SECONDARY INFECTION IN THE WARD TREATMENT OF INFLUENZA AND PNEUMONIA
EUGENE L. OPIE, M.D.; FRANCIS G. BLAKE, M.D.; JAMES C. SMALL, M.D.; AND
THOMAS M. RIVERS, M.D.
One of the most pressing problems that presented itself in the care of
influenza and pneumonia patients in the army cantonments during the
recent epidemic was the danger of secondary contact infection because of
the overcrowding of the base hospitals, nearly all of which were taxed
far beyond the limits of their capacity. That this danger was very real
was fully demonstrated by certain studies in ward infection that this
commission was able to make at Camp Pike[49]. It is the purpose of the
present section of the report to present these studies and to discuss
the means whereby this danger may be most successfully met.
It is perhaps well, first to define exactly what is meant by secondary
contact infection in influenza and pneumonia. In our experience at Camp
Pike it was found that a very large percentage of the pneumonias
following influenza were accompanied by secondary infection with
pneumococcus, some few being caused by hemolytic streptococcus. The
types of pneumococcus encountered were almost entirely those that are
found normally in the mouths of healthy men, approximately 85 per cent
being Types II atypical, III, and IV. It has been generally accepted
that infection with these types of pneumococci is usually
autogenous—that is, that under the proper conditions of lowered
resistance an individual becomes infected with the pneumococcus that he
carries in his own mouth. Many observations made during the course of
the present work have suggested that this is probably not so in many
instances and that the influenza patient may not be so much in danger
from the pneumococcus that he normally carries in his own mouth as he is
from that carried by his neighbor, in other words, he is in danger from
contact infection. The same considerations hold true with respect to
hemolytic streptococcus infection. Secondary contact infection in cases
of already existing pneumonia following influenza were found to occur
frequently. These were for the most part caused by hemolytic
streptococcus infection superimposed upon a pneumococcus pneumonia. Many
instances of double pneumococcus infection, however, either coincident
with or following one another were encountered.
Secondary Infection with S. Hemolyticus in Pneumonia
Pneumonia caused by streptococci was repeatedly observed[50] during the
pandemic of influenza which occurred in 1889–90. With clearer
recognition of the characters which distinguish varieties of
streptococci several observers have shown that secondary infection with
hemolytic streptococci may occur during the course of pneumonia and
though definite evidence has been lacking have suggested that it may be
acquired within hospital wards. That a similar secondary infection with
S. hemolyticus in pneumococcus pneumonias following influenza occurred
not infrequently at Camp Pike during the epidemic was shown by
bacteriologic studies made during life and at autopsy in a considerable
series of cases. During the early days of the epidemic of influenza,
secondary streptococcus infection was almost entirely limited to certain
wards which were opened for the care of the rapidly increasing number of
patients with pneumonia. During this period these wards were
overcrowded, organization was incomplete, and the opportunities for
transfer of infection from patient to patient were almost unlimited. The
spread of streptococcus contagion and its fatal effect may be clearly
brought out by comparison of these wards with wards that had long been
organized for the care of patients with pneumonia.
Ward 3 had been in use for the care of patients with pneumonia for some
time prior to the outbreak of influenza. It was provided with sheet
cubicles and conducted by medical officers, nurses and enlisted men
accustomed to the care of patients with pneumonia, ordinary precautions
being taken against transfer of infection from one patient to another.
The data in Table XVII show the average number of patients in the ward,
the number of new cases of pneumonia admitted, and the number of deaths
among patients admitted during the corresponding period, for three
periods of ten days each from September 6 to October 5. The types of
infection in fatal cases as determined by cultures taken at autopsy are
also shown.
TABLE XVII
PNEUMONIA IN WARD 3
═════╤════════╤════════╤═════════════╤═════════════════════════════════════
│AVERAGE │ NUMBER │TOTAL DEATHS │ CULTURES AT AUTOPSY
│ NUMBER │ OF │ AMONG │
│ OF │PATIENTS│ PATIENTS │
│PATIENTS│ADMITTED│ ADMITTED │
│IN WARD │ │ DURING THE │
│ │ │CORRESPONDING│
│ │ │ PERIOD │
─────┼────────┼────────┼──────┬──────┼────────────┬───────────┬────────────
„ │ „ │ „ │NUMBER│ PER│PNEUMOCOCCUS│ S.│UNDETERMINED
│ │ │ │ CENT│ │HEMOLYTICUS│(NO AUTOPSY)
─────┼────────┼────────┼──────┼──────┼────────────┼───────────┼────────────
Sept.│ 18.6│ 11│ 3│ 27.2│ 3│ 0│ 0
6–15 │ │ │ │ │ │ │
Sept.│ 46.1│ 52│ 16│ 30.7│ 13│ 1│ 2
16–25│ │ │ │ │ │ │
Sept.│ 58.6│ 23│ 8│ 34.7│ 5│ 1│ 2
26–Oct.│ │ │ │ │ │ │
5 │ │ │ │ │ │ │
─────┴────────┴────────┴──────┴──────┴────────────┴───────────┴────────────
During the period from September 6 to 15, just prior to the outbreak of
influenza in epidemic proportions, the ward had an average population of
18.6 patients. The total number of new patients admitted was 11, of whom
3 died, a mortality of 27.2 per cent. All these cases were pneumococcus
pneumonias as determined by bacteriologic examination of the sputum at
time of admission. The 3 fatal cases showed pneumococcus infection at
autopsy. During the second period, from September 16 to 25, with the
outbreak of the epidemic of influenza, the ward rapidly filled with new
cases of pneumonia, attaining an average population of 46.1 patients. Of
the 52 new cases admitted 16 died, a mortality of 30.7 per cent. Again
all the cases admitted during this period in which bacteriologic
examination of the sputum was made, were found to be pneumococcus
pneumonias with one exception. This case, admitted on September 21 and
dying two days later, had a hemolytic streptococcus pneumonia.
