Rubert W. (Rubert William) Boyce.

Yellow fever and its prevention : a manual for medical students and practitioners online

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careful manuscript records of the diseases prevalent amongst
the troops and sailors similar to those which have been
preserved in Freetown.

There has been, however, a strong opinion expressed by
many of the experienced traders that the disease which has
proved rapidly fatal to the white man on several occasions, and


which had at the time been attributed to a malignant form of
malaria, was, in all probability, yellow fever. This view is much
strengthened by the outbreak of yellow fever which took place
in Bonny in 1899, an d by the undoubted cases, in my opinion,
of yellow fever which occurred in Lagos in 1893- 1894 and again
in 1905 and in 1906.

I will now briefly record the outbreaks and supposed
outbreaks of the disease in some of the chief towns of Southern
Nigeria, in order that the student may realise why I consider
yellow fever endemic in Southern Nigeria at the present

time : —

Yellow Fever in Southern Nigeria

Warri. — The medical officer reports that a tradition exists
that there was a yellow fever outbreak at the European factories
about the years i860- 1870.

Calabar. — An undoubted case occurred in the years 1890-

Bonny. — 1873: Several deaths were recorded which might
have been due to yellow fever.

In 1883 it is stated that an outbreak of yellow fever occurred
due to importation from Freetown.

In 1 890- 1 89 1 a very serious outbreak is recorded of what
was unquestionably yellow fever. The medical officer, Dr
Parker, was certain that it was genuine yellow fever. The
description of the symptoms are such as to leave no doubt as to
the nature of the disease. The disease was thought by some to
be malignant malaria, and was attributed to the pulling down of
an old factory ; others maintained that it was introduced in the
straw and litter on a ship coming from South America.

The natives were not affected. There were 1 1 cases and 9
deaths amongst the population of 15 white men.

Dr A. J. Brown, who was in Bonny at the time, informs me
that he attended two of the cases. The symptoms were head-
ache, pain, great prostration, albuminuria, yellowness, persistent
black vomiting.


Dr Parker, who was the medical officer at the time, stated
that he was convinced that the disease was yellow fever.

He subsequently contracted the disease and died.

Dr MacDonald, Bonny, has furnished me with notes of a
suspicious case which occurred in 1909, six weeks after arrival in
Bonny. The diagnosis at the time was " gastritis and jaundice."
No malarial parasites were, however, found in the specimens of
blood which were repeatedly examined.

From numerous inquiries which I have made there can be
no doubt that yellow fever occurred in Lagos in a virulent form
from 1 894- 1 895. Thus, I have it on reliable authority that 17
members of a mission arrived from England in Lagos on
13th December 1893. Of these, 5 had died by the end of
January 1894. In addition, a resident missionary, and the
young child of another missionary, had also died. The cases
presented the classical symptoms of yellow fever. According to
Ott, cases were reported at Lagos in 1896. This is confirmed
by Dr Hopkins who saw 2 cases in that year.

At Sapele, in 1898- 1899, there were a considerable number
of suspicious deaths; and in 1907 an outbreak of a severe type
of fever was recorded at Widah.

Examination of the medical notes in the hospital at Lagos
convinces me that genuine well-marked cases of yellow fever
occurred in the years 1902- 1905 ; there were also many mild

The symptoms recorded are violent headache and body
pains, high temperature, slow pulse, suppression of urine, black
vomit, and coma, terminating fatally. In 1905 the symptoms
recorded could hardly be those of any other disease but yellow
fever, yet the diagnosis made at the time included " fever and
gastritis" and "fever and morbus cordis" — a diagnosis which
Ott also states was made in Togoland. I am therefore strongly
of opinion that in Lagos one of the causes of mortality in the
past has undoubtedly been yellew fever. When it is recollected
how little is known of the fevers amongst the 60,000 native


inhabitants of Lagos, and when it is understood that by far the
most abundant mosquito is the Stegomyia, it is not unreasonable
to assume that the natives in all probability suffer from a mild
type of yellow fever, and that, therefore, yellow fever is endemic.
Further evidence in favour of this contention is furnished by
the admitted frequent presence of yellow fever in Dahomey and
Togoland close by (see these colonies). It must also be
recollected that, just as in the case of Sierra Leone, the infected
Stegomyia were not destroyed by fumigation, but were left to
propagate the disease.


