History of Nursing in Pacific Canada

The Vancouver Medical Association Bulletin: July, 1954 Vancouver Medical Association Jul 31, 1954

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 T H E
BULLETIN
OF
The Vancouver Medical Association
EDITOR
dr. j. h. MacDermot
EDITORIAL BOARD
DR.  E.  F.  CHRISTOPHERSON
DR.   H.  A.  DesBRISAY
Publisher and Advertising Manager
W. E. G. MACDONALD
DR.   J.   H.  B.   GRANT
Dr. j. l. McMillan
VOLUME XXX.
JULY, 1954
NUMBER 10
Dr. J. Howard Black
President
OFFICERS 1954-55
Dr. F. S. Hobbs
Vice-President
Dr. D. S. Munroe
Past President
Dr. R. A. Gilchrist
Hon. Treasurer
i Dr. G. E. Langley
Hon. Secretary
Additional Members of Executive:
Dr. A. F. Hardyment Dr. Paul Jackson
TRUSTEES
Dr. G. H. Clement Dr. Murray Blair Dr. W. J. Dorrance
Auditor: R. H. N.  Whiting, Chartered Accountant
SECTIONS
Eye, Ear, Nose and Throat
Dr. W. Ronald Taylor Chairman Dr. R. S. Grimmett Secretary
Paediatric
Dr. E. S. James Chairman Dr. G. R. Gayman Secretary
Orthopaedic and Traumatic Surgery
Dr. W. H. Fahrni Chairman Dr. J. W. Sparkes... Secretary
Neurology and Psychiatry
Dr. T.  G. B. Caunt.
.Chairman
^
Dr. J. R. Wilson Secretary
Radiology
Dr. H. H. Brooke Chairman Dr. S. Miller Secretary
STANDING COMMITTEES
Library
Dr. R. J. Cowan, Chairman; Dr. W. F. Bie, Secretary; Dr. D. W. Moffat ;
Dr. C. E. G. Gould; Dr. W. C. Gibson; Dr, M. D. Toung.
Summer School
Dr. Max Frost, Chairman: Dr. E. A. Jones. Secretary; Dr. S. L. Williams;
Dr. J. A. Elliot ; Dr. Robert Goublay ; Dr. G. C. Walsh
Medical Economics
Dr. E. A. Jones, Chairman; Dr. W. Fowler, Dr. F. W. Hurlburt, Dr. R. Langston,
Dr. Robert Stanley, Dr. Charles Battle, Dr. S. Kaplan
Credentials
Dr. J. C. Grimson, Dr. E. O. McCoy, Dr. D. S. Munroe
V.O.N. Advisory Committee
Dr. D. M. Whitelaw, Dr. R. Whitman, Dr. R. A. Stanley
Representative to the Vancouver Board of Trade (Health Committee) : Dr. F. S. Hobbs
Representative to the Greater Vancouver Health League: Dr. F. S. Hobbs
Published   monthly   at  Vancouver,   Canada.     Authorized   as   second   class  mail,   Post   Office  Department,
Ottawa, Ont.
Page 389 For the Peptic Ulcer Patient
BEDEVILED BY NIGHT PAIN
AMPHOJEL
ALUMINUM   HYDROXIDE  GEL
AMPHOJEL helps patients sleep by neutralizing acid promptly . . .
promoting pain relief through the night. A double dose at bedtime
will effectively control "night pain" in most patients.
AMPHOJEL is a double gel—one reactive, for immediate buffering of gastric
acid; the other, demulcent, for prolonged coating of the gastric mucosa—
protection for the granulation tissue in the ulcer crater.
»il <Ti__t
Available: Amphojel Plain—Bottles of 12 fl. ozs. and 1 Imp. Gal.
Amphojel Unflavoured—Bottles of 12 fl. ozs.
Amphojel with Magnesium Trisilicate—
Bottles of 12 fl. ozs.
Amphojel with Mineral Oil—Bottles of 12 fl. ozs. and
1 Imp. Gal.
Amphojel Tablets—Bottles of 50 and 500
Page 390 HOSPITAL CLINICS
VANCOUVER  GENERAL  HOSPITAL
Regular Weekly Fixtures in the Lecture Hall
Monday, 8:00 a.m.—Orthopaedic Clinic.
Monday, 12:15 p.m.—Surgical Clinic.
Tuesday—9:00 a.m.—Obstetrics and Gynaecology Conference.
Wednesday, 9:00 a.m.—Clinicopathological Conference.
Thursday, 9:00 a.m.—Medical Clinic.
12:00 noon—Clinicopathological Conference on Newborns.
Friday, 9:00 a.m.—Paediatric Clinic.
Saturday,  9:00 a.m.—Neurosurgery Clinic.
ST. PAUL'S   HOSPITAL
Regular Weekly Fixtures
2nd Monday of each month—2 p.m - Tumour Clinic
Tuesday—9-10 a.m Paediatric Conference
Wednesday—9-10 a.m :„ - Medical Clinic
Wednesday—11-12 a.m 1 Obstetrics and Gynaecology Clinic
Alternate Wednesdays—12 noon Orthopaedic Clinic
Alernate Thursdays—11 a.m Pathological Conference (Specimens and Discussion)
Friday—8  a.m Clinico-Pathological Conference
(Alternating with Surgery)
Alternate Fridays—8 a.m . Surgical Conference
Friday—9 a.m Dr. Appleby's Surgery Clinic
Friday—11 a.m Interesting Films Shown in X-ray Department
SHAUGHNESSY  HOSPITAL
Regular Weekly Fixtures ^r
Tuesday, 8:30 a.m.—Dermatology. Monday, 11:00 a.m.—Psychiatry.
Wednesday, 10:45 a.m.—General Medicine. ^     Friday, 8:30 a.m.—Chest Conference.
Wednesday, 12:30 p.m.—Pathology. Friday, 1:15 p.m.—Surgery.
BRITISH  COLUMBIA  CANCER  INSTITUTE
2656 Heather Street
Vancouver 9, B.C.
SCHEDULE OF CLINICS—1953
MONDAY—9:00 a.m.-10:00 a.m.—Nose and Throat Clinic.
TUESDAY—9:00 a.m.-10:00 a.m.—Clinical Meeting.
10:30-12:00 noon—Lymphoma Clinic.
THURSDAY—11:00 a.m.-12:00 noon—Gynaecological Clinic.
DAILY—11:45 a.m.-12:45 p.m.—Therapy Conference.
Page 391 m pregnancy |jj
a new comprehensive
formula
for optimal nutritive
support
PRENGRAN
Squibb Vitamin Mineral Supplement
Prengran  is  the   new,   comprehensive  Squibb   Vitamin
Mineral Supplement which offers protective amounts of ^
vitamins and minerals considered useful in a dietary supplement for expectant mothers. Dosage: 1 capsule t.i.d.
Supply: Bottles of 100 and 500 capsules.
1 Capsule t.i.d.
The Prengran formula:
supplies:
Vitamin A                       *_&
6,000 I.U.
Vitamin D
800 I.U.
Menadione (vitamin K analog)
0.3 mg.
Thiamine Mononitrate
3 mg.
Riboflavin
3 mg.
Pyridoxine Hydrochloride
1 mg.
Niacinamide
15 mg.
Panthenol
5 mg.
Vitamin B& activity
10 mcgm.
Folic Acid
2 mg.
Ascorbic Acid
100 mg.
Calcium (elemental)
459 mg.
(as dicalcium phosphate)
Phosphorus (elemental)
354 mg.
Desiccated Liver
300 mg.
Iron (elemental)
15 mg.
(equiv. to ferrous sulfate, exsic.)
51 mg.
PRENGRAN is a registered trademark of E. R. Squibb & Sons of Canada, Limited,
2245 Viau Street, Montreal
Squibb
Page 392 Some years ago the medical profession of British Columbia made history by inaugurating what has now become the Medical Services Association, M.S.A. for short.
It is worthwhile to recall the fact that this plan was originally devised, sponsored and
underwritten entirely by the medical profession, a small group of members actually
guaranteeing the scheme financially.
The rest is history. The scheme was well and soundly planned, and has become a
major industry in British Columbia, and has been of great benefit to all concerned,
doctors, employed persons, and employers of labour. But, under the terms of its charter,
its operations are limited in several ways, and to make changes in its regulations would
by now be almost impossible.
Accordingly, a new scheme is now on foot, the Medical Services Institute, which,
it is hoped, will fill the gaps and supply the needs which are left unsatisfied by the
M.S.A. This M.S.I., as it is called for short, will do three things. It will take in
employees in industry who are not covered by M.S.A. The latter cannot insure groups
of less than ten individuals. M.S.I, will take from one to nine. This alone will open a
very big field for the new plan in which to operate.  This group will get M.S.A. coverage.
Next, it will take over those who for various reasons are dropped from M.S.A.,
by cessation of work and so on, and so enable people who have come to value the prepaid plan idea, and depend on it, to continue membership in a prepaid plan.
With regard to this group, and to certain other groups, the M.S.I, will at first
give only partial coverage, i.e., illness requiring hospital care, since this will make it
considerably cheaper.   Full coverage  (i.e., house and office calls)  will not be given at'
first, though as the plan develops and it is appreciably feasible, these will be added.
Its third function will be to look after members of other Canadian prepaid plans
who have come to B.C. Here again, coverage will at first be limited, and will be more
like the coverage these other plans give.
Undoubtedly, M.S.I, will, either now or later, be available by the individual family
or unit.   Just how this will be worked out is a matter for arrangement.
Here again, the medical profession is asked, as a group, to underwrite this plan.
The B.C. Division has advanced $10,000 towards the initial steps to be taken. As
happened before, the money is put up by th_ medical profession, and we assume the risk,
if any, of failure, though this is not seriously contemplated. Since we, as a profession,
are assuming the risk, we, as a profession, are in complete control at the outset, and the
Board of Directors is predominantly medical, as M.S.A. was at first.
Every medical man in the Province is asked to participate in this scheme, and so far
nearly a thousand men have declared their willingness to do so. In order to
conform with the regulations laid down by the Commissioner of Insurance, from 75 to
80% of the practising profession must so sign. As soon as this is done, the scheme will
start full operations.  We hope that ^those who have delayed signing will delay no longer.
