
installed in a doctor's consulting room.
It is, therefore, not to be wondered at
that it has achieved great popularity, and
has been Very generally advocated and
—Sir Henry Gauvain, M. D., M. Chir.
(Cantab)., in his introduction to J.
Bell Ferguson's "The Quartz Mercury Vapour Lamp."
internationally for his contribu'
tions to medical literature, particularly
with reference to ultraviolet therapy.
In England, at Hay ling Island and Alton,
he has combined the work of Finsen
and Rollier, and utilizes both natural
and artificial sources of light; the arti'
hcial source because he realizes that atmos'
pheric conditions in that climate are not
comparable to those of a Swiss village some
4700 feet above sea level.
When selecting equipmentfor
ultraviolet therapy, consider the
Uviarc, as used in all Victor
Quartz Mercury Vapor Lamps.
The Uviarc, or so-called burner,
is designed solely for one form
of therapy—ultraviolet—and
accordingly its spectrum is out'
standingly rich in radiations of
3100 Angstrom units or shorter,
i. e., falling in that portion of
Showing Interior of Reflecting Hood of
Victor Air~Cooled Quartz Lamp.
Note how this design minimizes inter'
ference to the reflection of rays.
the ultraviolet region where the maximum biologic effects are realized.
Consider, too, the consistent operation of the
Uviarc for hours at a time without attention; no smoke, no soot,
no fire hazard. From the standpoint of economy, consider the
large quantity of ultraviolet
radiations in proportion to the
electrical input, which in turn
means also the conservation of
time by shortening considerably the treatment period for a
given dosage; furthermore, no
special wiring is required for
its installation.
Write for booklet: "A Few Facts Pertinent to the Consideration of
Artificial Sources of Ultraviolet Radiations."
Victor X*Ray Corporation of Canada, Ltd*
^Manufacturers of the Coolidge Tube
and complete line of X'Ray Apparatus
524 Medical Arts Building, Montreal
Motor Transportation Bldg., Vancouver
Physical Therapy Apparatus, TSlectro-
cardiographs,  and other Specialties
2 College Street, Toronto
Medical Arts Bldg., Winnipeg
Is a Habit
Accuracy is a habit which can only be acquired by years of keen concentration. Our
pharmacists are able to concentrate on the
work of dispensing because they are not
obliged to leave the dispensary to wait on
customers in the store.
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Florists' Supplies and Funeral Designs a Specialty
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Connecting all three stores.
Brown Bros* & Co. Ltd.
In this issue we present to our readers a paper of somewhat unusual
character. Through the kindness of Dr. C. S. McKee we are enabled
to publish some interesting details of a disease in cattle which has been
the cause of a great deal of economic loss and which has hitherto baffled
all attempts at investigation.
Although the subject of this paper may appear somewhat foreign to
the interests of the readers of a medical journal, as a contribution to the
study of comparative medicine we feel that it is of considerable importance.
It is possible, nay indeed probable, that much natural experimental
work is going on in the lower animals which could be made to yield information of value to the investigation and control of disease in the
human family.
While, so far as we are aware, there is nothing in the diseases which
afflict mankind immediately comparable to the subject of this paper,
our readers will see that the same general problems are present, the same
methods of investigation useful. And as is becoming increasingly the
case in human disease, workers are turning more and more frequently to
the theory that deficiency factors may be of greater importance and that
over a wider field than we have hitherto been willing to concede.
This paper and the changing yiewpoint which has gradually come
over the minds of the authors in the course of their investigation well
illustrate the probability that invasion and infection may not contain the
whole story of disease. There is a static as well as a dynamic aspect.
Moreover the term "deficiency" will have to carry a wider concept.
Not only is the food factor including vitamines concerned. Deficiency
in oxygen supply or distribution produces effects which have not yet
received their due meed of consideration. Deficiency in the digestive
juices or in their composition. Deficiency in the secretion of the endocrine glands. At any rate the word will be a useful variant from the
.word "toxic."
Dr. McKee tells us that the disease under discussion is characterized
post mortem by a thickened, ulcerated bladder, from which the bleeding,
which lends its name to the disease, arises. The kidneys are not affected
and the problem is to account for the condition of the bladder.
Research work was at one time undertaken by the Federal Government, but abandoned at the time of the war.
The disease prevails on bench lands from north of the Fraser river
into Northern Oregon. Eastward it is found to a distance of 60 to 65
miles from the coast and is not present on low-lying or prairie farms.
A Study of the Pacific Coast Type of Red Water in 63 Head
of High Producing Holstein Frtesian Cattle on
Fernhill Farm, Abbotsford, B. C.
By John R. McKee, B.A., and C. S. McKee, M.D.
Paper read at a meeting of Animal Husbandry and Agronomy experts
and Dominion and Provincial Veterinarians on January 7th, 1928.
The writers have jointly suffered severe loss on account of the prevalence of "The Pacific Coast Type of Red Water" which in eight years
Page 55 1
has practically wiped out a herd of 63 valuable Holstein Friesians. During this time every precaution was taken to counteract the effect of the
disease and naturally, much attention was paid to the affected animals.
In the following report we offer some observations, particularly in connection with early symptoms and evidence of pathological changes taking
place in the animal long before Red Water itself appears, which to the
best of our knowledge have not been recorded before. It may be stated
also that animals sold from affected areas to non-affected areas do not
develop Red Water, even in cases where they have shown signs of these
early symptoms, whereas corresponding animals remaining on the affected
areas have invariably succumbed. Once Red Water has appeared, an
animal never recovers.