I think I have brought forward sufficient evidence based
upon accurate records, clinical and historical, written by men
of admitted ability and experience in yellow fever, to conclusively
prove that yellow fever has been of far more frequent occurrence
than is usually supposed on the West Coast. That, in fact, it
has appeared annually over a very large number of years
practically, as my figures show for the last hundred years.

A few gaps of a few years have occurred, such as between
1852 and 1858, 1868 and 1872, 1873 and 1878, 1878 and 1883,
1884 and 1890.

But from 1890 to the present date I am of opinion from
the data which I have examined that there is an unbroken

During the whole hundred years there is no large interval
which would make it reasonable to suppose that yellow fever
had completely died out on the coast.

In my opinion this evidence is so strong that we are obliged
to assume that the disease is endemic upon the West African
coast for at least the last hundred years.

The question now therefore arises, by whom has the virus
been kept up ?

In the first place, we know positively that the transmitting
agent, the Stegomyia y is present in overwhelming quantity. It


only remains to prove how a continuous source of infection has
been maintained.

To those who would adopt the theory of importation, it would
mean a continuous importation from, say, the West Indies,
Central, or South America, and there is no history of such

Therefore, in my opinion, the most reasonable explanation
is the one which has proved correct in the West Indies, Central,
and South America ; and is adopted by the most recent English,
French, and German investigators in yellow fever, namely, that
the disease exists amongst the natives in a mild form ; in other
words, that it is endemic.

A little consideration will show that the whites have not
been the source of the continuous infection for the reason
that the total number of whites on the whole West African
coast has never been large enough to admit of continuous
keeping up of the virus ; the whites are in the very small

Therefore, precisely as in the case of the sister disease,
malaria, the continuous or endemic source of infection is the
comparatively dense native population of the West Coast.

The evidence which I have brought forward also conclusively
points both in English, French, and German colonies to a vast
amount of mistaken diagnosis. Yellow fever was not suspected
in its mild form, and it was not found out, it was only discovered
when fatal cases made their appearance, and, as my evidence
shows, these cases were as often as not mistaken for other
diseases. These same mistakes in diagnosis have occurred over
and over again in yellow fever countries, especially in the

I therefore conclude from the evidence that a comparatively
large number of deaths and mild cases have occurred from
yellow fever in the past and which have been attributed to
malaria, chiefly the "bilious remittent fever." Most authorities
upon yellow fever are agreed that in a very large number of



instances " bilious remittent fever " is another name for yellow

It must be recollected that it is only in this year that effective
sulphur fumigation of the infected Stegomyia has been attempted
on the West Coast after outbreaks.

Therefore infected Stegomyia were left in the past to live on
and to carry infection into a succeeding year.

Finally : —

(i) The historical record of outbreaks and sporadic cases, as
recorded above ;

(2) Mistaken diagnosis ; and

(3) The absence of any destruction of infected Stego?nyia in
the past, is evidence overwhelmingly in favour of the disease
being endemic on the coast, and of its having been repeatedly
mistaken for other diseases or entirely overlooked.

Tears in which Yellow Fever has appeared in Sporadic or
Epidemic Form in West Africa

Note. — These figures are based upon documents, official reports, and
published memoranda carefully examined by the author.































18 16






























— .















In this chapter I desire to draw attention to the various types
of yellow fever, those forms, more especially, which often pass
unrecognised because of the mildness of their symptoms ; but
which nevertheless are the means of keeping up a constant
infection, and are the source of the more typical severe forms of
fever which attack non-immunes and new arrivals.

The study of infectious diseases teaches us that until we are
in possession of some simple scientific clinical test, such, for
example, as the finding of a protozoon or bacterium in the
blood, or in a tissue, or until we possess a serum reaction as in
the case of typhoid, there must exist immense difficulty as to
the diagnosis of the true nature of any disease in its early

The young medical officer will experience this difficulty in
deciding what is and what is not yellow fever. The same
difficulty crops up in every disease. Were we in a position to
diagnose early the very mild forms of typhoid, scarlet fever,
diphtheria, etc., the prevalence of these diseases in Europe to-day
would be far different.