This is no untried scheme. Apart from the long and arduous hours of planning
and preparation, by our best minds, that this has entailed, the history of M.S.A. and
indeed of all prepaid plans throughout Canada, is an assurance that M.S.I., too, will be
a success. It will fill a definite need, it will help to ensure the best of medical care to a
great many people, it will hasten the day when prepaid medical care will be jtvailable
to all, and it will represent a very great contribution by the medical profession to the
improvement of health conditions in British Columbia.
We have repeatedly endorsed this sort of prepaid health care. We know its value,
not only to ourselves, but even more to those who are beneficiaries. It is up to each one
of us to do his or her share, and right now this is best done by signing the agreement
to participate in the plan.
Page 395 SUMMER LIBRARY HOURS
Monday to Friday SSll - 9:00 a.m. to 5:00 p.m.
Saturday   9:00 a.m. to  1:00 p.m.
Recent Accessions
Surgical Practice of the Lahey Clinic by the Staff Members of the Clinic, 1951.
Child Psychiatry by Leo Kanner, 1953.
Resuscitation of the Newborn by J. D. Russ, 1953.
Connective Tissue edited by Charles Ragon—Transactions of  the Third and Fourth
Conferences, 1952 and 1953.
Sterility by Walter W. Williams, 1953.
Official History of the Canadian Medical Services, 1939-45, edited by Wm. R. Feasby.
The Unique Influence of Johns Hopkins University on American Medicine by R. H.
Shyrock, 1953. Sill
Prospects in Psychiatric Research by J. M. Tanner, 1953.
British Medical Practice and Science by G. F. Petrie, 1953.
Vesalius on the Human Brain by Charles Singer, 1952.
Emotional Factors in Skin Disease by Eric Wittkower and Russell Brian, 1953.
Transactions of the American Proctologic Society, 1953.
Fanconi and Wallgren's Textbook of Pediatrics edited by W. R. F. Collis, 1952.        i
A Surgeon's Life by Ferdinand Sauerbruch, 1953.
Reconstruction Surgery and Traumatology edited by Max Lange, 1953.
Pediatric Clinics of North America, Symposium on Clinical Advances in Poliomyelitis,
May, 1954.
The British Medical Directory v. I and II, 1954.
Forensic Psychiatry by Henry A. Davidson, 1952.
Surgical Clinics of North America, New Technique in Surgery, April, 1954.
Medical Clinics of North America, New Technique in Surgery, April, 1954.
Medical Clinics of North America, Differential Diagnosis of Internal Diseases, May, 1954.
The Management of Abdominal Operations, edited by Rodney Maingot, 1953, second
edition.
Ulcerative Colitis by Bryan N. Brooke, 1954.
Peripheral  Nerve Injuries,  Principles  of  Diagnosis  by  Webb  Haymaker  and  Barnes
Woodhall, 1953.
Principles of Refraction by S. J. Beach, 1952.
Cardiovascular Surgery by Gerald H. Pratt, 1954.
Rudolph Virchow, Doctor, Statesman and Anthropologist, by Edwin H. Ackerknecht,
1953.
Epilepsy and the Functional Anatomy of the Human Brain by Wilder Penfield and
Herbert Jasper, 1954.
Pediatric Gynecology by G. C. Schauffler, third edition, 1953.
Page 396 VANCOUVER MEDICAL ASSOCIATION
LIBRARY RULES
1. Journals are not to be taken away from the Library until one month following date
received or until the copy is no longer current.
2. Books and journals are loaned out for a period of fourteen days.
3. It is imperative that members sign for each book or journal | borrowed from the
Library in the book provided for that purpose on the counter, and also enter each
book and journal on their return.
4. No member shall loan a borrowed book or journal to another member.
5. Members are asked not to replace volumes on the shelves.
6. Members failing to return books or journals within two weeks will be notified by
theXibrarians that the time limit has expired. If the book or publication in question
is riot returned within a reasonable period of time, the Library Committee will send
a bill covering the price of the missing volume. If this is not paid, the matter will
be referred to the Executive Committee of the Vancouver Medical Association.
7. Members are expected to pay for the replacement of lost volumes or periodicals.
8. The Librarians are authorized to refuse to loan any old books or journals which are
out of print, and certain designated books which are in constant use for reference in
the Library.
Approved Seniorships are still available at St. Paul's Hospital, Vancouver, B.C., in
Surgery, Medicine and Obstetrics & Gynaeology. Physicians interested should apply to
the Interne Committee, St. Paul's Hospital.
^
pf        FOR SALE
Office Equipment of Modern Medical Office
Phone PA. 1053
DESIRABLE OFFICE FOR RENT
In a medical building located on Broadway west—central—close to
V.M.A. Library. Furnished or unfurnished consulting room, examining
room. Shares waiting room and business office with an Internist.
Bright, clean, attractive. Rent reasonable. Information if interested
—Phone CEdar 4188.
Page 397 ACUTE STAPHYLOCOCCUS ENTERITIS
By DRS. B. B. MOSCOVICH and W. H. CHASE
A problem of considerable importance in the chemotherapy of infectious diseases
has been the development and dissemination of resistant strains of bacteria. In this
respect, the Micrococcus pyogenes (staphylococcus) has acquired considerable and
increasing prominence in the medical literature. It is the purpose of this paper to bring
special attention to the fact that resistant strains of staphylococci when present in the
gastrointestinal tract may produce reactions varying from mild to very severe and fatal
involvement. My interest in this subject was stimulated by a recent fulminating fatal
case of staphylococcal enteritis as follows:
Mr. P. C, age 61, white male, was admitted to the Vancouver General Hospital on
July 8th, 1953, with complaints of: (1) Reduction in the size of stool and increase in
the frequency of bowel movements for 3 months. (2) Haemorrhoids since November,
1952. These complaints became steadily worse and he therefore reported for examination in June, 1953. He gave a history of occasional blood streaked stools in the past three
months. There was no weight loss, anorexia, or dyspepsia. His main complaint was
that of narrow, ribbon-Lke stools of 3 months duration.
Ba Enema revealing an obstruction at the junction of the
descending and sigmoid loops.
In his past history, in 1943, following a drinking episode he had an attack of
colitis requiring hospitalization for ten days. In 1948, he developed a large carbuncle
on the back of his neck requiring surgery and antibiotic therapy. This illness lasted
two months, and it was at this time he developed a skin eruption diagnosed as. a reaction
to sulfonamides.  He was advised that he was sensitive to this drug, and to avoid its use.
The personal history and the rest of the functional enquiry was noncontributory.
His general condition on examination was good, with the cardiovascular and respiratory
Page 398 systems revealing no evidence of organic disease. The blood pressure was 120/70. The
abdomen was slightly protruberant with no masses, guarding, or rigidity. The liver and
spleen were nonpalpable. There was no lymphadenopathy. Special examination revealed:
Haemoglobin 95% (13.8 grams); W.B.C. 8950 with a normal differential; coagulogram
normal; N.P.N, and liver function tests normal; the stool was negative for occult
blood, parasites and ova. The electrocardiogram was within normal limits. The
sigmoidoscopic examination revealed no mucosal lesion, but a constricted area was
encountered at about 15 cms. Moderate sized hemorrhoids were present. The chest
x-ray was normal. Barium enema (see picture 1) revealed an obstruction at the junction
of the descending and sigmoid loops. A long irregular, narrow, tapering contraction of
the bowel lumen was visualized at this site. It measured approximately 3 x/z cms. The
margins, particularly the proximal face, did not present a sharply defined or overhanging
border. The contours of the segments were fixed, and did not alter following evacuation
or on the post evacuation or inflation films. No distension of the large bowel above
the lesion, or small bowel dilatation in keeping with down-stream obstruction could be
detected. The x-ray conclusion was that of obstruction to the retrograde passage of
the barium with a deformity in keeping with an annular area of carcinoma. A second
less likely possibility to be considered was that of constriction secondary to diverticulitis
in view of the tapering, imperfectly demarcated contours of the lesion. This x-ray was
repeated after a course of antispasmodics with no change in the findings.
With the above clinical picture, a tentative diagnosis of carcinoma of the sigmoid
was considered, although an inflammatory lesion could not be excluded. Operation
was planned. As the patient gave a history of sensitivity to sulfonamides, his bowel
preparation was begun with Neomycin July 14th, 4 grams being given in the first
dose, and 1 gram subsequently the same day. The next day, July 15th, he had neomycin
gram I q.i.d. The patient was operated on July 16th by Dr. Rocke Robertson, at which
time an extensive lesion involving the sigmoid was found. There was no evidence of
liver metastases or enlarged nodes. After ligation of the inferior mesenteric artery at
the aorta, a resection from the rectal ampulla to the transverse colon was carried out.
An end to end anastomosis was effected without difficulty, and a transverse colostomy
in the right upper quadrant was fashioned but not opened. The patient received 1500
cc. of blood in the operating room, and in his intravenous that evening he received Yz
gram of terramycin.
H S   £*H
Gross picture of Small Intestine—showing membrane formation. This could be peeled off to the underlying submucosa.
To the right of this,' the mucosa was completely, denuded and
intensely haemorrhagic.
Following the operation, the patient did fairly well although on the first postoperative day he ran more fever than one might expect—up to  102°.   His abdomen
Page 399 was moderately distended. His general condition, however, was well maintained. He
received 3000 cc. of intravenous fluid with vitamins B and C added, and two doses of i
Yz gram of terramycin. The urinary output that day was 1000 cc. On July 18th the
patient showed much abdominal distention, and a temperature elevation to 103°. His
colostomy was opened first thing in the morning, and it drained "copiously" with a i
large amount of gas and liquid material. A Levine tube had been inserted the previous
night, and there was some drainage from this tube during the night. However, by the.
next morning in addition to this drainage, he began to vomit about the tube. Copious
drainage and some amounts of emesis (July 18th) indicated an upward revision of the
planned 3000 cc. of intravenous fluid, and 5000 cc. were ordered, terramycin J4 gram
being given in 2 of the bottles. As the day progressed, the patient became more toxic,
restless and uncooperative. At 8:00 p.m. his temperature rose to 105°, and then he
suddenly went into collapse. Seen at this time, his blood pressure was barely obtainable,
his pulse rapid (in the region of 140), he was clammy and pale. Chest examination was
essentially negative. The electrocardiogram showed no abnormality. The patient was
markedly dehydrated, distended, and there was very profuse drainage from the colostomy and suction. It was felt that the patient might have an acute electrolyte deficiency
in association with his dehydration, or else might be suffering from a toxic enteritis
related to his terramycin therapy. The latter was discontinued, and penicillin and
streptomycin were ordered. A cut-down was inserted, and blood was given very quickly
plus large amounts of electrolyte containing fluid, these being normal saline 2000 cc,
5% sodium chloride 200 cc, and large doses of neosynephrine in these fluids. At the
end of two hours the patient's general condition had markedly improved, blood pressure
and pulse were of good quality and seemed to stabilize. Approximately three hours later
(3:00 a.m.), the patient again went into collapse. Three bottles of blood restored the
blood pressure. July 19th found the patient's condition grave. His temperature was
105 and pulse 120. It was noted that green mucoid material was being passed per
colostomy, and likewise per anun. There were copious amounts of Levine tube drainage.