We submit the report, sincerely hoping that our contribution may
seem of sufficient importance to cause a reopening of the investigation
previously undertaken in connection with this disease, which constitutes
a serious economic problem to many dairy farmers in British Columbia.
situation, sou. and crop conditions
The farm is situated on high land about 3% miles north and east
of the town of Abbotsford, B. C. The soil, a brown loam with a depth
of from 1 inch to 7 inches, is fertile and well watered, producing splendid
crops of clover, roots and corn. Grain has been grown only as a cover
crop for small seeds, on account of difficulties in threshing, and has
shown satisfactory growth. The subsoil consists of a blue clay. The
land lies in several benches and faces in a general direction of north and
west. Mostly cleared from 1912 on, clearing ended in 1924 and it is to
be noted that as no new land was brought under the plow the disease
progressed more rapidly.
All roughage produced on the farm has been fed to the animals, but
concentrates ( including grain) have been purchased. Occasionally small
quantities of roughage, some bedding straw, and on one occasion a large
quantity of alfalfa hay were obtained from outside.
Seven Holstein grades were purchased in the summer of 1919. A
few months later a registered bull calf was secured. Since then, and
until the spring of 1924, additions were made to the herd by purchase
of springing cows and heifers (mostly high-priced pure-breds), all young
animals, none over 5 years of age.
The first case of Red Water appeared in the fall of 1921—two years
and some months after the arrival of the first cows. A second animal
showed the red urine a few months later and in 4 years, five out of the
original seven cows had become affected (two had died from other
causes). Four died from Red Water by the spring of 1923, one lived
until May, 1924.
Since the first appearance of Red Water every animal has become
affected sooner or later.    In practically all cases the purchased cows re-
Page 56 mained normal in appearance during their first lactation period and gave
satisfactory quantities of milk. Many cows milked sixty pounds on
twice-a-day milking and several more than that on three-times-a-day
(all on R.O.P.) On second an dthird freshening they never came up
to their first showing. In fact, the best never gave more than 40-50
pounds per day with identical feed, care and other conditions. In most
cases they rapidly drpoped down to 25-30 pounds per day.
Generally in two or three months after their second calving the cows
became unthrifty, their coats rough and dry looking, and they showed
a distant tendency to lose flesh. No drop or rise in temperature. They
usually went off feed for two or three days, lying down and refusing to
eat. A distinct but transitory jaundice could be seen lasting ten or
twelve days and then disappearing only to recur later on from time to
time. The natural yellow pigmentation of the skin seemed to become
unhealthy and unnatural. The change in pigmentation seemed to extend
also to the eye. There is, particularly in the more heavily pigmented
animals, a natural brown in the iris, even extending into the white. In
affected cases this coloring took on a muddy appearance, and the eyes did
not look as bright and inquisitive as they do normally.
Our first observation was that a cow would remain about two or
three years without showing signs of bloody urine. After that she would
live from one to three years. Many of the high-priced animals were
kept until they died, in the vain hope that resistant calves might be
obtained from them.
Later this conception had to be changed in that "the period of
affection" shortened as time advanced. The last "case" on the farm is
typical in this respect; the cow in question showed the first indications
of trouble eighteen months after coming to the farm; three months later
she gave certain signs (red urine); she is already passing small clots of
blood, and, unless there is a deviation from other cases, she will die
before the first of June this year, 1928.
With one single exception, the period of affection, as indicated
before, has become shorter since the disease first appeared. This exception, or respite, refers to the winter of 1924-25, when alfalfa hay and
straw, purchased from outside, were fed to the cows. No new cases of
Red Water developed that winter. The cows which were already definitely affected continued to retrogress, but the others did better. The
four calves which were raised during this period made better gains and
progress than calves raised at any other time. But, subsequently they
all died from Red Water.
Most of the first calves born on this farm died from haemorrhagic
septicemia. There were some few that lived, however. These few early
calves were observed particularly closely during their early period of development. They were, however, rather small for the breed. In these
animals red urine appeared at around three years of age, just appearing
previous to their second freshening. These animals lived until the fall
of 1927, six and five years respectively.
Page 57 The calves that came from this time on, however, show some very
interesting symptoms. At birth they appeared quite normal, whether
their dams were showing Red Water or not—nor did it matter whether
their dams had just been purchased and given birth to a calf carried previous to coming to the farm or had carried the calf here for full
time. For the first six weeks in all cases and in some cases for five or
six months the calves were fed whole milk. After that they were
changed to skim milk, with a mixture of ground oats and oil cake meal
fed dry.    Hay (grown on the place) was before them all the time.
From six weeks of age onwards (with four exceptions—fed on
alfalfa hay, purchased during the winter of 1924-25) the calves did
not thrive. By the time they were three months of age their coats had
become rough and dry. They were small for their age, and continued to
be so.
These calves seemed to show distinct signs of "jaundice." The pigment of the skin seemed an unnatural yellow. The eyes were muddy
looking and seemed to have an unnatural brownish yellow pigmentation,
not very pronounced but noticeable. In those born during 1922-23
Red Water appeared just previous to first calving.
From 1924 on, in those calves bred on the place, Red Water often
appeared at six or seven months; sometimes it would clear, and again
show just previous to freshening. They never lived to freshen again.
Of those calves in utero, when the dam was purchased, the Red Water
usually appeared just previous to first freshening. They died, usually
in two to three months after freshening.