Fortunately, though quite by accident, he was placed in a bed at one end
of the porch and no transmission of streptococcus infection to other
cases in the ward took place. At autopsy 13 cases showed pneumococcus
infection; the foregoing case, hemolytic streptococcus. During the third
period from September 26 to October 5 the ward became even more crowded,
having an average of 58.6 patients; 23 new cases were admitted, 8 of
whom died, a mortality of 34.7 per cent. Autopsy showed that 5 of these
were pneumococcus pneumonias and 1 was caused by hemolytic streptococcus
infection. It is noteworthy that the death rate from pneumonia gradually
increased as the ward became more and more crowded. This may possibly be
attributed in part to the increasing severity of the pneumonia during
the early days of the influenza epidemic. That it was in part directly
due to secondary contact infection with pneumococcus will be shown when
the transmission of pneumococcus infection is discussed. In spite of the
overcrowding of the ward the introduction of 2 cases of streptococcus
pneumonia did not cause an outbreak of streptococcus infection. Whether
this was due to precautions taken against the transfer of infection or
was merely a matter of good luck is difficult to say, in view of the
fact that a considerable amount of transfer of pneumococcus infection
from one patient to another did occur.
Ward 8 had long been used for the care of colored patients with
pneumonia. As in Ward 3 cubicles were in use and ordinary precautions
against the transfer of infection were used. The data are presented in
Table XVIII.
TABLE XVIII
PNEUMONIA IN WARD 8
═══════╤════════╤════════╤═════════════╤═════════════════════════════════════
│AVERAGE │ NUMBER │TOTAL DEATHS │ CULTURES AT AUTOPSY
│ NUMBER │ OF │ AMONG │
│ OF │PATIENTS│ PATIENTS │
│PATIENTS│ADMITTED│ ADMITTED │
│IN WARD │ │ DURING THE │
│ │ │CORRESPONDING│
│ │ │ PERIOD │
───────┼────────┼────────┼──────┬──────┼────────────┬───────────┬────────────
„ │ „ │ „ │NUMBER│ PER │PNEUMOCOCCUS│ S. │UNDETERMINED
│ │ │ │ CENT │ │HEMOLYTICUS│(NO AUTOPSY)
───────┼────────┼────────┼──────┼──────┼────────────┼───────────┼────────────
Sept. │ │ │ │ │ │ │
6–20 │ 25.5│ 18│ 2│ 11.1│ 2│ 0│ 0
Sept. │ 46.1│ 59│ 20│ 33.9│ 10│ 1│ 9
21–Oct.│ │ │ │ │ │ │
5 │ │ │ │ │ │ │
───────┴────────┴────────┴──────┴──────┴────────────┴───────────┴────────────
During the period from September 6 to 20, prior to the outbreak of
influenza in epidemic proportions among the colored troops, the ward had
an average population of 25.5 patients; 18 new cases of pneumonia were
admitted during this period, all of whom were pneumococcus pneumonias as
determined by bacteriologic examination of the sputum at time of
admission to the ward. Only 2 died, a mortality of 11.1 per cent,
autopsy cultures showing pneumococcus in both cases. All these patients
were treated on the porch of the ward while they were acutely sick.
During the second period from September 21 to October 5, when the
influenza epidemic was at its height, the ward rapidly filled with
active cases of pneumonia and became distinctly crowded. It contained an
average of 46.1 patients, but had actually reached a population of 64
patients at the end of the period. Of the 59 new cases admitted, 20
died, a mortality of 33.9 per cent, 10 with pneumococcus pneumonia, one
with hemolytic streptococcus pneumonia. In 9 there was no autopsy. The
conditions in Ward 8 were quite analogous to those in Ward 3. In spite
of the overcrowding during the second period no outbreak of secondary
infection with S. hemolyticus occurred, but secondary pneumococcus
infection did occur as will be shown below.
In contrast with these two wards are Wards 1 and 2 in which widespread
secondary contact infection with S. hemolyticus took place. Ward 2 was
opened September 26, at the beginning of the period when 20 new wards
for pneumonia were organized. From September 26 to October 1 the cubicle
system was not in use, the ward was crowded, organization was imperfect,
and few precautions were taken to prevent transfer of infection from one
patient to another. On October 2 the cubicle system was installed and
precautions against transfer of infection were instituted. The data are
shown in Table XIX.
TABLE XIX
PNEUMONIA IN WARD 2
═════╤════════╤═════════╤═════════════╤═════════════════════════════════════
│ │ │TOTAL DEATHS │
│AVERAGE │ │ AMONG │
│ NUMBER │NUMBER OF│ PATIENTS │
│ OF │PATIENTS │ ADMITTED │ CULTURES AT AUTOPSY
│PATIENTS│ADMITTED │ DURING THE │
│IN WARD │ │CORRESPONDING│
│ │ │ PERIOD │
─────┼────────┼─────────┼──────┬──────┼────────────┬───────────┬────────────
„ │ „ │ „ „ │NUMBER│ PER │PNEUMOCOCCUS│ S. │UNDETERMINED
│ │ │ │ CENT │ │HEMOLYTICUS│(NO AUTOPSY)
─────┼────────┼─────────┼──────┼──────┼────────────┼───────────┼────────────
Sept.│ 10│ 10 40│ 27│ 67.5│ 0│ 23│ 4
26 │ │ │ │ │ │ │
Sept.│ 27│ 17 „ │ „ │ „ │ „ │ „ │ „
27 │ │ │ │ │ │ │
Sept.│ 40│ 13 „ │ „ │ „ │ „ │ „ │ „
28 │ │ │ │ │ │ │
─────┼────────┼─────────┼──────┼──────┼────────────┼───────────┼────────────
Sept.│ 51│ 12 17│ 6│ 35.3│ 2│ 2│ 2
29 │ │ │ │ │ │ │
Sept.│ 49│ 1 „ │ „ │ „ │ „ │ „ │ „
30 │ │ │ │ │ │ │
Oct. │ 43│ 4 „ │ „ │ „ │ „ │ „ │ „
1 │ │ │ │ │ │ │
─────┼────────┼─────────┼──────┼──────┼────────────┼───────────┼────────────
Oct. │ 47│ 6 10│ 4│ 40.0│ 2│ 1│ 1
2 │ │ │ │ │ │ │
Oct. │ 42│ 0 „ │ „ │ „ │ „ │ „ │ „
3 │ │ │ │ │ │ │
Oct. │ 41│ 4 „ │ „ │ „ │ „ │ „ │ „
4 │ │ │ │ │ │ │
─────┴────────┴─────────┴──────┴──────┴────────────┴───────────┴────────────
During the first three days 40 patients with pneumonia were admitted to
the ward. Of these 40 patients, 27 died, a mortality of 67.5 per cent.