The picture was very suggestive of an acute enterocolitis with a profound toxemia.
At this stage, swabs were taken from the colostomy, and an abdominal paracentesis was
carried out revealing a straw-coloured fluid with fibrin flecks in it. The smears were
examined by Dr. W. H. Cockcroft of the Bacteriology Dept. and he repdrted "very
many staphylococci in with specimens." It was therefore felt that the patient had
Staphylococcal Enterocolitis and Peritonitis. He was given the following treatment:
Massive doses of aqueous penicillin, bacitracin and staphylococcal antitoxin. The
patient's condition became steadily worse, and he died in a state of shock at 1:45 a.m.,
July 20, 1953, 12 days after admission and 3 days postoperatively.
An autopsy was performed on July 20th, ten hours after death. There was no
oedema nor palpable lymph nodes. There was a left paramedian surgical incision with
sutures in place. A Mikulicz colostomy was present in the right upper quadrant. The
heart and lungs revealed no gross abnormalities, no pus in the bronchi, and no gross
evidence of pneumonia. The pulmonary circulation, trachea and bronchi were clear.
There was no evidence of recent or old myocardial infarction. The peritoneal cavity
contained one litre of thin bloody fluid. There was a thin fibrinous exudate over the
large and small bowel. The gastric mucosa contained many small ulcers and many small
areas of hemorrhage. (Picture 2.) The stomach was not dilated. The entire small intestine
was moderately dilated, and when opened contained large amounts of plasma-like fluid.
The mucosa was entirely lost or shedding in the form of sheets of yellow, friable, gelatinous material. The underlying wall was intensely hemorrhagic. Towards the ileum
this process gradually petered out, so that the mucosa around the ilea-caecal valve
appeared essentially normal. The wall of the caecum and ascending colon was ©edematous and soft, and injected vessels could be seen through it. The colostomy was in good
condition. The remaining colon was collapsed and contained a moderate amount of
mucopurulent material. The rectal anastomosis was intact and in good condition. In
the wall of the colon, immediately above the anastomosis, there were several small
diverticula whose orifices measured approximately 1  mm. in diameter, and extending
Page 400 1 cm. through the bowel wall. There was no gross evidence of inflammation about the
diverticula. The rectum contained a large amount of green mucoid material. The
mesentery of the large and small bowel revealed no abnormality. The spleen weighed
100 grams, and the pulp was extremely mushy and purplish red. The kidneys were
flabby, weighing 170 and 180 grams. The capsule stripped easily to reveal an injected
cortical surface. On the cut sections, the parenchyma bulged slightly, and the cortical
striations were moderately increased.
_!_?*•   i ***
_l * _.* • I
Micro photo graph of Small Intestine showing complete necrosis
of mucosa with membrane formation.   Colonies of bacteria
are present in the overlying exudate.   Note line of separation
in the upper submucosa (H. & E. Low Former).
The microscopic examination revealed: (1) Stomach—The section through the
gastric ulcer reveals coagulation necrosis of the mucosa with several bacterial colonies
present. There is haemorrhage into the lamina propria and marked congestion of the
vessels in the wall beneath. (2) Jejunum (pictures 3 and 4)—There is a shedding of
endothelium down to the lamina propria. A heavy infiltration of round cells, leukocytes
and eosinophils is seen. The slough consists of a network of fibrin containing acute
inflammatory cells and many bacterial colonies. (3) Ileum—The mucosa is fairly intact
although a heavy infiltration of chronic inflammatory cells is present. (4) Kidneys—
A marked degeneration of distal and proximal convoluted tubules with complete loss
of nuclei by chromatolysis. The tubular spaces are filled with debris. This degeneration
is patchy in nature. Some tubular systems are intact and their associated glommeruli
contained R.B.C. in the capillaries. The medulla is congested with dilated vessels. A
few hyaline casts are present in the collecting tubules and loops of Henle.
Bacteriological study revealed: (a) Gramstain on the surgical specimen revealed
a few gram positive cocci (staphylococcus or fecal streptococcus), (b) Smear from
colostomy revealed many gram positive cocci, (c) Peritoneal fluid revealecKa heavy
growth of pure culture of staphlococcus aureus sensitive to Chloromycetin,, neomycin,
and bacitracin; less sensitive to aureomycin and terramycin. This fluid separated into
fairly clear supernatant level, and a small clot. The clot was a mixture of pus cells
and staphylococci. The supernatant fluid contained staphylococci and exotoxin with
lysis of rabbit cells, 1/80 to 1/160. (d) Bowel contents showed heavy growth of
^staphylococci, coagulate positive, with sensitivity as mentioned above.
Page 401 The incidence of events in this case was rapid and fulminating. Symptoms of
nausea, vomiting, abdominal discomfort and distention were noted on the second postoperative day. The opening of the colostomy on the second postoperative day was
followed by tremendous outpouring of fluids and gas, and a steadily mounting rise in
temperature. Soon after occurred the most striking feature of all, and that was a
rapidly progressing circulatory collapse. Despite heroic supportive measures the patient
went into irreversible and fatal shock, dying 72 hours after his operation. The preoperative preparation in this case consisted of neomycin. Postoperatively he received
terramycin, and later penicillin, streptomycin and bacitracin. With the smears from
the colostomy and from the peritoneal fluid revealing staphylococci, the diagnosis of
staphylococcal enteritis and peritonitis with toxemia was made, but at this stage treatment failed to stem the downhill course. The autopsy and further bacteriological
studies verified the diagnosis as a membranous enteritis. In retrospect the neomycin
probably cleared the majority of bacteria from the gastrointestinal tract. The staphylococci were the first organisms in the gastrointestinal tract in any numbers, setting
up a jejunitis, ileitis, and peritonitis. There may have been some staphylococci in the
mouth at the time of operation, and if these were disseminated, the oral neomycin
would not help, as it is not appreciably absorbed in the gut. The organism isolated was
only slightly sensitive to aureomycin and terramycin. In view of the clinical picture,
the gross and histologic findings, it was logical to postulate that the fulminating rapidly
progressing diarrhoea was caused by bacterial infection, namely the coagulase positive
haemolytic staphylococci.
Discussion: During the past few years reports have been published regarding
staphylococcus enteritis as a complication of antibiotic therapy. Finland1 in 1950
referred to the increasing occurrence of antibiotic resistant staphylococcal infections,
and reported what apparently is a new disease entity, namely "Staphylococcal Dysentery". He observed several patients under treatment with aureomycin and terramycin
with severe diarrhoea in which the stools showed cultures of coagulase pdsitive haemolytic
staphylococcus aureus. Since then, numerous reports have appeared showing similar
adverse effects to other antibiotics particularly streptomycin and penicillin. A recent
comprehensive review by Prissik on "Antibiotic Resistant Staphylococci and Related
Infections" presents various causes for the increasing incidence of resistant strains.
Ths complication is not caused by hypersensitivity to the drug by the patient, but is
produced by the effect of these antibiotics on normal fecal flora. Most of the fecal
bacteria consists of organisms of the Escherichia coli and aerobacter aerogenes group,
together with groups represented by Bacteroides, Clostridium and Proteus. In minor
numbers are found Pseudomonas, yeasts, enterococci, and saprophytic micrococci.
When terramycin3 or aureomycin4 is given a decrease in the total number of bacteria
in the intestinal tract occurs during the first few hours. After the first few hours,
important changes occur. Escherichia coli rapidly decreases in number, and becomes
practically absent by the 4th day after onset of antibiotic therapy. The organisms often
the Proteus or Pyocyaneus group, which are usually resistant to ordinary amounts of
terramycin or aureomycin, increase in a reciprocal fashion. This increase becomes
extremely rapid by the end of the fourth day, after which these organisms are predominant in the stool. Therefore a period occurs usually about the 4th day, when the total
number of bacteria in the intestinal content is extremely small. The next step in the
alteration of the bacterial flora of the host by the use of antibiotics is superinfections.
Resistant organisms, if present or if implanted from the environment, can propagate
in any areas of the body to which they have access. At present more than 30% of
all strains of staphylococcus are resistant to terramycin and aureomycin5. If a patient
who is receiving one of these antibiotic agents happens to have such a resistant type
of organism in his intestine, the stage is set for possible disaster. At first, the organism
in question is present only in small numbers because growth is retarded by means of
competition for nutritidn from the much greater number of other bacteria present.
However, as mentioned above on the 4th day the total number of bacteria in the}
intestinal tract is extremely small, and micrococci therefore take advantage of this
Page 402 situation and multiply very rapidly. It is reported that 40% of strains of staphylococcus produce quantities of potent endotoxin and a characteristic syndrome may
be produced.
Other causes suggested by Prissik in the incidence of resistant strains are bacterial
stimulation and host susceptibility. It has been established that low concentration of
antibiotics can actually stimulate the growth of bacteria in vitro. It brings to mind
the old pharmacologic law which states that "sublethal amounts of drugs may act as
stimulants." This is true for both sensitive and resistant strains of bacteria. If this
also occurs in the body, clinical infections might be expected at sites where bacteria
are ordinarily filtered out and held in check by body mechanisms such as the urinary
tract, the lungs, and the intestines. Dearing and Heilman6 showed that resistant strains
of staphylococcus developing in the hospital population was associated with an acute,
and often fatal enteritis. Cultures of the micrococci were obtained in nearly all of
their 44 cases, and the bacteria were found resistant to all antibiotics except erythromycin. They suggested that the enteritis was the result of the staphylococcus growing
in profusion in the intestinal tract, owing to the inhibition of the normal flora by antibiotics. They noted that many of the patients harbored the organism in the nasopharynx, and suggested that downward invasion occurred.