Of those calves born on this place in late 1925 and the spring of
1926, none lived to freshen. They were very poor and unthrifty. Red
Water usually first appeared at six to seven months. They never cleared,
and died or were slaughtered (when just about dead) at from 10-20
Of the last calves born on the place and kept, (late 1926-spring of
1927) one died at just over one year of age, the other at 11 months.
In connection with this, it may be of interest to note, that these
calves at all times ate their bedding, which was straw purchased from a
farm on Sumas Prairie. They would leave "good" home grown hay to
eat this. This was particularly noticeable at all times. And many cows
ate dirt the first thing after leaving the barn for pasture in the morning.
The only calves that seemed to thrive at all, were those fed alfalfa
hay during the winter of 1924-25.
Three bulls were used on this farm. The first one lived for four
years and did not come under observation as to the first occurrence of
the disease.    Very shortly after the first red urine appeared he was dead.
The next bull used was one born on the place. He was sold as a
yearling to a farmer on Matsqui Prairie and was small for his age. He
was repurchased as a.two-year-old for use here. When repurchased he
was in nice shape and fairly well grown.    He was kept in a pen by him-
Page58 self and never allowed to run out to pasture. He had a small run about
150 feet square to play in. He was fed hay, roots and ensilage grown
on the place, and a good ration of ground oats and oil-cake meal which
was purchased. About 18 months later the first signs of approaching
Red Water appeared. The bloody urine showed, and a few months later
he died.
The last bull used was also one born on this place. This bull presents a rather interesting study. The first six months of his life, he was
fed as the other calves—on hay, grain and milk—the hay grown here.
He was, however, an animal of outstanding type and of excellent record
backing—(over 800 pounds fat for his three nearest dams and 23,000
pounds milk). All his life he was never allowed to run out. At" first
alfalfa hay was purchased and fed to him after he was six months of age.
He was fed liberally on grain. He received a good allowance of mangels
or ensilage grown here. This was kept up until he was two years old,
and he was fat and sleek, full of life and did well. At two years he was
transferred to a small shed with a yard 20 x 25 feet attached. The
ground here had been previously dug and limed. He was from now on
fed on roughages grown on this farm plus his usual grain ration. Six
months later the prognosis was Red Water. A year or so later the first
Red Water appeared, and in a few months he was dead.
The bulls go quickly after the Red Water first appears.
The cows on this farm were always well fed and cared for, particularly so from the spring of 1924 until the end. They were brushed
daily in the winter. The barn was kept clean and the cows well bedded.
Water was before them in automatic fountains. In the cold weather
(a few weeks) the fountains were shut off and water fed from pails.
This water was warmed. The source of water supply is a spring coming
out of the rock about 2,000 feet up the hill back of the farm. It is
piped down.    The water is soft, cold and pure.
The animals were fed roughage grown on this farm at all times,
with the exception of the winter of 1924-25, when alfalfa hay and some
stra wwas purchased and fed. During this winter no new cases of Red
Water developed and the calves did much better.
During the summer months care was always taken to see that the
cows had ample feed when pastures were short. The silos were never
allowed to become empty. A summer silo of peas and oats was filled in
July and some clover was blown in. This was very good feed and relished by all the stock. Either clover, oats or oats and peas were fed to
supplement this silage. In August and September there was always
ample after grass to carry the stock into winter in grand shape. Usually
a little silage was fed after the middle of September to supplement the
pasture. Grain was always fed in ample quantities to both milking and
dry stock. In fact to many of the Red Water animals, grain in excess
of what normally would be required was fed. This heavy grain feeding
seemed to make no difference to the course of the disease. Quite often, in
fact, some of the diseased cows would refuse their grain for a day or so.
The blood and urine were examined many times for the presence of
bacteria or protozoa. The urine was particularly well examined, both of
apparently normal and diseased cows. No signs of bacteria or of protozoa were at any time in evidence. The possibility of its being a lepto-
spira involving the liver has not been excluded.
Since this was started no haemorrhagic septicemia has appeared. The
Red Water went on as before. This may be excluded by the fact that
after our first losses, all animals were inoculated, the calves ten days
after birth.
Several mineral mixtures were tried. The first consisted of calcium
carbonate, bone-meal, ferrous carbonate and iodized salt. No difference
in the course of the disease was noted. Also a mineral mixture put out
by the Triangle Chemical Company was tried. The cows refused to eat
their grain wth which this was mixed at first. They ate it finally, but
the use of the mixture was discontinued as the stuff smelt like bone-
meal fertilizer and had an offensve taste. A first-class quality of bone-
meal flour was then fed, with a little ground limestone and iodized salt.
No difference was ever noted in the course of the disease.
This was a preparation secured from Dr. Milton of Chilliwack. The
cows were drenched three times daily before feeding in December, 1925,
for 14 days. Eight animals were so treated. In seven cases of young
heifers, the Red Water temporarily disappeared (for about two months).
All animals treated became very sick and went off their feed. When the
disease again appeared similar treatment had no effect on these same
animals. Some milking cows were also treated. It had no effect on the
disease. The cows quit milking, however. Several other farmers in the
neighborhood tried it on mature anmals, but reported that it did not
relieve the cows treated.
It may be well to state here that other iron, lead and arsenical salts
were tried, with no effect on the course of the disease.
Therefore in view of the facts as herein presented—that as time
went on, the land became more intensively cultivated and no new land
was brought under cultivation; that the cows purchased lived for shorter
and shorter periods; that the calves died earlier and earlier in life; that
the severity of the disease increased, we have come to the conclusion that
this type of Red Water is a deficiency disease. We believe that the
liver is involved some time before the appearance of the red urine, which
in our opinion is the terminal point of the disease.