In the majority of cases a diagnosis is not made until the
well-marked, severe, or as they are termed " classical " signs
of the disease in question have declared themselves. So it is
with yellow fever.

It is for these reasons that it is very essential to study what
are the uncomplicated symptoms produced by the bite of the



Stegomyia, and then to analyse and see if in nature there are
diseases which present similar or closely similar symptoms.

I have endeavoured to bring out these points in the following
account. It will serve as an introduction to those more severe
symptoms met with in yellow fever, which are regarded as
" typical " of that disease.

It is a golden rule in analysing any disease, to, where
possible, direct in the first instance attention to experiments or
direct observations. Unfortunately a large number of tropical
diseases are still based upon a most hazy and inaccurate patho-
logical foundation.

In yellow fever, however, thanks to the experimental
work of Finlay, Reed, Carroll, and other American observers, we
have a very definite foundation to build upon.

I. — Experimental Yellow Fever

The reason why the Reed Commission did not hesitate to
make direct Stegomyia inoculations in man, was because as they
state, Finlay had shown as the result of 90 inoculations that
little danger resulted from the bites of infected Stegomyia. In
other words, Finlay found that in 18 per cent of his inoculation
experiments there resulted a very benign form of yellow fever.
The American Commission made a series of very carefully
recorded observations, and in 12 cases were able to produce
yellow fever in its milder type. The following are some
typical examples : —

CASE V. — Infected 19th January. On the 23rd took to bed
with feeling of lassitude and headache ; temperature 99-2°; pulse
78. Later in the day these symptoms increased, and were severe
headache, chill, eyes and face flushed ; temperature 100 G ; pulse
104 ; still later headache increased with marked backache,
vomited once; temperature 103-6°; pulse no.

At the end of 42 hours albumin appeared in the urine.
The sclerae became jaundiced on the second day, and by the
fourth day this had extended to other parts of the body.

FlG. 6. — Temperature and pulse curve
(dotted lower curve) from an experi-
mental case of infection by the
Stegomyia. There is an early remis-
sion in the temperature curve on the
second day. The pulse falls from
the end of the first day, and does not
follow the temperature. — GuiTERAS.

[To face X'- 100.


The symptoms did not increase, and on the seventh day the
temperature was normal.

Diagnosis. — Yellow fever of moderate severity.

Case VI. — C. W., American, non-immune, aged twenty-
seven, with his full consent was at 9.30 A.M., 31st January, bitten
by two of the three mosquitos that had been applied to the
foregoing Case V. The interval that had elapsed since their
contamination was therefore 51 days. The subject remained
well until 12 o'clock noon, 3rd February, when he complained
of heaviness in his legs and some supra-orbital pain. His
temperature at this hour was 99° F. and pulse 70. At 1.30 P.M.,
it had risen to ioo° F., and at 5 p.m. to ioo-6° F., and pulse to 84.
The primary rise of fever, which was somewhat fluctuating in
character, did not reach its height until at the end of 24 hours,
noon, 4th February, when temperature was 102-4° an d the
pulse 92. The facies was now suggestive of yellow fever.
Remission occurred at the end of 45 hours and lasted for about
one day. The secondary rise was slight in character, the tempera-
ture falling to normal on the morning of the sixth day. The
case was very mild in character. Albumin appeared at the
end of 75 hours (beginning of fourth day); it never amounted
to more than a distinct trace and disappeared on the eighth
day. There was no occular jaundice, and although the gums
were injected and swollen, there was no haemorrhage at any
time. The patient perspired freely throughout the attack.
Convalescence was rapid. The subject had been in quarantine
for the period of 6 days prior to inoculation.