In a recent paper Fairlie and Kendall7 described 5 cases of fatal Staphylococcal
Enteritis following penicillin and streptomycin therapy. Haemolytic staphylococcus
aureaus was isolated from the stools or intestines of all, except one, which yielded
profeus vulgaris. Fever and diarrhoea were described as the cardinal initial clinical
features, with shock, oliguria and azotemia occurring later. The authors suggested
that simple suppression of intestinal flora permitting overgrowth of staphylococci or
possibly another organism does not appear to be sufficient explanation for this complication. They mentioned other factors, including the introduction of another strain
of staphylococcus or the stimulation of toxin production by staphylococcus under the
influence of antibiotics.
Wakefield and Sommers8 in a recent article reported 3 fatal cases of staphylococcal
enteritis in surgical patients. They had received four or more antibiotic reagents postoperatively. Autopsy revealed fibrinous, membranous enteritis from which a haemolytic
staphylococcus aureus was isolated bacteriologically in two cases. In one case where
sensitivity tests were done, the staphylococcus was found to be resistant to all the
antibiotics.
Epidemiological studies have shown that resistant stapyhlococcal infection is much
more common among patients who have been in hospital for some time, than in new
patients or outpatients. Hayhoe and Whitehead9 in an attempt to trace the source of
infection examined the "carrier state" of the staff of their hospital. This study revealed
that 75% of the staff were carrying staphylococcus pyogenes, and that 83% of the
carriers were carrying penicillin resistant strains. Cairns and Summers10 reported that
with increasing time in hospital the proportion of resistant strains rose, and that this
effect was seen with the time spent in hospital, rather than with the presence or
absence of previous penicillin therapy.
In contrast to the above reports of stapylococcal enteritis in which a definite
bacterial infection has been shown to be the cause of the condition, are the reports by
Dixon and Weisman11 and others, on the condition of "acute pseudomembranous enteritis or enterocolitis" following intestinal surgery. This condition has been described as
far back as 1893, and numerous reports have appeared over the year. The clinical
manifestations are similar to those of the above mentioned case, and at autopsy there
is an acute enteritis of varying degree which may involve the gastrointestinal tract
anywhere from the esophagus to the anus, although it is most prominent in the small
intestine. The histological feature is that of inflammation, necrosis, and ulceration of
the mucosa with oedema and varying degrees of inflammatory infiltration in the sub-
mucosa. The precipitating or inciting factor of this serious illness is unknown. The
cultures of enteric pathogens are usually negative. This suggests that pseudomembranous.enteritis may be the initial pathological condition, and that infection occurs second-
Page 403 arily, probably aided by antibiotics. Recent reports show that the incidence of pseudomembranous enteritis is not increasing, while that of staphylococcal enteritis appears to be
increasing. This may suggest that the two diseases are not closely related, except in that
their pathology, i.e. the reaction of the bowel, is similar. Klechner, Bargan and Baggin-
stoss12 described 14 cases of acute pseudomembranous enteritis which were not preceded
by operative procedures. They referred to a paper by Penner and Berheim13 who attributed the disease to stasis of the splanchnic circulation resulting from shock causing
increased permeability of the intestinal mucosa to bacteria or to toxins.
Terplan and his co-workers in a recent article describes 8 cases of staphylococcal
enteritis following surgery. All these cases had received antibiotics. Bacterial investigation revealed no evidence of pathogenic enteric micro organisms, that is typhoid,
paratyphoid, and dysentery. They were impressed by the fact that the clinical features
were strikingly similar in all cases and that the picture was observed from the first to
the fourth postoperative day. The fact that the condition occurred in patients in the
same ward raised the question of an extrinsic infection acquired within, the hospital.
At postmortem, direct smear from the mucosa of the small intestine revealed gram
positive cocci, and the cultures revealed colonies of the haemolytic staphylococci,
enterococci, B pyocyaneus and B proteus. In addition, they were able by bacterioscopic
analysis of histologic slides of small and large intestines to disclose gram positive cocci
within the inflammatory membrane exudate covering the mucosa of the intestine. They
stressed the fact that technical precautions are necessary to conserve proper material
at once and without contamination for future bacteriologic and histologic studies.
They stressed also the importance of culturing fecal material a_4 exudate from the
intestinal mucosa on blood agar in addition to the usual media for the Salmonella and
Shigella groups. Care is necessary in carrying out postmortem analysis in cases of
diarrhoea in general. In desquamative catarrh the diagnosis rests largely on the analysis
of the intestinal content and the most superficial parts of the mucosa. The gross
appearance of the intestinal coat, in desquamative processes, once the.diarrhoeal content
is washed off, does not always disclose an acute inflammatory state and my be considered
as normal. The jejunum seemed to be particularly involved in most of his cases, and
the inflammation of the mucosa was either desquamative, catarrhal, or only superficially
pseudomembranous. The inflammatory reaction was in general restricted to the mucosa
and submucosa.
The incidence and seriousness of staphylococcus enteritis makes it important for
one to review the means at hand in the prevention and control of stapylococcal infections. It is important for one to include the recognition of such a, complication as an
explanation for unexplained fever and diarrhoea in a patient receiving antibiotics. Recognition should be followed by prompt withdrawal of antibiotics, and where indicated or
possible the use of antibiotics to which the staphylococcus is sensitive, e.g., erythromycin.
Frequent sputum, nose and throat and stool cultures should be carried out. However,
under no conditions should the physician await the outcome of cultures before the
method of treatment is changed. As already mentioned this illness is fulminating,
explosive in nature. The associated disturbance in fluids and electrolyte balance, the
circulatory collapse and shock demands prompt and heroic supportive measures. When
severe infections with antibiotic resistant staphylococci occur, consideration may well
be given to the use of antitoxin15. With the arrival of chemotherapeutic agents, the
immunological approach to treatment was almost entirely put aside. The properties of
staphylococcus antitoxin have been found to include the power to neutralize the
haemolysins and the pathogenic effects of the lethal and dermonecrotic factors in the
cells and tissues of laboratory animals. The use of antitoxin is limited, however. The
necessity for early diagnosis and institution of antitoxin serum therapy is advocated
in the treatment of acute and generalized staphylococcal infections,' but it is not
recommended for the obviously moribund patient.
SUMMARY
A case o£ fatal enteritis due to coagulase positive haemolytic staphylococcus aureus,
with autopsy findings, has been presented.   This case demonstrates the dangers inherent
Page 404 111 in the use of antibiotics for intestinal sterilization. Normally the intestinal flora are
kept in well regulated balance by symbiotic relationship which cannot be disturbed
with impunity. The use of wide-spectrum antibiotics in this case, so upset this balance
that bacteria not affected or bacteria invading from the upper respiratory tract multiplied in profusion. This case is unusual in that the staphylococcus isolated produced a
toxin that was demonstrated by haemolysis of rabbit's cells. This toxin was obviously
easily absorbed through the denuded intestine, and together with the large amounts
of plasma-like fluid which leaked from the intestinal wall, accounted for the death
of the patient with marked pyrexia and shock. This is not a case of so-called pseudomembranous enteritis where bacteria do not predominate. The prolonged state of shock
which preceded the death of this patient accounted for the picture of early lower
nephron nephrosis found in the kidneys. Chronic diverticulitis of the rectosigmoid
caused the constricting lesion which on x-ray so resembled a neoplasm. On the basis of
this case and from a review of the literature, the following important facts stand out:
(1) There is a steady increase in the occurrence of Antibiotic-Resistant Staphylococcal Infections.
(2) It is generally agreed that the increasing incidence is largely an outcome of:
(a)   Widespread arid often indiscriminate use of antibiotics, and (b) cross infections
from carriers and clinically infected persons among the hospital personnel and patients.
(3) Staphylococcal enteritis should be kept in mind as a possibility in any patient
receiving antibiotics. The condition is a true bacteriologic and medical emergency
and prompt recognition is necessary to save the life of the patient.
REFERENCES
1. Finland, M., Bull. New York Acad. Med., 1951, 27:199.
Jackson, G. G., and Finland, M., Arch. Int. Med., 1951, 88:446.
2. Prissick, F. H., Am. J.M.Sc, 1953, 225:299.
3. Rivera, J. A., and Shorov, V. M., Gastroenterology, 1951, 17:546. ll_l
4. Jacob, S., Schweinburg, F. B., and Rutenburg, A. M., Society for Exp. Bio. and Medicine, 1951, 78:121.
5. Minnesota Medicine, 1953, 36:63.
6. Dearing, W. H., and Heilman, F. R., Proc Staff Meet. Mayo Clinic, 1953, 28:121.
7. Fairlie, C. W, and Kendall, R. E., J.A.M.A., 1953, 2:153.
8. Wakefield, R. D., and Sommers, S. C, Ann. of Surgery,  1953,  138:249.
9. Hayhoe, F. G. J., and Whithead, J E. M., Lancet, 1949, 2:1120.
10. Cairns, H. J. F., and Summers, G. A. C., Lancet, 1950, 1:446.
11. Dixon, C. F., and Weismann, R. E., Surg. Clin, of N.A., 1948, 999.
12. Kleckner, M. S., Bargen, J. A., and Raggenstoss, A. H., Proc. Staff Meet. Mayo Clinic, 1953, 28:313.
13. Penner, A., and Bernheim, A. I., Arch. Path. 1939, 27:966.
14. Terplan, K., Paine, J. R., Sheffer, J., Egan, R., and Lansky, H., Gastroenterology,  1953, 24:476.
15. Dolman, C. E., Can. Med. Ass. J., 1934, 30:601^
We wish to express sincere appreciation to Dr. H. Taylor, Department of Pathology
of Vancouver General Hospital tfor his help and for the photos of the pathologicaV
specimens; and to Dr. H. Spiro for the x-rays.
AVAILABLE NOW
Doctors' offices, four rooms with common reception room, suitable
for small clinic or two medical men. Will decorate to suit' tenant.
Growing residential area.