Cultures at autopsy showed that 23 of these died with hemolytic
streptococcus infection, none of pneumococcus infection. In four there
was no autopsy. To appreciate the full significance of these figures it
must be emphasized that these patients at time of admission to the ward
in no way differed from those admitted to Ward 3 during the
corresponding period and were not in any sense selected cases. The type
of infection in 9 of these patients had been determined by bacteriologic
examination of the sputum just prior to or immediately after admission
to the ward before opportunity for secondary contact infection in this
ward had occurred. All 9 were shown to have pneumococcus pneumonia free
from hemolytic streptococci at that time. All 9 died, 7 with secondary
streptococcus infection as shown by cultures taken at autopsy, 1 with a
secondarily acquired Pneumococcus Type III infection—sputum showed a
Pneumococcus Type IV on admission—and in 1 there was no autopsy. In view
of the fact that bacteriologic examination of the sputum in cases of
pneumonia following influenza had shown that the large majority of them
were due to pneumococcus infection, it is probable that most of the
other cases of pneumonia admitted to this ward were pneumococcus
pneumonias at time of admission, and that they acquired the
streptococcus infection after admission.
During the next three days 17 new patients were admitted, of whom 6
died, a mortality of 35.3 per cent. Cultures at autopsy showed
pneumococcus infection in 2, streptococcus in 2. It is noteworthy that
the porch was first put into use on September 29. Of the 12 patients
admitted on this date, 8 were treated throughout the acute stage of
their illness on the porch. Of these 8 patients but one died, of a
Pneumococcus Type IV infection and none became infected with S.
hemolyticus. From October 4 to October 6, 10 patients were admitted, of
whom 4 died. Cultures at autopsy showed pneumococcus infection in 2,
hemolytic streptococcus in 1.
The widespread prevalence of hemolytic streptococcus infection in this
ward as compared with its almost entire absence in Wards 3 and 8 is very
striking. Cultures made during life and at autopsy have shewn clearly
that it was due to rapid spread of contagion throughout the ward. The
almost unlimited opportunities for transfer of infection from patient to
patient, during the first six days the ward was in use, undoubtedly
greatly facilitated this spread. From the data available it is
impossible to state exactly when and by which patients hemolytic
streptococcus infection was introduced into the ward, but it must have
been very early since the death rate was very high from the beginning,
and the first 23 cases coming to autopsy died with streptococcus
infection.
Ward 1 was opened on September 24. From that date until October 2 no
cubicles were in use and few precautions were taken against transfer of
infection. On October 2 cubicles were installed and ordinary precautions
to prevent transfer of infection were instituted. On October 6 the ward
was closed to further admissions. The data presented in Table XX are
divided into two periods, because on September 29 and 30, 4 patients
with streptococcus pneumonia were admitted to the ward.
TABLE XX
PNEUMONIA IN WARD 1
═══════╤════════╤════════╤═════════════╤═════════════════════════════════════
│AVERAGE │ NUMBER │TOTAL DEATHS │ CULTURES AT AUTOPSY
│ NUMBER │ OF │ AMONG │
│ OF │PATIENTS│ PATIENTS │
│PATIENTS│ADMITTED│ ADMITTED │
│IN WARD │ │ DURING THE │
│ │ │CORRESPONDING│
│ │ │ PERIOD │
───────┼────────┼────────┼──────┬──────┼────────────┬───────────┬────────────
„ │ „ │ „ │NUMBER│ PER │PNEUMOCOCCUS│ S. │UNDETERMINED
│ │ │ │ CENT │ │HEMOLYTICUS│(NO AUTOPSY)
───────┼────────┼────────┼──────┼──────┼────────────┼───────────┼────────────
Sept. │ 35.8│ 34│ 11│ 32.3│ 5│ 3│ 3
24–29 │ │ │ │ │ │ │
Sept. │ 55.3│ 40│ 24│ 60.0│ 6│ 14│ 4
30–Oct.│ │ │ │ │ │ │
5 │ │ │ │ │ │ │
───────┴────────┴────────┴──────┴──────┴────────────┴───────────┴────────────
During the first period from September 24 to 29 the ward contained an
average of 35.8 patients, being only moderately crowded; 34 cases of
pneumonia were admitted, of whom 11 died, a mortality of 32.3 per cent.
It is noteworthy that deaths among this group which occurred prior to
September 30 were due to pneumococcus infection with one exception, a
patient entering the ward on September 26 and dying the following day.
Of the other 2 patients in this group who died with hemolytic
streptococcus pneumonia, 1 was admitted to the ward on September 25, was
shown to be free from S. hemolyticus on September 30, and died on
October 12 with a secondarily acquired streptococcus pneumonia and
empyema; the other was admitted on September 29 with streptococcus
pneumonia and died the following day.