From what has been previously stated it would seem fairly conclusive
that deficiency of some kind must exist, and unless this conference reaches
other conclusions it is respectfully suggested that investigations should
Page 60 be carried out along the following main lines in order that this important
economical problem may be solved:
1. A survey establishing areas involved and losses sustained in at
least ten specific areas.    (Widely distributed areas).
2. An examination of soils in the districts affected.
3. Chemical analysis of water, soils and feed (with special reference to Ca, K, P, Mg, Mn) grown upon the soils in question.
4. Feeding experiments with a sufficient number of cows so that
comparative results may be obtained.
(a) From feed grown on "deficiency" land.
(b) From feed grown on unaffected areas.
(c) From a combination of feed from affected and unaffected areas.
(d) With different kinds of drinking water.
Blood chemistry—Ca, P, K, Cholesterol, Mg, Sugar, NPN.
A series of animals should be taken to the farm and one killed every
four months and sections of the livers taken.
Star—Grade   Holstein.    Purchased   August   as   a   springer.
Case Histories
By John R. McKee, B.A.
late September, 1919—a bull which was vealed.
(a) Calved October, 1921—heifer.
(b) Calved December,  1922—heifer.
She showed signs of red water shortly after her second calving
(November-December, 1921). She gave birth to another calf in December, 1922, and as the Red Water was affecting her production severely,
she was shortly after butchered.
(a) Grade—born October, 1921. Was a mother of bulls throughout her life. She showed signs of Red Water shortly before her second
calving. It cleared up after this calving. Red Water again appeared
just before her next freshening. Never entirely cleared thereafter. Died
October, 1927. P.M.—Liver badly adherent to diaphragm—elongated
downwards—felt tough and leathery. Bladder, usual Red Water type.
Other organs seemed normal.
(b) Star—born December, 1922. Freshened four times with the
following calves:
*(bl)   Heifer—Grade II.—born February, 1925.
*(b2)  Heifer—Little Star—born December, 1925.
Her next calf, born October, 1926, was a monster and in May, 1927,
she aborted.
As a calf she did not thrive well. Was small. Coat always rough.
Calved at 23  months.    Just previous to this first calving she showed
* These dates are correct.    I bred a number of my grade cows when they first came
around in order to have them.freshen sooner for the purpose of balancing my herd.
Page 61 . . . every day
. . . every night!
ClThroughout the year we are always ready
to serve the Physician and his patients.
C^Co-operation with the medical profession
has always been one of the fundamentals
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618 Georgia Street West - Vancouver bloody urine. The urine cleared until three months before next freshening. It never cleared thereafter. The rest of her life she kept going
down hill until she died from Red Water in November, 1927. P.M.—
Liver badly adherent to diaphragm—elongated downwards—felt tough
and leathery. Bladder, usual Red Water type. Other organs seemed
(bl)—Grade II.—born February, 1925. Small unthrifty calf.
Was bred and gave birth to a bull. Showed Red Water previous to calving. Was bred again. Died of Red Water before next calf was born.
No. P.M.
(b2) Little Star-—born December, 1925. Was a small and unthrifty calf. Passed bloody urine at 11 or 12 months. Died before she
was bred ,aged 20 months. P.M.—Liver as usual. Bladder typical.
Other organs seemed normal.
II. Mandy—Grade  Holstein.    Purchased  August,   1919.    Calved  No
vember, 1919, a mother of bulls. Gave birth to one daughter.
Do not know when she first showed signs of Red Water.
Died March, 1925. P.M.—Liver very badly adherent to diaphragm and spleen. Seemed to be general adhesions all around
the liver, which was elongated and tough. Bladder very badly
ulcerated and hard.
(a) Little Mandy. Born April, 1924. Grew fairly well. Was
fed purchased hay in the summer of 1924 as our own had run out.
Was not allowed out of the barn. Fed purchased alfalfa winter of
1924-25 plus roots and ensilage grown on the place. Thrived well. Was
turned out with the herd to pasture in the spring of 1925. Became unthrifty by the summer. Was bred in the fall of 1925. Did not grow
much the winter of 1925-26. It was observed that she looked very
poorly when put in the barn in the fall of 1925. She showed a muddi-
ness of eye and looked yellow. Told my brother she would develop Red
Water before the winter was out. In March, 1925, she passed bloody
urine. Calved July, 1926. Died end of August, 1926. P.M.—As
III. Hejelkje Rooker—Purebred   Holstein.    Purchased  February,   1920.
Calved June,   1920—bull—(a)   Fernhill Rooker Posch.
Aborted, 1921 and 1922.
Calved March, 1924—heifer (b) Fernhill Hejelkje Korndyke.
Calved March, 1925—heifer  (c) not registered.
This cow first showed Red Water in the spring of 1923. Usual
development.    Died September, 1925.    P.M.—As usual.
(a) Bull—Fernhill Rooker Posch, born June, 1920. Raised to a
yearling. Sold to a lowland farm. Repurchased at 2 years of age for
service in our herd. Noticed him rather rough looking in the spring of
1924. Red Water appeared in June, 1924. Died September, 1924.
No P.M.
Page 62 (b) Heifer—Fernhill Hejelkje Korndyke, born March, 1924. Never
thrived. Was rough looking. Seemed yellow. Was so small she was
not bred at the usual time. In April, 1926, showed bloody urine. Met
with an accident and was destroyed. P.M.—Liver not adherent. Was
tough and leathery to the touch.    Bladder showed ulcers.