For Further Information, Phone the Publisher, MA. 7729
Page 405 THE CAUSE OF STROKES
S. E. C. TURVEY, M.D.
"Only a stroke." How often have house physicians thus replied to the query
about new and interesting patients on their ward! I once made that answer unwittingly
to that greatest of neurological teachers, Sir Gordon Holmes, and the subsequent two-
hour clinic left everyone dazed with what was known, and particularly what was not
known about strokes. Until recently a stroke was considered to be due to haemorrhage,
thrombosis or embolism. However, it has become embarrassingly apparent that this
is a naive simplification of the problem, and shows how prone we are to regard the
nervous system as a structure with laws of its own, which render it immune to the
pathological reactions to damage such as all other tissues show. The problem is not a
minor one. Each year in the United States it is estimated 170,000 people die from
strokes. This is three times the number who died from diabetes and tuberculosis
combined. And it does not reveal the 1,800,000 who are handicapped by those milder
strokes which do not kill.
Walshe9 has written: "It is, perhaps, those scientific notions that we take most
readily for granted, and receive upon authority with the greatest assurance, that are
most apt to repay examination from time to time, and that upon occasion are found
wanting when brought to the touchstone of correspondence with facts. The more
abstract such a notion the greater the probability that this will be so. Further, in
continued currency, abstract ideas seem to harden so easily into concrete facts, and
mental constructs come to pass muster for natural phenomena." And elsewhere he
comments10 on the license we take with the nervous system, "a license to speculative
and abstract thinking about it that we would be wary of in respect of any other
tissue".
If it be true, and I believe it is, that few neurologists have a catholicity of interest
in arid knowledge of internal medicine, then the converse is also true. The problem of
the stroke lies between these two disciplines, which are ideally one and the same but
too often are estranged by specialism. The pathologist and physiologist as usual should
provide the fusing knowledge, but here again the limitation of the fields of specialism
has been a hindrance.
If we excluded such obviously intracerebral conditions as congenital aneurysms,
thrombo-angiitis obliterans, obstructions of cerebral venous outflow, and trauma, it
was presumed that the symptoms of the stroke were due to an obstruction or rupture
of a cerebral artery. Certainly an embolus may obstruct an artery causing widespread
death of tissue, but usually this is not the cause where one or two small arteries are
obstructed, with the clinical picture of immediate and profound symptoms but a
good measure of recovery. Nor can we consider thrombosis and haemorrhage to be
universally valid hypotheses; it has been practically an impossibility to demonstrate a
rupture of the artery in spite of extensive and repeated researches by competent neuropathologists using serial sections over the last thirty years; and in many strokes, no
thrombosis of an artery can be demonstrated even by the most meticulous pathologists.
Thus, gross occlusion or rupture of the arteries cannot be postulated as the invariable
cause and we may well ask, "Why should they be?" For nowhere else in the body do
the blood vessels commonly react in such a manner.
In hypertensive hyaline arteriolopathy where one would expect the conditions to
be peculiarly propitious for intra-arterial thrombosis, it is a rare finding as the initial
event in the disease (Scheinker7). The perpetuation of these concepts in medical
teaching is amazing, lacking all pathological proof as they do. A similar state of
affairs exists concerning the phrase, "cerebral arteriosclerosis". For years it has been
only a convenient waste-bin in which all sorts of psychiatric and neurological scraps
are gathered. There has been negligible correlation of clinical states with experimental
and pathological facts. Every middle-aged or elderly person has a degree of arteriosclerosis, and though admittedly it may, and usually does, diminish the arterial flow
of blood,  the passive role of the arteries alone, in  the production of symptoms in
Page 406 thrombosis and haemorrhage, is dubious indeed. As elsewhere in the body, the blood
continues to flow through the lurnina of the arteries until another complicating factor
arises, and this new factor is not primarily an arterial factor. It is a melancholy
reflection whether "cerebral arteriosclerosis", as a diagnostic term, is ever justified;
and indeed it is dubious if hardening of cerebral arteries is the chief or even basic
factor in the ageing process of the brain.
The diagnosis of cerebrovascular spasm is intimately concerned with the problem
of strokes. The neural control of the intracerebral vessels is undoubtedly weaker than
that of the systemic vessels, but it is an active mechanism in migraine, in the cerebral
type of carotid sinus syndrome, with cerebral embolism, under the action of certain
drugs, in blood pressure. It may produce temporary or prolonged vasoconstriction,
vasodilatation or vasoparalysis. If the action is mild and of short duration, only fleeting
symptoms result, but if severe and prolonged it may result in permanent cerebral
damage. However the systemic blood pressure is the most important factor in the
regulation of intracranial circulation and venous pressure. It is worthy of repeated
emphasis that the cerebral circulation is intimately and strongly influenced by the
mechanisms of extracerebral circulation. Concerning another factor in vasomotor
interdependence, McQueen, Browne and Walker have recently written: "It is of
interest that the central vasomotor mechanisms are not affected by the state of the
peripheral vascular system. Even with an arterial pressure of 200mm. of mercury, the
responses to brain stimulation are the same as obtained with a normal blood pressure.
Although the afferent vasomotor regulatory systems are intact, they do not seem to
modulate the activity of the central pressor systems. This is of interest in the consideration of hyperpiesia in man, for if the same principles apply to human being as
in the dog, any factor chronically elevating the arterial pressure may not be compen-:
sated by the central vasomotor regulation. But on the other hand, all stresses upon the
central mechanisms will cause rises in the blood pressure as if it were a ndrmal level."
Recently Wilson et al. in a series of 542 cases in which an acute cerebral vascular
accident was demonstrated at necropsy, the past medical history, clinical examination
or autopsy revealed evidence of cardiovascular insufficiency in 451  (83%).
Thus pathological facts, clinical observations and physiological principles form
the basis of a reasonable hypothesis: That in the majority of strokes there is not only
evidence of cardiovascular disease, but of inadequate maintenance of total and constant
blood flow to the cerebral tissues.  (Schaller.)
This ^discussion shall be limited to the so-called "cerebral thrombosis", with or
without hypertension. In 1939 Villaret and Cachera8, using an experimental window
in the skull showed that the venous and qapillary effects following obstruction of a
cerebral artery (as by an embolus5) were more severe and extensive than the arterial
effects. The veins and capillaries were dilated and engorged and the flow of blood
might even be reversed. This functional disorder was not localized to the affected area
but was widespread throughout the cerebral hemisphere and if it was severe would
cause those symptoms of loss of cerebral function from Which the patient recoviers.
(Of course, if the blocked artery is large, sudden death results.) This diminution in
venous flow results in reduced oxygen supply to the wall of* the vein as well as the
surrounding cerebral parenchyma. There follows in turn an increased permeability
of the vessel wall first to fluid, then to protein and finally to cells (Landis, 19286).
The arteries or arterioles play no part in this early picture. This would be expected
as the vein has a delicate wall with no elastic strengthening tissue and was never
intended to bear stress or strain. The retinal haemorrhages in hypertension are from
venules and illustrate this susceptibility of the veins to bleed after prolonged obstruction3. Focal areas of necrosis and haemorrhagic softening occur in perivenous areas,
and result in the familiar picture of "ball-haemorrhage". This may progress to massive
cerebral haemorrhage, but much more frequently it is absorbed and results in an area
of focal softening.
In hypertension the small and medium veins are frequently atrophied and fibrosed,
or have segments of varying lengths which are greatly narrowed or may be grossly
Page 407 dilated in other areas. Aring has suggested that "this attenuation of venules in longstanding hypertension, particularly in cases that have suffered cerebral symptpmatology,
possibly represents the difference between the occurrence of haemorrhage and thrombosis in a given case." Cerebral haemorrhage may occur without venular atrophy, but
when it does it appears that the noxa must be rather overwhelming in nature1.
In arteriosclerosis and arteriolosclerosis the lumen of the artery is narrowed but,
as emphasized before, actual obstruction is uncommonly found though areas of focal
softening, "ball" or massive haemorrhage are not uncommon. Therefore, the old term
cerebral thrombosis should properly be cerebral softening, and this is only one stage in
the production of "ball" and massive haemorrhages. Even in 1929 Cobb and Hubbard
concluded that venous pathology was the underlying etiology of _11 three5. Many
clinicians have emphasized this relationship since then. In hypertension the arterioles
carry the main burden at first, but when they fail to "hold the line" more pressure is
transmitted via an inadequate heart to the veins and capillaries with vasodilatation or
vasopara lysis. If there is no hypertension, a failing heart may cause diminution of
cerebral circulation with hypoxia of the walls of the veins, the same effect as caused
by increased venous and capillary pressure.
In TABLE 1 a summary of the possible clinical mechanisms preceding strokes
is outlined.
TABLE 1
Summary
With Hypertension:
1. Slow shift of burden from arterioles to veins—slow left ventricular failure,
then right ventricular failure—venous engorgement;
2. Sudden shift of burden from arterioles or heart to veins—if myocardial infarction or any sudden left ventricular failure occurs—right ventricular failure—
venous engorgement;
With Normal Blood Pressure:
1. Arteriosclerotic cardiac failure (slow) of left ventricle—right ventricular
failure—burden shifted to veins;
2. Arteriosclerotic cardiac disease with sudden failure (e.g. myocardial infarction)—right ventricular failure—venous engorgement.
ILLUSTRATIVE CLINICAL OBSERVATIONS
Case 1
Male aet. 60: His illness began two years prior to death with dyspnoea on exertion, Blood Pressure 190/110, no oedema. The electrocardiograph showed myocardial
damage. Seven months later he developed a left hemiparesis with complete recovery in
two weeks (B.P. 185/115). Six months later he had an.attack of hypertensive encephalopathy and was unconscious for two days (B.P. 215/115-120) and the electrocardiograph showed further myocardial damage. He recovered from the cerebral
symptoms but was increasingly short of breath. Five months before death he had an
attack in which he was unconscious for two days and was confused and aphasic for
eight days but again he recovered completely.|l; (B.P. 225/120). Retinal venous
haemorrhages were present. Finally he had sudden agonizing praecordial pain and in two
hours was unconscious and had right hemiplegia.  He died in five hours.
Post Mortem
There was moderate cerebral hypertensive arteriolopathy with thickening and
hyalinization of the entire wall of the arterioles and perivascular fibrosis; cerebral
arteriosclerosis (grade 2); numerous areas of focal cortical softening, recent and old;
a discrete "ball" haemorrhage, 1" in diameter, in the left cerebrum; atrophic thinning of the walls of the small veins, some of which were dilated and engorged with
blood, and some had attenuated lumina, and the walls of some had undergone necrosis.