During the second period from September 30 to October 5 the ward
contained an average of 55.3 patients, being very overcrowded; 40 new
cases of pneumonia were admitted of whom 24 died, a mortality of 60 per
cent. Cultures taken at autopsy showed that 6 died of pneumococcus
pneumonia, 14 with hemolytic streptococcus infection. As in Ward 2,
patients admitted to this ward were in no way selected and were
probably, as experience has shown, in large part pneumococcus pneumonias
at time of admission. The widespread dissemination of hemolytic
streptococcus and its fatal effect following the introduction of the
organism on September 29 and 30 is only too evident.
TABLE XXI
SECONDARY INFECTION WITH PNEUMOCOCCUS TYPE II
═════════════╤═════════╤═════════╤══════════════╤══════════════════════
NAME │ BED │ADMITTED │PNEUMOCOCCUSIN│ SECONDARY INFECTION
│OCCUPIED │ │ SPUTUM ON │
│ │ │ ADMISSION │
─────────────┼─────────┼─────────┼──────────────┼─────────┬────────────
„ │ „ │ „ │ „ │ DATE │PNEUMOCOCCUS
│ │ │ │ │ AT AUTOPSY
─────────────┼─────────┼─────────┼──────────────┼─────────┼────────────
Pvt. Wolfe │No. 6 │Sept. 17 │IV │Sept. 23 │II[51]
Pvt. Pullam │No. 5 │Sept. 9 │IV │Sept. 24 │II
Pvt. Swain │No. 3 │Sept. 16 │II │ │
─────────────┴─────────┴─────────┴──────────────┴─────────┴────────────
Secondary Infection with Pneumococcus in Pneumonia
The foregoing studies have shown that hemolytic streptococcus infection
may spread by contagion throughout an entire ward with great rapidity.
Other observations have demonstrated that pneumococcus infection may be
transmitted in the same way. Only three instances of this nature will be
cited. The first occurred in Ward 3 (Table XXI). Between September 6 and
16 no cases of pneumonia caused by Pneumococcus Type II had been
admitted to the ward. On September 16 Pvt. Swain was admitted to the
ward and placed in Bed 3. Bacteriologic examination of his sputum showed
that his pneumonia was caused by Pneumococcus Type II. At this time Pvt.
Pullam, who had been admitted to the ward on September 9 with a
pneumococcus Type IV pneumonia, occupied Bed 5 separated from Bed 3 by
one intervening bed. He had had his crisis on September 14 and was doing
well, his temperature being normal. On September 24 he developed a
second attack of pneumonia and died on September 30. Cultures at autopsy
showed Pneumococcus Type II in heart’s blood and lung, Pneumococcus Type
II and B. influenzæ in the right bronchus. Pvt. Wolfe was admitted to
the ward with bronchopneumonia on September 17 and placed in Bed 6 next
to Pvt. Pullam. Pneumococcus Type IV and B. influenzæ were found in his
sputum. His temperature had fallen to normal by lysis on September 21
and he was doing well. On September 23 his temperature suddenly rose and
he developed a second attack of pneumonia. Pneumococcus Type II was
isolated by blood culture on this date. He recovered. In both instances
Pneumococcus Type II was acquired after the admission of a patient with
a Pneumococcus Type II pneumonia, the opportunity for contact infection
having been favored by the association of these patients in adjoining
beds.
TABLE XXII
SECONDARY INFECTION WITH PNEUMOCOCCUS TYPE II
═════════════╤═════════╤══════════╤════════════╤═══════════════════════
│ BED │ │PNEUMOCOCCUS│
NAME │OCCUPIED │ ADMITTED │IN SPUTUM ON│ SECONDARY INFECTION
│ │ │ ADMISSION │
─────────────┼─────────┼──────────┼────────────┼──────────┬────────────
„ │ „ │ „ │ „ │ DATE │PNEUMOCOCCUS
│ │ │ │ │ AT AUTOPSY
─────────────┼─────────┼──────────┼────────────┼──────────┼────────────
Pvt. Smith │No. 26 │Sept. 18 │II │ │II
Pvt. Thompson│No. 28 │Sept. 17 │Atyp. II │Sept. 21 │II
Pvt. Linehan │No. 30 │Sept. 16 │IV │Sept. 26 │II
─────────────┴─────────┴──────────┴────────────┴──────────┴────────────
The second instance is almost identical and occurred on the opposite
side of Ward 3 at about the same time (Table XXII). Pvt. Linehan was
admitted on September 16 and placed in Bed 30. Pneumococcus Type IV was
found in his sputum. Pvt. Thompson was admitted the following day with a
Pneumococcus II atypical pneumonia and placed in Bed 28. The next day
Pvt. Smith was admitted and placed in Bed 26. Pneumococcus Type II was
found in his sputum. On September 19 Pvt. Thompson recovered by crisis
and was doing well. On September 21 he had a chill, his temperature rose
to 104.4° F. and he developed a second attack of pneumonia. He died on
September 29; cultures at autopsy showing Pneumococcus Type II in
heart’s blood and left pleural cavity, Pneumococcus Type II and B.
influenzæ in bronchus and lung. Pvt. Linehan had begun to improve on
September 24 and his temperature was falling by lysis. On September 26
he became worse, developed signs of pericarditis and died on September
30. Cultures from lungs and bronchus at autopsy showed Pneumococcus Type
II and B. influenzæ. In both instances the fatal secondary infection
with Pneumococcus Type II was undoubtedly acquired from Pvt. Smith in
the nearby bed.