(c) Heifer calf—not registered, born March, 1925. Very small
and weedy looking. Never grew much. Looked sick and jaundiced
all the time. Eye not clear and bright. Showed Red Water in August,
1925 at 6 months of age. Cleared. Sold her cheap to farmer on Sutnas
Prairie. (He know she had Red Water). She died of Red Water on
his place sometime in summer of 1926.
IV. Countess Canary  Mercedes—Pure-bred  Holstein.    Purchased  Sep
tember,   1920.    Aborted   and   again   aborted.    Calved   April,
1923—twin heifers.
(a) Fernhill Canary Segis  (twin), born April, 1923.
(b) Fernhill Canary Segis Girl (twin), born April, 1923.
This cow showed Red Water just previous to this calving in April,
1923.    She died in August, 1924.
P.M.—Liver badly adherent—bladder as usual.
(a) Fernhill Canary Segis (twin), born April, 1923. This animal
was a mother of bulls and aborted. She had one daughter, (a) not registered. Born June, 1925. The heifer showed Red Water just before her
first calving in June, 1925. From then on she passed bloody urine.
She lived until August, 1927, when she aborted. Her Red Water then
became so severe that I shot her.    P.M.—As usual.
(al) Heifer calf—unregistered. Born June, 1925. Small, but did
not do badly. Coat fairly rough. Was fed purchased alfalfa hay
as a calf. Sold her at 23 months to a farmer on Sumas Prairie.
She never, to my knowledge, passed bloody urine. She looked to me,
however, as if she was going down with Red Water. Later her coat
became harsh and dry, unhealthy looking yellow pigmentation appearing
and eye becoming muddy looking. I am watching her at her new home.
She has been there now for 3 months. Her present owner informed me
(February 23, 1928) that she was picking up and looking fine, no signs
of Red Water.
(b) Fernhill Canary Segis Girl (twin), born April, 1923. She was
a mother of bulls. Did not thrive very well as a calf. Did
not breed her until nearly three years old. She showed Red Water when
just over two years of age. Never cleared. She calved in February,
1926. She did not milk very much. She was killed in May, 1926 for
examination. P.M.—The liver was not adherent. Was not of normal
color. Felt tough and leathery. Section of the liver showed gross inflammation and destruction.     (Round cell infiltration).
V. Colantha   Walker  Beauty—Pure-bred  Hblstein,purchased   August,
Calved October, 1922—heifer, (a) Fernhill Colantha Walker.
Page 6} Calved February, 1924—heifer, (b) not registered.
Calved February, 1925—heifer, (c) not registered.
Calved February, 1926—bull, stillborn.
This was a big heavy producing cow with a very strong constitution.
She had great depth and heart. She milked well during her first lactation. .
In the fall of 1924 it was noticed that she seemed unwell. Made a
close examination. Cow appeared jaundiced. Was off feed. Eye seemed muddy. She dropped from 40 pounds of milk a day down to 17-18
pounds of milk a day in about 6 weeks. Recovered from her illness and
got on feed again.    Did not milk well again, 15-16 pounds daily.
She calved again in February, 1925. Did not milk well, only 45
pounds when fresh—dropped in 3 months to 30 pounds. Red Water
appeared in the summer of 1925. She seemed to throw it off. Did not
milk well,, even on good grass.
She calved again February, 1926, and was never bred again. Red
Water became worse. She did not milk at all well, only 37 pounds at
freshening and did not come up in the spring on good grass. She kept
her flesh well, but was fed very heavily on grain. She dropped, in spite
of good grass to about 25 pounds daily and gradually dried off. She was
kept to see what would happen. Fed heavily on grain, but she kept getting worse and worse, until in fall of 1927 she was sold to the butcher
for her hide.    No. P.M.
(a) Fernhill Colantha Walker, born October, 1922. Did not thrive
well as a calf. Was bred late. Calved February, 1925 (a bull which
was vealed). Milked very poorly. Was very thin and could barely
stagger around. Recovered slightly but was not bred again. Died June,
1926.    P.M.—As usual.    Very severe liver adhesions.
(b) Heifer calf—unregistered. Born February, 1924. Was small
and unthrifty. No Red Water. Sold January, 1926. Is still alive and
doing well.
(c) Heifer calf—unregistered. Born February, 1925. Did not
grow well. Small and unthrifty. Looked jaundiced and eye seemed
muddy. Passed bloody urine in August, 1925. Cleared. Was sold
January, 1926. Die dof Red Water later in year. (The owner does
not remember the date of her death. She had Red Water, he knew, and
he took a chance).
VI.    Nikomekl  Butter   Girl—pure-bred   Holstein.    Purchased   August,
Calved October, 1922, bull.    Died of haemorrhagic septicemia.
Calved November, 1923, bull, Fernhill Douglas Seg/s.
Calved February, 1925, twin heifers  (sold as calves).
All other calves bulls and vealed.
She milked well during her first lactation. After she again freshened,   she  soon  became   poor  and   rough.    Afterwards   milked   poorly
Page 64 always.    In the fall of 1924, she first passed bloody urine.    She became
steadily worse and died August, 1927.    P.M.—As usual.