CASE VII. — J. H., American, non-immune, aged twenty-six,
with his full consent was bitten at 1 1 A.M., 6th February 1901,
by the same two mosquitos that had 6 days previously bitten
Case VI. Fifty-seven days had therefore elapsed since the insects
had been contaminated by biting a case of yellow fever. He
remained well until 12 o'clock noon, 9th February, when he
experienced slight chilly sensations, accompanied by yawning.
At this hour his temperature was ioo° F. and pulse 72. At
3 P.M., temperature 98-8°, pulse 72. Says that he feels " out of
sorts" but has no headache. At 5.30 P.M. his temperature was


100-6° F., pulse 78. He was not seen until 7.30 p.m., when he
complained of backache and severe general headache, more
intense through the frontal region. Eyes much injected,
photophobia very marked, face flushed. He was stretching and
yawning constantly, complained of nausea, and vomited a small
quantity of partially digested food. The height of the primary
fever was reached at 3 P.M., 10th February, i.e. 22 hours after
the commencement of the attack, when the temperature was
102-8° and the pulse 98. Remission of the fever to 99-4°, and
the pulse to 74, occurred at 6 A.M., nth February, making the
duration of the primary paroxysm 36 hours. Twenty-four
hours after the remission had occurred, the temperature had
risen to 102-4° with a pulse of 70. The fever continued to
steadily increase until midnight of 12th February, when a
temperature of 105° F. was recorded, with a pulse of 90. The
subsequent course was that of a case of severe yellow fever.
Slight oozing of blood from the gums occurred as early as the
third day. Ocular jaundice, beginning on the third day became
later very distinct, and was associated with general jaundice.
Albumin, however, did not appear until the sixth day. The
fever subsided on the ninth day, and was followed by a slow
convalescence. The subject had been in strict quarantine for
a period of 78 days prior to inoculation.

Cases of Yellow Fever Produced by the Injection of Blood
(Reed, Carroll, and Agramonte)

CASE I. — W. J., American, non-immune, aged twenty-seven
— in quarantine since 20th December 1900 — with his full consent
at n A.M., 4th January 1 901, was injected subcutaneously with
2 c.c. of blood taken from the general circulation of a case of
mild yellow fever at the beginning of the second day of the
disease and having a temperature of ioo-8° F. The subject,
who had been in strict quarantine at the station for a period of
45 days, remained in his usual health until the early morning of
8th January, when he complained of slight frontal headache.
At 6 A.M. his temperature was 98-2° F., and pulse 70 ; 9 A.M.,
temperature 98-8° F., pulse 95 ; frontal headache increased,
with slight, chilly sensations in the feet and lower extremities.
There was some congestion of the eyes, and his usual florid


complexion was heightened in colour. At 10.15 A - M - tempera-
ture 100-6° F., pulse 97 ; complains of some pain in the lumbar
region. At 11.20 a.m., temperature 101-4° F., pulse 99. The
height of the febrile paroxysm was reached at 3 P.M. the same
day when the temperature was 103-4° F., and pulse 108. The
facial expression was now characteristic of yellow fever. The
eyes were deeply injected and watery and the face much
suffused. Photophobia moderate, frontal headache and backache
severe. The skin was moist. The remission occurred at the
end of 24 hours — 9 A.M., 9th January — when the temperature
had fallen to 99-4° F. and the pulse 86. The subsequent history
was that of a case of yellow fever of moderate severity. Albumin
was found in the urine at the end of the sixty-first hour. There
was some bleeding from the gums on the third day and moderate
ocular jaundice on the fourth day. Fever disappeared on the
morning of the seventh day.

Case II. — W. O., American, non-immune, aged twenty-
eight, in quarantine since 20th December 1900. On 8th January
1901 at 9 P.M., with his full consent, he was given, by subcutane-
ous injection, 1-5 c.c. of blood taken from the median cephalic vein
of Case I. just 12 hours after the beginning of the attack, and
when the temperature was 102-4° F- — that is, just after the first
febrile paroxysm began to decline. The subject remained in
his usual condition the following two days.

nth January 1901. — Six a.m. his temperature was 98-9° F.
and pulse 70. He complained of being disturbed by dreams
during the night and had some frontal headache. At 9 A.M.
temperature 100° F., pulse 77. At 10.15 A.M. temperature
ioi-4°F., pulse 76. Eyes decidedly congested and face moder-
ately suffused. At 12 o'clock noon, when the temperature had
risen to 103-2° F. and the pulse 102, the height of the primary
paroxysm had been reached. Headache and backache were
now much complained of. The facial expression was character-
istic. The remission occurred at the end of 24 hours, lasted one
day, and was followed by a very moderate secondary fever. A
distinct trace of albumin was found in the urine passed at
2 A.M., 1 2th January, 17 hours after the attack began. A few
hyaline casts were also present. Slight bleeding from the gums.


occurred on the second and third days of sickness. The
character of the attack in this case was very mild. The
albumin, which at no time amounted to more than a distinct
trace, did not disappear, however, until 24th January.