Page 408 NO OBSTRUCTION OF ANY ARTERY OF ARTERIOLE WAS FOUND. The
heart showed thrombotic obstruction of the descending branch of the anterior coronary
artery with advanced sclerosis of the coronary arteries.
Case 2
Female aet. 61: Three years prior to death she had a small myocardial infarction,
proven by the electrocardiograph. Mild diabetes Was discovered at this time and remained well controlled. Two days after this thrombosis she developed left hemiplegia
with recovery in six weeks. Blood Pressure 225/110. She remained well until five days
before death when she had a severe substernal pain lasting an hour. Blood Pressure
115-125/85-95; pulse faint, pallor, sweating. Electrocardiograph-infarction of the
posterior wall of the left ventricle.
Two days later she became unconscious with a left hemiplegia and died in forty-
eight hours. Retinal haemorrhages and areas of exudate were present. Blood pressure
during last twenty-four hours was 165/120.
Post Mortem
Marked cerebral arteriosclerosis and mild hypertensive arteriolopathy; "ball"
haemorrhage lr/2" in diameter in right cerebrum; THERE WAS NO OBSTRUCTION
OF ANY ARTERY. In the area around the "ball" haemorrhage there were seven?
changes in the walls of the veins, cheifly generalized thinning, distention, areas of
necrosis and rupture; peri-venous haemorrhages. One area of old softening, l/z" in
diameter, was present in the right frontal region in which there was dense gliosis
replacing the parenchyma.
Heart—massive recent infarction on posterior wall of the left ventricle distal to
it an area of scar tissue \l/z" in diameter indicating a previous infarction; advanced
coronary sclerosis.
In this patient two episodes of myocardial infarction were followed by hemiplegia
not due to arterial obstruction or embolism, but most likely due to venous disease.
Case 3
Male aet. 58: Four years before death, he began to complain of fatiguability and
mild dyspnoea on effort. He had no angina or oedema. Blood Pressure 140/95. Electrocardiograph—low amplitude in all leads; occasional extrasystoles. Retinal arteries were
sclerosed. Two years before death he had a period lasting three days during which he
was confused, mildly dysarthric and aphasic, and there was failure of voluntary sustained ocular fixation to the right but no other paresis. Blood Pressure 110/80. Heart—
no enlargement, murmurs or arrhythmias. He recovered in three weeks. The diagnosis
was an "area of softening of the left froiital lobe with widespread disturbance of
vasomotricity beyond the area of the original venous pathology." Electrocardiograph—
evidence of myocardial damage, more marked than previously but no definite evidence
of infarction.
A year before death he had a period of confusion and dysarthria with weakness of
the right arm and leg, lasting three weeks but clearing entirely. He was more dyspnoeic
but had no oedema or angina. A week before death he suddenly had an acute praecordial
pain with dyspnoea, cyanosis and pulmonary oedema. In a few hours he was comatose
and never rallied.
At Post Mortem examination there was a "ball" haemorrhage in the right cerebrum;
an area of previous softening with scarring in the left frontal lobe; arteriosclerosis,
grade 2; four smaller areas of softening in the cortex, three on the left, one on right.
THERE WAS NO OBSTRUCTION OF ANY. ARTERY OR ARTERIOLE.
Case 4
Male aet. 56: He was in excellent health until nine months ago. His activities had
been intense, both physically and emotionally. He had never had any dyspnoea or angina
and his blood pressure had been 130-140/80-90 for ten years. Suddenly he had a severe
myocardial infarction. While in bed three weeks later he began to be dyspnoeic on the
slightest effort.  His blood pressure was 120/85.   A week later he developed a complete
Page 409 motor aphasia and a mild right-hemi-paresis. The aphasia has remained unchanged but
the hemiparesis disappeared in two to three months. The dyspnoea of effort improved so
that he could walk a mile easily until seven months after the onset of his illness, when
it recurred and he developed oedema of his ankles. His resting blood pressure was 95/60.
There were no murmurs or arrhythmias. The electrocardiograph was not improved.
He received no cardiac therapy during his illness.
A month later he died in another city, within 20 hours after the sudden onset of
unconsciousness and left hemiplegia. No post mortem examination was obtained. The
course of this patient's illness illustrates one of the frequent tragedies of omission, the
neglect of preventive treatment of strokes.
Case 5
A male aet. 64: Developed acute rheumatic fever at the age of sixteen and was
invariably refused life insurance because "both valves of his heart were damaged".
However, he had no further episodes of rheumatic infection and remained active and
well until three years prior to his death. His first symptom was dyspnoea on climbing
a moderate incline. After three months he had to give up golf and then began to be
dyspnoeic on ordinary walking.  He had no oedema.  The examination showed:
(a) Retinal arteries—sclerosed (Grade 2).
(b) Heart—
1. Apex beat—1" outside mid-clavicular line; poor response to effort;  no
arrhythmias;
2. Frequent extrasystoles, mitral and aortic systolic and diastolic murmurs,
grade 2.
3. Blood pressure 135/75.
(c) Electrocardiograph—showed a moderate degree of myocardial damage.
The descending gradient of the myocardial failure was interrupted by four episodes
of acute congestive failure with oedema and enlarged liver, and in three of these he had
cerebrovascular accidents—a left hemiparesis, a three-day spell of coma followed by
confusion and nominal aphasia for four weeks, and a period of coma lasting two days
with a mild left hemiparesis lasting two weeks.. He recovered from all of these except
for loss of interest and "drive", spells of somnolence and irritability. The last four
months of his life were without event except that he required diuretics and other cardiac
treatment constantly.   He died suddenly.
Permission could be obtained to examine, post mortem, only the brain. THERE
WAS NO EVIDENCE OF EMBOLUS OR OBSTRUCTION OF ANY ARTERY.
There was a recent massive "ball" haemorrhage (1^4"x3") in the left parieto-occipital
region. There were four areas of focal softening, three on the right and one on the left,
affecting the cerebral cortex and the subcortical white matter to a depth of l/z cm.
There was a similar area in the right cerebellar lobe. Microscopically these showed gross
gliosis. There were changes in the veins in the areas surrounding these areas—thinning
of the walls of some, marked narrowing or widening of the lumina, actual atrophy
in others.   Otherwise, the veins were generally engorged and dilated.
Conclusion:
Until recent times, a stroke was thought by clinicians and pathologists to be
caused by haemorrhage, thrombosis or embolism. Certainly some are due to rupture of
the arteries and to emboli, but pathological proof of the etiological role of the arteries
in causing the "ball" haemorrhage and the so-called thrombosis is meagre indeed. The
role of the systemic cardiovascular mechanism and especially that of the cerebral veins,
is outlined.
The catastrophe of a stroke has been accepted as inevitable. Specific remedies have
rarely been recommended or considered. Surely, as the pathological changes are an end-
result and not a cause (except in embolism), the causes should be explored in order
to prevent them.  The stroke is a tragic reminder of the intimately integrated unit that
Page 410 is the body, and that it is not a multiplicity of isolated units in its reactivity to noxious
stimuli. :
The general neurocirculatory state is more important than the local, and often
hypothetical, spastic and thrombotic states.
BIBLIOGRAPHY
1.   Aring, C. D.,  (1945) Brain 68, 28.
2. , Ryder, H. W., Roseman, E., Rosenbaum, M.,  and Ferris, E. B., Jr.,   (1941)   Arch.
Neurology and Psychiatry, 46, 649.
3. Ballantyne, A. J.  (1943), Irish, J., Med. Science Sixth Series No. 214, 551.
4. Cobb, S., and Hubbard, J. P.,  (1929)   American Journal of Medical Sciences, 178, 693.
5. Fleming, H. W., and Naflfziger, H.  C,   (1927)   Journal of the American Medical Association,  89,
1484.
6. Landis, E. M., (1928) American Journal of Physiology, 83, 528.
MacQueen, Browne, Walker, (1954) Neurology, 4, 1, 1.
7. Scheinker, I. M., Arch. Path. 36, 289, September, 1953.
8. Vilkret, M., and Cachera, R., (1939) * _es Embolies Cerebrales", Paris, 133.
9. Wilshe, F. M. R., (1942) Brain, 65-3.
10. Walshe, F. M. R.,  (1947) Brain, 75, 93.
11. Wilson, Rupp, Riggs and Wilson,  (1951)  J.A.M.A. Volume 145, number 16, 1227.
1
MISS FIRMIN
Died June, 1954
It is with a great sense of personal loss that we record the passing of our
old friend, Miss Firrnin, who was for many years our highly-valued Librarian
in the Library of the Vancouver Medical Association. We shall probably never
realize fully just how much she did to make this the great Library that it has
become. v
Miss Firrnin was a very fine person, and those of us who worked with her
in past years acquired for her an immense respect, as well as a very deep affection. She had a complete integrity of mind as well as of character. She hated
compromise or insincerity—but apart from these, she never attempted to
impose her own standards on anyone else, and was tolerant of the human weaknesses of us all. She had, too, a sense of humour which made acquaintance with
her a very delightful thing.
She was a very hard worker, and all her work was admirably done, without
fuss, but with an excellent finish. One could never ask too much of her, and
she never seemed tired. She loved books, read widely and had excellent literary
taste, and we think her work as Librarian was a joy to her. It certainly was a
joy to us. The Bulletin of the Vancouver Medical Association, in its early days,
owed a very great deal to her work, and it was always one of her chief interests.
So, for many reasons, we mourn her loss—and look back on her as one of
our most valued friends and associates. To her family we extend our sincere
condolences and sympathy.
Page 411 A CASE OF IATROGENIC HEART DISEASE
By DR. L. MIRABEL
The patient was a stout housewife of 64 who had three previous hospital admissions for "heart trouble". She was seen this time in what appeared to be a typical
attack of cardiac infraction with severe praecordial pain radiating to left arm and
unrelieved by several injections of morphine and "Demerol".
Her blood pressure on admission was 222/130—clinically her heart was not
enlarged and no gross retinal changes were found.
She said that all her attacks would begin with "clicking in her right temple, soon
followed by either dizziness or else true rotatory vertigo (on this point her description
varied on different occasions) and profuse sweating. Over the last two years chest
pain would follow some of the attacks. She was told by her physicians that her blood
pressure "jumped up and down".
The electrocardiogram taken on admission and repeated the next day was interpreted as within normal limits. The blood pressure over the next few weeks ranged
between   110/80  and  150/110.