(a) Bull—Fernhill Douglas Segis, born November, 1923. Did
poorly as a calf. The in spring of 1924 I started feeding him purchased
alfalfa and lots of grain. Also he was fed roots and ensilage grown on
the place. This feeding was continued until he was 2 years old. He
was never out of the barn till then. He was fat and sleek, full of life,
a beautiful animal in every way. In the fall of 1925 I put him in a
pen with a small yard 20 ft. by 25 ft which I dug and limed. From
then on I fed him home grown feed entirely. In 6 months he lost his
sleekness; his coat became rough and dry; his skin tough and his eye
muddy. He grew quite a bit, however. He was fed 10 pounds of grain
a day, 30 pounds of roots—i nsummer about 25 pounds of ensilage
instead of roots. All the hay he could eat was given him. He began
to get mean and I had his horns cut off in the spring of 1927. H ebe-
came dangerously mean. I watched closely, suspecting Red Water some
time previously. In September, 1927, he passed bloody urine. He died
in November, 1927, just four years of age.    No P.M.
VII.    Colony Girl Newman—Pure-bred Holstein, purchased  1924.
Calved June, 1924—heifer (a) Fernhilb Aggie De Kol.
Calved April, 1925—heifer (b) Fernhill Posch Newman.
Calved April,  1926 and 1927, bulls—vealed.
This cow did extremely well her first lactation. Milked over 90
pounds a day part of the time—tested 3.4 (on R.O.P.) She calved again
in April, 1925. She did well at first, but in about 3 months she dropped
very materially. Her coat became a little rough. She calved again in
April, 1926. She did not do very well—only 55 pounds when fresh.
In a few months (on clover pasture up to her belly) she dropped to about
20 pounds daily. She looked unwell. Her eye was not clear. (She was
a black cow and it was difficult to be sure of her skin pigmentation).
The prognosis was for Red Water. She calved again in April, 1927.
She passed bloody urine in May, 1927. She was sold in November,
1927 to a farmer on Sumas Prairie who was gambling on a calf from
her. She calved in March, 1928, and is going down hill. Calf is doing
(a) Fernhill Aggie De Kol, bom June, 1924. Did fairly well as
a calf. Was fed purchased alfalfa hay the first winter, and came on
well. She was bred. Went to pasture with the herd the summer of
1925 and that winter was fed a home grown ration plus purchased
grain. She did not do well. She showed Red Water just previous to
calving in July, 1926. She developed a tumor in her udder and was
butchered.    P.M.—Liver tough—not adherent.    Ulcers on bladder.
(b) Fernhill Posch Newman, born April, 1925. She never did well
as a calf—coat and other symptoms as usual. Red Water appeared in
August, 1926. Cleared. Did not breed as she was small. In February, 1927, Red Water again appeared and gradually became more
severe. She died in September, 1927. P.M.—Liver adherent to diaphragm.
Bladder badly ulcerated.
Page 65 VIII. Teussie Victoria Echo 2nd—Pure-bred Holstein, purchased September, 1924.
Calved October, 1924, heifer (a) Fernhill Victoria Ormsby.
Calved September, 1925, bull—vealed.
Calved September, 1926, heifer  (b)   unregistered.
Calved July, 1927, heifer (sold).
Did fairly well until December, 1926, when she dropped in her
milk. She became rough and unthrifty looking. In October, 1927, she
looked jaundiced and her eye became muddy. She passed bloody urine
in December, 1927. She is still alive but the disease is very severe—
clotting is already apparent and she is rapidly losing ground. She eats
dirt whenever let out of the barn (February, 1928). She died in August, 1928.    P.M.—Liver not adherent, though tough and thickened.
(a) Fernhill Victoria Ormsby, born October, 1924. Her history
is the same as that of the others. She showed Red Water at about a year.
Gradually became worse. Was bred. Calved February, 1927, and died
of Red Water in April, 1927.    P.M.—As usual.
(b) Heifer calf—unregistered. Born September, 1926. Was very
poor and unthrifty. All signs of Red Water from 3 months of age.
Passed bloody urine at 6 months. Died of Red Water November, 1927.
P.M.—As usual.
IX. Thorndale Creamo Posch—purchased October, 1924.
Calved December, 1924—bull, vealed.
Calved December, 1925—heifer (a)  unregistered.
Calved November, 1926—heifer  (b)   unregistered.
Calved September, 1927—heifer (sold).
Usual course. Was sold to a man on Sumas Prairie who is gambling
on a calf.    Is still alive but passing bloody urine.*
(a) Heifer calf—sold at 2 years. No Red Water but has shown
all preliminary signs.    Is doing well now and is under observation.
(b) Heifer calf, born November, 1926. Very poor and unthrifty—
ill all the time—eye muddy. Red Water appeared at 5 months. Died
September, 1927. P.M.—Liver not adherent. Was tough and very
hard.    Not a good color.
X. Etta Banostine Canary—pure-bred Holstein, purchased September,
(a) Freshened October 15, 1924—heifer.
(b) Freshened October,  1925—bull—vealed.
(c) Freshened November,  1926—bull—vealed.
This cow was never a good milker and was very particular as to her
food, though not a good feeder. She wa snot bred after her calving
in 1926 and did not show signs of Red Water until spring of 1928.
In August she first passed blood and was killed September, 1928 .
* Has died since this report was written.
Page 66 (a) Fernhill Banostine McKmley. Born October 15th, 1924.
Grew slowly and never attained full size. When fully matured was
smaller than her mother. She was bred and gave birth to a heifer calf
(al) September 7th, 1927. This heifer (a) was a much heavier milker
than her dam but was not bred again. She showed early symptoms in
the spring of 1928 and passed Red Water first August, 1928, about the
same time as her dam and was killed September, 1928.
(a) Fernhill Banostine Segis. This calf was fed on purchased hay
and grain until sold in March, 1928. She grew rapidly and gives every
promise of being a fine animal.