The third instance occurred in Ward 8 (Table XXIII). Pvts. Lewis and
Scott were admitted on September 21 and were placed in adjoining beds,
50 and 51. Lewis showed Pneumococcus Type I in his sputum, Scott
Pneumococcus II atypical. The following day Pvts. Pighee, Jones, and
Columbus were admitted and given Beds 48, 49 and 53 respectively. All
showed Pneumococcus II atypical in the sputum. Pvt. Lewis with
Pneumococcus Type I pneumonia recovered by crisis on September 29. His
temperature remained normal until October 2 when it suddenly rose to
104.2° F. He developed a second attack of pneumonia and died on October
8. Cultures at autopsy from heart’s blood and lung showed Pneumococcus
II atypical, from the bronchus Pneumococcus II atypical and B.
influenzæ. It is, of course, impossible to say from which one of his
neighbors Pvt. Lewis acquired his second pneumococcus infection.
TABLE XXIII
SECONDARY INFECTION WITH PNEUMOCOCCUS II ATYPICAL
═════════════╤═════════╤══════════╤════════════╤═══════════════════════
│ BED │ │PNEUMOCOCCUS│
NAME │OCCUPIED │ ADMITTED │IN SPUTUM ON│ SECONDARY INFECTION
│ │ │ ADMISSION │
─────────────┼─────────┼──────────┼────────────┼──────────┬────────────
„ │ „ │ „ │ „ │ DATE │PNEUMOCOCCUS
│ │ │ │ │ AT AUTOPSY
─────────────┼─────────┼──────────┼────────────┼──────────┼────────────
Pvt. Pighee │No. 48 │Sept. 22 │Atyp. II │ │
Pvt. Jones │No. 49 │Sept. 22 │Atyp. II │ │
Pvt. Lewis │No. 50 │Sept. 21 │I │Oct. 2 │Atyp. II
Pvt. Scott │No. 51 │Sept. 21 │Atyp. II │ │
Pvt. Columbus│No. 53 │Sept. 22 │Atyp. II │ │
─────────────┴─────────┴──────────┴────────────┴──────────┴────────────
It is noteworthy that these instances of secondary contact infection
with pneumococci occurred in wards where every precaution was supposedly
taken to prevent transfer of infection from one patient to another. It
is true however that the wards were greatly overcrowded at the time.
Many other instances of secondary pneumococcus infection in cases of
pneumonia following influenza were encountered in which it was
impossible to trace the source of infection, many combinations of
different types of pneumococcus being found. There were two instances in
which Pneumococcus Type IV was found in the sputum by inoculation of
white mice shortly after onset of pneumonia, whereas secondary infection
with other types was found at autopsy, one with Pneumococcus Type II,
one with Pneumococcus Type III. In 2 cases by inoculation of white mice,
two types of pneumococcus were found simultaneously in the sputum
coughed from the lung, in one Pneumococcus Types III and IV, in the
other Pneumococcus Types I and IV. There were 5 cases in which two types
of pneumococcus were found in cultures at autopsy as shown in Table
XXIV. Combined pneumococcus infections of this nature are almost never
encountered in pneumonia occurring under normal conditions in the
absence of epidemic influenza.
TABLE XXIV
MIXED PNEUMOCOCCUS INFECTIONS IN PNEUMONIA
═════════════════╤═════════════════════════════════════════════════════
NAME │ CULTURES AT AUTOPSY
─────────────────┼─────────────────┬─────────────────┬─────────────────
„ │ HEART’S BLOOD │ BRONCHUS │ LUNGS
─────────────────┼─────────────────┼─────────────────┼─────────────────
Pvt. Gal. │ │Pn. Type III │Pn. Type III
│ │B. influenzæ │Pn. Type IV
│ │Staphylococcus │B. influenzæ
─────────────────┼─────────────────┼─────────────────┼─────────────────
Pvt. Sug. │Pn. Type III │Pn. Type III │Pn. Type III
│ │Pn. Type IV │Pn. Type IV
│ │B. influenzæ │B. influenzæ
│ │Staphylococcus │
─────────────────┼─────────────────┼─────────────────┼─────────────────
Pvt. Hig. │S. hemolyticus │ │Pn. Type II
│ │ │Pn. Type IV
│ │ │S. hemolyticus
│ │ │Staph. aureus
─────────────────┼─────────────────┼─────────────────┼─────────────────
Pvt. Can. │Pn. Type I │ │Pn. Type III
│ │ │S. hemolyticus
─────────────────┼─────────────────┼─────────────────┼─────────────────
Pvt. Fer. │Sterile │Pn. Type IV │Pn. Type I
│ │B. influenzæ │Pn. Type IV
│ │Staphylococcus │B. influenzæ
─────────────────┴─────────────────┴─────────────────┴─────────────────
The foregoing data show that infection with one type of pneumococcus may
readily be superimposed upon or closely follow infection with another
type. Cases have been cited in which it was clearly demonstrated that
this was due to contact infection. It is furthermore evident that
pneumonia caused by one type of pneumococcus affords no reliable
immunity against pneumonia caused by another type. The same conditions
that favored the spread of hemolytic streptococcus infection also
favored the transfer of pneumococcus infection from patient to patient.
Secondary Contact Infection in Influenza
The material so far presented has dealt with contact infection in cases
of pneumonia following influenza. That a similar contact infection in
cases of influenza treated in crowded hospital wards is responsible in
considerable degree for the development of pneumonia in cases of
influenza seems quite probable. It has already been stated that this
pneumonia was found in large part to be caused by infection with types
of pneumococcus that are found in the mouths of normal individuals. It
has been fairly definitely established by Stillman[52] that lobar
pneumonia caused by pneumococcus Types I and II is in all probability
due to contact infection, and definite instances of such infection by
Pneumococcus Type II have been reported above. In a recent communication
Stillman[53] has furthermore shown that of the various groups of
Pneumococcus II atypical those most frequently associated with pneumonia
are rarely found in normal mouths, while those infrequently associated
with pneumonia are more commonly found. Whether similar considerations
will hold true for pneumococci of Group IV can only be determined by
further investigation. It has been stated that certain observations made
during the course of this work have suggested that cases of pneumonia
which complicate influenza may be due to contact rather than to
autogenous infection. The data available are far too limited to
establish this fact and it would require a very extensive study to
furnish conclusive evidence.