Her previous admission chart was obtained and it was noted that the electrocardiogram taken on that occasion and repeated once was considered to be within
normal limits. Nevertheless the patient was treated with prolonged anti-coagulant
administration. Neither on this nor on the previous occasion was there any fever or
raised sedimentation rate.
The negative EGG's in the third and fourth attacks of "cardiac infraction"
virtually ruled out that diagnosis. The history of "dizziness", etc., preceding the pain
was noted as "strange", but in view of the elevation of diastolic blood pressure on
admission the tentative suggestion of pheochromocytoma, with functional coronary
insufficiency during attacks, was made and investigation instituted. This proved to be
entirely negative.
In the meantime the patient appeared to be making satisfactory progress apart
from frequent complaints of "whacking" and "clicking" originating in the right
temple. This was not related either to the pulse rate or to chewing movements of the
jaw. She attributed her symptoms to her "blood pressure" and maintained that she
could always tell when it was high—which claim was disproved on several occasions.
On the seventh hospital day examination of the central nervous system showed
some impairment of hearing on the right, weakness of the right upper and lower limbs,
without evidence of pyramidal tract injury or of diminished tendon jerks; hemi-
heypoaestheaesia from the forehead down on the right; non-sensory ataxia of the right
upper limb, and patchy loss of vibration sense in the right lower limb.
It was noted that the presence of all the signs on the right side instead of crossing
over below the cranial nerve level was not easily accounted for in terms of an intracranial space-occupying lesion.
A neurologist called in consultation had little difficulty diagnosing anxiety
neurosis with hysterical overlay. While awaiting his visit the patient developed
several new signs and forgot some others, showing also some inherently contradictory
signs such as complete anaesthesia to pinprick with preservation of the hot and cold
sensation in the same area.
The search for an organic diagnosis was therefore abandoned and both the patient
and her physician were coming to grips with reality. Behind them there was a backlog
of four hospital admissions with expensive treatment, investigation and medical care.
Over several days the following story was elicited. The patient used to be a nurse
before her marriage and had seen patients with coronary artery disease. Her husband
died ten years previously, of cardiac infarction. Six years later she fell and fractured
her tibia and patella. She spent some months in hospital, had several operations and
suffered much pain.
Two years later she fell again and fractured her left hip. She spent six months
in hospital.   She was told that in all likelihood she would never be able to walk and
Page 412 that "she should be grateful that she still had a leg there at all".   However, she made
a fight of it and eventually began walking, though with a permanent limp.
Both accidents occurred while the patient was alone in the house and on both
occasions she was found unconscious on the floor.
For some time she has been having occasional dizzy feelings. This had not been
worrying her unduly, but after the second accident the attacks became increasingly
frequent and disabling. She felt that another accident could happen during one of
these and was not seldom left by herself. She was told that her blood pressure was
causing the symptoms and soon had to be admitted to hospital after a severe attack.
On discharge she was told that in all likelihood her high blood pressure had damaged
her heart and that she must not lift heavy objects, reach with her hands above her
head or wash floors. All of these orders she disobeyed, feeling extremely guilty, living
in fear of retribution for her trespasses.
The punishment soon came in the shape of another attack of dizziness, this time
followed by pain in the chest radiating to the left arm. On discharge she was told that
it was* not certain if she had a clot in her heart artery or not, but in any case her
activities must be curtailed even more severely.
Soon afterwards she moved to another town. One day the news came that her
son had been shot accidentally. The whole family was in turmoil over the news, no
one had much time for the patient who began feeling her "pressure going up again".
One afternoon she was left alone in the house, brooding, when it occurred to her that
she did not know any physicians in town on whom she could call " should something
happen to me". Finally she recalled a name and dialled the office for an appointment.
The receptionist told her that there was no chance for an appointment for a week.
"When I heard that, terrible dizziness came over me, the receiver dropped from my
hand, and I became unable to speak. The next thing I remember is the oxygen tent in
the hospital."
A dramatic rescue involving police and inhalator squad was effected—the patient
actually was perfectly conscious and clear-minded on admission as the record showed.
As already related a definite diagnosis of cardiac infarction was reached this time
and the patient enjoined to spend her remaining days in a chair. Her hobby used to
be rug-knitting and she was very proud of her skill. She asked her physician if she
could knit and was told:   "Yes, if you can do it without using your hands."
She used to stay in town at the homes of her three daughters, but now travelling
by car was out of the question. She became a permanent charge of her only unmarried
daughter. This girl had to forego both going out with her fiance "as we did not dare
leave mother alone".
The fourth attack came during another period of family stress, when a little
granddaughter had to come to live with them and naturally demanded much of the
daughter's attention.
The patient had good grounds for developing anxiety. She started with dizziness:
not an uncommon symptom in anxious people of all ages with or without hypertension.
Soon she learned that her labile blood pressure was the dause and developed "heart
consciousness". Through careful coaching by leading questions, aided by her memories
of nursing and of her husband's illness she learned to give a fair imitation of cardiac
infraction, fundamentally aimed at the termination of her constant dread of ever being
left alone. Finally when told she had no heart disease she developed a complicated
neurological syndrome, referred to her right side—the side from which her pseudo-
Meniere's syndrome originated.
The rehabilitation was slow and probably will never be complete. She was
reminded that her accidents had nothing to do with the "dizzy spells". Her fears
were brouht into the open and the mechanism of her symptoms explained. Eventually
she gave up the "blood pressure" as the cause of her ills and announced that she found
a way of stopping the spells by exerting pressure at a certain spot in front of her right
ear.
WjM Page 413 Within the last seven months she has been travelling, walking, going out to see
friends and enjoying life as much as any woman her age.
Discussion.
The first comment to be made is that ignoring a doubtful case of heart disease
causes less harm than giving a positive diagnosis on insufficient grounds. The exaggerated
fear of missing an organic diagnosis has already been responsible for creating thousands
of unwarranted cardiac invalids. To a layman the diagnosis of heart disease is fraught
with the fear of sudden death, and should not be given lightly; not even when reassurance and comfort are conveyed and certainly not when only prohibitions and gloom
are dispensed.
A cardiac infarct which does not produce unequivocal signs in a repeated twelve-
lead electrocardiogram is unlikely to lead to rupture of the heart, just as a doubtful
systolic murmur in a young man will not cause sudden death on a playing field. We
had just as well face the unpredictability of the coronary artery disease: a "cardiac
cripple" may live to bury his physician, while another patient may fall dead on the
doctor's doorstep after being given a clean bill of health. Frank admission of our lack
of knowledge detracts less from our prestige than gloomy and mistaken forecasts.
There is no evidence that prohibition of a reasonable amount of physical activity
adjusted individually extends the life of a cardiac by one single day. If the patient
has angina his activities should be adjusted to his exercise-pain threshold- If after
recovery from cardiac infarction the patient has no symptoms there is little reason to
interfere with his enjoyment of life within reasonable limits, whatever his T waves
are doing. In fact more often the patient needs to be encouraged not to fold up and
submit himself to the tender care of his relations who like the old people safely in bed
and out of harm's way. Certainly sedentary life, preoccupied with thoughts of death,
and with overeating as the only consolation, does not appear conducive to longevity.
It would be interesting to know how many of the physicians who recommend this
mode of life to their patients would accept it for themselves if faced with a choice.
Fundamentally a form of insurance is being taken out: "If the patient dies in spite of
my precautions they cannot blame me; if he does not, they will praise me for insuring
his survival by burying him alive."
Discovery and universal availability of the sphygmomanometer has proved to be
a mixed blessing. Everyone accepts that there should be the short and the tall amongst
us, but every small or transient deviation from the arbitrary "normal blood pressure"
is labelled hypertension—a disease practically synonymous with strokes to a layman.
In Fishberg's1 words, the situation is that: "Many persons .' . . would have been more
fortunate if they had never learned of their hypertension. As things are, however, it
is almost always necessary to tell an individual . . . for he is very apt to learn it from
another source and then his confidence in his physician is destroyed."
W. Evans2 defines hypertension as diastolic blood pressure of 110 or above, on
three different occasions. This definition, although probably too rigid for the younger
age groups, can be taken as a good working rule on the old. The height of systolic
blood pressure is of no consequence—many old people with inelastic, atheromatous
aorta have high systolic readings with normal diastolic, without for that reason being
hypertensive. Even if true hypertension is present it is doubtful if treatment is warranted in the absence of advanced retinal cardiac, renal or cerebral damage. Certainly
older age groups and especially women tolerate their hypertension well. And if one
does not intend to treat (assuming that effective treatment is available) there is little
reason to make the patient disease-conscious.
Stewart3 has shown that two large groups of hypertensive with 120 or higher
diastolic readings, symptoms such as headache and dizziness were present in 75%
of those who knew of their disease and in only 10% of those who dig! npt (mostly
cases of malignant hypertension). In the first group the headache, had all the usual
characteristics of anxiety tension headache, and developed soon after the patients became
acquainted with the diagnosis.   Thus it is doubtful if any symptoms can be attached
Page 414 §f&ij to benign essential hypertension per se—but certainly symptoms of doctor-provoked
anxiety are only too common.
L. Mirabel, G.B., Ch.B., M.R.C.D.   (Ed.)
Bibliography.
1A. Fishberg, "Hypertension & Nephritis," 1946.
2W. Evans, "Cardiology," Butterworth, 1947.
|| McD. G. Stewart, "Lancet" I,  1985,  1261.
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Page 415 1?
PUBLIC HEALTH AND MENTAL HEALTH NEWS
G. F. AMYOT, M.D., D.P.H.,
Deputy Minister of Health, Province of British Columbia
A. M. GEE, M.D.,
Director, Mental Health Services, Province of British Columbia
SYPHILIS TODAY
From Division of V. D. Control
Introduction
Syphilis was the scourge of Europe for over 400 years prior to the discovery of
the causative organism of this disease by Schaudinn and Hoffman in 1905. In the
following year, 1906, Wassermann, Neisser and Bruck introduced their complement
fixation test which first permitted the serologic diagnosis of syphilis. With the attainment of these two excellent diagnostic procedures the groundwork was laid for a
similar advance in therapy. Within three years Ehrlich announced his discovery of
salvarsan which at that time was heralded as the answer to syphilis—but which was
soon found to fall short of the mark that had been hoped for by its originators.