XI. Ormsby Queen Colantha. Purchased Holstein. Purchased September, 1924. Half sister of No. X. and No. VIII. Very heavy milker
and fine dairy cow. Died of Red Water October 19th, 1927. She was
a mother of bulls and is only put in here for purposes of comparison
with her half sisters Etta Banostine Canary and Teussie Victoria Echo
2nd, the three animals being purchased and brought to the farm at the
same time.
Pathological Reports
from the Pathological Department, Vancouver General Hospital.
March 28,  1928.
S-27-743, 744—Cow's Spleen and Liver.
(Cow born on farm out of a mother with Red Water).
Macroscopical Examination: . Specimen consists of a portion of
liver, on one surface of whch is a rather dense, hyaline-appearing structure which grossly has the appearance of a portion of cyst wall. A
small portion of what is evidently spleen, is also present. There is
otherwise nothng particularly remarkable about the specimen.
Microscopical Examination: A number of sectons were taken
through the spleen and liver and in the former beyond a moderate
degree of congestion and some slight increase in the fibrous connective
tissue trabeculae, nothing of note is apparent. The liver, however, shows
many areas of dense hyaline fibrosis which is not at all of the scirrhous
type but is of a diffuse type which completely destroys any growth of
liver cells in these particular parts. Many capillary channels are present in these areas and diffuse small round and plasma cell infiltration.
Although these plasma cells are not well defined nor typical, it is possible
that these may be degenerated hepatic cell nuclei. In these fibrous
areas, scattered canalicular structures are seen which are probably bile
ducts. Throughout the less fibrotic liver tissue, very extreme congestion is seen, with atrophy of liver cells, leaving vacuolated spaces where
they formerly were, giving the appearance somewhat of a fatty infiltration, but it is the former, i.e., cyanotic atrophy due to passive venous congestion. In the portal spaces there is some increase in the fibrous
connective tissue but no special inflammatory cell infiltration. There is
nothing of a specific nature in any of the sections examined and it is
probably a process that in the liver at least, has its port of entry in the
portal spaces, but through which component part of the portal spaces—
bile, duct, artery or vein—is a question.
Page 67 S-28-2350—Portions of Cow's Liver.
Shows little of note grossly.
Microscopical Examination: A number of sections were taken
through the different areas and these show the central veins to be
filled with a pinkish-staining material, homogeneous for the most
part. There seems to be increased fibrosis in the portal spaces, with a
moderate small round cell infiltration, and moderate congestion throughout the parenchyma. Subcapsularly, layers of liver cells are seen which
have a rather vacuolated appearance somewhat resembling a fatty degeneration, but one cannot say definitely that it is such. Otherwise,
little of note is apparent.
H. H. Pitts, M.D.
As we had no more cattle to kill we turned to guinea pigs as a
possible experimental animal to use in feeding tests. If they responded
in any like way in the nature of similar liver changes, a less expensive
and more rapid method of investigation was hoped for.
In May, 1928, half our breeding stock of guinea pigs was taken
from Vancouver to the farm. It may be said here that those left in
Vancouver did as well as usual.
In July it was noticed that the animals at the farm were not thriving, although given all the fresh clover and carrots they could eat. All
the young born up to this time lived, but after the middle of July all
young were killed and eaten by the older animals. From this date until
October, a guinea pig from the farm was brought down every couple of
weeks, killed and sections made of the liver, with the general picture
given in the autopsy findings appended. About the middle of October
the animals began to die off and the remainder were brought back to
Vancouver. Of those so dying, the ones showing most degeneration of
the liver were born on the farm.
Some of the guinea pigs brought back were put in a cage in which
there were some newly born animals from those never out of the city.
These young were promptly killed and eaten by the farm animals, but
after a few days on the hay, etc., used for our normal feeding, no further deaths occurred and no more eating of the young. In fact some
young have been born amongst the animals brought in from the farm
and they are growing normally.
Further feeding experiments as well as blood and tissue chemistry
work are in course of preparation now.
Pathological Reports: Numerous examinations have been made
by Dr. H. H. Pitts, of the Pathological Department of the Vancouver
General Hospital, of the livers of these guinea pigs. A typical
reports says "the liver cells stand out rather clearly as far as their
borders are concerned as a rather reticulated network in the centre of
Page 68 which well formed nuclei are seen. The protoplasm is, however, not
so well preserved and shows quite extensive vacuolation, probably a fatty
change. The central veins are not particularly congested and there is no
evidence of any inflammatory infiltration in the portal spaces or elsewhere."     (S-28-2309).
On one guinea pig's liver (a guinea pig born on the farm) the
report says "there seems to be more of a definite fatty-appearing infiltration so vacuolated as to give the cells a crescentric appearance or so
called "signet ring" morphology. Extensive passive venous congestion
is also apparent."
NOTE:—The writers wish to thank Prof.  P.  A.   Boving for his constant aid in the
many changes they made in their feeding methods.
Report on the "Second International Congress of Radiology"
Stockholm, 1928.
Dr. C. W. Prowd
The Second International Congress of Radiology was held in Stockholm, Sweden, in July, 1928. The first held in London three years previously paved the way and, in a measure, set the pace for the Stockholm
meeting. Thes recent congress was largely attended and gathered together over twelve hundred delegates from all parts of the world. The
papers were read in one of three official languages—German, French or
English—the Swedes, with characteristic generosity, relegating their
own language to the background. The German group was the largest,
Russia second with France, British Isles and Italy well represented. More
than one hundred registered from the United States of America. One
cannot speak too highly of the splendid organization and complete arrangements. The President, Dr. Gosta Forssell of Stockholm, and his
committee, reflected the Swedish efficiency and hospitality everywhere
One must note particularly the thoroughness and care with which
the Information Bureau handled what at times approached a miniature
"Tower of Babel," presided over by a score of Swedish women and girls,
equally at ease in any language. Charming in manner and appearance
they won the favor and plaudits of all present—not excepting your two
representatives from Vancouver.