Certain general observations have suggested this point of view. It is
well recognized that the incidence of pneumonia in patients with
influenza has been much higher where overcrowding has existed. It would
seem probable that this has been in large part due to the greater
opportunity for the dissemination of organisms capable of producing
pneumonia and the consequently increased opportunity for secondary
contact infection among patients treated under such conditions. The not
infrequent occurrence of influenzal pneumonia due to combined infections
of the different types of pneumococci, hemolytic streptococci,
staphylococci, and other bacteria, instances of which have been cited,
is in harmony with this view, especially since pneumonia under ordinary
conditions is rarely found to be associated with mixed infections of
this nature. It is true that healthy individuals occasionally carry more
than one type of pneumococcus simultaneously in the mouth, though this
is very infrequent, and autogenous infection occurring in such
individuals might account in some instances for the mixed pneumococcus
infections encountered. By way of analogy it has been clearly shown in
other studies by the Commission on the relation of hemolytic
streptococcus carriers to the complications of measles, that secondary
infection of the respiratory tract with S. hemolyticus is in very large
part due to contact infection, the chronic carrier rarely developing
complications due to this organism.
To obtain further light on this question the type of pneumococcus
present in the mouths of 46 consecutive cases of early uncomplicated
influenza was determined by the mouse inoculation method at time of
admission to the receiving ward of the hospital before the patients had
been associated, with the purpose of determining if cases among this
group which subsequently developed pneumonia might be shown to have
acquired a pneumococcus which they did not carry at time of admission.
This group of patients was treated in a special ward set apart for the
purpose. The patients were assigned to beds in rotation and confined in
bed until thoroughly convalescent. Beds were well separated and
cubicles, masks and gowns were in use. Cultures were made from the ward
personnel. By these procedures an accurate record was kept of all
sources of pneumococcus infection. The types of pneumococcus found in
the mouths of these patients at time of admission are shown in Table
XXV.
TABLE XXV
TYPES OF PNEUMOCOCCI IN THE MOUTHS OF INFLUENZA PATIENTS
═══════════════════════════════════════════════════════════════════════
PNEUMOCOCCUS NUMBER PER CENT
───────────────────────────────────────────────────────────────────────
Pneumococcus, Type I 0 0
Pneumococcus, Type II 0 0
Pneumococcus, II atypical 1 2.2
Pneumococcus, Type III 0 0
Pneumococcus, Group IV 25 54.3
No pneumococci found 20 43.5
───────────────────────────────────────────────────────────────────────
Only 1 patient in this group developed pneumonia. At time of admission
he had no pneumococcus in his mouth as determined by inoculation of a
white mouse with his sputum. Examination of the sputum by the same
method at time of onset of pneumonia three days after admission showed
Pneumococcus Type III. The only ascertainable source of infection in
this case was one of the ward attendants who carried Pneumococcus Type
III in his throat in sufficiently large numbers to be demonstrable by
direct culture and who frequently came in contact with the patient. In
this instance the development of pneumonia was probably due to contact
infection. An extensive study of this nature would be necessary to
determine in what proportion of cases pneumonia following influenza is
caused by secondary contact infection and in what proportion to
autogenous infection. It is at least evident that contact infection with
a type of pneumococcus found in the mouth of normal individuals may
occur in influenza and be responsible for the development of pneumonia.
Therefore every precaution should be taken to prevent it.
Methods for the Prevention of Secondary Contact Infection in Influenza
and Pneumonia
The methods at present in vogue for preventing the spread of contagion
in wards devoted to the care of patients with influenza and pneumonia
may be briefly enumerated: The separation of patients by means of sheet
or screen cubicles, the wearing of masks and gowns by the ward personnel
and to some extent by convalescent patients who are up and about the
ward, and in some hospitals the separation of streptococcus carriers
from noncarriers as determined by throat culture at time of admission.
That these methods are of some value in preventing spread of infection
cannot be denied, and it is probable that they are fairly effective
under ordinary conditions when conscientiously carried out. That they
inevitably break down in the presence of an overwhelming epidemic when
hospital wards become overcrowded is only too evident. Under such
conditions the sheets hung between the beds are constantly being
displaced and are slight proof against a patient’s curiosity as to the
identity and condition of the man in the adjoining bed; masks cannot be
worn by patients seriously ill with pneumonia, during the very time when
they are most dangerous and in greatest danger and those worn by the
ward personnel are very rarely sufficiently well made to prevent spread
of contagion by droplet infection as the studies of Haller and
Colwell[54] and Doust and Lyon[55] have shown; the separation of
streptococcus carriers from noncarriers as at present carried out cannot
keep pace with the ever increasing influx of patients nor with the
rapidity of the spread of the hemolytic streptococcus, in part because
of the time required to make the bacteriologic diagnosis, in part
because the amount of work involved cannot be accomplished by the
laboratory personnel available. That this is so will be shown in data
presented below. Not only do these methods break down in the face of an
epidemic, but they often provide a false sense of security.
In searching for a solution of the problem it is essential to have the
following considerations clearly in mind. Every patient with influenza
must be considered a potential source of pneumococcus or hemolytic
streptococcus infection for his neighbor until he is proved otherwise by
bacteriologic examination. Every person engaged in the care of patients
with respiratory diseases must also be regarded as a potential source of
danger. Pneumonia cannot be regarded as one disease but must be looked
upon as a group of different diseases, with more or less similar
physical signs and symptoms, it is true, but caused by a considerable
variety of bacteria, infection with any one of which not only provides
no protection against infection with another, but may even render the
individual more susceptible to secondary infection. Therefore, every
patient with pneumonia must be regarded as an actual source of danger to
his neighbor, at least until it is established that he has the same type
of infection. All these considerations are especially true in the
presence of influenza, for it has become evident that many organisms
readily gain access to the lung and produce pneumonia in patients with
influenza which under ordinary circumstances fail to cause disease of
the respiratory organs.