No paper should omit mention of the arsenical and heavy metal era in the treatment of syphilis. With the introduction of salvarsan for the treatment of syphilis
Ehrlich was responsible for a new concept in medicine now referred to as chemotherapy,
i.e., the phenyl arsenoxides are known to act on spirochetes directly, presumably by
blocking the essential—SH group. In other words, by the administration of salvarsan,
neoarsphenamine or mapharsen the physician was able to bring about a clinical and
biologic result due to the specific action of a chemical on the responsible organism,
treponema pallidum. The use of the arsenicals and bismuth was not without risk however and the lengthy period of treatment required made it impossible to achieve the
best therapeutic response. A large percentage of patients were reluctant or unable to
continue with the 18 months or so required to ensure a satisfactory response. Because
of this large inadequately treated group, relapses were common. |
Expert opinion today admits that penicillin is the treatment of choice and has
now completely replaced arsenic, bismuth and mercury for all stages of syphilis. This
therapeutic concept cannot be denied when the facts that are well knownrto all are
considered. The etiologic organism, the Treponema Pallidum, has not as yet shown any
tendency to be drug-resistant; in fact it still remains as the most susceptible organism
to penicillin in the bacteriological spectrum.
Therapy
In June of 1943 Mahoney, Arnold and Harris demonstrated that penicillin was
effective in early syphilis. Initially this drug showed promise of being the answer to a
rapid cure for syphilis as well as being non-toxic in comparison with the hazardous
older forms of therapy, such as the arsenicals and bismuth.
In summary, it might be stated that six million units of a long acting form of
penicillin over a period of ten days is considered adequate treatment of early, early
latent or syphilis in pregnancy. A total of twelve million units of a similar type of
penicillin over twenty days is adequate therapy for late symptomatic syphilis (e.g., with
cutaneous, osseous, central nervous system or cardiovascular complications).
The corticosteroids have also found a place in the treatment of this strange and
stubborn disease. By the use of topically applied cortisone or hydrocortisone to the
acute inflammatory ocular lesions of congenital syphilitic interstitial keratitis we have
completely revolutionized the outlook for this disease which has hitherto been remarkably resistant. Both corticotropin and cortisone have recently been mentioned to have
a beneficial effect in the management of the late manifestations of tabes dorsalis. As
yet, however, the results have not been conclusive.
Page 416 Diagnosis
Prior to 1949 the diagnosis of syphilis was based on: darkfield examination of the
suspected lesion to determine the presence or absence of the treponema pallidum,
clinical signs and symptoms suggestive of syphilis and the non-specific standard serologic
tests, i.e., the complement fixation test (e.g., Kolmer modification of the original
Wassermann) and the precipitation tests (e.g., Kahn). The standard serologic tests are
biologically non-specific. By this it is meant that the antigens used in the various
complement fixation and flocculation reactions are prepared from non-syphilitic, normal
mammalian tissues, such as beef heart. The nature of the reacting substance in the blood
serum, reagin, has not been fully determined. Reagin has no demonstrable spirochaetal
reactions as have true antibodies. Because of this biologic non-specificity such tests as
the complement fixation (Kolmer Wassermann) and flocculation (Kahn) frequently
were reported as positive and in many cases over one-third of all such positive results
were due to causes other than syphilis, e.g., lupus erythematosus, infectious mononucleosis, recent vaccination, upper respiratory infections, etc.
Because of this serious sero-diagnositc short-coming in cases of latent syphilis the
introduction of the treponemal immobilization (T.P.I.) test by Nelson and Mayer in
1949 served as the most important development in the past five years. This test thus
allows recognition of the biologic false positive test from syphilis. The use of the T.P.I,
test under appropriate conditions permits the physician to answer the age-old question
"does the patient have syphilis?"
Patients displaying the chronic biologic false positive phenomena should be examined thoroughly to rule out the possibility of serious underlying disease, e.g., lupus
erythematosus. In the recent past the medical profession has been led to believe that
the presence of a persistent biologic false positive reaction was innocuous in the light
of preesnt knowledge, but this is not true.
Unfortunately, neither the Division of Laboratories nor the Division of V.D.
Control is able to have the T.P.I, test performed on an unlimited number of serologic
samples because of the inadequate laboratory facilities that exist in Canadja for the
performance of this test. However, in a limited number of cases which present a real
diagnostic problem the Division of V.D. Control is able to have the test done by the
Department of Health of the Province of Ontario.
Epidemiology
It can be seen, therefore, that recent years have brought with them remarkable
advances in the diagnosis and treatment of venereal disease. However, neither society
nor individuals will derive appreciable benefit unless these advances in medical science
can be applied to infected persons early in the course of their disease. Each year a large
number of persons are infected with syphilis, but do not begin treatment until the
latent or late stages, if at all. It is apparent, therefore, that intensive epidemiological
effort must be expended to find these hitherto unknowta cases.
At the present time, three principal case-finding methods are in general use—
education, mass screening, and contact tracing. Education is an effective means for
bringing a large number of persons to voluntary treatment and has been pushed to the
utmost since 193 6 when Parran blasted syphilis into social consciousness. As might be
expected, mass screening tests bring in the bulk of the latent (symptomless) syphilis,
but lose their effectiveness as the prevalence of the disease declines. Contact investigation, therefore, remains as a selective process that brings to examination only persons
exposed to known cases of V.D. While the possibilities of this method were indicated
by Bierhoff as early as 1910, the practicability of this technique was not generally
accepted until the classical observations of Munson, Brumfield, and Sniith, in the early
'30s graphically demonstrated the "transmission sequence of syphilis", and its mode of
spread by a series of local outbreaks. These workers emphasized the patience, tact, and
energy necessary to successful tracing of contacts and pointed out the important place
of the physician in these studies which "cannot be done successfully by nurses and
social workers alone."
Page 417 Numerous studies into the epidemiologic phases of venereal disease have been carried
on in the Provincial Division of V.D. Control, Vancouver, B.C. These studies have
clearly demonstrated several important considerations which determine the success or
otherwise of an epidemiologic program.   Thus, it is important:-
(1) To obtain all sexual contacts to the known case by careful interviewing and questioning on the part of the epidemiologist or private physician.
(2) To bring all suspected contacts under examination, and treatment if necessary,
within a matter of hours prior to the infection being passed to a third party.
(3) To recognize the importance of the female as a potential carrier, particularly of
gonorrhoea, and to understand the importance of treating her on epidemiological
grounds as such, because of the difficulties associated with the bacteriological diagnosis of venereal disease in women.
Conclusion
This short paper has sought to trace the therapeutic and diagnostic advances that
have been achieved over the past fifty years. During this period of time penicillin as a
specific anti-syphilitic agent has been proven. The previously used non-specific standard
serologic tests have been modified to increase their sensitivity and specificity. And most
recently the addition of the T.P.I, test as a specific serologic diagnostic aid has at last
bridged a gap of ignorance that had been with us for many years.
One of the last problems of syphilis that has refused to bow before modern
medical technology has been our inability, satisfactorily, to maintain a growth of the
Treponema Pallidum on artificial media. When this problem is solved the next great
advance may be in the field of immunology and may well usher in mass protective
programs for our populations.
Finally, V.D. spreads as a rule directly from person to person, so that the physician
does not need to worry about vectors and intermediate hosts. The basic problem is
therefore to find new cases. Apart from educational and screening techniques of case-
finding, the private physician can do much towards successful control over these diseases
by recognizing the part which he plays in the contact tracing program thus enabling
it to achieve its best results through the application of the three simple precepts outlined
above.
REPLACEMENT OF KAHN TEST BY VDRL TEST
From Division of Laboratories
Over the past few weeks the Central Laboratories in Vancouver have replaced the
Kahn test by a test developed by the Venereal Disease Rlesearch Laboratory (VDRL)
of the United States Public Health Service. After extensive trials, the Laboratories are
in accord with the claims made by other authorities that the VDRL test is superior to
the Kahn test in specificity. At their annual conference in Ottawa last December, the
Provincial Laboratory Directors agreed to adopt the VDRL test in place of the Presumptive and Standard Kahn tests; and the change now being effected is in line with
this resolution.
The VDRL test, like the familiar Kahn test, involves a precipitation reaction. The
Kolmer-Wassermann complement fixation test will continue to be done on all specimens
giving a positive or doubtful precipitation reaction. The terminology hitherto used in
reporting reactions, viz. POSITIVE, DOUBTFUL and NEGATIVE, will be unchanged
and will carry the same significance as before.
The branch laboratories will probably change over to similar procedures within
the next few months.-
COMBINED REQUISITION AND REPORT FORMS
A new report form has also been adopted.  This step again conforms with the views
of the Laboratory Directors' Conference that a combined requisition and report form
presents many advantages. When completing the requisition part of this form physicians
should bear in mind that they are in effect addressing the report to themselves.
Page 418 leu/3  an
d   ifoted
We would like to include your district medical news in the "News and Notes"
column of the "Bulletin". Will you kindly write in some of the recent meetings, elections, births or marriages, etc., and mail to Dr. J. L. McMillan, 1401 West Broadway,
Vancouver, B.C.
Drs. J. L. M. Anderson, D. A. Hewitt, George McKenzie, and A. W. Perry of
Victoria spent a week in Los Angeles observing the Polio Therapy in various centres.
Dr. R. E. Burns of Victoria has taken a post in the Department of Dermatology,
Henry Ford Hospital, Detroit.
Dr. Kemble Greenwood, formerly of England, is now practising dermatology in
Victoria.
Dr. John Harvey, formerly of Vancouver, is in Victoria practising neuro-surgery.
Dr. Brock Chisholm, former Director-General of WHO, addressed the Victoria
Medical Society at a recent meeting on the World Health Organization.
BIRTHS
Born to Dr. and Mrs. R. Spicer, of Victoria, a daughter.
Born to Dr. and Mrs. Mark Roach, of Victoria, a daughter.
Born to Dr. and Mrs. D. Longridge, of Victoria, a daughter.
Born to Dr. and Mrs. David Claman, of Vancouver, a son.
Born to Dr. and Mrs. J. G. Gillis, of Vancouver, a son.
Born to Dr. and Mrs. Gordon Westgate, of Vancouver, a daughter.
MARRIAGES
Dr. Maurice Young, to Mrs. Kay Long, both of Vancouver.
*
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Kingsway at llth Ave. — Telephone EMerald 2161
Vancouver 10,  B.C.
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Page 420

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