Every phase of Radiology—technical, diagnostic and therapeutic
received its share of papers and discussion. The many problems of diagnostic procedure and interpretation were crystallized in world opinion.
International standardization in radium and x-ray therapeutics were
brought definitely nearer. The papers, proceedings and resolutions of
the congress will be published in two special volumes of "Acta Radio-
logica" soon off the press.
Two resolutions of outstanding importance were adopted by the
Stockholm Congress. One, standardized protective measures for x-ray
and radium workers, the other defined an international unit of measurement for radiation dosage.
Page 69 The necessity of increased protection and improved working conditions for x-ray and radium operators in all countries is recognized.
The Continent is in advance of America in these measures. The hospital
space and room arrangement, also the measure of protection in x-ray
equipment is in many cases in striking contrast to our limited space
and conditions of work.
Standardization of x-ray dosage and an international measuring
unit will make duplication of treatment and comparison of results more
accurate and simple.
Continental hospitals and clinics, as a rule, devote much space,
equipment and personnel to their x-ray and radium departments and
there is a keen appreciation of the growing importance and necessity of
their diagnostic and therapeutic measures.
The comprehensive report and demonstration by Dr. Gosta Forssell
and his associates on "Therapeutic methods and results at Radium-
hemmet" was one of the best offered. Over one hundred cases were
presented. The history, method of treatment and result was given in
each case. The cancer groups considered most favorable are cutaneous
cancer, cancer of the lip, cancer of the oral cavity, cancer of the uterus
and sarcoma.
The following summary is of interest:
"Of a total of applicants of 207 cases of cancer of the skin of the
face from the years 1910-1915, inclusive, 142 have remained healed,
which means a percentage of absolute cure of 68 per cent. If, however,
we count only technically operable cases, the figure for relative cure is
78 per cent.
In lip cancer we have obtained a permanent healing in 45 cases of
a total number of applicants of 66, that is in 68 per cent, of the cases.
For the operable cases the percentage of relative cure was 86.
In cancer, of the mouth we have got a five years' healing in 71
cases of 113, that is a figure of relative cure of 62 per cent, of all cases
radiologically treated.
In cancer of the uterine cervix our absolute healing figure is 22.4
per cent, by a total number of applicants of 500.
Of 145 operable and border-line cases 67 have obtained a five years'
healing, corresponding to a relative cure of 46.2 per cent.
In 234 inoperable cases of cervix cancer five years' healing is reached
in 16.7 per cent, of the cases treated.
In cancer of the uterine body the figure of absolute healing is 43.5
per cent. (20 out of 46 cases), and the relative performance 60%, or
a 5 years' healing in 15 of 25 operable cases.
Of the total of 543 cases of sarcoma treated at the "Radiumhemmet"
during the period 1910-1922, 181, or one-third were free from symptoms when reexamined in 1925. Of the 238 primary tumors treated by
radiotherapy only 58, 24 per cent., have remained free from symptoms.
Page 70 I will also mention that the results of our comparison between the
final achievements of surgery and radiotherapy as regards the treatment
of malignant tumors is as follows:
In those types of tumour that offer a fair chance of obtaining a primary healing by radiological treatment, the duration of the healing obtained by radiotherapy is, both as regards the relative and the absolute
performance, in every way comparable to the results obtained by surgery.
When primary healing—immediate freedom from symptoms—has
once been secured by radiotherapy, the percentage of recurrences in most
of those forms of tumour is lower than after primary surgical healing,
and in none of the groups comprised in this inquiry is it higher than the
percentage of recurrences following radical operation.
The duration of the period of latency is very much the same for
recurrences after radiological treatment as for recurrences after radical
operation. Most of the recurrences occur during the first and second
years after primary healing, the majority of them during the first year.
After the third year there are only scattered instances of recurrence.
After the fifth year they are rare; still, cases have occurred as late
as in the eight and ninth years. After the ninth year our material does
not show any recurrence.
In radiotherapy of tumours the palliative effect plays at least as important a part as the curative effect.
Our system of after-observation gets its strongest support from the
fact that the Government, in conformity with a decision of the Swedish Parliament, defrays the travelling expenses of all poor patients to
and from the hospital. This makes the maintenance of a personal observation and control possible in most instances. With a few exceptions
we have been able to keep constant track of all our cases for the last
fifteen years."
The Third International Congress of Radiology meets in Paris in
1931. Those who contemplate the Paris Congress would do well to
include Northern Europe and especially Scandinavian countries in the
itinerary, both from a scientific and recreational point of view.
.Page 71 128
Total  Population   (Estimated)    ,  142,150
Asiatic   Population   (Estimated)      10,940
Rate per  1000  of Population
Total   Deaths   	
Asiatic   Deaths   ^  -	
Deaths—Residents only  	
Male        180
Female    181
Stillbirths—not included* in above 	
Deaths under one year of age 	
Death   rate   per   1,000   Births	
November 1st
Scarlet Fever  	
Scarlet  Fever 	
Typhoid  Fever
iber, 1928
r, 1928
to 15th
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Page 72 Ii
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