Since secondary infection in respiratory disease is undoubtedly spread
in large part by droplet and contact infection, the prevention of
secondary infection must depend upon the elimination of these methods of
transmission. Three solutions present themselves: (1) Ward treatment
with absolute elimination of overcrowding and much wider separation of
patients than has hitherto been deemed necessary; (2) segregation of
patients according to type of bacterial infection; (3) effective
individual isolation of every patient.
It has been clearly shown that treatment of influenza and pneumonia in
overcrowded wards even with the use of such precautions to prevent
transfer of infection as cubicles, masking of attendants and patients,
etc., is attended by serious danger of contact infection and that such
infection will almost inevitably occur. This is not at all surprising
when it is remembered that we are treating in the same ward, in the case
of pneumonia, a group of what are in reality entirely different
diseases, all of which may be transmitted from one patient to another,
and in the case of influenza a group of individuals who carry a variety
of potentially pathogenic bacteria. No one would expect to treat cases
of scarlet fever, measles, and diphtheria together in a hospital ward
without having contact infection result. Among patients ill with
influenza and postinfluenzal pneumonia, certainly streptococcus
pneumonia and to some extent pneumococcus pneumonia may be transmitted
quite as readily as any of these diseases. In view of these
considerations it must be apparent if ward treatment of these diseases
is to be continued without respect to type of bacterial infection, not
only that overcrowding is absolutely contraindicated but also that much
wider separation of patients than has hitherto been regarded as
necessary is imperative. Furthermore, beds should be separated by
permanent cubicles that cannot readily be displaced. Patients should be
confined to their cubicles until thoroughly convalescent and when up and
about should not be allowed to enter cubicles occupied by patients still
sick. Medical officers, nurses and attendants who come into contact with
the patients should use the same rigid precautions that are used in the
care of patients with typhoid or erysipelas or meningitis with the
additional use of means to prevent droplet infection of the patients,
always bearing in mind that the respiratory tract in patients with
influenza or postinfluenzal pneumonia is as susceptible to secondary
infection as the postpartum uterus or an open surgical wound. In other
words, the most rigid aseptic technic should be maintained. The
recognition of a case of streptococcus pneumonia in a ward should be an
indication for immediate quarantine of the ward until it has been shown
by bacteriologic examination that there is no longer danger of spread of
streptococcus contagion. This is done in the case of meningitis or
diphtheria, neither of which diseases is comparable with streptococcus
pneumonia in rapidity of spread or in resulting fatality.
Segregation of patients in wards according to type of bacterial
infection while theoretically an improvement over the indiscriminate
mixing of patients with many different types of infection presents many
practical difficulties which make it impossible to carry out in the
presence of an overwhelming epidemic. It is quite obvious that grouping
of influenzal patients on the basis of the types of pneumococci that
they carry in their mouths is impossible since the great majority of
mouth pneumococci belong to Group IV and comprise a heterologous
immunologic group. The separation of influenza patients who carry S.
hemolyticus from those who do not would appear to offer a more hopeful
field. Since we cannot make an immediate distinction between
streptococcus carriers and noncarriers by inspection of the patient,
this procedure requires the taking of throat cultures at time of
admission to the hospital, the holding of patients for eighteen to
twenty-four hours in receiving wards until the bacteriologic diagnosis
has been made, and their subsequent distribution to streptococcus and
nonstreptococcus wards. This is feasible when the admission rate is low
and the number of streptococcus carriers found at time of admission is
small. In the presence of an influenza epidemic it immediately becomes
impossible to carry out in base hospitals as now constituted, since the
demand for beds under such conditions at once converts a large part of
the hospital into a group of receiving wards with little room remaining
for subsequent separation of patients. The amount of bacteriologic work
involved at once becomes prohibitive and the time required to make the
bacteriologic diagnosis defeats its purpose since it allows the spread
of hemolytic streptococcus to occur in the receiving wards during the
interval.
The foregoing statements are based on results obtained in an attempt to
separate streptococcus carriers from noncarriers in a limited group of
cases of influenza at Camp Pike, the investigation being conducted
during a secondary wave of influenza between November 27 and December 5.
A special group of five wards consisting of one receiving ward and four
distributing wards were set aside for the study. Cubicles, masks and
gowns were in use and the wards were not crowded. The personnel on these
wards did not carry S. hemolyticus in their throats. Patients entering
the receiving ward were assigned to beds in rotation. Throat cultures
were made on blood agar plates at time of admission. The plates were
examined promptly the next morning, the diagnosis of S. hemolyticus
being made by the characteristic hemolytic colonies and microscopic
examination of stained smears. By this method a report reached the
receiving ward at 9:30 a.m. and patients were promptly evacuated to the
streptococcus and nonstreptococcus wards, where they were again assigned
to beds in rotation, remaining confined in bed until convalescent.
Confirmation of all strains of hemolytic streptococcus was subsequently
carried out by isolation in pure culture, bile solubility test, and
hemolytic test with washed sheep corpuscles. All cases free from
hemolytic streptococci at time of admission who were sent to the “clean”
wards were recultured daily throughout the period of study, those
acquiring a hemolytic streptococcus being transferred to a streptococcus
ward as soon as the bacteriologic diagnosis was made. The results are
shown in Table XXVI.
TABLE XXVI
S. HEMOLYTICUS IN CASES OF INFLUENZA
══════════╤══════════╤═══════════════════╦═════════════════════════════
DATE │ PATIENTS │THROAT CULTURES ON ║ “CLEAN” CASES ACQUIRING S.