CASE III. — W. F., American, non-immune, aged twenty -three,
was, with his full consent, at 1 P.M., 22nd January 1901,
injected subcutaneously with 0-5 c.c. of blood taken on the second
day from the general circulation of a severe case of yellow fever,
which was fatal on the seventh day of the disease. The patient's
temperature when the blood was withdrawn was 103 F. and
pulse 90°. The subject remained well during the following day,
24th January ; at 6 A.M. his temperature was 98-4° F. and pulse 78.
He partook of a hearty breakfast at 6.30 A.M. which he vomited
soon afterwards. At 7 A.M. he complained of dizziness and
general lassitude ; temperature 98-4° F., pulse yS. At 9 A.M.
chilliness complained of, but there is no record of temperature
or pulse. At 9.30 A.M. temperature ioo-6° F., pulse 82. Frontal
headache well marked. Eyes already injected and face slightly
suffused. At 10.30 A.M. temperature ioi-2°F. and pulse 86.
An hour later his temperature was 102-6° F. and pulse 82. The
height of the primary paroxysm was reached at 1 P.M. when the
temperature was 102-8° F. and pulse 98. At this hour photo-
phobia was well marked, and constant complaint made of severe
frontal headache and backache, together with pains in the lower
extremities. The skin was moist The remission occurred at
the end of 36 hours. The subsequent course was that of
a case of yellow fever of moderate severity. With the return of
the secondary fever there was present sharp backache and
headache. Albumin appeared in the urine at the end of 57J
hours. Ocular jaundice was present on the third day and there-
after until convalescence. The gums did not bleed, although
they were swollen and injected. Fever subsided on the sixth
day, and albumin disappeared on the eighth day.

CASE IV. — J. H. A., American, non-immune, aged twenty-
two, with his full consent, received subcutaneously, at 12.15 p - M ->
25th January 1901, 1 c.c. of blood taken from the median
cephalic vein of Case III. just 27! hours after the commence-
ment of the latter's attack of yellow fever; temperature


ioo-6° F. The subject remained in his usual condition during
26th and 27th January, except that on the afternoon of the last
mentioned date he complained of occipital headache. This was
present on the following morning, 28th January ; otherwise he
felt well. His temperature at noon was 98-6° F. and pulse 6$.
Occipital headache continued. He partook of dinner with fair
appetite. He was not seen again until 3 P.M. In the mean-
while, at 1.1 5 P.M., the patient states that, while sitting alone in
his tent, he began to feel cold, and that this was quickly followed
by a decided chill with increase of headache. He noted the
hour in writing at the time. At 3 P.M. his temperature was
103-6° F. and pulse 120. The eyes were intensely congested
and face deeply suffused. The patient was very restless, and
complained bitterly of occipital headache and backache. Photo-
phobia was very marked. He vomited several times within the
next 2 hours. Skin hot and dry. The height of the primary
paroxysm was reached at 3.30 P.M., at which hour the tempera-
ture was 104-2° F. and pulse 120. The subsequent history was
one of severe yellow fever. There was no remission of the fever
until the fourth day, when the temperature fell to ioi-2°F.
Now, for the first time, the patient ceased to complain of
occipital headache and backache. Albumin appeared at the
end of i8| hours (7.30 A.M., 29th January). A few hyaline
casts were also present at this time. The specimen of urine
passed at 6.40 A.M., 30th January, contained albumin one-
twentieth by volume, and many fine and coarse granular,
bile-tinted casts. Ocular jaundice appeared on the third day.
The skin of the face and of the anterior part of the neck and
thorax was tinted on the fourth day. This rapidly became
intensified and general. The secondary fever lasted about 30
hours, the temperature falling to 97-2° F. at 12 o'clock (mid-
night) of the fifth day. Marked fluctuations of temperature
continued until the eleventh day of illness. Recovery was

Online LibraryRubert W. (Rubert William) BoyceYellow fever and its prevention : a manual for medical students and practitioners → online text (page 8 of 30)