│ ADMITTED │ ADMISSION. S. ║ HEMOLYTICUS IN THE HOSPITAL
│ TO │ HEMOLYTICUS: ║
│RECEIVING │ ║
│ WARD │ ║
──────────┼──────────┼─────────┬─────────╫─────────┬─────────┬─────────
„ │ „ │ + │ − ║WHILE IN │WHILE IN │ TOTAL
│ │ │ ║REC. WARD│ “CLEAN” │
│ │ │ ║ │ WARD │
──────────┼──────────┼─────────┼─────────╫─────────┼─────────┼─────────
Nov. 27 │ 12│ 4│ 8║ 0│ 2│ 2
Nov. 28 │ 8│ 2│ 6║ 0│ 1│ 1
Nov. 29 │ 17[56]│ 8│ 9║ 1│ 2│ 3
Nov. 30 │ 11│ 2│ 9║ 3│ 0│ 3
Dec. 1 │ 10│ 5│ 5║ 0│ 0│ 0
Dec. 2 │ 37│ 16│ 21║ 1│ 1│ 2
Dec. 3 │ 21│ 8│ 13║ 0│ 2│ 2
Dec. 4 │ 32[56]│ 11│ 21║ 4│ 2│ 6
Dec. 5 │ 17│ 10│ 7║ 5│ 0│ 5
──────────┼──────────┼─────────┼─────────╫─────────┼─────────┼─────────
Totals │ 165│ 66│ 99║ 14│ 10│ 24
──────────┴──────────┴─────────┴─────────╨─────────┴─────────┴─────────
One hundred and sixty-five cases were admitted to the receiving ward
during the period of study as cases of influenza. Of these, 137 had
influenza; 4 of those with influenza had pneumonia at time of admission,
23 had acute follicular tonsillitis, 3 epidemic cerebrospinal
meningitis, 1 scarlet fever, and 1 Vincent’s angina. Sixty-six cases (40
per cent) showed hemolytic streptococcus in the throat at time of
admission and were sent to the streptococcus wards; 99 cases (60 per
cent) were negative for hemolytic streptococcus on admission, and of
these 91 were sent to the “clean” influenza wards. Twenty-four of these
clean cases subsequently became positive for S. hemolyticus. It is
especially noteworthy that 14 of them acquired a hemolytic streptococcus
during the short period that they were held in the receiving ward
awaiting the report of the culture taken at time of admission, the first
culture taken shortly after admission to the “clean” wards being
positive. This result was undoubtedly due to the fact that these cases
were unavoidably associated in the receiving ward with many carriers of
hemolytic streptococcus. It is evident that cases which were supposedly
free from streptococci but which in reality had picked up the organism
in the receiving ward were constantly being sent to the “clean” wards.
It is furthermore evident that if the precaution had not been taken of
reculturing all clean cases on day of admission to the “clean” wards and
daily thereafter these wards would soon have become saturated with
hemolytic streptococci. Even under these conditions, 10 cases, after
varying periods in the “clean” wards, acquired the organism in their
throats. When it is stated that it required the full time of two men
under very special conditions to carry out this work in a very limited
number of cases and that it failed to keep “clean” wards free from
hemolytic streptococci, it is only too apparent that the efficient
separation of carriers from noncarriers in the presence of an epidemic
of influenza is an impossible task.
The segregation of pneumococcus pneumonias following influenza according
to type of infection is obviously impossible, since they are caused by
an almost unlimited variety of immunologic types as far as present
knowledge goes.
Even the efficient separation of streptococcus pneumonias from
pneumococcus pneumonias would require a considerable team of workers and
the closest cooperation between laboratory and ward staffs, so that no
case of pneumonia would be sent to a pneumonia ward until the
bacteriologic diagnosis had been made. In our experience this is rarely
considered feasible even under ordinary conditions, and in the presence
of an epidemic is nearly impossible because of the volume of work
involved and the delay necessitated by bacteriologic methods. It is,
nevertheless, absolutely essential if highly fatal ward epidemics of
streptococcus pneumonia are to be prevented.
In view of the considerations discussed above, it is believed that the
clear and most fundamental indication for the management of epidemic
respiratory diseases in the army is to scatter patients as widely as
possible instead of following the time-honored custom of concentrating
them. In brief, abandon open ward treatment and adopt effective
individual isolation of every case, maintaining as strict a quarantine
as is demanded in other highly contagious and infectious diseases. The
adoption of a strict aseptic technic in the handling of these patients
is an evident corollary. Only by this means can the serious and highly
fatal secondary hospital infections, which occur in influenza and
pneumonia when these diseases are present in epidemic form, be
prevented.
The prevention of secondary infection, prior to admission to the
hospital, is another and more difficult problem. That opportunity for
secondary contact infection in cases of influenza before patients reach
the hospital is great seems unquestionable, since many cases have
already developed these infections at time of admission. During the
epidemic patients were crowded in regimental infirmaries, in ambulances,
and in the receiving office of the hospital with every opportunity for
droplet infection present. No study has been made of this question, but
it seems reasonable that the same methods of prevention should apply,
namely, effective separation of patients.
It is not within the scope of this paper to discuss details of method,
but anything that is possible becomes feasible as soon as sufficient
evidence can be brought to bear that it is a necessity. In the present
instance it would seem that any means that can be used to reduce
materially the terrific toll taken by respiratory diseases is an
absolute necessity.
Summary
1. Secondary contact infection with pneumococci not infrequently occurs
in patients with pneumonia following influenza when they are treated in
hospital wards.
2. Secondary contact infection with S. hemolyticus readily occurs in
patients with pneumonia and may spread rapidly throughout an entire ward
with highly fatal results.
3. Secondary contact infection may be responsible for the development of
pneumonia in patients with influenza.
4. Ward treatment of these diseases is fraught with serious danger which
is greatly increased by overcrowding, by imperfect separation of
patients by cubicles, and by imperfect aseptic technic of medical
officers, nurses, and attendants.
5. It is probable that secondary contact infection can be effectively
prevented only by individual isolation and strict quarantine of every
patient.